Drug Database
CA

cannabidiol (Xalex 10)

✓ Approved

RAMM Pharma · CNR1

What is cannabidiol?

cannabidiol is a therapeutic agent developed by RAMM Pharma. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesXalex 10
CompanyRAMM Pharma
Molecular TargetCNR1, TRPV1, GPR55
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, RAMM Pharma

Mechanism of Action

Molecular Targets

cannabidiol acts on 3 molecular targets:

CNR1cannabinoid receptor 1 (CNR, CB1A)
TRPV1transient receptor potential cation channel subfamily V member 1 (VR1)
GPR55G protein-coupled receptor 55 (LPIR1)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

cannabidiol is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Nervous system disordersEpilepsy✓ Approved

Related Research Articles

PubMedJournal of cannabis research2026-11-11

The effect of organic amendments on cannabidiol yield and topsoil health (0-10 cm) in floral hemp (Cannabis sativa L.) production system.

Atoloye Idowu I, Rai Dipti D, George Ashlee A, Massie Pippin P et al.

Compost and cover crops enhance soil health and crop productivity in agricultural systems, yet their integration as soil management strategies in floral hemp (Cannabis sativa L.) production remains underexplored. Understanding these effects is critical for optimizing cannabidiol yield while building soil health. In a two-year field study in north-central North Carolina, USA, we evaluated the effects of compost, cover crops, and their combination, and a non-fertilized control on soil health and cannabidiol yield in two floral hemp cultivars, Spectrum and Therapy. The experiment utilized a randomized complete block split-plot design with soil health indicators and agronomic parameters measured across multiple growth stages. Treatment effects varied substantially by year and cultivar. In 2021, compost produced the highest cannabidiol yields for both cultivars-1.1 to 2.6 times greater than control and cover crop treatments. By 2022, compost-cover crop treatment had the highest yields for Spectrum, while Therapy responded minimally to amendments. Organic amendments increased soil organic carbon by 15%, total nitrogen by 20%, and microbial activity by 25%, particularly in year two. Mid-vegetative leaf nitrogen concentration emerged as a strong predictor of yield, explaining 52% of dry inflorescence and 40% of cannabidiol yield variation. Principal component analysis revealed that compost and compost-cover crop treatments clustered with enhanced soil biological indicators (soil organic carbon, total nitrogen, soil test biological activity, and permanganate oxidizable carbon) and higher yields, though year-specific environmental conditions resulted in distinct response patterns. Compost and combined compost-cover crop amendments improved soil health metrics, with benefits accumulating by year two. Cover crops alone provided minimal advantage. The effectiveness of organic amendments depends on cultivar selection and environmental conditions, necessitating multi-year evaluations to develop reliable management recommendations for CBD hemp production systems.

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PubMedJournal of cannabis research2026-11-11

A human microbiota-associated translational mouse model reveals sex-specific responses to cannabidiol and cannabigerol.

Keohane Eva E, Poehlein Lance L, Chaparro Jacqueline M JM, Wrigley Scott D SD et al.

Cannabidiol (CBD) and cannabigerol (CBG) are non-psychoactive phytocannabinoids with therapeutic potential, yet their effects on host physiology and interactions with the gut microbiome remain poorly defined. Here, we used a translational mouse model colonized with human-associated microbiotas to investigate the effects of oral CBD and CBG intervention on microbial composition, endocannabinoid signaling, and intestinal protein expression. While neither phytocannabinoids altered overall gut microbiome diversity, both induced sex-specific shifts in bacterial taxa associated with mucin utilization and short-chain fatty acid production. Circulating concentrations of CBD were higher than those of CBG, and females exhibited higher plasma phytocannabinoid concentrations than males. Males treated with CBD had elevated anandamide (AEA) levels, potentially reflecting inhibition of fatty acid amide hydrolase, consistent with upregulation of serine protease inhibitors observed in ileal proteomes. Females also accumulated more subcutaneous adipose tissue with both CBD and CBG treatment resulting in greater total CBD storage in this depot. Collectively, these findings suggest sex-specific interactions between phytocannabinoids, the endocannabinoid system, and the gut microbiome, underscoring the importance of considering biological sex in cannabinoid research and informing personalized therapeutic strategies.

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PubMedBiochemical and biophysical research communications2026-11-10

Cannabidiol abrogates the atypical enlargement of mitochondria in Tafazzin-deficient B-lymphoblastoid cells.

