Shenzhen Zhongge Biotechnology Co. Ltd. has synthesized tyrosine-protein phosphatase non-receptor type 1 (PTPN1; PTP-1B) and/or PTPN2 (TCPTP) inhibitors reported to be useful for the treatment of cancer, obesity, atherosclerosis, type 1 diabetes, type 2 diabetes, neurodegeneration, metabolic syndrome and inflammatory bowel disease, among others.
Shionogi & Co. Ltd. has divulged glucagon-like peptide 1 receptor (GLP-1R) agonists reported to be useful for the treatment of obesity and diabetes type 2.
Jnana Therapeutics Inc. has synthesized sodium-dependent neutral amino acid transporter B(0)AT1 (SLC6A19) inhibitors reported to be useful for the treatment of amino acid metabolism disorders, amino acid transport disorders and metabolic and nutritional genetic disorders, among others.
Obesity is a chronic disorder tied to other disorders such as hyperglycemia, type 2 diabetes or cardiovascular disease, among others. Recent findings have suggested that EphB tyrosine kinase receptor and its ligand, ephrin B, may be involved in insulin signaling.
A small molecule could provide a new therapeutic approach against organ fibrosis. Using genome-wide association (GWA) assays, a group of researchers from the Westmead Institute for Medical Research in Sydney identified Mer tyrosine kinase (MERTK) as a candidate to study fibrosis and showed that its inhibition with the experimental compound reduced this condition in mouse models’ liver, kidneys and lungs. “There were some studies on the role of MERTK in liver fibrosis, but its therapeutic potential for various organ fibrosis has not been explored before. This study provides unequivocal evidence that MERTK is a potent nodal regulator of fibrosis supported by detailed mechanistic studies,” the senior author Mohammed Eslam told BioWorld.
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as nonalcoholic fatty liver disease, shows different occurrence between sexes, being less prevalent in premenopausal women than in men or postmenopausal women.
It has been previously demonstrated that insulin-reactive B cells act as antigen-presenting cells to promote type 1 diabetes by stimulating pathogenic T cells and leading to destruction of insulin-producing beta cells of pancreatic islets.