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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)
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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

PubMedJournal of cannabis research2026-11-11

A human microbiota-associated translational mouse model reveals sex-specific responses to cannabidiol and cannabigerol.

Keohane Eva E, Poehlein Lance L, Chaparro Jacqueline M JM, Wrigley Scott D SD et al.

Cannabidiol (CBD) and cannabigerol (CBG) are non-psychoactive phytocannabinoids with therapeutic potential, yet their effects on host physiology and interactions with the gut microbiome remain poorly defined. Here, we used a translational mouse model colonized with human-associated microbiotas to investigate the effects of oral CBD and CBG intervention on microbial composition, endocannabinoid signaling, and intestinal protein expression. While neither phytocannabinoids altered overall gut microbiome diversity, both induced sex-specific shifts in bacterial taxa associated with mucin utilization and short-chain fatty acid production. Circulating concentrations of CBD were higher than those of CBG, and females exhibited higher plasma phytocannabinoid concentrations than males. Males treated with CBD had elevated anandamide (AEA) levels, potentially reflecting inhibition of fatty acid amide hydrolase, consistent with upregulation of serine protease inhibitors observed in ileal proteomes. Females also accumulated more subcutaneous adipose tissue with both CBD and CBG treatment resulting in greater total CBD storage in this depot. Collectively, these findings suggest sex-specific interactions between phytocannabinoids, the endocannabinoid system, and the gut microbiome, underscoring the importance of considering biological sex in cannabinoid research and informing personalized therapeutic strategies.

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PubMedThe international journal of neuropsychopharmacology2026-11-10

The Relationship Between Manic Episodes and Serum Endocannabinoid Levels in Bipolar Disorder.

Özel Sarpkan S, Görgülü Yasemin Y, Topuz Ruhan Deniz RD

Endocannabinoids are involved in biological processes relevant to mood regulation, and altered circulating levels have been reported in bipolar disorder (BD). However, serum endocannabinoid levels have not previously been examined across mania and remission within the same patients and compared with healthy controls. This study evaluated serum palmitoylethanolamide (PEA), oleoylethanolamide (OEA), 2-arachidonoylglycerol (2-AG), anandamide (AEA), and C-reactive protein (CRP) levels in patients with BD during manic episodes and remission and in healthy controls. Fifty-one patients diagnosed with BD, manic episode, according to DSM-5-TR criteria, and 49 healthy controls were included. After discharge, 32 patients who attended outpatient follow-up visits were re-evaluated during remission. Serum PEA, OEA, 2-AG, AEA, and CRP levels were measured in all participants. Patients with BD were additionally assessed using the Young Mania Rating Scale, Hamilton Depression Rating Scale, and Positive and Negative Syndrome Scale. Serum PEA and OEA levels were significantly lower during manic episodes than in healthy controls. During remission, serum PEA and OEA levels did not differ significantly from those of healthy controls. In within-patient comparisons between manic episodes and remission, only serum PEA levels were significantly lower during manic episodes. This is the first study to assess serum endocannabinoid levels in patients with BD during both manic episodes and remission, together with healthy controls. PEA and OEA levels were significantly lower during mania and returned to values comparable to healthy controls during remission. These findings suggest that endocannabinoid-related mechanisms may have potential as future biomarkers and therapeutic targets in mood regulation.

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PubMedFrontiers in pharmacology2026-11-05

Live combined bifidobacterium attenuates rivaroxaban-associated colonic bleeding in mice: evidence for a substantial gut microbiota-dependent component.

Chen Xiaowen X, Lin Yuze Y, Huang Youqi Y, Zeng Linghong L et al.

