In both acute myeloid leukemia (AML) and synovial sarcoma (SS), targeting BRD9 disrupts oncogenic transcriptional programs, including MYC, leading to reduced proliferation and induction of apoptosis. Researchers from Pamplona Therapeutics (Shenzhen) Co. Ltd. reported the discovery and preclinical efficacy profile of XYD-270, a BRD9-targeting PROTAC, in models of SS and AML.
Researchers from the Chinese Academy of Sciences reported the design and preclinical characterization of YCH-3971, a selective PARP1 inhibitor developed for the treatment of BRCA-mutated tumors.
Researchers from GSK plc and collaborators described the identification of MMV-1581361, a PfATP4 inhibitor, and its efficacy in models of malaria. The compound originates from MMV-020136, following structure-activity relationship studies to optimize antimalarial activity.
Atopic dermatitis (AD) is an inflammatory skin disease accompanied by pruritus, for which IL-13 and IL-31 are clinically validated targets. Earendil Labs Inc. has developed a bispecific antibody targeting both IL-13 and IL-31, HX-16108, with an extended half-life.
Researchers from Specally (Wuhan) Life Technology Co. Ltd. have disclosed the discovery and preclinical profile of WWZ-11-098, a non-palbociclib-based, selective cyclin-dependent kinase 6 (CDK6) degrader in models of leukemia.
Fibroblast growth factor receptor 2 (FGFR2) is a transmembrane tyrosine kinase that regulates signaling pathways controlling cell survival and proliferation. Dysregulation of FGFR2, through amplification or activating mutations, contributes to tumor development, making it an attractive target for therapeutic intervention in oncology.
Researchers from Fudan University reported the development of CZL-077, a p300/CBP bromodomain inhibitor. p300 and CREB-binding protein (CBP) are closely related histone acetyltransferases that play central roles in regulating gene expression. Dysregulation of these proteins has been implicated in tumorigenesis and the development of therapy resistance.
Triple-negative breast cancer (TNBC) cells depend on the transcriptional kinases CDK12 and CDK13 to maintain DNA damage response gene expression and manage replication stress. Due to their functional overlap, inhibition of a single kinase may permit compensatory activity.
DNA polymerase θ (POLθ) is a specialized, error-prone DNA polymerase that promotes the repair of DNA double-strand breaks through theta-mediated end joining (TMEJ), an alternative pathway that operates independently of homologous recombination.
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