FCCP (370-86-5) is an extremely potent uncoupler of mitochondrial oxidative phosphorylation (IC50 = 20 nM).1 Induces apoptosis in a variety of cell lines.2 Inhibits wild type and mutant beta-amyloid production in embryonic kidney 293 cells expressing either wild-type or “Swedish” mutant APP.3 An important tool for inhibiting mitochondrial membrane potential.2,4 Cell permeable.
FCCP is a potent uncoupler of oxidative phosphorylation in mitochondria that disrupts ATP synthesis by transporting protons across cell membranes. At 40 μM, FCCP induces complete depolymerization of microtubules by increasing intracellular pH via the disruption of the mitochondrial H+ gradient and by decreasing the stability of microtubules by impairing the binding of microtubule-associated proteins.[Cayman Chemical]
ChEBI: A hydrazone that is hydrazonomalononitrile in which one of the hydrazine hydrogens is substituted by a p-trifluoromethoxyphenyl group.
A very potent uncoupler of oxidative phosphorylation in mitochondria.
FCCP is a protonophore (H+ ionophore) and uncoupler of oxidative phosphorylation in mitochondria. It is capable of depolarizing plasma and mitochondrial membranes. FCCP has been shown to have a number of effects on cellular calcium. It also is reported to inhibit a background K+ current and induce a small inward current, reduce pH by 0.1 unit, and induce a rise of intracellular [Na+]. FCCP stimulates Mg2+-ATPase activity, inhibits β-amyloid production, and mimics the effect of selective glutamate agonist N-methyl-D-aspartate (NMDA) on mitochondrial superoxide production.
fccp increases the rate of cellular o2 consumption. in pc-3 and du-145 prostate cancer cells, the compound could significantly decrease hypoxic as well as normoxic hif-1 transcriptional activity which was in part mediated by down-regulation of the oxygen labile hif-1α and hif-2α protein levels. during hypoxic as well as normoxic, it decreases the expression of hif target genes, vegf and vegf receptor-2. [2]
fccp reduces mitochondrial membrane potential and atp production in 8-cell mouse embryos. also, the number of inner cell mass cells decrease 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, 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]
[1] R BENZ S M. The molecular mechanism of action of the proton ionophore FCCP (carbonylcyanide p-trifluoromethoxyphenylhydrazone).[J]. Biophysical journal, 1983, 41 3: 381-398. DOI:
10.1016/s0006-3495(83)84449-x[2] I GAUTIER. A moderate but not total decrease of mitochondrial membrane potential triggers apoptosis in neuron-like cells.[J]. Neuroreport, 2000, 11 13: 2953-2956. DOI:
10.1097/00001756-200009110-00024[3] BRUCE P. CONNOP. Novel Effects of FCCP [Carbonyl Cyanide p-(Trifluoromethoxy)phenylhydrazone] on Amyloid Precursor Protein Processing[J]. Journal of Neurochemistry, 2001, 72 4: 1457-1465. DOI:
10.1046/j.1471-4159.1999.721457.x[4] T J COLLINS. Inositol 1,4,5-trisphosphate-induced Ca2+ release is inhibited by mitochondrial depolarization.[J]. Biochemical Journal, 2000, 347 Pt 2: 593-600. DOI:
10.1042/0264-6021:3470593
