10-Thiastearic Acid
目录号 : GC41873
A stearoyl CoA desaturase inhibitor
Cas No.:105099-89-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Heteroatom-substituted fatty acids have been observed to modulate the extension and desaturating of fatty acids, and to influence their distribution within phospholipids pools. 10-Thiastearic acid inhibits desaturation of radiolabeled stearate to oleate in rat hepatocytes and hepatoma cells by more than 80% at a concentration of 25 µM. This activity is associated with a hypolipidemic effect, making this 10-thiastearic acid a useful tool for evaluating new anti-obesity therapeutics.
| Cas No. | 105099-89-6 | SDF | |
| Canonical SMILES | CCCCCCCCSCCCCCCCCC(O)=O | ||
| 分子式 | C17H34O2S | 分子量 | 302.5 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 10 mg/ml,Ethanol: 10 mg/ml,PBS (pH 7.2): .15 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 | 3.3058 mL | 16.5289 mL | 33.0579 mL |
| 5 mM | 0.6612 mL | 3.3058 mL | 6.6116 mL |
| 10 mM | 0.3306 mL | 1.6529 mL | 3.3058 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。
10-Thiastearic Acid inhibits both dihydrosterculic acid biosynthesis and growth of the protozoan Crithidia fasciculata
J Biol Chem 1986 Sep 25;261(27):12441-3.PMID:3745198doi
10-Thiastearic Acid is a specific inhibitor of the biosynthesis of dihydrosterculic acid (9,10-methyleneoctadecanoic acid) in the trypanosomatid protozoan Crithidia fasciculata. A 50% inhibition of the biosynthesis of dihydrosterculate is observed in the presence of 4 microM 10-thiastearate in the protozoan growth medium, but little effect is seen on the distribution of the other fatty acids. In addition, the growth of the protozoa is slowed by the presence of 10-thiastearate, with 50% growth inhibition produced at about 10 microM. A possible mechanism of this inhibition and the implication of this result with regard to the design of antiprotozoal agents are discussed.
A Histoplasma capsulatum Lipid Metabolic Map Identifies Antifungal Targets
mBio 2021 Dec 21;12(6):e0297221.PMID:34809453DOI:10.1128/mBio.02972-21.
Lipids play a fundamental role in fungal cell biology, being essential cell membrane components and major targets of antifungal drugs. A deeper knowledge of lipid metabolism is key for developing new drugs and a better understanding of fungal pathogenesis. Here, we built a comprehensive map of the Histoplasma capsulatum lipid metabolic pathway by incorporating proteomic and lipidomic analyses. We performed genetic complementation and overexpression of H. capsulatum genes in Saccharomyces cerevisiae to validate reactions identified in the map and to determine enzymes responsible for catalyzing orphan reactions. The map led to the identification of both the fatty acid desaturation and the sphingolipid biosynthesis pathways as targets for drug development. We found that the sphingolipid biosynthesis inhibitor myriocin, the fatty acid desaturase inhibitor thiocarlide, and the fatty acid analog 10-Thiastearic Acid inhibit H. capsulatum growth in nanomolar to low-micromolar concentrations. These compounds also reduced the intracellular infection in an alveolar macrophage cell line. Overall, this lipid metabolic map revealed pathways that can be targeted for drug development. IMPORTANCE It is estimated that 150 people die per hour due to the insufficient therapeutic treatments to combat fungal infections. A major hurdle to developing antifungal therapies is the scarce knowledge on the fungal metabolic pathways and mechanisms of virulence. In this context, fungal lipid metabolism is an excellent candidate for developing drugs due to its essential roles in cellular scaffolds, energy storage, and signaling transductors. Here, we provide a detailed map of Histoplasma capsulatum lipid metabolism. The map revealed points of this fungus lipid metabolism that can be targeted for developing antifungal drugs.