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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

PubMedVeterinary record open2026-06-08

Effect of environmental temperature on oxidative status, inflammatory response and endocannabinoid system at oestrus in dairy cows.

Carbonari Alice A, Frattina Lorenza L, Burgio Matteo M, Cicirelli Vincenzo V et al.

Heat stress (HS) poses a significant challenge to dairy production under climate change, as it compromises fertility, productivity and overall health in cows. This seasonal observational cross-sectional study investigated how environmental temperature affects oxidative status, inflammatory responses and endocannabinoid system (ECS) in dairy cows, comparing winter and summer conditions. Sixty Italian Holstein cows, 20 per farm, were enrolled from three farms in southern Italy. In winter and summer, temperature‒humidity index (THI) was recorded using data loggers and blood samples were collected from each cow's coccygeal vein during oestrus. Serum samples were analysed to evaluate the oxidative status as reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP), inflammatory responses as tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-10, and ECS as anandamide (AEA) and 2-arachidonoylglycerol (2-AG). Temperature‒humidity index was significantly higher in summer than in winter (p < 0.001), confirming HS exposure. Anandamide levels showed no significant seasonal variation, while 2-AG concentrations were significantly reduced in summer compared to winter (p < 0.01). Oxidative stress increased in summer, with lower BAP (p < 0.05) and higher d-ROMs (p < 0.001). Tumour necrosis factor-alpha and IL-10 were significantly higher in summer than in winter (p < 0.001 and <0.05). The study demonstrates that summer HS could alter oxidative balance, stimulates inflammatory pathways and modulates ECS activity in dairy cows. Reduced 2-AG suggests potential ECS involvement in thermal-stress adaptation. These findings provide a foundation for future research on nutritional or management strategies aimed at improving resilience to HS.

PMID 42254555
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PubMedImmunity, inflammation and disease2026-06-04

Dandruff Is a Low-Grade Inflammatory Condition Featuring Hyperproliferative Keratinocytes, Interleukin-17-Producing T Cells, and N-Acyl Ethanolamines.

Kendall Alexandra C AC, Mohamed Karishma K, Linley Holly H, Koszyczarek Marta M MM et al.

Dandruff features epidermal scaling but lacks overt signs of inflammation, such as erythema. Characterisation of its inflammatory profile may improve understanding of the underlying inflammatory mechanisms and therefore indicate alternative approaches for treatment. Full-thickness scalp biopsies were sampled from healthy volunteers and those with dandruff. Immunohistochemistry for Ki67 and keratin 16 was used to examine keratinocyte proliferation and differentiation. Mass spectrometry lipidomics was applied to profile scalp skin barrier lipids and lipid mediators. The presence of immune cells and their cytokine production was examined by flow cytometry. Cytokine and chemokine levels in scalp skin were analysed by cytometric bead array. Increased keratinocyte proliferation and aberrant keratinocyte differentiation were observed in dandruff relative to healthy scalp; however, this epidermal dysregulation was not mirrored by alterations to barrier lipid levels. Decreased numbers of innate lymphoid cells and reduced expression of CD86 on antigen-presenting cells, were the few cellular alterations observed in dandruff scalp, suggesting dandruff only subtly changes major skin immune cell populations. Despite this, increased proportions of interleukin-17-producing T-cells and increased C-C Motif Chemokine Ligand 17 (CCL17) levels were observed in dandruff scalp, indicative of a low-grade, mixed Type-2/Type17 inflammatory response. Increased levels of N-acyl ethanolamines, including the endocannabinoid anandamide, as well as linoleoyl- and oleoyl-ethanolamine, were also observed in dandruff scalp which could be responsible for suppressing inflammation to sub-clinical levels. These findings indicate that, contrary to being a mere flaking disorder, dandruff involves an altered inflammatory environment consistent with low-grade inflammation.

PMID 42237451
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PubMedTranslational psychiatry2026-05-29

Enhancing anandamide signalling through fatty acid amide hydrolase inhibition: An update on the pharmacological strategy for treating psychiatric disorders.

Couttas Timothy A TA, Hoffmann Anna E AE, Jieu Beverly B, Golla Felix R FR et al.

