One-third of patients with acute myeloid leukemia (AML) present mutations in the FMS-like tyrosine kinase 3 (FLT3) gene. Several first- and next-generation FLT3 inhibitors are currently being used in AML management, but there is a need for new options able to achieve complete and sustained FLT3 signaling suppression.
Simultaneous inhibition of the phosphoinositide 3-kinase (PI3K) signaling pathway and histone deacetylase (HDAC) provides synergistic efficacy in the treatment of hematological malignancies.
SUMOylation is a post-translational modification implicated in DNA damage repair that has been linked to the lack of efficacy of some therapies commonly used for the treatment of leukemia.
Remix Therapeutics Inc. has closed a $60 million financing to advance its lead program, REM-422, into the clinic and for further advancement of a pipeline of RNA processing targeted therapeutics.
About 30% of patients with acute myeloid leukemia (AML) harbor mutations in the gene encoding receptor-type tyrosine-protein kinase FLT3 in the form of internal tandem duplication (ITD) or mutations in the tyrosine kinase domain.
Researchers from Epics Therapeutics SA presented preclinical data for EP-102, a novel small-molecule inhibitor of N6-adenosine-methyltransferase catalytic subunit (METTL3), being developed for the treatment of cancer.
Researchers from Hibercell Inc. recently presented preclinical data for HC-7366, a first-in-class direct activator of GCN2 (general control nonderepressible 2) currently in phase I development for the treatment of solid tumors (NCT05121948).
Nicotinamide phosphoribosyltransferase (NAmPRTase; Nampt) plays a central role in cancer metabolism as well as in metabolism in healthy tissues. Remedy Plan Therapeutics Inc. has presented data on the first hyperbolic Nampt inhibitor – RPT-1G – for the potential treatment of acute myeloid leukemia (AML).
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