CBP-93872

inhibits G2 checkpoint maintenance; structure in first source

Networked: 3 relevant articles (0 outcomes, 0 trials/studies)

1.	Neoplasms (Cancer) 01/01/2017 - "Treatment with CBP-93872 significantly increased cancer cell sensitivities to various chemotherapeutic agents tested through suppression of checkpoint activation. " 11/01/2011 - "Interestingly, CBP-93872 directly suppressed the growth of p53-mutated cancer cell lines with wild-type CDKN2A by eliciting G(1) arrest, but not CDKN2A-deleted and/or wild-type p53 lines. " 07/15/2014 - "Taken together, our results suggest that CBP-93872 is an inhibitor of maintenance of the DSB-specific G2 checkpoint and thus might be a strong candidate as the basis for a drug that specifically sensitizes p53-mutated cancer cells to DSB-inducing DNA damage therapy."
2.	Pancreatic Neoplasms (Pancreatic Cancer) 01/01/2017 - "The G2 checkpoint inhibitor CBP-93872 increases the sensitivity of colorectal and pancreatic cancer cells to chemotherapy." 01/01/2017 - "To examine the potential use of CBP-93872 for clinical applications, we analyzed the synergistic effects of platinum-containing drugs, oxaliplatin and cisplatin, pyrimidine antimetabolites, gemcitabine and 5-fluorouracil (5-FU), in combination with CBP-93872, on cell lethality in colorectal and pancreatic cancer cell lines. "
3.	Ataxia Telangiectasia (Louis Bar Syndrome) 01/01/2017 - "CBP-93872 suppresses maintenance of DNA double-stranded break-induced G2 checkpoint, by inhibiting the pathway between ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) activation. "

1.	Platinum
2.	Fluorouracil (Carac)
3.	DNA (Deoxyribonucleic Acid)
4.	Cisplatin (Platino)
5.	Antimetabolites
6.	Gemcitabine
7.	Oxaliplatin (Eloxatin)
8.	pyrimidine
9.	1,2- di- (4- sulfamidophenyl)- 4- butylpyrazolidine- 3,5- dione (DSB)