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Drug Database
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cannabidiol (Xalex 10)

✓ Approved

RAMM Pharma · CNR1

什么是 cannabidiol？

cannabidiol 是一种治疗药物，由RAMM Pharma研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Xalex 10
公司RAMM Pharma
分子靶点CNR1, TRPV1, GPR55
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, RAMM Pharma

作用机制

分子靶点

cannabidiol 作用于 3 个分子靶点：

CNR1cannabinoid receptor 1 (CNR, CB1A)
TRPV1transient receptor potential cation channel subfamily V member 1 (VR1)
GPR55G protein-coupled receptor 55 (LPIR1)
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

cannabidiol 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersEpilepsy✓ Approved

相关研究文献

PubMedJournal of psychopharmacology (Oxford, England)2026-08-05

CB1 receptor-enriched functional connectivity analysis revealed target-specific modulation by cannabidiol in early psychosis.

Lombardi Giada G, Shatalina Ekaterina E, O'Neill Aisling A, Wilson Robin R et al.

Cannabidiol (CBD) has emerged as a potential antipsychotic treatment, acting as a negative allosteric modulator of cannabinoid type-1 (CB1) receptors within the endocannabinoid system. Although previous neuroimaging studies have shown that CBD induces changes in aberrant brain activity and functional connectivity (FC) in psychosis, they have not directly integrated information about the spatial distribution of the molecular targets through which CBD may act. In this study, we aimed to investigate whether a single dose of CBD may acutely modulate CB1 receptor-enriched FC in patients with early psychosis and to compare these effects with healthy controls (HC). Thirteen patients with early psychosis (PSY) and 14 age- and sex-matched HC underwent resting-state functional magnetic resonance imaging (fMRI). Patients participated in a randomised, double-blind, placebo-controlled crossover study receiving 600 mg CBD (PSY-CBD) or matched placebo (PSY-PLB). CB1 receptor-enriched FC was computed using Receptor-Enriched Analysis of functional Connectivity by Targets (REACT), integrating Positron Emission Tomography (PET)-derived CB1 receptor maps with fMRI data. Three main findings emerged: (i) PSY-PLB showed increased CB1 receptor-enriched FC across multiple regions compared to HC; (ii) a single dose of CBD significantly reduced CB1 receptor-enriched FC of the right insular cortex relative to PLB; (iii) no differences were observed when CB1 receptor-enriched FC maps of PSY-CBD were compared with those of HC. Our findings support the potential of CBD to regulate CB1 receptor-enriched FC in early psychosis, providing mechanistic insight into its antipsychotic effects and highlighting REACT as a valuable tool for integrating molecular and functional imaging in psychiatric research.

PMID 42552898
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PubMedDer Nervenarzt2026-08-04

[Psychiatric aspects of commercially available products containing cannabidiol].

Gahr Maximilian M

Cannabidiol (CBD) has gained sustained public, medical, and scientific attention in recent years. The prevalence of use of commercially available products containing CBD (CPC) is correspondingly high. Overview of the benefits and risks of CPC, taking into account certain aspects related to CBD as a pharmaceutical active ingredient. Selective literature search in the PubMed database. Currently, only one primarily CBD-containing drug is approved in Germany (Epidyolex®). CBD demonstrates good safety and tolerability. Elevated transaminases, sedation, decreased appetite, diarrhea, sleep disturbances, infections, and weight loss are possible side effects. CBD modulates the endocannabinoid system and interacts with numerous other molecular targets. CBD is metabolized via CYP2C19, CYP3A4, and UGT. The potential for pharmacokinetic interactions with CBD has not been well studied, but is theoretically high. The potential for abuse of CBD is negligible when administered orally, but should be investigated more thoroughly for inhalation and higher-dose use. Studies have found significant discrepancies between the stated and actual CBD content in many CPC; THC was frequently detected. There is no evidence supporting the health benefits typically claimed by manufacturers for ≤ 4.3 mg of oral CBD/kg/day, but there are indications of significant hepatotoxicity at ≥ 4.3 mg of oralCBD/kg/day. There is no robust evidence of health benefits associated with CPC. However, given the levels of exposure, product deficiencies, and the EFSA safety concerns, it must be assumed that there are relevant health risks (particularly hepatotoxicity) associated with the use of CPC.

PMID 42550189
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PubMedNeoplasma2026-08-04

Neuroimmune treatment of advanced solid tumors: 3-year survival after angiotensin 1-7, pineal indoles, and cannabinoids.

Lissoni Paolo P, Monzon Alejandra A, Marroccoli Savino S, Di Fede Giuseppe G et al.

