D3 Bio Inc. secured $108 million in a series B financing round Dec. 9 to support its planned phase III program of lead oral KRAS G12C inhibitor, elisrasib (D3S-001).
Immuse Therapeutics Inc. has described heterocyclic compounds acting as leucine-rich repeat kinase 2 (LRRK2; dardarin) inhibitors reported to be useful for the treatment of cancer.
Nikang Therapeutics Inc. has divulged proteolysis targeting chimera (PROTAC) compounds comprising an E3 ubiquitin ligase binding moiety covalently linked to a cyclin-dependent kinase 2 (CDK2)- and/or CDK4-targeting moiety through a linker reported to be useful for the treatment of cancer.
Prelude Therapeutics Inc. has synthesized tyrosine-protein kinase JAK2 inhibitors reported to be useful for the treatment of cancer, myelofibrosis, essential thrombocythemia and graft-vs.-host disease.
While current treatments can prolong the life of many patients with the malignant bone cancer osteosarcoma, a substantial proportion have metastasis or recurrence. This highlights the need for more specific, targeted therapies against the disorder, yet the mechanism of pathogenesis is unclear and may be heterogeneous, so no drug targets have been definitively validated.
Oxford Biotherapeutics Ltd. has entered into a multiyear, multitarget strategic collaboration with GSK plc to discover novel antibody-based therapeutics for the treatment of cancer.
Ideaya Biosciences Inc. has submitted an IND application to the FDA for IDE-574, a KAT6/7 dual inhibitor with potential to treat hormone receptor-positive breast cancer and lung adenocarcinoma. A phase I trial of IDE-574 monotherapy is expected to begin in the first quarter of next year.
Akari Therapeutics plc has released new preclinical data indicating the therapeutic potential of AKTX-101 in pancreatic cancer driven by KRAS mutations. AKTX-101 is an antibody-drug conjugate (ADC) that delivers a novel RNA spliceosome modulating payload, PH1, into cancer cells that express TROP2.
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.
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