Beigene Ltd. struck a global licensing deal with CSPC Zhongqi Pharmaceutical Technology (Shijiazhuang) Co. Ltd. worth up to $1.5 billion for its phase I selective methionine adenosyltransferase 2A (MAT2A) inhibitor, SYH-2039, which is being explored for solid tumors.
SK Biopharmaceuticals Co. Ltd. and Proen Therapeutics Co. Ltd. joined hands in a research collaboration to advance up to two preclinical small protein-based radiopharmaceuticals by 2027 – the year SK Biopharmaceuticals aims to “become a leading radiopharma player” worldwide.
Iregene Therapeutics (Suzhou) Co. Ltd. has identified pyrazolecarbonyl piperazinone compounds acting as bone morphogenetic protein receptor type-1B (BMPR1B) inhibitors reported to be useful for the treatment of cancer and pulmonary hypertension.
B7H3 is a pan-cancer antigen considered a promising target for immunotherapy. However, targeting B7H3 using bispecific T-cell engagers (BiTEs) presents the problem of systemic toxicity.
SK Biopharmaceuticals Co. Ltd. has signed a research collaboration agreement with Proen Therapeutics Inc. to further extend its oncology research capability and expand its pipeline of radiopharmaceutical therapies.
Cathepsin G (CTSG) is overexpressed and aberrantly localized for antigen presentation on acute myeloid leukemia blasts and stem cells compared to normal hematopoietic progenitors. Earlier this year, Crossbow Therapeutics Inc. announced the nomination of its first development candidate, CBX-250, a TCR-mimetic (TCRm) bispecific T-cell engager (TCE) antibody targeting a CTSG peptide-human leukocyte antigen (pHLA) complex and CD3.
The lack of acute myeloid leukemia-specific antigens is one of the challenges for targeted immunotherapy together with on-target off-tumor toxicities due to the expression of the target in normal myeloid cells. A subset of T cells – Vδ2 T-cells – which represent ~5% of the T-cell population in healthy donors, are seen as part of emerging immunotherapeutic strategies.
In tumoral cells, the modulation of the G1/S phases of cell cycle is destabilized by amplification and high expression of cyclin E (CCNE) or by mutation or loss of retinoblastoma 1 (RB1) gene. Cancer cells meeting these characteristics have been sown to be highly sensitive to cyclin-dependent kinase 2 (CDK2) depletion.
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