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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

PubMedBehavioural brain research2026-08-30

N-Stearoyltyrosine Attenuates Ischemia-Reperfusion Injury by Inhibiting Caspase-Dependent Apoptosis and PARP-1/AIF-Mediated Parthanatos.

Yang Rui R, Ma Jing J, Le Kejia K, Lu Yang Y

Cerebral ischemia-reperfusion (I/R) injury induces neuronal death via caspase-dependent apoptosis and parthanatos, a poly (ADP-ribose) polymerase 1 (PARP-1)/apoptosis-inducing factor (AIF)-mediated caspase-independent pathway. Simultaneous inhibition of these pathways may provide enhanced neuroprotection. N-Stearoyltyrosine (NsTyr), a synthetic analogue of the endocannabinoid anandamide (AEA), exhibits neuroprotective effects in various models, however, its efficacy and mechanism in middle cerebral artery occlusion (MCAO) remain unclear. Neuronal oxygen-glucose deprivation/ reoxygenation (OGD/R) and rat MCAO models were employed to evaluate the neuroprotection of NsTyr. Neuronal viability and apoptosis were assessed using MTT assay, flow cytometry, TUNEL staining, and Hoechst 33342 staining. The cognitive impairment was evaluated using the Morris water maze. Mitochondrial function and ultrastructure were eassessed by JC-1 assay and transmission electron microscopy (TEM). Expression levels of key apoptotic-related proteins were determined by immunoblotting. Intracellular NAD⁺ and ATP levels were measured to assess PARP-1 activity. NsTyr significantly improved neuronal survival, reduced apoptosis, and ameliorated cognitive deficits in both in vitro and in vivo models. Mechanistically, NsTyr preserved mitochondrial integrity, maintained the Bcl-2/Bax balance, suppressed cytochrome c release and caspase-3 activation, and inhibited nuclear translocation of AIF. Concurrently, NsTyr attenuated PARP-1 overactivation, preserved NAD⁺ and ATP levels, and thereby suppressed parthanatos. These findings demonstrate that NsTyr confers potent neuroprotection against I/R injury by dual inhibition of caspase-dependent apoptosis and PARP-1/AIF-mediated parthanatos through the maintenance of mitochondrial integrity, supporting its potential as a therapeutic candidate for ischemic stroke.

PMID 42669348
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PubMedPharmaceuticals (Basel, Switzerland)2026-08-27

Neuropharmacology of Cannabinoids: A Comprehensive Review of Preclinical and Clinical Evidence for Hemp-Derived Extracts and Active Compounds.

Odonkor Charles A CA, Karpe David A DA, Siddique Muhammad Uzair MU, Abd-Elsayed Alaa A

Cannabis sativa contains more than 120 phytocannabinoids, with Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) being the best characterized. This review synthesizes preclinical and clinical evidence on hemp-derived extracts, cannabinoids, and active compounds. THC primarily acts as a partial agonist at cannabinoid receptor type 1 (CB1) and type 2 (CB2), producing psychoactive, appetite-stimulating, antiemetic, and analgesic effects. CBD is non-intoxicating and has a multimodal profile involving CB1 negative allosteric modulation, CB2 inverse agonism or antagonism, inhibition of anandamide inactivation, and activity at 5-HT1A receptors, transient receptor potential channels, GPR55, and peroxisome proliferator-activated receptor gamma. Preclinical models of Parkinson's disease, Alzheimer's disease, Huntington's disease, epilepsy, and pain support anti-inflammatory, antioxidant, anti-excitotoxic, and glial-modulating mechanisms, but clinical translation remains uneven. The strongest evidence supports FDA-approved cannabidiol for Lennox-Gastaut syndrome, Dravet syndrome, and tuberous sclerosis complex, and THC-based agents for refractory chemotherapy-induced nausea and vomiting and AIDS-related anorexia. Moderate-certainty evidence supports nabiximols for multiple sclerosis spasticity and small benefits in selected chronic neuropathic pain populations. Evidence remains insufficient or negative for acute pain, insomnia, most psychiatric disorders, and many promoted indications. Key risks include cannabis use disorder, cognitive and psychiatric effects, cardiovascular events, sedation, high-dose CBD hepatotoxicity, and drug interactions. Rigorous, long-term, product-standardized trials are needed.

