Cloperastine fendizoate (Hustazol) inhibits the hERG K+ currents in a concentration-dependent manner (IC50: 27 nM).

Dimethindene (Dimetindeno) is a selective antagonist of H1 receptor and blocks K+ current. Dimethindene exhibits antihistamine and anticholinergic effects.

Phe-Met-Arg-Phe, amide acetate dose dependently (ED50=23 nM) activates a K+ current in the peptidergic caudodorsal neurons. This peptide appears to localize with neuropeptide Y in some regions of the brain.

KV4 channel blocker. Blocks A-type K+ current (ISA) in mouse cerebellar granule neurons. The accessory dipeptidyl peptidase-like proteins (DPP) 6 and 10 are required for blockade.

Zonisamide-13C2,15N is intended for use as an internal standard for the quantification of zonisamide by GC- or LC-MS. Zonisamide is an antiepileptic agent.1 It selectively inhibits the repeated firing of sodium channels (IC50 = 2 μg/ml) in mouse embryo spinal cord neurons and inhibits spontaneous channel firing when used at concentrations greater than 10 μg/ml.2 In rat cerebral cortex neurons, zonisamide (1-1,000 μM) inhibits T-type calcium channels with a maximum reduction of 60% of the calcium current.3 Zonisamide inhibits H. pylori recombinant carbonic anhydrase (CA) and the human CA isoforms I, II, and V with Ki values of 218, 56, 35, and 21 nM, respectively.4,5 In mice, it has anticonvulsant activity against maximal electroshock seizure (MES) and pentylenetetrazole-induced maximal, but not minimal, seizures (ED50s = 19.6, 9.3, and >500 mg/kg, respectively). Zonisamide (40 mg/kg, p.o.) prevents MPTP-induced decreases in the levels of dopamine , but not homovanillic acid or dihydroxyphenyl acetic acid , and increases MPTP-induced decreases in the dopamine turnover rate in mouse striatum in a model of Parkinson's disease.6 Formulations containing zonisamide have been used in the treatment of partial seizures in adults with epilepsy. |1. Masuda, Y., Ishizaki, M., and Shimizu, M. Zonisamide: Pharmacology and clinical efficacy in epilepsy. CNS Drug Rev. 4(4), 341-360 (1998).|2. Rock, D.M., Macdonald, R.L., and Taylor, C.P. Blockade of sustained repetitive action potentials in cultured spinal cord neurons by zonisamide (AD 810, CI 912), a novel anticonvulsant. Epilepsy Res. 3(2), 138-143 (1989).|3. Suzuki, S., Kawakami, K., Nishimura, S., et al. Zonisamide blocks T-type calcium channel in cultured neurons of rat cerebral cortex. Epilepsy Res. 12(1), 21-27 (1992).|4. Nishimori, I., Vullo, D., Minakuchi, T., et al. Carbonic anhydrase inhibitors: Cloning and sulfonamide inhibition studies of a carboxyterminal truncated α-carbonic anhydrase from Helicobacter pylori. Bioorg. Med. Chem. Lett. 16(8), 2182-2188 (2006).|5. De Simone, G., Di Fiore, A., Menchise, V., et al. Carbonic anhydrase inhibitors. Zonisamide is an effective inhibitor of the cytosolic isozyme II and mitochondrial isozyme V: Solution and X-ray crystallographic studies. Bioorg. Med. Chem. Lett. 15(9), 2315-2320 (2005).|6. Yabe, H., Choudhury, M.E., Kubo, M., et al. Zonisamide increases dopamine turnover in the striatum of mice and common marmosets treated with MPTP. J. Pharmacol. Sci. 110(1), 64-68 (2009).

17R(18S)-EpETE is an oxylipin and a cytochrome P450 metabolite of eicosapentaenoic acid .1,217R(18S)-EpETE is an activator of large-conductance calcium-activated potassium (BKCa) channels, increasing the potassium current amplitude by 15-fold in isolated rat cerebral artery vascular smooth muscle cells (VSMCs) at +60 mV when used at a concentration of 50 nM.2It has negative chronotropic effects in isolated neonatal rat cardiomyocytes (NRCMs; EC50= ~1-2 nM) and prevents calcium-induced increases in the spontaneous beating of NRCMs.3,4 1.Schwarz, D., Kisselev, P., Ericksen, S.S., et al.Arachidonic and eicosapentaenoic acid metabolism by human CYP1A1: Highly steroselective formation of 17(R), 18(S)-epoxyeicosatetraenoic acidBiochem. Pharmacol.67(8)1445-1457(2004) 2.Lauterbach, B., Barbosa-Sicard, E., Wang, M.H., et al.Cytochrome P450-dependent eicosapentaenoic acid metabolites are novel BK channel activatorsHypertension39(2 Pt. 2)609-613(2002) 3.Falck, J.R., Wallukat, G., Puli, N., et al.17(R),18(S)-Epoxyeicosatetraenoic acid, a potent eicosapentaenoic acid (EPA) derived regulator of cardiomyocyte contraction: Structure-activity relationships and stable analoguesJ. Med. Chem.54(12)4109-4118(2011) 4.Arnold, C., Markovic, M., Blossey, K., et al.Arachidonic acid-metabolizing cytochrome P450 enzymes are targets of omega-3 fatty acidsJ. Biol. Chem.285(43)32720-32733(2010)

Phe-met-arg-phe amide trifluoroacetate is an activator of K+ current with an ED50 of 23nm on the fundus nerve.

