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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

PubMedThe Journal of pharmacology and experimental therapeutics2026-10-14

Antinociceptive interaction of Δ9-tetrahydrocannabinol and cannabidiol in a humanized mouse model of sickle cell disease.

Mabou Tagne Alex A, Ajeigbe Olufunke Florence OF, Avalos Heidi C HC, Galvani Francesca F et al.

Sickle cell disease (SCD) is characterized by recurrent, debilitating pain. Opioid analgesics are routinely used in its management, but limited efficacy and pervasive side effects prompt many patients with SCD to seek alternatives, including cannabis. Prior work has shown that 2 major cannabis constituents, Δ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD), exert antinociceptive effects in HbSS-BERK mice, a model of SCD. The present study investigated the pharmacological interaction between these 2 agents and characterized the effects associated with repeated coadministration. Fixed-ratio isobolographic analyses demonstrated that Δ9-THC and CBD produced dose-dependent antinociception following acute coadministration. Fixed-ratio isobolographic analyses showed that the experimentally determined median effective dose of the mixture was lower than the theoretical additive dose, but the difference was not statistically significant, supporting an additive antinociceptive interaction. Repeated coadministration maintained antinociceptive efficacy over 14 days and reduced SCD-evoked anxiety-like behavior in one cohort but did not improve recognition-memory deficits. Liquid chromatography-tandem mass spectrometry analyses revealed that repeated coadministration increased plasma CBD concentrations, produced a modest increase in Δ9-THC exposure, and markedly elevated circulating levels of the endocannabinoid 2-arachidonoyl-sn-glycerol. Molecular analyses of spinal cord tissue showed that HbSS-BERK mice exhibited increased oxidative stress (malondialdehyde, MDA) and proinflammatory signaling (interleukin [IL]-1β mRNA), with no change in anti-inflammatory signaling (IL-10 mRNA). Following 14 days of treatment, CBD reduced MDA and IL-1β transcription, whereas Δ9-THC reduced MDA and increased IL-10. Notably, the combination treatment simultaneously reduced oxidative stress, suppressed IL-1β, and enhanced IL-10. Together, these findings demonstrate an additive antinociceptive interaction between Δ9-THC and CBD and sustained efficacy during repeated administration in SCD mice. SIGNIFICANCE STATEMENT: Chronic pain in sickle cell disease remains difficult to treat, and many patients use cannabis despite limited understanding of how its constituents interact to produce analgesia. This study demonstrates that the 2 major phytocannabinoids in cannabis, Δ9-tetrahydrocannabinol and cannabidiol, produce additive antinociceptive effects in a humanized mouse model of sickle cell disease, and their combined efficacy is maintained during repeated administration without detectable tolerance.

PMID 42874273
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PubMedAlcohol and alcoholism (Oxford, Oxfordshire)2026-10-14

Effects of cannabidiol on risky decision-making and autonomic function in alcohol use disorder.

McGuire Ellen E, Hurzeler Tristan T, Logge Warren W, Watt Joshua J et al.

To examine the effects of cannabidiol (CBD) on psychophysiological responding and risky decision-making in individuals with alcohol use disorder (AUD). In a double-blind, placebo-controlled crossover trial, 18 participants with AUD completed the Columbia Card Task (CCT) following administration of CBD and placebo. Skin conductance responses (SCR) and high-frequency heart rate variability (HF-HRV) were assessed as indices of autonomic responding during task performance. Risk-taking was indexed by the number of cards selected on the CCT. CBD did not significantly affect SCR (P = .16, pBH = .326) or risky decision-making on the CCT (P > .63, pBH = 0.67). However, CBD significantly increased HF-HRV (β = 0.53, SE = 0.19, P = .005; pBH = 0.020). There was no evidence that the relationships between HF-HRV or SCR and risky decision-making differed between CBD and placebo conditions (drug × HF-HRV: P = .92; drug × SCR: P = .958; both pBH = .958). CBD increased HF-HRV but did not significantly alter SCR, risky decision-making, or the relationship between autonomic responses and risky decision-making. These findings suggest that CBD influences autonomic responding during task performance, although the functional significance of this effect remains uncertain. The modest sample size and relatively healthy, non-treatment-seeking sample may have limited the ability to detect broader physiological and behavioural effects.

