北京若生智能科技有限公司
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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

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.

PMID 42925024
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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.

PMID 42909680
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PubMedFASEB bioAdvances2026-10-17

Microbiome-Endocannabinoidome Crosstalk as an Immunometabolic Rheostat in Inflammatory Disease.

Maghembe Reuben S RS, Damian Donath D, Bahati Samweli S, Makaranga Abdalah A

Chronic inflammatory diseases reflect disrupted coordination among microbial ecology, epithelial barriers, lipid signaling, and immunity. The microbiome-endocannabinoidome (eCBome) axis is already recognized as a regulator of metabolism, permeability, and inflammatory tone; the unresolved issue is how to distinguish direct crosstalk from parallel or associative changes. This review therefore operationalizes the axis as an immunometabolic rheostat defined by five measurable domains: microbial functions and metabolites, compartment-specific eCBome ligands and enzymes, barrier integrity and microbial translocation, immune-cell programming, and tissue or clinical outcomes. We distinguish classical endocannabinoids (anandamide and 2-arachidonoylglycerol) from the endocannabinoid-related N-acylethanolamines palmitoylethanolamide and oleoylethanolamide, which act prominently through PPARα, TRPV1, GPR119, and related pathways. Evidence is appraised as direct causal, mechanistically supportive, associative, or hypothesis-generating. The strongest causal foundation links microbiota manipulation to intestinal eCBome tone, permeability, and metabolic endotoxemia, while disease-specific evidence is most developed in obesity-associated inflammation and inflammatory bowel disease. Engineered Lactobacillus paracasei platforms that produce PEA or OEA in situ provide particularly informative proof-of-concept because they couple a defined microbial perturbation to lipid-mediator release, receptor-dependent barrier effects, and inflammatory or metabolic outcomes. By contrast, evidence in MASLD/MASH, neuroinflammation, and systemic autoimmunity remains more compartment-dependent and heterogeneous. Clinical translation must account for the psychiatric toxicity that ended centrally active CB1 antagonism with rimonabant, the target and off-target complexity of FAAH/MAGL inhibition, and limitations of surrogate barrier biomarkers. A causal roadmap should combine gnotobiotic and loss-of-function models, isotope tracing, organoids, and gut-on-chip systems with tissue-resolved lipidomics and longitudinal, biomarker-enriched human trials.

PMID 42889337
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PubMedAnimals : an open access journal from MDPI2026-10-16

Molecular Mechanisms Underlying α-Linolenic Acid-Enhanced Reproductive Performance in Male Blue Foxes.

Yuan Chongshan C, Qi Shuai S, Tian Yu Y, Cao Wenhui W et al.

α-Linolenic acid (ALA), an essential n-3 polyunsaturated fatty acid, exerts critical effects on animal reproductive function. However, the molecular mechanisms by which dietary ALA regulates reproductive performance in male blue foxes remain largely unclear. In the present study, 16 male blue foxes of similar age and condition were assigned to four dietary groups (n = 4 per group) receiving a basal diet supplemented with 0, 0.5, 1.25, or 2 g/kg of ALA. q-PCR validation further confirmed that medium-dose ALA supplementation significantly upregulated mRNA levels of steroid synthesis-related genes (StAR, LHCGR, INSL3) and antioxidant gene GPX3, while inhibiting the calcium-signaling gene GRIN1. Untargeted liquid chromatography-mass spectrometry (LC-MS) metabolomics of seminal plasma and RNA-seq transcriptomics of testicular tissue were combined to explore the underlying molecular pathways of ALA in terms of its modulating male blue fox reproduction. A total of eight significantly altered seminal plasma metabolites were screened out through metabolomics: mainly arachidonic acid, anandamide, oxaloacetic acid, guanine, lactic acid, dihydrodaidzein, stearic acid, and valylisoleucine. Transcriptomic analysis identified seven differentially expressed genes (DEGs), including FRAS1, COL1A1, CDH17, CLDN4, CTH, KYAT1, and GRIN1, enriched in three core KEGG pathways: ECM-receptor interaction, cell-adhesion molecules and selenocompound metabolism. Spearman correlation analysis revealed extensive significant correlations between seminal-plasma differential metabolites and testicular genes, indicating complicated metabolite-gene crosstalk. Collectively, appropriate dietary ALA remodels the seminal-plasma metabolic microenvironment, stabilizes testicular tissue structure, enhances gonadal antioxidant capacity and facilitates testicular steroidogenesis, thereby improving the reproductive potential of male blue foxes. This study elucidates the nutritional regulatory mechanism of ALA in breeding male blue foxes and provides theoretical references for the application of ALA as a functional feed additive in the production of canines.

