Outcome Research Guide

Immune modulation, explained simply with PubMed links

This page translates Immune modulation research into plain English: what scientists studied, what kind of evidence exists, where the source links are strong or limited, and which PubMed records support each bucket.

Launch set page

Read Evidence Overview Open Source Table

106research sources

53evidence buckets

PubMedlinked references

What this page is

A plain-English research page about Immune modulation. It explains what researchers studied and links the PubMed or DOI sources.

How to use it

Read the overview first. If a sentence matters to you, open the PubMed link or source table below it.

Important limit

This page is education, not medical advice, dosing advice, or a recommendation to use cannabinoids.

Evidence Rows 131

Traceable statements carried into the source table.

Human Evidence 2

Rows where human participants, patients, or clinical evidence are visible.

Mechanisms 67

Biology, target, enzyme, receptor, or pharmacology rows.

Safety / Limits 10

Safety, tolerability, uncertainty, or insufficient-evidence context.

Evidence Overview

Immune modulation has research behind it, but the bucket matters.

This page currently indexes 106 research sources across 53 evidence bucket(s). Read it as a map of what researchers have studied, not as a single bottom-line instruction. PMID 10469884

Human evidence 2 evidence rows

Human studies are separated from preclinical and mechanistic evidence so a reader can see where people were actually studied. PMID 10469884

Mechanisms 67 evidence rows

Mechanistic rows explain biological plausibility, receptor activity, enzyme activity, or pharmacology; they do not automatically prove an outcome in people. PMID 10469884

Safety and limits 10 evidence rows

Safety, tolerability, product quality, impairment, interactions, and higher-risk contexts stay visible instead of being treated as footnotes. PMID 10469884

Evidence Buckets

What the Immune modulation research is usually about

Jump to source-backed table

CB2

Immune modulation appears in rows about CB2 mechanisms. It currently draws from 19 research source(s), and mechanistic evidence should stay separate from human-outcome evidence. PMID 10469884

Skin and inflammatory dermatology

Immune modulation appears in rows studying Skin and inflammatory dermatology. It currently draws from 9 research source(s), so the population, dose, route, and endpoint should be checked before reading across contexts. PMID 41680865

PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms

Immune modulation appears in rows studying PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms. It currently draws from 5 research source(s), so the population, dose, route, and endpoint should be checked before reading across contexts. PMID 35176443

CB1

Immune modulation appears in rows about CB1 mechanisms. It currently draws from 4 research source(s), and mechanistic evidence should stay separate from human-outcome evidence. PMID 34050525

CB2

Immune modulation appears in rows about CB2 mechanisms. It currently draws from 4 research source(s), and mechanistic evidence should stay separate from human-outcome evidence. PMID 30639103

Inflammation-related outcomes

Immune modulation appears in rows studying Inflammation-related outcomes. It currently draws from 4 research source(s), so the population, dose, route, and endpoint should be checked before reading across contexts. PMID 33998900

Reader Map

Evidence buckets before the source table

Grouped for readability

Bucket	Plain-English meaning	Evidence posture	Starting source
CB2	Grouped source-backed rows focused on CB2, collapsed into one reader-facing bucket before the full source table.	Mechanistic research summary: insufficient (5), mechanistic or pharmacological (14)	PMID 10469884
Skin and inflammatory dermatology	Grouped source-backed rows focused on Skin and inflammatory dermatology, collapsed into one reader-facing bucket before the full source table.	Mechanistic research summary: insufficient (2), mechanistic or pharmacological (7)	PMID 41680865
PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms	Grouped source-backed rows focused on PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms, collapsed into one reader-facing bucket before the full source table.	Mechanistic research summary: insufficient (3), mechanistic or pharmacological (2)	PMID 35176443
CB1	Grouped source-backed rows focused on CB1, collapsed into one reader-facing bucket before the full source table.	Mapped evidence with interpretation limits: insufficient (4)	PMID 34050525
CB2	Grouped source-backed rows focused on CB2, collapsed into one reader-facing bucket before the full source table.	Mechanistic research summary: insufficient (1), mechanistic or pharmacological (3)	PMID 30639103
Inflammation-related outcomes	Grouped source-backed rows focused on Inflammation-related outcomes, collapsed into one reader-facing bucket before the full source table.	Mechanistic research summary: insufficient (2), mechanistic or pharmacological (2)	PMID 33998900
Safety, risk, adverse events, and formulation concerns	Grouped source-backed rows focused on Safety, risk, adverse events, and formulation concerns, collapsed into one reader-facing bucket before the full source table.	Mapped evidence with interpretation limits: insufficient (4)	PMID 33013414
SEA biology, metabolism, physiology, or safety-relevant mechanisms	Grouped source-backed rows focused on SEA biology, metabolism, physiology, or safety-relevant mechanisms, collapsed into one reader-facing bucket before the full source table.	Preclinical research summary: insufficient (1), preclinical (3)	PMID 24874648

Safety Reading Notes

Read safety context beside the research guide.

The Immune modulation source set includes safety-context rows around PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms. Public reading should keep these rows beside the benefit-oriented buckets, because product identity, dose, route, population, impairment, interactions, and adverse-event context can change what a study means. PMID 10469884

Mechanistic research summary: insufficient (3), mechanistic or pharmacological (2)

PubMed For Dummies Article

Immune modulation Evidence Review: the long-form source walk-through

Quick read

Immune modulation currently has 131 source-backed evidence row(s), so this page should be read as a research guide rather than a single conclusion. PMID 10469884
The evidence classes most visible in the row language are mechanistic or pharmacological (69), insufficient (54), preclinical (6), and preliminary human (2). PMID 41680865
The study-design language most visible in the row language is Narrative or expert review (44), Animal study (43), Cellular or in vitro study (31), and other mapped categories (5). PMID 37332213
The repeated topics are CB2 (26), Skin and inflammatory dermatology (16), Cannabinoids and immune modulation research outcomes (9), Inflammation-related outcomes (8), and other mapped categories (72), which tells the reader where to start opening PubMed and DOI links. PMID 33998900

Start with the research question

Immune modulation is built from 131 source-backed evidence row(s) and 106 research source(s). The current evidence classes read as mechanistic or pharmacological (69), insufficient (54), preclinical (6), and preliminary human (2), and the study-design language most often reads as Narrative or expert review (44), Animal study (43), Cellular or in vitro study (31), and other mapped categories (5). PMID 10469884

The row-level question is not simply whether Immune modulation is "good" or "bad." The useful question is what each row studied, what evidence class it received, and whether the source is close to the reader's actual question. The most repeated row topics are CB2 (26), Skin and inflammatory dermatology (16), Cannabinoids and immune modulation research outcomes (9), Inflammation-related outcomes (8), and other mapped categories (72). PMID 41680865

Human evidence 2 rows

Rows involving human participants, patients, or clinical source language. These rows are closer to everyday reader questions, but still depend on population, dose, route, comparator, and endpoint. PMID 35910331

Preclinical evidence 6 rows

Animal, cellular, or model-based rows. These can explain why a topic is being studied, but they should not be read as human-health instructions. PMID 41213439

Mechanistic evidence 67 rows

Rows about receptors, enzymes, channels, metabolism, binding, signaling, or pharmacology. These explain plausibility without proving a consumer outcome. PMID 37083031

Limits and uncertainty 64 rows

Rows where safety, tolerability, risk, product limits, or insufficient evidence need to stay visible next to the rest of the article. PMID 36342776

The lane labels are not a quality score. They are a reading method: keep human evidence, preclinical evidence, mechanisms, and uncertainty in separate mental boxes before deciding what a source can actually support. PMID 25655949

Where this page has the most source density

The largest bucket surfaced for this page is CB2. That does not automatically mean the topic is settled; it means this is where the current source trail is densest. The next visible bucket is Skin and inflammatory dermatology, which gives readers another way to see what the literature repeatedly circles. PMID 10469884

Source density should be read with evidence posture. A bucket can contain many rows and still be limited if the studies are indirect, mixed, preclinical, product-specific, or mostly review-level. The paragraphs below name the buckets directly and keep each explanation connected to a source record. PMID 41680865

Bucket chapters: what the literature is circling

CB2

19 research sources 19 rows (869-925) Mechanistic research summary: insufficient (5), mechanistic or pharmacological (14)

Immune modulation appears in rows about CB2 mechanisms. It currently draws from 19 research source(s), and mechanistic evidence should stay separate from human-outcome evidence. PMID 10469884

Read this bucket as mechanism or pharmacology context. Mechanisms can make the biology easier to understand, but they are not the same thing as a demonstrated effect in people. PMID 10469884

Evidence row 869
Cannabinoids modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 receptor pharmacology, ligand binding, selectiv... PMID 10469884
Evidence row 925
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, mic... PMID 41740200

Skin and inflammatory dermatology

9 research sources 9 rows (525-533) Mechanistic research summary: insufficient (2), mechanistic or pharmacological (7)

Read this bucket as mechanism or pharmacology context. Mechanisms can make the biology easier to understand, but they are not the same thing as a demonstrated effect in people. PMID 41680865

Evidence row 525
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: skin, dermatology, i... PMID 41680865
Evidence row 533
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: skin, derm... PMID 40568800

PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms

5 research sources 5 rows (1106-1112) Mechanistic research summary: insufficient (3), mechanistic or pharmacological (2)

Read this bucket as safety context first. It belongs beside any benefit-oriented rows because risk, route, dose, product quality, co-exposures, and population can change what a source means. PMID 35176443

Evidence row 1106
PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or pati... PMID 35176443
Evidence row 1112
PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; st... PMID 10785541

CB1

4 research sources 4 rows (842-850) Mapped evidence with interpretation limits: insufficient (4)

Immune modulation appears in rows about CB1 mechanisms. It currently draws from 4 research source(s), and mechanistic evidence should stay separate from human-outcome evidence. PMID 34050525

Read this bucket as mechanism or pharmacology context. Mechanisms can make the biology easier to understand, but they are not the same thing as a demonstrated effect in people. PMID 34050525

Evidence row 842
Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, p... PMID 34050525
Evidence row 850
Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain,... PMID 15550444

CB2

4 research sources 4 rows (876-917) Mechanistic research summary: insufficient (1), mechanistic or pharmacological (3)

Immune modulation appears in rows about CB2 mechanisms. It currently draws from 4 research source(s), and mechanistic evidence should stay separate from human-outcome evidence. PMID 30639103

Read this bucket as mechanism or pharmacology context. Mechanisms can make the biology easier to understand, but they are not the same thing as a demonstrated effect in people. PMID 30639103

Evidence row 876
Endocannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signalin... PMID 30639103
Evidence row 917
Endocannabinoids modulates CB2; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuro... PMID 24877594

Inflammation-related outcomes

4 research sources 4 rows (587-597) Mechanistic research summary: insufficient (2), mechanistic or pharmacological (2)

Read this bucket as mechanism or pharmacology context. Mechanisms can make the biology easier to understand, but they are not the same thing as a demonstrated effect in people. PMID 33998900

Evidence row 587
CBG studied for Inflammation-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: inflammation-related or immune outcom... PMID 33998900
Evidence row 597
CBG studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: inflammation-related or... PMID 40362835

Safety, risk, adverse events, and formulation concerns

4 research sources 4 rows (327-342) Mapped evidence with interpretation limits: insufficient (4)

Immune modulation appears in rows studying Safety, risk, adverse events, and formulation concerns. It currently draws from 4 research source(s), so the population, dose, route, and endpoint should be checked before reading across contexts. PMID 33013414

Evidence row 327
CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concer... PMID 33013414
Evidence row 342
CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure:... PMID 38904694

SEA biology, metabolism, physiology, or safety-relevant mechanisms

4 research sources 4 rows (1188-1201) Preclinical research summary: insufficient (1), preclinical (3)

Immune modulation appears in rows studying SEA biology, metabolism, physiology, or safety-relevant mechanisms. It currently draws from 4 research source(s), so the population, dose, route, and endpoint should be checked before reading across contexts. PMID 24874648

Evidence row 1188
SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome meas... PMID 24874648
Evidence row 1201
SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: preclinical (outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms). PMID 33434116

Human evidence, mechanisms, and safety are different lanes

This page currently separates human evidence (2 row(s)), mechanistic evidence (67 row(s)), and safety/tolerability context (10 row(s)). That separation is the heart of the site. Mechanistic evidence can make a topic biologically interesting, but it should not silently become a human outcome. PMID 10469884

