Pentanoic acid
目录号 : GC33901
Pentanoicacid是一种短链脂肪酸，是细菌代谢产物，与过敏性皮肤病有关系。Pentanoicacid能够激活ROCK信号通路。
Cas No.:109-52-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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Cell experiment: |
PAM212 murine keratinocytes are derived from BALB/c mouse skin. PAM212 cells are cultured in alpha minimal essential medium containing 10% heat-inactivated fetal bovine serum, penicillin G (15 μg/mL), and streptomycin (50 μg/mL) in a humidified atmosphere of 5% CO2/95% air at 37°C. Cells seeded at 50,000 cells/mL are grown for 24 h in culture medium. Cells are stimulated with Pentanoic acid for an appropriate period. Pretreatment with Y-27632, a highly potent and selective inhibitor of Rho-associated, coiled-coil containing protein kinase (ROCK), is carried out for 1 h, whereas pretreatment with YM-254890, a specific Gq/11 inhibitor, is carried out for 30 min[1]. |
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References: [1]. Mizuno N, et al. Pentanoic acid induces thymic stromal lymphopoietin production through Gq/11 and Rho-associated protein kinase signaling pathway in keratinocytes. Int Immunopharmacol. 2017 Sep;50:216-223. |
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Pentanoic acid, a short-chain fatty acid, is a product of bacterial metabolism and are associated with allergic skin disorders. Pentanoic acid activates ROCK signaling pathway.
Pentanoic acid, a short-chain fatty acid, is a product of bacterial metabolism and are associated with allergic skin disorders. Pentanoic acid (0-2 mM) strongly and dose-dependently induces thymic stromal lymphopoietin (TSLP) production in PAM212 cells. Pentanoic acid slightly induces the expression of Tnfa, Il1b and Il6 mRNA, but does not induce the protein levels of TNF-α expression. Pentanoic acid (2 mM) induced-TSLP production in keratinocytes is not related to FFAR2 and FFAR3, but mediated by activating ROCK signaling pathway, and is competetely inhibited by co-inhibition of Gq/11 and the ROCK signaling pathway[1].
[1]. Mizuno N, et al. Pentanoic acid induces thymic stromal lymphopoietin production through Gq/11 and Rho-associated protein kinase signaling pathway in keratinocytes. Int Immunopharmacol. 2017 Sep;50:216-223.
| Cas No. | 109-52-4 | SDF | |
| Canonical SMILES | OC(CCCC)=O | ||
| 分子式 | C5H10O2 | 分子量 | 102.13 |
| 溶解度 | DMSO : ≥ 100 mg/mL (979.14 mM); H2O : 5 mg/mL (48.96 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 | 9.7914 mL | 48.9572 mL | 97.9144 mL |
| 5 mM | 1.9583 mL | 9.7914 mL | 19.5829 mL |
| 10 mM | 0.9791 mL | 4.8957 mL | 9.7914 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。
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.
Mechanism of Inactivation of Neuronal Nitric Oxide Synthase by (S)-2-Amino-5-(2-(methylthio)acetimidamido)Pentanoic acid
J Am Chem Soc 2015 May 13;137(18):5980-9.PMID:25874809DOI:10.1021/jacs.5b01202.
Nitric oxide synthase (NOS) catalyzes the conversion of l-arginine to l-citrulline and the second messenger nitric oxide. Three mechanistic pathways are proposed for the inactivation of neuronal NOS (nNOS) by (S)-2-amino-5-(2-(methylthio)acetimidamido)Pentanoic acid (1): sulfide oxidation, oxidative dethiolation, and oxidative demethylation. Four possible intermediates were synthesized. All compounds were assayed with nNOS, their IC50, KI, and kinact values were obtained, and their crystal structures were determined. The identification and characterization of the products formed during inactivation provide evidence for the details of the inactivation mechanism. On the basis of these studies, the most probable mechanism for the inactivation of nNOS involves oxidative demethylation with the resulting thiol coordinating to the cofactor heme iron. Although nNOS is a heme-containing enzyme, this is the first example of a NOS that catalyzes an S-demethylation reaction; the novel mechanism of inactivation described here could be applied to the design of inactivators of other heme-dependent enzymes.
