4-Pentenoic acid
(Synonyms: 4-戊烯酸) 目录号 : GC60524
4-Pentenoic acid (Allylacetic acid, 3-vinylpropionic acid, 4-penten-1-oic acid), a flavouring ingredient, is used to inhibit fatty acid oxidation in rat heart mitochondria.
Cas No.:591-80-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
4-Pentenoic acid (Allylacetic acid, 3-vinylpropionic acid, 4-penten-1-oic acid), a flavouring ingredient, is used to inhibit fatty acid oxidation in rat heart mitochondria.
| Cas No. | 591-80-0 | SDF | |
| 别名 | 4-戊烯酸 | ||
| Canonical SMILES | C=CCCC(O)=O | ||
| 分子式 | C5H8O2 | 分子量 | 100.12 |
| 溶解度 | DMSO : 100 mg/mL (998.80 mM; Need ultrasonic); H2O : 65 mg/mL (649.22 mM; Need ultrasonic) | 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 | 9.988 mL | 49.9401 mL | 99.8801 mL |
| 5 mM | 1.9976 mL | 9.988 mL | 19.976 mL |
| 10 mM | 0.9988 mL | 4.994 mL | 9.988 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。
Chemoenzymatic Halocyclization of 4-Pentenoic acid at Preparative Scale
ACS Sustain Chem Eng 2020 Feb 24;8(7):2602-2607.PMID:32117647DOI:10.1021/acssuschemeng.9b07494.
The scale-up of chemoenzymatic bromolactonization to 100 g scale is presented, together with an identification of current limitations. The preparative-scale reaction also allowed for meaningful mass balances identifying current bottlenecks of the chemoenzymatic reaction.
Metabolism of 4-Pentenoic acid and inhibition of thiolase by metabolites of 4-Pentenoic acid
Biochemistry 1983 Apr 12;22(8):1827-32.PMID:6133549DOI:10.1021/bi00277a013.
The metabolism of 4-Pentenoic acid, a hypoglycemic agent and inhibitor of fatty acid oxidation, has been studied in rat heart mitochondria. Confirmed was the conversion of 4-Pentenoic acid to 2,4-pentadienoyl coenzyme A (CoA), which either is directly degraded via beta-oxidation or is first reduced in a NADPH-dependent reaction before it is further degraded by beta-oxidation. At pH 6.9, the NADPH-dependent reduction of 2,4-pentadienoyl-CoA proceeds 10 times faster than its degradation by beta-oxidation. At pH 7.8, this ratio is only 2 to 1. The direct beta-oxidation of 2,4-pentadienoyl-CoA leads to the formation of 3-keto-4-pentenoyl-CoA, which is highly reactive and spontaneously converts to another 3-ketoacyl-CoA derivative (compound X). 3-Keto-4-pentenoyl-CoA is a poor substrate of 3-ketoacyl-CoA thiolase (EC 2.3..1.16) whereas compound X is not measurably acted upon by this enzyme. The effects of several metabolites of 4-Pentenoic acid on the activity of 3-ketoacyl-CoA thiolase were studied. 3,4-Pentadienoyl-CoA is a weak inhibitor of this enzyme that is protected against the inhibition by acetoacetyl-CoA. The most effective inhibitor of 3-ketoacyl-CoA thiolase was found to be 3-keto-4-pentenoyl-CoA, which inhibits the enzyme in both a reversible and irreversible manner. The reversible inhibition is possibly a consequence of the inhibitor being a poor substrate of 3-ketoacyl-CoA thiolase. It is concluded that 4-Pentenoic acid is metabolized in mitochondria by two pathways. The minor yields 3-keto-4-pentenoyl-CoA, which acts both as a reversible and as a irreversible inhibitor of 3-ketoacyl-CoA thiolase and consequently of fatty acid oxidation.
