TRC160334 is a hydroxylase inhibitor of hypoxia-inducible factor (HIF). It is employed in research about ischemia/reperfusion injury.

TRC160334 (100~400 μΜ; 4 hours; Hep3B cells) results in dose-dependent stabilization of nuclear HIF-1[1]. TRC160334 (75~300 μM; 4 hours; Hep3B cells) results in dose-dependent transcriptional activation of HIF-1. TRC160334 shows a dose-dependent expression of HIF target genes such as EPO and adrenomedullin[1]. Western Blot Analysis[1]Cell Line: Hep3B cells Concentration: 100~400 μΜ Incubation Time: 4 hours Result: Resulted in dose-dependent stabilization of nuclear HIF-1.

TRC160334 (0.1 and 0.3 mg/kg; i.p.) significantly reduces serum creatinine and blood urea nitrogen[1]. TRC160334 (0.3 and 0.6 mg/kg; i.p.) shows reducing trends for acute tubular necrosis[1]. TRC160334 significantly reduces the rise in electrolyte excretion dose dependently. Preischemic treatment with TRC160334 results in a pronounced induction of HSP70 in kidneys by 6 hours while postischemic treatment with TRC160334 results in a pronounced induction of HSP70 in kidneys by 12 hours as compared with the respective vehicle control[1]. Animal Model: Sprague-Dawley male rats (250–300 g)[1]Dosage: 0.1 and 0.3 mg/kg Administration: I.p. Result: Significantly reduced serum creatinine and blood urea nitrogen. Animal Model: Sprague-Dawley male rats (250–300 g)[1]Dosage: 0.3 and 0.6 mg/kg Administration: I.p. Result: Showed reducing trends for acute tubular necrosis.