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Type
HazMat fee for 500 gram (Estimated)
Excepted Quantity
USD 0.00
Limited Quantity
USD 15-60
Inaccessible (Haz class 6.1), Domestic
USD 80+
Inaccessible (Haz class 6.1), International
USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic
USD 100+
Accessible (Haz class 3, 4, 5 or 8), International
Stimulator of Interferon Genes (STING) is a cytosolic DNA sensing pathway, as a proximal event required for optimal type I interferon production, dendritic cell activation, and priming of CD8+ T cells against tumor-associated antigens[1]. 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[1]. 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 log10 reduction is observed in the bacterial count. The developed model validates the enhanced antibacterial activity of combination therapy[2]. 99mTc-MIBI signals in the hearts of SD rats administered CCCP (4 mg/kg intraperitoneally) or vehicle is also measured. 99mTc-MIBI signals decrease in rat hearts administered CCCP, and the ATP content, as measured by 31P magnetic resonance spectroscopy, decreased simultaneously. To investigate whether CCCP decreased the 99mTc-MIBI signals in rats, the radioisotope activity of excised heart tissue from rats administered CCCP was analyzed. At 180 min after 99mTc-MIBI injection, the 99mTc-MIBI signals from the hearts in the CCCP group are significantly lower than those in the vehicle group[3]. CCCP is the most commonly used inducer of mitophagy in mammalian cells and is thought to exert its effects by reducing the mitochondrial membrane potential[4].
CCCP 细胞实验
Cell Line
Concentration
Treated Time
Description
References
GV oocytes
1 µM
0.5 hours
CCCP treatment activated the PRKN-mediated mitophagy pathway and resulted in meiotic arrest at the MI stage
Autophagy. 2022 Mar;18(3):643-660.
Wheat root cells
10 µM
1 hour
To study the effect of CCCP on cytokinin accumulation in root cells, the results showed that CCCP treatment decreased cytokinin accumulation in root cells but increased both flow from the roots and accumulation in the shoots.
J Exp Bot. 2014 Jun;65(9):2287-94.
MRC5 cells
25 µM
2 hours
CCCP treatment significantly increased mitolysosome formation and promoted VZV replication but attenuated IFN production.
Cell Death Dis. 2024 Jan 6;15(1):16.
HaCaT cells
25 µM
2 hours
CCCP treatment significantly increased mitolysosome formation and promoted VZV replication but attenuated IFN production.
Cell Death Dis. 2024 Jan 6;15(1):16.
293T cells
10 µM
2 hours
CCCP treatment induced mitochondrial damage, manifested as mitochondrial membrane rupture and vacuolization
Autophagy. 2022 Mar;18(3):643-660.
SH-SY5Y cells
20 µM
2 hours
To investigate the role of AMBRA1 in the PINK1-PRKN signaling pathway after CCCP treatment, results showed that AMBRA1 downregulation leads to reduced PINK1 stability and mitophagy.
Autophagy. 2022 Aug;18(8):1752-1762.
HeLa cells
20 µM
2 hours
To investigate the role of AMBRA1 in the PINK1-PRKN signaling pathway after CCCP treatment, results showed that AMBRA1 downregulation leads to reduced PINK1 stability and mitophagy.
Autophagy. 2022 Aug;18(8):1752-1762.
Yeast cells
2 µM
20 minutes
To test the direct inhibitory effect of CCCP on TbAQP2 glycerol permeability, results showed that CCCP directly inhibits TbAQP2 glycerol permeability in the single-digit micromolar range.
Cells. 2020 Oct 21;9(10):2335.
Human induced pluripotent stem cell-derived dopaminergic neurons
10 µM
48 hours
To evaluate the effect of CCCP-induced mitochondrial damage on healthy neurons, it was found that healthy neurons responded to CCCP by clearing impaired mitochondria, and this process was accelerated by USP30 inhibition.
Cell Death Dis. 2024 Jan 15;15(1):52.
PARK2 knockout neurons
10 µM
48 hours
To evaluate the effect of CCCP-induced mitochondrial damage on PARK2 knockout neurons, it was found that PARK2 knockout neurons showed an impaired mitophagic response to CCCP, but USP30 inhibition promoted mitophagy in PARK2 knockout neurons.
Cell Death Dis. 2024 Jan 15;15(1):52.
Vascular smooth muscle cells (A10)
2 µM
5 minutes and 20 minutes
CCCP increased the cellular ADP/ATP ratio and activated AMPK after 5 and 20 minutes.
Br J Pharmacol. 2016 Nov;173(21):3145-3158.
GT1-7 cells
10 µM
6 hours
CCCP was used for mitochondrial depolarization to assess its impact on the mitochondrial network. Results showed that CCCP led to a significant decrease in mitochondrial volume, indicating that the network likely underwent fragmentation prior to observation.
Cells. 2023 Jun 27;12(13):1726.
CCCP 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
Aged mice
Intraperitoneal injection
1 µM
Every other day for one month
ML098 treatment improved oocyte quality and fertility in aged mice
Autophagy. 2022 Mar;18(3):643-660.
Rat
POI model
Intraperitoneal injection
2 mg/kg
Every other day for 15 days
CCCP inhibited the ability of BMSCs-MOX treatment to regulate mitophagy and exacerbated Cy-induced ovarian injury.
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