Rivaroxaban, a direct oral anticoagulant (DOAC), is widely prescribed for the prevention and treatment of thromboembolic disorders. However, its use is associated with an increased risk of gastrointestinal bleeding, the mechanisms of which remain incompletely understood. Effective strategies to relief such bleeding are also lacking. Because the gut microbiota plays a critical role in maintaining intestinal homeostasis, we investigated whether probiotics could mitigate anticoagulant-related bleeding and explored the underlying mechanisms. Using a rivaroxaban-induced mouse model of colonic bleeding, we found that treatment with live combined Bifidobacterium reduced occult blood in the feces, alleviated damage to colon tissue, and lowered serum levels of the inflammatory cytokines tumor necrosis factor-α and chemokine ligand 5. Integrated 16S rRNA sequencing and untargeted metabolomic analyses showed that LCB treatment was accompanied by alterations in the gut microbial community and fecal metabolic profile. Following antibiotic-mediated microbiota depletion, the overall ameliorative effect of LCB was attenuated, although partial responses, including a reduction in CXCL5, were retained. These findings support a substantial microbiota-dependent component of the full ameliorative phenotype. Untargeted metabolomic analysis identified a metabolite feature putatively annotated as anandamide that showed a nominal decrease following rivaroxaban administration and a nominal increase after LCB treatment. However, these differences did not remain significant after false discovery rate (FDR) correction and were therefore considered exploratory. The same feature also showed a nominal increase following LCB treatment in antibiotic-treated mice without corresponding restoration of the overall ameliorative phenotype, suggesting that this metabolic change alone was insufficient to account for the observed effects. To our knowledge, the present study provides initial evidence that LCB administered after the onset of fecal occult bleeding ameliorates rivaroxaban-associated colonic injury in mice. Collectively, these findings suggest that the overall ameliorative effect of LCB has a substantial gut microbiota-dependent component, whereas the putative anandamide signal represents a hypothesis-generating metabolic association that requires targeted quantitative and functional validation.

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PubMedMolecular psychiatry2026-10-31

Identification of fluid endocannabinoid and sphingolipid biomarkers in schizophrenia. A machine learning approach toward clinical value.

Hoffmann Anna E AE, Allwright Michael M, Guennewig Boris B, Rohleder Cathrin C et al.

Schizophrenia (SCZ) diagnosis relies on subjective clinical evaluation, with symptoms often overlapping between psychiatric conditions, hindering early intervention, and creating an urgent need for objective, accessible biomarkers. Lipids, especially endocannabinoid system (ECS) and sphingolipid metabolism members, are promising candidates given their implication in SCZ pathogenesis and measurability in accessible biofluids, with minimally invasive procedures. Our study conducted the first comprehensive crossover of endocannabinoids (eCBs) and sphingolipids in matched cerebrospinal fluid (CSF) and serum samples from antipsychotic-naïve SCZ patients (SCZnaïve, n = 49), antipsychotic-treated patients (SCZtreat, n = 56), and healthy volunteers (HVs, n = 51). The machine learning Integrated Disease Explanation and Risk Scoring (IDEARS) platform was applied to eCBs, N-acylethanolamines, ceramides, and sphingomyelins quantified using liquid chromatography-tandem mass spectrometry, identifying key discriminatory features across biofluids and conditions (CSF AUC: SCZnaïve = 0.87, SCZtreat = 0.94; serum AUC: SCZnaïve = 0.87, SCZtreat = 0.90). Anandamide emerged as the top CSF feature in SCZnaïve patients, showing significantly elevated levels (q = 0.010) compared to HVs. Notably, though not statistically significant under conventional statistics, IDEARS identified anandamide as a top ten serum feature. Additionally, elevated sphingadiene backbone (d18:2) sphingolipids were conserved between the CSF and serum of SCZnaïve (q < 0.05), highlighting their potential as peripheral surrogate markers. Treatment-specific ceramide patterns were also evident, with elevated C16-C18 and reduced long-chain (>C24) species potentially reflecting antipsychotic metabolic effects. Our results support the involvement of the ECS and sphingolipid imbalances in SCZ, highlighting the potential of machine learning for novel biomarker discovery, including stratification across biofluids, and therapeutic monitoring toward more objective psychiatric care.

PMID 42963368
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PubMedPhytotherapy research : PTR2026-10-25

Toll-Like Receptor 4 Signaling in Natural N-Acylethanolamines and Derivative NAE-Like Compounds: Mechanisms and Implications for Neuroimmune and Inflammatory Processes in a Systematic Search Approach.

