Kidney and the endocannabinoid system
Blood flow, salt and water balance, and excretion.
Blood flow, salt and water balance, and excretion. Where the cannabinoid receptors CB1 and CB2 sit in this region, what they do there, and what is actually known about CBD; at three levels for Everyone, Students and Experts, with sources.
Kidneys and urinary tractCB1 very low · CB2 very low (Human Protein Atlas)Last updated:
What's on this page?
Interactive 3D · real anatomy and real data
Where in your body are the cannabinoid receptors?
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Regions
How to read it Choose a region, or tap a glowing point on the map.
- Solid light is the CB1 receptor, a ring is CB2. Each region has its own color; the color only tells regions apart.
- The strength of the light is the receptor gene level measured in human tissue (Human Protein Atlas). That is why the liver’s point is dim: a healthy liver has few receptors.
- With the layer selector above you can also see other receptors, the enzymes that make and break down endocannabinoids, and the liver enzymes that break down CBD and THC.
- Every piece of information shows its source and the type of evidence (human, animal, cell). You can change the reading level above.
- Drag to rotate. Use the + and − buttons to zoom; on a computer, Ctrl or ⌘ with the scroll wheel, on a phone, two fingers.
Kidney: RNA level of the receptor gene in human tissue (tissue consensus data). RNA for both receptors is very low across the whole organ; CB1 is concentrated in certain tubule cells (human tissue study). Human Protein AtlasHuman tissue
| Receptor | Gene | RNA (nTPM) | Level |
|---|---|---|---|
| CB1 | CNR1 | 0.6 | very low |
| CB2 | CNR2 | 0 | very low |
What does it do there?
Across the kidney as a whole, RNA for both receptors is measured as very low, but CB1 is concentrated in certain cells. In the human kidney, CB1 was found clearly in the cells of the first coiled tubule (proximal tubule), where 70–80% of the filtered fluid is reabsorbed, and of the second coiled tubule (distal tubule), as well as in the intercalated cells of the collecting ducts; the distribution was similar in adult and fetal kidney. The same study did not find CB2; another study, however, reported that CB2 was reduced in kidney samples from people with advanced diabetic kidney disease. So findings on CB2 in the kidney do not agree. According to a review, CB1 is the leading endocannabinoid receptor in the kidney. Human Protein AtlasHuman tissueSampaio 2015Cell / labLarrinaga 2010Human tissueRein 2024AnimalBarutta 2011Human tissueAnimalCell / labJenkin 2013Cell / labAnimalArceri 2023Review
The kidney is rich in anandamide and the enzymes that break it down; according to a review, this system may regulate blood flow in the kidney and the reabsorption of salt and water in the tubules. In rats, anandamide widened the kidney's small arteries (arterioles), and CB1 played a role in this: blood flow to the kidney increased, the filtration rate decreased, and blood pressure did not change. In mice, anandamide given into the inner part of the kidney (medulla) increased urine volume and salt excretion; a substance that blocks CB1 abolished this effect. In mice, however, the large amounts of dilute urine caused by a synthetic CB1 stimulant fit with a disruption not of the kidney but of the water-retaining hormone signal from the brain (vasopressin). Ritter 2016ReviewDeutsch 1997AnimalCell / labKoura 2004AnimalRitter 2012AnimalRitter 2021AnimalLi and Wang 2006AnimalSampaio 2015Cell / labRein 2024Animal
In kidney diseases with a buildup of scar tissue (fibrosis), CB1 rose markedly in kidney samples from people with IgA nephropathy, diabetes and acute interstitial nephritis. In mouse and rat models of diabetes and obesity, increased CB1 signaling in the kidney contributed to inflammation, scar tissue and damage to the filter cells (podocytes); stimulating CB2 in the kidney, on the other hand, worked in the direction of reducing this damage. In cultured human filter cells, stimulating CB1 reduced proteins specific to these cells (nephrin, podocin); blocking CB1 prevented this. In mice, deleting CB1 only in the proximal tubule markedly eased obesity-related fat buildup and dysfunction in the kidney. Lecru 2015Human tissueAnimalCell / labTam 2016ReviewBarutta 2010AnimalJourdan 2014AnimalCell / labUdi 2017AnimalCell / labBarutta 2011Human tissueAnimalCell / lab
