Harnessing the non-complement role of factor H and properdin for cardiovascular and onco-immunotherapeutics

Factor H  in complement activation inhibit the assembly of the alternative pathway C3 and C5 convertase enzymes via competition with factor B for C3b binding . Factor H facilitates the disassembly of the convertases by displacing bound factor Bb 9decay accelerating activity. Factor H has shown to generate non-complement pathways in essential biological processes such as regulation of circadian rhythms as well as factors in blood clotting along with pregnancy and what not… What significance factor H holds as a biomarker for cardiovascular diseases and implications in therapeutics remains a billion dollar question to be investigated…