Asandeutertinib (Osimertinib-d3, AZD-9291-d3) is an orally administered, ATP-competitive, irreversible, deuterated third-generation Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor (EGFR TKI) and a deuterium-stabilized derivative of osimertinib, with the potential to treat advanced EGFR-mutated NSCLC.

Asandeutertinib (Osimertinib-d3, AZD-9291-d3) is an orally administered, ATP-competitive, irreversible, deuterated third-generation Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor (EGFR TKI) and a deuterium-stabilized derivative of osimertinib, with the potential to treat advanced EGFR-mutated NSCLC.

ES9-17 is a potent, selective and reversible inhibitor of Clathrin-mediated endocytosis (CME). It bind to the N-terminal domain (nTD) of the clathrin heavy chain (CHC), inhibiting the uptake of FM4-64 and of several CME cargos in Arabidopsis.

ES9-17 is a potent, selective and reversible inhibitor of Clathrin-mediated endocytosis (CME). It bind to the N-terminal domain (nTD) of the clathrin heavy chain (CHC), inhibiting the uptake of FM4-64 and of several CME cargos in Arabidopsis.

ES9-17 is a potent, selective and reversible inhibitor of Clathrin-mediated endocytosis (CME). It bind to the N-terminal domain (nTD) of the clathrin heavy chain (CHC), inhibiting the uptake of FM4-64 and of several CME cargos in Arabidopsis.

KRAS-533 is a potent agonist of KRAS that binds to the GTP/GDP-binding pocket and prevents the hydrolysis of GTP, leading to accumulation of active GTP-bound KRAS. This triggers both apoptotic and autophagic cell death pathways in cancer cells, leading to potent suppression of mutant KRAS lung cancer in vitro and in animal models.

KRAS-533 is a potent agonist of KRAS that binds to the GTP/GDP-binding pocket and prevents the hydrolysis of GTP, leading to accumulation of active GTP-bound KRAS. This triggers both apoptotic and autophagic cell death pathways in cancer cells, leading to potent suppression of mutant KRAS lung cancer in vitro and in animal models.

KRAS-533 is a potent agonist of KRAS that binds to the GTP/GDP-binding pocket and prevents the hydrolysis of GTP, leading to accumulation of active GTP-bound KRAS. This triggers both apoptotic and autophagic cell death pathways in cancer cells, leading to potent suppression of mutant KRAS lung cancer in vitro and in animal models.

CL075 (3M002) is a selective agonist of TLR8 with immunomodulatory properties. It primes human neutrophils by activating signaling pathways, including p47phox phosphorylation and p38MAPK, leading to enhanced reactive oxygen species (ROS) production and contributing to immune defense.

CL075 (3M002) is a selective agonist of TLR8 with immunomodulatory properties. It primes human neutrophils by activating signaling pathways, including p47phox phosphorylation and p38MAPK, leading to enhanced reactive oxygen species (ROS) production and contributing to immune defense.