Human evidence still depends on population, dose, route, duration, product identity, and endpoint. Safety rows belong in the same reading path as benefit-oriented rows because formulation, co-exposures, prescription medications, impairment context, and higher-risk populations can change how close a source is to a reader's question. PMID 41680865

What this does and does not mean

It means the page has a traceable source trail. It does not mean every bucket has the same clinical strength. PMID 39596290
It means mechanisms, animal models, human studies, safety rows, and insufficient-evidence rows are being kept visible as separate evidence types. PMID 17828291
It does not turn a preclinical mechanism into a consumer recommendation, and it does not treat one product, dose, route, or population as interchangeable with another. PMID 40016352

How to use the source table

The source-backed evidence table below is the audit trail. Each row keeps a public sentence connected to a source record when a PubMed ID or DOI is available. If a sentence feels important, the reader should be able to click through, inspect the study type, and decide whether the source is close to the question they care about. PMID 10469884

This is why the public page is intentionally layered. The top gives the reader a fast orientation. The bucket table groups repeated rows into readable topics. The article body explains the buckets using the actual evidence-row language. The source notes below walk through every evidence row before the source table repeats the technical trace. PMID 41680865

Source-reading checklist for Immune modulation

Open the linked PubMed or DOI record. PMID 36746342
Check whether the source studied humans, animals, cells, chemistry, pharmacology, product testing, or a review of prior literature. PMID 35176443
Compare the source product, dose, route, population, and endpoint to the question being asked. PMID 34607960
Look for safety, tolerability, drug-interaction, impairment, pregnancy, pediatric, psychiatric, cardiovascular, and product-quality context before treating the bucket as settled. PMID 37962860
Return to the evidence table when the article summary sounds too broad; the row is the audit unit. PMID 12648025

Source Notes

Immune modulation source-by-source reading notes

These notes pull every evidence row on this page into the readable article body before the source table repeats the audit trail. Each note keeps the row language beside the PubMed or DOI link when available.

