Venetoclax has shown good results for adult acute myeloid leukemia (AML) in combination with azacitidine, but there is increasing evidence of inherent and acquired resistance. High expression of nicotinamide phosphoribosyltransferase (NAMPT) has been associated with cancer aggressiveness and poor prognosis due to increased nicotinamide metabolism.
Sumitomo Pharma Co. Ltd. is developing the Menin (MEN1)-myeloid/lymphoid or mixed-lineage leukemia (MLL) interaction inhibitor DSP-5336 (enzomenib) for the treatment of MLL-rearranged acute myeloid leukemia.
Apollo Therapeutics Ltd. has developed APL-4098, a small-molecule general control nonderepressible 2 (GCN2) inhibitor for the potential treatment of AML.
ENL-YEATS is an epigenetic reader that sustains transcriptional programs essential for AML, whereas FLT3 mutations, present in approximately 30% of patients, drive malignant proliferation. Dual inhibition of ENL-YEATS and FLT3 may therefore more effectively disrupt complementary drivers of leukemogenesis than FLT3 targeting alone.
The Schlafen (SLFN) family of interferon-inducible genes, involved in the regulation of immune and antiviral responses, has recently attracted attention for the development of novel anticancer therapies.
Leukogene Therapeutics Inc.’s lead product candidate LTI-214 (M2T-CD33) has been awarded orphan drug designation by the FDA for the treatment of acute myeloid leukemia (AML).
Amphista Therapeutics Ltd. has nominated AMX-883, a selective and orally bioavailable degrader of BRD9, as its first clinical development candidate. AMX-883 is being advanced for the treatment of acute myeloid leukemia (AML), with an IND application planned for early next year.
Acute myeloid leukemia (AML) is an aggressive blood cancer with poor clinical outcomes and high mortality rates, primarily driven by drug resistance and relapse. Increasing evidence has confirmed dysregulated cellular metabolism as a tumor hallmark with crucial roles in tumor growth, progression and drug resistance.
Charm Therapeutics Ltd. has closed an oversubscribed series B funding round, raising $80 million to advance its next-generation menin inhibitor into clinical development. Current menin inhibitors show promise in acute myeloid leukemia (AML) treatment but are limited by the rapid emergence of resistance mutations that cause treatment failure.
In a study published recently in Cancer Immunology, Immunotherapy journal, researchers from Jiangsu Province Hospital and colleagues investigated the impact of targeting the TP53-induced glycolysis and apoptosis regulator (TIGAR) on T-cell function and antitumor immunity in acute myeloid leukemia.
.webp?height=488&t=1670008838&width=650 "Acute myeloid leukemia")