Chan John Z JZ, Groh Mishi M, Musa Musa M, Sciaini German G et al.

Barth Syndrome (BTHS) is a rare, X-linked disorder caused by the loss of function of Tafazzin, an enzyme responsible for the remodelling of cardiolipin. Although neutropenia is the best-characterized immunological deficit in BTHS, recent studies have also demonstrated deficiencies in B-cell and T-cell populations. BTHS patient-derived B-lymphoblastoid cells have been widely used to investigate the mitochondrial abnormalities associated with the disease. Our group, and others, have previously reported alterations in mitochondrial cristae architecture and the presence of abnormally enlarged mitochondria in these cells. Recently, we demonstrated that treatment of BTHS B-lymphoblastoids with the phytocannabinoid cannabidiol (CBD) restores maximal respiratory capacity, total cardiolipin content, the ratio of monolysocardiolipin to cardiolipin, and cell growth. However, the effects of CBD in restoring other mitochondrial parameters, including the relative abundance of various electron transport chain (ETC) proteins, and the profile of cardiolipin fatty acyl species, were ineffective or incomplete. Building on these findings, the present study aimed to examine whether CBD altered mitochondrial morphology and dynamics in Tafazzin-deficient B-lymphoblastoid cells. Using transmission electron microscopy, we found that CBD reversed the mitochondrial enlargement in BTHS B-lymphoblastoid cells but had no significant effect on cristae architecture. CBD fully reversed the elevated phosphorylation of Drp1 at the fission-inhibitory Ser637 site, strongly suggesting that the reduction in mitochondrial enlargement following CBD treatment involves the modulation of mitochondrial fission. Our results support the notion that cardiolipin composition, not just content, is important for mitochondrial ultrastructure in mammalian cells, and also supports a role for CBD in regulating mitochondrial dynamics.

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PubMedEuropean journal of pharmacology2026-11-10

Chronic Topical Water-Soluble Cannabidiol Formulation Reduces Intraocular Pressure and Corneal Mechanical Sensitivity in DBA/2J Mice.

Garcia Miguel M MM, Paniagua Nancy A NA, Rodríguez-Rivera Carmen C, Paradas Paola S PS et al.

Glaucoma is a multifactorial neurodegenerative disease and a leading cause of irreversible blindness worldwide. Although elevated intraocular pressure (IOP) is the main modifiable risk factor, current therapies often fail to fully prevent disease progression and may cause ocular discomfort. Cannabidiol (CBD) has attracted increasing interest due to its anti-inflammatory, analgesic and vasoregulatory properties, yet its ocular effects remain controversial, partly due to formulation-dependent limitations and short-term administration paradigms. We evaluated a novel water-soluble topical CBD formulation in a spontaneous murine model of glaucoma (DBA/2J mice), using CD-1 mice as a non-glaucomatous comparator strain. IOP, tear production, corneal mechanical sensitivity and body weight were assessed longitudinally in conscious animals following acute and chronic CBD administration (once or twice daily). Contralateral untreated eyes were analyzed to investigate potential systemic or bilateral effects. Following an initial transient IOP increase, topical CBD progressively induced a significant and sustained reduction of IOP in the treated eyes of DBA/2J mice, particularly during chronic twice-daily administration. IOP changes in contralateral eyes were smaller and inconsistent, supporting a predominantly local ocular effect. CBD also increased corneal touch threshold in DBA/2J mice, indicating reduced corneal mechanical sensitivity, with effects persisting after treatment withdrawal. Tear production and body weight were not significantly affected in either strain, suggesting good ocular and systemic tolerability. Overall, chronic topical administration of a water-soluble CBD formulation lowered IOP and modulated corneal sensitivity in a strain-dependent manner. These findings support CBD as a potential adjunctive therapeutic strategy targeting both ocular hypertension and sensory dysfunction.

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PubMedJournal of inflammation research2026-11-10

Isoform-Selective and Context-Dependent Modulation of Nitric Oxide Synthase by Cannabidiol: A Mechanistic Review of Preclinical Evidence in Neurological and Neuropathic Disorders.