Evidence row 35
CBC studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: inflammation-related or pain-related outcomes). PMID 41680865
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Anti-inflammatory and analgesic potential of minor cannabinoids in vivo.
Evidence row 36
CBC studied for Inflammation-related outcomes; evidence class: preclinical (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: inflammation-related or pain-related outcomes). PMID 37332213
Evidence class: preclinical; Study design: Animal study. Source: The Mechanism of Cannabichromene and Cannabidiol Alone Versus in Combination in the Alleviation of Arthritis-Related Inflammation.
Evidence row 64
CBG studied for Pain-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: pain-related outcomes). PMID 33998900
Evidence class: insufficient; Study design: Systematic review. Source: The Effects of Cannabinoids on Pro- and Anti-Inflammatory Cytokines: A Systematic Review of In Vivo Studies.
Evidence row 68
CBG studied for Pain-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: pain-related outcomes). PMID 35910331
Evidence class: insufficient; Study design: Narrative or expert review. Source: Acidic Cannabinoids Suppress Proinflammatory Cytokine Release by Blocking Store-operated Calcium Entry.
Evidence row 72
CBC studied for Inflammation-related outcomes; evidence class: preliminary human (outcome measure: inflammation-related or pain-related outcomes). PMID 41213439
Evidence class: preliminary human. Source: Therapeutic potential of cannabidiol-rich Cannabis sativa to mitigate the severity of inflammation and pain: A pre-clinical study.
Evidence row 137
CBDA studied for nausea-related or inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: nausea-related or inflammation-related outcomes). PMID 37083031
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Antiviral activities of hemp cannabinoids.
Evidence row 139
CBDA studied for nausea-related or inflammation-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; outcome measure: nausea-related or inflammation-related outcomes). PMID 36342776
Evidence class: insufficient. Source: Medical Cannabis Use and Inflammatory Cytokines and Chemokines Among Adult Chronic Pain Patients.
Evidence row 143
CBDA studied for nausea-related or inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: nausea-related or inflammation-related outcomes). PMID 25655949
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: The effect of phytocannabinoids on airway hyper-responsiveness, airway inflammation, and cough.
Evidence row 157
CBG studied for safety, adverse-event, impairment, or formulation-specific concerns; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: safety, adverse-event, impairment, or formulation-specific concerns). PMID 39596290
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Exploring Cannabidiol (CBD) and Cannabigerol (CBG) Safety Profile and Skincare Potential.
Evidence row 204
THC modulates receptor, target, or pharmacology mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: receptor, target, or pharmacology mechanisms). PMID 17828291
Evidence class: insufficient; Study design: Narrative or expert review. Source: The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin.
Evidence row 268
Endocannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 40016352
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Astrocytic cannabinoid receptor 1 promotes resilience by dampening stress-induced blood-brain barrier alterations.
Evidence row 269
THC studied for Cannabinoids and immune modulation research outcomes; evidence class: preclinical (population or model: Pediatric, adolescent, or developmental context mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 36746342
Evidence class: preclinical; Study design: Animal study. Source: Maternal immune activation impairs endocannabinoid signaling in the mesolimbic system of adolescent male offspring.
Evidence row 270
PEA studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 35176443
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Palmitoylethanolamide dampens neuroinflammation and anxiety-like behavior in obese mice.
Evidence row 271
Endocannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 34607960
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Phospholipase Cγ2 regulates endocannabinoid and eicosanoid networks in innate immune cells.
Evidence row 272
Endocannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 37962860
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Impact of Chronic Moderate Exercise on Immune Cells and Cytokine Levels in Rats: Focus on the Endocannabinergic Pathway.
Evidence row 273
THC studied for Cannabinoids and immune modulation research outcomes; evidence class: insufficient (population or model: Pregnancy, lactation, or reproductive context mentioned; study design: Narrative or expert review; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 12648025
Evidence class: insufficient; Study design: Narrative or expert review. Source: Pharmacokinetics and pharmacodynamics of cannabinoids.
Evidence row 274
Cannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 39334169
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Modulation of cannabinoid receptor 2 alters neuroinflammation and reduces formation of alpha-synuclein aggregates in a rat model of nigral synucleinopathy.
Evidence row 275
Cannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 37164044
Evidence class: insufficient; Study design: Narrative or expert review. Source: CB2 receptor in the CNS: From immune and neuronal modulation to behavior.
Evidence row 276
Cannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: Cannabinoids and immune modulation research outcomes). PMID 16596771
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoid receptor signaling.
Evidence row 277
THC studied for receptor, target, or pharmacology mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: receptor, target, or pharmacology mechanisms). PMID 37083031
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Antiviral activities of hemp cannabinoids.
Evidence row 278
THC studied for receptor, target, or pharmacology mechanisms; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: receptor, target, or pharmacology mechanisms). PMID 38162115
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabigerolic Acid (CBGA) Inhibits the TRPM7 Ion Channel Through its Kinase Domain.
Evidence row 293
THC studied for Endocannabinoids and endocannabinoid-like lipids research topics; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: Endocannabinoids and endocannabinoid-like lipids research topics). PMID 19833407
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoid activation of peroxisome proliferator-activated receptors: potential for modulation of inflammatory disease.
Evidence row 327
CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns). PMID 33013414
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabis Contaminants Limit Pharmacological Use of Cannabidiol.
Evidence row 340
CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns). PMID 41008526
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabidiol in Skin Health: A Comprehensive Review of Topical Applications in Dermatology and Cosmetic Science.
Evidence row 341
CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns). PMID 33851375
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabis sativa and Skin Health: Dissecting the Role of Phytocannabinoids.
Evidence row 342
CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: safety, risk, adverse-event, or formulation-specific concerns). PMID 38904694
Evidence class: insufficient; Study design: Cellular or in vitro study. Source: Potential of cannabidiol as acne and acne scar treatment: novel insights into molecular pathways of pathophysiological factors.
Evidence row 345
Endocannabinoids studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns). PMID 36439142
Evidence class: insufficient; Study design: Narrative or expert review. Source: Sebaceous immunobiology - skin homeostasis, pathophysiology, coordination of innate immunity and inflammatory response and disease associations.
Evidence row 346
Endocannabinoids studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns). PMID 19608284
Evidence class: insufficient; Study design: Narrative or expert review. Source: The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities.
Evidence row 369
CBD modulates endocannabinoid enzyme activity or metabolic mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: endocannabinoid enzyme activity or metabolic mechanisms). PMID 40750820
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Hepatotoxicity evaluation of cannabidiol, cannabinol, cannabichromene and cannabigerol using a human quad culture liver chip.
Evidence row 372
CBD modulates endocannabinoid enzyme activity or metabolic mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: endocannabinoid enzyme activity or metabolic mechanisms). PMID 38904421
Evidence class: insufficient; Study design: Narrative or expert review. Source: Metabolism and liver toxicity of cannabidiol.
Evidence row 490
THC studied for Appetite and metabolic outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: appetite or metabolic outcomes). PMID 12608509
Evidence class: insufficient; Study design: Narrative or expert review. Source: Orexigenic and anabolic agents.
Evidence row 494
THC studied for Appetite and metabolic outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: appetite or metabolic outcomes). PMID 26929669
Evidence class: insufficient; Study design: Narrative or expert review. Source: Clinical utility of dronabinol in the treatment of weight loss associated with HIV and AIDS.
Evidence row 514
CBN studied for safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns; evidence class: insufficient (population or model: Pediatric, adolescent, or developmental context mentioned; study design: Narrative or expert review; outcome measure: safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns). PMID 27428345
Evidence class: insufficient; Study design: Narrative or expert review. Source: [Cannabis: Effects in the Central Nervous System. Therapeutic, societal and legal consequences].
Evidence row 516
CBN studied for safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns). PMID 36228902
Evidence class: insufficient; Study design: Cellular or in vitro study. Source: Evaluation of the anti-inflammatory effects of selected cannabinoids and terpenes from Cannabis Sativa employing human primary leukocytes.
Evidence row 519
CBN modulates receptor, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: receptor, target, metabolic, or pharmacology mechanisms). PMID 16596770
Evidence class: insufficient; Study design: Narrative or expert review. Source: Pharmacological actions of cannabinoids.
Evidence row 525
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 41680865
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Anti-inflammatory and analgesic potential of minor cannabinoids in vivo.
Evidence row 526
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 37764262
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Anti-Inflammatory Effects of Minor Cannabinoids CBC, THCV, and CBN in Human Macrophages.
Evidence row 527
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 39275884
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Cannabinol modulates the endocannabinoid system and shows TRPV1-mediated anti-inflammatory properties in human keratinocytes.
Evidence row 528
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 36228902
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Evaluation of the anti-inflammatory effects of selected cannabinoids and terpenes from Cannabis Sativa employing human primary leukocytes.
Evidence row 529
CBN studied for Skin and inflammatory dermatology; evidence class: insufficient (study design: Narrative or expert review; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 38673788
Evidence class: insufficient; Study design: Narrative or expert review. Source: Phytocannabinoids: Exploring Pharmacological Profiles and Their Impact on Therapeutical Use.
Evidence row 530
CBN studied for Skin and inflammatory dermatology; evidence class: insufficient (study design: Narrative or expert review; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 27435265
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoids, inflammation, and fibrosis.
Evidence row 531
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 41478536
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Phytocannabinoids as anti-inflammatory agents: Synergistic effects when combined with Cannabis sativa L. matrices.
Evidence row 532
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 40580876
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Preclinical evaluation of cannabidiolic acid as a neuroprotective agent in TDP-43 transgenic mice, an experimental model of amyotrophic lateral sclerosis.
Evidence row 533
CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes). PMID 40568800
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Distinct Interactions of Cannabinol and Its Cytochrome P450-Generated Metabolites with Receptors and Sensory Neurons.
Evidence row 542
CBG studied for safety, tolerability, adverse-event, impairment, toxicity, or formulation-specific concerns; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: safety, tolerability, adverse-event, impairment, toxicity, or formulation-specific concerns). PMID 39596290
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Exploring Cannabidiol (CBD) and Cannabigerol (CBG) Safety Profile and Skincare Potential.
Evidence row 565
CBG modulates receptor, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: receptor, target, metabolic, or pharmacology mechanisms). PMID 33998900
Evidence class: insufficient; Study design: Systematic review. Source: The Effects of Cannabinoids on Pro- and Anti-Inflammatory Cytokines: A Systematic Review of In Vivo Studies.
Evidence row 571
CBG modulates receptor, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: receptor, target, metabolic, or pharmacology mechanisms). PMID 42105814
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoids in autoimmune diseases: mechanistic insights and translational challenges.
Evidence row 587
CBG studied for Inflammation-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: inflammation-related or immune outcomes). PMID 33998900
Evidence class: insufficient; Study design: Systematic review. Source: The Effects of Cannabinoids on Pro- and Anti-Inflammatory Cytokines: A Systematic Review of In Vivo Studies.
Evidence row 592
CBG studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: inflammation-related or immune outcomes). PMID 40818359
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Cannabigerol attenuates liver fibrosis via AMPK activation: Regulation of lipid metabolism, inflammation, and hepatic stellate cell activation.
Evidence row 593
CBG studied for Inflammation-related outcomes; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: inflammation-related or immune outcomes). PMID 35614947
Evidence class: insufficient; Study design: Narrative or expert review. Source: Medical Cannabis Activity Against Inflammation: Active Compounds and Modes of Action.
Evidence row 597
CBG studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: inflammation-related or immune outcomes). PMID 40362835
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabigerol Alleviates Liver Damage in Metabolic Dysfunction-Associated Steatohepatitis Female Mice via Inhibition of Transforming Growth Factor Beta 1.
Evidence row 606
CBG studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, or topical inflammatory outcomes). PMID 39596290
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Exploring Cannabidiol (CBD) and Cannabigerol (CBG) Safety Profile and Skincare Potential.
Evidence row 610
CBG studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Human clinical study; outcome measure: skin, dermatology, or topical inflammatory outcomes). PMID 35056807
Evidence class: mechanistic or pharmacological; Study design: Human clinical study. Source: In Vitro and Clinical Evaluation of Cannabigerol (CBG) Produced via Yeast Biosynthesis: A Cannabinoid with a Broad Range of Anti-Inflammatory and Skin Health-Boosting Properties.
Evidence row 611
CBG studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: skin, dermatology, or topical inflammatory outcomes). PMID 39851511
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Anti-Inflammatory Effects of Cannabigerol In Vitro and In Vivo Are Mediated Through the JAK/STAT/NFκB Signaling Pathway.
Evidence row 619
CBG studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, or topical inflammatory outcomes). PMID 27094344
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Differential effectiveness of selected non-psychotropic phytocannabinoids on human sebocyte functions implicates their introduction in dry/seborrhoeic skin and acne treatment.
Evidence row 622
CBG studied for Appetite and metabolic outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: appetite-related, weight, glucose, or metabolic outcomes). PMID 42105814
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoids in autoimmune diseases: mechanistic insights and translational challenges.
Evidence row 670
CBC modulates receptor, transporter, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Animal model mentioned; study design: Animal study; outcome measure: receptor, transporter, target, metabolic, or pharmacology mechanisms). PMID 39769302
Evidence class: insufficient; Study design: Animal study. Source: Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.
Evidence row 681
CBC modulates receptor, transporter, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: receptor, transporter, target, metabolic, or pharmacology mechanisms). PMID 38950639
Evidence class: insufficient; Study design: Cellular or in vitro study. Source: Selected phytocannabinoids inhibit SN-38- and cytokine-evoked increases in epithelial permeability and improve intestinal barrier function in vitro.
Evidence row 684
CBC studied for Pain-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: pain-related outcomes). PMID 41680865
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Anti-inflammatory and analgesic potential of minor cannabinoids in vivo.
Evidence row 685
CBC studied for Pain-related outcomes; evidence class: preclinical (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: pain-related outcomes). PMID 37332213
Evidence class: preclinical; Study design: Animal study. Source: The Mechanism of Cannabichromene and Cannabidiol Alone Versus in Combination in the Alleviation of Arthritis-Related Inflammation.
Evidence row 687
CBC studied for Pain-related outcomes; evidence class: preliminary human (outcome measure: pain-related outcomes). PMID 41213439
Evidence class: preliminary human. Source: Therapeutic potential of cannabidiol-rich Cannabis sativa to mitigate the severity of inflammation and pain: A pre-clinical study.
Evidence row 707
CBC studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, antimicrobial, or topical inflammatory outcomes). PMID 27094344
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Differential effectiveness of selected non-psychotropic phytocannabinoids on human sebocyte functions implicates their introduction in dry/seborrhoeic skin and acne treatment.
Evidence row 708
CBC studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: skin, dermatology, antimicrobial, or topical inflammatory outcomes). PMID 39769302
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.
Evidence row 716
