Newco Outrun Therapeutics Ltd. has raised $10 million in a seed round to develop small-molecule E3 ubiquitin ligase inhibitors that prevent programmed protein degradation. The lead program targeting an E3 ligase that tags a tumor suppressor protein for destruction will now advance to preclinical development.
Genescience Pharmaceuticals Co. Ltd. has described fused ring kinesin-like protein KIF18A inhibitors reported to be useful for the treatment of cancer.
Oncopia Therapeutics Inc. (dba Proteovant Therapeutics Inc.) has divulged protein cereblon (CRBN) ligands and its PROTACs reported to be useful for the treatment of cancer.
Researchers at CNCCS Scarl (Collezione Nazionale Dei Composti Chimici E Centro Screening) and IRBM SpA have disclosed tyrosine-protein phosphatase non-receptor type 11 (PTPN11; PTP-2C; SHP2) inhibitors reported to be useful for the treatment of cancer, Noonan and Leopard syndrome.
Crossfire Oncology BV has disclosed CFON-026, a potent, highly selective and macrocyclic noncovalent inhibitor of wild-type (WT) Bruton tyrosine kinase (BTK) and all clinically relevant BTK resistance mutations, with best-in-class potential for the treatment of cancer.
Researchers from Dong-A Socio Holdings Co. Ltd. presented a first-in-class Src homology 2 domain-containing phosphatase 1 (SHP1) allosteric inhibitor, SB-8091, being developed as an anticancer agent.
Rac1 is a small GTPase, the hyperactivation of which is linked to tumor progression and drug resistance. The oncogenic variant Rac1b has been shown to be overexpressed in cancers, such as colorectal cancer (CRC), and it has also been correlated with poor prognosis and CRC resistance to oxaliplatin.
In tumors with amino acid deprivation, eIF-2α kinase GCN2 is activated and triggers a signaling response to promote cell survival and proliferation. This is important in high metabolically active hematological cancers, such as acute myeloid leukemia (AML).
Cross talk between macrophages and tumor cells could modulate cachexia in pancreatic cancer patients. A group of scientists from the University of Oklahoma has discovered a new pathway that promoted muscle wasting after the recruitment of this immune cell in the tumor microenvironment, activating cachexia-inducing factors. Macrophage depletion and the inhibition of this signaling could be developed as a therapeutic target for this condition.
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