Javier O. Rivera-Reyes

The discovery of regulated cell death (RCD) revolutionized chemotherapy. With caspase-dependent apoptosis initially being thought to be the only form of RCD, many drug development strategies aimed to synthesize compounds that turn on this kind of cell death. While yielding a variety of drugs, this approach is limited, given the acquired resistance of cancers to these drugs and the lack of specificity of the drugs for targeting cancer cells alone. The discovery of non-apoptotic forms of RCD is leading to new avenues for drug design. Evidence shows that ferroptosis, a relatively recently discovered iron-based cell death pathway, has therapeutic potential for anticancer application. Recent studies point to the interrelationship between iron and other essential metals, copper and zinc, and the disturbance of their respective homeostasis as critical to the onset of ferroptosis. Other studies reveal that several coordination complexes of non-iron metals have the capacity to induce ferroptosis. This collective knowledge will be assessed to determine how chelation approaches and coordination chemistry can be engineered to program ferroptosis in chemotherapy.

The electrocatalytic reduction of carbon dioxide (CO₂) into added-value products is a promising alternative to completing the cycle of atmospheric CO₂. We report two new platinum complexes—a salen-like naphthalene (PtL1) and a hydroxy-substituted salpn naphthalene (PtL2)—that are capable of activating CO₂ to produce carbon monoxide (CO). The predominant keto tautomer of the non-innocent ligands was determined using DFT calculations and UV-Vis spectroscopy. The PtL2 complex has a CO Faradaic efficiency >40% in the presence of water as a sacrificial proton source at −2.5 V vs. Fc/Fc⁺. The addition of the hydroxy group in combination with water as a proton source decreased the reduction potential and increased the CO formation tenfold when compared to PtL1.