Terfenadine

50679-08-8

C32H41NO2

DMSO : >= 50 mg/mL (106.01 mM); H2O : < 0.1 mg/mL (insoluble)

Membrane Transporter/Ion Channel; Immunology/Inflammation; GPCR/G Protein; Apoptosis; Protein Tyrosine Kinase/RTK; Apoptosis; Membrane Transporter/Ion Channel; Neuronal Signaling

Terfenadine ((+/-)-Terfenadine) is a potent open-channel blocker of hERG with an IC₅₀ of 204 nM^[1]. Terfenadine, an H1 histamine receptor antagonist, acts as a potent apoptosis inducer in melanoma cells through modulation of Ca²⁺ homeostasis. Terfenadine induces ROS-dependent apoptosis, simultaneously activates Caspase-4, -2, -9 and inducts p73, Noxa^[2]. IC50 & Target: IC50: 204 nM (hERG)^[1] In Vitro: Terfenadine ((+/-)-Terfenadine) (4-20 uM; 24 hours) induces dose and time-dependent apoptosis on A375 melanoma cells. The IC₅₀ after 24 h of TEF treatment in complete medium was 10.4 uM for A375 cells, 9.9 uM for Hs294T cells and 9.6 for HT144 cells^[2].
Terfenadine (2-10 uM; 8 hours) induces dose-dependent cytotoxicity^[2].
Terfenadine (10 uM; 8 hours) causes a massive vacuolization of the cytoplasm and autophagic vacuoles of both double and multiple membranes and at various stages. Terfenadine induces autophagy by ROS-dependent and -independent mechanisms^[2].
Terfenadine (10 uM; 8-28 hours) increases p53, p73, p21 and Noxa protein levels in cells in complete medium^[2].
In Vivo: Terfenadine (p.o.; 40 mg/kg; for 16 days) produces a significant inhibition of tumour growth rate and enhances the anti-cancer effect of EPI in chemo-resistant NSCLC xenograft models^[3].