Complement 3a (C3a) receptor agonist binds the G protein-coupled C3a receptors (C3aRs) in the immune system complement pathway.[1] Activation of C3aR prevents neutrophils from being mobilized in a model of intestinal ischemia-reperfusion injury. [2] C3aRs are expressed on neural progenitor cells and immature neurons in adult mice. C3a stimulates differentiation of neural progenitor cells in vitro.[3] [4]

Reference:
[1]. Klos, A., Wende, E., Wareham, K.J., et al. International union of basic and clinical pharmacology. LXXXVII. Complement peptide C5a, C4a, and C3a receptors. Pharmacol. Rev. 65(1), 500-543 (2013).
[2]. Wu, M.C.L., Brennan, F.H., Lynch, J.P.L., et al. The receptor for complement component C3a mediates protection from intestinal ischemia-reperfusion injuries by inhibiting neutrophil mobilization. Proc. Natl. Acad. Sci. USA 110923), 9439-9444 (2013).
[3]. Rahpaymai, Y., Hietala, M.A., Wilhelmsson, U., et al. Complement: A novel factor in basal and ischemia-induced neurogenesis. EMBO J. 25(6), 1364-1374 (2006).
[4]. Shinjyo, N., Stahlberg, A., Dragunow, M., et al. Complement-derived anaphylatoxin C3a regulates in vitro differentiation and migration of neural progenitor cells. Stem Cells 27(11), 2824-2832 (2009).