C3aR antagonists, SB290157 and JR14a, could block these effects, attenuating proteinuria, electron-dense deposition, foot process width and glomerular basement membrane thickening, also alleviating plasma C3a levels and overexpression of C3aR.[57] An experimental rat model of MN demonstrated that the disease could be ameliorated by blocking the alternative pathway with LNP023, a highly potent FB inhibitor, as evidenced by a marked reduction in proteinuria, improvement of overall histopathology score, and attenuation of glomerulopathy.[58]. Here, C3AR1 is linked to lipoprotein glomerulopathy.