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Caspases, a family of cysteine proteases, plays a key role in the pathogenesis of ischemic brain injury. Caspase-3 is involved in mechanisms that determine cell death. In the human, the gene is expressed in neurodegenerative disorders, including stroke and Alzheimer disease, as well as in normal brain tissue. It has been proposed that caspase-3 inhibitors might be effective in stroke and its complications. A novel approach to post-ischemic neuronal death involves the inhibition of caspases, in particular caspase-3. It has been proposed that caspase-3 inhibitors could be effective in reducing ischemic brain injury in a number of studies. Moreover, other death-related mechanisms, such as apoptosis, autophagy, necrosis and the caspase-independent cell death, have been recently under investigation for their potential in the treatment of cerebral ischemia. There are two types of caspase-3 inhibitors in clinical development: peptide and non-peptide inhibitors. The first group of caspase-3 inhibitors is derived from peptides of proteins that are the substrates of caspase-3, namely caspase-3 inhibitors target the caspase-3-activating complex. The second group of inhibitors, such as LEVD-CHO and QVD-OPh, do not target the caspase-3-activating complex and instead inhibit only active caspase-3 itself. In vitro and in vivo experimental evidence has shown that the two types of caspase-3 inhibitors are neuroprotective in models of brain ischemia. However, in clinical studies with patients affected by stroke, the two types of caspase-3 inhibitors were not able to reduce ischemic stroke. The aim of this review is to show the rationale of caspase-3 inhibitors in neuroprotection, summarize the results of the clinical trials performed so far and to discuss possible future directions.Q:

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