6151-40-2
Chemical Structure
Quinidine hydrochloride monohydrate
- CAS No.: 6151-40-2
- Formula:C20H27ClN2O3
- Molecular Weight:378.89
IUPAC Name: (S)-(6-methoxyquinolin-4-yl)((1S,2R,4S,5R)-5-vinylquinuclidin-2-yl)methanol hydrochloride hydrate
InChIKey: SGVZDMWHXVXUBY-KAIFKDDSSA-N
SMILES: C=C[C@H]1C[N@](CC[C@H]1C2)[C@@]2([H])[C@@H](O)C3=CC=NC4=CC=C(OC)C=C34.[H]Cl.[H]O[H]
Biological Activity: Quinidine hydrochloride monohydrate is an orally active antiarrhythmic agent. Quinidine hydrochloride monohydrate reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine hydrochloride monohydrate exerts sustained block and open-channel block effects on IK(f). Quinidine hydrochloride monohydrate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine hydrochloride monohydrate can be used in studies related to uterine sarcoma and seizures[1][2][3][4].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
Quinidine hydrochloride monohydrate | 99.97% | Quinidine hydrochloride monohydrate is an orally active antiarrhythmic agent. Quinidine hydrochloride monohydrate reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine hydrochloride monohydrate exerts sustained block and open-channel block effects on IK(f). Quinidine hydrochloride monohydrate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine hydrochloride monohydrate can be used in studies related to uterine sarcoma and seizures. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
|
|
Quinidine hydrochloride monohydrate (Standard) | ≥98% | Quinidine hydrochloride monohydrate (Standard) is the analytical standard of Quinidine hydrochloride monohydrate (HY-B1302). This product is intended for research and analytical applications. Quinidine hydrochloride monohydrate is an orally active antiarrhythmic agent. Quinidine hydrochloride monohydrate reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine hydrochloride monohydrate exerts sustained block and open-channel block effects on IK(f). Quinidine hydrochloride monohydrate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine hydrochloride monohydrate can be used in studies related to uterine sarcoma and seizures. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
References
- [1]. Lee SY, et al. Hydrocinchonine, cinchonine, and quinidine potentiate paclitaxel-induced cytotoxicity and apoptosis via multidrug resistance reversal in MES-SA/DX5 uterine sarcoma cells. Environ Toxicol. 2011 Aug;26(4):424-31. [Content Brief]
- [2]. Kehl SJ, et al. Quinidine-induced inhibition of the fast transient outward K+ current in rat melanotrophs. Br J Pharmacol. 1991;103(3):1807-1813. [Content Brief]
- [3]. Moody DE, et al. Quinidine inhibits in vivo metabolism of amphetamine in rats: impact upon correlation between GC/MS and immunoassay findings in rat urine. J Anal Toxicol. 1990;14(5):311-317. [Content Brief]
- [4]. Jamali H, et al. Effect of dextromethorphan/quinidine on pentylenetetrazole- induced clonic and tonic seizure thresholds in mice. Neurosci Lett. 2020;729:134988. [Content Brief]
