Figure 2: Growth factor receptor inhibition. (a) Immuno-modulatory mechanism for monoclonal antibodies. Binding of monoclonal antibodies (mAbs) to a specific target on a tumour cell can cause either complement-dependent cytotoxicity (CDC) by the interaction of C1q complement factor with the CH2 constant region of the mAb, which leads to the activation of complement classical pathway and induces the formation of a membrane-attack complex (MAC) for the lysis of tumour cells or antibody-dependent cellular cytotoxicity (ADCC) by the interaction of CH3 region of the mAbs with FcγRIIIa expressed by effector cells (macrophages or NK cells) which leads to phagocytosis by macrophages or undergo cytolysis by NK cells. C3b, which is generated during CDC, can facilitate phagocytosis and cytolysis through its interaction with macrophage or natural killer (NK) cell. This effect is termed as complement-dependent cell-mediated cytotoxicity (CDCC). (b) Small-molecule receptor tyrosine kinase inhibitor interaction to its specific site. Small-molecule tyrosine kinase inhibitors (TKIs) function as ATP analogues to compete with ATP for their binding site and block the receptor mediated downstream signaling.