Abcam, ab120504, Flecainide, Sodium channel blocker

Size: 10mg / 50mg
MW 414.34 Da, Purity >99%. Sodium channel blocker. Class IC antiarrhythmic agent. Inhibits fast Na + current in cardiac muscle in a use- and concentration-dependent manner. Also inhibits cardiac ryanodine receptors. Orally-active.
Key facts
CAS number:54143-55-4,
Purity:>99%,
Form:SolidSee storage information,
Molecular weight:414.34 Da,
Molecular formula:C17H20F6N2O3,
PubChem:3356,
Nature:Synthetic,
Solubility:Soluble in ethanol to 100 mMSoluble in DMSO to 50 mM,
Biochemical name:Flecainide,
Biological description:Sodium channel blocker. Class IC antiarrhythmic agent. Inhibits fast Na+ current in cardiac muscle in a use- and concentration-dependent manner. Also inhibits cardiac ryanodine receptors. Orally-active.,
Canonical smiles:C1CCNC(C1)CNC(=O)C2=C(C=CC(=C2)OCC(F)(F)F)OCC(F)(F)F,
InChi:InChI=1S/C17H20F6N2O3/c18-16(19,20)9-27-12-4-5-14(28-10-17(21,22)23)13(7-12)15(26)25-8-11-3-1-2-6-24-11/h4-5,7,11,24H,1-3,6,8-10H2,(H,25,26),
InChiKey:DJBNUMBKLMJRSA-UHFFFAOYSA-N,
IUPAC Name:N-(piperidin-2-ylmethyl)-2,5-bis(2,2,2-trifluoroethoxy)benzamide

Properties and Storage Information:
Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions-+4°C, Storage information-Store under desiccating conditions, The product can be stored for up to 12 months

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
The target proteins CACNA1C Kv4.2/KCND2 Nav1.5/SCN5A H-ERG CaV1.3 and CACNA1F are important ion channels that facilitate the movement of ions such as calcium potassium and sodium across cell membranes. These channels play an important role in generating and regulating action potentials within various cell types most notably in cardiac tissue and neurons. CACNA1C also known as CaV1.2 has a molecular mass of approximately 240 kDa and is expressed widely including in the heart brain and skeletal muscle. Kv4.2/KCND2 and H-ERG part of the potassium channel family contribute to cell repolarization whereas Nav1.5/SCN5A a sodium channel initiates action potential in cardiac cells. CaV1.3 and CACNA1F are calcium channels that are important for synaptic transmission and are expressed predominantly in sensory cells of the eye which is essential for vision.
Biological function summary
These ion channels regulate cellular excitability and facilitate signal transmission. CACNA1C and its counterparts which are often part of larger channel complexes coordinate with accessory proteins to modulate channel activity. Kv4.2 participates in the rapid repolarization phase of the cardiac action potential whereas Nav1.5 provides the influx of sodium necessary for the depolarization phase. CaV1.3 and CACNA1F are integral to calcium ion influx that triggers synaptic vesicle release in auditory and retinal cells. These biological functions are critical for proper cardiac rhythm and neuronal communication.
Pathways
These ion channels are integral to the cardiac action potential pathway and calcium signaling pathway. CACNA1C is part of the L-type calcium current within these pathways. Kv4.2 and Nav1.5 are closely associated with the cardiac action potential pathway controlling heart rate and rhythmicity. H-ERG participates in cardiac repolarization and its dysfunction is linked to arrhythmogenic pathways. These pathways involve intricate interactions with other proteins like KCNQ1 and RyR2 which further mediate cardiac and neuronal excitability.
Mutations or dysfunction in these ion channels can lead to severe cardiac and neurological conditions. CACNA1C mutations are associated with Timothy syndrome characterized by long QT intervals in cardiac electrophysiology and has a relationship with the protein calmodulin in calcium regulation. Malfunctions in Nav1.5 are critically linked to Brugada syndrome a genetic condition that results in irregular heartbeats. H-ERG abnormalities are implicated in long QT syndrome impacting cardiac rhythm and this condition involves interactions with KCNQ1. These disorders emphasize the importance of normal channel function for maintaining cardiac and neurological health.