Ropivacaine is a member of the amino amide class of local anesthetics and is supplied as the pure S-(-)-enantiomer. It produces effects similar to other local anesthetics via reversible inhibition of sodium ion influx in nerve fibers. Ropivacaine is less lipophilic than bupivacaine and is less likely to penetrate large myelinated motor fibers, resulting in a relatively reduced motor blockade. Thus, ropivacaine has a greater degree of motor-sensory differentiation, which could be useful when the motor blockade is undesirable. The reduced lipophilicity is also associated with decreased potential for central nervous system toxicity and cardiotoxicity. Ropivacaine is indicated for the production of local or regional anesthesia for surgery and for acute pain management.

Quinidine is a pharmaceutical agent that acts as a class I antiarrhythmic agent (Ia) in the heart. It is a stereoisomer of quinine, originally derived from the bark of the cinchona tree. The drug causes increased action potential duration, as well as a prolonged QT interval. Like all other class I antiarrhythmic agents, quinidine primarily works by blocking the fast inward sodium current (INa). Quinidine's effect on INa is known as a 'use-dependent block'. This means at higher heart rates, the block increases, while at lower heart rates, the block decreases. The effect of blocking the fast inward sodium current causes the phase 0 depolarization of the cardiac action potential to decrease (decreased Vmax). Quinidine also blocks the slowly inactivating, tetrodotoxin-sensitive Na current, the slow inward calcium current (ICA), the rapid (IKr) and slow (IKs) components of the delayed potassium rectifier current, the inward potassium rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and Ito. Quinidine is also an inhibitor of the cytochrome P450 enzyme 2D6 and can lead to increased blood levels of lidocaine, beta blockers, opioids, and some antidepressants. Quinidine also inhibits the transport protein P-glycoprotein and so can cause some peripherally acting drugs such as loperamide to have central nervous system side effects, such as respiratory depression if the two drugs are coadministered. Quinidine can cause thrombocytopenia, granulomatous hepatitis, myasthenia gravis, and torsades de pointes, so is not used much today. Torsades can occur after the first dose. Quinidine-induced thrombocytopenia (low platelet count) is mediated by the immune system and may lead to thrombocytic purpura. A combination of dextromethorphan and quinidine has been shown to alleviate symptoms of easy laughing and crying (pseudobulbar affect) in patients with amyotrophic lateral sclerosis and multiple sclerosis. This drug is marketed as Nuedexta in the United States. Intravenous quinidine is also indicated for the treatment of Plasmodium falciparum malaria. However, quinidine is not considered the first-line therapy for P. falciparum. The recommended treatments for P. falciparum malaria, according to the Toronto Notes 2008, are a combination of either quinine and doxycycline or atovaquone and proguanil (Malarone). The drug is also effective for the treatment of atrial fibrillation in horses.

A sulfide ion is composed of a lone sulfur atom. Its charge is negative two, giving sulfides this formula: S^2-. Sulfide is a strong base, so solutions of sulfide in water are basic, due to hydrolysis. One well-known ionic compound with a sulfide ion is H_2S. The infamous rotten-egg smell often associated with sulfur originates from this compound. Sodium sulfide nonahydrate is used in the formation of surface functionalized cadmium sulfide quantum dots.

Clofilium is a quaternary ammonium compound that acts as potassium channel blocker. Clofilium is a class III agent. Clofilium increases atrial and ventricular effective refractory period without changing conduction time and, despite no apparent change in premature ventricular complex frequency, it can abolish the ability to induce ventricular tachycardia by programmed stimulation and is also well tolerated.

IVABRADINE, (-)- is an (R)-enantiomers of Ivabradine. IVABRADINE, (-)- produced a concentration-dependent block of hKv1.5 channels. S 16260 (R configuration) and S 16257 (S configuration) of Ivabradine were equipotent in reducing the spontaneous firing of rabbit sinus node preparations, but S 16260 induced significant prolongations of action potential duration of ventricular preparation (guinea pig papillary muscle and rabbit purkinje fibers), contrary to S 16257. These in vitro data have been confirmed by in vivo studies in anesthetized pigs showing the equipotence of the two isomers in reducing the heart rate, the absence of effect of S 16257 on the QT interval corrected for heart rate (QTc) in contrast with S 16260 which induced a dose-dependent increase in the QTc, indicating a direct effect on ventricular repolarization.

PAP-1 (5-(4-phenoxybutoxy)psoralen) is the selective inhibitor of Kv1.3, voltage-gated K+ channel, that is highly expressed in cell membranes of activated effector memory T cells (TEM). The blockade of Kv1.3 results in membrane depolarization and inhibition of TEM proliferation and function. PAP-1 is 23-fold selective over Kv1.5, 33- to 125-fold selective over other Kv1-family channels, and 500- to 7500-fold selective over Kv2.1, Kv3.1, Kv3.2, Kv4.2, HERG, calcium-activated K+ channels, Na+, Ca2+, and Cl- channels. PAP-1 does not exhibit cytotoxic or phototoxic effects, is negative in the Ames test, and affects cytochrome P450-dependent enzymes only at micromolar concentrations. PAP-1 potently inhibits the proliferation of human TEM cells and suppresses delayed-type hypersensitivity, a CD4+ T cell-mediated reaction, in rats when administered intraperitoneally or orally. PAP-1 further effectively treats allergic contact dermatitis, a CD8+ T cell-mediated reaction.

(R)-Ropivacaine (Dextroropivacaine) is a voltage-dependent potassium channel blocker with local anesthetic activity. (S)-Ropivacaine is a medication used for the production of local or regional anesthesia for surgery and for acute pain management. Ropivacaine shows a difference in channel blockade between two enantiomers, and R-Ropivacaine shows greater cardiotoxicity than (S)-Ropivacaine. (R)-Ropivacaine is the impurity in commercial formulations of Ropivacaine.

AVE-0118 is a Kv1.5 blocker which was developed by Aventis Pharma for the treatment of cardiovascular diseases. The drug reached phase II of clinical trilas in patients with atrial fibrillation, however its development was terminated.