Student level: terms and cell types
In HPA tissue data, the kidney shows CNR1 at 0.6 and CNR2 at 0 nTPM. The proximal tubule is the part of the nephron where 70–80% of the filtrate is reabsorbed. In adult and fetal human kidney, RT-PCR showed CB1 mRNA and no CB2 mRNA; on western blot and immunohistochemistry, CB1 protein was clearly positive in proximal and distal convoluted tubule cells and in the intercalated cells of the collecting duct, and CB2 protein was negative in all samples. In mice, too, CB1 antibodies labeled cells in the collecting duct that did not carry AQP2, most likely intercalated cells. By contrast, in biopsies of advanced diabetic nephropathy, CB2 was reported to be reduced and podocytes to carry CB2; a human proximal tubule cell line (HK-2) had CB2, which fell with high albumin. According to a review, CB1 is the more prominent endocannabinoid receptor in the kidney. Human Protein AtlasHuman tissueSampaio 2015Cell / labLarrinaga 2010Human tissueRein 2024AnimalBarutta 2011Human tissueAnimalCell / labJenkin 2013Cell / labAnimalArceri 2023Review
The kidney is rich in AEA and AEA-degrading enzymes; according to a review, the system may play a role in renal blood flow and hemodynamics and in tubular sodium and fluid reabsorption. In rats, AEA dilated in vitro perfused juxtamedullary afferent arterioles; the effect was blocked by NO synthase inhibition (L-NAME) and the CB1 antagonist SR141716A. In another rat study, AEA dilated the afferent arteriole through CB1 and non-CB1 receptors, and the efferent arteriole more through CB1; as a result, GFR fell, renal blood flow rose, and mean arterial pressure did not change. In mice, AEA is richer in the medulla than in the cortex, FAAH is higher in the cortex and COX-2 in the medulla; AEA given into the medulla increased urine volume and Na⁺ and K⁺ excretion, and this effect was blocked by the selective COX-2 inhibitor celecoxib. The effect on urine and salt excretion of AEA given into the outer medulla was blocked by rimonabant; CB1 was shown in the thick ascending limb (TAL), and cannabinoids reduced Na⁺ efflux in TAL cells by suppressing Na⁺-K⁺-ATPase. In a pig kidney tubule cell line (LLC-PK1), too, CB1 and TRPV1 regulated Na⁺/K⁺-ATPase activity. In rats, however, the diuretic effect of methanandamide given into the medulla was not abolished by a CB1 or TRPV1 antagonist but was abolished by renal denervation. In mice, the CB1 agonist WIN55,212-2 produced acute diabetes insipidus with dilute urine; when given together with desmopressin, urine was concentrated to the maximum level, which fits with central rather than nephrogenic diabetes insipidus. Ritter 2016ReviewDeutsch 1997AnimalCell / labKoura 2004AnimalRitter 2012AnimalRitter 2021AnimalLi and Wang 2006AnimalSampaio 2015Cell / labRein 2024Animal
CB1 expression rose markedly in biopsies of IgA nephropathy, diabetes and acute interstitial nephritis. In the mouse unilateral ureteral obstruction (UUO) model, CB1 was among the most upregulated genes, 2-AG rose significantly in the fibrotic kidney, and genetic or pharmacological inactivation of CB1 markedly reduced fibrosis; CB1 increased in myofibroblasts with TGF-β1 stimulation. In diabetic mice, CB1 rose in the glomerulus, mainly in podocytes; CB1 blockade reduced albuminuria and prevented the loss of nephrin, podocin and ZO-1. In ZDF rats, glomerular CB1 increased; in cultured human podocytes, the CB1 agonist ACEA, angiotensin II or high glucose increased CB1 and desmin expression and reduced podocin and nephrin; CB1 blockade or CNR1 silencing prevented this. Proximal-tubule-specific CB1 deletion did not prevent obesity in mice but markedly eased fat accumulation, dysfunction, inflammation and fibrosis in the kidney. In diabetic mice, the CB2 agonist AM1241 reduced albuminuria and podocyte protein loss. According to a review, in these rodent models CB1 contributes to oxidative stress, inflammation and fibrosis, while stimulating renal CB2 reduces the harmful effects. Lecru 2015Human tissueAnimalCell / labTam 2016ReviewBarutta 2010AnimalJourdan 2014AnimalCell / labUdi 2017AnimalCell / labBarutta 2011Human tissueAnimalCell / lab
