MTK458 (25 µM) increases PINK1-mediated mitophagy to enhance clearance of intramitochondrial aggregates in Hela cells induced ΔOTC and YFP-Parkin[1].
MTK458 (0.1-25 µM) clears pS129 α-synuclein aggregates (12-250 kDa) in a dose-dependent manner in DIV9 and DIV12[1].
MTK458 (0-13 µM, 10 days) reduces α-synuclein pathology and the mitochondrial stress marker pUb in iPSC neurons[1].
MTK458 (50 mg/kg, p.o., daily, 6 months) drives clearance of pathologic α-synuclein in a dose-dependent manner in the stratum of mice injected with α-synuclein preformed fibrils (PFFs)[1].
MTK458 (50 mg/kg, p.o., 6 doses, 5 days) decreases plasma pS65-Ubiquitin (pUb) in wild-type Sprague-Dawley rats[1].
References:
[1]. Chin RM, et al. Pharmacological PINK1 activation ameliorates Pathology in Parkinson's Disease models. bioRxiv [Preprint]. 2023 Feb 15:2023.02.14.528378.
