CBC studied for Skin and inflammatory dermatology; evidence class: insufficient (outcome measure: skin, dermatology, antimicrobial, or topical inflammatory outcomes). PMID 41121423
Evidence class: insufficient. Source: Targeting the antioxidant, antimicrobial and anti-inflammatory activity of non-psychotropic Cannabis sativa L.: a comparison with chemotype V.
Evidence row 721
CBC studied for neurobehavioral, mood, neural stem cell, or neurogenesis outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: neurobehavioral, mood, neural stem cell, or neurogenesis outcomes). PMID 41680865
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Anti-inflammatory and analgesic potential of minor cannabinoids in vivo.
Evidence row 727
CBC studied for neurobehavioral, mood, neural stem cell, or neurogenesis outcomes; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: neurobehavioral, mood, neural stem cell, or neurogenesis outcomes). PMID 39769302
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.
Evidence row 734
THCV studied for Appetite and metabolic outcomes; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: appetite-related or metabolic outcomes). PMID 37108282
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Tetrahydrocannabivarin (THCV) Protects Adipose-Derived Mesenchymal Stem Cells (ASC) against Endoplasmic Reticulum Stress Development and Reduces Inflammation during Adipogenesis.
Evidence row 763
THCV modulates receptor, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: receptor, target, metabolic, or pharmacology mechanisms). PMID 17828291
Evidence class: insufficient; Study design: Narrative or expert review. Source: The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin.
Evidence row 786
THCV studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: inflammation-related or immune outcomes). PMID 36559009
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Phytocannabinoids Act Synergistically with Non-Steroidal Anti-Inflammatory Drugs Reducing Inflammation in 2D and 3D In Vitro Models.
Evidence row 808
THC modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 receptor pharmacology, ligand binding, or signaling mechanisms). PMID 16596770
Evidence class: insufficient; Study design: Narrative or expert review. Source: Pharmacological actions of cannabinoids.
Evidence row 810
THC modulates CB1; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: CB1 receptor pharmacology, ligand binding, or signaling mechanisms). PMID 35489334
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabinoid receptor 1 antagonist genistein attenuates marijuana-induced vascular inflammation.
Evidence row 817
Cannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 receptor pharmacology, ligand binding, or signaling mechanisms). PMID 10469884
Evidence class: insufficient; Study design: Narrative or expert review. Source: Pharmacology of cannabinoid receptor ligands.
Evidence row 842
Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain, cognition, or synaptic mechanisms). PMID 34050525
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoid-based therapy as a future for joint degeneration. Focus on the role of CB2 receptor in the arthritis progression and pain: an updated review.
Evidence row 846
Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain, cognition, or synaptic mechanisms). PMID 16570099
Evidence class: insufficient; Study design: Narrative or expert review. Source: The pharmacology of cannabinoid receptors and their ligands: an overview.
Evidence row 849
Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain, cognition, or synaptic mechanisms). PMID 31461639
Evidence class: insufficient; Study design: Narrative or expert review. Source: Therapeutic potential of cannabinoid receptor 2 in the treatment of diabetes mellitus and its complications.
Evidence row 850
Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain, cognition, or synaptic mechanisms). PMID 15550444
Evidence class: insufficient; Study design: Narrative or expert review. Source: The endocannabinoid system: physiology and pharmacology.
Evidence row 863
THC modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms). PMID 17828291
Evidence class: insufficient; Study design: Narrative or expert review. Source: The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin.
Evidence row 869
Cannabinoids modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms). PMID 10469884
Evidence class: insufficient; Study design: Narrative or expert review. Source: Pharmacology of cannabinoid receptor ligands.
Evidence row 876
Endocannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms). PMID 30639103
Evidence class: mechanistic or pharmacological. Source: Crystal Structure of the Human Cannabinoid Receptor CB2.
Evidence row 885
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms). PMID 34774714
Evidence class: mechanistic or pharmacological. Source: Cannabinoid Receptor Type 2 Agonist Reduces Morphine Tolerance via Mitogen Activated Protein Kinase Phosphatase Induction and Mitogen Activated Protein Kinase Dephosphorylation.
Evidence row 891
Cannabinoids modulates CB2; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms). PMID 37349984
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoid CB2 receptor orthologues; in vitro function and perspectives for preclinical to clinical translation.
Evidence row 895
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 39334169
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Modulation of cannabinoid receptor 2 alters neuroinflammation and reduces formation of alpha-synuclein aggregates in a rat model of nigral synucleinopathy.
Evidence row 897
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 38662453
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Type 2 cannabinoid receptor expression on microglial cells regulates neuroinflammation during graft-versus-host disease.
Evidence row 899
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 39173999
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabinoid CB2 receptors enhance high-fat diet evoked peripheral neuroinflammation.
Evidence row 901
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 36475439
Evidence class: mechanistic or pharmacological. Source: Cannabinoid receptor 2 evolutionary gene loss makes parrots more susceptible to neuroinflammation.
Evidence row 902
Endocannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 37061199
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabinoid CB2 receptors modulate alcohol induced behavior, and neuro-immune dysregulation in mice.
Evidence row 903
Endocannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 18615177
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: The cannabinoid CB2 receptor as a target for inflammation-dependent neurodegeneration.
Evidence row 904
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 30666359
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabinoid receptor 2 activation mitigates lipopolysaccharide-induced neuroinflammation and sickness behavior in mice.
Evidence row 907
THC modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 26824325
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Up-regulation of immunomodulatory effects of mouse bone-marrow derived mesenchymal stem cells by tetrahydrocannabinol pre-treatment involving cannabinoid receptor CB2.
Evidence row 909
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 38751621
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Enantiomeric Agonists of the Type 2 Cannabinoid Receptor Reduce Retinal Damage during Proliferative Vitreoretinopathy and Inhibit Hyperactive Microglia In Vitro.
Evidence row 910
Cannabinoids modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 20236042
Evidence class: insufficient; Study design: Narrative or expert review. Source: The development of cannabinoid CBII receptor agonists for the treatment of central neuropathies.
Evidence row 911
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 12823482
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Induction of CB2 receptor expression in the rat spinal cord of neuropathic but not inflammatory chronic pain models.
Evidence row 913
THC modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 36583304
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabidiol-rich non-psychotropic Cannabis sativa L. oils attenuate peripheral neuropathy symptoms by regulation of CB2-mediated microglial neuroinflammation.
Evidence row 915
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Pediatric, adolescent, or developmental context mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 40332343
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Effects of CB2 Receptor Modulation on Macrophage Polarization in Pediatric Inflammatory Bowel Disease.
Evidence row 916
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 41383775
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: CB2 cannabinoid receptor-specific therapeutic antibody agonists for treatment of chemotherapy-induced peripheral neuropathy.
Evidence row 917
Endocannabinoids modulates CB2; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 24877594
Evidence class: insufficient; Study design: Narrative or expert review. Source: What we know and do not know about the cannabinoid receptor 2 (CB2).
Evidence row 918
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 40791361
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Cannabinoid Receptor 2 Activating Antibodies: A Promising Therapeutic Strategy for Macrophage-Driven Fibro-Inflammatory Diseases.
Evidence row 919
Cannabinoids modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 40943579
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoid Receptor 2 (CB2) in Macrophages: A Promising Clinical Target for Immune Disorders.
Evidence row 921
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 41310604
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabinoid receptor 2 affect the inflammatory response in periodontitis by regulating macrophage M1/M2 polarization.
Evidence row 923
Cannabinoids modulates CB2; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 32471272
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabinoid Receptor Type 2: A Possible Target in SARS-CoV-2 (CoV-19) Infection?
Evidence row 924
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 39538989
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Cannabinoid receptor type 2 agonist GP1a attenuates macrophage activation induced by M. bovis-BCG by inhibiting NF-κB signaling.
Evidence row 925
Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms). PMID 41740200
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Cannabinoid receptor 2 activating antibodies: A promising therapeutic strategy for macrophage-driven fibro-inflammatory diseases.
Evidence row 937
Endocannabinoids modulates GPR55; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: GPR55 receptor activity, binding, signaling, or pharmacology). PMID 31527410
Evidence class: insufficient; Study design: Narrative or expert review. Source: The Endocannabinoid System of Animals.
Evidence row 942
CBD modulates GPR55; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: GPR55 receptor activity, binding, signaling, or pharmacology). PMID 41560741
Evidence class: insufficient; Study design: Narrative or expert review. Source: Epilepsy, neuroinflammation and cannabidiol What do we know thus far?
Evidence row 946
THC modulates GPR18; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: GPR18 receptor activity, binding, signaling, or pharmacology). PMID 32365486
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Computational Investigations on the Binding Mode of Ligands for the Cannabinoid-Activated G Protein-Coupled Receptor GPR18.
Evidence row 949
THC modulates GPR18; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: GPR18 receptor activity, binding, signaling, or pharmacology). PMID 29902723
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Structure-activity relationships of imidazothiazinones and analogs as antagonists of the cannabinoid-activated orphan G protein-coupled receptor GPR18.
Evidence row 952
Endocannabinoids modulates GPR18; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: GPR18 receptor activity, binding, signaling, or pharmacology). PMID 29098189
Evidence class: insufficient; Study design: Narrative or expert review. Source: An Update on Non-CB1, Non-CB2 Cannabinoid Related G-Protein-Coupled Receptors.
Evidence row 954
Endocannabinoids modulates GPR18; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: GPR18 receptor activity, binding, signaling, or pharmacology). PMID 30871175
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Protective Effect of N-Arachidonoyl Glycine-GPR18 Signaling after Excitotoxical Lesion in Murine Organotypic Hippocampal Slice Cultures.
Evidence row 973
THC modulates TRPV1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: TRPV1 channel activity, desensitization, binding, signaling, or pharmacology). PMID 16596770
Evidence class: insufficient; Study design: Narrative or expert review. Source: Pharmacological actions of cannabinoids.
Evidence row 978
CBD modulates TRPV1; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV1 channel activity, desensitization, binding, signaling, or pharmacology). PMID 37199723
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.
Evidence row 980
Endocannabinoids modulates TRPV1; evidence class: insufficient (population or model: Animal model mentioned; study design: Narrative or expert review; outcome measure: TRPV1 channel activity, desensitization, binding, signaling, or pharmacology). PMID 36222019
Evidence class: insufficient; Study design: Narrative or expert review. Source: Endocannabinoid signaling in microglia.
Evidence row 991
CBD modulates TRPV2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV2 channel activity, binding, signaling, or pharmacology). PMID 37199723
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.
Evidence row 1001
CBD modulates TRPV2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV2 channel activity, binding, signaling, or pharmacology). PMID 36747846
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.
Evidence row 1009
CBD modulates TRPV3; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV3 channel activity, binding, signaling, dermatology-relevant mechanism, or pharmacology). PMID 37199723
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.
Evidence row 1010
CBD modulates TRPV3; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV3 channel activity, binding, signaling, dermatology-relevant mechanism, or pharmacology). PMID 36747846
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.
Evidence row 1014
Cannabinoids modulates TRPV3; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: TRPV3 channel activity, binding, signaling, dermatology-relevant mechanism, or pharmacology). PMID 26845556
Evidence class: insufficient; Study design: Systematic review. Source: A Systematic Review of Plant-Derived Natural Compounds for Anxiety Disorders.
Evidence row 1026
Cannabinoids modulates TRPV4; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV4 channel activity, binding, signaling, or pharmacology). PMID 41802611
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Peripheral cannabinoid receptor activation attenuates frostbite-induced chronic pain via modulation of TRP channels, neuroinflammation, and autophagy.
Evidence row 1046
CBD modulates TRPA1; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: TRPA1 channel activity, desensitization, binding, signaling, or pharmacology). PMID 32873774
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Cannabidiol (CBD): a killer for inflammatory rheumatoid arthritis synovial fibroblasts.
Evidence row 1102
OEA studied for OEA biology, receptor pharmacology, feeding, metabolism, physiology, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: OEA biology, receptor pharmacology, feeding, metabolism, physiology, or safety-relevant mechanisms). PMID 32142797
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: GPR119 Is a Potent Regulator of Human Sebocyte Biology.
Evidence row 1106
PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms). PMID 35176443
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: Palmitoylethanolamide dampens neuroinflammation and anxiety-like behavior in obese mice.
Evidence row 1107
PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms). PMID 39714723
Evidence class: insufficient; Study design: Narrative or expert review. Source: Mechanisms and clinical applications of palmitoylethanolamide (PEA) in the treatment of neuropathic pain.
Evidence row 1109
PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms). PMID 40563990
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Palmitoylethanolamide: A Multifunctional Molecule for Neuroprotection, Chronic Pain, and Immune Modulation.
Evidence row 1111
PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms). PMID 28215162
Evidence class: insufficient; Study design: Narrative or expert review. Source: Gut-brain Axis: Role of Lipids in the Regulation of Inflammation, Pain and CNS Diseases.
Evidence row 1112
PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms). PMID 10785541
Evidence class: insufficient; Study design: Narrative or expert review. Source: Cannabimimetic fatty acid derivatives in cancer and inflammation.
Evidence row 1134
NADA studied for NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms). PMID 24644287
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: The endocannabinoid/endovanilloid N-arachidonoyl dopamine (NADA) and synthetic cannabinoid WIN55,212-2 abate the inflammatory activation of human endothelial cells.
Evidence row 1142
NADA studied for NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms). PMID 33568652
Evidence class: mechanistic or pharmacological; Study design: Cellular or in vitro study. Source: Anti-inflammatory dopamine- and serotonin-based endocannabinoid epoxides reciprocally regulate cannabinoid receptors and the TRPV1 channel.
Evidence row 1168
DHEA / synaptamide studied for DHEA/synaptamide biology, receptor or signaling mechanisms, metabolism, physiology, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: DHEA/synaptamide biology, receptor or signaling mechanisms, metabolism, physiology, or safety-relevant mechanisms). PMID 27809877
Evidence class: mechanistic or pharmacological; Study design: Animal study. Source: N-Docosahexaenoylethanolamine ameliorates LPS-induced neuroinflammation via cAMP/PKA-dependent signaling.
Evidence row 1188
SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms). PMID 24874648
Evidence class: insufficient; Study design: Narrative or expert review. Source: Roles of fatty acid ethanolamides (FAE) in traumatic and ischemic brain injury.
Evidence row 1194
SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: preclinical (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms). PMID 38279735
Evidence class: preclinical; Study design: Animal study. Source: N-Stearoylethanolamine Exerts Cardioprotective Effects in Old Rats.
Evidence row 1199
SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: preclinical (population or model: Animal model mentioned; study design: Animal study; outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms). PMID 19873884
Evidence class: preclinical; Study design: Animal study. Source: [Anti-inflammatory effect of N-stearoylethanolamine in experimental burn injury in rats].
Evidence row 1201
SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: preclinical (outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms). PMID 33434116
Evidence class: preclinical. Source: Exploring the Utility of Hair Endocannabinoids for Monitoring Homeostasis in Bonobos.