PMID 42873665
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PubMedFrontiers in pharmacology2026-10-14

Protective effects of cannabidiol against acute stress: behavioral responses and corticosterone concentrations in female Wistar rats.

Uršič Matjaž M, Karaer Mina Cansu MC, Gregorič Alenka A, Vake Tilen T et al.

Cannabidiol (CBD) has been widely investigated for its potential anxiolytic and stress-modulating effects. This study evaluated whether CBD reduces the stress response induced by acute restraint stress in rats. Thirty-six female Wistar rats were randomly assigned to six groups. Four experimental groups received CBD at different doses (2, 10, 20, and 100 mg/kg), while two control groups received the placebo (CBD vehicle medium-chain triglycerides). Sixty minutes after administration, the animals treated with CBD and one placebo-treated group (stressed control group) were subjected to 60 min of restraint stress. The other placebo-treated group (nonstressed control group) was not subjected to restraint stress. Subsequently, all animals were tested in the open field (OF) for 30 min. Immediately after the OF test, blood samples were collected for corticosterone analysis. Plasma corticosterone concentrations were determined using a commercial ELISA kit. In the OF, distance traveled differed significantly between groups, although no significant differences were observed among the different CBD doses. Compared with stressed control rats, CBD-treated rats spent more time in the center of the OF arena, suggesting reduced anxiety-like behavior. Plasma corticosterone concentrations did not differ significantly between groups. At 90 min after the onset of stress (30 min after the end of restraint stress), corticosterone concentrations did not differ between CBD-treated and untreated rats. CBD showed no effect on locomotor activity but increased center time, suggesting anxiolytic-like effects. Further studies are needed to clarify the underlying mechanisms.

PMID 42871897
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PubMedPhysiology & behavior2026-10-14

The effect of concurrent application of the deep brain stimulation of the nucleus accumbens and cannabidiol injection during extinction period on reinstatement of METH-induced conditioned place preference in extinguished rats.

Mohammadi Mahsa M, Zendehdel Morteza M, Haghparast Abbas A

Methamphetamine (METH) is a potent stimulant drug that significantly alters the function of the central nervous system (CNS). METHS's abuse may be linked with a variety of psychiatric disorders, primarily by affecting the reward system. Cannabidiol (CBD), a primary cannabinoid component of the Cannabis plant, has been shown to affect the reward system, suggesting it for modulating addictive behaviors. On the other hand, deep brain stimulation (DBS) of the nucleus accumbens (NAc), one of the most significant brain regions implicated in mediating rewards, is effective in alleviating drug-seeking behaviors. The present research aimed to evaluate the effects of low-frequency DBS, CBD, and a combination of both on the extinction and reinstatement of METH-induced conditioned place preference (CPP). CBD was injected into the lateral ventricle at doses of 2.5, 5, and 10 μg/5 μL, and low-frequency DBS (10 Hz, for 30 minutes) was administered to the NAc, both during the extinction phase. The results showed CBD (10 µg/5 µL) or DBS facilitated extinction. DBS decreased mean extinction latency but did not differ significantly from CBD (10 µg/5 µL) alone. The combination groups at all tested CBD doses showed reduced mean extinction latency compared with the control groups; only the 10 µg/5 µL combination group differed significantly from DBS alone. However, neither CBD (10 µg/5 µL) alone nor DBS altered the CPP score on the reinstatement day. Combination of DBS and CBD administration (at all doses) significantly decreased the CPP score on the reinstatement day. In conclusion, it can be suggested that CBD may be beneficial for alleviating METH-induced reinstatement in combination with DBS, while both alone had no effect.

