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Olaparib effectively acts on Brca1; p53 for breast tumors (intraperitoneally injected at a dose of 50mg/kg daily), but against HR deficient Ecad; p53 has no effect on breast tumors. Olaparib had no dose-limiting toxicity in tumor-carrying mice. Olaparib is already used to treat tumors with BRCA mutations, such as ovarian, breast, and prostate cancers. In addition, Olaparib was selective in inhibiting ATM-deficient tumor cells, suggesting that Olaparib could be used as a potential agent for treating ATM-mutated lymphoid tumors.
Uses of bimatoprost.
Olaparib is a PARP inhibitor that also acts on BRCA1 or BRCA2 mutations. Olaparib has little effect on anchor-1, and IC50 value is greater than that of OLaparib. The concentration of Olaparib at 30-100nM acts on SW620 cells and inactivates PARP-1. Compared with BRCA1 and BRCA2-sufficient cell lines (Hs578T,MDA-MB-231,T47D), BRCA1-deficient cell lines (MDA-MB-463[1] and HCC1937) were over-sensitive to Olaparib, which inhibited PARP and blocked base excisation repair. Resulting in strong sensitivity of KB2P cells to Olaparib. The result is a shift from a single strand break to a double strand break during DNA replication, thus activating the BRCA2-dependent recombination pathway.
Preparation of bimatoprost.
Product Method of bimatoprost.
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