On October 16, 2017 NATURE COMMUNICATIONS published an article named «A novel Fer/FerT targeting compound selectively evokes metabolic stress and necrotic death in malignant cells." The authors of the publication credited ChemDiv with developing the new inhibitor.
A newly developed inhibitor of Fer and FerT, E260, selectively evokes metabolic stress in cancer cells by imposing mitochondrial dysfunction and deformation, and an onset of energy-consuming autophagy which decreases the cellular ATP level. Notably, Fer was also found to disrupt the association between PARP-1 and E260, thereby leading to PARP-1 activation. The cooperative intervention with these metabolic pathways leads to energy crisis and necrotic death in malignant, but not in normal human cells, and to the suppression of tumor growth in vivo. Thus, E260 is a new anti-cancer agent which imposes metabolic stress and cellular death in cancer cells.
We, at ChemDiv, are proud that our discovery chemistry platform helped the authors achieve such remarkable results.
You can find the full article article at
https://www.nature.com/articles/s41467-017-00832-w.
About ChemDivChemDiv is a recognized global leader in drug discovery solutions. Over the past 25+ years the ChemDiv team has delivered hundreds of leads, drug candidates and new drug approvals in the areas of CNS, oncology, virology, inflammation, immunology, cardio and metabolic diseases to its pharma, biotech and academic partners around the globe. ChemDiv’s integrated drug discovery and risk-share collaborative platforms allow for an accelerated, cost-effective R&D process aimed at rapidly bringing a project from target ID to Phase 3 clinical candidate and beyond.
http://www.chemdiv.com/
On October 16, 2017 NATURE COMMUNICATIONS published an article named «A novel Fer/FerT targeting compound selectively evokes metabolic stress and necrotic death in malignant cells." The authors of the publication credited ChemDiv with developing the new inhibitor.A newly developed inhibitor of Fer and FerT, E260, selectively evokes metabolic stress in cancer cells by imposing mitochondrial dysfunction and deformation, and an onset of energy-consuming autophagy which decreases the cellular ATP level. Notably, Fer was also found to disrupt the association between PARP-1 and E260, thereby leading to PARP-1 activation. The cooperative intervention with these metabolic pathways leads to energy crisis and necrotic death in malignant, but not in normal human cells, and to the suppression of tumor growth in vivo. Thus, E260 is a new anti-cancer agent which imposes metabolic stress and cellular death in cancer cells.We, at ChemDiv, are proud that our discovery chemistry platform helped the authors achieve such remarkable results.You can find the full article article at https://www.nature.com/articles/s41467-017-00832-w. About ChemDivChemDiv is a recognized global leader in drug discovery solutions. Over the past 25+ years the ChemDiv team has delivered hundreds of leads, drug candidates and new drug approvals in the areas of CNS, oncology, virology, inflammation, immunology, cardio and metabolic diseases to its pharma, biotech and academic partners around the globe. ChemDiv’s integrated drug discovery and risk-share collaborative platforms allow for an accelerated, cost-effective R&D process aimed at rapidly bringing a project from target ID to Phase 3 clinical candidate and beyond. http://www.chemdiv.com
