Aboleris Pharma has closed a €27.3 million (US$28.7 million) series A financing, funds it plans to put toward progressing into the clinic a monoclonal antibody against a novel T-cell target with “first-in-class potential” to treat rheumatoid arthritis. The Gosselies, Belgium-based company’s antibody, ABO-21009, is designed to “rebalance” the immune system by inhibiting CD45RC, a protein expressed on the surface of a subset of disease-causing T cells.
The interleukin-17 (IL-17) family is involved in innate immunity regulation and plays a crucial role in inflammatory and autoimmune disorders by sustaining inflammation during the onset and progression of diseases such as rheumatoid arthritis (RA), psoriasis or inflammatory bowel disease (IBD). Researchers from the University of Naples have reported on a new biological entity, Ab-IPL-IL-17, that displays potent anti-inflammatory activity in preclinical testing.
Researchers from Anhui Medical University presented the discovery and preclinical evaluation of new vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitors as potential therapeutic candidates for rheumatoid arthritis.
Eli Lilly and Co.’s phase II data with LY-3462817 (peresolimab), a monoclonal antibody (MAb) that functions as a PD-1 agonist for rheumatoid arthritis (RA), juiced hopes for the approach being tried by a handful of firms.
Lynk Pharmaceuticals Co. Ltd. raised ¥200 million (US$28 million) in a series C1 financing round to accelerate the clinical development of its second-generation and third-generation JAK inhibitors for cancer and autoimmune diseases.
Lynk Pharmaceuticals Co. Ltd. raised ¥200 million (US$28 million) in a series C1 financing round to accelerate the clinical development of its second-generation and third-generation JAK inhibitors for cancer and autoimmune diseases.
CD38 is an enzyme with NAD-depleting and intracellular signaling activity expressed on the cell surface, in intracellular compartments and in mitochondria, and is linked to inflammatory and autoimmune diseases. Studies in CD38-deficient mice have revealed that these animals develop a type of collagen-induce arthritis (CIA) which suggests a link between CD38 and CIA pathogenesis.
