Researchers from SL Bigen Inc. and collaborators presented the preclinical characterization of BM-205, a novel entity of engineered MSCs designed to exert antitumor functions.
By comparing the transcriptomic profile of tissue regeneration after induced damage in the small intestine and colon with their transcriptomic landscape in their steady state, researchers have identified a pathway that unlinks tissue regeneration from tumorigenesis.
Arovella Therapeutics Ltd. is heading toward the clinic with its lead product, ALA-101, which consists of a chimeric antigen receptor (CAR) targeting CD19 and invariant natural killer T (iNKT) cells.
Genesis Therapeutics Inc. has divulged phosphatidylinositol 3-kinase alpha (PI3Kα) (H1047R mutant) inhibitors reported to be useful for the treatment of cancer.
Matchpoint Therapeutics Inc. has synthesized new diazepino-thieno-quinoxaline compounds acting as MAP kinase-activated protein kinase 2 (MAPKAPK2; MK2) inhibitors reported to be useful for the treatment of cancer and inflammatory disorders.
Nimbus Saturn Inc. has identified proteolysis targeting chimeras (PROTACs) comprising an E3 ubiquitin ligase-binding moiety covalently linked to a mitogen-activated protein kinase kinase kinase kinase 1 (MAP4K1; HPK1; MEKKK1)-targeting moiety linked via a linker.
Investigators from the University of Turin have developed and characterized a new murine immunocompetent model of Usp18-knockout leiomyosarcoma (LMS). LMS is a rare malignant soft tissue cancer with limited therapeutic options when in advanced stages.
Compared to normal tissues, where the expression of ULBP2/5/6 protein is restricted, in non-small-cell lung cancer (NSCLC), head and neck cancer and squamous urothelial carcinoma, the levels of ULBP2/5/6 remain high even following relapse from standard-of-care therapies and is retained in metastatic lesions. Besides, these squamous cell cancers showed a high proportion of CD2+ tumor-infiltrating lymphocytes compared to other co-stimulatory receptors.
Investigators from Duke University hypothesized that hirudin-like protease inhibitors could be generated by linking exosite-binding aptamers with small-molecule active site inhibitors, thus generating more potent “EXACT” inhibitors.
RSS
