Salt-inducible kinase 2 (SIK2) is a serine/threonine kinase that regulates transcriptional programs in myeloid cells by phosphorylating transcriptional coregulators. In macrophages, SIK2 promotes the expression of proinflammatory cytokines and contributes to the balance between inflammatory and regulatory responses. Researchers from Nimbus Therapeutics LLC presented the preclinical efficacy of NTX-147, a SIK2 selective inhibitor, in ex vivo models of ulcerative colitis (UC).
Boehringer Ingelheim Ltd. has acquired an exclusive license for a preclinical small-molecule program from Sitryx Therapeutics Ltd. The program offers a novel oral immunometabolic approach to modulating disease-driving immune cells with potential for multiple autoimmune and inflammatory disease indications.
GSK plc will pay Frontier Biotechnologies Inc. $40 million up front and up to $963 million in milestone payments to license two of Frontier’s small interfering RNA-based assets in the field of immunology.
Haisco Pharmaceutical Group Co. Ltd. has synthesized new cyclic peptides acting as interleukin-23 receptor (IL-23R) antagonists potentially useful for the treatment of inflammatory bowel disease and psoriasis.
Researchers from Shanghai Ailux Biotechnology Co. Ltd. have disclosed preclinical data regarding their humanized bispecific antibody ALX-001 targeting TL1A and IL-23 for the potential treatment of immune-mediated inflammatory diseases (IMIDs).
Hangzhou Innogate Pharma Co. Ltd. has reported cyclic GMP-AMP synthase (MB21D1; cGAS) inhibitors. They are described as useful for the treatment of Aicardi-Goutieres syndrome, psoriasis, rheumatoid arthritis, systemic lupus erythematosus, myasthenia gravis, multiple sclerosis, myocardial infarction and Parkinson’s disease, among others.
Chugai Pharmaceutical has reported a new humanized antibody (Ab, SOF-10) that targets latent TGF-β1 and selectively blocks protease- and integrin αVβ8-mediated latent TGF-β1 activation.
In the inflamed joints of rheumatoid arthritis, CD4+ T lymphocytes accumulate lipid droplets that make them vulnerable and promote their death, thereby amplifying joint inflammation. A study led by scientists at Mayo Clinic and Stanford University suggests that blocking the formation of these lipid droplets or their contents could offer a therapeutic strategy for this condition.
Scientists from Adlai Nortye Biopharma Co. Ltd. and Adlai Nortye Pte Ltd. have prepared and tested proteolysis targeting chimera (PROTAC) compounds comprising an E3 ubiquitin ligase-binding moiety coupled to a signal transducer and activator of transcription 6 (STAT6)- or STAT3-targeting moiety.
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