Adnan Azeez Aboomaima Wiqar W, Hasan Burhan Abbas A, Aziz Abu Omaima Hiba Adnan HA, Mahmoudi Ali A

Nitric oxide (NO), produced by nitric oxide synthase (NOS) isoforms, plays a dual role in the central nervous system. Cannabidiol (CBD), a non-psychoactive phytocannabinoid, has shown promise as a neuroprotective and anti-inflammatory agent. This narrative review examines the complex interactions between CBD and NOS isoforms, including neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) variants, and discusses how these may contribute to its neuroprotective and analgesic properties. Preclinical evidence, primarily from cellular and animal models, indicates that CBD can reduce excessive NO production, particularly by inhibiting iNOS in neuroinflammatory conditions. However, the effects of CBD on nNOS are context-dependent and cannot be characterized simply as inhibitory: while CBD may attenuate pathological nNOS-mediated excitotoxicity in some models, nNOS-derived NO is also required for CBD-induced analgesia in certain neuropathic pain models, where nNOS activation and downstream NO signaling contribute to antinociception. The strongest preclinical evidence supports CBD-mediated suppression of pathological iNOS expression and NO production in neuroinflammatory conditions. The effects of CBD on nNOS are context-dependent and cannot be characterized simply as inhibitory: while CBD may attenuate pathological nNOS-mediated excitotoxicity in some models, nNOS-derived NO is also required for CBD-induced analgesia in certain neuropathic pain models, where nNOS activation and downstream NO signaling contribute to antinociception. Similarly, evidence for eNOS-mediated vascular benefits in the CNS remains preliminary and largely derived from peripheral studies, and cerebrovascular eNOS effects require further investigation. We review the potential therapeutic implications of these interactions in neurological conditions such as Alzheimer's disease, multiple sclerosis, depression, and neuropathic pain. The review also addresses antioxidant and anti-nitrosative benefits of CBD, pharmacokinetic challenges, and research gaps, including the need for clinical trials with biomarkers to validate NOS-related findings. By integrating molecular, preclinical, and translational perspectives, this review provides insights into the context-dependent and isoform-selective modulation of NOS by CBD, emphasizing that the strength of evidence varies by isoform, with iNOS and nNOS modulation being better established than eNOS-related effects.

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PubMedBMC complementary medicine and therapies2026-11-10

The role of cannabidiol treatment in reducing HER2 expression and inducing ER stress-mediated apoptosis in HER2-positive breast cancer.

Çakmak Eser E, Bi̇lgi̇ci̇ Bi̇rşen B

Cannabidiol (CBD) has attracted attention as a potential anticancer agent due to its observed efficacy, particularly in breast cancer. However, the exact molecular pathway through which it exerts its anticancer effects remains unknown. The present study aimed to investigate the effects of CBD on the HER2 receptor, endoplasmic reticulum (ER) stress signaling pathway, and apoptosis in HER2-positive breast cancer cells, as well as to examine the effect of trastuzumab (TZB), used in treatment, on the ER stress signaling pathway. For this purpose, SKBR3 cells were treated with CBD at three different concentrations (9.38, 18.75, and 37.5 µM), TZB at 62.5 µg/mL, and two combinations of TZB and CBD (18.75 µM CBD + 62.5 µg/mL TZB and 37.5 µM CBD + 62.5 µg/mL TZB). Cell proliferation was assessed using real-time cell analysis, while expression levels of ER stress-associated genes were measured by qPCR. Apoptosis was analyzed by Annexin V/PI flow cytometry. Findings revealed that CBD, TZB, or their combination were associated with reduced cell proliferation, significant activation of ER stress pathways, and increased apoptosis, while CBD was associated with marked downregulation of HER2 gene expression. Treatment with 9.38 µM CBD, 18.75 µM CBD, 37.5 µM CBD, 62.5 µg/mL TZB, 18.75 µM CBD + 62.5 µg/mL TZB, and 37.5 µM CBD + 62.5 µg/mL TZB significantly increased GRP78, PERK, IRE1, ATF6, eIF2A, ATF4, CHOP, and XBP1s gene expression levels, and significantly decreased HER2 gene expression at all doses except 62.5 µg/mL TZB. All doses significantly increased the total number of apoptotic cells and were associated with significantly reduced cell viability. The present findings demonstrated that both TZB and CBD are associated with activation of the ER stress response and induction of apoptosis in HER2-positive breast cancer cells, and that CBD is associated with downregulation of HER2 receptor gene expression. Collectively, our results indicate that CBD may have potential as an adjunct or alternative strategy in HER2-positive breast cancer, although further in vivo studies are required to evaluate the efficacy and safety of its combination with low-dose TZB.

PMID 43004316
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