Peptide directorySkin, immune & repair

C3a

The fragment released at the centre of every complement cascade.

Related medicinesPegcetacoplan

Where it comes from

Made in
Made in blood whenever C3 is cleaved, by any of the three complement pathways; C3 itself comes mostly from the liver
Sent out by
Infection, immune complexes, tissue damage, and contact with artificial surfaces such as dialysis membranes
Acts on
  • Mast cells and basophils (histamine release)
  • Eosinophils
  • Macrophages
  • Smooth muscle

What it does

  • Releases histamine and contracts smooth muscle, the anaphylatoxin effect
  • Calls eosinophils and mast cells
  • Switched off within seconds by carboxypeptidase N, which clips its last arginine (C3a-desArg)
  • Dampens some neutrophil responses, so it is not simply pro-inflammatory

In medicine

  • Measured in research in sepsis, asthma and after cardiac bypass
  • Pegcetacoplan binds C3 itself and is approved for paroxysmal nocturnal haemoglobinuria 2 and for geographic atrophy of the retina 3; blocking C3 stops C3a being made at all

Beyond the body’s own use

  • C3a receptor blockers are laboratory tools, used in models of asthma, lupus and brain injury. No medicine acts on this receptor 1
  • Its clipped form, C3a-desArg, is also called acylation-stimulating protein and tells fat cells to store triglyceride, a second life with nothing to do with inflammation 4

Sources

  1. Klos et al., The role of the anaphylatoxins in health and disease, Molecular Immunology 2009
  2. Pegcetacoplan (Empaveli), FDA application NDA 215014
  3. Pegcetacoplan (Syfovre), FDA application NDA 217171
  4. Rezvani et al., Acylation stimulating protein in the metabolic states, Journal of Physiology 2024

This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.