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Quinidine hydrochloride monohydrate is a clinical anti-arrythmic drug which is also a potent blocker of K+ channel with an IC50 of 19.9 μM. IC50: 19.9 μM (K+ channel)[1]

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[1].

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[2].

[1]. Wrighton DC, et al. Mechanism of inhibition of mouse Slo3 (KCa 5.1) potassium channels by quinine, quinidine and barium. Br J Pharmacol. 2015 Sep;172(17):4355-63. [2]. Cheng KI, et al. Application of quinidine on rat sciatic nerve decreases the amplitude and increases the latency of evoked responses. J Anesth. 2014 Aug;28(4):559-68.

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