Bifunctional protein derived from blood-feeding ticks that specifically prevents complement-mediated C5 activation and acts as a scavenger for inflammatory modulators such as leukotriene B4 (LTB4). C5 and LTB4 binding activities are independent (PubMed:23625922). Inhibits classical and alternative pathways of complement activation by preventing the cleavage of complement C5 by both classical and alternative C5 convertases (PubMed:15699138) (Probable). Inhibits complement in all species tested (rabbit, rat, guinea pig, mouse, pig, and human) (PubMed:27018802). Also binds fatty acids such as palmitoleic acid and ricinoleic acid, as well as inflammatory modulators LTB4 (and presumably arachidonic acid (AA)) that may be sequestered to interfere with the host inflammatory response (PubMed:23625922). Does not bind to leukotriene C4 and thromboxane B2 (PubMed:23625922). In vivo, when tested on the mouse model of immune complex-induced acute lung injury (IC-ALI), shows a potent inhibitory activity of the pathology, equally dependent on both C5 inhibition and LTB4 binding for full activity (PubMed:23625922). Interacts with complement C5. Expressed in salivary glands. Is currently under several clinical trials by Akari therapeutics under the name Nomacopan (previously Coversin). Is in phase I to treat recalcitrant atopic keratoconjunctivitis (AKC) (PubMed:34116700). Is in phase III to treat bullous pemphigoid (BP). Is in phase III to treat severe pediatric hematopoietic stem cell transplant-related thrombotic microangiopathy (HSCT-TMA). In addition, is also under preclinical trials to treat complement-driven inflammatory diseases, such as atypical hemolytic uremic syndrome (aHUS), paroxysmal nocturnal hemoglobinuria (PNH), age-related macular degeneration (AMD) and uveitis, thrombotic microangiopathy (TMA), and paroxysmal nocturnal hemoglobinuria (PNH). Belongs to the calycin family. Lipocalin subfamily.