PMID 42882953
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PubMedBiochemical and biophysical research communications2026-10-11

Stage-dependent expression of CB1 and CB2 receptors and their vascular effects during the progression of diet-induced atherosclerosis.

Álvarez-Valadez María Del Rosario MDR, Virgen-Ortiz Adolfo A, Rodríguez-Hernández Alejandrina A, Limón-Miranda Saraí S et al.

Cardiovascular diseases (CVDs) remain the leading cause of global mortality, with ischemic heart disease and stroke representing the most common clinical manifestations. Atherosclerosis, a chronic inflammatory disorder of the arterial wall, constitutes the primary pathological basis of these conditions. Recent studies have implicated the endocannabinoid system (ECS), which includes cannabinoid receptors CB1 and CB2, their endogenous ligands, and metabolic enzymes, in the pathophysiology of atherosclerosis. In the present study, we explored the molecular and functional interactions between the ECS and diet-induced atherosclerosis in Wistar rats. Our results show distinct expression patterns of CB1 and CB2 receptors in the aortic wall, with significant downregulation observed in the advanced stages of atherosclerosis. Functional assays demonstrated stage-dependent vascular responses to selective CB1 and CB2 agonists, indicating that modulation of the ECS influences vascular tone and blood pressure. Additionally, biochemical analysis of endocannabinoids and their catabolic enzymes, including 2-arachidonoylglycerol (2-AG)/monoacylglycerol lipase (MAGL) and anandamide (AEA)/fatty acid amide hydrolase (FAAH), revealed dynamic alterations throughout the course of disease progression. These findings underscore the critical role of the ECS in vascular homeostasis and suggest that cannabinoid-based therapeutic strategies may hold potential for the management of atherosclerotic cardiovascular disease.

PMID 42858650
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PubMedFrontiers in cell and developmental biology2026-10-11

Integrated lipidomic and transcriptomic profiling of imiquimod-induced psoriasiform dermatitis.

Wisniewski Eva E, Du Wenwen W, Himelstein Jenna A JA, Szanda Gergő G et al.

Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and immune dysregulation. Emerging clinical and experimental evidence suggests that endogenous lipid (endolipid) signaling systems, including the endocannabinoid system (ECS), represent a promising therapeutic target to treat psoriasis; however, comprehensive characterization of small-molecule endolipids and related proteins in psoriatic skin and their relationship to systemic changes remains limited. Here, we used the imiquimod (IMQ)-induced mouse model of psoriasis to perform combined lipidomic and transcriptional profiling of endolipid signaling in both skin and plasma. Targeted lipidomics revealed a striking divergence between tissues: most endolipids increased in inflamed skin but decreased in plasma, including the canonical ECS lipids anandamide and 2-arachidonoylglycerol. In contrast, selected lipid species, including taurine-conjugated metabolites (both N-acyl taurines and bile acids), were elevated in both tissues, indicating pathway-specific regulation. Targeted transcriptional analysis of whole skin showed reduced expression of key endolipid biosynthetic enzymes (Napepld, Dagla, Daglb) and the cannabinoid receptor Cnr1, while Cnr2 and ECS-related metabolic enzymes remained unchanged. Additional alterations were observed in transcripts involved in related endolipid signaling (Trpv1, Trpv4, Ppara, Pparg, Gpr55), bile acid metabolism (Fxr, Bsep, Fabp4, Fabp5, Cyp27a1, Cyp8b1), and inflammatory pathways (Cox-2). To resolve this apparent discrepancy between lipid levels and gene expression, we performed compartment-specific analyses of epidermal and dermal layers. These revealed a predominantly suppressive epidermal response across multiple ECS-related proteins, contrasted by a more variable dermal profile with selective preservation or upregulation, particularly of Cnr2. Together, these findings demonstrate that psoriasiform inflammation is associated with compartment-specific remodeling of endolipid signaling across skin and systemic compartments, underscoring the functional heterogeneity of epidermal and dermal layers. This dataset provides novel insights into the dysregulation of endolipid signaling systems in psoriasis and provides a foundation for the development of spatially informed, lipid-based therapeutic strategies.

PMID 42856670
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