HERG Inhibitors

E-4031 dihydrochloride acts as a HERG channel blocker by engaging with the channel's voltage-sensing domains, leading to altered gating properties. Its unique molecular architecture, featuring a flexible linker and diverse functional groups, facilitates strong interactions with the lipid bilayer, influencing membrane dynamics. The compound demonstrates notable binding kinetics, with a slow dissociation rate that prolongs its inhibitory effects on ion flow, highlighting its potential for modulating channel activity.

Nifekalant Hydrochloride exhibits distinctive interactions with the HERG potassium channel, primarily through its specific binding to the channel's pore region. This compound's unique structural features, including a rigid core and multiple polar substituents, enhance its affinity for the channel, resulting in significant alterations to ion conductance. Its reaction kinetics reveal a rapid association rate, contributing to its effective modulation of channel function and influencing cardiac repolarization dynamics.

Terfenadine interacts with the HERG potassium channel by stabilizing its open conformation, which leads to prolonged ion flow. Its unique molecular architecture, characterized by a bulky aromatic system and flexible side chains, facilitates specific interactions with channel residues. This compound exhibits slow dissociation kinetics, allowing for sustained channel modulation. Additionally, its lipophilic nature enhances membrane permeability, influencing cellular ion homeostasis.

Threo Ifenprodil hemitartrate exhibits a distinctive affinity for the HERG potassium channel, promoting a unique binding interaction that alters channel dynamics. Its structural features, including a chiral center and specific functional groups, enable selective engagement with channel sites, influencing gating mechanisms. The compound demonstrates notable reaction kinetics, with a propensity for prolonged channel occupancy, which may affect ion conductance and cellular excitability. Its hydrophilic characteristics contribute to solubility, impacting its interaction with lipid membranes.

Sertindole interacts with the HERG potassium channel through a unique binding mechanism that stabilizes the open state of the channel. Its molecular structure, characterized by specific aromatic rings and nitrogen-containing moieties, facilitates selective interactions with channel residues, influencing ion flow. The compound exhibits distinct reaction kinetics, with a slower dissociation rate, which may enhance its effects on cardiac repolarization. Additionally, Sertindole's lipophilicity affects its membrane permeability and distribution within cellular environments.

Quinidine blocks HERG channels, reducing potassium efflux and prolonging cardiac repolarization, which can result in QT interval prolongation.

Amiodarone inhibits HERG channels, slowing repolarization and suppressing arrhythmias by blocking potassium efflux.

Verapamil blocks HERG channels and inhibits calcium influx, leading to decreased heart rate and reduced contractility.

Diltiazem inhibits HERG channels and calcium influx, reducing cardiac contractility and controlling arrhythmias by slowing conduction.

Bepridil blocks HERG channels, calcium channels, and sodium channels, effectively preventing arrhythmias by prolonging cardiac action potentials.