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    Cannabidiol
    Information
    CAS No. 13956-29-1 Price $238 / 20mg
    Catalog No.CFN99444Purity>=98%
    Molecular Weight314.5 Type of CompoundPhenols
    FormulaC21H30O2Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Our products had been exported to the following research institutions and universities, And still growing.
  • University of Eastern Finland (Finland)
  • Chiang Mai University (Thailand)
  • Universiti Kebangsaan Malaysia (Malaysia)
  • Universidade Católica Portuguesa (Portugal)
  • Korea Food Research Institute(KF... (Korea)
  • University of Wuerzburg (Germany)
  • Charles University in Prague (Czech Republic)
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  • Indian Institute of Science (India)
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    Biological Activity
    Description: Cannabidiol has a potent anti-arthritic effect in collagen-induced arthritis through its combined immunosuppressive and anti-inflammatory actions, it has a pharmacological profile similar to that of atypical antipsychotic drugs. Cannabidiol exerts a combination of neuroprotective, anti-oxidative and anti-apoptotic effects against beta-amyloid peptide toxicity, and that inhibition of caspase 3 appearance from its inactive precursor, pro-caspase 3, by cannabidiol is involved in the signalling pathway for this neuroprotection. Cannabidiol may have great therapeutic potential in the treatment of diabetic complications, and perhaps other cardiovascular disorders, by attenuating oxidative/ nitrative stress, inflammation, cell death and fibrosis.
    Targets: JNK | MAPK | P450 (e.g. CYP17) | TNF-α | COX | NF-kB | Caspase | 5-HT Receptor
    In vivo:
    Epilepsy Behav. 2013 Dec;29(3):574-7.
    Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy.[Pubmed: 24237632]
    Severe childhood epilepsies are characterized by frequent seizures, neurodevelopmental delays, and impaired quality of life. In these treatment-resistant epilepsies, families often seek alternative treatments. This survey explored the use of Cannabidiol-enriched cannabis in children with treatment-resistant epilepsy.
    METHODS AND RESULTS:
    The survey was presented to parents belonging to a Facebook group dedicated to sharing information about the use of Cannabidiol-enriched cannabis to treat their child's seizures. Nineteen responses met the following inclusion criteria for the study: a diagnosis of epilepsy and current use of Cannabidiol-enriched cannabis. Thirteen children had Dravet syndrome, four had Doose syndrome, and one each had Lennox-Gastaut syndrome and idiopathic epilepsy. The average number of antiepileptic drugs (AEDs) tried before using Cannabidiol-enriched cannabis was 12. Sixteen (84%) of the 19 parents reported a reduction in their child's seizure frequency while taking Cannabidiol-enriched cannabis. Of these, two (11%) reported complete seizure freedom, eight (42%) reported a greater than 80% reduction in seizure frequency, and six (32%) reported a 25-60% seizure reduction. Other beneficial effects included increased alertness, better mood, and improved sleep. Side effects included drowsiness and fatigue. Our survey shows that parents are using Cannabidiol-enriched cannabis as a treatment for their children with treatment-resistant epilepsy. Because of the increasing number of states that allow access to medical cannabis, its use will likely be a growing concern for the epilepsy community. Safety and tolerability data for Cannabidiol-enriched cannabis use among children are not available.
    CONCLUSIONS:
    Objective measurements of a standardized preparation of pure Cannabidiol are needed to determine whether it is safe, well tolerated, and efficacious at controlling seizures in this pediatric population with difficult-to-treat seizures.
    J Trace Elem Med Biol. 2013 Oct;27(4):355-63.
    Protective effect of cannabidiol against cadmium hepatotoxicity in rats.[Pubmed: 23993482]

    METHODS AND RESULTS:
    The protective effect of Cannabidiol, the non-psychoactive component of Cannabis sativa, against liver toxicity induced by a single dose of cadmium chloride (6.5 mgkg(-1) i.p.) was investigated in rats. Cannabidiol treatment (5 mgkg(-1)/day, i.p.) was applied for five days starting three days before cadmium administration. Cannabidiol significantly reduced serum alanine aminotransferase, and suppressed hepatic lipid peroxidation, prevented the depletion of reduced glutathione and nitric oxide, and catalase activity, and attenuated the elevation of cadmium level in the liver tissue resulted from cadmium administration. Histopathological examination showed that cadmium-induced liver tissue injury was ameliorated by Cannabidiol treatment. Immunohistochemical analysis revealed that Cannabidiol significantly decreased the cadmium-induced expression of tumor necrosis factor-α, cyclooxygenase-2, nuclear factor-κB, caspase-3, and caspase-9, and increased the expression of endothelial nitric oxide synthase in liver tissue.
