Loss of effective DNA repair correlates with carcinogenesis; conversely, an upregulation of DNA repair is often seen in cancer cells in response to DNA-damaging agents such as platinum-based chemotherapy and radiation. The capacity of cancer cells to identify and repair the damage caused by therapeutic assault is a major driver of acquired resistance and therefore limits the effectiveness of these conventional treatment approaches. Therefore, pharmacological targeting of DNA repair proteins may increase the efficacy of current treatments and overcome the risk of therapeutic resistance. Furthermore, the concept of synthetic lethality, whereby loss of function of either one of two interrelated genes is not lethal but loss of both genes results in cell death, provides a promising platform for pharmacological targeting of DNA repair genes. Endonucleases are enzymes, which are involved in several DNA repair pathways and act to cleave either damaged DNA or nucleotide by-products of repair, thus facilitating progression to DNA synthesis and ligation.[1]

[1] R. Doherty and S. Madhusudan. DNA Repair Endonucleases: Physiological Roles and Potential as Drug Targets. J Biomol Screen. 2015 Aug;20(7):829-41.

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2137 APE1 Inhibitor III Inhibitor of apurinic/apyrimidinic endonuclease 1 (APE1) €110.00
2136 AR03 Inhibitor of apurinic/apyrimidinic endonuclease 1 (APE1) €105.00
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3027 FEN1 inhibitor 1 Potent flap endonuclease-1 (FEN1) inhibitor €135.00
1656 Irestatin 9389 IRE1 inhibitor; UPR inhibitor €125.00
2821 PFM01 Inhibitor of MRE11 endonuclease €70.00
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