Dodecanedioic acid is a human endogenous metabolite that targets metabolic pathways involved in energy metabolism. It functions as an EC 1.1.1.1 (alcohol dehydrogenase) inhibitor. As a dicarboxylic acid, it participates in the β-oxidation pathway and can be metabolized to produce energy. The compound is an alpha,omega-dicarboxylic acid and a dicarboxylic fatty acid. Its role as an energy substrate makes it relevant for studies of metabolic disorders, including diabetes and obesity.

In vitro studies have shown that dodecanedioic acid can be utilized as an energy substrate by various cell types. It is involved in metabolic pathways intermediate to those of lipids and carbohydrates. The compound's ability to serve as an alternative energy source has been investigated in the context of metabolic diseases. It has been shown to modulate energy metabolism and may have effects on mitochondrial function. The compound's role as an alcohol dehydrogenase inhibitor suggests it may affect alcohol metabolism pathways.

In five NIDDM patients with good metabolic control (HbA1C 5.0-6.2%, off metformin for 3 days) and five healthy controls, a continuous intravenous infusion of 46.6 mmol dodecanedioic acid (as 0.4 M sodium salt solution in saline) was administered over 195 min at a constant rate of 0.24 mmol/min. Plasma glucose levels significantly decreased in NIDDM patients from 7.8 ± 0.6 mM (basal) to 5.4 ± 0.8 mM at the end of the 360-min study period (P<0.05), reaching normal range, while no significant change occurred in controls (4.7 ± 0.1 to 4.4 ± 0.04 mM). [1]
Plasma insulin levels did not change significantly in either group, indicating that C12 does not stimulate insulin secretion. [1]
Plasma lactate concentration significantly decreased in NIDDM patients from 3.5 ± 0.2 to 1.5 ± 0.1 mM (P<0.001), while no change was observed in controls. Blood pyruvate increased in NIDDM patients from 26.0 ± 11.6 to 99.5 ± 14.9 μM (P<0.01), with no significant change in controls. [1]
Free fatty acids (FFA) decreased in diabetic patients from 1,500 ± 250 to 875 ± 341 μM (ns), while controls had basal FFA 750 ± 128 μM. [1]
Plasma ketone bodies (β-hydroxybutyrate + acetoacetate) did not change significantly in either group (controls: 235 ± 6 to 241 ± 7 μmol; NIDDM: 240 ± 5 to 246 ± 6 μmol). [1]
Indirect calorimetry showed no significant increase in VO₂ consumption, indicating minimal thermogenic effect. The nonprotein respiratory quotient (npRQ) decreased basally to 0.78 ± 0.02 in NIDDM, close to the theoretical RQ for C12 oxidation (0.77), suggesting C12 oxidation. [1]
No significant reduction in basal plasma glucose was observed in NIDDM patients during saline infusion (control experiment). [1]
In vivo, dodecanedioic acid has been studied for its effects on energy metabolism and metabolic disorders. As a human endogenous metabolite, it is naturally present in the body and participates in normal metabolic processes. The compound has been investigated as a potential therapeutic agent for metabolic diseases, including diabetes and obesity, due to its role as an alternative energy substrate. Studies have examined its effects on glucose and lipid metabolism in animal models of metabolic disease.

In cell-free biochemical assays, dodecanedioic acid is evaluated for its inhibitory activity against alcohol dehydrogenase (EC 1.1.1.1). Enzyme activity assays measure the compound's ability to inhibit the conversion of alcohols to aldehydes or ketones. The compound's role as a metabolic intermediate is studied using in vitro enzyme systems that reconstitute fatty acid oxidation pathways. These assays help elucidate the compound's mechanism of action in energy metabolism.

Cellular assays for dodecanedioic acid involve evaluating its effects on energy metabolism in various cell lines. The compound's ability to serve as an alternative energy substrate is assessed by measuring cellular oxygen consumption, ATP production, and metabolic flux. Studies have investigated its effects on mitochondrial function and fatty acid oxidation in hepatocytes, adipocytes, and other cell types. The compound's effects on glucose metabolism and insulin sensitivity are also studied in cellular models of metabolic disease.

Five patients with non-insulin-dependent diabetes mellitus (NIDDM) and five healthy controls (matched for gender, age, and BMI) participated. NIDDM patients were treated with oral hypoglycemic agents (metformin 850 mg ×2 daily) which was stopped 3 days before the experiment; short-acting human insulin was administered before meals during that period. After an overnight fast, a continuous intravenous infusion of dodecanedioic acid (0.4 M sodium salt solution in saline) was administered at a constant rate of 0.24 mmol/min for 195 min using an electric syringe pump. Infusion solutions were sterilized through 0.25 μm Millipore filters before administration. Blood samples (8 mL) were taken every 15 min for 360 min. Heparinized blood was centrifuged, and plasma was frozen at -20°C. Aliquots (5 mL) were used for pyruvate analysis. Twenty-four-hour urine was collected in containers with 0.1% sodium azide. Indirect calorimetry was continuously performed starting 45 min before and for 600 min after the infusion using a Deltatrac apparatus. [1]
Animal studies for dodecanedioic acid typically involve models of metabolic disease, including diet-induced obesity, diabetes, and dyslipidemia. The compound is administered orally or intraperitoneally to evaluate its effects on energy metabolism, glucose homeostasis, and lipid profiles. Pharmacokinetic parameters are derived from plasma concentration-time curves after administration. Studies have examined the compound's effects on body weight, insulin sensitivity, and metabolic markers in rodent models.

