COMING SOON: C5a/C5a-desArg/C5 (C5a C-term)

C5a is a 74–amino acid polypeptide derived from the N-terminus of the C5 α-chain and represents one of the most potent anaphylatoxins generated during complement activation. In circulation, C5a is rapidly converted by serum carboxypeptidases into the more stable but still biologically active derivative C5a-desArg. In humans C5a exerts its biological effects primarily through two seven-transmembrane receptors: C5aR1 (CD88) and C5aR2 (C5L2/GPR77). These receptors are widely expressed, particularly on immune cells such as neutrophils, macrophages, monocytes, and T cells. Activation of C5aR1 initiates G-protein–coupled signalling pathways that stimulate the production of pro-inflammatory cytokines including TNF-α, IL-1β, IL-6, and IL-8. Through these signalling pathways, C5a induces smooth muscle contraction, increases vascular permeability, promotes mast cell and basophil degranulation, and stimulates the release of lysosomal enzymes. In addition, it acts as a powerful chemoattractant, directing these cells to migrate to sites of inflammation.

Although these responses are essential for host defence, excessive C5a generation contributes to the pathogenesis of numerous inflammatory and immune-mediated diseases, including sepsis, ischemia-reperfusion injury, autoimmune disorders, and cardiovascular disease. Consequently, the C5–C5a axis has emerged as an important therapeutic target. Inhibition of complement activation at the level of C5, using eg eculizumab, prevents the generation of C5a and the formation of the terminal complement complex. This makes complement inhibition a promising strategy for controlling complement-driven inflammation.

Antibody HM1159 is, at least but not limited to, applicable in the following applications: ELISA, BLI and western blotting. Please, Contact Hycult Biotech for further information.