Quinidine hydrochloride

Research use only, not for human use.

An optical isomer of quinine, extracted from the bark of the Cinchona tree and similar plant species.

An optical isomer of quinine, extracted from the bark of the Cinchona tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular action potential, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission. (In Vitro):Quinidine hydrochloride monohydrate blocks WT mSlo3 (KCa5.1) channels with an IC50 of 19.9±1.41 μM and Hill slope of 1.15±0.15 (n=7). Again, the potency of inhibition by Quinidine hydrochloride monohydrate is higher for F304Y mSlo3 (IC50 of 2.42±0.60 μM, n=9, P<0.005; Hill slope of 0.98±0.12), but lower with R196Q mSlo3 (IC50 of 38.4±6.77 μM, n=5, P<0.001; Hill slope of 1.05±0.16). The inhibition of F304Y mSlo3 by Quinidine hydrochloride monohydrate is observed to have some time dependence.(In Vivo):Direct application of Quinidine hydrochloride monohydrate on the sciatic nerve produces a dose-related decrease in amplitude at ascending somato-sensory evoked potential (SSEP) and descending compound muscle action potentials (CMAP) when comparing baseline with other time points, or when comparing the experimental left limb to the right contra-lateral glucose-treated limb. The latencies of SSEPs and CMAP potentials after Quinidine hydrochloride monohydrate applications are increased compare to baseline and the contralateral side.

Quinidine hydrochloride monohydrate blocks WT mSlo3 (KCa5.1) channels with an IC50 of 19.9±1.41?μM and Hill slope of 1.15±0.15 (n=7). Again, the potency of inhibition by Quinidine hydrochloride monohydrate is higher for F304Y mSlo3 (IC50 of 2.42±0.60?μM, n=9, P<0.005; Hill slope of 0.98±0.12), but lower with R196Q mSlo3 (IC50 of 38.4±6.77?μM, n=5, P<0.001; Hill slope of 1.05±0.16). The inhibition of F304Y mSlo3 by Quinidine hydrochloride monohydrate is observed to have some time dependence.

Direct application of Quinidine hydrochloride monohydrate on the sciatic nerve produces a dose-related decrease in amplitude at ascending somato-sensory evoked potential (SSEP) and descending compound muscle action potentials (CMAP) when comparing baseline with other time points, or when comparing the experimental left limb to the right contra-lateral glucose-treated limb. The latencies of SSEPs and CMAP potentials after Quinidine hydrochloride monohydrate applications are increased compare to baseline and the contralateral side.

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Cell Cycle/DNA Damage

Potassium Channel

Potassium Channel| Sodium Channel

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6151-40-2

378.89

C20H27ClN2O3

>98% (HPLC)

DMSO: 10 mM

COC1=CC2=C(C=CN=C2C=C1)[C@@H]([C@H]3C[C@@H]4CCN3C[C@@H]4C=C)O.O.Cl

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(-20℃)

With Ice Pack

≥ 2 years