| References: |
Oltipraz, as a chemoprotective agent, induces Phase II detoxification enzyme activity in a Nrf2-dependent manner. 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. 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. 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. In rats on a CDAA diet, Oltipraz attenuate the progression of nonalcoholic steatohepatitis-related fibrosis. For the detailed information of Oltipraz, the solubility of Oltipraz in water, the solubility of Oltipraz in DMSO, the solubility of Oltipraz in PBS buffer, the animal experiment (test) of Oltipraz, the cell expriment (test) of Oltipraz, the in vivo, in vitro and clinical trial test of Oltipraz, the EC50, IC50,and affinity,of Oltipraz, For the detailed information of Oltipraz, the solubility of Oltipraz in water, the solubility of Oltipraz in DMSO, the solubility of Oltipraz in PBS buffer, the animal experiment (test) of Oltipraz, the cell expriment (test) of Oltipraz, the in vivo, in vitro and clinical trial test of Oltipraz, the EC50, IC50,and affinity,of Oltipraz, Please contact DC Chemicals. |
