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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

PubMedCell biochemistry and biophysics2026-09-18

A Potentially Protective Role for NRF2 in Endocannabinoid-Mediated Oxidative Stress in Human Coronary Artery Endothelial Cells.

Haas Michael J MJ, Champagne Kareen K, Gupta Nidhi N, Velarde Andrew A et al.

Excess oxidative and endoplasmic reticulum (ER) stress disrupt cellular homeostasis and promote cardiovascular disease (CVD). The endocannabinoids anandamide and 2-arachidonoyl glycerol and the potent cannabinoid Δ9-tetrahydrocannabinol increase oxidative stress and ER stress in endothelial cells. However, it remains unclear whether endocannabinoids have intrinsic capacity to ameliorate oxidative stress. In human coronary artery endothelial cells (HCAEC), anandamide, 2-arachidonoyl glycerol, and tunicamycin increased superoxide generation and nuclear factor erythroid 2-related factor 2 (NRF2) mRNA and NRF2-dependent reporter gene activity. High anandamide, 2-arachidonoyl glycerol, and tunicamycin levels also increased lipid peroxidation. Furthermore, anandamide increased NRF2-responsive hemeoxygenase 1 (HO1), thioredoxin reductase 1 (TRX1), and NAD(P)H dehydrogenase quinone 1 (NQO1) mRNA. This effect was mediated by protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK); PERK silencing utilizing siRNA suppressed NRF2 induction by anandamide and tunicamycin. In contrast, activating transcription factor 6 (ATF6) and inositol requiring enzyme 1α (IRE1α ) silencing had no effect on NRF2 mRNA or NRF2 target gene expression in tunicamycin and anandamide-treated cells. Likewise, the PERK inhibitor GSK2606414 prevented NRF2 induction by anandamide and tunicamycin while treatment with Ceapin A7 (an ATF6 inhibitor) or GSK2850163 (an IRE1α inhibitor) did not. In conclusion, endocannabinoid-related ER stress increased superoxide generation accompanied by compensatory increase in production of antioxidant enzymes thereby highlighting the cross talk between ER stress and oxidative stress.

PMID 42758439
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PubMedJournal of affective disorders2026-09-15

Plasma endocannabinoid levels in bipolar disorder: Differences between manic and euthymic states and the impact of cannabis use.

Ochandiano Iñaki I, Powlowski Pavel P, Andreu Helena H, Olivier Luis L et al.

The endocannabinoid system (ECS) is a key regulator of mood homeostasis, but its longitudinal dynamics during an acute manic episode until the clinical recovery in bipolar disorder (BD) and the specific influence of cannabis use remain poorly characterized. We conducted a longitudinal study of 23 patients with BD I followed from acute mania (T0) to clinical stabilization (T1). Plasma AEA and 2-AG were quantified via LC-MS/MS at T0 and T1. Patients were divided into cannabis users and non-cannabis users for further analyses. Linear mixed-effects models assessed the interaction between cannabis use and timepoint on endocannabinoid (eCB) trajectories. Non-cannabis users exhibited a significant decline in both anandamide (AEA) and 2-arachidonoglycerol (2-AG) levels during the transition to euthymia (p < 0.05). In contrast, cannabis users showed a disrupted trajectory with no significant reduction in eCB tone despite clinical improvement (Cannabis x Timepoint interaction: AEA p = 0.016; 2-AG p = 0.029). In both groups of BD patients, eCB levels were not associated with sociodemographic factors and symptom severity measured by Young Mania Rating Scale (YMRS). Our findings suggest that circulating eCBs (AEA and 2-AG) may serve as a key state-transition biomarker from mania to clinical stabilization in BD. This intrinsic regulation could be disrupted by cannabis use, which might hinder recovery from manic episodes. Specifically addressing cannabis use and monitoring eCBs levels may play a crucial role to help returning to a biological balance and may support clinical stability in BD patients.

PMID 42735776
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PubMedPsychopharmacology2026-09-14

Anandamide blocks spatial memory reconsolidation in male rats through a CB1 receptor dependent mechanism.

Queiroz Ruliam R, Marchiori Crisleine C, Rosas Heitor Kraushaar HK, Medeiros Isabella Sayuri Shiguehara ISS et al.