PMID 42653650
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PubMedNeuropharmacology2026-08-26

Enhancement of 2-arachidonoylglycerol but not anandamide signaling in the ventral tegmental area selectively increases the choice to respond to reward-predictive incentive cues in male rats.

Leigh Martin P K MPK, Colangelo Jaqlyn J, Feja Malte M, Suarez Mauricio M et al.

Mesolimbic endocannabinoid (eCB) signaling impacts reward-seeking behaviors that rely on incentive salience. We previously showed that systemic enhancement of 2-arachidonoylglycerol (2-AG) using the monoacylglycerol lipase (MAGL) inhibitor MJN110 robustly decreased the latency of responding to reward-predictive incentive cues (ICs) and collecting the reward, as well as the choice to respond to the IC. Here we sought to determine the contribution of the endocannabinoids 2-AG and anandamide in the ventral tegmental area (VTA) in mediating incentive salience processes. We microinfused MJN110 or PF3845, a fatty acid amide hydrolase (FAAH) inhibitor, into the VTA to increase 2-AG and anandamide, respectively in male rats. These rats were trained to nosepoke during an 8-sec audiovisual IC to receive a 10% sucrose reward. We found that while intra-VTA PF3845 had little effect on responding to the IC, intra-VTA MJN110 specifically increased only the choice to respond without impacting the vigor (e.g., rapidity) of the response towards either the IC or the sucrose reward itself. This contrasts with our previous work in which systemic MJN110 treatment enhanced choice, and vigor to both the IC and reward. Further, the intra-VTA MJN110 enhancement of responding to ICs was blocked by the CB1 receptor antagonist rimonabant. Our results suggest that increasing 2-AG, but not anandamide, in the VTA selectively enhances the choice to respond to cues predicting a reward. However, the effects of systemic MJN110 in enhancing the vigor of responding cannot be attributed to VTA 2-AG signaling.

PMID 42648566
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PubMedJournal of fungi (Basel, Switzerland)2026-08-26

Anandamide Targets Membrane Integrity in Non-Albicans Candida: A Novel Antifungal Approach.

Wolfson Goldie G, Steinberg Doron D, Polacheck Itzhack I, Korem Maya M

Fungal infections remain a major threat to human health, with non-albicans Candida (NAC) species causing more than half of all clinical cases and many strains gaining resistance to current treatments rapidly. Previously, N-arachidonoyl ethanolamine (anandamide, AEA) has been studied and shown to possess antibacterial and antifungal properties against various bacteria and Candida albicans. Given the previous findings, we aim here to expand the current preliminary research on AEA to investigate its antifungal activities against clinically relevant NAC species in vitro: Candida glabrata, Candida parapsilosis, and Candidaozyma auris. The minimum inhibitory concentration (MIC) and growth curve analysis determined planktonic inhibition. MTT metabolic assay and ATP production via BacTiter-Glo luminescence assay evaluated biofilm formation. Membrane fluidity, polarization and efflux pump activity were examined using fluorescence probes Laurdan, DiS-C3(3), and Rhodamine 6G, respectively. Reactive oxygen species (ROS) were assessed using DCFH-DA. Biofilm architecture and cell viability were analyzed by spinning disk confocal microscopy (SDCM). AEA reduced MIC values and slowed planktonic growth, while MTT and ATP assays demonstrated a pronounced dose-dependent reduction in biofilm metabolic activity. Membrane-targeted effects revealed increased fluidity and permeability at 125 µg/mL. Notably, AEA rapidly impaired efflux pump activity and induced intracellular ROS production. This effect was accompanied by reduced cell viability, increased proportions of PI-positive cells, and enhanced intracellular dye retention, as confirmed by SDCM. Together, these findings demonstrate that AEA exerts antifungal activity by disrupting membrane integrity and associated cellular functions and provide the first comparative characterization of species-specific membrane and oxidative stress responses to AEA across three major clinically relevant multidrug-resistant NAC species.

