NZ-66

NZ-66 exhibits ULK1 agonist activity comparable to that of BL-918 (HY-124729 ) in cell-free in vitro kinase assays^[1].
NZ-66 (1 μM; 18 h) retains ULK1 agonist activity and induces functional autophagy in PANC-1 cells, as evidenced by increased phosphorylation level of ULK1, altered LC3 processing, decreased p62 level, and enhanced formation of autophagosomes/autolysosomes^[1].
NZ-66 (1 μM; 18 h) recruits ULK1 to the outer mitochondrial membrane in PANC-1 cells. This process depends on free TSPO receptors and is enhanced by CCCP-induced mitochondrial damage^[1].
NZ-66 (1.25-10 μM; 1-18 h) induces mitophagy in SH-SY5Y cells in a TSPO-dependent manner, and its activity is enhanced by mitochondrial damage without relying on mitochondrial membrane depolarization^[1].
NZ-66 (1 μM; 18 h)-induced mitophagy depends on the activity of ULK1/2, which is evidenced by the absence of Mfn2 degradation and the lack of LC3-mitochondria colocalization in ULK1/2 double-knockout mouse embryonic fibroblasts (ULK1/2 DKO MEFs)^[1].
NZ-66 (1 μM; 18 h) induces mitophagy in fibroblasts from Parkinson's disease patients with PINK gene knockout, and this process is independent of the PINK1/PARKIN pathway; this is evidenced by the degradation of Mfn2 without activation of phosphorylated ubiquitin (Ser65) and the colocalization of ULK1 with mitochondria^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.