With years of ample experiences in drug development, our scientists are confident in providing a full range of SB 290157 development services to promote the development for complement related biopharmaceuticals. We offer turn-key or ala carte services customized to our client’s needs.
SB 290157-C3aR Antagonist
SB 290157, N2-[(2,2-diphenylethoxy)acetyl]-L-arginine, is a high affinity, selective, and competitive C3aR antagonist that has inhibiting activity on C3aR in a variety of cell systems, including a calcium mobilization assay in transfected RBL cells, a β-lactamase assay in CHO-NFAT-bla-Gα16 cells and an enzyme-release assay in differentiated U-937 cells. It blocks C3a-induced C3aR internalization in a concentration-dependent manner. And SB 290157 is selective for the C3aR that it did not antagonize the C5aR or other chemotactic G protein-coupled receptors. There is a continuing need for the development of this small molecule C3aR antagonists.
Fig.1 The balance of C3a actions determines the disease phenotype. (Liam G. 2015)
Effect on Anti-OVA Polyclonal Antibody-induced Arthritis
Rheumatoid arthritis (RA) is an autoimmune disease characterized by polyarticular joint inflammation with leukocytic recruitment into synovial fluid and tissue, eventually leading to cartilage and bone destruction. Neutrophil infiltration into the synovial membrane is one of the hallmarks of active RA and plays a pivotal role in the pathogenesis of synovial inflammation. SB 290157 can inhibit the induction of arthritis by lowering the level of joint swelling, neutrophil migration, and IL-1 β production. The current findings suggested that C3a may be involved in the aggravation of arthritis by using SB 290157. Therefore, SB 290157 is effective in the inhibition of arthritis.
Inhibition of Expression of Muc5ac-induced Asthma
Mucus hypersecretion by airway epithelium and airway obstruction due to mucus plugs contribute significantly to the pathology of asthma and can result in a fatal outcome. Airway mucus is composed mainly of mucin glycoproteins, specialized airway epithelial cells, called goblet cells, which are the major source of mucins in the proximal airway. Of the 20 known human mucin genes, attention has focused predominantly on the gel-forming secreted mucins MUC5AC, because its mRNA is well expressed in normal airway tissues and their gene products have been identified in mucus from the lungs of patients with asthma. SB 290157 is capable of inhibiting the expression of Muc5ac by biding C3aR, which is recognized as a novel mechanism for regulating goblet cells and Muc5ac production in airway obstruction in asthma.
Based on our advanced SB 290157 development services strategy and well-developed complement therapeutics platforms, Creative Biolabs is confident in proving customized SB 290157 development services against a variety of complement component, especially for those which are essential for complement activities. Please contact us for more information or a detailed quotation.
Reference
1. Coulthard, L. G.; Woodruff, T. M. Is the complement activation product C3a a proinflammatory molecule? Re-evaluating the evidence and the myth. The Journal of Immunology. 2015, 194(8), 3542-3548.
For Research Use Only.
Related Sections:
