base excision repair

Methoxyamine HCl (Methoxyamine) covalently binds to apurinic/apyrimidinic (AP) DNA damage sites and inhibits base excision repair (BER), which may result in an increase in DNA strand breaks and apoptosis. Methoxyamine is an orally bioavailable small molecule inhibitor with potential adjuvant activity. This agent may potentiate the anti-tumor activity of alkylating agents.

Niraparib, also know as MK-4827, is an inhibitor of poly (ADP-ribose) polymerase (PARP) with potential antineoplastic activity. MK4827 inhibits PARP activity, enhancing the accumulation of DNA strand breaks and promoting genomic instability and apoptosis. The PARP family of proteins detect and repair single strand DNA breaks by the base-excision repair (BER) pathway.

Pamiparib is a highly potent and selective PARP inhibitor. BGB-290 selectively binds to PARP and prevents PARP-mediated repair of single-strand DNA breaks via the base-excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks, pro

Niraparib hydrochloride (MK-4827 hydrochloride) is an inhibitor of poly (ADP-ribose) polymerase (PARP) with potential antineoplastic activity. By inhibiting PARP activity, niraparib hydrochloride increases DNA strand breaks, leading to genomic instability and apoptosis. The PARP family of proteins detects and repairs single-strand DNA breaks via the base-excision repair (BER) pathway.

TIQ-A is a PARP1 inhibitor which involved in DNA single-strand break repair via the base excision repair pathway. PARP1 is triggered by DNA damage and its excessive activation has been proposed as a causative factor in many pathological conditions includi

Pamiparib, also known as BGB-290, is a highly potent and selective PARP inhibitor with favorable drug metabolism and pharmacokinetic properties. BGB-290 selectively binds to PARP and prevents PARP-mediated repair of single-strand DNA breaks via the base-excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks, promotes genomic instability, and eventually leads to apoptosis. BGB-290 may both potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance.

APE1-IN-2 (compound AP1), a Pt(IV) proagent, selectively targets the essential base excision repair protein apurinic apyrimidinic endonuclease 1 (APE1). Exhibiting anticancer properties, APE1-IN-2 prompts the intracellular accumulation of platinum and initiates the activation of DNA damage response and apoptosis pathways [1].

NTPO trisodium induces DNA damage and fragmentation, activating ATR-mediated cell cycle checkpoints. Its DNA damaging effects are mitigated by base excision repair (BER) but not by nucleotide excision repair (NER) [1].