Efficacy in Animal Models
The compound displayed cell-rescuing effects in various models of apoptotic neuronal death, as well as in rodent and non-rodent animal models of neurodegeneration. Omigapil rescues in vitro PC12 cells from rotenone toxicity, β-amyloid toxicity, nutrition withdrawal, and lactacystin. Additionally, omigapil can prevent NMDA and kainate receptor excitotoxicity in rat cortical neurons as well as toxicity from cytosine arabinoside (ara C) in cerebellar granule cells. Omigapil also rescues rat oligodendrocytes from AMPA receptor excitotoxicity and rat embryonic mesencephalic (midbrain) dopaminergic cells from toxicity by MPP+/MPTP. In human neuroblastoma (PAJU) cells, omigapil can also prevent toxicity from rotenone and GAPDH overexpression. Omigapil has an active concentration range from about 10−12 M to 10−5 M, with a maximum at about 10−9 M. Omigapil prevents neurodegeneration in both unilateral carotid occlusion/transient hypoxia and facial motor neuron axotomy animal models as well as mouse models of progressive motor neuronopathy, MPTP, and oxidopamine. Omigapil also prevents the death of nigrostriatal dopaminergic neurons in monkeys treated with MPTP to mimic Parkinson's disease symptoms. While omigapil was able to prevent programmed cell death for high-risk cells and prevent deterioration of concomitant motor deficits associated with Parkinson's symptoms, omigapil was unable to reverse pre-existing Parkinson's symptoms in MPTP monkeys.
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