Expert level: method notes and numbers
Kidney: RNA level of the receptor gene in human tissue (tissue consensus data). RNA for both receptors is very low across the whole organ; CB1 is concentrated in certain tubule cells (human tissue study). Human Protein AtlasHuman tissue
Method note
Location. Larrinaga 2010: adult and fetal human kidney; RT-PCR, western blot, immunohistochemistry; sample size not in the abstract. Barutta 2011: biopsies of advanced diabetic nephropathy, early experimental diabetes (mouse) and cultured podocytes (species not in the abstract); the CB2 agonist AM1241 for 14 weeks. Jenkin 2013: HK-2 cells and diabetic rat kidney (CB2 did not change in rat kidney lysate). Human CB2 findings conflict (Larrinaga: protein negative in all samples; Barutta: reduced in biopsies, meaning present); antibody and sample differences are not discussed in the abstracts. Lecru 2015: UUO in mice, microarray; the quantitative value of the increase in human biopsies is not in the abstract. Larrinaga 2010Human tissueBarutta 2011Human tissueAnimalCell / labJenkin 2013Cell / labAnimalLecru 2015Human tissueAnimalCell / lab
Blood flow and salt and water. Koura 2004: Sprague-Dawley rat, anandamide 15, 150 and 1500 pmol/kg; in the presence of AM251, only 15 pmol/kg increased GFR and RBF; blood-perfused juxtamedullary nephron technique; CB1 mRNA in the afferent arteriole, and on immunohistochemistry in the afferent and efferent arterioles. Deutsch 1997: rat kidney homogenate, renal endothelial and mesangial cells (CB1 mRNA in endothelium, CB1 and CB2 mRNA in mesangial cells); anandamide 1 µM. Ritter 2012: mouse, intramedullary AEA 15–60 nmol/kg/min, little effect on mean arterial pressure. Ritter 2021: isolated mouse TAL tubules. Li and Wang 2006: Wistar rat, intramedullary methanandamide; urine flow increased by 64% on the same side and 62% on the opposite side, sodium excretion did not change. Rein 2024: mouse, WIN55,212-2. The mechanism of the increase in urine differs between studies (CB1, COX-2 and prostamides, a renal nerve reflex, central vasopressin). Koura 2004AnimalDeutsch 1997AnimalCell / labRitter 2012AnimalRitter 2021AnimalLi and Wang 2006AnimalRein 2024Animal
CBD, THC and kidney function. The measured GFR study in the label: 39 healthy people, 7.5 mg/kg twice daily for 7 days in the study, iohexol clearance; in the same study, estimated GFR based on serum creatinine and cystatin C fell by 5%, and 24-hour urine creatinine clearance by 10%. The FDA label has no renal impairment subsection; EMA product information 5.2: in mild (CLcr 50–80), moderate (30 to <50) and severe (<30 mL/min) renal impairment, Cmax and AUC did not change after a single 200 mg dose; end-stage kidney disease was not studied. Tayo 2020: n = 8 in each group, 48-hour sampling; geometric mean ratio of Cmax 0.68–1.35. Sønderskov 2025: randomized and open-label; single dose of oromucosal spray (5.4 mg THC + 5 mg CBD); 29 people with stage 4–5 chronic kidney disease, 20 healthy; median THC AUC 2.76 in healthy people, 4.16 in stage 4, 4.31 h·ng/mL in stage 5; dizziness score at 1.5 hours higher in the patient groups. The difference between the two human studies may relate to dose, product (pure CBD vs. THC + CBD) and patient group; the abstracts do not discuss this. Pan 2009: mouse, cisplatin, assessment at hour 72; CBD dose not in the abstract. Didik 2025: immortalized human podocytes; concentrations and comparison with blood levels not in the abstract. Epidiolex label (FDA)Official drug labelEpidyolex product information (EMA)Official drug labelTayo 2020Human · clinical studySønderskov 2025Human · clinical studyPan 2009AnimalDidik 2025Cell / lab
The adrenal gland is a separate region; here the two kidneys light up together.
What is known about CBD?
