Absorption, Distribution and Excretion
This study investigated the intestinal absorption and hepatic uptake of medium-chain fatty acids (MCFAs) in six pigs. A permanent fistula was implanted in the duodenum of the pigs, with catheters inserted into the portal vein, carotid artery, and hepatic vein, respectively. Decanoic acid (octyl esterified) was injected into the duodenum 1 hour later. Blood samples were collected periodically over 12 hours, and the content of unesterified decanoic acid was analyzed. Decanoic acid levels in portal venous blood rapidly increased after the start of infusion (consistent with previously reported data in dogs and mice) and exhibited a biphasic time course with two peaks (at 15 minutes and 75–90 minutes, respectively). 54% of decanoic acid was recovered from the portal venous blood samples. The amount of unesterified MCFA absorbed by the liver per hour was close to the amount absorbed from the intestine via the portal vein, indicating that the liver is the primary site of MCFA metabolism in pigs. /Cecapanoic acid forms medium-chain triglycerides with octyl esterification/ This study investigated the effect of pancreatic enzyme secretion on intestinal absorption of medium-chain fatty acids (MCFAs) in three pigs. The pancreatic duct was ligated (causing exocrine pancreatic insufficiency), and a permanent fistula was established, with catheters inserted into the portal vein and carotid artery. A mixture of decanoic acid and triglycerides was injected into the duodenum 1 hour later. Blood samples were collected within 8 hours, and the content of unesterified decanoic acid was analyzed. Decanoic acid levels rose slowly after the start of infusion, peaking after 90 to 120 minutes. This contrasts with previous findings… previous studies showed that healthy pigs reached peak blood concentrations after 15 minutes. This indicates that pancreatic lipase activity is not the pathway for medium-chain fatty acid (MCFA) deesterification. 27% of decanoic acid was recovered from the portal venous bloodstream. While this percentage is lower than previous findings, it confirms that more than one pathway is involved, as decanoic acid production was not completely inhibited. /Cecaprylic acid esterifies with caprylic acid to form medium-chain triglycerides/
The effect of triglyceride structure on intestinal absorption was investigated. Triglycerides are composed of caprylic acid (C8), capric acid (C10), and linoleic acid (C18:2) (existing in structured oils, with C8 and C10 located at sn-1 and sn-3 positions, respectively; or in random oils, with the three acids randomly distributed). The absorption of these three acids varies; when C18:2 occupies the sn-2 position, its absorption rate in structured oils is the highest. When the probability of the two short-chain fatty acids occupying the sn-2 position is about 33%, their absorption rate in randomized oils is the highest.
(14)C-labeled fatty acids (including 240 mg of capric acid) were administered to lactating rabbits via cannulation. The animals were sacrificed 24 hours later, and mammary gland lipids were analyzed. Capric acid was extensively metabolized. After degradation into C2 units, it was resynthesized, resulting in uniform alternating labeling of C2-C10 fatty acids, while the carboxyl terminus of C12-C18 fatty acids had an excess of (14)C. Fatty acids β-oxidized to C12 (but not below C12) are also present in mammary lipids. For more complete data on the absorption, distribution, and excretion of decanoic acid (8 types), please visit the HSDB record page. Metabolism/Metabolites This study investigated the intestinal absorption and hepatic uptake of medium-chain fatty acids (MCFAs) in six pigs. A permanent fistula was implanted in the duodenum of the pigs, and catheters were inserted into the portal vein, carotid artery, and hepatic vein. Decanoic acid (caprylylated) was injected into the duodenum for 1 hour. Blood samples were collected periodically over 12 hours, and the content of unesterified decanoic acid was analyzed… The amount of unesterified medium-chain fatty acids (MCFAs) absorbed by the liver per hour was close to the amount absorbed from the intestine via the portal vein, indicating that the liver is the main site of MCFA metabolism in pigs. /Cecapanoic acid forms medium-chain triacylglycerols with caprylylated octanoic acid/ Decanoic acid is metabolized via the 13-oxidation pathway, producing C8 and C6 dicarboxylic acids (caprylic acid and adipic acid) in rats. Decanoic acid metabolism also produces ketone bodies in rats, rabbits, dogs, piglets, and goats. Starvation, high-fat feeding, and experimental diabetes activate lipid metabolism, increasing the degree of ketosis in rats. ω-oxidation has been reported to lead to the excretion of sebacic acid and the occurrence of chain elongation reactions. Decanoic acid metabolism is rapid; in humans orally administered [1-14C]decanoic acid, approximately 52% of the radioactivity is recovered within 2.5 to 4 hours.
(14)C-labeled fatty acids (including 240 mg of decanoic acid) were administered via cannulation to lactating rabbits. The animals were sacrificed 24 hours later, and mammary lipids were analyzed. Decanoic acid was extensively metabolized. It was degraded to C2 units and then resynthesized, resulting in a uniform alternating labeling of C2-C10 fatty acids, while the C12-C18 fatty acids had excess (14)C at the carboxyl terminus. Fatty acids that were β-oxidized to C12 (but not lower) were also present in mammary lipids. Decanoic acid (decanoic acid) is rapidly metabolized via the β-oxidation pathway to produce C8 and C6 dicarboxylic acids (T29). Medium-chain acyl-CoA dehydrogenase (MCAD) is responsible for the dehydrogenation step in the β-oxidation process of 6- to 12-carbon fatty acids in mitochondria. Fatty acid β-oxidation provides energy after the body's glucose and glycogen reserves are depleted. This typically occurs during prolonged fasting or illness, when calorie intake is reduced and energy demand increases. β-oxidation of long-chain fatty acids produces two-carbon molecules: acetyl-CoA and reducing equivalents NADH and FADH₂. NADH and FADH₂ enter the electron transport chain for ATP synthesis. Acetyl-CoA enters the tricarboxylic acid cycle and also synthesizes ATP via electron transport and substrate-level phosphorylation. When the supply of acetyl-CoA (from fatty acid β-oxidation) exceeds the Krebs cycle's ability to metabolize acetyl-CoA, excess acetyl-CoA molecules are converted into ketone bodies (acetoacetic acid and β-hydroxybutyrate) in the liver by HMG-CoA synthase. Ketone bodies can also be used as energy, especially for the brain and heart; in fact, after the third day of fasting, ketone bodies become the primary energy source for these two organs. (Wikipedia)