Chlorahololide C is a potent and selective potassium channel blocker, it exerts potent and selective inhibition on the delayed rectifier (I(K)) K(+) current with the IC(50) value of 3.6 +/- 10.1 mu M.

slow delayed rectifier K+ current (IKs) blocker

Linopirdine (DuP 996) is a TRPV1 agonist. Linopirdine is an orally active and selective M-type K+ current (IM; Kv7; KCNQ Channels) inhibitor (IC50: 2.4 μM). Linopirdine is a cognitive enhancer. It acts by stimulating release of acetylcholine and other neurotransmitters.Linopirdine is a putative cognition-enhancing drug that increases acetylcholine release in rat brain tissue.

Phe-Met-Arg-Phe, amide dose dependently (ED50=23 nM) activates a K+ current in the peptidergic caudodorsal neurons. This peptide appears to localize with neuropeptide Y in some regions of the brain.

Almokalant is a class III antiarrhythmic drug, acts as a potassium channel blocker. And it inhibits a specific component (Ikr) of the time-dependent delayed rectifier K+ current.

F 15845 is a blocker of the persistent sodium current prevents consequences of hypoxia in rat femoral artery. F15845 has been shown to selectively inhibit the persistent sodium current of Nav1.5[1] exerting cardioprotective effects following ischemia. In vitro testing showed minimal effects of F15845 on other important ion channels of the heart, including major Ca2+ and K+ channels.[1] This characteristic is thought to account for the limited effect of F15845 to change other heart parameters such as basal cardiac function, hemodynamic functions and ventricular fibrillation. F15845 was also shown to exert improved effects when the membrane potential was depolarized,[1] by acting on the extracellular side of the channel.

Propafenone (Propafenonum) is only found in individuals that have used or taken this drug. It is an antiarrhythmia agent that is particularly effective in ventricular arrhythmias. It also has weak beta-blocking activity. The drug is generally well tolerated. The electrophysiological effect of propafenone manifests itself in a reduction of upstroke velocity (Phase 0) of the monophasic action potential. In Purkinje fibers, and to a lesser extent myocardial fibers, propafenone reduces the fast inward current carried by sodium ions, which is responsible for the drugs antiarrhythmic actions. Diastolic excitability threshold is increased and effective refractory period prolonged. Propafenone reduces spontaneous automaticity and depresses triggered activity. At very high concentrations in vitro, propafenone can inhibit the slow inward current carried by calcium but this calcium antagonist effect probably does not contribute to antiarrhythmic efficacy.

Sematilide hydrochloride (CK-1752) is a class III antiarrhythmic. It is a selectively delayed rectifier K+ current (IKr) channel blocker. It inhibits rapidly activating Ik in guinea pig atrial myocytes, resulting in the prolongation of refractoriness and action potential duration.

Sematilide is a blocker of selective IKr channel.

1. Resibufogenin (Bufogenin) is a cytotoxic steroid isolated from the Chinese drug ChanSu. 2. Resibufogenin can inhibit rectifier potassium current ( I K ) and transient potassium current ( I A ), it has pathological effects on central nervous system. 3. Resibufogenin corrects hypertension in a rat model of human preeclampsia, it not only prevents the advent of hypertension and proteinuria, but also the development of intrauterine growth restriction.4. Resibufogenina's major metabolic pathway in the human liver is CYP3A4 dominantly mediated 5β-hydroxylation .

LY303511, an inactive analogue of LY294002, is a mTOR inhibitor and no inhibition for PI3-K.

Irdabisant hydrochloride (CEP-26401) is a selective, orally active, and blood-brain barrier (BBB) penetrant histamine H3 receptor (H3R) inverse agonist/inverse agonist, demonstrating high affinity with K*i values of 7.2 nM and 2.0 nM for rat and human H3R respectively. It exhibits relatively low hERG current inhibitory activity, with an IC*50 of 13.8 μM. This compound has been shown to enhance cognition and promote wakefulness in rat social recognition models, suggesting potential applications in schizophrenia or cognitive impairment research.

AmmTX3 TFA, a peptide toxin derived from Androctonus mauretanicus scorpion venom, functions as a selective blocker of the K_v4 channel. It inhibits the A-type K^+ current with an inhibition constant (K_i) of 131 nM [1] [2].

Cloperastine hydrochloride (HT-11 hydrochloride) is a type of flavonoid.

Ibutilide Fumarate (U70226E) is the fumarate salt form of ibutilide, a class III antiarrhythmic agent. Ibutilide exerts its effect by activating a slow, inward, predominately sodium current rather than by blocking outward potassium currents. This results in prolongation of atrial and ventricular action potential duration and refractory periods. Ibutilide slightly decreases the sinus rate and atrioventricular (AV) conduction and produces a dose-related prolongation of the QT interval.

Flecainide is a medication used to prevent and treat abnormally fast heart rates. This includes ventricular and supraventricular tachycardias.

Zonisamide (AD 810), a sulfonamide anticonvulsant, is approved for use as an adjunctive treatment in adults with partial-onset seizures. It may inhibit a carbonic anhydrase although this is not one of the main mechanisms of action. Zonisamide may act by blocking repetitive firing of voltage-gated sodium channels results in a reduction of T-type calcium channel currents, or by binding allosterically to GABA receptors. This latter action may lower the uptake of the inhibitory neurotransmitter GABA while increasing the uptake of the excitatory neurotransmitter glutamate.

Zonisamide sodium is a 1,2 benzisoxazole derivative. It is the first agent of this chemical class to be developed as an antiepileptic drug.