TAVNEOS is an oral, selective inhibitor of the C5a receptor1,2
Activation of the alternative complement system plays a crucial role in the pathogenesis of ANCA‑associated vasculitis.3


Complement System
A central mediator of immunothrombosis and vascular necroinflammation in anti‑neutrophil cytoplasmic autoantibody (ANCA)‑associated vasculitis. There are 3 pathways of the complement system: classical, lectin, and alternative.4,5

Alternative Pathway
Believed to be crucial in the pathogenesis of ANCA‑associated vasculitis.3

Complement Peptides
In particular, C5 activation leads to the formation of complement peptides C5a and C5b. C5b fuels the formation of the membrane attack complex (MAC) that is essential for host defense, whereas C5a acts as a potent chemoattractant that recruits immune cells to the site of tissue injury. In ANCA‑associated vasculitis, C5a binds to C5a receptors (C5aR) on neutrophils, causing the release of destructive mediators that chronically inflame and eventually damage vascular tissues and the organs fed by those blood vessels.3-6

TAVNEOS
TAVNEOS is an antagonist of C5aR. TAVNEOS blocks C5a-mediated neutrophil activation and migration, and is not believed to impact the formation of the MAC. However, the precise mechanism by which TAVNEOS exerts its effect in patients with ANCA‑associated vasculitis has not been definitively established.1,4

Priming
Neutrophils are primed (partially activated) by a combination of factors, including the inflammatory milieu of cytokines produced in response to an infection or another event.3

Neutrophil Activation and NETosis
ANCA binds to target antigens on the cell surface of neutrophils. This causes them to activate and ultimately produce additional C5a. ANCA‑induced neutrophil activation also results in NETosis (an explosion‑like form of neutrophil death during which neutrophils expel their chromatin and granular content into the extracellular space).4-6

Microvascular Necroinflammation Loop
Occurs between neutrophils and the complement system. The ANCA‑induced activation of neutrophils generates C5a, which, in turn, increases neutrophil recruitment and priming, and intensifies the inflammatory response. This can lead to tissue damage and other clinical manifestations of ANCA‑associated vasculitis.3-5,7