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Description

A cell-permeable, orally available triazole-class antifungal agent that, in addition to its known inhibitory activity against fungal cytochrome P450 14-alpha-demethylase, also acts as an effective Hh signaling inhibitor (IC50 ~0.8 µ,M against SHHN-induced Gli transcription activity in Shh-Light2 cells) in a Ptch-independent manner (IC50 ~0.9 µ,M against Ptch promoter-mediated transcription activity in murine Ptch-/- fibroblasts), presumably by binding smoothened (smo) at a site distinct from that targeted by cyclopamine (Cat. No. 239803) and SAG (Cat. No. 566660), as Itraconazole does not compete with BODIPY-cyclopamine binding, and it alters only the magnitude, but not the EC50, of SAG-induced Gli transcription activity in Shh-Light2 cells. Shown to effectively suppress Hh pathway-dependent growth of both engrafted medulloblastoma and endogenous basal cell carcinoma in mice in vivo (37.5 to 100 mg/kg/12 hr, p.o.) in a reversible manner., A cell-permeable, orally available triazole-class antifungal agent that, in addition to its known inhibitory activity against fungal cytochrome P450 14-alpha-demethylase, also acts as an effective Hh signaling inhibitor (IC50 ~ 0.8 µ,M against SHHN-induced Gli transcription activity in Shh-Light2 cells) in a Ptch-independent manner (IC50 ~ 0.9 µ,M against Ptch promoter-mediated transcription activity in murine Ptch-/- fibroblasts), presumably by binding smoothened (smo) at a site distinct from that targeted by cyclopamine (Cat. No. 239803) and SAG (Cat. No. 566660), as Itraconazole does not compete with BODIPY-cyclopamine binding, and it alters only the magnitude, but not the EC50, of SAG-induced Gli transcription activity in Shh-Light2 cells. Shown to effectively suppress Hh pathway-dependent growth of both engrafted medulloblastoma and endogenous basal cell carcinoma in mice in vivo (37.5 to 100 mg/kg/12 hr, p.o.) in a reversible manner.