A proposed model for drug-dependent antibody binding to an epitope on a platelet glycoprotein. Left: Antibodies capable of causing drug-dependent thrombocytopenia react weakly with an epitope on a glycoprotein. The KA for this interaction is too small to allow significant numbers of antibody molecules to bind in the absence of drug. Right: Drug contains structural elements that are complementary to charged or hydrophobic domains (H) on the glycoprotein epitope and the complementarity determining region (CDR) of the antibody. Drug interacts with the target protein and antibody to improve the “fit” between the two proteins, increasing the KA to a value that permits binding to occur at levels of antibody, antigen and drug achieved in the circulation after ingestion of the drug. Reprinted with permission from Bougie DW et al. Blood. 2006;108:922–927.11)