Inactivation Mechanism of Neuronal Nitric Oxide Synthase by ( S)-2-Amino-5-(2-(methylthio)acetimidamido)Pentanoic acid: Chemical Conversion of the Inactivator in the Active Site
Inorg Chem 2021 Jul 5;60(13):9345-9358.PMID:34137256DOI:10.1021/acs.inorgchem.1c00046.
Neuronal nitric oxide synthase (nNOS) is one of the three isoforms of nitric oxide synthase (NOS). The other two isoforms include inducible NOS (iNOS) and endothelial NOS (eNOS). These three isoforms of NOS are widely present in both human and other mammals and are responsible for the biosynthesis of NO. As an essential biological molecule, NO plays an essential role in neurotransmission, immune response, and vasodilation; however, the overproduction of NO can cause a series of diseases. Thus, the selective inhibition of three isoforms of NOS has been considered to be important in treating related diseases. The active sites of the three enzymes are highly conserved, causing the selective inhibition of the three enzymes to be a great challenge. (S)-2-Amino-5-(2-(methylthio)acetimidamido)Pentanoic acid (1) has been experimentally proved to be a selective and time-dependent irreversible inhibitor of nNOS, and three pathways, including sulfide oxidation, oxidative dethiolation, and oxidative demethylation, have been suggested. In this work, we performed quantum mechanics/molecular mechanics calculations to verify the chemical conversion of inactivator 1. Although we agree with the previously suggested chemical transformation process, our calculations demonstrated that there are lower energy pathways to accomplish both oxidative dethiolation and oxidative demethylation. These three branching reactions are competitive, but only dethiolation and demethylation reactions can generate inhibitory intermediates. As a powerful time-dependent irreversible inhibitor of nNOS, the key sulfur atom and middle imine are all necessary. Our calculation results not only verified the chemical reaction of inhibitor 1 occurring in the enzymatic active site but also explained the inactivation mechanism of inhibitor 1. This is also the first verified example of the heme-enzyme-catalyzed S-demethylation mechanism.
2,5-Bis-(2-hydroxybenzoylamino)Pentanoic acid, a salicylic acid-metabolite isolated from chicken: characterization and independent synthesis
Bioorg Med Chem Lett 2003 Feb 10;13(3):335-7.PMID:12565924DOI:10.1016/s0960-894x(02)01021-1.
From excreta of chickens that had been treated with sodium salicylate, a new compound was detected and identified as a double conjugated ornithine metabolite. The structural assignment of this metabolite was further confirmed by an independent efficient 3-step synthesis from ornithine.
The effects of 4-pentenoic and Pentanoic acid on the hypoxic rat atria
Arch Int Physiol Biochim 1989 Oct;97(5):375-80.PMID:2480093DOI:10.3109/13813458909104550.
When exposed to hypoxia, the isolated rat atria released lactate into the bathing medium and underwent a rise in resting tension and a decline of the contractions frequency. In some of them, it also occurred a complete cessation of the pacemaker activity. Atria from 24-h fasted rats, when compared to those from fed ones, exhibited a lower lactate output, a higher rise in resting tension, a faster decay of the contraction frequency and an increased occurrence of atrial arrest. In both the fed and fasted rats atria, some triacylglycerol lipolysis remained throughout the hypoxic incubation. Addition of 2 mM 4-pentenoic acid abolished the lipolytic activity and reduced lactate output in both groups of atria. In the fed rats atria it also accelerated the decrease of the pacemaker frequency. Pentanoic acid reduced lactate output in both groups of atria and in those from fed rats it did not alter lipolysis but increased the rise in resting tension, the decline of the pacemaker frequency and the occurrence of atrial arrest. Present data indicate that although 4-pentenoic acid inhibits fatty acid oxidation and endogenous lipolysis, it was not able to reduce the noxious effects of hypoxia. Since the effects of 4-pentenoic acid were rather similar to those of fasting and Pentanoic acid, they might be ascribed to the accumulation of its own oxidative metabolites which could be detrimental for the hypoxic atria.