PMID 42874832
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PubMedPsychopharmacology2026-10-14

Is it safe-and ethical-to prescribe THC to youth?

Crippa José Alexandre S JAS, Hallak Jaime E C JEC

The medical use of cannabis-derived products in children and adolescents has expanded beyond established indications for purified cannabidiol (CBD), with increasing investigation of CBD-rich extracts containing Δ9-tetrahydrocannabinol (THC) for neuropsychiatric conditions. Although preliminary studies suggest potential symptomatic benefits, the evidence remains limited by small samples, heterogeneous formulations, short follow-up, and insufficient assessment of long-term neurodevelopmental outcomes. Unlike CBD, THC directly activates CB1 receptors as a partial agonist, a pharmacological property underlying both its therapeutic and psychoactive effects. Following oral administration, THC undergoes extensive first-pass metabolism to the psychoactive metabolite 11-hydroxy-THC, with substantial interindividual variability in pharmacokinetics and pharmacodynamics supporting individualized dosing according to clinical response and tolerability. Experimental studies raise concerns regarding THC exposure during neurodevelopment, while observational studies associate frequent, high-potency recreational cannabis use with cognitive impairment, psychosis, and other adverse psychiatric outcomes. These findings cannot be directly extrapolated to regulated medicinal cannabinoid use, which differs substantially in product composition, dosing, administration, therapeutic indication, and clinical monitoring. Nevertheless, long-term neurodevelopmental safety data for medicinal THC exposure in children and adolescents remain limited. These uncertainties must be weighed against the consequences of inadequately treated disease, particularly severe drug-resistant epilepsy. Accordingly, the risk-benefit assessment of THC-containing products should be individualized, considering disease severity, treatment refractoriness, available evidence-based alternatives, therapeutic response, and tolerability. Long-term prospective studies and improved patient-selection strategies are needed to better define the role of THC-containing medicinal products in pediatric populations.

PMID 42873220
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PubMedFrontiers in pharmacology2026-10-14

Cannabinoids in oncology: pharmacology, clinical applications, and translational perspectives.

Safran Emma E, Safran Howard H, Kim Stanley S

Cannabis and cannabinoid products are increasingly used by patients with cancer for symptom management and supportive care. Although cannabis is widely used to alleviate cancer- and treatment-related symptoms, many patients also believe that it possesses direct anticancer activity. This review provides a comprehensive pharmacologic and clinical assessment of cannabinoids in oncology, integrating the endocannabinoid system, cannabinoid receptor signaling, pharmacokinetics, therapeutic applications, adverse effects, drug-drug interactions, and emerging antitumor research. The strongest clinical evidence supports selected cannabinoid preparations for refractory chemotherapy-induced nausea and vomiting, whereas evidence for cancer-related pain, appetite stimulation, sleep disturbance, anxiety, and opioid-sparing effects remains limited or inconsistent. Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) differ substantially in receptor pharmacology, psychoactive effects, metabolism, and toxicity, with important implications for product selection, dosing, and interactions with anticancer and supportive-care medications. Preclinical studies demonstrate antiproliferative, proapoptotic, antiangiogenic, and immunomodulatory effects across multiple tumor models; however, cannabinoid signaling is highly context dependent and may also promote tumor progression in selected settings. Human evidence for direct anticancer activity remains sparse, consisting predominantly of small early-phase studies and observational data, with no established improvement in tumor response, progression-free survival, or overall survival. Particular caution is warranted regarding neuropsychiatric and cardiovascular toxicity, pharmacokinetic drug interactions, and the potential influence of cannabis on immune checkpoint inhibitor outcomes. Overall, cannabinoids have defined but limited roles in supportive oncology, while their direct antitumor potential remains investigational. Future studies should prioritize standardized formulations, pharmacologically informed dosing, rigorous randomized designs, clinically meaningful endpoints, and biomarker-based approaches to define therapeutic benefit and risk.

PMID 42870966
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