CCCP (Carbonyl Cyanide m-Chlorophenylhydrazone) is an oxidative phosphorylation (OXPHOS) inhibitor and mitochondrial proton carrier uncoupler. CCCP inhibits the activation of STING and its downstream signaling molecules TBK1 and IRF3.

METHODS: Human cervical cancer cells HeLa were treated with CCCP (20 μM) for 30 min, and the effect on the mitochondria-labeled fluorescent dye DiOC6 was observed using live cell fluorescence microscopy.
RESULTS: CCCP-induced loss of mitochondrial membrane potential resulted in efflux of DiOC6 from mitochondria into the cytoplasm and subsequent localization to punctate structures. [1]
METHODS: Mouse alveolar epithelial cells, MLE-12, were treated with CCCP (10-50 μM) for 2-18 h. The expression levels of the target proteins were examined by Western Blot.
RESULTS: CCCP caused a dose- and time-dependent conversion of LC3-I to LC3-II. [2]

METHODS: To assay in vivo activity, CCCP (5 mg/kg) was administered as a single intraperitoneal injection to adult and aged C57BL/6J mice, and hearts were collected 12 h later.
RESULTS: Under CCCP-treated conditions, more mitochondria bound to autophagic vesicles were found in the hearts of adult but not aged mice. [3]
METHODS: To assay in vivo activity, CCCP (1 mg/kg) was administered intraperitoneally to mt-Rosella mice once a day for three days.
RESULTS: Mitochondrial fragments were readily visible on the hearts of CCCP-treated mice, and these fragments were trapped in lysosomes for degradation.CCCP induced mitochondrial autophagy. [4]