Yaoya Technology (Shanghai) Co. Ltd. has disclosed tyrosine-protein kinase BTK inhibitors reported to be useful for the treatment of cancer, rheumatoid arthritis, lupus erythematosus, lupus nephritis, multiple sclerosis, asthma and Sjogren's syndrome.
Shanghai Apeiron Biotechnology Co. Ltd. has disclosed triheterocyclic compounds acting as protein mono-ADP-ribosyltransferase TIPARP inhibitors and thus reported to be useful for the treatment of cancer.
Researchers from Biomea Fusion Inc. presented preclinical data for the novel covalent menin inhibitor, BMF-219, after being evaluated in models of diffuse large B-cell lymphoma (DLBCL) and multiple myeloma (MM).
Applied Pharmaceutical Science Inc. has described new proto-oncogene tyrosine-protein kinase receptor Ret, (V804M mutant) and (G810R mutant) inhibitors reported to be useful for the treatment of cancer and irritable bowel syndrome.
The prognostic role of complement inhibitor CSMD1 was assessed in 1,507 patients with glioma from three different datasets. Results of the bioinformatical analysis suggested that high expression of CSMD1 was associated with increased overall survival and disease-free survival, as well as lower tumor grade.
A metabolite derived from the airway microbiome, indole-3-acetic acid (IAA), could become a potential therapeutic candidate for chronic obstructive pulmonary disease (COPD). Researchers at South China Normal University (SCNU) have shown how IAA prevents lung function decline by reducing inflammation, apoptosis and emphysema through IL-22 in the interaction between macrophages and alveolar epithelial cells.
Academy of Military Medical Sciences (AMMS) has divulged 3C-like proteinase (viral) and 3C protease (viral) inhibitors reported to be useful for the treatment of viral infections.
Sirnaomics Ltd. reported progress with its Galahead RNAi delivery platform for developing novel therapeutic products focused on complement-related diseases.
Preserving beta-cell mass and expansion is a key point in diabetes. Prolonged hyperglycemia may lead to glucose toxicity, which impairs insulin production and secretion, promoting a cycle with increasing glucose concentrations that promote a decline of beta-cell function and eventually their death.