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.
With its launch barely three years in the rearview mirror, Remix Therapeutics Inc. has inked its second potential $1 billion pharma collaboration, drawing Roche Holding AG to the table with the promise of its RNA processing platform and the potential to develop small-molecule therapeutics targeting the underlying drivers of disease. At the same time, the Watertown, Mass.-based firm added $60 million in a venture round, bringing its total financing to date to $201 million.
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).
Senti Biosciences Inc. has received clearance of its IND application from the FDA for SENTI-202, an off-the-shelf chimeric antigen receptor natural killer (CAR-NK) cell therapy product candidate designed to selectively target and eliminate CD33- and/or FLT3-expressing hematologic malignancies, such as acute myeloid leukemia (AML) and myelodysplastic syndrome, while sparing healthy bone marrow cells.
MYB is a transcription factor essential for cell proliferation and differentiation, and is regarded as a target for cancer therapy because it is overexpressed in many different tumor types such as adenoid cystic carcinoma (ACC), acute myeloid leukemia (AML) or T-cell acute lymphoblastic leukemia, among others.
