KT-333 is a first-in-class, potent, and selective heterobifunctional degrader of STAT3 that recruits the VHL E3 ligase for ubiquitin-proteasome-mediated degradation. It induces robust antitumor activity in preclinical models of ALK⁺ anaplastic large cell lymphoma (ALCL).

KT-333 is a first-in-class, potent, and selective heterobifunctional degrader of STAT3 that recruits the VHL E3 ligase for ubiquitin-proteasome-mediated degradation. It induces robust antitumor activity in preclinical models of ALK⁺ anaplastic large cell lymphoma (ALCL).

ART0380 (IACS-030380) is a potent and selective, orally bioavailable inhibitor of ATR kinase, with an IC50 of 51.7 nM effectively inhibiting the enzyme activity of the ATR-ATRIP complex. It functions as an ATP-competitive inhibitor, binding to the ATP pocket of ATR, where ATP would typically bind. It interacts with the hinge through its morpholine oxygen […]

ART0380 (IACS-030380) is a potent and selective, orally bioavailable inhibitor of ATR kinase, with an IC50 of 51.7 nM effectively inhibiting the enzyme activity of the ATR-ATRIP complex. It functions as an ATP-competitive inhibitor, binding to the ATP pocket of ATR, where ATP would typically bind. It interacts with the hinge through its morpholine oxygen […]

ART0380 (IACS-030380) is a potent and selective, orally bioavailable inhibitor of ATR kinase, with an IC50 of 51.7 nM effectively inhibiting the enzyme activity of the ATR-ATRIP complex. It functions as an ATP-competitive inhibitor, binding to the ATP pocket of ATR, where ATP would typically bind. It interacts with the hinge through its morpholine oxygen […]

ART0380 (IACS-030380) is a potent and selective, orally bioavailable inhibitor of ATR kinase, with an IC50 of 51.7 nM effectively inhibiting the enzyme activity of the ATR-ATRIP complex. It functions as an ATP-competitive inhibitor, binding to the ATP pocket of ATR, where ATP would typically bind. It interacts with the hinge through its morpholine oxygen […]

APX2009 is a second-generation redox-specific inhibitor of APE1/Ref-1, an essential enzyme in the base excision repair (BER) pathway. APX2009 effectively reduces breast cancer cell proliferation and colony formation.

APX2009 is a second-generation redox-specific inhibitor of APE1/Ref-1, an essential enzyme in the base excision repair (BER) pathway. APX2009 effectively reduces breast cancer cell proliferation and colony formation.

APX2009 is a second-generation redox-specific inhibitor of APE1/Ref-1, an essential enzyme in the base excision repair (BER) pathway. APX2009 effectively reduces breast cancer cell proliferation and colony formation.

APX2009 is a second-generation redox-specific inhibitor of APE1/Ref-1, an essential enzyme in the base excision repair (BER) pathway. APX2009 effectively reduces breast cancer cell proliferation and colony formation.