Carboxyatractyloside (potassium salt)
(Synonyms: 羧基苍术苷) 目录号 : GC43141
An inhibitor of ADP/ATP translocases
Cas No.:35988-42-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Carboxyatractyloside is a natural heteroglucoside produced in some plants, including A. gummifera. Carboxyatractyloside prevents mitochondrial ATP synthesis by inhibiting ADP/ATP translocases, which are responsible for the exchange of adenine di- and triphosphates across the inner mitochondrial membrane.
| Cas No. | 35988-42-2 | SDF | |
| 别名 | 羧基苍术苷 | ||
| Canonical SMILES | C=C([C@H](CC1)C2)[C@H](O)[C@@]32CC[C@]4([H])C(C([O-])=O)(C([O-])=O)C[C@@H](O[C@@H]5[C@@H]([C@H]([C@@H]([C@@H](CO)O5)OS(=O)(O)=O)OS(=O)(O)=O)OC(CC(C)C)=O)C[C@@]4(C)[C@@]31[H].[K+].[K+] | ||
| 分子式 | C31H44O18S2•2K | 分子量 | 847 |
| 溶解度 | Water: 10 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.1806 mL | 5.9032 mL | 11.8064 mL |
| 5 mM | 0.2361 mL | 1.1806 mL | 2.3613 mL |
| 10 mM | 0.1181 mL | 0.5903 mL | 1.1806 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Matrix volume measurements challenge the existence of diazoxide/glibencamide-sensitive KATP channels in rat mitochondria
J Physiol 2003 Mar 15;547(Pt 3):893-902.PMID:12562892DOI:10.1113/jphysiol.2002.035006.
A mitochondrial sulphonylurea-sensitive, ATP-sensitive K+ channel (mitoKATP) that is selectively inhibited by 5-hydroxydecanoate (5-HD) and activated by diazoxide has been implicated in ischaemic preconditioning. Here we re-evaluate the evidence for the existence of this mitoKATP by measuring changes in light scattering (A520) in parallel with direct determination of mitochondrial matrix volumes using 3H2O and [14C]sucrose. Incubation of rat liver and heart mitochondria in KCl medium containing Mg2+ and inorganic phosphate caused a decrease in light scattering over 5 min, which was accompanied by a small (15-30 %) increase in matrix volume. The presence of ATP or ADP in the buffer from the start greatly inhibited the decline in A520, whilst addition after a period of incubation (1-5 min) induced a rapid increase in A520, especially in heart mitochondria. Neither response was accompanied by a change in matrix volume, as measured isotopically. However, the effects of ATP and ADP on A520 were abolished by Carboxyatractyloside and bongkrekic acid, inhibitors of the adenine nucleotide translocase (ANT) that lock the transporter in two discrete conformations and cause distinct changes in A520 in their own right. These data suggest that rather than matrix volume changes, the effects of ATP and ADP on A520 reflect changes in mitochondrial shape induced by conformational changes in the ANT. Furthermore, we were unable to demonstrate either a decrease in A520 or increase in matrix volume with a range of ATP-sensitive K+ channel openers such as diazoxide. Nor did glibencamide or 5-HD cause any reduction of matrix volume, whereas the K+ ionophore valinomycin (0.2 nM), produced a 10-20 % increase in matrix volume that was readily detectable by both techniques. Our data argue against the existence of a sulphonylurea-inhibitable mitoKATP channel.
Regulation of glycolysis in rat aorta
Am J Physiol 1984 Jul;247(1 Pt 1):C107-14.PMID:6204540DOI:10.1152/ajpcell.1984.247.1.C107.
Certain factors that might contribute to the regulation of the rate of glycolysis by rat aorta were investigated. Rat aortic rings were incubated with [14C]glucose, and the release of [14C]lactate was determined. There was good agreement between the lactate production estimated by enzymatic assay and by [14C]lactate release, suggesting that almost all the lactate produced under our experimental conditions was derived from exogenous glucose. When the glucose concentration in the medium was 10 mM or higher, the rate of glucose transport did not limit the rate of lactate production. In most cases studies were done both aerobically and anaerobically. In Hanks' Balanced Salt Solution the aerobic rate of lactate production was 18% of the anaerobic rate. We tested the effects on glycolysis of agents that alter ATP generation by mitochondria or ATP splitting by Na+-K+-ATPase or the mitochondrial ATPase. Under aerobic conditions, ouabain (5 mM) caused a 54% decrease in lactate production, and gramicidin (5 micrograms/ml) caused a 45% increase. Under anaerobic conditions, neither ouabain nor gramicidin affected lactate production. Aerobically dinitrophenol (25 microM) and Carboxyatractyloside (0.5 mM) caused substantial increases in lactate production, 72 and 98% respectively. Under anaerobic conditions the effects of dinitrophenol and Carboxyatractyloside were much smaller, with dinitrophenol causing a 15% increase and Carboxyatractyloside a 12% decrease in lactate production. Increasing the concentration of phosphate in the incubation medium caused marked increases in lactate production. Both aerobically and anaerobically, shifting from 1.3 to 50 mM phosphate in the incubation medium caused a 3.5-fold increase in lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)
The role of ATP in the cytostructure of the hepatocytes
J Cell Biochem 1987 Feb;33(2):127-36.PMID:3571339DOI:10.1002/jcb.240330207.
We have previously described the preparation of hepatocytes from which the plasma membrane was removed by digitonin treatment. Such "nude" cells were found to be very stable in sucrose media containing above 50 mM NaCl or KCl, but they disintegrate near instantly in salt-free media, liberating nuclei, mitochondria, and other organelles. We show here that disintegration occurs at a physiologic pH and in the presence of oxygen. Disintegration was blocked by rotenone, oligomycin, KCN, and Carboxyatractyloside, establishing that oxidative phosphorylation and ATP generation is essential for disintegration to occur. The addition of ATP, GTP, ITP, or ADP (but not AMP) in the presence of the inhibitors, induced breakdown. Taxol, an inhibitor of tubulin depolymerization and phalloidin, a drug that stabilizes actin fibers, prevented disintegration in salt-free media. The effect of these drugs was counteracted by the addition of ATP. Our results show that two conditions are essential to induce the disintegration of the nude cell: media of low ionic strength, and ATP generation. The ATP effect is likely to be of physiological significance, suggesting role of ATP generation in affecting polymerization of cytoskeletal elements.