Memory reconsolidation is a process through which previously consolidated memories become temporarily labile after retrieval and require molecular mechanisms, including protein synthesis and degradation, to be stabilized again. The endocannabinoid system, particularly cannabinoid receptors CB1 and CB2, has been implicated in several forms of learning and memory. However, the specific role of CB1 receptors in the regulation of protein turnover during spatial memory reconsolidation remains incompletely understood. Therefore, this study investigated whether cannabinoid receptor activation in the hippocampal CA1 region influences the reconsolidation of spatial memory. Spatial memory was evaluated using the Morris water maze task. After training, animals underwent an early non-reinforced test session 24 hours later to reactivate the previously acquired spatial memory. Immediately after this retrieval session, anandamide (AEA) or oleamide, a CB1 receptor agonist, was bilaterally infused into the CA1 region of the hippocampus. To investigate the involvement of CB1 receptors, some animals received a CB1 receptor antagonist together with the agonists. Additional experiments evaluated whether the amnesic effects of oleamide were dependent on protein degradation mechanisms and whether activation of CB1 receptors could modulate the effects produced by inhibition of protein synthesis. Bilateral administration of AEA and oleamide into the hippocampal CA1 region immediately after memory retrieval impaired the reconsolidation of spatial memory, producing anterograde amnesia. Oleamide primarily affected the early long-term phase of spatial memory, whereas AEA impaired later phases of memory. The disruptive effect on memory reconsolidation was prevented by co-administration of a CB1 receptor antagonist, indicating that the observed effects were mediated by CB1 receptor activation. Furthermore, the amnesic effect induced by oleamide was dependent on protein degradation mechanisms. Conversely, the impairment caused by inhibition of protein synthesis could be reversed through inverse activation of CB1 receptors. These findings indicate an interaction between CB1 receptor signaling and the molecular mechanisms responsible for protein turnover during memory reconsolidation. The findings demonstrate that CB1 cannabinoid receptors in the hippocampal CA1 region play a direct role in the reconsolidation of spatial memory. Activation of these receptors can interfere with memory stabilization after retrieval by modulating protein degradation and protein synthesis mechanisms. Therefore, the endocannabinoid system, particularly CB1 receptor signaling, appears to be an important regulator of the molecular processes underlying the persistence and modification of long-term spatial memories.

PMID 42734663
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PubMedEJNMMI reports2026-09-13

Cannabinoid type 1 receptor availability imaging in attention-deficit/hyperactivity disorder using [18F]MK-9470 positron emission tomography: study protocol of the CB1-ADHD study.

Miederer Isabelle I, Schofer Marina Louise ML, Ruckes Christian C, Retz Wolfgang W et al.

Attention deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by attentional deficits, hyperactivity and impulsivity that often persists into adulthood. While dysfunction of dopaminergic neurotransmitter systems has been observed, underlying mechanisms remain incompletely understood. Current treatments with methylphenidate and amphetamines show limited long-term effectiveness and do not address broader clinical needs. The endocannabinoid system represents a promising therapeutic target. Cannabinoid type 1 (CB1) receptors are highly concentrated in the prefrontal cortex and striatum, brain regions central to ADHD pathophysiology. The "dual pathway model of ADHD" describes deficits in inhibition-related executive functions and reward-related functions, both mediated by fronto-striatal networks. Striatal CB1 receptor availability correlates negatively with impulsivity. Given the interaction between dopaminergic and endocannabinoid systems, CB1 receptors may play a key role in ADHD pathogenesis. This controlled study will investigate CB1 receptor availability in ADHD using positron emission tomography (PET) with the CB1-selective radiotracer [18F]MK-9470. The primary outcome is the CB1 receptor distribution volume (VT) in the striatum. Secondary outcomes include CB1 receptor availability in prefrontal cortex and other ADHD-relevant brain regions, plasma concentrations of endocannabinoids (anandamide, 2-arachidonoylglycerol), and validated neuropsychological assessments of attention and impulsivity. We will compare three groups (n = 34 each): medication-naïve participants with ADHD, methylphenidate-treated participants with ADHD, and healthy controls. Statistical analysis will employ ANOVA with post-hoc comparisons and correlation analyses between neuroimaging and behavioral measures. N/A, as this is a study protocol. This first investigation of the endocannabinoid system in ADHD will provide crucial insights into disease mechanisms and identify potential therapeutic targets. Results may inform development of novel cannabinoid-based treatments and improve evidence-based therapeutic strategies for ADHD management. German Clinical Trials Register (DRKS-ID: DRKS00037526, Registration date: 25 September 2025).