Toxicity Summary
Studies have shown that caprylic acid (OA) and decanoic acid (DA) impair the function of glycolysis and the citric acid cycle, increase hepatic oxygen consumption, and inhibit certain activities of respiratory chain complexes and creatine kinase in the rat brain (A15454, A15455). These fatty acids have also been shown to induce oxidative stress in the brain (A15456). Experiments have shown that OA and DA impair mitochondrial energy homeostasis in the brain, which may be at least partly the basis of the neuropathology of MCADD. (A15457) Toxicity Data
LD50: 3730 mg/kg (oral, rat) (MSDS) LD50: 1770 mg/kg (skin, rabbit) (MSDS) Interactions This study investigated the effects of sodium decanoate and sodium caprylic acid on transcellular permeation pathways in rats. The results showed that only sodium decanoate significantly increased the release of membrane phospholipids, while protein release remained unchanged in the presence of sodium decanoate or sodium caprylate compared to the control group, indicating that the degree of membrane disruption was insufficient to explain the extent of permeability enhancement. The perturbation effects of sodium decanoate and sodium caprylate on the membrane were detected by fluorescence polarization using brush border membrane vesicles prepared from the colon (whose protein and lipid components were labeled with fluorescent probes). Sodium decanoate interacted with membrane proteins and lipids, while sodium caprylate primarily interacted with proteins, leading to membrane perturbation. Decanoate increased the release of 5(6)-carboxyfluorescein previously contained in brush border membrane vesicles, while caprylate had no such effect. These results suggest that decanoate enhances permeability across cellular pathways by perturbing membrane structure. /Sodium Decanoate/
Skin permeation rates were determined in vitro using human skin samples. Six model compounds with different physicochemical properties were dissolved in propylene glycol, and their permeation rates were investigated in the presence and absence of various fatty acids, including decanoic acid and neodecanoic acid. Both decanoic acid and neodecanoic acid increased the skin diffusion rate of four out of six model compounds, but only decanoic acid increased the penetration rate of propylene glycol…
In vitro experiments showed that adding 0.5% decanoic acid increased the human skin penetration rate of the analgesic (buprenorphine) by 3.5 times.
The promoting effect of decanoic acid on the intestinal absorption of benzyl sulfonylurea (PSP) was studied in rats. Decanoic acid and its 2-hydroxy derivatives promoted the absorption of PSP to varying degrees; once the promoter was completely absorbed, PSP was no longer absorbed. The enhanced absorption was associated with the ability to chelate calcium ions.
For more complete data on interactions of decanoic acid (7 compounds in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in rats: 3320 mg/kg
Oral LD50 in rats: 3730 mg/kg /mixed isomers/
Oral LD50 in rats: 15800 mg/kg /5% decanoic acid dissolved in 40% (w/w) ethanol/
Intravenous LD50 in mice: 129 mg/kg
For more complete non-human toxicity data for decanoic acid (6 types), please visit the HSDB record page.

