Product Description
The 1G9-CP119 monoclonal antibody is a recombinant, chimeric version of the original 1G9 antibody. The variable domain sequences are identical but the constant region sequences are switched from Mouse IgG1, kappa to mouse IgG2a, kappa. Additionally, 1G9-CP119 contains LALA-PG mutations in the heavy chain Fc fragment rendering it unable to bind endogenous murine Fcgamma receptors or C1q to induce antibody-dependent, cell-mediated cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC). The LALA-PG variant has demonstrated significantly reduced effector function, C1q binding and C3 fixation compared to other common silencing mutations such as the LALA and DANG variants while retaining favorable biophysical and manufacturing properties. Silencing of anti-TIGIT effector function has been shown to retain checkpoint-blocking activity while minimizing Fc-driven depletion of immune cells and promoting antitumor immunity. The highly controlled sequence and lack of genetic drift in recombinant antibodies provide more reliable and reproducible results over hybridoma derived antibodies. The 1G9-CP119 antibody reacts with mouse TIGIT (T cell immunoreceptor with Ig and ITIM domains). TIGIT is a 26 kDa, type I transmembrane protein and a member of the poliovirus receptor (PVR) family. TIGIT has been found to be expressed on follicular T helper cells in mice while in humans its expressed by many T cell subsets including activated T cells, follicular T helper cells, memory T cells, and regulatory T cells as well as on NK cells. TIGIT can interact with certain members of the PVR and PVR-like families, including PVR, PVRL2, PVRL3, CD155, and CD112. TIGIT is thought to negatively regulate NK and T cell activation. Binding TIGIT on T cells by dendritic cells results in their differentiation into a tolerogenic phenotype, with increased secretion of IL-10 and diminished production of IL-12. TIGIT knock-out mice are more susceptible to autoimmune disease.
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