Endocannabinoids (eCBs) are lipid-derived neuromodulators that regulate numerous neurophysiological processes by modulating synaptic transmission. Synthesised on demand in response to increased postsynaptic intracellular calcium or activation of postsynaptic G-protein coupled receptors, eCBs are rapidly degraded, resulting in transient, tightly regulated signalling. Dysregulation in the endocannabinoid system (ECS), including altered peripheral and central eCB concentrations and/or cannabinoid-1 receptor (CB1R) expression, has been observed across psychiatric syndromes, including major depressive disorder, psychotic disorders, and post-traumatic stress disorder (PTSD). These associations have prompted growing interest in pharmacological strategies targeting the ECS. Though medical cannabis is increasingly prescribed for psychiatric symptoms, its clinical use remains controversial due to limited high-quality evidence, psychotropic side effects, and regulatory constraints. An alternative is to enhance the signalling of a principal eCB, anandamide (AEA), potentially offering more physiologically constrained CB1R engagement, by inhibiting fatty acid amide hydrolase (FAAH), the main enzyme degrading AEA and its congener, N-acylethanolamines (NAE), oleoylethanolamide (OEA) and palmitoylethanolamide (PEA). This review consolidates recent clinical evidence for FAAH inhibitors, examining their influence on AEA, safety and efficacy in ameliorating symptoms across a range of psychiatric conditions, including depression, anxiety, PTSD, and cannabis use disorder (CUD). Presently, only two compounds, PF-04457845 (JZP150) and JNJ-42165279, have progressed to Phase II trials, demonstrating modest clinical benefit in CUD, with no efficacy in PTSD or osteoarthritis pain. Herein, we discuss emerging insights, safety considerations, broader mechanistic implications, and future directions for FAAH-targeted therapeutics, advocating for a precision medicine approach to realise their potential in the treatment of psychiatric disorders.

PMID 42209468
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PubMedInternational journal of molecular sciences2026-05-27

Short Communication: The Peripheral Cannabinoid CB1 Receptor Antagonist AM6545 Modifies Cardiovascular Effects of Endocannabinoids in DOCA-Salt Rats.

Remiszewski Patryk P, Schlicker Eberhard E, Grzęda Emilia E, Weresa Jolanta J et al.

Peripherally restricted ('second-generation') cannabinoid CB1 receptor (CB1R) antagonists have been suggested to have therapeutic potential in numerous diseases. However, their effects on the cardiovascular system require further research. The peripheral CB1R antagonist AM6545 failed to modify the decrease in blood pressure (BP) elicited by inhibition of anandamide degradation in spontaneously hypertensive rats. The aims of the present study were to examine the effect of AM6545 on BP and its interaction with endocannabinoid-evoked effects in deoxycorticosterone acetate (DOCA)-salt rats. For this purpose, we applied methanandamide (MethAEA), a stable analogue of anandamide, and URB597, an inhibitor of its degradation, in urethane-anesthetized animals. AM6545 did not affect BP by itself. MethAEA elicited a biphasic effect (a rise in BP, followed by its fall); both phases were antagonized by AM6545. URB597 induced a monophasic hypotensive effect, which was abolished by AM6545 in DOCA-salt rats but further enhanced in control animals. AM6545 also unmasked an additional increase in BP after URB597 in both groups of rats. In conclusion, AM6545 modifies the cardiovascular effects of endocannabinoids in hypertension in a model-dependent manner. The cardiovascular effects of CB1R antagonists should be carefully evaluated when assessing their potential therapeutic significance, as they may unmask an increase in BP.

PMID 42196427
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PubMedBiomedicines2026-05-27

The Endocannabinoid System in Neuropsychiatric Disorders: Mechanisms, Dysregulation and Therapeutic Potential.

