For research use only. Not for use in humans.
Molecular Weight(MW): 471.67
Terfenadine is an antihistamine, generally completely metabolizes to the active form fexofenadine in the liver by the enzyme cytochrome P450 CYP3A4 isoform.
Purity & Quality Control
|Description||Terfenadine is an antihistamine, generally completely metabolizes to the active form fexofenadine in the liver by the enzyme cytochrome P450 CYP3A4 isoform.|
Terfenadine is equipotent to quinidine as a blocker of the delayed rectifier potassium current in isolated feline myocytes.  Terfenadine inhibits the human ether-a-go-go related gene (HERG) encoded channels expressed in Xenopus oocytes at nanomolar concentrations in a use- and voltage-dependent fashion.  Terfenadine (2 μM) blocks the steady-state maximum current at 0 mV by 65% in Xenopus oocytes. Terfenadine block is dose dependent and equally potent on the maximal steady-state and tail currents, its Kd values are 350 nM and 390 nM, respectively. Terfenadine blocks Kv1.5 (a member of the Kv1 subfamily of voltage-dependent K+ channels) in human atrial myocytes and in the human embryonic kidney cell expression system. Terfenadine (10 μM) produces a dose-dependent block with a 60% reduction of steady-state current in Xenopus oocytes.  Terfenadine is oxidated into oxidative N-dealkylation to 4-(hydroxydiphenylmethyl)-piperidine and oxidation of a tert-butyl methyl group to a primary alcohol, which is subsequently oxidized to a carboxylic acid, which is markedly inhibited by gestodene, a selective mechanism-based inactivator of P-450 3A enzymes but not by any of several other P-450 inhibitors.  Terfenadine significantly increases action potential duration of guinea pig myocytes. Terfenadine potently blocks the rapidly activating component of the delayed rectifier, IKr, with IC50 values of 1.5 nM and 50 nM, respectively. Terfenadine (10 μM) blocks the slowly activating component of the delayed rectifier, IKs (58.4%), and the inward rectifier, IK1 (20.5%). 
|In vivo||Terfenadine (1.0 to 3.0 mg/kg, i.v.) significantly prolongs the QTc interval and ventricular effective refractory period in chloralose-anesthetized dogs. |
|In vitro||DMSO||94 mg/mL warmed (199.29 mM)|
|Ethanol||27 mg/mL warmed (57.24 mM)|
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