HC-7366, is a First-in-Human modulator of General controlled nonderepressible 2 (GCN2) that activates GCN2. It demonstrates anti-metastatic efficacy, reducing lung metastases and exhibits anti-tumor activity.

HC-7366, is a First-in-Human modulator of General controlled nonderepressible 2 (GCN2) that activates GCN2. It demonstrates anti-metastatic efficacy, reducing lung metastases and exhibits anti-tumor activity.

MS8709 (EX-A11295) is a first-in-class G9a/GLP proteolysis targeting chimera (PROTAC) degrader, that induces G9a/GLP degradation in a concentration, time, and ubiquitin-proteasome system (UPS)-dependent manner, and does not alter the mRNA expression of G9a/GLP over other methyltransferases. It displays superior cell growth inhibition in prostate, leukemia, and lung cancer cells over parent G9a/GLP inhibitors.

MS8709 (EX-A11295) is a first-in-class G9a/GLP proteolysis targeting chimera (PROTAC) degrader, that induces G9a/GLP degradation in a concentration, time, and ubiquitin-proteasome system (UPS)-dependent manner, and does not alter the mRNA expression of G9a/GLP over other methyltransferases. It displays superior cell growth inhibition in prostate, leukemia, and lung cancer cells over parent G9a/GLP inhibitors.

MS8709 (EX-A11295) is a first-in-class G9a/GLP proteolysis targeting chimera (PROTAC) degrader, that induces G9a/GLP degradation in a concentration, time, and ubiquitin-proteasome system (UPS)-dependent manner, and does not alter the mRNA expression of G9a/GLP over other methyltransferases. It displays superior cell growth inhibition in prostate, leukemia, and lung cancer cells over parent G9a/GLP inhibitors.

MS8709 (EX-A11295) is a first-in-class G9a/GLP proteolysis targeting chimera (PROTAC) degrader, that induces G9a/GLP degradation in a concentration, time, and ubiquitin-proteasome system (UPS)-dependent manner, and does not alter the mRNA expression of G9a/GLP over other methyltransferases. It displays superior cell growth inhibition in prostate, leukemia, and lung cancer cells over parent G9a/GLP inhibitors.

R16(NSC29869, Nrf2-IN-3) is an inhibitor of NRF2 (nuclear factor erythroid 2-related factor 2) that selectively binds KEAP1 mutants and restores their NRF2-inhibitory function by repairing the disrupted KEAP1/NRF2 interactions. It significantly enhances the sensitivity of KEAP1-mutated tumor cells to cisplatin and gefitinib.

R16(NSC29869, Nrf2-IN-3) is an inhibitor of NRF2 (nuclear factor erythroid 2-related factor 2) that selectively binds KEAP1 mutants and restores their NRF2-inhibitory function by repairing the disrupted KEAP1/NRF2 interactions. It significantly enhances the sensitivity of KEAP1-mutated tumor cells to cisplatin and gefitinib.

R16(NSC29869, Nrf2-IN-3) is an inhibitor of NRF2 (nuclear factor erythroid 2-related factor 2) that selectively binds KEAP1 mutants and restores their NRF2-inhibitory function by repairing the disrupted KEAP1/NRF2 interactions. It significantly enhances the sensitivity of KEAP1-mutated tumor cells to cisplatin and gefitinib.

R16(NSC29869, Nrf2-IN-3) is an inhibitor of NRF2 (nuclear factor erythroid 2-related factor 2) that selectively binds KEAP1 mutants and restores their NRF2-inhibitory function by repairing the disrupted KEAP1/NRF2 interactions. It significantly enhances the sensitivity of KEAP1-mutated tumor cells to cisplatin and gefitinib.