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Decanoic acid Sale

(Synonyms: 癸酸) 目录号 : GC33602

Capric acid (DA, Decanoic acid, Decylic acid), a component of medium-chain triclycerides occurring naturally in coconut oil and palm kernel oil, contributes to seizure control through direct AMPA receptor inhibition. Capric acid is also a modulating ligand for PPARs. Due to its specific melting range the product may be solid, liquid, a solidified melt or a supercooled melt.

Decanoic acid Chemical Structure

Cas No.:334-48-5

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产品描述

Capric acid (DA, Decanoic acid, Decylic acid), a component of medium-chain triclycerides occurring naturally in coconut oil and palm kernel oil, contributes to seizure control through direct AMPA receptor inhibition. Capric acid is also a modulating ligand for PPARs. Due to its specific melting range the product may be solid, liquid, a solidified melt or a supercooled melt.

[1] Katrin Augustin, et al. Epilepsia. 2018 Nov;59(11):e172-e178. [2] Raghu R V Malapaka, et al. J Biol Chem. 2012 Jan 2;287(1):183-95.

Chemical Properties

Cas No. 334-48-5 SDF
别名 癸酸
Canonical SMILES CCCCCCCCCC(O)=O
分子式 C10H20O2 分子量 172.27
溶解度 DMSO : ≥ 130 mg/mL (754.63 mM) 储存条件 Store at RT
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1 mg 5 mg 10 mg
1 mM 5.8048 mL 29.0242 mL 58.0484 mL
5 mM 1.161 mL 5.8048 mL 11.6097 mL
10 mM 0.5805 mL 2.9024 mL 5.8048 mL
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Research Update

Decanoic acid Stimulates Autophagy in D. discoideum

Cells 2021 Oct 29;10(11):2946.PMID:34831171DOI:10.3390/cells10112946.

Ketogenic diets, used in epilepsy treatment, are considered to work through reduced glucose and ketone generation to regulate a range of cellular process including autophagy induction. Recent studies into the medium-chain triglyceride (MCT) ketogenic diet have suggested that medium-chain fatty acids (MCFAs) provided in the diet, Decanoic acid and octanoic acid, cause specific therapeutic effects independent of glucose reduction, although a role in autophagy has not been investigated. Both autophagy and MCFAs have been widely studied in Dictyostelium, with findings providing important advances in the study of autophagy-related pathologies such as neurodegenerative diseases. Here, we utilize this model to analyze a role for MCFAs in regulating autophagy. We show that treatment with Decanoic acid but not octanoic acid induces autophagosome formation and modulates autophagic flux in high glucose conditions. To investigate this effect, Decanoic acid, but not octanoic acid, was found to induce the expression of autophagy-inducing proteins (Atg1 and Atg8), providing a mechanism for this effect. Finally, we demonstrate a range of related fatty acid derivatives with seizure control activity, 4BCCA, 4EOA, and Epilim (valproic acid), also function to induce autophagosome formation in this model. Thus, our data suggest that Decanoic acid and related compounds may provide a less-restrictive therapeutic approach to activate autophagy.

RIFM fragrance ingredient safety assessment, Decanoic acid, CAS Registry Number 334-48-5

Food Chem Toxicol 2020 Oct 15;144 Suppl 1:111465.PMID:32640335DOI:10.1016/j.fct.2020.111465.

The existing information supports the use of this material as described in this safety assessment. Decanoic acid was evaluated for genotoxicity, repeated dose toxicity, reproductive toxicity, local respiratory toxicity, phototoxicity/photoallergenicity, skin sensitization, and environmental safety. Data on the target material and from read-across analog nonanoic acid (CAS # 112-05-0) show that Decanoic acid is not expected to be genotoxic. Data on read-across analog octanoic acid (CAS # 124-07-2) provide a calculated MOE >100 for the repeated dose and reproductive toxicity endpoints. Based on the existing data, Decanoic acid does not present a concern for skin sensitization under the current, declared levels of use. The phototoxicity/photoallergenicity endpoints were evaluated based on UV spectra; Decanoic acid is not expected to be phototoxic/photoallergenic. The local respiratory toxicity endpoint was evaluated using the TTC for a Cramer Class I material, and the exposure to Decanoic acid is below the TTC (1.4 mg/day). The environmental endpoints were evaluated; Decanoic acid was found not to be PBT as per the IFRA Environmental Standards, and its risk quotients, based on its current volume of use in Europe and North America (i.e., PEC/PNEC), are <1.

