| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | HeLa, MCF-7，U2OS cells |
Preparation Method | Human cell lines were sequentially incubated for 24 h in media containing varying concentrations of mitomycin C, followed by 24 h in media containing RI-1. Cells were then allowed to grow in drug-free media for an additional 7–9 days. |
Reaction Conditions | 24h，15 μM, 25 μM |
Applications | In all three cell types, RI-1 significantly sensitized cells to MMC. The magnitude of sensitization was calculated as a function of the concentration of MMC required to kill 50% of cells. The magnitude of sensitization achieved with 25 uM RI-1 was 2.5-3 fold, depending on the cell type. These data suggest that RI-1 can specifically interfere with RAD51 functions in human cancer cells, thereby rendering them more susceptible to the lethal effects of oncologic treatment[1]. |
Animal models | Female BALB/c nude mice (6 weeks) |
Preparation Method | Mice bearing MDA-MB-157 xenografts with a tumor volume of 100mm3(±50), was then randomly grouped and treated by intraperitoneal injection every 3 days for 30 days with RI-1 (50 mg/kg), ABT888 (25 mg/kg), a combination of RI-1 and ABT888, or no treated. Tumors were taken 8 hours after last drug administration for immunofluorescence assay. |
Dosage form | 50 mg/kg，every 3 days for 30 days |
Applications | The combination of ABT888 and RI-1 resulted in significant inhibition of tumor growth.The combination of ABT888 and RI-1 showed a slower growth and a decreased tumor weight of tumors. |
| 产品描述 | RI-1 is a RAD51 inhibitor, with IC50ranging 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[1].RI-1 sensitizes cells to DNA damage by directly and specifically disrupting HsRAD51.RI-1covalently attaches to HsRAD51 protein, thereby inhibiting the ability of RAD51 to form filaments on ssDNA. RI-1 can inhibit sub-nuclear accumulation of HsRAD51 protein at sites of DNA damage, and this inhibitory activity sensitizes various cancer cell types to cross-linking chemotherapy[1]. In HeLa, MCF-7 and U2OS cells, RI-1 significantly sensitized cells to MMC. The magnitude of sensitization achieved with 25uM RI-1 was 2.5-3fold, depending on the cell type. These data suggest that RI-1 can specifically interfere with RAD51 functions in human cancer cells, thereby rendering them more susceptible to the lethal effects of oncologic treatment[1].In Huh7 and HCCLM3 cells,XRCC2 overexpression accelerates mtDNA level recovery, but treatment with RI-1 can deplete RAD51 and prevent mtDNA level recovery[3]. Rad51 inhibitor RI-1 to inhibit the HR in oocytes. 60 μM RI-1 exposure has no obvious effects on the PBE（polar body extrusion） rates of normal oocytes[4]. Ri-1 reduced γ-H2AX foci in G2 phase cells and resulted in elevated levels of unrepaired DNA double-strand breaks 6 hours after radiation[5].VS tumors expressed RAD51. VS may evade radiation injury by entering cell cycle arrest and upregulating RAD51-dependent repair of radiation-induced double-stranded breaks in DNA. Although there was variability in responses among individual primary VS cells, RAD51 inhibition with RI-1 reduced RAD51-dependent DNA repair to enhance radiation toxicity in VS cells[6] In an MDA-MB-157 breast cancer model, mice were randomly assigned to one of four groups to receive vehicle, ABT888, RI-1, or combination of ABT888 and RI-1. The combination of ABT888 and RI-1 resulted in significant inhibition of tumor growth.The combination of ABT888 and RI-1 showed a slower growth and a decreased tumor weight of tumors[2] References: |
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