北京若生智能科技有限公司
Drug Database
AN

anandamide (anandamide)

✓ Approved

Yissum · CNR1

什么是 anandamide？

anandamide 是一种治疗药物，由Yissum研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名anandamide
公司Yissum
分子靶点CNR1, CNR2
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, Yissum

作用机制

分子靶点

anandamide 作用于 2 个分子靶点：

CNR1cannabinoid receptor 1 (CNR, CB1A)
CNR2cannabinoid receptor 2 (CX5, CB-2)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

anandamide 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Psychiatric disordersAnorexia nervosa✓ Approved
Psychiatric disordersBulimia nervosa✓ Approved

相关研究文献

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
阅读全文 →
PubMedThe Journal of physiology2026-09-03

N-Arachidonoyl-phosphatidylethanolamide phospholipase D activation by muscarinic receptors.

Murataeva Natalia N, Schmitt Connor C, Hyman Elyssa E, Wager-Miller Jim J et al.

The endogenous cannabinoid signalling system consists of G protein-coupled receptors, messengers - 2-arachidonoylglycerol (2-AG) and anandamide - and enzymatic machinery to synthesize and metabolize these messengers. Anandamide is physiologically important, but its synthesis is incompletely understood. N-Arachidonoyl-phosphatidylethanolamide phospholipase D (NAPE-PLD) synthesizes acylethanolamines, including anandamide, but how is NAPE-PLD activated? We used genetically encoded G protein-coupled receptor based (GRAB) sensors for endocannabinoids (eCBs) and immunohistochemistry to investigate. Human embryonic kidney 293 (HEK293) cells natively express Gq-coupled muscarinic M3 receptors. The muscarinic agonist oxotremorine-M stimulated the GRABeCB sensor only when HEK293 cells were cotransfected with NAPE-PLD. This signal was reduced by the NAPE-PLD inhibitor LEI401 and required both phospholipase C and internal calcium stores. Gq-coupled mGluR5 glutamate receptors effectively substitute for M3 receptors. Thus M3 receptors stimulate NAPE-PLD synthesis of acylethanolamines such as anandamide via Gq signalling pathways resembling those for 2-arachidonoylglycerol. Parasympathetic activation stimulates tearing and salivation via M3 receptors on myoepithelial cells. The cannabinoid signalling system may act as a feedback inhibitor to inhibit acetylcholine release, but the identity and source of the endogenous cannabinoid messenger are uncertain. NAPE-PLD and M3 proteins colocalize in myoepithelial cells; fatty acid amide hydrolase (FAAH) resides in glandular acinar cells. Oxotremorine-M stimulation of lacrimal or submandibular salivary glands co-cultured with HEK293-GRABeCB cells stimulated GRABeCB responses. This response was diminished by LEI401 and was also present in cells expressing GRABAEA, an anandamide-specific sensor, but not those expressing GRAB2AG. We conclude that muscarinic M3 receptors stimulate NAPE-PLD to produce anandamide in cell lines and exocrine glands. This means of stimulating anandamide synthesis may play many roles in the body. KEY POINTS: The cannabinoid signalling system plays important roles in the body and in doing so makes use of two endogenous messengers, 2-arachidonoylglycerol (2-AG) and anandamide. The regulation of anandamide synthesis is still poorly understood. This study demonstrates that muscarinic Gq-coupled GPCRs can stimulate anandamide production by activating the enzyme N-arachidonoyl-phosphatidylethanolamide phospholipase D (NAPE-PLD) and further shows that this occurs natively in salivary and lacrimal glands. Muscarinic Gq-coupled G protein-coupled receptor (GPCR) activation of NAPE-PLD to induce anandamide synthesis may play many roles in the body.

PMID 42687141
阅读全文 →
PubMedBMC medicine2026-09-02

Endocannabinoid dynamics across marathon and ultramarathon running: evidence from two field studies.

Siebers Michael M, Huvermann Dana D, Siebers Christoph C, Canales-Romero Deborah D et al.

Endocannabinoid (eCB) signaling has been implicated in the physiological and affective responses to endurance exercise, including phenomena such as the runner's high. However, although humans have the capacity to run for several hours and even days, evidence regarding eCB signaling is largely limited to exercise bouts shorter than 60 min. Consequently, the temporal dynamics of eCB signaling during prolonged running and the accompanying acute affective responses remain unclear. This study investigated eCB signaling during long-distance running and following a 45-minute break. Two studies were conducted: In Study 1, 19 trained runners completed both a marathon and a duration-matched walking session, with repeated blood sampling every 14 km during the marathon and after a 45-minute recovery. In Study 2, 36 ultramarathon runners completed races of 100 km, 160 km, or 230 km and provided blood samples before and after their respective races. Plasma concentrations of anandamide (AEA), 2-arachidonoylglycerol (2-AG), 1-AG, arachidonic acid (AA), and palmitoylethanolamide (PEA) were quantified by a standardized liquid chromatography/multiple reaction monitoring assay. Euphoria, anxiety, and pain were assessed as core features of the runner's high using visual analog scales. AEA increased progressively throughout the marathon and remained elevated after 45 min, whereas walking elicited only modest changes. In line, after all ultramarathon distances AEA levels were increased compared with baseline. By contrast, an increase in 2-AG during exercise was observed only in the regular marathon, where concentrations rose significantly during the later stages of running and into early recovery. Elevated post-race 2-AG levels were also observed following all ultramarathon distances, consistent with a delayed, recovery-related response. Marathon running was associated with higher euphoria and lower anxiety than walking, while pain increased after 28 km of running. Ultramarathon running increased pain, reduced anxiety, and did not significantly alter euphoria post-exercise. Together, these findings show robust, time-dependent changes in circulating eCB concentrations during and after prolonged endurance running, as well as gradual increases in AEA during walking. These eCB dynamics occurred alongside acute affective changes during sustained endurance exercise.

PMID 42681668
阅读全文 →
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
阅读全文 →
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
阅读全文 →
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
阅读全文 →

注册免费账户还可查看另外 4811 篇文献

免费注册查看全部文献 →

了解更多anandamide