PMID 42646143
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PubMedJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2026-08-25

Baihe Dihuang decoction activates cannabinoid type 2 receptor to regulate microglial polarization and alleviate anxiety-like behavior in chronic restraint stress mice.

Qiaoyun Luo L, Yuanshan Han H, Yang Liu L, Lin Tang T et al.

To investigate the anxiolytic effects of Baihe Dihuang decoction (, BDD) and its underlying molecular mechanisms, focusing on cannabinoid type 2 receptor (CB2R)-mediated regulation of microglial polarization and the toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) signaling pathway. A total of 60 male C57BL/6J mice were randomly divided into six groups (n= 10 per group): control group, model group, diazepam (2 mg/kg) group, high-dose BDD (16 g/kg) group, low-dose BDD (8 g/kg) group, and high-dose BDD (16 g/kg) combined with CB2R antagonist AM630 (1 mg/kg) group. Except for the control group, all other groups were subjected to chronic restraint stress (CRS) to establish an anxiety model. Anxiety-like behaviors were assessed using the open field test, light-dark box test, and elevated plus maze. Serum levels of interleukin (IL)-1β, IL-6, IL-10, and IL-4 and amygdala concentrations of 2-arachidonoylglycerol (2-AG) and anandamide (AEA) were quantified by enzyme-linked immunosorbent assay. Hematoxylin and eosin, Nissl, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining were used to evaluate neuronal damage in the amygdala. Immunofluorescence staining was employed to assess microglial polarization and CB2R expression. The expression levels of CB2R and downstream signaling molecules TLR4/MyD88/NF-κB in the amygdala were determined by quantitative polymerase chain reaction and Western blot. BDD significantly alleviated CRS-induced anxiety-like behaviors and reduced neuronal damage in the amygdala. It downregulated pro-inflammatory cytokines IL-1β, IL-6 and upregulated anti-inflammatory cytokines IL-10, IL-4 in serum while increasing 2-AG and AEA levels in the amygdala. Furthermore, BDD promoted microglial polarization toward the M2 phenotype and enhanced CB2R expression, while suppressing the TLR4/MyD88/NF-κB signaling pathway. The administration of the CB2R antagonist AM630 reversed these effects, confirming the essential role of CB2R activation in the anxiolytic and neuroprotective effects of BDD. BDD treatment activated CB2R, which in turn modulated microglial polarization in the amygdala viathe TLR4/MyD88/NF-κB signaling pathway, thereby alleviating anxiety-like behaviors and exerting neuro-protective effects.

PMID 42639765
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PubMedNature reviews. Endocrinology2026-08-19

Endocannabinoids and related lipids in host metabolism-gut microbiome signalling.

Silvestri Cristoforo C, Di Marzo Vincenzo V

Over the past two decades, it has become clear that the two endocannabinoids, anandamide and 2-arachidonoyl-glycerol, are only the tip of an iceberg of a larger signalling system composed of hundreds of chemically similar fatty acid derivatives, including 2-monoacylglycerols, N-acylethanolamines and other N-acylamines. Unlike the endocannabinoids, these lipids only seldom bind the two cannabinoid receptors, of which CB1 is now recognized as a major player in both the central and peripheral control of energy metabolism. They modulate instead the activity of other G-protein-coupled receptors, as well as of ligand-activated ion channels and nuclear receptors, which also regulate energy intake, accumulation and expenditure. Bacteria inhabiting the gut as part of the intestinal microbiome also produce endocannabinoid-like molecules capable of activating host receptors in vitro. These discoveries led to current research into potential bi-directional communication between this 'extended endocannabinoid system', or endocannabinoidome, and the gut microbiome. Ongoing studies are investigating how this axis might control energy metabolism, particularly in response to diet.

PMID 42613356
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