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Bulleyaconitine A
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Product Name Bulleyaconitine A
Price: $60 / 20mg
CAS No.: 107668-79-1
Catalog No.: CFN99720
Molecular Formula: C35H49NO10
Molecular Weight: 643.8 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Source: The roots of Aconitum kusnenzoffii Reichb.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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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 / $30.8 / In-stock
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Bulleyaconitine A is an analgesic and antiinflammatory drug, it has several potential targets, including voltage-gated Na+ channels. It displays long-acting local anesthetic properties in vitro and in vivo, it has been approved for the treatment of chronic pain and rheumatoid arthritis in China, it has the suppressive effect on some immune function of Balb/c mice.
Targets: NO | Sodium Channel
In vitro:
Anesthesiology. 2007 Jul;107(1):82-90.
Bulleyaconitine A isolated from aconitum plant displays long-acting local anesthetic properties in vitro and in vivo.[Pubmed: 17585219]
Bulleyaconitine A (BLA) is an active ingredient of Aconitum bulleyanum plants. Bulleyaconitine A has been approved for the treatment of chronic pain and rheumatoid arthritis in China, but its underlying mechanism remains unclear.
METHODS AND RESULTS:
The authors examined (1) the effects of Bulleyaconitine A on neuronal voltage-gated Na channels in vitro under the whole cell patch clamp configuration and (2) the sensory and motor functions of rat sciatic nerve after single Bulleyaconitine A injections in vivo. Bulleyaconitine A at 10 microm did not affect neuronal Na currents in clonal GH3 cells when stimulated infrequently to +50 mV. When stimulated at 2 Hz for 1,000 pulses (+50 mV for 4 ms), Bulleyaconitine A reduced the peak Na currents by more than 90%. This use-dependent reduction of Na currents by Bulleyaconitine A reversed little after washing. Single injections of Bulleyaconitine A (0.2 ml at 0.375 mm) into the rat sciatic notch not only blocked sensory and motor functions of the sciatic nerve but also induced hyperexcitability, followed by sedation, arrhythmia, and respiratory distress. When Bulleyaconitine A at 0.375 mm was coinjected with 2% lidocaine (approximately 80 mm) or epinephrine (1:100,000) to reduce drug absorption by the bloodstream, the sensory and motor functions of the sciatic nerve remained fully blocked for approximately 4 h and regressed completely after approximately 7 h, with minimal systemic effects.
CONCLUSIONS:
Bulleyaconitine A reduces neuronal Na currents strongly at +50 mV in a use-dependent manner. When coinjected with lidocaine or epinephrine, Bulleyaconitine A elicits prolonged block of both motor and sensory functions in rats with minimal adverse effects.
In vivo:
Exp Neurol. 2015 Nov;273:263-72.
Bulleyaconitine A depresses neuropathic pain and potentiation at C-fiber synapses in spinal dorsal horn induced by paclitaxel in rats.[Pubmed: 26376216 ]
Paclitaxel, a widely used chemotherapeutic agent, often induces painful peripheral neuropathy and at present no effective drug is available for treatment of the serious side effect.
METHODS AND RESULTS:
Here, we tested if intragastrical application of Bulleyaconitine A (BLA), which has been approved for clinical treatment of chronic pain in China since 1985, could relieve the paclitaxel-induced neuropathic pain. A single dose of BLA attenuated the mechanical allodynia, thermal hyperalgesia induced by paclitaxel dose-dependently. Repetitive administration of the drug (0.4 and 0.8 mg/kg, t.i.d. for 7 d) during or after paclitaxel treatment produced a long-lasting inhibitory effect on thermal hyperalgesia, but not on mechanical allodynia. In consistency with the behavioral results, in vivo electrophysiological experiments revealed that spinal synaptic transmission mediated by C-fiber but not A fiber was potentiated, and the magnitude of long-term potentiation (LTP) at C-fiber synapses induced by the same high frequency stimulation was ~50% higher in paclitaxel-treated rats, compared to the naïve rats. Spinal or intravenous application of BLA depressed the spinal LTP, dose-dependently. Furthermore, patch clamp recordings in spinal cord slices revealed that the frequency but not amplitude of both spontaneous excitatory postsynaptic current (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) in lamina II neurons was increased in paclitaxel-treated rats, and the superfusion of BLA reduced the frequency of sEPSCs and mEPSCs in paclitaxel-treated rats but not in naïve ones.
