HypaconitineCAS# 6900-87-4 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 6900-87-4 | SDF | Download SDF |
| PubChem ID | 51307 | Appearance | White powder |
| Formula | C33H45NO10 | M.Wt | 615.71 |
| Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
| Solubility | DMSO : 50 mg/mL (81.21 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) | ||
| SMILES | CC(=O)OC12C3C(CC(C3OC(=O)C4=CC=CC=C4)(C(C1O)OC)O)C56C(CCC7(C5C(C2C6[NH+](C7)C)OC)COC)OC.[Br-] | ||
| Standard InChIKey | QJUUTBMHIVNBSD-MNEZKBEBSA-N | ||
| Standard InChI | InChI=1S/C33H45NO10.BrH/c1-17(35)44-33-21-19(14-31(38,28(42-6)26(33)36)27(21)43-29(37)18-10-8-7-9-11-18)32-20(40-4)12-13-30(16-39-3)15-34(2)25(32)22(33)23(41-5)24(30)32;/h7-11,19-28,36,38H,12-16H2,1-6H3;1H/t19-,20?,21-,22?,23?,24-,25-,26?,27?,28+,30?,31-,32?,33-;/m1./s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| 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 | Blocking effects of hypaconitine and aconitine on nerve action potentials in phrenic nerve-diaphragm muscles of mice.[Pubmed: 2385329]Neuropharmacology, 1990, 29(6):567-72.The mechanisms of neuromuscular blockade by Hypaconitine and aconitine were investigated electrophysiologically in isolated phrenic nerve-diaphragm muscles of mice.
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| In vivo | Effect of hypaconitine combined with liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo.[Pubmed: 23058053]J Pharm Pharmacol. 2012 Nov;64(11):1654-8.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.
Effect of hypaconitine combined with liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo.[Pubmed: 23058053 ]J Pharm Pharmacol. 2012 Nov;64(11):1654-8.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.
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| Kinase Assay | Microsomal cytochrome P450-mediated metabolism of hypaconitine, an active and highly toxic constituent derived from Aconitum species.[Pubmed: 21550385 ]Toxicol Lett. 2011 Jul 4;204(1):81-91.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.
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| Animal Research | Hypaconitine-induced QT prolongation mediated through inhibition of KCNH2 (hERG) potassium channels in conscious dogs.[Pubmed: 25800797 ]J Ethnopharmacol. 2015 May 26;166:375-9.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.
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Hypaconitine Dilution Calculator
Hypaconitine Molarity Calculator
| 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 necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Hypaconitine-induced QT prolongation mediated through inhibition of KCNH2 (hERG) potassium channels in conscious dogs.[Pubmed:25800797]
J Ethnopharmacol. 2015 May 26;166:375-9.
ETHNOPHARMACOLOGICAL RELEVANCE: 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. MATERIAL AND METHODS: 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. RESULTS: 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. CONCLUSION: These data suggest that Hypaconitine inhibits KCNH2 potassium channels and this effect might be the molecular mechanism underlying QT prolongation in conscious dogs.
Anti-inflammatory activity of diterpene alkaloids from Aconitum baikalense.[Pubmed:24770754]
Bull Exp Biol Med. 2014 Mar;156(5):665-8.
We compared anti-inflammatory activity of individual diterpene alkaloids isolated from Aconitum baikalense (napelline, songorine, Hypaconitine, mesaconitine, 12-epinapelline N-oxide) under conditions of acute inflammation of different genesis. The tested substances showed high antiexudative activity comparable with that of sodium diclofenac. Unlike nonsteroidal anti-inflammatory drugs, diterpene alkaloids exerted no ulcerogenic effect.
Effect of hypaconitine combined with liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo.[Pubmed:23058053]
J Pharm Pharmacol. 2012 Nov;64(11):1654-8.
OBJECTIVES: 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: 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. KEY FINDINGS: 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.
Microsomal cytochrome P450-mediated metabolism of hypaconitine, an active and highly toxic constituent derived from Aconitum species.[Pubmed:21550385]
Toxicol Lett. 2011 Jul 4;204(1):81-91.
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. 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. 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.
Blocking effects of hypaconitine and aconitine on nerve action potentials in phrenic nerve-diaphragm muscles of mice.[Pubmed:2385329]
Neuropharmacology. 1990 Jun;29(6):567-72.
The mechanisms of neuromuscular blockade by Hypaconitine and aconitine were investigated electrophysiologically in isolated phrenic nerve-diaphragm muscles of mice. 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. 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.
