Absorption, Distribution and Excretion
The rate of intestinal absorption and hepatic uptake of medium chain fatty acids (MCFA) was investigated in 6 pigs. The pigs were fitted with a permanent fistula in the duodenum, and catheters in the portal vein, carotid artery and hepatic vein. Decanoic acid (esterified with octanoic acid) was infused into the duodenum for 1 hr. Regular blood samples were taken over 12 hr and analysed for non-esterified decanoic acid content. Decanoic acid levels in portal vein blood rose sharply after the beginning of the infusion (confirming data previously reported for dogs and rats), and showed a bi-phasic time course with 2 maximum values (at 15 min and 75 to 90 min). 54% of the decanoic acid was recovered in portal blood samples. The amt of non-esterified MCFA taken up per hr by the liver were close to those absorbed from the gut via the portal vein, showing that the liver is the main site of MCFA metabolism in pigs. /Decanoic acid esterified with octanoic acid as medium-chain triacylglycerols/
The influence of pancreatic enzyme secretion on the intestinal absorption of medium-chain fatty acids (MCFA) was investigated in 3 pigs. The pancreatic ducts were ligated (so producing exocrine pancreatic deficiency) and fitted with a permanent fistula, and catheters fitted in the portal vein and carotid artery. The decanoic acid triacylglycerol mixture was infused into the duodenum for 1 hr. Blood samples were taken over 8 hr and analysed for non-esterified decanoic acid content. Decanoic acid level incr slowly after the start of the infusion, reaching a max after 90 to 120 min. This contrasts with previous studies ... where healthy pigs reached a max blood concn after 15 min. This indicates that pancreatic lipase activity is not the pathway for de-esterification of MCFA. 27% of the decanoic acid was recovered from the portal blood flow. This is lower than seen previously, but confirms that more than one pathway is involved as decanoic acid production was not completely suppressed. /Decanoic acid esterified with octanoic acid as medium-chain triacylglycerols/
The influence of triglyceride structure on intestinal absorption was investigated. The triglycerides were composed of octanoic (C8), decanoic (C10) and linoleic (C18:2) acids (either as a structured oil, with the C8 and C10 at the sn-1 and sn-3 positions, or as a randomized oil, with the 3 acids in a random distribution). Absorption of the 3 acids varied; absorption of the C18:2 was highest from the structured oil, when it occupied the sn-2 position. Absorption of the 2 shorter chain fatty acids was highest from the randomized oil, when both acids occupied the sn-2 position approximately 33% of the time.
(14)C-labelled fatty acids (including 240 mg decanoic acid) were fed by intubation into lactating rabbits. The animals were killed 24 hr later, and the mammary gland lipids were analyzed. Decanoic acid was extensively metabolized. Resynthesis after degradation to C2 units led to uniform alternate labelling in the C2-C10 acids, whereas C12-C18 acids had an excess of (14)C at the carboxyl end. Acids formed by beta-oxidation down to C12 (but not below) were also present in the mammary gland lipids.
For more Absorption, Distribution and Excretion (Complete) data for DECANOIC ACID (8 total), please visit the HSDB record page.

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Metabolism / Metabolites
The rate of intestinal absorption and hepatic uptake of medium chain fatty acids (MCFA) was investigated in 6 pigs. The pigs were fitted with a permanent fistula in the duodenum, and catheters in the portal vein, carotid artery and hepatic vein. Decanoic acid (esterified with octanoic acid) was infused into the duodenum for 1 hr. regular blood samples were taken over 12 hr and analysed for non-esterified decanoic acid content ... The amt of non-esterified MCFA taken up per hr by the liver were close to those absorbed from the gut via the portal vein, showing that the liver is the main site of MCFA metabolism in pigs. /Decanoic acid esterified with octanoic acid as medium-chain triacylglycerols/
Capric acid is metabolized by the 13-oxidative pathway, giving rise to C8- and C6-dicarboxylic acids (suberic and adipic acids) in rats. Capric acid metabolism also produced ketone bodies in rats, rabbits, dogs, piglets, and goats. Activation of lipid metabolism by starvation, fat-feeding, and experimental diabetes increased the extent of ketosis in rats. omega-Oxidation, leading to the excretion of sebacic acid, and chain elongation reactions have been reported. Metabolism of capric acid is rapid; in humans given [1-14C]decanoic acid orally, about 52% of the radioactivity was recovered within 2.5 to 4 hr.
(14)C-labelled fatty acids (including 240 mg decanoic acid) were fed by intubation into lactating rabbits. The animals were killed 24 hr later, and the mammary gland lipids were analyzed. Decanoic acid was extensively metabolized. Resynthesis after degradation to C2 units led to uniform alternate labelling in the C2-C10 acids, whereas C12-C18 acids had an excess of (14)C at the carboxyl end. Acids formed by beta-oxidation down to C12 (but not below) were also present in the mammary gland lipids.
Capric acid (decanoic acid) is rapidly metabolized by the β-oxidative pathway, giving rise to C8- and C6-dicarboxylic acids (T29). The enzyme MCAD (medium-chain acyl-CoA dehydrogenase) is responsible for the dehydrogenation step of fatty acids with chain lengths between 6 and 12 carbons as they undergo beta-oxidation in the mitochondria. Fatty acid beta-oxidation provides energy after the body has used up its stores of glucose and glycogen. This typically occurs during periods of extended fasting or illness when caloric intake is reduced, and energy needs are increased. Beta-oxidation of long chain fatty acids produces two carbon units, acetyl-CoA and the reducing equivalents NADH and FADH2. NADH and FADH2 enter the electron transport chain and are used to make ATP. Acetyl-CoA enters the Krebs Cycle and is also used to make ATP via the electron transport chain and substrate level phosphorylation. When the supply of acetyl-CoA (coming from the beta-oxidation of fatty acids) exceeds the capacity of the Krebs Cycle to metabolize acetyl-CoA, the excess acetyl-CoA molecules are converted to ketone bodies (acetoacetate and beta-hydroxybutyrate) by HMG-CoA synthase in the liver. Ketone bodies can also be used for energy especially by the brain and heart; in fact they become the main sources of energy for those two organs after day three of starvation. (Wikipedia)