Effects of pentanoic acid and 4-Pentenoic acid on the intracellular fluxes of acetyl coenzyme A in Tetrahymena
J Biol Chem 1975 Jun 10;250(11):4067-72.PMID:805136doi
Cultures of Tetrahymena pyriformis were incubated for 1 hour with a mixture of acetate, pyruvate, and pentanoate with only one substrate labeled at a time and with the position of the label chosen so that [1-14-C]acetyl coenzyme A was an early product of the metabolism of each substrate. The appearance of label in CO2, lipids, glycogen, glutamate, and alanine were measured and results interpreted in terms of a previously developed three-compartment model of metabolism, which was found to quantitatively describe the data even when two of the flux rates (the flux of acetyl-CoA from the peroxisomal to the outer mitochondrial compartment and from the outer mitrochondrial to the inner mitochondrial compartment) were set equal to zero. This reduction in the number of independent parameters leads to the model being overdetermined and to a probably unique fit of the three-compartment model tof the present data and to previous data when octanoate was the fatty acid substrate. Pentanoate was metabolized to a greater extent than octanoate and did not inhibit growth. Pentanoate inhibited acetate utilization in both the inner mitochondrial and peroxisomal compartments as indicated by a reduction in the incorporation of label from [1-14-C]acetate into lipids and into CO2, but there was no difference in oxidation of [2-14-C]pyruvate when pentanoate was the fatty acid substrate as compared to octanoate. Glyconeogenesis was inhibited when pentanoate was substituted for octanoate. Similar experiments were performed on cells treated with 4-Pentenoic acid. The effects of 4-Pentenoic acid were essentially the same whether octanoate or pentanoate was the fatty acid substrate, i.e. inhibition of glyconeogenesis from all labeled substrates and inhibition of [2-14-C]pyruvate oxidation. The results indicate that the effects of pentanoate are largely confined to the peroxisomal and the inner mitochondrial compartments whereas the effects of 4-Pentenoic acid are confined to the peroxisomal and outer mitochondrial compartments.
Effects of 4-Pentenoic acid on renal phosphate and calcium excretion in the dog
Am J Physiol 1976 Jul;231(1):216-21.PMID:961862DOI:10.1152/ajplegacy.1976.231.1.216.
The effects of 4-Pentenoic acid (4-PA) on renal excretion of phosphate and calcium were studied in anesthetized mongrel dogs. The major metabolic action of 4-PA is inhibition of long-chain fatty acid oxidation. In intact dogs undergoing modest saline diuresis, 4-PA caused significant decrease in the percentage of filtered phosphate reabsorbed. No statistically significant calciuria was observed. Similar results were observed in intact dogs undergoing more brisk saline diuresis as well as in acutely and chronically thyroparathyroidectomized dogs. However, when results were pooled, both phosphate and calcium excretions were significantly increased. The results are interpreted as demonstrating the importance of fatty acid oxidation in providing energy for the work of tubular phosphate reabsorption. Either the energy source for calcium reabsorption differs from fatty acid oxodation, or calcium reabsorption is less sensitive to changes in energy sources. The action of 4-PA is independent of the forces involved in saline diuresis and of parathyroid hormone.
In vivo formation of the thiol conjugates of reactive metabolites of 4-ene VPA and its analog 4-Pentenoic acid
Drug Metab Dispos 1993 Nov-Dec;21(6):1098-106.PMID:7905390doi
The terminal olefin metabolite of valproic acid (VPA), 4-ene VPA, is an analog of the experimental hepatotoxin 4-Pentenoic acid and is believed to play a role in the hepatotoxicity of VPA. The formation of glutathione and N-acetylcysteine conjugates of the putative electrophilic metabolites of 4-ene VPA and 4-Pentenoic acid was studied in vivo in the rat. Animals were treated intraperitoneally with the sodium salts of VPA, 4-ene VPA, (E)-2,4-diene VPA, 4-pentenoic or (E)-2,4-pentadienoic acids, and methylated bile and urine extracts were analyzed by LC/MS/MS and GC/MS techniques. The alpha,beta-unsaturated reactive metabolite of 4-Pentenoic acid, 3-oxo-4-pentenoic acid, was isolated and identified as its thiol conjugates. In contrast, 3-oxo-4-ene VPA or its thiol conjugates could not be demonstrated as metabolites even though synthetic standards were available to facilitate their detection. Isolation of the thiol conjugates of 3-oxo-4-pentenoic acid provides the first direct spectroscopic evidence for the in vivo formation of the metabolite of 4-Pentenoic acid considered responsible for the irreversible inhibition of fatty acid metabolism. The biliary and urinary metabolite profiles of 4-ene VPA and 4-Pentenoic acid revealed basic differences between the in vivo metabolism of these two unsaturated carboxylic acids.