Cfhr2 Inhibitors

Chemical inhibitors of Cfhr2 act through diverse mechanisms to modulate the complement system, to which Cfhr2 is a key contributor. Eculizumab, for instance, binds to the complement protein C5, preventing its cleavage and effectively inhibiting the formation of the membrane attack complex (MAC), thereby indirectly limiting the regulatory role of Cfhr2 in this terminal part of the complement cascade. Compstatin, on the other hand, targets complement component C3, a central protein in the complement system, and by doing so, it indirectly inhibits the regulatory function of Cfhr2, which interacts with and modulates C3 activation. Similarly, PMX-53 acts by blocking the C5a receptor, and since Cfhr2 contributes to the complement activation that produces C5a, PMX-53 also indirectly reduces the influence of Cfhr2 on these downstream effects.

Other chemical inhibitors operate by targeting different aspects of the complement system, indirectly affecting Cfhr2 function. Nafamostat, a serine protease inhibitor, impedes the activation of essential complement proteases, such as C1r, C1s, and factor D; this has the effect of indirectly inhibiting Cfhr2's role in the initial stages of the complement activation process. K76 COOH, like Compstatin, inhibits C3 convertase activity, thereby also indirectly inhibiting Cfhr2's regulatory function. Arsenic trioxide can lead to the depletion of complement components, which in turn can suppress the regulatory capacity of Cfhr2 within the complement system. Cobra Venom Factor employs a unique strategy by forming a stable alternative pathway C3 convertase, depleting complement components and, as a consequence, inhibiting Cfhr2 function. Chemicals such as Epigallocatechin gallate (EGCG) and Curcumin express their inhibitory effects on Cfhr2 by interfering with the activation of the classical complement pathway, a system where Cfhr2 plays a regulatory role. Auranofin is reported to inhibit the activation of the entire complement system, thus affecting the function of Cfhr2, while LY294002 downregulates the PI3K/Akt pathway, which has potential connections to the inflammatory response and complement system, thereby indirectly influencing Cfhr2's regulatory actions.