The average 24-hour urinary excretion of dodecanedioic acid was 3.0 ± 0.8 mmol in NIDDM patients and 3.1 ± 0.1 mmol in controls, corresponding to approximately 6.5% and 6.7% of the administered dose (46.6 mmol), respectively. This low urinary excretion is due to tubular reabsorption. [1]
Plasma C12 concentration reached a peak after 135 min of infusion in both groups (1.2 ± 0.2 μM in both). Area under the curve (AUC) of plasma C12 was 279.9 ± 42.7 μmol in NIDDM and 219.7 ± 14.0 μmol in controls (P = ns). [1]
Urinary urea loss over 24 h was 4.8 ± 1.0 g in NIDDM and 5.1 ± 1.1 g in controls (within normal range, ns). [1]
Pharmacokinetic data for dodecanedioic acid show that it is water-soluble and can be absorbed and metabolized through normal metabolic pathways. As an endogenous metabolite, it is naturally present in the body and is metabolized through β-oxidation. The compound has a molecular weight of 230.30 g/mol with a formula of C12H22O4. It is a medium-chain dicarboxylic acid that can be utilized as an energy source. The SMILES notation is OC(=O)CCCCCCCCCCC(O)=O.

Interactions
At a concentration of 1.0 mmol, dicarboxylic acids reduced the neuromuscular inhibitory effect of 10⁻⁶ mmol D-tuboCularine in isolated rat hemidiaphragmatic nerve. The β-oxidation rate of dodecanoic acid in rat liver homogenate was determined by simultaneously measuring the change in the rate of incubation of C6-C12 dicarboxylic acids with dodecanoic acid over time. In clofibrate-treated rat liver homogenate, the β-oxidation rate of C8-C12 dicarboxylic acids was significantly increased. 2.0 mmol cyanide did not inhibit the β-oxidation rate but slightly increased it in homogenates from normal rats and clofibrate-treated rats. These results strongly suggest the presence of β-oxidation of dicarboxylic acids in the peroxisome.

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No significant adverse effects or toxicity were reported. Urinary nitrogen loss was within normal range. The infusion was well tolerated. No mention of LD50, hepatotoxicity, nephrotoxicity, or other toxicity parameters. [1]
Dodecanedioic acid is considered to have low toxicity as it is a human endogenous metabolite. It is naturally present in the body and participates in normal metabolic processes. The compound is water-soluble and is metabolized through normal fatty acid oxidation pathways. No significant toxicity has been reported for this endogenous metabolite. Standard safety precautions for handling laboratory chemicals apply.

[1]. The metabolic effect of dodecanedioic acid infusion in non-insulin-dependent diabetic patients. Nutrition. 1998 Apr;14(4):351-7.

Dodecanoic acid is an α,ω-dicarboxylic acid, a product of the oxidation of the methyl group in dodecane to the corresponding carboxylic acid. It is an EC 1.1.1.1 (alcohol dehydrogenase) inhibitor and a human metabolite. It is an α,ω-dicarboxylic acid and dicarboxylic acid fatty acid, the conjugate acid of dodecanoic acid ester (2-), derived from the hydride of dodecane. Dodecanoic acid has been reported in fruit flies, humans, and several other organisms with relevant data. See also: Nylon 612 (molecular weight 14000) (monomer); Nylon 612 (molecular weight 18000) (monomer).

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Dodecanedioic acid (C12) is a dicarboxylic acid that serves as an alternate fuel substrate. Its β-oxidation yields acetyl-CoA and succinyl-CoA, the latter entering the Krebs cycle and potentially supporting gluconeogenesis. In NIDDM patients, C12 infusion decreased plasma glucose to normal range without affecting insulin levels, reduced lactate, and increased pyruvate, suggesting increased gluconeogenesis from pyruvate and glycogen formation. C12 has very low urinary excretion (≈6.5-6.7%) compared to other dicarboxylic acids like sebacate (up to 45%), making it more suitable for clinical use. It is water-soluble, can be administered intravenously, and has minimal thermogenic effect. Potential clinical applications include parenteral nutrition and treatment of NIDDM where glucose oxidation is impaired. [1]
DDodecanedioic acid is a human endogenous metabolite and an EC 1.1.1.1 (alcohol dehydrogenase) inhibitor. It is a straight-chain dicarboxylic acid that serves as an alternative energy substrate, facilitating energy metabolism between lipids and carbohydrates. The compound belongs to the class of organic compounds known as medium-chain fatty acids. It has been investigated for potential therapeutic applications in metabolic diseases, including diabetes and obesity. The CAS number is 693-23-2. The compound is for research use only and not for human use.

C12H22O4

230.3

230.151

693-23-2

Dodecanedioic acid-d20;89613-32-1;Dodecanedioic acid-d4;97543-02-7

12736

White to off-white solid powder

1.1±0.1 g/cm3

394.0±0.0 °C at 760 mmHg

127-129 °C(lit.)

216.6±17.7 °C

0.0±1.9 mmHg at 25°C

1.475

2.92

2

4

11

16

179

0

TVIDDXQYHWJXFK-UHFFFAOYSA-N

InChI=1S/C12H22O4/c13-11(14)9-7-5-3-1-2-4-6-8-10-12(15)16/h1-10H2,(H,13,14)(H,15,16)

dodecanedioic acid

1,10-Decanedicarboxylic acid 1,12-Dodecanedioic acid 1,10-Dicarboxydecane

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 : ~100 mg/mL (~434.22 mM)
H2O : < 0.1 mg/mL

Solubility in Formulation 1: 2.5 mg/mL (10.86 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 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: ≥ 2.5 mg/mL (10.86 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 25.0 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: ≥ 2.5 mg/mL (10.86 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 25.0 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.)