CONCLUSIONS:
Taken together, we provide novel evidence that BLA attenuates paclitaxel-induced neuropathic pain and that depression of spinal LTP at C-fiber synapses via inhibiting presynaptic transmitter release may contribute to the effect.
Anesth Analg. 2008 Oct;107(4):1397-405.
Use of bulleyaconitine A as an adjuvant for prolonged cutaneous analgesia in the rat.[Pubmed: 18806059]
Bulleyaconitine A (BLA) is an analgesic and antiinflammatory drug isolated from Aconitum plants. BLA has several potential targets, including voltage-gated Na+ channels. We tested whether BLA elicited long-lasting cutaneous analgesia, when co-injected with lidocaine and epinephrine, as a model for prolonged infiltration anesthesia.
METHODS AND RESULTS:
The local anesthetic properties of BLA were assessed by the patch-clamp technique in HEK293t cells expressing Nav1.7 and Nav1.8 neuronal Na+ channels, both crucial for nociception. Drug solutions (0.6 mL) were injected subcutaneously via rat shaved dorsal skin. Inhibition of the cutaneous trunci muscle reflex was evaluated by pinpricks. Skin cross-sections were stained with hematoxylin and eosin or with antibodies against PGP9.5. BLA at 10 microM interacted minimally with resting or inactivated Nav1.7 and Nav1.8 Na+ channels when infrequently stimulated to +50 mV for 3 ms. However, when stimulated at 2 Hz for 1000 pulses, their peak Na+ currents were >90% reduced by BLA. This use-dependent inhibition was not significantly reversed after 15-min washing. Complete nociceptive blockade after injection of lidocaine (0.5%)/epinephrine (1:200,000) lasted for approximately 1 h in rats; full recovery occurred after approximately 6 h. Co-injection of 0.125 mM BLA with lidocaine/epinephrine increased the duration of complete nociceptive blockade to 24 h. Full recovery occurred after approximately 6 days. Skin histology including peripheral nerve fibers appeared unaffected by BLA.
CONCLUSIONS:
BLA inhibits Nav1.7 and Nav1.8 Na+ currents in a use-dependent manner. Co-injection of BLA at
Bulleyaconitine A Description
Source: The roots of Aconitum kusnenzoffii Reichb.
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 1.5533 mL 7.7664 mL 15.5328 mL 31.0655 mL 38.8319 mL
5 mM 0.3107 mL 1.5533 mL 3.1066 mL 6.2131 mL 7.7664 mL
10 mM 0.1553 mL 0.7766 mL 1.5533 mL 3.1066 mL 3.8832 mL
50 mM 0.0311 mL 0.1553 mL 0.3107 mL 0.6213 mL 0.7766 mL
100 mM 0.0155 mL 0.0777 mL 0.1553 mL 0.3107 mL 0.3883 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
Animal Research:
Chinese Journal of New Drugs & Clinical Remedies, 2007, 26(10):755-8.
Inhibitory effect of bulleyaconitine A on some immune function in Balb/c mice.[Reference: WebLink]
To determine the effect of Bulleyaconitine A(BLA)on some immune functions of mice.
METHODS AND RESULTS:
:Balb/c mice were divided randomly into control group,BLA groups(0.08,0.16,0.32 mg·kg~(-1),intramuscularly),and hydrocortisone(10 mg·kg~(-1))group,and drugs were given for 7d.After mice were sacrificed on d7,spleen-and thymus-index were recorded,and lymphocytes proliferation were tested.The levelof total IgG in serum was measured by ELISA method.Phagocytosis of peritoneal macrophages(MΦ)was tested with neutral-red phagocytosis assay.Nitric oxide(NO)in supernatants of macrophages was detected by nitrate reductase method.BLA 0.32 mg·kg~(-1)inhibited T-and B-lymphocytes proliferations(P0.01) and NO in supernatants(P0.05).BLA 0.16 and 0.32 mg·kg~(-1)lowered the thymus-index(P0.05,P0.01) with the suppression of phagocytosis function of MΦ(P0.05,P0.01).BLA also reduced the total IgG in serum(P0.05,P0.01).
CONCLUSIONS:
BLA had the suppressive effect on some immune function of Balb/c mice.
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