Anti-TCC, Mouse, mAb 12C3, biotinylated

The monoclonal antibody 12C3 targets the C9 neoantigen within the Mouse Terminal Complement Complex (TCC), marking a critical juncture in complement system activation. The convergence of complement pathways leads to the formation of a C5 convertase, catalyzing the transition to the terminal pathway. Unlike earlier stages that rely on enzymatic cleavage, the terminal pathway is driven by conformational shifts upon sequential binding of components C6 through C9. This cascade results in the assembly of the TCC or Membrane Attack Complex (MAC), instrumental in cell lysis and stimulating various cellular responses, including the release of inflammatory mediators. Unique neoantigens, not found in the individual native components, emerge in both membrane-bound and fluid-phase forms of the TCC. This indicates ongoing complement activity. Clinically, the presence of TCC in mouse plasma or tissue serves as a biomarker for complement activation, with elevated levels indicating heightened immune response. TCC can be a focal point for diagnostic and therapeutic that approach immune-mediated diseases. References Carpanini, S.M. et al, Terminal complement pathway activation drives synaptic loss in Alzheimer's disease models, 2022. Acta Neuropathol Commun, 6,10(1):99 Zelek, W.M. et al, Brain-penetrant complement inhibition mitigates neurodegeneration in an Alzheimer's disease mouse model, 2025. Brain, 6,148(3):941-954.