<p>The mechanisms of neuroprotection include antioxidant protection of neurons, increased synthesis of growth factors, optimization of mitochondrial bioenergetics, restoration of homeostasis of neurotransmitters and calcium ions, and inhibition of inflammation, necrosis, and apoptosis. All these mechanisms directly or indirectly involve the cyclosporine-sensitive calcium-dependent mitochondrial pore. Opening of the pore leads to the release of cytochrome C from mitochondria and apoptosis. Inhibition of pore opening prevents mitochondrial damage and is a mechanism of cytoprotection. The role of pore opening inhibitors is important not only in neuroprotection, but also in cardio- and hepatoprotection and in protecting cells from various types of electro-magnetic radiation. Herein, clinically approved pharmacological drugs and those in preclinical and clinical trials that regulate the opening of the mitochondrial pore are reviewed. The main attention is paid to cyclosporine A as a promising neuroprotector and inhibitor of P-glycoprotein, the level of expression of which in the blood-brain barrier affects the bioavailability of psychotropic drugs. The megestrol acetate derivative gestobutanoyl (butagest), an inhibitor of the pore and an inhibitor of P-glycoprotein, is of interest for further study as a neuroprotector</p>