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anandamide (anandamide)

✓ Approved

Yissum · CNR1

What is anandamide?

anandamide is a therapeutic agent developed by Yissum. It is approved for therapeutic indications via unknown.

Drug Profile

Brand Namesanandamide
CompanyYissum
Molecular TargetCNR1, CNR2
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Yissum

Mechanism of Action

Molecular Targets

anandamide acts on 2 molecular targets:

CNR1cannabinoid receptor 1 (CNR, CB1A)
CNR2cannabinoid receptor 2 (CX5, CB-2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

anandamide is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Psychiatric disordersAnorexia nervosa✓ Approved
Psychiatric disordersBulimia nervosa✓ Approved

Related Research Articles

PubMedCannabis and cannabinoid research2026-07-17

Oral Medicinal Cannabis Does Not Alter Plasma Levels of Endocannabinoid-Related N-Acylethanolamines in Fibromyalgia Patients: Findings from a Randomized Placebo-Controlled Trial.

Kurlyandchik Inna I, Van Crugten Jacoba J, Lauche Romy R, Tiralongo Evelin E et al.

Fibromyalgia syndrome (FMS) involves central sensitization and possible endocannabinoid system dysfunction, with medicinal cannabis increasingly investigated as a treatment. We assessed whether chronic oral 1:1 THC:CBD alters plasma endocannabinoid-related N-acylethanolamines (NAEs)-palmitoylethanolamide (PEA), oleoylethanolamide (OEA), and stearoylethanolamide (SEA)-in FMS. In a single-center, randomized, double-blind, placebo-controlled pilot trial, 24 women with FMS were allocated to cannabis oil (10 mg/mL THC and CBD) or placebo. Plasma samples were collected at five timepoints between enrollment and week 12 (over 16 weeks), ∼10-14 h after evening dosing, under fasting conditions. NAEs were quantified by ultra-high-performance liquid chromatography mass spectrometer. Repeated-measures analysis of variance tested main effects of time and group, and their interaction; Greenhouse-Geisser corrections were applied as required. Effect sizes were reported as partial eta squared. ACTRN12623000345684. Twenty-two participants completed the trial (n = 11 per group). Plasma anandamide and 2-AG were below limits of detection and excluded from analyses. Mean plasma PEA, OEA, and SEA remained stable across all timepoints in both groups, with no significant effects of time, group, or time × group interaction (all p > 0.05). Effect sizes were minimal (partial η2 ≤ 0.06), indicating negligible influence of medicinal cannabis on peripheral NAEs. Despite clinical benefits observed with this treatment, peripheral NAEs were unchanged, suggesting they may have limited utility as biomarkers for monitoring therapeutic response to this formulation in FMS. These preliminary findings support investigation of alternative mechanisms, likely driven by central rather than peripheral processes.

PMID 42464432
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PubMedJournal of cannabis research2026-07-17

Cannabichromene (CBC): a comprehensive review of biosynthesis, pharmacology, therapeutic potential, and translational perspectives.

Elbouzidi Amine A, Baraich Abdellah A, Haddou Mounir M, El Hachlafi Naoufal N et al.

Cannabis sativa L. produces a chemically diverse array of over 150 phytocannabinoids, of which cannabichromene (CBC) represents the fourth most abundant constituent in many chemovars, yet remains profoundly underexplored relative to its structural congeners delta-9-tetrahydrocannabinol (THC), cannabidiol (CBD), and its precursor cannabigerol (CBG). Unlike THC, CBC is non-psychoactive and lacks the intoxicating central effects associated with THC, positioning it as a particularly attractive candidate for therapeutic development. This comprehensive review critically examines the current state of knowledge on CBC, encompassing its biosynthetic origin through the polyketide and mevalonate/methylerythritol phosphate pathways, the enzymatic conversion of cannabigerolic acid (CBGA) to cannabichromenic acid (CBCA) by CBC synthase (CBCAS), and subsequent spontaneous and thermally accelerated decarboxylation. We survey the natural occurrence and distribution of CBC across Cannabis chemovars, the genetic and environmental determinants of its accumulation, and the advanced extraction, isolation, and analytical methodologies employed for its characterization. The pharmacokinetic profile of CBC, including absorption, distribution, hepatic metabolism via cytochrome P450 enzymes, and elimination, is discussed in the context of its notably low oral bioavailability. The molecular pharmacology of CBC is examined in depth, highlighting its unique receptor interaction profile: minimal direct engagement with CB1/CB2 cannabinoid receptors, potent agonism at transient receptor potential channels (TRPV1, TRPA1, TRPV3, TRPV4), and indirect modulation of endocannabinoid tone through inhibition of anandamide reuptake. We evaluate the preclinical evidence supporting its anti-inflammatory, analgesic, antimicrobial, anticancer, neuroprotective, antidepressant, and dermatological activities, and contextualize these findings within the entourage effect framework. The toxicological safety profile, drug-drug interaction potential, and regulatory landscape are critically assessed. Finally, we identify translational challenges, including formulation limitations, the absence of clinical trials, and regulatory fragmentation, and propose future research directions encompassing nanotechnology-based delivery systems, synthetic biology platforms for sustainable production, multi-omics integration, and precision medicine approaches. This review establishes CBC as a high-potential but critically understudied phytocannabinoid deserving of accelerated preclinical and clinical investigation.

