CCCP
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Cat.No：IC2490 Solarbio
CAS：555-60-2
Storage：Powder:2-8℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year
Purity：≥98%
Appearance：Yellow to brown Solid
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> Small Molecule Compounds > Reaction Substrate & Physicochemical Detection > CCCP
Product Information
| CAS | 555-60-2 |
| Name | CCCP |
| Molecular Formula | C9H5ClN4 |
| Molecular Weight | 204.62 |
| Solubility | Soluble in DMSO ≥100mg/mL |
| Purity | ≥98% |
| Appearance | Yellow to brown Solid |
| Storage | Powder:2-8℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year |
| EC | EINECS 209-103-7 |
| MDL | MFCD00001848 |
| SMILES | N#C/C(C#N)=N/NC1=CC=CC(Cl)=C1 |
| InChIKey | UGTJLJZQQFGTJD-UHFFFAOYSA-N |
| InChI | InChI=1S/C9H5ClN4/c10-7-2-1-3-8(4-7)13-14-9(5-11)6-12/h1-4,13H |
| PubChem CID | 2603 |
| Background | CCCP is an oxidative phosphorylation uncoupler. |
| Biological Activity | CCCP是氧化磷酸化解偶联剂，是线粒体质子载体解偶联剂，可增加线粒体膜对质子的通透性，从而破坏线粒体膜电位。[1-3] |
| In Vitro | CCCP抑制由各种类型的STING途径激活剂诱导的IFN-β产生。 CCCP通过破坏STING和TBK1的结合来抑制STING，TBK1和IRF3的磷酸化。 CCCP抑制STING及其下游信号分子TBK1和IRF3的激活，但不抑制STING易位至核周区域。 CCCP损害STING和TBK1之间的相互作用，同时引发线粒体分裂。重要的是，关键线粒体裂变调节因子Drp1的敲除恢复了STING活性，表明CCCP通过DRP1介导的线粒体断裂下调STING途径。破坏膜电位的质子载体CCCP抑制DMXAA触发的STING信号传导途径。 CCCP大大抑制了DMXAA处理的RAW264.7细胞和MEF中IFN-β的产生[1]。 |
| In Vivo | 使用相同剂量的3mg / kg.bw各CCCP和PPEF。在两种情况下，在细菌负荷中观察到1个对数减少。然而，当3mg / kg.bw的PPEF与3mg / kg.bw的CCCP组合使用时，在细菌计数中观察到6log10的减少。所开发的模型验证了联合治疗的增强的抗菌活性[2]。还测量了施用CCCP(4mg / kg腹膜内)或载体的SD大鼠心脏中的.99mTc-MIBI信号。在施用CCCP的大鼠心脏中99mTc-MIBI信号减少，并且通过31P磁共振光谱法测量的ATP含量同时降低。为了研究CCCP是否减少大鼠中的99mTc-MIBI信号，我们分析了来自施用CCCP的大鼠的切除的心脏组织的放射性同位素活性。在99mTc-MIBI注射后180分钟，来自CCCP组心脏的99mTc-MIBI信号显著低于载体组[3]。 |
| Cell Experiment | 稳定表达STING(1.5×105)的MEF(5×105)，Raw264.7细胞(1×106)和HeLa细胞用DMXAA(100μg/ mL)刺激2或3小时，或用c-di转染-GMP(5μM)，cGAMP(5μg/ mL)或聚(dA：dT)(2μg/ mL)，持续6小时。 CCCP(50μM)与DMXAA(100μg/ mL)共同处理，或在处理c-di-GMP或poly(dA：dT)的情况下处理最后5小时[1]。 |
| Animal Experiment | 小鼠[2]雌性Balb / c小鼠n = 6，每个给药组20-25g，在4天和1天前腹膜内注射环磷酰胺150mg / kg.bw和100mg / kg.bw，使其中性粒细胞减少。对细菌感染。将0.1mL的10 6 CFU / mL细菌悬浮液注射到右后大腿肌肉中。感染后2小时，用PPEF(3 mg / kg.bw)，CCCP(3 mg / kg.bw)和PPEF + CCCP(3 mg / kg.bw + 3 mg / kg.bw)联合治疗小鼠通过单次静脉推注溶解于0.1mL无菌水中。抗菌给药后二十四小时，人道地处死小鼠。无菌收集每只小鼠的右大腿肌肉，均质化并连续稀释并加工用于定量培养。大鼠[3]将大鼠随机分成三组。在12.5MBq(337.8μCi)99mTc-MIBI注射剂量(n = 6)后15分钟对一组进行安乐死。另外两组在相同剂量的99mTc-MIBI注射后90分钟通过腹膜内(ip)注射施用4mg / kg CCCP(CCCP组; n = 7)或媒介物(媒介物组; n = 7)并在之后安乐死另外90分钟(99mTc-MIBI注射后180分钟)。切下心脏并称重，用自动伽马计数器测量放射性在110和170keV之间。校正99mTc-MIBI信号的物理衰减(半衰期= 6小时)。 |
| Data Literature Source | [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. |
| Unit | Bottle |
| Specification | 10mg 25mg 50mg |
是一种氧化磷酸化抑制剂，是线粒体质子载体解偶联剂，可增加线粒体膜对质子的通透性，从而破坏线粒体膜电位。常用作一种阳性对照来诱导细胞凋亡，并配合线粒体膜电位检测探针JC-1（货号：IJ0300）来进行相关研究。
推荐工作浓度（仅供参考）: 10-100µM。初次实验可进行凋亡诱导20min，随后进行JC-1线粒体膜电位丧失检测，呈绿色荧光。
Remark：These protocols are for reference only. Solarbio does not independently validate these methods.
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