Scuteri Damiana D, Guida Francesca F, Bagetta Giacinto G, Maione Sabatino S et al.

N-acylethanolamines (NAEs) are endogenous fatty acid amides structurally related to the endocannabinoid anandamide and function as bioactive lipid mediators with broad regulatory roles in inflammation and neuroinflammation. Among pattern-recognition receptors, Toll-like receptor 4 (TLR4) occupies a central position in innate immune surveillance, sensing pathogen-associated molecular patterns, such as lipopolysaccharide (LPS), as well as damage-associated molecular patterns. Upon ligand engagement, TLR4 triggers both MyD88- and TRIF-dependent signaling cascades, leading to NF-κB activation and the transcriptional induction of pro-inflammatory cytokines and Type I interferons. Within this family, classical NAEs, such as palmitoylethanolamide (PEA), and structurally distinct NAE-like derivatives represent two partially overlapping but pharmacodynamically different groups of bioactive compounds. Classical NAEs, including palmitoylethanolamide (PEA), primarily exert their anti-inflammatory actions through activation of peroxisome proliferator-activated receptors and related nuclear pathways. In contrast, NAE-like compounds with distinct scaffolds, such as 2-pentadecyl-2-oxazoline (C15OXA) and N-palmitoyl-D-glucosamine (PGA), may interact with the TLR4/MD-2 complex and modulate receptor activation more proximally, as suggested by cell-based functional assays and computational modeling. PRISMA-guided analyses across experimental models of colitis, LPS-induced systemic inflammation, and alcohol binge exposure consistently demonstrate the anti-inflammatory efficacy of PGA and C15OXA, identifying TLR4 as a pivotal mechanistic node underlying their activity. Together, these findings delineate distinct yet partially convergent pharmacodynamic profiles among endogenous NAEs and naturally occurring NAE-like compounds, supporting their potential relevance as natural-product-inspired pharmacological strategies for the modulation of TLR4-associated inflammatory and neuroinflammatory processes.

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PubMedMolecular biology reports2026-10-23

Cannabidiol in Alzheimer's disease: evidence-weighted molecular mechanisms and translational challenges.

Sura Sreenivasulu S, Jagadeesan Saravanan S, Masrudin Siti Saleha SS, Moklas Mohamad Aris Mohd MAM et al.

Alzheimer's disease (AD) is a complex, progressive neurodegenerative disorder in which amyloid-β accumulation, tau dysregulation, neuroinflammation, oxidative stress, mitochondrial dysfunction, synaptic loss and neurodegeneration interact to drive memory loss and cognitive decline. Despite advances in symptomatic therapies and anti-amyloid agents, clinical benefit remains modest, supporting interest in polypharmacological approaches. Cannabidiol (CBD) is a non-psychotropic phytocannabinoid that interacts with several signalling systems relevant to AD, including cannabinoid-related pathways, peroxisome proliferator-activated receptor-γ (PPARγ), transient receptor potential vanilloid 1 (TRPV1) channels, 5-HT1A signalling, fatty acid-binding proteins involved in anandamide transport, GPR55 and adenosine transporters. The most consistent preclinical findings indicate that CBD attenuates neuroinflammatory and oxidative responses and improves selected behavioural outcomes. Evidence for amyloid-related effects is supportive but heterogeneous. Direct evidence for tau modulation has expanded in transgenic and chemically induced models, but findings remain model-dependent, whereas mitochondrial rescue and adult hippocampal neurogenesis are less firmly established. Methodological variability in CBD source, formulation, dose, route, treatment window, sex, age and outcome selection limits direct comparison between studies. Work on other cannabinoids and CBD:Δ9-THC combinations is discussed for context, and current evidence does not establish CBD as a disease-modifying treatment in AD. Overall, current preclinical evidence supports continued investigation of CBD as a multi-target neuroprotective candidate in AD, provided that future studies use standardized, mechanism-focused and translationally relevant designs. This review compares preclinical evidence across pathological domains and identifies translational research priorities.

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