The approved CBD medicine leaves the body mostly in the feces; excretion through the kidneys is a minor route. According to the label of an oral THC medicine, by contrast, about half of a labeled dose was found in the feces and 10–15% in the urine within three days; even after a single dose, breakdown products were measured at low levels in urine and feces for longer than five weeks. The approved CBD medicine can raise blood creatinine by about 10% within the first two weeks after starting; in healthy adults this rise reversed. In a separate study in healthy volunteers, the kidney's filtration rate was measured directly and did not change; according to the label, the rise in creatinine is not caused by reduced filtration. Epidiolex label (FDA)Official drug labelEpidyolex product information (EMA)Official drug labelOral THC capsule label (FDA)Official drug label
Two small studies in people with reduced kidney function gave different results. In 24 people with mild, moderate or severe kidney impairment, after a single dose of the approved CBD medicine there was no significant difference from healthy people in blood levels of CBD and its breakdown products, and no notable CBD was measured in urine; people with end-stage kidney disease were not studied. In 29 people with advanced (stage 4 and 5) chronic kidney disease, however, after a single dose of an oromucosal spray containing THC and CBD, total exposure to THC, CBD and their breakdown products was higher than in healthy people; the differences between individuals were large. In the laboratory, CBD reduced the kidney damage caused by a cancer drug (cisplatin) in mice; in immortalized human filter cells, on the other hand, long-term CBD exposure increased intracellular calcium in a dose-dependent way and led to cell damage and death. These last two findings are animal and cell experiments. Tayo 2020Human · clinical studyEpidyolex product information (EMA)Official drug labelSønderskov 2025Human · clinical studyPan 2009AnimalDidik 2025Cell / lab
No effect found Insufficient evidence
In the guide: Diabetes and CBD
Research has not shown that CBD helps with this. If you are considering CBD, you can talk with your doctor or pharmacist, including about the medicines you take.
Check drug interactions · Safety
Which receptor and enzyme genes are read in this region?
Values in this region for the genes in the map's layer selector: besides CB1 and CB2, the other targets of cannabinoids, the enzymes that make and break down endocannabinoids, and the liver enzymes that break down CBD and THC.
| Gene | What does it do? | Here | Tissue where it is read the most |
|---|---|---|---|
| Receptors | |||
| CB1 CNR1 | Cannabinoid receptor | 0.6 | cerebral cortex (18.6) |
| CB2 CNR2 | Cannabinoid receptor | 0.0 | spleen (8.4) |
| TRPV1 | Heat and chili pepper sensor · ion channel | 7.2 | liver (21.8) |
| GPR55 | Long an "orphan" receptor · in the cell membrane | 0.0 | testis (4.4) |
| PPARγ PPARG | Gene switch · in the cell nucleus | 14.7 | adipose tissue (153.2) |
| 5-HT1A HTR1A | Serotonin receptor · in the cell membrane | 0.0 | hippocampal formation (6.1) |
| TRPV2 | Relative of TRPV1 · ion channel | 4.6 | lung (29.5) |
| Endocannabinoid enzymes | |||
| NAPE-PLD NAPEPLD | Makes anandamide | 13.9 | kidney (13.9) |
| FAAH | Breaks down anandamide | 20.2 | testis (46.0) |
| DAGLα DAGLA | Makes 2-AG | 1.4 | cerebral cortex (12.3) |
| DAGLβ DAGLB | Makes 2-AG | 4.7 | adrenal gland (15.2) |
| MGL MGLL | Breaks down 2-AG | 72.1 | adipose tissue (161.3) |
| ABHD6 | Breaks down 2-AG | 33.2 | liver (60.7) |
| ABHD12 | Breaks down 2-AG | 42.1 | epididymis (125.2) |
| Enzymes that break down CBD and THC | |||
| CYP3A4 | Breaks down CBD and THC | 4.2 | liver (3,367.1) |
| CYP2C19 | Breaks down CBD | 0.0 | liver (178.0) |
| CYP2C9 | Breaks down THC | 2.1 | liver (1,607.6) |
RNA level shows how much the gene is read in this tissue; it does not directly show the amount of protein or how active an enzyme is. Human Protein Atlas (layers)Human tissue
Identifiers and citation
- Kidney
- Kidney · MeSH D007668 · UBERON 0002113 · Wikidata Q9377
- Receptors
- CB1 (CNR1, UniProt P21554) · CB2 (CNR2, UniProt P34972)
How to cite: cbd.school editorial team. Kidney and the endocannabinoid system. Endocannabinoid system 3D map, cbd.school. Last updated October 24, 2026. https://cbd.school/learn/endocannabinoid-system-map/bobrek/
The body model is derived from BodyParts3D (DBCLS, CC BY 4.0) and Z-Anatomy (CC BY-SA 4.0); receptor levels from Human Protein Atlas v25 (CC BY 4.0). The map, text and downloaded images are CC BY-SA 4.0. An independent expert review has not been done yet. All licenses
Other pages of the map
Overview: what the endocannabinoid system is, the feedback brake at the synapse, CBD's targets, lesson mode, data and licenses.
