| Description |
TRC160334 is a hypoxia-inducible factor (HIF) hydroxylase inhibitor. TRC160334 can be used for the research of ischemia/reperfusion injury[1].
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| Related Catalog |
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| Target |
HIF hydroxylase[1]
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| In Vitro |
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.
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| In Vivo |
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.
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| References |
[1]. Jamadarkhana P, et al. Treatment with a novel hypoxia-inducible factor hydroxylase inhibitor (TRC160334) ameliorates ischemic acute kidney injury. Am J Nephrol. 2012;36(3):208-218.
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