Figure 8. Schematic model of CRP conformational changes and C10M's in vitro and in vivo anti‐inflammatory effects.

Exposed phospholipids (PL) in activated cell membranes (e.g., endothelial cells or platelets) or microvesicles contain PC head groups derived from LPC and PE head groups derived from lysophosphatidylethanolamine (LPE), which bind to the PC/PE binding sites on the B‐face of pCRP, thereby anchoring pCRP to the membrane surface. Once bound to the activated membrane, pCRP dissociates into pCRP* and ultimately mCRP. This pro‐inflammatory conformational change results in the activation of leukocytes and endothelial cells as well as NETosis and contributes substantially to renal ischemia/reperfusion injury (IRI) and transplant rejection. Administration of C10M prevents the conformational change of pCRP toward pCRP*/mCRP, the consequent pro‐inflammatory cellular effects and reduces renal IRI and transplant rejection.