Sources
Show 26 references
- Human Protein Atlas v25: tissue RNA consensus data (rna_tissue_consensus.tsv, HPA and GTEx, nTPM) and brain region data (rna_brain_region_hpa.tsv, nTPM), CNR1 (ENSG00000118432) and CNR2 (ENSG00000188822); v25.proteinatlas.org, file date November 6, 2025, downloaded October 24, 2026. Uhlén M et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419. License CC BY 4.0. PMID 25613900 · doi:10.1126/science.1260419 Human tissue
- Sampaio LS, Taveira Da Silva R, Lima D et al. The endocannabinoid system in renal cells: regulation of Na(+) transport by CB1 receptors through distinct cell signalling pathways. Br J Pharmacol. 2015;172(19):4615-25. PMID 25537261 · doi:10.1111/bph.13050 Cell / lab
- Larrinaga G, Varona A, Pérez I et al. Expression of cannabinoid receptors in human kidney. Histol Histopathol. 2010;25(9):1133-8. PMID 20607655 · doi:10.14670/HH-25.1133 Human tissue
- Rein JL, Mackie K, Kleyman TR, Satlin LM. Cannabinoid receptor type 1 activation causes a water diuresis by inducing an acute central diabetes insipidus in mice. Am J Physiol Renal Physiol. 2024;326(6):F917-F930. PMID 38634131 · doi:10.1152/ajprenal.00320.2022 Animal
- Barutta F, Piscitelli F, Pinach S et al. Protective role of cannabinoid receptor type 2 in a mouse model of diabetic nephropathy. Diabetes. 2011;60(9):2386-96. PMID 21810593 · doi:10.2337/db10-1809 Human tissueAnimalCell / lab
- Jenkin KA, McAinch AJ, Briffa JF et al. Cannabinoid receptor 2 expression in human proximal tubule cells is regulated by albumin independent of ERK1/2 signaling. Cell Physiol Biochem. 2013;32(5):1309-19. PMID 24280624 · doi:10.1159/000354529 Cell / labAnimal
- Arceri L, Nguyen TK, Gibson S et al. Cannabinoid Signaling in Kidney Disease. Cells. 2023;12(10):1419. PMID 37408253 · doi:10.3390/cells12101419 Review
- Ritter JK, Li G, Xia M, Boini K. Anandamide and its metabolites: what are their roles in the kidney? Front Biosci (Schol Ed). 2016;8(2):264-77. PMID 27100705 · doi:10.2741/s461 Review
- Deutsch DG, Goligorsky MS, Schmid PC et al. Production and physiological actions of anandamide in the vasculature of the rat kidney. J Clin Invest. 1997;100(6):1538-46. PMID 9294122 · doi:10.1172/JCI119677 AnimalCell / lab
- Koura Y, Ichihara A, Tada Y et al. Anandamide decreases glomerular filtration rate through predominant vasodilation of efferent arterioles in rat kidneys. J Am Soc Nephrol. 2004;15(6):1488-94. PMID 15153559 · doi:10.1097/01.asn.0000130561.82631.bc Animal
- Ritter JK, Li C, Xia M et al. Production and actions of the anandamide metabolite prostamide E2 in the renal medulla. J Pharmacol Exp Ther. 2012;342(3):770-9. PMID 22685343 · doi:10.1124/jpet.112.196451 Animal
- Ritter JK, Ahmad A, Mummalaneni S et al. Mechanism of Diuresis and Natriuresis by Cannabinoids: Evidence for Inhibition of Na+-K+-ATPase in Mouse Kidney Thick Ascending Limb Tubules. J Pharmacol Exp Ther. 2021;376(1):1-11. PMID 33087396 · doi:10.1124/jpet.120.000163 Animal
- Li J, Wang DH. Differential mechanisms mediating depressor and diuretic effects of anandamide. J Hypertens. 2006;24(11):2271-6. PMID 17053550 · doi:10.1097/01.hjh.0000249706.42230.a8 Animal
- Lecru L, Desterke C, Grassin-Delyle S et al. Cannabinoid receptor 1 is a major mediator of renal fibrosis. Kidney Int. 2015;88(1):72-84. PMID 25760323 · doi:10.1038/ki.2015.63 Human tissueAnimalCell / lab