PMID 42464425
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PubMedNutrients2026-07-15

Gut Microbiota Composition and Plasma Metabolomic Profile Are Associated with Amyloid Pathology and Cognitive Performance in Patients with Mild Cognitive Impairment.

Mora-Ortiz Marina M, Cardelo Magdalena P MP, Porras-Pérez Esther E, Serrán-Jiménez Alejandro A et al.

The gut-brain axis and systemic metabolic dysregulation are increasingly implicated in Alzheimer's disease (AD) pathogenesis. This study aimed to characterize gut microbiota and plasma metabolomic profiles associated with amyloid pathology and cognitive impairment in patients with mild cognitive impairment (MCI). A cross-sectional multi-omics baseline analysis was performed in 47 MCI patients enrolled in a randomized, double-blind, crossover dietary intervention trial (NCT05029765). Gut microbiota composition was assessed by 16S rRNA sequencing (n = 47), and plasma metabolomics by untargeted LC-MS/MS (n = 45 after exclusion of two PCA-defined metabolomic outliers). Patients were stratified according to plasma amyloid-beta 42/40 ratio (BA42/40) and ADAScog11 score, representing complementary biomarkers of amyloid burden and cognitive impairment, respectively. Higher amyloid burden and worse cognitive performance were associated with significant gut microbiota alterations, including increased alpha diversity and distinct beta diversity profiles. Differential abundance analyses consistently showed enrichment of Bacteroides-associated taxa and Akkermansia, alongside depletion of short-chain fatty acid-producing genera such as Faecalibacterium, Blautia, and Phascolarctobacterium. Plasma metabolomics identified a coherent signature associated with elevated BA42/40, characterized by accumulation of secondary bile acid sulfates and depletion of sphingolipids, neuroactive steroids, and anti-inflammatory lipid mediators, including pregnenolone sulfate, resolvin E1, and anandamide. A valid OPLS-DA discriminant model was obtained for BA42/40, whereas no predictive model was achieved for ADAScog11. Critically, this dissociation, characterized by significant microbiota differences but no metabolomic separation for ADAScog11, is itself an informative finding, suggesting that gut microbiota dysbiosis and plasma metabolomic alterations are not equally coupled to both dimensions of MCI pathophysiology. MCI patients with greater amyloid pathology and cognitive impairment exhibited gut microbiota dysbiosis. However, metabolic associations were observed only for BA42/40, but not for ADAScog11. These findings provide a mechanistic framework for evaluating the impact of Mediterranean diet and probiotic interventions in the longitudinal phase of the trial.

PMID 42451200
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PubMedNeuroscience and biobehavioral reviews2026-07-11

The CB1 receptor as a convergence hub linking stress, sleep and appetite regulation: An integrative neurobiological model.

da Rosa Rafaela Aparecida RA, de Pontes Lauro Rodriguez LR, Pablos Alethéia Buosi AB, Kreffta Gabriela S GS

The endocannabinoid system (ECS) plays a central role in the regulation of stress, sleep, feeding behavior, and energy metabolism. This conceptual review proposes a neurobiological model in which cannabinoid type 1 receptor (CB1) signaling acts as a convergence mechanism linking these physiological domains. Evidence from neuroendocrinology, chronobiology, and cannabinoid pharmacology indicates that CB1 signaling participates in the regulation of hypothalamic-pituitary-adrenal (HPA) axis activity, circadian fluctuations in endocannabinoid tone, and neural circuits involved in energy homeostasis, reward processing, and feeding behavior. Stress-related HPA-axis activation modifies the availability of anandamide (AEA) and 2-arachidonoylglycerol (2-AG), thereby influencing stress responsivity and feeding behavior. Similarly, sleep restriction and circadian disruption alter the temporal dynamics of endocannabinoids and are associated with increased hunger, preference for highly palatable foods, and greater metabolic vulnerability. In addition, CB1-modulating ligands such as Δ⁹-tetrahydrocannabinol (Δ⁹-THC), cannabigerol (CBG), and noladin ether may influence food intake through mechanisms dependent on dose, biological context, and cell type, involving proopiomelanocortin (POMC) neurons, β-endorphin signaling, reward circuits, and mitochondrial adaptations related to uncoupling protein 2 (UCP2). Enzymatic regulation of endocannabinoid tone by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), together with individual genetic factors, may further shape susceptibility to metabolic, affective, and sleep-related phenotypes. Collectively, these observations support a model in which CB1 signaling connects stress, sleep, reward, and feeding behavior within the broader endocannabinoidome. This model remains hypothesis-generating and requires prospective translational validation.

