B02 | RAD51 inhibitor

B02 chemical structure

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RAD51 is a key protein involved in homologous recombination that plays a critical role in the repair of DNA double-strand breaks (DSB) and interstrand cross-links (ICL).1 B02 (1290541-46-6) was identified in a high-throughput screen using a DNA strand exchange assay and was found to specifically inhibit human RAD51 (IC50=27.4 µM) but not its E. coli homolog (RecA)1. It sensitizes multiple myeloma cells to doxorubicin2 and  potentiates breast cancer cell killing by therapeutic agents in mouse models3.  B02 induces a heat-shock protein mediated cellular response that positively regulates the conversion of rcDNA to cccDNA via the authentic intracellular amplification pathway in human hepatoma cells.4

References/Citations:

  1. Huang et al. (2011), Identification of specific inhibitors of human RAD51 recombinase using high-throughput screening; ACS Chem. Biol., 6 628
  2. Alagpulinsa et al. (2014), A Small-Molecule Inhibitor of RAD51 Reduces Homologous Recombination and Sensitizes Multiple Myeloma Cells to Doxorubicin; Front. fOncol., 4 289
  3. Huang and Mazin (2014), A Small Molecule Inhibitor of Human RAD51 Potentiates Breast Cancer Cell Killing by Therapeutic Agents in Mouse Xenografts; PLoS One, 9 e100993
  4. Tang et al. (2023), Heat Shock Protein Family A Member 1 Promotes Intracellular Amplification of Hepatitis B Virus Covalently Closed Circular DNA; J. Virol., 97 e0126122
1290541-46-6, B-02, B02, B02 supplier, RAD51 inhibitor

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Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee

RAD51 is a key protein involved in homologous recombination that plays a critical role in the repair of DNA double-strand breaks (DSB) and interstrand cross-links (ICL).1 B02 (1290541-46-6) was identified in a high-throughput screen using a DNA strand exchange assay and was found to specifically inhibit human RAD51 (IC50=27.4 µM) but not its E. coli homolog (RecA)1. It sensitizes multiple myeloma cells to doxorubicin2 and  potentiates breast cancer cell killing by therapeutic agents in mouse models3.  B02 induces a heat-shock protein mediated cellular response that positively regulates the conversion of rcDNA to cccDNA via the authentic intracellular amplification pathway in human hepatoma cells.4

References/Citations:

  1. Huang et al. (2011), Identification of specific inhibitors of human RAD51 recombinase using high-throughput screening; ACS Chem. Biol., 6 628
  2. Alagpulinsa et al. (2014), A Small-Molecule Inhibitor of RAD51 Reduces Homologous Recombination and Sensitizes Multiple Myeloma Cells to Doxorubicin; Front. fOncol., 4 289
  3. Huang and Mazin (2014), A Small Molecule Inhibitor of Human RAD51 Potentiates Breast Cancer Cell Killing by Therapeutic Agents in Mouse Xenografts; PLoS One, 9 e100993
  4. Tang et al. (2023), Heat Shock Protein Family A Member 1 Promotes Intracellular Amplification of Hepatitis B Virus Covalently Closed Circular DNA; J. Virol., 97 e0126122