New insights into the mechanisms of the ketogenic diet

Curr Opin Neurol 2017 Apr;30(2):187-192.PMID:28141738DOI:10.1097/WCO.0000000000000432.

Purpose of review: High-fat, low-carbohydrate ketogenic diets have been used for almost a century for the treatment of epilepsy. Used traditionally for the treatment of refractory pediatric epilepsies, in recent years the use of ketogenic diets has experienced a revival to include the treatment of adulthood epilepsies as well as conditions ranging from autism to chronic pain and cancer. Despite the ability of ketogenic diet therapy to suppress seizures refractory to antiepileptic drugs and reports of lasting seizure freedom, the underlying mechanisms are poorly understood. This review explores new insights into mechanisms mobilized by ketogenic diet therapies. Recent findings: Ketogenic diets act through a combination of mechanisms, which are linked to the effects of ketones and glucose restriction, and to interactions with receptors, channels, and metabolic enzymes. Decanoic acid, a component of medium-chain triclycerides, contributes to seizure control through direct α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor inhibition, whereas drugs targeting lactate dehydrogenase reduce seizures through inhibition of a metabolic pathway. Ketogenic diet therapy also affects DNA methylation, a novel epigenetic mechanism of the diet. Summary: Ketogenic diet therapy combines several beneficial mechanisms that provide broad benefits for the treatment of epilepsy with the potential to not only suppress seizures but also to modify the course of the epilepsy.

Organo-Soluble Decanoic Acid-Modified Ni-Rich Cathode Material LiNi0.90Co0.07Mn0.03O2 for Lithium-Ion Batteries

ACS Appl Mater Interfaces 2022 Apr 13;14(14):16348-16356.PMID:35353483DOI:10.1021/acsami.2c02797.

Ni-rich layered oxides as cathode materials deliver a higher capacity than those used currently, in hopes of improving the energy density of Li-ion batteries. However, the surface residual alkali and the interfacial parasitic reactions caused by the rich nickel bring a series of problems such as surface slurrying, structure deterioration, mechanical fracture, and capacity decay. Herein, different from the common surface coating strategies with inorganics, an organo-soluble acid modification approach is proposed to meet the challenges. For LiNi0.90Co0.07Mn0.03O2 (NCM90), Decanoic acid can react with the residual lithium salts on the surface to form an organic lithium salt-dominant modification layer. During cycling, an organic lithium-involved cathode/electrolyte interface (CEI) layer is rapidly formed. Specially, the solubility of Decanoic acid in the organic electrolyte makes the CEI layer keep strong interaction with NCM90, thin but effective. Consequently, the modified NCM90 exhibits notable performances in terms of structural stability, mechanical integrity, and capacity retention.

Decanoic acid modification enhances the antibacterial activity of PMAP-23RI-Dec

Eur J Pharm Sci 2021 Feb 1;157:105609.PMID:33141035DOI:10.1016/j.ejps.2020.105609.

Antimicrobial peptides are a new type of antibacterial drugs with a broad antibacterial spectrum. Based on our previous research, PMAP-23RI-Dec was designed by modifying the C-terminal of PMAP-23RI with Decanoic acid. In this study, we measured the antibacterial activity, stability, hemolysis, and cytotoxicity of PMAP-23RI-Dec. The mechanism of PMAP-23RI-Dec on biofilm and cell membranes were also studied. The results show that PMAP-23RI-Dec exhibited high antibacterial activity and stability, but the hemolytic activity and cytotoxicity of PMAP-23RI-Dec were not enhanced. Moreover, PMAP-23RI-Dec could inhibit biofilm formation at low concentrations, and enhance the killing effect on bacteria by changing the permeability of their cell membranes. Finally, PMAP-23RI-Dec reduced Pseudomonas aeruginosa GIM1.551 and Staphylococcus aureus ATCC25923 damage to organs, and showed superior efficacy against peritonitis. PMAP-23RI-Dec also reduced the scope of abscess and alleviated wound infections. Our research indicated that PMAP-23RI-Dec is a new antibacterial agent with potential clinical application.