Source Trail

Source-backed evidence table and references

106 research sources

This section is the technical source layer under the overview. It keeps grouped evidence buckets, evidence rows, PubMed or DOI links, related pages, and references visible for audit and revision.

Plain-Language Summary

This outcome page summarizes cannabinoid-related evidence connected to Immune modulation. The current ledger contributes 131 evidence row(s) from 106 source(s).

Identity

Canonical name: immune-modulation
Type: outcome
Subtype: Not recorded
Description: Not recorded

Evidence Snapshot

Evidence rows: 131
Sources: 106
Evidence classes: insufficient (54), mechanistic or pharmacological (69), preclinical (6), preliminary human (2)
Draft sections: human evidence (2), mechanistic evidence (67), preclinical evidence (6), safety (10), uncertainty (46)

Key Draft Sections

Human evidence: 2 evidence row(s).
Safety and tolerability: 10 evidence row(s).
Uncertainty and gaps: 46 evidence row(s).
Preclinical evidence: 6 evidence row(s).
Mechanistic evidence: 67 evidence row(s).

Compounds Studied With This Outcome

Subject	Relationship	Object Or Focus	Evidence Summary	Sources	Evidence Rows
Cannabinoids	studied for	Cannabinoids and immune modulation research outcomes	Mechanistic research summary: insufficient (2), mechanistic or pharmacological (1)	3	3 rows (274-276)
Cannabinoids	modulates	CB1	Mapped evidence with interpretation limits: insufficient (1)	1	817
Cannabinoids	modulates	CB2	Mechanistic research summary: insufficient (5), mechanistic or pharmacological (14)	19	19 rows (869-925)
Cannabinoids	modulates	TRPV3	Mapped evidence with interpretation limits: insufficient (1)	1	1014
Cannabinoids	modulates	TRPV4	Mechanistic research summary: mechanistic or pharmacological (1)	1	1026
CBC	studied for	Inflammation-related outcomes	Developed but mixed human research summary: mechanistic or pharmacological (1), preclinical (1), preliminary human (1)	3	3 rows (35-72)
CBC	studied for	neurobehavioral, mood, neural stem cell, or neurogenesis outcomes	Mechanistic research summary: mechanistic or pharmacological (2)	2	2 rows (721-727)
CBC	studied for	Pain-related outcomes	Developed but mixed human research summary: mechanistic or pharmacological (1), preclinical (1), preliminary human (1)	3	3 rows (684-687)
CBC	modulates	receptor, transporter, target, metabolic, or pharmacology mechanisms	Mapped evidence with interpretation limits: insufficient (2)	2	2 rows (670-681)
CBC	studied for	Skin and inflammatory dermatology	Mechanistic research summary: insufficient (1), mechanistic or pharmacological (2)	3	3 rows (707-716)
CBD	modulates	endocannabinoid enzyme activity or metabolic mechanisms	Mechanistic research summary: insufficient (1), mechanistic or pharmacological (1)	2	2 rows (369-372)
CBD	modulates	GPR55	Mapped evidence with interpretation limits: insufficient (1)	1	942
CBD	studied for	safety, risk, adverse-event, or formulation-specific concerns	Mapped evidence with interpretation limits: insufficient (4)	4	4 rows (327-342)
CBD	modulates	TRPA1	Mechanistic research summary: mechanistic or pharmacological (1)	1	1046
CBD	modulates	TRPV1	Mechanistic research summary: mechanistic or pharmacological (1)	1	978
CBD	modulates	TRPV2	Mechanistic research summary: mechanistic or pharmacological (2)	2	2 rows (991-1001)
CBD	modulates	TRPV3	Mechanistic research summary: mechanistic or pharmacological (2)	2	2 rows (1009-1010)
CBDA	studied for	nausea-related or inflammation-related outcomes	Mechanistic research summary: insufficient (1), mechanistic or pharmacological (2)	3	3 rows (137-143)
CBG	studied for	Appetite and metabolic outcomes	Mapped evidence with interpretation limits: insufficient (1)	1	622
CBG	studied for	Inflammation-related outcomes	Mechanistic research summary: insufficient (2), mechanistic or pharmacological (2)	4	4 rows (587-597)
CBG	studied for	Pain-related outcomes	Mapped evidence with interpretation limits: insufficient (2)	2	2 rows (64-68)
CBG	modulates	receptor, target, metabolic, or pharmacology mechanisms	Mapped evidence with interpretation limits: insufficient (2)	2	2 rows (565-571)
CBG	studied for	safety, adverse-event, impairment, or formulation-specific concerns	Mechanistic research summary: mechanistic or pharmacological (1)	1	157
CBG	studied for	safety, tolerability, adverse-event, impairment, toxicity, or formulation-specific concerns	Mechanistic research summary: mechanistic or pharmacological (1)	1	542
CBG	studied for	Skin and inflammatory dermatology	Mechanistic research summary: mechanistic or pharmacological (4)	4	4 rows (606-619)
CBN	modulates	receptor, target, metabolic, or pharmacology mechanisms	Mapped evidence with interpretation limits: insufficient (1)	1	519
CBN	studied for	safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns	Mapped evidence with interpretation limits: insufficient (2)	2	2 rows (514-516)
CBN	studied for	Skin and inflammatory dermatology	Mechanistic research summary: insufficient (2), mechanistic or pharmacological (7)	9	9 rows (525-533)
DHEA / synaptamide	studied for	DHEA/synaptamide biology, receptor or signaling mechanisms, metabolism, physiology, or safety-relevant mechanisms	Mechanistic research summary: mechanistic or pharmacological (1)	1	1168
Endocannabinoids	studied for	Cannabinoids and immune modulation research outcomes	Mechanistic research summary: mechanistic or pharmacological (3)	3	3 rows (268-272)
Endocannabinoids	modulates	CB1	Mapped evidence with interpretation limits: insufficient (4)	4	4 rows (842-850)
Endocannabinoids	modulates	CB2	Mechanistic research summary: insufficient (1), mechanistic or pharmacological (3)	4	4 rows (876-917)
Endocannabinoids	modulates	GPR18	Mechanistic research summary: insufficient (1), mechanistic or pharmacological (1)	2	2 rows (952-954)
Endocannabinoids	modulates	GPR55	Mapped evidence with interpretation limits: insufficient (1)	1	937
Endocannabinoids	studied for	safety, risk, adverse-event, or formulation-specific concerns	Mapped evidence with interpretation limits: insufficient (2)	2	2 rows (345-346)
Endocannabinoids	modulates	TRPV1	Mapped evidence with interpretation limits: insufficient (1)	1	980
NADA	studied for	NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms	Mechanistic research summary: mechanistic or pharmacological (2)	2	2 rows (1134-1142)
OEA	studied for	OEA biology, receptor pharmacology, feeding, metabolism, physiology, or safety-relevant mechanisms	Mechanistic research summary: mechanistic or pharmacological (1)	1	1102
PEA	studied for	Cannabinoids and immune modulation research outcomes	Mechanistic research summary: mechanistic or pharmacological (1)	1	270
PEA	studied for	PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms	Mechanistic research summary: insufficient (3), mechanistic or pharmacological (2)	5	5 rows (1106-1112)
SEA	studied for	SEA biology, metabolism, physiology, or safety-relevant mechanisms	Preclinical research summary: insufficient (1), preclinical (3)	4	4 rows (1188-1201)
THC	studied for	Appetite and metabolic outcomes	Mapped evidence with interpretation limits: insufficient (2)	2	2 rows (490-494)
THC	studied for	Cannabinoids and immune modulation research outcomes	Preclinical research summary: insufficient (1), preclinical (1)	2	2 rows (269-273)
THC	modulates	CB1	Mechanistic research summary: insufficient (1), mechanistic or pharmacological (1)	2	2 rows (808-810)
THC	modulates	CB2	Mechanistic research summary: insufficient (1), mechanistic or pharmacological (2)	3	3 rows (863-913)
THC	studied for	Endocannabinoids and endocannabinoid-like lipids research topics	Mapped evidence with interpretation limits: insufficient (1)	1	293
THC	modulates	GPR18	Mechanistic research summary: mechanistic or pharmacological (2)	2	2 rows (946-949)
THC	modulates	receptor, target, or pharmacology mechanisms	Mapped evidence with interpretation limits: insufficient (1)	1	204
THC	studied for	receptor, target, or pharmacology mechanisms	Mechanistic research summary: mechanistic or pharmacological (2)	2	2 rows (277-278)
THC	modulates	TRPV1	Mapped evidence with interpretation limits: insufficient (1)	1	973
THCV	studied for	Appetite and metabolic outcomes	Mechanistic research summary: mechanistic or pharmacological (1)	1	734
THCV	studied for	Inflammation-related outcomes	Mechanistic research summary: mechanistic or pharmacological (1)	1	786
THCV	modulates	receptor, target, metabolic, or pharmacology mechanisms	Mapped evidence with interpretation limits: insufficient (1)	1	763

