FCCP 是一种线粒体中氧化磷酸化解偶联剂，能够诱导 PINK1 激活，促进 Parkin 在 Ser65 位点磷酸化。

FCCP, a potent uncoupler of oxidative phosphorylation in mitochondria, transport protons across cell membranes leading to disrupts ATP synthesis.

FCCP treatment induces a very rapid 2-fold increase in intracellular Ca2+ concentration that is accompanied by a strong protein synthesis rate inhibition. The translation inhibition correlates with an increased phosphorylation of the α subunit of eIF2 (eIF2α) and a 1.7-fold increase in the double-stranded RNA-dependent protein kinase activity[1]. FCCP treatment also mildly decreases ATP and reactive oxygen species levels. It increases the expression of mitochondrial genes such as Tfam and COXIV while inducing morphological features of quiescent mouse HSCs and abrogating TGF-β signal transduction[2].

FCCP significantly reduces mitochondrial membrane potential and ATP production in 8-cell mouse embryos and the number of inner cell mass cells within blastocysts with unchanged blastocyst development. This perturbed embryonic mitochondrial function is concomitant with reduced birth weight in female offspring following embryo transfer, which persists until weaning. Although FCCP-treated males also exhibits reduced glucose tolerance as female, but their insulin sensitivity and adiposity gain between 4 and 14 weeks is unchanged. Reducing mitochondrial function and, thus, decreasing ATP output in the precompacting embryo can influence offspring phenotype[3].

Protein synthesis rate is assayed in 24-mm diameter multi-well dishes with fresh medium containing 0.175 Ci/mmol of [3H]methionine (200 μM), for 30 min at 37°C. PC12 cells are treated with FCCP for different period of times. (Only for Reference)

370-86-5

C10H5F3N4O

254.17

Trifluoromethoxy carbonylcyanide phenylhydrazone;Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone

DMSO:25.4 mg/mL (100 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years