RI-1RI-1
MedChemExpress (MCE)
HY-15317
415713-60-9
99.83%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Room temperature in continental US
may vary elsewhere.
RI-1 is a RAD51 inhibitor, with IC50s ranging from 5 to 30 μM. RI-1 binds covalently to the surface of RAD51 protein at cysteine 319. RI-1 inactivates RAD51 by directly binding to a protein surface that serves as an interface between protein subunits in RAD51 filaments. RI-1 can disrupt homologous recombination in human cells.
RI-1 (1-50 μM
24 h) specifically inhibits homologous recombination (HR) in U2OS cells and stimulates single-strand annealing (SSA) in HEK293 cells[1].?RI-1 (5-20 μM
30 min) inhibits HsRAD51 in a concentration-dependent manner[1].?RI-1 (20 μM
8 h) disrupts the formation of RAD51 foci after DNA damage in immortalized human fibroblasts[1].?RI-1 (15-25 μM
24 h) sensitizes human cancer cells (HeLa, MCF-7 and U2OS) to cross-linking chemotherapy[1].
RI-1 (50 mg/kg
i.p. every 3 d for 30 d) significantly reduces triple negative breast cancer (TNBC) tumor growth in mice[2].
IC50: 5-30 μM (RAD51)[1] In Vitro RI-1 (1-50 μM
24 h) specifically inhibits homologous recombination (HR) in U2OS cells and stimulates single-strand annealing (SSA) in HEK293 cells[1].?RI-1 (5-20 μM
30 min) inhibits HsRAD51 in a concentration-dependent manner[1].?RI-1 (20 μM
8 h) disrupts the formation of RAD51 foci after DNA damage in immortalized human fibroblasts[1].?RI-1 (15-25 μM
24 h) sensitizes human cancer cells (HeLa, MCF-7 and U2OS) to cross-linking chemotherapy[1]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> RI-1 Related Antibodies
| | | |
| | | | | |
[1]. Budke B, et, al. RI-1: a chemical inhibitor of RAD51 that disrupts homologous recombination in human cells. Nucleic Acids Res. 2012 Aug
40(15):7347-57. [Content Brief]
[2]. Shi Y, et, al. DAXX, as a Tumor Suppressor, Impacts DNA Damage Repair and Sensitizes BRCA-Proficient TNBC Cells to PARP Inhibitors. Neoplasia. 2019 Jun
21(6):533-544. [Content Brief]