Source-Backed Evidence Table

Evidence Row	Statement	Source
35	CBC studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: inflammation-related or pain-related outcomes).	Anti-inflammatory and analgesic potential of minor cannabinoids in vivo.PubMed 41680865 DOI 10.1186/s42238-025-00384-7
36	CBC studied for Inflammation-related outcomes; evidence class: preclinical (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: inflammation-related or pain-related outcomes).	The Mechanism of Cannabichromene and Cannabidiol Alone Versus in Combination in the Alleviation of Arthritis-Related Inflammation.PubMed 37332213 DOI 10.1097/sap.0000000000003547
64	CBG studied for Pain-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: pain-related outcomes).	The Effects of Cannabinoids on Pro- and Anti-Inflammatory Cytokines: A Systematic Review of In Vivo Studies.PubMed 33998900 DOI 10.1089/can.2020.0105
68	CBG studied for Pain-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: pain-related outcomes).	Acidic Cannabinoids Suppress Proinflammatory Cytokine Release by Blocking Store-operated Calcium Entry.PubMed 35910331 DOI 10.1093/function/zqac033
72	CBC studied for Inflammation-related outcomes; evidence class: preliminary human (outcome measure: inflammation-related or pain-related outcomes).	Therapeutic potential of cannabidiol-rich Cannabis sativa to mitigate the severity of inflammation and pain: A pre-clinical study.PubMed 41213439 DOI 10.1016/j.jep.2025.120856
137	CBDA studied for nausea-related or inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: nausea-related or inflammation-related outcomes).	Antiviral activities of hemp cannabinoids.PubMed 37083031 DOI 10.1042/cs20220193
139	CBDA studied for nausea-related or inflammation-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; outcome measure: nausea-related or inflammation-related outcomes).	Medical Cannabis Use and Inflammatory Cytokines and Chemokines Among Adult Chronic Pain Patients.PubMed 36342776 DOI 10.1089/can.2022.0143
143	CBDA studied for nausea-related or inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: nausea-related or inflammation-related outcomes).	The effect of phytocannabinoids on airway hyper-responsiveness, airway inflammation, and cough.PubMed 25655949 DOI 10.1124/jpet.114.221283
157	CBG studied for safety, adverse-event, impairment, or formulation-specific concerns; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: safety, adverse-event, impairment, or formulation-specific concerns).	Exploring Cannabidiol (CBD) and Cannabigerol (CBG) Safety Profile and Skincare Potential.PubMed 39596290 DOI 10.3390/ijms252212224
204	THC modulates receptor, target, or pharmacology mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: receptor, target, or pharmacology mechanisms).	The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin.PubMed 17828291 DOI 10.1038/sj.bjp.0707442
268	Endocannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes).	Astrocytic cannabinoid receptor 1 promotes resilience by dampening stress-induced blood-brain barrier alterations.PubMed 40016352 DOI 10.1038/s41593-025-01891-9
269	THC studied for Cannabinoids and immune modulation research outcomes; evidence class: preclinical (population or model: Pediatric, adolescent, or developmental context mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes).	Maternal immune activation impairs endocannabinoid signaling in the mesolimbic system of adolescent male offspring.PubMed 36746342 DOI 10.1016/j.bbi.2023.02.002
270	PEA studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes).	Palmitoylethanolamide dampens neuroinflammation and anxiety-like behavior in obese mice.PubMed 35176443 DOI 10.1016/j.bbi.2022.02.008
271	Endocannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes).	Phospholipase Cγ2 regulates endocannabinoid and eicosanoid networks in innate immune cells.PubMed 34607960 DOI 10.1073/pnas.2112971118
272	Endocannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes).	Impact of Chronic Moderate Exercise on Immune Cells and Cytokine Levels in Rats: Focus on the Endocannabinergic Pathway.PubMed 37962860 DOI 10.1089/jir.2023.0120
273	THC studied for Cannabinoids and immune modulation research outcomes; evidence class: insufficient (population or model: Pregnancy, lactation, or reproductive context mentioned; study design: Narrative or expert review; outcome measure: Cannabinoids and immune modulation research outcomes).	Pharmacokinetics and pharmacodynamics of cannabinoids.PubMed 12648025 DOI 10.2165/00003088-200342040-00003
274	Cannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: Cannabinoids and immune modulation research outcomes).	Modulation of cannabinoid receptor 2 alters neuroinflammation and reduces formation of alpha-synuclein aggregates in a rat model of nigral synucleinopathy.PubMed 39334169 DOI 10.1186/s12974-024-03221-5
275	Cannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: Cannabinoids and immune modulation research outcomes).	CB2 receptor in the CNS: From immune and neuronal modulation to behavior.PubMed 37164044 DOI 10.1016/j.neubiorev.2023.105226
276	Cannabinoids studied for Cannabinoids and immune modulation research outcomes; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: Cannabinoids and immune modulation research outcomes).	Cannabinoid receptor signaling.PubMed 16596771 DOI 10.1007/3-540-26573-2_2
277	THC studied for receptor, target, or pharmacology mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: receptor, target, or pharmacology mechanisms).	Antiviral activities of hemp cannabinoids.PubMed 37083031 DOI 10.1042/cs20220193
278	THC studied for receptor, target, or pharmacology mechanisms; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: receptor, target, or pharmacology mechanisms).	Cannabigerolic Acid (CBGA) Inhibits the TRPM7 Ion Channel Through its Kinase Domain.PubMed 38162115 DOI 10.1093/function/zqad069
293	THC studied for Endocannabinoids and endocannabinoid-like lipids research topics; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: Endocannabinoids and endocannabinoid-like lipids research topics).	Cannabinoid activation of peroxisome proliferator-activated receptors: potential for modulation of inflammatory disease.PubMed 19833407 DOI 10.1016/j.imbio.2009.09.007
327	CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns).	Cannabis Contaminants Limit Pharmacological Use of Cannabidiol.PubMed 33013414 DOI 10.3389/fphar.2020.571832
340	CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns).	Cannabidiol in Skin Health: A Comprehensive Review of Topical Applications in Dermatology and Cosmetic Science.PubMed 41008526 DOI 10.3390/biom15091219
341	CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns).	Cannabis sativa and Skin Health: Dissecting the Role of Phytocannabinoids.PubMed 33851375 DOI 10.1055/a-1420-5780
342	CBD studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: safety, risk, adverse-event, or formulation-specific concerns).	Potential of cannabidiol as acne and acne scar treatment: novel insights into molecular pathways of pathophysiological factors.PubMed 38904694 DOI 10.1007/s00403-024-03131-9
345	Endocannabinoids studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns).	Sebaceous immunobiology - skin homeostasis, pathophysiology, coordination of innate immunity and inflammatory response and disease associations.PubMed 36439142 DOI 10.3389/fimmu.2022.1029818
346	Endocannabinoids studied for safety, risk, adverse-event, or formulation-specific concerns; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: safety, risk, adverse-event, or formulation-specific concerns).	The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities.PubMed 19608284 DOI 10.1016/j.tips.2009.05.004
369	CBD modulates endocannabinoid enzyme activity or metabolic mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: endocannabinoid enzyme activity or metabolic mechanisms).	Hepatotoxicity evaluation of cannabidiol, cannabinol, cannabichromene and cannabigerol using a human quad culture liver chip.PubMed 40750820 DOI 10.1038/s41598-025-12846-2
372	CBD modulates endocannabinoid enzyme activity or metabolic mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: endocannabinoid enzyme activity or metabolic mechanisms).	Metabolism and liver toxicity of cannabidiol.PubMed 38904421 DOI 10.1080/26896583.2024.2366741
490	THC studied for Appetite and metabolic outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: appetite or metabolic outcomes).	Orexigenic and anabolic agents.PubMed 12608509 DOI 10.1016/s0749-0690(02
494	THC studied for Appetite and metabolic outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: appetite or metabolic outcomes).	Clinical utility of dronabinol in the treatment of weight loss associated with HIV and AIDS.PubMed 26929669 DOI 10.2147/hiv.s81420
514	CBN studied for safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns; evidence class: insufficient (population or model: Pediatric, adolescent, or developmental context mentioned; study design: Narrative or expert review; outcome measure: safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns).	[Cannabis: Effects in the Central Nervous System. Therapeutic, societal and legal consequences].PubMed 27428345
516	CBN studied for safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: safety, tolerability, sedation, adverse-event, impairment, or formulation-specific concerns).	Evaluation of the anti-inflammatory effects of selected cannabinoids and terpenes from Cannabis Sativa employing human primary leukocytes.PubMed 36228902 DOI 10.1016/j.fct.2022.113458
519	CBN modulates receptor, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: receptor, target, metabolic, or pharmacology mechanisms).	Pharmacological actions of cannabinoids.PubMed 16596770 DOI 10.1007/3-540-26573-2_1
525	CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Anti-inflammatory and analgesic potential of minor cannabinoids in vivo.PubMed 41680865 DOI 10.1186/s42238-025-00384-7
526	CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Anti-Inflammatory Effects of Minor Cannabinoids CBC, THCV, and CBN in Human Macrophages.PubMed 37764262 DOI 10.3390/molecules28186487
527	CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Cannabinol modulates the endocannabinoid system and shows TRPV1-mediated anti-inflammatory properties in human keratinocytes.PubMed 39275884 DOI 10.1002/biof.2122
528	CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Evaluation of the anti-inflammatory effects of selected cannabinoids and terpenes from Cannabis Sativa employing human primary leukocytes.PubMed 36228902 DOI 10.1016/j.fct.2022.113458
529	CBN studied for Skin and inflammatory dermatology; evidence class: insufficient (study design: Narrative or expert review; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Phytocannabinoids: Exploring Pharmacological Profiles and Their Impact on Therapeutical Use.PubMed 38673788 DOI 10.3390/ijms25084204
530	CBN studied for Skin and inflammatory dermatology; evidence class: insufficient (study design: Narrative or expert review; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Cannabinoids, inflammation, and fibrosis.PubMed 27435265 DOI 10.1096/fj.201600646r
531	CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Phytocannabinoids as anti-inflammatory agents: Synergistic effects when combined with Cannabis sativa L. matrices.PubMed 41478536 DOI 10.1016/j.jep.2025.121134
532	CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Preclinical evaluation of cannabidiolic acid as a neuroprotective agent in TDP-43 transgenic mice, an experimental model of amyotrophic lateral sclerosis.PubMed 40580876 DOI 10.1016/j.biopha.2025.118288
533	CBN studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, inflammatory, or immune-modulation outcomes).	Distinct Interactions of Cannabinol and Its Cytochrome P450-Generated Metabolites with Receptors and Sensory Neurons.PubMed 40568800 DOI 10.1021/acs.jmedchem.5c00938
542	CBG studied for safety, tolerability, adverse-event, impairment, toxicity, or formulation-specific concerns; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: safety, tolerability, adverse-event, impairment, toxicity, or formulation-specific concerns).	Exploring Cannabidiol (CBD) and Cannabigerol (CBG) Safety Profile and Skincare Potential.PubMed 39596290 DOI 10.3390/ijms252212224
565	CBG modulates receptor, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: receptor, target, metabolic, or pharmacology mechanisms).	The Effects of Cannabinoids on Pro- and Anti-Inflammatory Cytokines: A Systematic Review of In Vivo Studies.PubMed 33998900 DOI 10.1089/can.2020.0105
571	CBG modulates receptor, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: receptor, target, metabolic, or pharmacology mechanisms).	Cannabinoids in autoimmune diseases: mechanistic insights and translational challenges.PubMed 42105814 DOI 10.1016/j.bcp.2026.118032
587	CBG studied for Inflammation-related outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: inflammation-related or immune outcomes).	The Effects of Cannabinoids on Pro- and Anti-Inflammatory Cytokines: A Systematic Review of In Vivo Studies.PubMed 33998900 DOI 10.1089/can.2020.0105
592	CBG studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: inflammation-related or immune outcomes).	Cannabigerol attenuates liver fibrosis via AMPK activation: Regulation of lipid metabolism, inflammation, and hepatic stellate cell activation.PubMed 40818359 DOI 10.1016/j.biopha.2025.118463
593	CBG studied for Inflammation-related outcomes; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: inflammation-related or immune outcomes).	Medical Cannabis Activity Against Inflammation: Active Compounds and Modes of Action.PubMed 35614947 DOI 10.3389/fphar.2022.908198
597	CBG studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: inflammation-related or immune outcomes).	Cannabigerol Alleviates Liver Damage in Metabolic Dysfunction-Associated Steatohepatitis Female Mice via Inhibition of Transforming Growth Factor Beta 1.PubMed 40362835 DOI 10.3390/nu17091524
606	CBG studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, or topical inflammatory outcomes).	Exploring Cannabidiol (CBD) and Cannabigerol (CBG) Safety Profile and Skincare Potential.PubMed 39596290 DOI 10.3390/ijms252212224
610	CBG studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Human clinical study; outcome measure: skin, dermatology, or topical inflammatory outcomes).	In Vitro and Clinical Evaluation of Cannabigerol (CBG) Produced via Yeast Biosynthesis: A Cannabinoid with a Broad Range of Anti-Inflammatory and Skin Health-Boosting Properties.PubMed 35056807 DOI 10.3390/molecules27020491
611	CBG studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: skin, dermatology, or topical inflammatory outcomes).	Anti-Inflammatory Effects of Cannabigerol In Vitro and In Vivo Are Mediated Through the JAK/STAT/NFκB Signaling Pathway.PubMed 39851511 DOI 10.3390/cells14020083
619	CBG studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, or topical inflammatory outcomes).	Differential effectiveness of selected non-psychotropic phytocannabinoids on human sebocyte functions implicates their introduction in dry/seborrhoeic skin and acne treatment.PubMed 27094344 DOI 10.1111/exd.13042
622	CBG studied for Appetite and metabolic outcomes; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: appetite-related, weight, glucose, or metabolic outcomes).	Cannabinoids in autoimmune diseases: mechanistic insights and translational challenges.PubMed 42105814 DOI 10.1016/j.bcp.2026.118032
670	CBC modulates receptor, transporter, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Animal model mentioned; study design: Animal study; outcome measure: receptor, transporter, target, metabolic, or pharmacology mechanisms).	Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.PubMed 39769302 DOI 10.3390/ijms252413539
681	CBC modulates receptor, transporter, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: receptor, transporter, target, metabolic, or pharmacology mechanisms).	Selected phytocannabinoids inhibit SN-38- and cytokine-evoked increases in epithelial permeability and improve intestinal barrier function in vitro.PubMed 38950639 DOI 10.1016/j.tiv.2024.105888
684	CBC studied for Pain-related outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: pain-related outcomes).	Anti-inflammatory and analgesic potential of minor cannabinoids in vivo.PubMed 41680865 DOI 10.1186/s42238-025-00384-7
685	CBC studied for Pain-related outcomes; evidence class: preclinical (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: pain-related outcomes).	The Mechanism of Cannabichromene and Cannabidiol Alone Versus in Combination in the Alleviation of Arthritis-Related Inflammation.PubMed 37332213 DOI 10.1097/sap.0000000000003547
687	CBC studied for Pain-related outcomes; evidence class: preliminary human (outcome measure: pain-related outcomes).	Therapeutic potential of cannabidiol-rich Cannabis sativa to mitigate the severity of inflammation and pain: A pre-clinical study.PubMed 41213439 DOI 10.1016/j.jep.2025.120856
707	CBC studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: skin, dermatology, antimicrobial, or topical inflammatory outcomes).	Differential effectiveness of selected non-psychotropic phytocannabinoids on human sebocyte functions implicates their introduction in dry/seborrhoeic skin and acne treatment.PubMed 27094344 DOI 10.1111/exd.13042
708	CBC studied for Skin and inflammatory dermatology; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: skin, dermatology, antimicrobial, or topical inflammatory outcomes).	Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.PubMed 39769302 DOI 10.3390/ijms252413539
716	CBC studied for Skin and inflammatory dermatology; evidence class: insufficient (outcome measure: skin, dermatology, antimicrobial, or topical inflammatory outcomes).	Targeting the antioxidant, antimicrobial and anti-inflammatory activity of non-psychotropic Cannabis sativa L.: a comparison with chemotype V.PubMed 41121423 DOI 10.1186/s42238-025-00336-1