[1]. New insights into the mechanisms of the ketogenic diet. Curr Opin Neurol. 2017 Apr;30(2):187-192.

[2]. Decanoic acid inhibits mTORC1 activity independent of glucose and insulin signaling. Proc Natl Acad Sci U S A. 2020 Sep 22;117(38):23617-23625.

[3]. Decanoic Acid Exerts Its Anti-Tumor Effects via Targeting c-Met Signaling Cascades in Hepatocellular Carcinoma Model. Cancers (Basel). 2023 Sep 22;15(19):4681.

[4]. Seizure control by decanoic acid through direct AMPA receptor inhibition. Brain. 2016 Feb;139(Pt 2):431-43.

[5]. Selective production of decanoic acid from iterative reversal of β-oxidation pathway. Biotechnol Bioeng. 2018 May;115(5):1311-1320.

Therapeutic Uses
Medium-chain triglycerides (MCTs) are a class of triglycerides primarily composed of caprylic acid (C8) and decanoic acid (C10) fatty acids, with smaller amounts of hexanoic acid (C6) and lauric acid (C12) fatty acids. MCTs are widely used in parenteral nutrition for individuals requiring supplemental nutrition and are increasingly used in food, pharmaceuticals, and cosmetics. For children with epilepsy that is uncontrolled by medication, MCT (medium-chain triglyceride) diet therapy appears to have achieved significant efficacy. The MCT diet is an emulsion primarily composed of caprylic acid (81%), but also contains 15% decanoic acid…/medium-chain triglycerides/
/EXPL THER/…Clinical conditions requiring total parenteral nutrition (TPN) are associated with insulin-mediated metabolic processes…decanoic acid is a potent insulin stimulant in an isolated perfused mouse islet model. Treatment for patients with inherited disorders of mitochondrial long-chain fatty acid β-oxidation aims to provide an adequate energy source to maintain normal growth and development, while preventing adverse reactions caused or resulting from metabolic decompensation. Standard treatment focuses on preventing lipid mobilization due to fasting and supplementing the diet with medium-chain triglycerides (MCTs) to bypass long-chain metabolic blockade. Currently available MCT preparations are mainly in the form of even-chain fatty acids, primarily a mixture of caprylic and capric acids… The even-chain medium-chain fatty acids (MCFAs) in MCT preparations can reduce the accumulation of potentially toxic long-chain metabolites during fatty acid oxidation (FAO)… /Cecapric Acid/
For more complete data on the therapeutic uses of decanoic acids (6 types), please visit the HSDB record page.

C10H20O2

172.27

172.146

334-48-5

Decanoic acid-d3;102611-15-4;Decanoic acid-d19;88170-22-3;Decanoic acid-d5;1219803-00-5;Decanoic acid-d2;62716-49-8

2969

Colorless to off-white <27°C powder,>32°C liquid

0.9±0.1 g/cm3

269.6±3.0 °C at 760 mmHg

27-32 °C(lit.)

121.8±11.9 °C

0.0±0.6 mmHg at 25°C

1.443

3.96

1

2

8

12

110

0

CCCCCCCCCC(O)=O

GHVNFZFCNZKVNT-UHFFFAOYSA-N

InChI=1S/C10H20O2/c1-2-3-4-5-6-7-8-9-10(11)12/h2-9H2,1H3,(H,11,12)

decanoic acid

Capric acid; 1-Nonanecarboxylic acid; Decanoic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ≥ 130 mg/mL (~754.63 mM)

Solubility in Formulation 1: ≥ 2.17 mg/mL (12.60 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.7 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.17 mg/mL (12.60 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.7 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.17 mg/mL (12.60 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.7 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)