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    Bullatine A
    CAS No. 1354-84-3 Price $218 / 20mg
    Catalog No.CFN90228Purity>=98%
    Molecular Weight343.51Type of CompoundAlkaloids
    FormulaC22H33NO2Physical DescriptionPowder
    Download     COA    MSDSSimilar structuralComparison (Web)
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    According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
    Size /Price /Stock 10 mM * 1 mL in DMSO / $78.3 / In-stock
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  • Biological Activity
    Description: Bullatine A possesses anti-rheumatic, anti-inflammatory and anti-nociceptive effects, may be used for the treatment of neurodegenerative diseases such as arthritis. Bullatine A produces antinociception without induction of tolerance and inhibits morphine antinociceptive tolerance, and provide pharmacological basis for concurrent bullatine A and morphine treatment for chronic pain and morphine analgesic tolerance.
    Targets: NOS | IL Receptor | NO | P2X receptor
    In vitro:
    Brain Res Bull. 2013 Aug;97:81-5.
    Bullatine A, a diterpenoid alkaloid of the genus Aconitum, could attenuate ATP-induced BV-2 microglia death/apoptosis via P2X receptor pathways.[Pubmed: 23769848 ]
    Bullatine A (BLA), a diterpenoid alkaloid of the genus Aconitum, possesses anti-rheumatic, anti-inflammatory and anti-nociceptive effects. The mechanism underlying the effects was examined in the present study.
    The effect of BLA on extracellular ATP induced cell death/apoptosis and pro-inflammatory cytokines release were investigated using BV-2 microglia cell line. The mediation/efficacy of inflammatory cytokines and P2X receptors was evaluated by detecting the mRNA levels of iNOS, IL-6, IL-1β and P2X receptors, respectively. The results demonstrated that BV-2 cells could be damaged after incubation with higher dose of ATP, leading to activation of pro-inflammatory cytokines, transcriptional activation of iNOS and overproduction of NO via activation of P2X receptor. The BLA (1-50μM) potently inhibits ATP-induced BV-2 cell death/apoptosis and P2X receptor-mediated inflammatory responses via selectively suppressing the up-regulation of P2X7 receptor mRNA.
    Since P2X7 receptors have an important role in immune and pain response, inflammation and inflammatory disease, this discovery of BLA as a potent P2X7 antagonist indicated that BLA may be a potential useful candidate for the treatment of neurodegenerative diseases such as arthritis.
    Zhongguo Zhong Yao Za Zhi. 2008 Mar;33(5):513-6.
    Effects of volatile oil of Rhizoma zingiberis and other two kinds of volatile oil on percutaneous penetration of bullatine A via hairless mouse skin in vitro[Pubmed: 18536371]
    To investigate the effects of volatile oils of Rhizoma Acori Tatarinowii (RAT), Semen Myristicae (SM) and Pericarpium Citri Reticulatae (PCR) on percutaneous penetration of Bullatine A via hairless mouse skin in vitro.
    By an improved Franz diffusion, the effects of three kinds of volatile oils on the percutaneous penetration of Bullatine A were observed and compared with Azone, and the cumulative amount of Bullatine A was determined by HPLC. The penetration enhancement ratios of Bullatine A with 7% volatile oil RAT and SM, 5% volatile oil of PCR and 3% Azone were 6.52, 6.74, 2.18, 6.03, respectively.
    The volatile oil of RAT, SM and PCR enhance permeation of Bullatine A, effectively.
    In vivo:
    J Neuroinflammation. 2016 Aug 30;13(1):214.
    Bullatine A stimulates spinal microglial dynorphin A expression to produce anti-hypersensitivity in a variety of rat pain models.[Pubmed: 27577933]
    Aconiti brachypodi Radix (Xue-shang-yi-zhi-hao) has been prescribed to manage chronic pain, arthritis, and traumatic injuries. Bullatine A, a C20-diterpenoid alkaloid, is one of its principle effective compounds. This study aimed to investigate the anti-hypersensitivity of Bullatine A in a variety of rat pain models and explore its mechanisms of action.
