[CAS NO. 555-60-2] CCCP
PRODUCTS SPECIFICATIONS [555-60-2]
DESCRIPTION [555-60-2]
Overview
| MDL | - |
|---|---|
| Molecular Weight | 204.62 |
| Molecular Formula | C9H5ClN4 |
| SMILES | N#C/C(C#N)=N/NC1=CC=CC(Cl)=C1 |
38 Publications Citing Use of MCE
- [1]Nature. 2019 Nov;575(7782):375-379.
- [2]Cell Res. 2021 Jun;31(6):703-712.
- [3]J Clin Invest. 2020 Jun 1;130(6):3253-3269.
- [4]Autophagy. 2021 Dec 10;1-19.
- [5]Autophagy. 2021 Jul 7;1-18.
- [6]Autophagy. 2021 Nov;17(11):3622-3643.
- [7]Proc Natl Acad Sci U S A. 2021 Aug 31;118(35):e2023909118.
- [8]Cell Rep. 2023 Jan 30;42(2):112033.
- [9]Cell Rep. 2023 Jan 31;42(1):112011.
- [10]Clin Transl Med. 2020 Nov;10(7):e228.
- [11]Cancer Lett. 2022 May 26;541:215752.
- [12]J Exp Clin Cancer Res. 2018 Sep 5;37(1):218.
- [13]Anal Chem. 2019 Sep 3;91(17):11409-11416.
- [14]J Nanobiotechnology. 2020 Mar 18;18(1):52.
- [15]Sci Signal. 2021 Mar 9;14(673):eaax7942.
- [16]Cell Death Dis. 2022 Oct 26;13(10):899.
- [17]Cell Death Dis. 2022 Jul 6;13(7):583.
- [18]J Neuroinflammation. 2022 Apr 12;19(1):87.
- [19]Clin Sci (Lond). 2019 Aug 14;133(15):1759-1777.
- [20]Mol Carcinog. 2022 Sep 19.
- [21]Cell Biosci. 2022 Nov 4;12(1):180.
- [22]FASEB J. 2020 Feb;34(2):2055-2074.
- [23]Biochem Pharmacol. 2022 Feb 19;198:114948.
- [24]Int J Biol Sci. 2022; 18(13):5168-5184.
- [25]Int J Biol Sci. 2022 Aug 8;18(13):5168-5184.
- [26]Sci Rep. 2020 Feb 20;10(1):3078.
- [27]Exp Cell Res. 2021 Jan 21;112493.
- [28]Virol Sin. 2022 Aug 4;S1995-820X(22)00136-5.
- [29]Spectrochim Acta A Mol Biomol Spectrosc. 2020 Jan 5;224:117456.
- [30]Biochem Biophys Res Commun. 2019 Apr 30;512(2):269-275.
- [31]FEBS Open Bio. 2021 Aug 4.
- [32]Bioengineered. 2022 Feb;13(2):3486-3502.
- [33]Exp Ther Med. 2023 Feb 10.
- [34]Research Square Print. November 28th, 2022.
- [35]Research Square Print. 2022 Sep.
- [36]Patent. US20200268864A1.
- [37]Fish Shellfish Immunol. 2020 Sep;104:663-672.
- [38]Department of life sciences, Humboldt university. 2019 Feb.
Summary
CCCP is an oxidative phosphorylation ( OXPHOS ) uncoupler. CCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation [1] .
In Vitro
CCCP inhibits IFN-β production induced by various types of the STING pathway activators. CCCP suppresses the phosphorylation of STING, TBK1, and IRF3 via disrupting the association of STING and TBK1. CCCP inhibits activation of STING and its downstream signaling molecules, TBK1 and IRF3, but not STING translocation to the perinuclear region. CCCP impairs the interaction between STING and TBK1 and concomitantly triggers mitochondria fission. Importantly, the knockout of the crucial mitochondria fission regulator Drp1 restored the STING activity, indicating that CCCP down-modulates the STING pathway through DRP1-mediated mitochondria fragmentation. The protonophore CCCP that disrupts membrane potential suppresses the DMXAA-triggered STING signaling pathway. CCCP drastically suppresses the production of IFN-β in DMXAA-treated RAW264.7 cells and MEFs
[1]
.
As low as 1 μM CCCP is enough to induce mitocytosis. In cells treated with 10 μM CCCP, which is the dose used for inducing mitophagy, mitocytosis is barely induced. Mechanistically, mitocytosis requires positioning of damaged mitochondria at the cell periphery, which occurs because damaged mitochondria avoid binding to inward motor proteins
[4]
.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
The same dosage of 3 mg/kg.bw each of CCCP and PPEF is used. In both the cases 1 log reduction is observed in the bacterial load. However, when 3 mg/kg.bw of PPEF is used in combination with 3 mg/kg.bw of CCCP, 6 log 10 reduction is observed in the bacterial count. The developed model validates the enhanced antibacterial activity of combination therapy [2] . 99m Tc-MIBI signals in the hearts of SD rats administered CCCP (4 mg/kg intraperitoneally) or vehicle is also measured. 99m Tc-MIBI signals decrease in rat hearts administered CCCP, and the ATP content, as measured by 31 P magnetic resonance spectroscopy, decreased simultaneously. To investigate whether CCCP decreased the 99m Tc-MIBI signals in rats, we analyzed the radioisotope activity of excised heart tissue from rats administered CCCP. At 180 min after 99m Tc-MIBI injection, the 99m Tc-MIBI signals from the hearts in the CCCP group are significantly lower than those in the vehicle group [3] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Appearance
Solid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
| Powder | -20°C | 3 years |
|---|---|---|
| 4°C | 2 years | |
| In solvent | -80°C | 6 months |
| -20°C | 1 month |
Solvent & Solubility
DMSO : 50 mg/mL ( 244.36 mM ; Need ultrasonic)
H 2 O : < 0.1 mg/mL (ultrasonic;warming;heat to 60°C) (insoluble)
Stock Solutions
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 4.8871 mL | 24.4355 mL | 48.8711 mL |
| 5 mM | 0.9774 mL | 4.8871 mL | 9.7742 mL |
| 10 mM | 0.4887 mL | 2.4436 mL | 4.8871 mL |
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1.
References
- [1] Kwon D, et al. Carbonyl cyanide 3-chlorophenylhydrazone (CCCP) suppresses STING-mediated DNA sensing pathway through inducing mitochondrial fission. Biochem Biophys Res Commun. 2017 Aug 30. pii: S0006-291X(17)31704-7.
- [2] Sinha D, et al. Synergistic efficacy of Bisbenzimidazole and Carbonyl Cyanide 3-Chlorophenylhydrazonecombination against MDR bacterial strains. Sci Rep. 2017 Mar 17;7:44419.
- [3] Kawamoto A, et al. Measurement of technetium-99m sestamibi signals in rats administered a mitochondrial uncoupler and in a rat model of heart failure. PLoS One. 2015 Jan 16;10(1):e0117091.
- [4] Kondapalli C, et al. PINK1 is activated by mitochondrial membrane potential depolarization and stimulates Parkin E3 ligase activity by phosphorylating Serine 65. Open Biol. 2012 May;2(5):120080.
- [5] Haifeng Jiao, et al. Mitocytosis, a migrasome-mediated mitochondrial quality-control process. Cell. 2021 May 27;184(11):2896-2910.e13.
Synonyms