PMID 42431566
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PubMedBrain, behavior, and immunity2026-07-11

Neuroimmune lipidome dysregulation in major depressive disorder: A meta-analysis of peripheral endocannabinoid and N-acylethanolamine signaling.

Yaseen Muhammad M, Chen Wei-Jen WJ, Chang Jane Pei-Chen JP, Liu Wen Chun WC et al.

Major depressive disorder (MDD) is a prevalent psychiatric condition characterized by substantial biological heterogeneity. Evidence suggests that the endocannabinoid system (ECS), which regulates stress responses, emotional processing, and neuroimmune signaling, may contribute to depression pathophysiology. However, clinical studies examining circulating endocannabinoids (eCBs) and N-acylethanolamines (NAEs) in MDD have produced inconsistent findings. We therefore conducted a systematic review and meta-analysis to quantify peripheral alterations in eCBs and NAEs in individuals with MDD. Following PRISMA guidelines, case-control and cross-sectional studies comparing circulating levels of eCBs and NAEs between patients with MDD and healthy controls were identified. Standardized mean differences (SMDs) with 95 % confidence intervals (CIs) were calculated using a random-effects model. Between-study heterogeneity was assessed by using Cochran's Q test and further explored in subgroups analysis. Nine studies, including 514 individuals with MDD and 417 healthy controls, met the inclusion criteria. Patients with MDD exhibited significantly higher circulating levels of anandamide (AEA; SMD = 0.32, 95 % CI: 0.10 - 0.54, p < 0.01) and palmitoylethanolamide (PEA; SMD = 0.35, 95 % CI: 0.04 - 0.65, p = 0.03) compared with controls, whereas no significant differences were observed for 2-arachidonoylglycerol (2-AG) or oleoylethanolamide (OEA). Subgroup analyses indicated that the elevation in AEA levels were more pronounced among medicated patients and individuals with psychiatric comorbidities. These findings suggest selective alterations in ECS-related lipid mediators in individuals with MDD and support dysregulation of the ECS-NAE signaling axis in depression. Circulating lipid signaling molecules such as AEA and PEA may represent potential peripheral biomarkers of MDD, although longitudinal and mechanistic studies are needed to clarify the influence of treatment and comorbidities.

PMID 42431383
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PubMedMolecular neurobiology2026-07-10

Photoreceptor preservation by FAAH inhibition in a murine model of retinitis pigmentosa.

Magalhães Camila Feitosa CF, de Freitas Azevedo-Repossi Rafael R, de Almeida-Pereira Luana L, Crisóstomo Millena Costa MC et al.

Retinitis pigmentosa is a hereditary neurodegenerative disease characterized by gradual photoreceptor loss, often leading to blindness. The murine model Pde6brd10/rd10 (rd10) reproduces key features of retinitis pigmentosa (RP) and is widely used to evaluate therapeutic strategies. Anandamide is an endocannabinoid ligand degraded by fatty acid amide hydrolase (FAAH), whose levels have been shown to be increased in retinopathies. In this study, endocannabinoid signaling was pharmacologically augmented in rd10 mice to prolong photoreceptor survival. FAAH is present both in rd10 and C57Bl/6 retinas, with no differences in expression by qPCR or immunofluorescence analysis. To increase levels of endocannabinoid ligands URB597 (FAAH inhibitor), was administered daily by intraperitoneal injection (0.3 mg/kg), from P13 to P18 or P24. At P19, URB597 increased peripheral photoreceptor cell number by 35% and ONL thickness by 27%, with no effect in the central retina. At P25, peripheral photoreceptor number increased by 28%, although ONL thickness was unchanged. FAAH inhibition reduced TUNEL-positive cells in the peripheral retina by 50% and 53% at P19 and P25, respectively. No changes to reactive gliosis markers and microglia cells following FAAH inhibition were observed by assessing GFAP fluorescence intensity and Iba-1+ cell counts either in central or peripheral retina in both ages studied. Treatment with URB597 led to a 30% reduction in reactive oxygen species content at P19. Together, these data indicate a neuroprotective role of the endocannabinoid system in the context of photoreceptor degeneration in retinitis pigmentosa.

PMID 42429887
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