The bromodomain and extraterminal domain (BET) family of proteins are involved in cell cycle regulation and for this reason are considered therapeutic targets in cancer therapeutics.
Acute myeloid leukemia (AML) presents high recurrence and low survival rates due to drug resistance and different gene mutations that contribute to the difficulty of being cured. Cyclin-dependent kinase 8 (CDK8) is a key oncogenic driver in AML and thus considered a therapeutic target worth exploring.
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.
.webp?height=488&t=1670008838&width=650 "Acute myeloid leukemia")