PMID 42728455
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PubMedEuropean journal of pharmacology2026-09-10

Diminazene aceturate-induced relaxation in isolated rat thoracic aorta: Contribution of cannabinoid and vanilloid signaling.

Okcay Yagmur Y, Rumanli Zeliha Z, Avci Emre E, Vural Ismail Mert IM

The renin-angiotensin system (RAS) is a key regulator of cardiovascular homeostasis, and its alternative ACE2/Ang (1-7) axis exerts vasodilatory, anti-inflammatory, and antifibrotic effects. Functional crosstalk between the RAS and the endocannabinoid system (ECS) has been suggested. In this study, we investigated the relaxant effects of diminazene aceturate (DIZE), an experimental ACE2 activator, in endothelium-denuded rat thoracic aorta and evaluated the contribution of the ECS, TRPV1 receptors, along with tissue ACE2 and Ang (1-7) levels. Thoracic aortic rings isolated from 30 male Wistar albino rats were mechanically denuded of endothelium and mounted in organ baths under standard conditions. Following phenylephrine-induced precontraction, cumulative concentrations of DIZE were applied in the absence or presence of the CB1 receptor antagonist AM251, the CB2 receptor antagonist AM630, the TRPV1 antagonist capsazepine, the FAAH inhibitor URB597, or anandamide. The effects of DIZE on electrical field stimulation (EFS)-induced neurogenic relaxation responses were examined. ACE2 and Ang-(1-7) levels in thoracic aortic tissue were measured by ELISA. DIZE produced marked concentration-dependent relaxation in endothelium-denuded aortic rings. This effect was not significantly altered by CB1, CB2, or TRPV1 receptor antagonism, whereas anandamide and URB597 enhanced DIZE-induced relaxation. DIZE also augmented EFS-induced neurogenic relaxation, an effect reversed by AM630, while anandamide and URB597 suppressed the DIZE response. Although DIZE did not significantly change tissue ACE2 or Ang-(1-7) levels, the findings indicate an interaction with the ECS at multiple levels. These results suggest that DIZE may represent a promising therapeutic candidate in cardiovascular conditions associated with endothelial dysfunction.

PMID 42722055
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PubMedTranslational psychiatry2026-09-04

Longitudinal changes in endocannabinoids and clinical course of adolescent non-suicidal self-injury.

Ferger Marc D MD, Brodesser Susanne S, Kaess Michael M, Koenig Julian J

Non-suicidal self-injury (NSSI) in adolescents has previously been linked to alterations in the endocannabinoid system. While increasing evidence supports endocannabinoid levels as potential biomarker in psychiatric care, little is known about their longitudinal trajectories over the course of treatment or in predicting clinical symptoms. This is the first study to investigate endocannabinoids in a longitudinal cohort of patients with NSSI, exploring associations with the development of symptoms over time. Plasma endocannabinoids and NSSI, using the German version of the Self-Injurious Thoughts and Behaviors Interview (SITBI-G), were assessed in n = 47 female adolescents with NSSI at both baseline and after one year of treatment (follow-up). Associations between endocannabinoid levels and clinical symptoms over time were analyzed. Anandamide (AEA) significantly decreased from baseline to follow-up while 2-arachidonoylglycerol (2-AG) increased after one year. While lower AEA levels have previously been reported in adolescents with NSSI, this longitudinal study found that AEA decreased over one year despite an overall improvement in NSSI symptoms. The overall pattern suggests that changes in circulating endocannabinoids do not closely correspond to symptom improvement. These findings indicate that circulating endocannabinoid levels change over time in adolescents with NSSI, but their complex and partly inconsistent associations with clinical symptoms limit their clinical utility as biomarkers.

PMID 42693114
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