    Rat neuropathic pain, inflammatory pain, diabetic neuropathic pain, and bone cancer pain models were used. Dynorphin A and pro-inflammatory cytokines were measured in the spinal cord and cultured primary microglia. Double immunofluorescence staining of dynorphin A and glial and neuronal cellular markers was also measured in the spinal cord. Subcutaneous and intrathecal injection of Bullatine A dose-dependently attenuated spinal nerve ligation-, complete Freud's adjuvant-, diabetes-, and bone cancer-induced mechanical allodynia and thermal hyperalgesia, with the efficacies of 45-70 % inhibition, and half-effective doses of 0.9-1.9 mg/kg for subcutaneous injection. However, Bullatine A was not effective in blocking acute nociceptive response in the normal condition. Bullatine A specifically stimulated dynorphin A expression in microglia in the spinal cord in vivo and cultured primary microglia in vitro; the stimulatory effects were completely inhibited by the microglial inhibitor minocycline. In contrast, Bullatine A did not have an inhibitory effect on peripheral nerve injury- or lipopolysaccharide-induced pro-inflammatory cytokine expression. The spinal anti-allodynic effects of Bullatine A were entirely blocked by intrathecal injection of minocycline, the specific dynorphin A antiserum, and the selective k-opioid receptor antagonist.
    We, for the first time, demonstrate that Bullatine A specifically attenuates pain hypersensitivity, regardless of the pain models employed. The results also suggest that stimulation of spinal microglial dynorphin A expression mediates Bullatine A anti-nociception in pain hypersensitivity conditions.
    Bullatine A Description
    Source: The roots of Aconitum brachypodum Diels
    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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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.9111 mL 14.5556 mL 29.1112 mL 58.2225 mL 72.7781 mL
    5 mM 0.5822 mL 2.9111 mL 5.8222 mL 11.6445 mL 14.5556 mL
    10 mM 0.2911 mL 1.4556 mL 2.9111 mL 5.8222 mL 7.2778 mL
    50 mM 0.0582 mL 0.2911 mL 0.5822 mL 1.1644 mL 1.4556 mL
    100 mM 0.0291 mL 0.1456 mL 0.2911 mL 0.5822 mL 0.7278 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.
    Animal Research:
    J Ethnopharmacol. 2017 Jan 20;196:151-159.
    Concurrent bullatine A enhances morphine antinociception and inhibits morphine antinociceptive tolerance by indirect activation of spinal κ-opioid receptors.[Pubmed: 27989510 ]
    Bullatine A, a C20-diterpenoid alkaloid and one of the major effective ingredients in Aconiti brachypodi Radix (Xue-shang-yi-zhi-hao), can block pain hypersensitivity in a variety of rodent models through expression of spinal microglial dynorphin A. To assess the interaction between Bullatine A and morphine on antinociception in acute nociception and pain hypersensitivity states, with the exogenous synthetic dynorphin A as a comparison
    Spinal nerve ligation-induced neuropathic rats and naïve mice were used for assessing the acute and chronic interactions of Bullatine A/dynorphin A with morphine. Single subcutaneous injection of Bullatine A or dynorphin A(1-17) did not either alter formalin- and thermally (hot-plate and water immersion tests)-induced acute nociception or potentiate morphine antinociception in naïve mice. In contrast, Bullatine A dose-dependently inhibited formalin-induced tonic pain with the efficacy of 54% inhibition and the half-effective dose of 0.9mg/kg. Concurrent Bullatine A additively enhanced morphine antinociception. In neuropathic rats, the antinociceptive effects of multiple bidaily intrathecal injections of Bullatine A and dynorphin A remained consistent over 13 days, whereas morphine produced progressive and complete tolerance to antinociception, which was completely inhibited by concurrent Bullatine A and dynorphin A. A single intrathecal injection of Bullatine A and dynorphin A immediately reversed established morphine tolerance in neuropathic rats, although the blockade was a less degree in the thermally induced mouse acute nociceptive tests. The inhibitory effects of Bullatine A and dynorphin A on morphine tolerance were immediately and completely attenuated by intrathecal dynorphin A antibody and/or selective κ-opioid receptor antagonist GNTI.
    These results suggest that Bullatine A produces antinociception without induction of tolerance and inhibits morphine antinociceptive tolerance, and provide pharmacological basis for concurrent Bullatine A and morphine treatment for chronic pain and morphine analgesic tolerance.