721	CBC studied for neurobehavioral, mood, neural stem cell, or neurogenesis outcomes; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: neurobehavioral, mood, neural stem cell, or neurogenesis outcomes).	Anti-inflammatory and analgesic potential of minor cannabinoids in vivo.PubMed 41680865 DOI 10.1186/s42238-025-00384-7
727	CBC studied for neurobehavioral, mood, neural stem cell, or neurogenesis outcomes; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: neurobehavioral, mood, neural stem cell, or neurogenesis outcomes).	Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.PubMed 39769302 DOI 10.3390/ijms252413539
734	THCV studied for Appetite and metabolic outcomes; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: appetite-related or metabolic outcomes).	Tetrahydrocannabivarin (THCV) Protects Adipose-Derived Mesenchymal Stem Cells (ASC) against Endoplasmic Reticulum Stress Development and Reduces Inflammation during Adipogenesis.PubMed 37108282 DOI 10.3390/ijms24087120
763	THCV modulates receptor, target, metabolic, or pharmacology mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: receptor, target, metabolic, or pharmacology mechanisms).	The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin.PubMed 17828291 DOI 10.1038/sj.bjp.0707442
786	THCV studied for Inflammation-related outcomes; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: inflammation-related or immune outcomes).	Phytocannabinoids Act Synergistically with Non-Steroidal Anti-Inflammatory Drugs Reducing Inflammation in 2D and 3D In Vitro Models.PubMed 36559009 DOI 10.3390/ph15121559
808	THC modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 receptor pharmacology, ligand binding, or signaling mechanisms).	Pharmacological actions of cannabinoids.PubMed 16596770 DOI 10.1007/3-540-26573-2_1
810	THC modulates CB1; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: CB1 receptor pharmacology, ligand binding, or signaling mechanisms).	Cannabinoid receptor 1 antagonist genistein attenuates marijuana-induced vascular inflammation.PubMed 35489334 DOI 10.1016/j.cell.2022.04.005
817	Cannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 receptor pharmacology, ligand binding, or signaling mechanisms).	Pharmacology of cannabinoid receptor ligands.PubMed 10469884
842	Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain, cognition, or synaptic mechanisms).	Cannabinoid-based therapy as a future for joint degeneration. Focus on the role of CB2 receptor in the arthritis progression and pain: an updated review.PubMed 34050525 DOI 10.1007/s43440-021-00270-y
846	Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain, cognition, or synaptic mechanisms).	The pharmacology of cannabinoid receptors and their ligands: an overview.PubMed 16570099 DOI 10.1038/sj.ijo.0803272
849	Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain, cognition, or synaptic mechanisms).	Therapeutic potential of cannabinoid receptor 2 in the treatment of diabetes mellitus and its complications.PubMed 31461639 DOI 10.1016/j.ejphar.2019.172628
850	Endocannabinoids modulates CB1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB1 neurobehavioral, appetite, metabolic, pain, cognition, or synaptic mechanisms).	The endocannabinoid system: physiology and pharmacology.PubMed 15550444 DOI 10.1093/alcalc/agh110
863	THC modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms).	The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin.PubMed 17828291 DOI 10.1038/sj.bjp.0707442
869	Cannabinoids modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms).	Pharmacology of cannabinoid receptor ligands.PubMed 10469884
876	Endocannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms).	Crystal Structure of the Human Cannabinoid Receptor CB2.PubMed 30639103 DOI 10.1016/j.cell.2018.12.011
885	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms).	Cannabinoid Receptor Type 2 Agonist Reduces Morphine Tolerance via Mitogen Activated Protein Kinase Phosphatase Induction and Mitogen Activated Protein Kinase Dephosphorylation.PubMed 34774714 DOI 10.1016/j.neuroscience.2021.11.007
891	Cannabinoids modulates CB2; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB2 receptor pharmacology, ligand binding, selectivity, or signaling mechanisms).	Cannabinoid CB2 receptor orthologues; in vitro function and perspectives for preclinical to clinical translation.PubMed 37349984 DOI 10.1111/bph.16172
895	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Modulation of cannabinoid receptor 2 alters neuroinflammation and reduces formation of alpha-synuclein aggregates in a rat model of nigral synucleinopathy.PubMed 39334169 DOI 10.1186/s12974-024-03221-5
897	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Type 2 cannabinoid receptor expression on microglial cells regulates neuroinflammation during graft-versus-host disease.PubMed 38662453 DOI 10.1172/jci175205
899	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid CB2 receptors enhance high-fat diet evoked peripheral neuroinflammation.PubMed 39173999 DOI 10.1016/j.lfs.2024.123002
901	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid receptor 2 evolutionary gene loss makes parrots more susceptible to neuroinflammation.PubMed 36475439 DOI 10.1098/rspb.2022.1941
902	Endocannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid CB2 receptors modulate alcohol induced behavior, and neuro-immune dysregulation in mice.PubMed 37061199 DOI 10.1016/j.bbr.2023.114439
903	Endocannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	The cannabinoid CB2 receptor as a target for inflammation-dependent neurodegeneration.PubMed 18615177 DOI 10.2174/157015907780866884
904	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid receptor 2 activation mitigates lipopolysaccharide-induced neuroinflammation and sickness behavior in mice.PubMed 30666359 DOI 10.1007/s00213-019-5166-y
907	THC modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Up-regulation of immunomodulatory effects of mouse bone-marrow derived mesenchymal stem cells by tetrahydrocannabinol pre-treatment involving cannabinoid receptor CB2.PubMed 26824325 DOI 10.18632/oncotarget.7042
909	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Enantiomeric Agonists of the Type 2 Cannabinoid Receptor Reduce Retinal Damage during Proliferative Vitreoretinopathy and Inhibit Hyperactive Microglia In Vitro.PubMed 38751621 DOI 10.1021/acsptsci.4c00014
910	Cannabinoids modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	The development of cannabinoid CBII receptor agonists for the treatment of central neuropathies.PubMed 20236042 DOI 10.2174/187152410790780145
911	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Induction of CB2 receptor expression in the rat spinal cord of neuropathic but not inflammatory chronic pain models.PubMed 12823482 DOI 10.1046/j.1460-9568.2003.02704.x
913	THC modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabidiol-rich non-psychotropic Cannabis sativa L. oils attenuate peripheral neuropathy symptoms by regulation of CB2-mediated microglial neuroinflammation.PubMed 36583304 DOI 10.1002/ptr.7710
915	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Pediatric, adolescent, or developmental context mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Effects of CB2 Receptor Modulation on Macrophage Polarization in Pediatric Inflammatory Bowel Disease.PubMed 40332343 DOI 10.3390/ijms26083720
916	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	CB2 cannabinoid receptor-specific therapeutic antibody agonists for treatment of chemotherapy-induced peripheral neuropathy.PubMed 41383775 DOI 10.1101/2025.11.26.690750
917	Endocannabinoids modulates CB2; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	What we know and do not know about the cannabinoid receptor 2 (CB2).PubMed 24877594 DOI 10.1016/j.smim.2014.04.002
918	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid Receptor 2 Activating Antibodies: A Promising Therapeutic Strategy for Macrophage-Driven Fibro-Inflammatory Diseases.PubMed 40791361 DOI 10.1101/2025.07.11.664477
919	Cannabinoids modulates CB2; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid Receptor 2 (CB2) in Macrophages: A Promising Clinical Target for Immune Disorders.PubMed 40943579 DOI 10.3390/ijms26178657
921	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid receptor 2 affect the inflammatory response in periodontitis by regulating macrophage M1/M2 polarization.PubMed 41310604 DOI 10.1186/s12903-025-07176-8
923	Cannabinoids modulates CB2; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid Receptor Type 2: A Possible Target in SARS-CoV-2 (CoV-19) Infection?PubMed 32471272 DOI 10.3390/ijms21113809
924	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid receptor type 2 agonist GP1a attenuates macrophage activation induced by M. bovis-BCG by inhibiting NF-κB signaling.PubMed 39538989 DOI 10.1093/jleuko/qiae246
925	Cannabinoids modulates CB2; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: CB2 immune, inflammatory, microglial, neuroinflammatory, pain, or tissue-injury mechanisms).	Cannabinoid receptor 2 activating antibodies: A promising therapeutic strategy for macrophage-driven fibro-inflammatory diseases.PubMed 41740200 DOI 10.1016/j.molpha.2026.100102
937	Endocannabinoids modulates GPR55; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: GPR55 receptor activity, binding, signaling, or pharmacology).	The Endocannabinoid System of Animals.PubMed 31527410 DOI 10.3390/ani9090686
942	CBD modulates GPR55; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: GPR55 receptor activity, binding, signaling, or pharmacology).	Epilepsy, neuroinflammation and cannabidiol What do we know thus far?PubMed 41560741 DOI 10.3389/fphar.2025.1749260
946	THC modulates GPR18; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: GPR18 receptor activity, binding, signaling, or pharmacology).	Computational Investigations on the Binding Mode of Ligands for the Cannabinoid-Activated G Protein-Coupled Receptor GPR18.PubMed 32365486 DOI 10.3390/biom10050686
949	THC modulates GPR18; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: GPR18 receptor activity, binding, signaling, or pharmacology).	Structure-activity relationships of imidazothiazinones and analogs as antagonists of the cannabinoid-activated orphan G protein-coupled receptor GPR18.PubMed 29902723 DOI 10.1016/j.ejmech.2018.05.050
952	Endocannabinoids modulates GPR18; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: GPR18 receptor activity, binding, signaling, or pharmacology).	An Update on Non-CB1, Non-CB2 Cannabinoid Related G-Protein-Coupled Receptors.PubMed 29098189 DOI 10.1089/can.2017.0036
954	Endocannabinoids modulates GPR18; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: GPR18 receptor activity, binding, signaling, or pharmacology).	Protective Effect of N-Arachidonoyl Glycine-GPR18 Signaling after Excitotoxical Lesion in Murine Organotypic Hippocampal Slice Cultures.PubMed 30871175 DOI 10.3390/ijms20061266
973	THC modulates TRPV1; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: TRPV1 channel activity, desensitization, binding, signaling, or pharmacology).	Pharmacological actions of cannabinoids.PubMed 16596770 DOI 10.1007/3-540-26573-2_1
978	CBD modulates TRPV1; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV1 channel activity, desensitization, binding, signaling, or pharmacology).	Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.PubMed 37199723 DOI 10.7554/elife.86166
980	Endocannabinoids modulates TRPV1; evidence class: insufficient (population or model: Animal model mentioned; study design: Narrative or expert review; outcome measure: TRPV1 channel activity, desensitization, binding, signaling, or pharmacology).	Endocannabinoid signaling in microglia.PubMed 36222019 DOI 10.1002/glia.24281
991	CBD modulates TRPV2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV2 channel activity, binding, signaling, or pharmacology).	Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.PubMed 37199723 DOI 10.7554/elife.86166
1001	CBD modulates TRPV2; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV2 channel activity, binding, signaling, or pharmacology).	Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.PubMed 36747846 DOI 10.1101/2023.01.27.525817
1009	CBD modulates TRPV3; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV3 channel activity, binding, signaling, dermatology-relevant mechanism, or pharmacology).	Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.PubMed 37199723 DOI 10.7554/elife.86166
1010	CBD modulates TRPV3; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV3 channel activity, binding, signaling, dermatology-relevant mechanism, or pharmacology).	Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.PubMed 36747846 DOI 10.1101/2023.01.27.525817
1014	Cannabinoids modulates TRPV3; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Systematic review; outcome measure: TRPV3 channel activity, binding, signaling, dermatology-relevant mechanism, or pharmacology).	A Systematic Review of Plant-Derived Natural Compounds for Anxiety Disorders.PubMed 26845556 DOI 10.2174/1568026616666160204121039
1026	Cannabinoids modulates TRPV4; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: TRPV4 channel activity, binding, signaling, or pharmacology).	Peripheral cannabinoid receptor activation attenuates frostbite-induced chronic pain via modulation of TRP channels, neuroinflammation, and autophagy.PubMed 41802611 DOI 10.1016/j.freeradbiomed.2026.02.059
1046	CBD modulates TRPA1; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: TRPA1 channel activity, desensitization, binding, signaling, or pharmacology).	Cannabidiol (CBD): a killer for inflammatory rheumatoid arthritis synovial fibroblasts.PubMed 32873774 DOI 10.1038/s41419-020-02892-1
1102	OEA studied for OEA biology, receptor pharmacology, feeding, metabolism, physiology, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: OEA biology, receptor pharmacology, feeding, metabolism, physiology, or safety-relevant mechanisms).	GPR119 Is a Potent Regulator of Human Sebocyte Biology.PubMed 32142797 DOI 10.1016/j.jid.2020.02.011
1106	PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms).	Palmitoylethanolamide dampens neuroinflammation and anxiety-like behavior in obese mice.PubMed 35176443 DOI 10.1016/j.bbi.2022.02.008
1107	PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms).	Mechanisms and clinical applications of palmitoylethanolamide (PEA) in the treatment of neuropathic pain.PubMed 39714723 DOI 10.1007/s10787-024-01623-8
1109	PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Cellular or in vitro model mentioned; study design: Cellular or in vitro study; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms).	Palmitoylethanolamide: A Multifunctional Molecule for Neuroprotection, Chronic Pain, and Immune Modulation.PubMed 40563990 DOI 10.3390/biomedicines13061271
1111	PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms).	Gut-brain Axis: Role of Lipids in the Regulation of Inflammation, Pain and CNS Diseases.PubMed 28215162 DOI 10.2174/0929867324666170216113756
1112	PEA studied for PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms; evidence class: insufficient (population or model: Human participants or patients mentioned; study design: Narrative or expert review; outcome measure: PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms).	Cannabimimetic fatty acid derivatives in cancer and inflammation.PubMed 10785541 DOI 10.1016/s0090-6980(00
1134	NADA studied for NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms).	The endocannabinoid/endovanilloid N-arachidonoyl dopamine (NADA) and synthetic cannabinoid WIN55,212-2 abate the inflammatory activation of human endothelial cells.PubMed 24644287 DOI 10.1074/jbc.m113.536953
1142	NADA studied for NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Human participants or patients mentioned; study design: Cellular or in vitro study; outcome measure: NADA biology, receptor or TRP-channel pharmacology, metabolism, physiology, or safety-relevant mechanisms).	Anti-inflammatory dopamine- and serotonin-based endocannabinoid epoxides reciprocally regulate cannabinoid receptors and the TRPV1 channel.PubMed 33568652 DOI 10.1038/s41467-021-20946-6
1168	DHEA / synaptamide studied for DHEA/synaptamide biology, receptor or signaling mechanisms, metabolism, physiology, or safety-relevant mechanisms; evidence class: mechanistic or pharmacological (population or model: Animal model mentioned; study design: Animal study; outcome measure: DHEA/synaptamide biology, receptor or signaling mechanisms, metabolism, physiology, or safety-relevant mechanisms).	N-Docosahexaenoylethanolamine ameliorates LPS-induced neuroinflammation via cAMP/PKA-dependent signaling.PubMed 27809877 DOI 10.1186/s12974-016-0751-z
1188	SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: insufficient (population or model: Cellular or in vitro model mentioned; study design: Narrative or expert review; outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms).	Roles of fatty acid ethanolamides (FAE) in traumatic and ischemic brain injury.PubMed 24874648 DOI 10.1016/j.phrs.2014.05.009
1194	SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: preclinical (population or model: Human participants or patients mentioned; study design: Animal study; outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms).	N-Stearoylethanolamine Exerts Cardioprotective Effects in Old Rats.PubMed 38279735 DOI 10.2174/0118746098275323231226073348
1199	SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: preclinical (population or model: Animal model mentioned; study design: Animal study; outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms).	[Anti-inflammatory effect of N-stearoylethanolamine in experimental burn injury in rats].PubMed 19873884
1201	SEA studied for SEA biology, metabolism, physiology, or safety-relevant mechanisms; evidence class: preclinical (outcome measure: SEA biology, metabolism, physiology, or safety-relevant mechanisms).	Exploring the Utility of Hair Endocannabinoids for Monitoring Homeostasis in Bonobos.PubMed 33434116 DOI 10.1086/712658