In a recent study, the exogenous administration of angiotensin 1-7 (Ang 1,7) together with melatonin, 5-methoxytryptamine, and cannabidiol increased 1-year survival in advanced cancer patients, underlining the utility of neuromodulation in oncology. We now report a single-arm interventional study to evaluate the effectiveness of introducing Ang 1-7 in the neuroimmune regime, including pineal indoles and cannabinoids. Two cohorts of patients with advanced solid tumors refractory to standard oncologic treatments and with an estimated life expectancy of less than six months were studied. The full neuroimmune regimen cohort consisted of 100 consecutive patients treated over the last three years with Ang 1-7, pineal indoles, and cannabinoids, while the comparator cohort included 212 consecutive patients treated between 2015 and 2019 with pineal indoles and cannabinoids alone. Gastroprotected capsules of Ang 1-7 coupled with cyclodextrin were administered at 0.5 mg p.o. twice/day. Melatonin (100 mg) and 5-methoxytryptamine (20 mg) were given p.o. at bedtime and in the early afternoon, respectively. Cannabidiol or cannabigerol (in the case of glioblastoma) was given at 20 mg p.o. twice/day. Clinical response, disease control, and overall survival, along with the lymphocyte-to-monocyte ratio, were evaluated. In the full regimen cohort, disease control was achieved in 67 of 100 patients, with objective tumor regression observed in 23%. In the comparator cohort, disease control was obtained in 111 of 212 patients, with objective regression in 8%. Three-year overall survival was significantly higher in the full regimen cohort (37%) compared with the comparator cohort (19%). Both treatments were associated with a significant increase in the lymphocyte-to-monocyte ratio, suggesting an improvement in systemic immune status. The addition of Ang 1-7 to a neuroimmune regimen combining pineal indoles and cannabinoids was associated with improved disease control and long-term survival in patients with end-stage solid tumors lacking effective therapeutic options.

PMID 42549589
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PubMedBiochemical and biophysical research communications2026-08-02

Cross-species causal gene mapping reveals brain-region-specific targets of Cannabidiol for post-traumatic stress disorder treatment.

Rao Hui H, Xie Guanbo G, Wu Ning N, Li Jin J et al.

Post-traumatic stress disorder (PTSD) involves hippocampal and prefrontal dysfunction. Cannabidiol (CBD) shows therapeutic promise, but its cell-type-specific and causal mechanisms remain unclear. We performed single-cell RNA sequencing of hippocampal and prefrontal cortices from PTSD mice, healthy controls, and CBD-treated PTSD mice. Genes dysregulated in PTSD and reversed by CBD were integrated with human PTSD GWAS and brain eQTL datasets using summary-data-based Mendelian randomization (SMR) to identify causal risk targets. Molecular docking assessed direct CBD-protein interactions. PTSD induced extensive transcriptional alterations, most prominent in excitatory neurons. SMR analysis identified 15 potential causal risk genes linked to PTSD. Among these, 7 high-confidence targets were confirmed to be transcriptionally responsive to CBD treatment. In the hippocampus, key causal targets included LYNX1 (OR = 0.75, 95% CI: 0.57-0.98, P = 0.038), RAB3C (OR = 1.291, 95% CI: 1.052-1.584, P = 0.015), MAGI2 (OR = 1.15, 95% CI: 1.00-1.31, P = 0.048), LINGO2 (OR = 1.48, 95% CI: 1.07-2.03, P = 0.017), and UNC5D (OR = 1.41, 95% CI: 1.03-1.93, P = 0.032). In the prefrontal cortex, identified targets were CNTN3 (OR = 0.78, 95% CI: 0.62-0.98, P = 0.036), IGSF21 (OR = 1.22, 95% CI: 1.04-1.42, P = 0.012). While SEPTIN3 (OR = 1.25, 95% CI: 1.01-1.56, P = 0.043) was identified as a causal risk gene, its expression was not reversed by CBD. Molecular docking indicated that all 15 SMR-identified candidates possess strong binding affinity to CBD, including RAB3C (-8.636 kcal/mol), CNTN3 (-7.216 kcal/mol), and LINGO2 (-6.222 kcal/mol), which suggests a direct pharmacological interaction. This study identifies causal, region-specific CBD targets in PTSD, providing a mechanistic basis for precision therapeutic interventions.

PMID 42542041
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PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-08-02

Ubiquitin-proteasome-dependent degradation of HIF-1α by cannabidiol disrupts pro-angiogenic synoviocyte-endothelial crosstalk in rheumatoid arthritis.