    CONCLUSIONS:
    It was concluded that Cannabidiol may represent a potential option to protect the liver tissue from the detrimental effects of cadmium toxicity.
    Cannabidiol Description
    Source: The herbs of Cannabis sativa.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

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    J Cell Biochem. 2018 Feb;119(2):2231-2239.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.1797 mL 15.8983 mL 31.7965 mL 63.593 mL 79.4913 mL
    5 mM 0.6359 mL 3.1797 mL 6.3593 mL 12.7186 mL 15.8983 mL
    10 mM 0.318 mL 1.5898 mL 3.1797 mL 6.3593 mL 7.9491 mL
    50 mM 0.0636 mL 0.318 mL 0.6359 mL 1.2719 mL 1.5898 mL
    100 mM 0.0318 mL 0.159 mL 0.318 mL 0.6359 mL 0.7949 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Kinase Assay:
    Free Radic Biol Med. 2014 Mar;68:260-7.
    Cannabidiol protects liver from binge alcohol-induced steatosis by mechanisms including inhibition of oxidative stress and increase in autophagy.[Pubmed: 24398069]
    Acute alcohol drinking induces steatosis, and effective prevention of steatosis can protect liver from progressive damage caused by alcohol. Increased oxidative stress has been reported as one mechanism underlying alcohol-induced steatosis.
    METHODS AND RESULTS:
    We evaluated whether Cannabidiol, which has been reported to function as an antioxidant, can protect the liver from alcohol-generated oxidative stress-induced steatosis. Cannabidiol can prevent acute alcohol-induced liver steatosis in mice, possibly by preventing the increase in oxidative stress and the activation of the JNK MAPK pathway. Cannabidiol per se can increase autophagy both in CYP2E1-expressing HepG2 cells and in mouse liver. Importantly, Cannabidiol can prevent the decrease in autophagy induced by alcohol.
    CONCLUSIONS:
    In conclusion, these results show that Cannabidiol protects mouse liver from acute alcohol-induced steatosis through multiple mechanisms including attenuation of alcohol-mediated oxidative stress, prevention of JNK MAPK activation, and increasing autophagy.
    Animal Research:
    J Psychopharmacol. 2013 Dec;27(12):1149-59.
    The role of 5-HT1A receptors in the anti-aversive effects of cannabidiol on panic attack-like behaviors evoked in the presence of the wild snake Epicrates cenchria crassus (Reptilia, Boidae).[Pubmed: 23926240]
    The potential anxiolytic and antipanic properties of Cannabidiol have been shown; however, its mechanism of action seems to recruit other receptors than those involved in the endocannabinoid-mediated system.
    METHODS AND RESULTS:
    It was recently shown that the model of panic-like behaviors elicited by the encounters between mice and snakes is a good tool to investigate innate fear-related responses, and Cannabidiol causes a panicolytic-like effect in this model. The aim of the present study was to investigate the 5-hydroxytryptamine (5-HT) co-participation in the panicolytic-like effects of Cannabidiol on the innate fear-related behaviors evoked by a prey versus predator interaction-based paradigm. Male Swiss mice were treated with intraperitoneal (i.p.) administrations of Cannabidiol (3 mg/kg, i.p.) and its vehicle and the effects of the peripheral pre-treatment with increasing doses of the 5-HT1A receptor antagonist WAY-100635 (0.1, 0.3 and 0.9 mg/kg, i.p.) on instinctive fear-induced responses evoked by the presence of a wild snake were evaluated.
    CONCLUSIONS:
    The present results showed that the panicolytic-like effects of Cannabidiol were blocked by the pre-treatment with WAY-100635 at different doses. These findings demonstrate that Cannabidiol modulates the defensive behaviors evoked by the presence of threatening stimuli, and the effects of Cannabidiol are at least partially dependent on the recruitment of 5-HT1A receptors.