Appetite and metabolic outcomes
CB1
CB2
CBC
CBD
CBDA
CBG
CBN
Cannabinoids
DHEA / synaptamide
Endocannabinoids
GPR18
GPR55
Inflammation-related outcomes
NADA
OEA
PEA
Pain-related outcomes
SEA
Skin and inflammatory dermatology

References

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[Cannabis: Effects in the Central Nervous System. Therapeutic, societal and legal consequences].PubMed 27428345
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Pharmacological actions of cannabinoids.PubMed 16596770 DOI 10.1007/3-540-26573-2_1
Anti-Inflammatory Effects of Minor Cannabinoids CBC, THCV, and CBN in Human Macrophages.PubMed 37764262 DOI 10.3390/molecules28186487
Cannabinol modulates the endocannabinoid system and shows TRPV1-mediated anti-inflammatory properties in human keratinocytes.PubMed 39275884 DOI 10.1002/biof.2122
Phytocannabinoids: Exploring Pharmacological Profiles and Their Impact on Therapeutical Use.PubMed 38673788 DOI 10.3390/ijms25084204
Cannabinoids, inflammation, and fibrosis.PubMed 27435265 DOI 10.1096/fj.201600646r
Phytocannabinoids as anti-inflammatory agents: Synergistic effects when combined with Cannabis sativa L. matrices.PubMed 41478536 DOI 10.1016/j.jep.2025.121134
Preclinical evaluation of cannabidiolic acid as a neuroprotective agent in TDP-43 transgenic mice, an experimental model of amyotrophic lateral sclerosis.PubMed 40580876 DOI 10.1016/j.biopha.2025.118288
Distinct Interactions of Cannabinol and Its Cytochrome P450-Generated Metabolites with Receptors and Sensory Neurons.PubMed 40568800 DOI 10.1021/acs.jmedchem.5c00938
Cannabinoids in autoimmune diseases: mechanistic insights and translational challenges.PubMed 42105814 DOI 10.1016/j.bcp.2026.118032
Cannabigerol attenuates liver fibrosis via AMPK activation: Regulation of lipid metabolism, inflammation, and hepatic stellate cell activation.PubMed 40818359 DOI 10.1016/j.biopha.2025.118463
Medical Cannabis Activity Against Inflammation: Active Compounds and Modes of Action.PubMed 35614947 DOI 10.3389/fphar.2022.908198
Cannabigerol Alleviates Liver Damage in Metabolic Dysfunction-Associated Steatohepatitis Female Mice via Inhibition of Transforming Growth Factor Beta 1.PubMed 40362835 DOI 10.3390/nu17091524
In Vitro and Clinical Evaluation of Cannabigerol (CBG) Produced via Yeast Biosynthesis: A Cannabinoid with a Broad Range of Anti-Inflammatory and Skin Health-Boosting Properties.PubMed 35056807 DOI 10.3390/molecules27020491
Anti-Inflammatory Effects of Cannabigerol In Vitro and In Vivo Are Mediated Through the JAK/STAT/NFκB Signaling Pathway.PubMed 39851511 DOI 10.3390/cells14020083
Differential effectiveness of selected non-psychotropic phytocannabinoids on human sebocyte functions implicates their introduction in dry/seborrhoeic skin and acne treatment.PubMed 27094344 DOI 10.1111/exd.13042
Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.PubMed 39769302 DOI 10.3390/ijms252413539
Selected phytocannabinoids inhibit SN-38- and cytokine-evoked increases in epithelial permeability and improve intestinal barrier function in vitro.PubMed 38950639 DOI 10.1016/j.tiv.2024.105888
Targeting the antioxidant, antimicrobial and anti-inflammatory activity of non-psychotropic Cannabis sativa L.: a comparison with chemotype V.PubMed 41121423 DOI 10.1186/s42238-025-00336-1
Tetrahydrocannabivarin (THCV) Protects Adipose-Derived Mesenchymal Stem Cells (ASC) against Endoplasmic Reticulum Stress Development and Reduces Inflammation during Adipogenesis.PubMed 37108282 DOI 10.3390/ijms24087120
Phytocannabinoids Act Synergistically with Non-Steroidal Anti-Inflammatory Drugs Reducing Inflammation in 2D and 3D In Vitro Models.PubMed 36559009 DOI 10.3390/ph15121559
Cannabinoid receptor 1 antagonist genistein attenuates marijuana-induced vascular inflammation.PubMed 35489334 DOI 10.1016/j.cell.2022.04.005
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Cannabinoid-based therapy as a future for joint degeneration. Focus on the role of CB2 receptor in the arthritis progression and pain: an updated review.PubMed 34050525 DOI 10.1007/s43440-021-00270-y
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Therapeutic potential of cannabinoid receptor 2 in the treatment of diabetes mellitus and its complications.PubMed 31461639 DOI 10.1016/j.ejphar.2019.172628
The endocannabinoid system: physiology and pharmacology.PubMed 15550444 DOI 10.1093/alcalc/agh110
Crystal Structure of the Human Cannabinoid Receptor CB2.PubMed 30639103 DOI 10.1016/j.cell.2018.12.011
Cannabinoid Receptor Type 2 Agonist Reduces Morphine Tolerance via Mitogen Activated Protein Kinase Phosphatase Induction and Mitogen Activated Protein Kinase Dephosphorylation.PubMed 34774714 DOI 10.1016/j.neuroscience.2021.11.007
Cannabinoid CB2 receptor orthologues; in vitro function and perspectives for preclinical to clinical translation.PubMed 37349984 DOI 10.1111/bph.16172
Type 2 cannabinoid receptor expression on microglial cells regulates neuroinflammation during graft-versus-host disease.PubMed 38662453 DOI 10.1172/jci175205
Cannabinoid CB2 receptors enhance high-fat diet evoked peripheral neuroinflammation.PubMed 39173999 DOI 10.1016/j.lfs.2024.123002
Cannabinoid receptor 2 evolutionary gene loss makes parrots more susceptible to neuroinflammation.PubMed 36475439 DOI 10.1098/rspb.2022.1941
Cannabinoid CB2 receptors modulate alcohol induced behavior, and neuro-immune dysregulation in mice.PubMed 37061199 DOI 10.1016/j.bbr.2023.114439
The cannabinoid CB2 receptor as a target for inflammation-dependent neurodegeneration.PubMed 18615177 DOI 10.2174/157015907780866884
Cannabinoid receptor 2 activation mitigates lipopolysaccharide-induced neuroinflammation and sickness behavior in mice.PubMed 30666359 DOI 10.1007/s00213-019-5166-y
Up-regulation of immunomodulatory effects of mouse bone-marrow derived mesenchymal stem cells by tetrahydrocannabinol pre-treatment involving cannabinoid receptor CB2.PubMed 26824325 DOI 10.18632/oncotarget.7042
Enantiomeric Agonists of the Type 2 Cannabinoid Receptor Reduce Retinal Damage during Proliferative Vitreoretinopathy and Inhibit Hyperactive Microglia In Vitro.PubMed 38751621 DOI 10.1021/acsptsci.4c00014
The development of cannabinoid CBII receptor agonists for the treatment of central neuropathies.PubMed 20236042 DOI 10.2174/187152410790780145
Induction of CB2 receptor expression in the rat spinal cord of neuropathic but not inflammatory chronic pain models.PubMed 12823482 DOI 10.1046/j.1460-9568.2003.02704.x
Cannabidiol-rich non-psychotropic Cannabis sativa L. oils attenuate peripheral neuropathy symptoms by regulation of CB2-mediated microglial neuroinflammation.PubMed 36583304 DOI 10.1002/ptr.7710
Effects of CB2 Receptor Modulation on Macrophage Polarization in Pediatric Inflammatory Bowel Disease.PubMed 40332343 DOI 10.3390/ijms26083720
CB2 cannabinoid receptor-specific therapeutic antibody agonists for treatment of chemotherapy-induced peripheral neuropathy.PubMed 41383775 DOI 10.1101/2025.11.26.690750
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Cannabinoid Receptor 2 Activating Antibodies: A Promising Therapeutic Strategy for Macrophage-Driven Fibro-Inflammatory Diseases.PubMed 40791361 DOI 10.1101/2025.07.11.664477
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Cannabinoid receptor type 2 agonist GP1a attenuates macrophage activation induced by M. bovis-BCG by inhibiting NF-κB signaling.PubMed 39538989 DOI 10.1093/jleuko/qiae246
Cannabinoid receptor 2 activating antibodies: A promising therapeutic strategy for macrophage-driven fibro-inflammatory diseases.PubMed 41740200 DOI 10.1016/j.molpha.2026.100102
The Endocannabinoid System of Animals.PubMed 31527410 DOI 10.3390/ani9090686
Epilepsy, neuroinflammation and cannabidiol What do we know thus far?PubMed 41560741 DOI 10.3389/fphar.2025.1749260
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Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.PubMed 37199723 DOI 10.7554/elife.86166
Endocannabinoid signaling in microglia.PubMed 36222019 DOI 10.1002/glia.24281
Cannabidiol sensitizes TRPV2 channels to activation by 2-APB.PubMed 36747846 DOI 10.1101/2023.01.27.525817
A Systematic Review of Plant-Derived Natural Compounds for Anxiety Disorders.PubMed 26845556 DOI 10.2174/1568026616666160204121039
Peripheral cannabinoid receptor activation attenuates frostbite-induced chronic pain via modulation of TRP channels, neuroinflammation, and autophagy.PubMed 41802611 DOI 10.1016/j.freeradbiomed.2026.02.059
Cannabidiol (CBD): a killer for inflammatory rheumatoid arthritis synovial fibroblasts.PubMed 32873774 DOI 10.1038/s41419-020-02892-1
GPR119 Is a Potent Regulator of Human Sebocyte Biology.PubMed 32142797 DOI 10.1016/j.jid.2020.02.011
Mechanisms and clinical applications of palmitoylethanolamide (PEA) in the treatment of neuropathic pain.PubMed 39714723 DOI 10.1007/s10787-024-01623-8
Palmitoylethanolamide: A Multifunctional Molecule for Neuroprotection, Chronic Pain, and Immune Modulation.PubMed 40563990 DOI 10.3390/biomedicines13061271
Gut-brain Axis: Role of Lipids in the Regulation of Inflammation, Pain and CNS Diseases.PubMed 28215162 DOI 10.2174/0929867324666170216113756
Cannabimimetic fatty acid derivatives in cancer and inflammation.PubMed 10785541 DOI 10.1016/s0090-6980(00
The endocannabinoid/endovanilloid N-arachidonoyl dopamine (NADA) and synthetic cannabinoid WIN55,212-2 abate the inflammatory activation of human endothelial cells.PubMed 24644287 DOI 10.1074/jbc.m113.536953
Anti-inflammatory dopamine- and serotonin-based endocannabinoid epoxides reciprocally regulate cannabinoid receptors and the TRPV1 channel.PubMed 33568652 DOI 10.1038/s41467-021-20946-6
N-Docosahexaenoylethanolamine ameliorates LPS-induced neuroinflammation via cAMP/PKA-dependent signaling.PubMed 27809877 DOI 10.1186/s12974-016-0751-z
Roles of fatty acid ethanolamides (FAE) in traumatic and ischemic brain injury.PubMed 24874648 DOI 10.1016/j.phrs.2014.05.009
N-Stearoylethanolamine Exerts Cardioprotective Effects in Old Rats.PubMed 38279735 DOI 10.2174/0118746098275323231226073348
[Anti-inflammatory effect of N-stearoylethanolamine in experimental burn injury in rats].PubMed 19873884
Exploring the Utility of Hair Endocannabinoids for Monitoring Homeostasis in Bonobos.PubMed 33434116 DOI 10.1086/712658

Immune modulation has research behind it, but the bucket matters.

What the Immune modulation research is usually about

CB2

Skin and inflammatory dermatology

PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms

CB1

CB2

Inflammation-related outcomes

Evidence buckets before the source table

Keep reading around this topic

Read safety context beside the research guide.

Immune modulation Evidence Review: the long-form source walk-through

Start with the research question

Where this page has the most source density

Bucket chapters: what the literature is circling

CB2

Skin and inflammatory dermatology

PEA biology, receptor or target pharmacology, inflammation, pain-related mechanisms, or safety-relevant mechanisms

CB1

CB2

Inflammation-related outcomes

Safety, risk, adverse events, and formulation concerns

SEA biology, metabolism, physiology, or safety-relevant mechanisms

Human evidence, mechanisms, and safety are different lanes

What this does and does not mean

How to use the source table

Source-reading checklist for Immune modulation

Immune modulation source-by-source reading notes

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References