| Field | Specification |
|---|---|
| Alternative names | Carbonyl cyanide 3-chlorophenylhydrazone; Carbonyl Cyanide m-Chlorophenylhydrazone |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C9H5ClN4 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
CCCP, also known as Carbonyl cyanide 3-chlorophenylhydrazone or Carbonyl Cyanide m-Chlorophenylhydrazone, is an uncoupler of oxidative phosphorylation (OXPHOS). It activates PINK1, leading to Parkin Ser65 phosphorylation[1]. It is supplied as a yellow to brown solid (C9H5ClN4, MW 204.62) at 98.12% purity.
Physical & Chemical Properties
| CAS Number | 555-60-2 |
|---|---|
| Molecular Formula | C9H5ClN4 |
| Molecular Weight | 204.62 g/mol |
| Purity | 98.12% |
| Appearance | Solid |
| Color | Yellow to brown |
| SMILES | N#C/C(C#N)=N/NC1=CC=CC(Cl)=C1 |
| Signaling Pathway | Neuronal Signaling; Autophagy; Immunology/Inflammation; Metabolic Enzyme/Protease; Anti-infection; Apoptosis |
| Solubility | In Vitro: DMSO: 50 mg/mL (244.36 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) H2O: < 0.1 mg/mL (insoluble) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 2 years; -20°C, 1 year. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 50 mg/mL (244.36 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
| H2O | < 0.1 mg/mL | insoluble |
Aliquot the stock solution and store it at -80°C (up to 2 years) or -20°C (up to 1 year); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.5 mg/mL (12.22 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Data provided by the manufacturer.
In Vitro
IFN-β production triggered by various STING pathway activators is inhibited by CCCP. By disrupting the association between STING and TBK1, CCCP suppresses phosphorylation of STING, TBK1, and IRF3. CCCP blocks activation of STING and its downstream signaling molecules, TBK1 and IRF3, yet does not block translocation of STING to the perinuclear region. CCCP also impairs the STING-TBK1 interaction and, at the same time, triggers mitochondria fission. Notably, knockout of Drp1, a key regulator of mitochondria fission, restored STING activity, which indicates that the STING pathway is down-modulated by CCCP via DRP1-mediated mitochondria fragmentation. CCCP is a protonophore that disrupts membrane potential, and it suppresses DMXAA-triggered STING signaling. In DMXAA-treated RAW264.7 cells and MEFs, CCCP drastically suppresses IFN-β production[1]. A CCCP concentration as low as 1 μM is sufficient to induce mitocytosis. In cells treated with 10 μM CCCP, the dose used to induce mitophagy, mitocytosis is barely induced. Mechanistically, mitocytosis requires damaged mitochondria to be positioned at the cell periphery, which happens because damaged mitochondria do not bind inward motor proteins[4].
In Vivo
CCCP and PPEF are each given at the same dosage of 3 mg/kg.bw. Either agent alone gives a 1 log reduction in bacterial load. When 3 mg/kg.bw PPEF is combined with 3 mg/kg.bw CCCP, however, the bacterial count falls by 6 log10. This model confirms the enhanced antibacterial activity of the combination therapy[2]. 99mTc-MIBI signals in the hearts of SD rats given CCCP (4 mg/kg intraperitoneally) or vehicle are also measured. In CCCP-treated rat hearts, 99mTc-MIBI signals decrease, and ATP content, measured by 31P magnetic resonance spectroscopy, decreases at the same time. To examine whether CCCP lowers the 99mTc-MIBI signals in rats, radioisotope activity is analyzed in excised heart tissue from CCCP-treated rats. At 180 min after 99mTc-MIBI injection, hearts from the CCCP group show significantly lower 99mTc-MIBI signals than hearts from the vehicle group[3].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Cell Assay[1]
Stimulate MEFs (5×105), Raw264.7 cells (1×106), and HeLa cells stably expressing STING (1.5×105) with DMXAA (100 μg/mL) for 2 or 3 h, or transfect them for 6 h with 5 μM c-di-GMP, 5 μg/mL cGAMP, or 2 μg/mL poly (dA:dT). Co-treat with CCCP (50 μM) alongside DMXAA (100 μg/mL), or add CCCP for the last 5 h when c-di-GMP or poly (dA:dT) is used[1].
Animal Administration[2][3]
Mice[2] Render female Balb/c mice (n=6 per dosing group, 20-25 g) neutropenic using 2 intraperitoneal cyclophosphamide injections (150 mg/kg.bw and 100 mg/kg.bw) given 4 days and 1 day before bacterial infection. Inject 0.1 mL of a 106 CFU/mL bacterial suspension into the right posterior thigh muscle. At 2 h post-infection, treat the mice with PPEF (3 mg/kg.bw), CCCP (3 mg/kg.bw), or the combination PPEF+CCCP (3 mg/kg.bw+3 mg/kg.bw), ; dissolve each in 0.1 mL sterile water and deliver as a single intravenous bolus. Twenty-four hours after antibacterial administration, euthanize the mice humanely. Aseptically collect the right thigh muscles from each mouse, homogenize, serially dilute, and process for quantitative cultures. Rats[3] Divide the rats randomly into three groups. Euthanize one group 15 min after injection of a 12.5 MBq (337.8 μCi) dose of 99mTc-MIBI (n=6). Inject the other two groups intraperitoneally (i.p.) with 4 mg/kg CCCP (CCCP group; n=7) or vehicle (vehicle group; n=7), 90 min after the same 99mTc-MIBI dose, and euthanize them after an additional 90 min (180 min after the 99mTc-MIBI injection). Excise and weigh the hearts, and measure radioactivity between 110 and 170 keV with an auto-well gamma counter. Correct 99mTc-MIBI signals for physical decay (half-life=6 h).
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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