Figure 2.

(1) Drug–CPE complex interacts with Claudin-4 receptors in brain metastatic tumor cells and forms a hexameric pore causing increases in influx of Ca²⁺, osmotic dysregulation, and membrane disruption (2), which leads to apoptosis or oncosis (3,4). Unbound drugs are delivered into tumor cells and further mediate cell destruction upon binding by exerting antitumor effects on cancer cells while (5,6) the modulation of growth factor signaling and nfKB increase cell death by decreasing cell proliferation and increasing expression of inflammatory cytokines and immune cells (7).