Background:

IC50: N/A

CCCP (carbonyl cyanide m-chlorophenyl hydrazine) is widely used uncoupler of oxidative phosphorylation.

The uncoupler of oxidative phosphorylation blocks ATP synthesis by collapsing the proton motive force.

In vitro: A genetic β-galactoside reporter system with a disk diffusion assay on MacConkey Lactose agar petri plates to monitor maintenance of the bacteriophage λ prophage state and viral induction in Escherichia coli K-12. It presented evidence that the phage λ major lytic promoters, pL and pR, are activated via cells containing the reporters following exposure to the energy poison CCCP. Requirement of expression of the λ lytic promoters in response to CCCP is host RecA function and an auto-cleavable CI repressor, as does SOS induction of the λ prophage occurring by a DNA damage-dependent pathway. CCCP-mediated activation of the λ lytic promoters required λ Cro function. CCCP does not modulate an sfi-lacZ SOS reporter [1]. The uncoupler CCCP blocks oxidative phosphorylation by damaging the proton gradient. An anion CCCP can bind a proton. but CCCP with a delocalized negative charge allows it to cross the lipid bilayer in the unprotonated form, while weak acids cross the hydrophobic membrane only when protonated. Many protons can be transported by one molecule of CCCP across the inner membrane. It is described that a genetic reporter system to monitor maintenance of the λ prophage state and viral induction, and evidence is presented that it activates the major leftward and rightward lytic promoters of the λ prophage that cells are exposed to the energy poison CCCP.

In vivo: So far, no study in vivo has been conducted.

Clinical trial: So far, no clinical study has been conducted.

Reference:
[1].  Thomason LC, Court DL. Evidence that bacteriophage λ lysogens may induce in response to the proton motive force uncoupler CCCP. FEMS Microbiol Lett. 2016 Feb;363(3).