QNZ was originally described as a potent inhibitor of NF-B activation (IC50 = 11 n) and TNF- production (IC50 = 7 nM).1,2 It indirectly inhibits the NF-B pathway via inhibition of store-operated calcium entry (SOC) and displayed neuroprotective effects in transgenic fly and mouse models of Huntingtons disease.3,4 Its target has been postulated to be heteromeric calcium channels containing TRPC1 as one of the subunits.4 QNZ reduced synaptic neuronal SOC and rescued dendritic spine loss in YAC128 striatal medium spiny neurons.5 QNZ has also been identified as a potent (IC50 = 25 nM complex 1 from Y.lipolytica, IC50 = 14 nm complex 1 from Bos Taurus heart mitochondria) and selective inhibitor of mitochondrial complex I.6 QNZ decreased PSEN1deltaE9-mediated nSOCE upregulation and rescued mushroom spines in PSEN1deltaE9-expressing neurons, which are linked to familial Alzheimers disease.7
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