- Tam J. The emerging role of the endocannabinoid system in the pathogenesis and treatment of kidney diseases. J Basic Clin Physiol Pharmacol. 2016;27(3):267-76. PMID 26280171 · doi:10.1515/jbcpp-2015-0055 Review
- Barutta F, Corbelli A, Mastrocola R et al. Cannabinoid receptor 1 blockade ameliorates albuminuria in experimental diabetic nephropathy. Diabetes. 2010;59(4):1046-54. PMID 20068137 · doi:10.2337/db09-1336 Animal
- Jourdan T, Szanda G, Rosenberg AZ et al. Overactive cannabinoid 1 receptor in podocytes drives type 2 diabetic nephropathy. Proc Natl Acad Sci U S A. 2014;111(50):E5420-8. PMID 25422468 · doi:10.1073/pnas.1419901111 AnimalCell / lab
- Udi S, Hinden L, Earley B et al. Proximal Tubular Cannabinoid-1 Receptor Regulates Obesity-Induced CKD. J Am Soc Nephrol. 2017;28(12):3518-3532. PMID 28860163 · doi:10.1681/ASN.2016101085 AnimalCell / lab
- EPIDIOLEX (cannabidiol) oral solution, US prescribing information (Jazz Pharmaceuticals), DailyMed setid 8bf27097-4870-43fb-94f0-f3d0871d1eec, SPL version 35 (effective May 29, 2026; on DailyMed June 15, 2026): sections 1, 2.1–2.6, 4, 5.1–5.5, 6.1, 7, 8.1, 8.2, 8.4, 8.5, 8.6, 9.2, 9.3, 11, 12.1, 12.2, 12.3, 13.1, 14.1–14.3, 17. Source Official drug label
- Epidyolex (cannabidiol) 100 mg/mL oral solution, European product information (SmPC; Jazz Pharmaceuticals Ireland Ltd), first authorization September 19, 2019, latest renewal July 26, 2024; sections 4.1, 4.2, 4.3, 4.4, 4.5, 4.6, 4.7, 4.8, 4.9, 5.1, 5.2, 5.3 and 9. Downloaded October 24–26, 2026. Source Official drug label
- Tayo B, Taylor L, Sahebkar F, Morrison G. A Phase I, Open-Label, Parallel-Group, Single-Dose Trial of the Pharmacokinetics, Safety, and Tolerability of Cannabidiol in Subjects with Mild to Severe Renal Impairment. Clin Pharmacokinet. 2020;59(6):747-755. PMID 31802404 · doi:10.1007/s40262-019-00841-6 Human · clinical study
- Sønderskov MB, Khatir DS, Kjærgaard KD et al. Pharmacokinetics and Side Effects of Δ9-Tetrahydrocannabinol and Cannabidiol in Patients with Different Stages of CKD. Kidney Int Rep. 2025;10(3):707-719. PMID 40225360 · doi:10.1016/j.ekir.2024.12.030 Human · clinical study
- Pan H, Mukhopadhyay P, Rajesh M et al. Cannabidiol attenuates cisplatin-induced nephrotoxicity by decreasing oxidative/nitrosative stress, inflammation, and cell death. J Pharmacol Exp Ther. 2009;328(3):708-14. PMID 19074681 · doi:10.1124/jpet.108.147181 Animal
- Didik S, Ahrari A, Taneja K et al. The effects of Cannabidiol on podocytes in vitro. Biochem Biophys Res Commun. 2025;784:152654. PMID 40967036 · doi:10.1016/j.bbrc.2025.152654 Cell / lab
- MARINOL (dronabinol) capsules, US prescribing information, DailyMed setid d0efeeec-640d-43c3-8f0a-d31324a11c68, SPL version 5 (effectiveTime February 14, 2023): sections 5.1, 5.2, 5.3, 5.5, 6.1, 7.1-7.4, 8.1, 8.5, 8.6, 9.2, 9.3, 11, 12.2, 12.3, 12.5, 17. Accessed October 24–26, 2026. Source Official drug label
- Human Protein Atlas v25: tissue RNA consensus data (rna_tissue_consensus.tsv, HPA and GTEx, nTPM), the 17 genes in the map's layer selector: CNR1, CNR2, TRPV1, GPR55, PPARG, HTR1A, TRPV2, NAPEPLD, FAAH, DAGLA, DAGLB, MGLL, ABHD6, ABHD12, CYP3A4, CYP2C19, CYP2C9; v25.proteinatlas.org/download/tsv/rna_tissue_consensus.tsv.zip, downloaded October 24, 2026. Uhlén M et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419. License CC BY 4.0. PMID 25613900 · doi:10.1126/science.1260419 Human tissue