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    Hypaconitine
    Information
    CAS No. 6900-87-4 Price $138 / 20mg
    Catalog No.CFN99200Purity>=98%
    Molecular Weight615.71Type of CompoundAlkaloids
    FormulaC33H45NO10Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Hypaconitine, an active and highly toxic constituent derived from Aconitum species, has anti-inflammatory activity, is widely used to treat rheumatism. It produced neuromuscular blockade by reducing the evoked quantal release, the mechanism of this effect was attributed mainly to blocking of the nerve compound action potential.
    Targets: P450 (e.g. CYP17) | Serine kinase | Potassium Channel
    In vitro:
    Neuropharmacology, 1990, 29(6):567-72.
    Blocking effects of hypaconitine and aconitine on nerve action potentials in phrenic nerve-diaphragm muscles of mice.[Pubmed: 2385329]
    The mechanisms of neuromuscular blockade by Hypaconitine and aconitine were investigated electrophysiologically in isolated phrenic nerve-diaphragm muscles of mice.
    METHODS AND RESULTS:
    Hypaconitine (0.08-2 microM) and aconitine (0.3-2 microM) depressed the nerve-evoked twitch tension, without affecting the contraction evoked by stimulation of the muscle. At the concentrations of Hypaconitine (up to 5 microM) and aconitine (up to 2 microM) that depressed the nerve-evoked twitch tension, the resting membrane potential of the muscle cells was unchanged. Hypaconitine (0.1-2 microM) and aconitine (2 microM) blocked the end-plate potential (epp), without affecting the amplitude of the miniature epp (mepp). The quantal content of end-plate potentials was decreased by these agents in parallel with the decrement in amplitude. The nerve compound action potential was inhibited by Hypaconitine (5 microM) and aconitine (2-10 microM), as well as by 1 microM tetrodotoxin (TTX). When the nerve compound action potential was completely blocked by 2 microM aconitine, the muscle action potential was unaffected, although 1 microM TTX suppressed both potentials to the same degree.
    CONCLUSIONS:
    These results indicate the neuromuscular blockade produced by Hypaconitine and aconitine were caused by reducing the evoked quantal release. The mechanism of this effect was attributed mainly to blocking of the nerve compound action potential.
    In vivo:
    J Pharm Pharmacol. 2012 Nov;64(11):1654-8.
    Effect of hypaconitine combined with liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo.[Pubmed: 23058053]
    To study the effects of Hypaconitine used alone and combined with liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of liquiritin on these Hypaconitine-induced effects.
    METHODS AND RESULTS:
    Adult Wistar rats were orally administered Hypaconitine (0.23, 0.69, 2.07 mg/kg per day), liquiritin (20 mg/kg per day), or Hypaconitine (2.07 mg/kg per day) plus liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by Hypaconitine used alone and combined with liquiritin. Although CaM mRNA expression level was inhibited by liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of Hypaconitine and liquiritin significantly reduced Hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation.
    CONCLUSIONS:
    The study indicated that Hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by Hypaconitine.
    J Pharm Pharmacol. 2012 Nov;64(11):1654-8.
    Effect of hypaconitine combined with liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo.[Pubmed: 23058053 ]
    To study the effects of Hypaconitine used alone and combined with liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of liquiritin on these Hypaconitine-induced effects.
    METHODS AND RESULTS:
    Adult Wistar rats were orally administered Hypaconitine (0.23, 0.69, 2.07 mg/kg per day), liquiritin (20 mg/kg per day), or Hypaconitine (2.07 mg/kg per day) plus liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by Hypaconitine used alone and combined with liquiritin. Although CaM mRNA expression level was inhibited by liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of Hypaconitine and liquiritin significantly reduced Hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation.
    CONCLUSIONS:
    The study indicated that Hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by Hypaconitine.
    Hypaconitine Description
    Source: The roots of Aconitum carmichaeli Debx.
    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 1.6241 mL 8.1207 mL 16.2414 mL 32.4828 mL 40.6035 mL
    5 mM 0.3248 mL 1.6241 mL 3.2483 mL 6.4966 mL 8.1207 mL
    10 mM 0.1624 mL 0.8121 mL 1.6241 mL 3.2483 mL 4.0604 mL
    50 mM 0.0325 mL 0.1624 mL 0.3248 mL 0.6497 mL 0.8121 mL
    100 mM 0.0162 mL 0.0812 mL 0.1624 mL 0.3248 mL 0.406 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:
    Toxicol Lett. 2011 Jul 4;204(1):81-91.
    Microsomal cytochrome P450-mediated metabolism of hypaconitine, an active and highly toxic constituent derived from Aconitum species.[Pubmed: 21550385 ]
    Hypaconitine (HA), an active and highly toxic constituent derived from Aconitum species, is widely used to treat rheumatism. Little is known about the hepatic cytochrome P450-catalyzed metabolism of HA.
    METHODS AND RESULTS:
    The present study investigated the metabolism of HA in vitro using male human liver microsomes (MHLMS). Chemical inhibitors of specific CYP enzymes, CYP-specific inhibitory monoclonal antibodies (mAbs), and cDNA-expressed CYP enzymes were used to confirm the enzyme subtypes involved in the metabolism. Liquid chromatography-high resolution mass spectrometry (LC-MS) was used to detect and identify metabolites. A total of 11 metabolites were identified in MHLMS incubations. The major metabolic pathways included demethylation (M1-M3), demethylation-dehydrogenation (M4-M6), hydroxylation (M7, M8), and didemethylation (M9-M11). M8 was identified as mesaconitine (MA), another active and highly toxic constituent of Aconitum.
    CONCLUSIONS:
    The results of chemical inhibition, monoclonal antibody inhibition, and cDNA-expressed CYP enzyme studies showed that the primary contributors toward HA metabolism were CYP3A4 and 3A5, with secondary contributions by CYP2C19, 2D6, and CYP2E1. CYP1A2 and 2C8 provided minor contributions.
    Animal Research:
    J Ethnopharmacol. 2015 May 26;166:375-9.
    Hypaconitine-induced QT prolongation mediated through inhibition of KCNH2 (hERG) potassium channels in conscious dogs.[Pubmed: 25800797 ]
    Hypaconitine is one of the main aconitum alkaloids in traditional Chinese medicines prepared with herbs from the genus Acotinum. These herbs are widely used for the treatment of cardiac insufficiency and arrhythmias. However, Acotinum alkaloids are known for their toxicity as well as their pharmacological activity, especially cardiotoxicity including QT prolongation, and the mechanism of this toxicity is not clear.
    METHODS AND RESULTS:
    In this study, Hypaconitine was administered orally to conscious Beagle dogs, and electrocardiograms were recorded by telemetry. Pharmacokinetic studies (6h) were conducted to evaluate the relationship between QT prolongation and exposure level. HEK293 cells stably transfected with KCNH2 (hERG) cDNA were used to examine the effects of Hypaconitine on the KCNH2 channel by using the manual patch clamp technique. In the conscious dogs, all doses of Hypaconitine induced QTcV (QT interval corrected according to the Van de Water formula) prolongation by more than 23% (67ms) of control in a dose-dependent manner. The maximum QTcV prolongation was observed at 2h after dosing. Maximum prolongation percentages were plotted against plasma concentrations of Hypaconitine and showed a strong correlation (R(2)=0.789). In the in vitro study in HEK293 cells, Hypaconitine inhibited the KCNH2 currents in a concentration-dependent manner with an IC50 of 8.1nM.
    CONCLUSIONS:
    These data suggest that Hypaconitine inhibits KCNH2 potassium channels and this effect might be the molecular mechanism underlying QT prolongation in conscious dogs.