Toxicity Summary
It has been demonstrated that octanoic (OA) and decanoic (DA) acids compromise the glycolytic pathway and citric acid cycle functioning, increase oxygen consumption in the liver and inhibit some activities of the respiratory chain complexes and creatine kinase in rat brain (A15454, A15455). These fatty acids were also shown to induce oxidative stress in the brain (A15456). Experiments suggest that OA and DA impair brain mitochondrial energy homeostasis that could underlie at least in part the neuropathology of MCADD. (A15457)

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Toxicity Data
LD50: 3730 mg/kg (Oral, Rat) (MSDS) LD50: 1770 mg/kg (Dermal, Rabbit) (MSDS)

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Interactions
The effects of sodium caprate and sodium caprylate on transcellular permeation routes were examined in rats. The release of membrane phospholipids was significantly increased only by caprate, while protein release did not change from the control in the presence of caprate or caprylate, indicating that the extent of membrane disruption was insufficient to account for the extent of the enhanced permeation. Using brush border membrane vesicles prepared from colon, with their protein and lipid component labeled by fluorescent probes, the perturbing actions of caprate and caprylate toward the membrane were examined by fluorescence polarization. Caprate interacted with membrane protein and lipids, and caprylate mainly with protein, causing perturbation to the membrane. The release of 5(6)-carboxyfluorescein previously included in brush border membrane vesicles was increased by caprate but not by caprylate. These results suggest that caprate enhances permeability via the transcellular route through membrane perturbation. /Sodium caprate/
Skin permeation rates were measured in vitro using human skin samples. 6 model cmpd of diverse physicochemical properties were dissolved in propylene glycol, and the permeation rates studied in the presence and absence of various fatty acids (including decanoic and neodecanoic acid). Both decanoic and neodecanoic acid increased the skin diffusivity of 4 of the 6 model cmpd, but only decanoic acid incr the permeation rate of propylene glycol ...
The in vitro human skin permeation rate of an analgesic (buprenorphine) was incr by a factor of 3.5 by the addition of 0.5% decanoic acid.
The enhancing action of decanoic acid on the intestinal absorption of phenosulfonphthalein (PSP) was studied in rats. Decanoic acid and 2 hydroxy derivatives enhanced PSP absorption to varying degrees; PSP was no longer absorbed once the enhancer had been completely absorbed. Absorption enhancement correlated with the ability to sequester calcium ions.
For more Interactions (Complete) data for DECANOIC ACID (7 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat oral 3320 mg/kg
LD50 Rat oral 3730 mg/kg /mix isomers/
LD50 Rat oral 15800 mg/kg /5% decanoic acid in 40% w/w ethanol/
LD50 Mouse iv 129 mg/kg
For more Non-Human Toxicity Values (Complete) data for DECANOIC ACID (6 total), 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 family of triglycerides, containing predominantly, caprylic (C(8)) and capric (C(10)) fatty acids with lesser amounts of caproic (C(6)) and lauric (C(12)) fatty acids. MCTs are widely used for parenteral nutrition in individuals requiring supplemental nutrition and are being more widely used in foods, drugs and cosmetics.
Children who suffer from seizures which are not controllable by drugs have apparently been successfully treated with MCT (medium chain triglyceride) diet. The MCT diet is an emulsion containing primarily (81%) octanoic acid, but also contains 15% decanoic acid ... /Medium chain triglyceride/
/EXPL THER/ ... The clinical situations requiring total parenteral nutrition (TPN) are associated with metabolic processes mediated by insulin ... Decanoic acid was a potent /insulin/ stimulator in /an isolated perfused mouse islet/ model.
/EXPL THER/ The treatment for patients with genetic disorders of mitochondrial long-chain fatty acid beta-oxidation is directed toward providing sufficient sources of energy for normal growth and development, and at the same time preventing the adverse effects that precipitate or result from metabolic decompensation. Standard of care treatment has focused on preventing the mobilization of lipids that result from fasting and providing medium-chain triglycerides (MCT) in the diet in order to bypass the long-chain metabolic block. MCTs that are currently available as commercial preparations are in the form of even-chain fatty acids that are predominately a mixture of octanoate and decanoate ... The even-numbered medium-chain fatty acids (MCFAs) that are found in MCT preparations can reduce the accumulation of potentially toxic long-chain metabolites of fatty acid oxidation (FAO) ... /Decanoate/
For more Therapeutic Uses (Complete) data for DECANOIC ACID (6 total), 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.)