c5a

C5a Anaphylatoxin (human) is a pro-inflammatory peptide that functions as a leukocyte chemoattractant, utilized in researching inflammation and immune responses, including allergic asthma [1] [2].

C5a Receptor Agonist (mouse, human) is a bioactive peptide derived from the C-terminus of the complement fragment 5 anaphylatoxin (C5a), functioning as an agonist for the C5a receptor. This peptide plays a role in mediating inflammatory responses by promoting chemotaxis, leukocyte degranulation, enhanced vascular permeability, and cytokine production. Its agonistic activity is critically dependent on the presence of cyclohexylalanine at position 5 and the d-isomer of Arg at the terminal position.

C5aR1 antagonist peptide, a biologically active linear peptide originating from the C-terminus of the chemokine complement fragment 5 anaphylatoxin (C5a), inhibits C5a binding and activity at human and rat C5a receptors. Overexpression of C5a is linked to various immunoinflammatory diseases, including arthritis, Alzheimer’s disease, cystic fibrosis, and systemic lupus erythematosus.

PMX-53 is a potent and orally active CD88 (C5aR) antagonist (IC50: 20 nM) and inhibits C5a-induced neutrophil myeloperoxidase release and chemotaxis with IC50 values of 22 nM and 75 nM, respectively. PMX-53 is also an agonist of Mas-related gene 2 (MrgX2).

PMX 205 acetate is an antagonist of complement C5a receptor (C5aR; CD88).

MUC5AC motif peptide is a 16-amino acid fragment of mucin 5.

PMX-53 is a Mas-related gene 2 (MrgX2) agonist and C5aR(CD88) antagonist. PMX-53 reduces atherosclerotic lesions in a mouse model of atherosclerosis, inhibits lung metastasis in a mouse breast cancer model, inhibits C5a-induced hypernociception in rats.

PMX-53, a macrocyclic complement 5a (C5a) peptidomimetic and C5a receptor antagonist (IC50 = 0.3 µM), effectively inhibits the C5a-induced secretion of myeloperoxidase (MPO) in isolated human polymorphonuclear leukocytes (PMNs). Administered orally at 10 mg/kg, PMX-53 mitigates vascular leakage, PMN infiltration, and the production of TNF-α and IL-6 in a rat peritoneal Arthus reaction model. Additionally, in a 3-nitropropionic acid (3-NP)-induced Huntington’s disease rat model, it alleviates body weight loss, anorexia, and striatal degeneration. Furthermore, at a dose of 3 mg/kg, PMX-53 decreases atherosclerotic lesion size and lipid content in ApoE-/- mice.