Chen Jing J, Li Gejing G, Zhao Fang F, Zhang Ye Y et al.

Cannabidiol (CBD), a major non-psychoactive phytocannabinoid derived from Cannabis sativa L., has shown therapeutic potential in rheumatoid arthritis (RA). However, the mechanisms by which CBD modulates synovial angiogenesis remain unclear. This study aimed to investigate whether CBD attenuates RA progression by suppressing synovial angiogenesis and to elucidate the underlying molecular mechanisms. An adjuvant-induced arthritis (AIA) rat model was established to evaluate the therapeutic effects of CBD in vivo using arthritis scoring, micro-CT, and histopathological, immunohistochemical, and immunofluorescence analyses. In vitro, cytotoxicity was determined using the CCK-8 assay, followed by evaluations of CBD's direct effects on the proliferation, migration, invasion, and inflammatory responses of RA fibroblast-like synoviocytes (RA-FLS) were evaluated, alongside Cell Counting Kit-8 (CCK-8) for cytotoxicity screening. Furthermore, the paracrine regulation of angiogenesis was assessed using a conditioned medium (CM) transfer system from hypoxia-stimulated RA-FLS applied to human umbilical vein endothelial cells (HUVECs). Molecular mechanisms were analyzed via Western blotting, RT-qPCR, ELISA, co-immunoprecipitation (Co-IP), molecular docking, and targeted proteasome inhibition (MG132). In vivo, CBD (5 and 10 mg/kg) treatment markedly alleviated joint inflammation, synovial angiogenesis, and structural bone destruction in AIA rats. In vitro, non-cytotoxic concentrations of CBD (2.4-4.8 μM) significantly suppressed aberrant RA-FLS proliferation, migration, invasion, and pro-inflammatory cytokine secretion. Mechanistically, CBD abrogated the hypoxia-induced accumulation of hypoxia-inducible factor-1α (HIF-1α) protein in RA-FLS without significantly altering HIF1A mRNA expression. This reduction was effectively reversed by MG132. Co-IP and molecular docking analyses revealed that CBD directly enhances the polyubiquitination of HIF-1α through stable structural interactions, driving a ubiquitin-proteasome-dependent degradation mechanism. Consequently, CBD dose-dependently decreased the extracellular secretion of vascular endothelial growth factor A (VEGFA) and angiopoietin-2 (ANG-2) from RA-FLS. Functionally, CM from CBD-treated RA-FLS disrupted the pro-angiogenic paracrine crosstalk-independent of direct CBD carryover-significantly impairing HUVEC migration, capillary-like tube formation, and downstream VEGFR2 (Tyr1175) phosphorylation. CBD attenuates RA pathogenesis not only by directly suppressing RA-FLS hyperactivity but also by severing the pro-angiogenic paracrine crosstalk between RA-FLS and endothelial cells. These effects are driven by the ubiquitin-proteasome-dependent degradation of HIF-1α in RA-FLS via direct structural engagement, which depletes VEGFA/ANG-2 production and subsequent endothelial VEGFR2 activation. These findings highlight CBD as a promising disease-modifying anti-angiogenic therapeutic agent for RA.

PMID 42542056
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PubMedPharmacology research & perspectives2026-08-01

The Relationship Between (Endo)cannabinoids, the Microbiome and Melanoma.

Javid Farideh A FA, Golčić Marin M, Hrkać Anja Harej AH, Belančić Andrej A

Despite advances in targeted and immunotherapy for melanoma, resistance to treatment and severe adverse effects pose significant challenges. This necessitates the development of new treatment strategies, and cannabinoids, because of the extensive preclinical evidence for their cytotoxic action on carcinoma cells in a variety of cancers, can offer a novel therapeutic option when used appropriately. Indeed, the potential therapeutic benefits of cannabinoids were formally recognized in the world and much more recently in the United Kingdom when cannabis-based medicinal products were moved from Schedule 1 of the Misuse of Drugs Regulations 2001 to Schedule 2 in 2018. This move further encouraged scientists to look at more applications of cannabinoids in different disorders. Although the potential psychoactivity of cannabis as a Schedule 1 drug hinders research, more research could focus on non-psychoactive components such as cannabidiol (CBD) and cannabigerol (CBG). This review summarizes some past and current research on the relationship between the cannabinoid system and the microbiome in patients with metastatic melanoma who undergo immunotherapy. The review also provides a comprehensive background on the function of the cannabinoid system in normal and diseased skin, as well as future directions in using cannabinoids as an adjunct to chemotherapeutics in the treatment of the disease.

PMID 42538621
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