mre11

PFM03 is an endonuclease inhibitor that specifically blocks Mre11 and is also able to reduce MRN endonuclease activity by 98%, blocking hMRN-mediated endonucleotomy and nuclear exocytosis processes on the protein-binding end of the 5 ' and 3 ' chains.

Mirin is a Mre11-Rad50-Nbs1 (MRN) complex inhibitor that inhibits MRN-dependent ATM activation without affecting ATM protein kinase activity. It also inhibits Mre11-associated exonuclease activity, thereby disrupting DNA double-strand break repair.Mirin induces cell cycle arrest in G1 phase.

PFM01 is an inhibitor of MRE11 endonuclease. PFM01 can regulate double-strand break repair (DSBR) by nonhomologous end-joining (NHEJ) versus homologous recombination (HR).

PFM39 is a selective MRE11 nucleic acid exonuclease inhibitor and Mirin analog that prolongs mitosis.PFM39 inhibits HR and alleviates repair defects caused by EXO1 BLM depletion.

MU1409 is an MRE11 nuclease inhibitor with an IC50 of 12.1 μM. It also inhibits FEN1 and EXO1, with IC50 values of 24.2 μM and 176.4 μM, respectively. MU1409 impacts cellular DNA repair and prevents the degradation of stalled replication forks in BRCA2-deficient cells, making it a promising candidate for studying BRCA2 mutation-induced cancers.

(Z)-Mirin is a potent Mre11–Rad50–Nbs1 (MRN) complex inhibitor, and inhibits Mre11-associated exonuclease activity.

Antitumor agent-96 (Compound D34) is a potent MRE11 inhibitor that down-regulates the homologous recombination (HR) pathway by binding to and suppressing the endonuclease functions of MRE11, thereby inducing apoptosis in CM cells [1].

MU147 is an MRE11 nuclease inhibitor and chemical probe with anticancer properties, exhibiting lethal effects on Ehrlich ascites tumor cells both in vivo and in vitro. It disrupts the MRE11 nuclease-dependent double-strand break repair mechanism without impairing ATM activation. Additionally, MU147 damages the degradation of nascent strands at stalled replication forks and selectively affects BRCA2-deficient cells.