Oltipraz is a potent Nrf2 activator and a potent inducer of Phase II detoxification enzymes, most notably glutathione-S-transferase (GST). Phase 3.
Description :
Oltipraz (RP 35972, NSC 347901) is a cancer chemopreventive agent with inhibitory effect on angiogenesis and tumor growth, inhibits insulin- or hypoxia-induced HIF-1α expression through an increase in ubiquitination; abrogates insulin-induced H(2)O(2) production, thereby preventing H(2)O(2)-enhanced HIF-1alpha expression and promoting its ubiquitination and degradation; inhibits HIF-1α activity and HIF-1α-dependent tumor growth both in vitro and in vivo.
Steatohepatitis
Oltipraz, as a chemoprotective agent, induces Phase II detoxification enzyme activity in a Nrf2-dependent manner. [1] In human HT29 colon cancer cells, oltipraz inhibits the induction of HIF-1α by insulin, hypoxia or CoCl2 by significantly accelerating degradation of HIF-1α protein. [2]
Oltipraz (500 mg/kg, p.o.) significantly reduces multiplicity of gastric neoplasia in wild-type mice by 55%, but has no effect on tumor burden in nrf2-deficient mice. [1] In BALB/c nude mice transplanted with HCT116 cells, Oltipraz (200 mg/kg, p.o.) inhibits tumor growth and angiogenesis via inhibition of HIF-1α. [2] In rats on a CDAA diet, Oltipraz attenuate the progression of nonalcoholic steatohepatitis-related fibrosis. [3]