Mušić Timur T, Turnšek Tamara Lah TL

The endocannabinoid system (ECS) is a fundamental regulator of brain and body homeostasis, integrating neural, immune, and stress-related signaling pathways. Dysregulation of ECS components, including cannabinoid receptors (CB1 and CB2), endocannabinoids such as anandamide (AEA) and 2-arachidonoylglycerol (2-AG), and their metabolic enzymes (FAAH and MAGL), has been increasingly implicated in the pathophysiology of neuropsychiatric disorders, including mood, anxiety, psychotic, stress-related, and eating disorders. Altered endocannabinoid signaling contributes to maladaptive stress responses, emotional dysregulation, and impaired synaptic plasticity, highlighting the role of the ECS as a core integrative mechanism. Therapeutic strategies targeting ECS, particularly through FAAH inhibition and the use of plant-derived cannabinoids, such as cannabidiol (CBD), show promise in restoring endogenous homeostasis while minimizing the adverse cognitive and affective effects associated with direct CB1 activation. ECS function and treatment response are further influenced by genetic polymorphisms in CNR1, CNR2, FAAH, and MGLL, as well as epigenetic mechanisms, including DNA methylation, histone modifications, and microRNA regulation. Despite these advances, clinical translation remains limited by interindividual variability, the complexity of ECS interactions, and the relatively small size of existing clinical studies. Future research integrating longitudinal clinical trials with multi-omics approaches is essential to support the development of evidence-based, personalized interventions. Overall, understanding ECS mechanisms and dysregulation provides a valuable framework for the development of targeted therapies in neuropsychiatric disorders.

PMID 42193293
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PubMedTranslational pediatrics2026-05-20

Transcriptome profile analysis of genes by RNA-sequencing in neonatal maternal separation rats with autistic-like behaviors.

Zhang Qing Q, Ma Jinhua J, Xu Boqing B, Li Xiaohuan X et al.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder marked by repetitive behaviors and difficulties in social interaction and communication. The pathogenesis of ASD remains poorly understood, and no definitive treatment is currently available. This study aimed to systematically identify key genes and signaling pathways involved in autistic-like behaviors by performing genome-wide transcriptional profiling on a neonatal maternal separation (NMS) rat model, thereby revealing the underlying molecular mechanisms. In this study, genome-wide transcriptional profiling of male Sprague-Dawley rats subjected to NMS, one of the animal models of ASD, was conducted via RNA sequencing (RNA-seq). The transcriptomic data were systematically analyzed to identify the key genes and pathways that are involved in autistic-like behaviors. Rats subjected to NMS exhibited autism-like behaviors. The RNA-seq data were derived from total RNA collected from both control (CON) and NMS rats. In the NMS group, there were 202 differentially expressed genes (DEGs) compared to the CON group, with 128 genes upregulated and 74 downregulated according to an adjusted P value of less than 0.05 as determined by DESeq software. Gene Ontology (GO) enrichment analysis revealed that the upregulated DEGs were most enriched in serotonergic synapse, transcription factor AP-1 complex, DNA-binding transcription factor activity, RNA polymerase, transcription regulatory region sequence-specific, tissue development, and response to xenobiotic stimulus. Conversely, the downregulated DEGs were primarily enriched in synapse, dendrite, neuron projection, postsynaptic membrane, axon terminus, neuropeptide binding, enkephalin receptor activity, oxidoreductase activity, oleamide hydrolase activity, anandamide amidohydrolase activity, amidase activity, nervous system development, neuron development, generation of neurons, neuron differentiation, neuron projection development, neurogenesis, and regulation of cell communication. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that the prominently enriched pathways included neuroactive ligand-receptor interaction, cAMP signaling pathway, PI3K/Akt signaling pathway, AGE/RAGE signaling pathway in diabetic complications, maturity onset diabetes of the young, estrogen signaling pathway, Th1 and Th2 cell differentiation, Th17 cell differentiation, and antigen processing and presentation. Gene interaction analysis identified 15 key central genes, including Jun, Fos, Smad3, Runx2, Klf4, Fosb, Atf3, Fn1, Ngfr, Egr2, Tagln, Ntrk1, Nos3, Gli1, and Notch3. This study examined the alterations in global gene expression in NMS rats and systematically identified the key genes and signaling pathways in rats subjected to NMS. These findings provide insights into the complex molecular mechanisms involved in autism-like behaviors and lay the groundwork for future ASD research. The study's sequence data have been archived in the Sequence Read Archive (https://dataview.ncbi.nlm.nih.gov/object/PRJNA1275822?reviewer=skc0d219fusapt07bptheggsdu).

PMID 42158647
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