(+)-Decanoylcarnitine
(+)-Decanoylcarnitine is an (S)-acylcarnitine derivative and a potent inhibitor of carnitine-acylcarnitine translocase, with an IC50 of 5 μM. (+)-Decanoylcarnitine acts as a competitive inhibitor of long-chain acylcarnitine transferase and (-)-carnitine palmityltransferase. (+)-Decanoylcarnitine blocks hepatic fatty acid oxidation, ketogenesis, oleate-induced activation of gluconeogenesis, as well as associated changes in acetyl-CoA, citrate, redox pair ratios, flavins and pyridine nucleotides. (+)-Decanoylcarnitine reverses ketosis in vivo, enhances insulin-mediated hypoglycemic effects in anesthetized animals, and reduces plasma ketone body levels when used in combination with insulin. (+)-Decanoylcarnitine can be used in studies related to diabetic ketoacidosis.
For research use only. We do not sell to patients.
- CAS No.: 25518-51-8
- Formula: C17H33NO4
- Molecular Weight:315.45
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
(+)-Decanoylcarnitine (compound 11b) belongs to (S)-acylcarnitine derivatives, and acts as a potent inhibitor of carnitine-acylcarnitine translocase with an IC50 value of 5 μM[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
(+)-Decanoylcarnitine (20 mg/mL; intravenous injection; infused over 10 min) reduces plasma ketone body levels by 609 μmol/100 mL within 2 hours in conscious alloxan-diabetic rats with ketoacidosis[1].
(+)-Decanoylcarnitine (20 mg/mL; intravenous injection; single injection duration of 2 min) reduces plasma ketone bodies more rapidly than insulin alone in unanesthetized, non-intubated alloxan-diabetic rats with ketoacidosis when used alone[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:Sprague-Dawley (male, initial weight ~130 g, weight ~100 g at experiment start, alloxan-induced diabetic ketoacidosis)[1]
-
Dosage:20 mg/mL
-
Administration:i.v.; 75 μl/min for 10 min then 10 μl/min until 2 h
-
Result:Reduced plasma ketone levels from an initial 1,502 μmol/100 mL to 262 μmol/100 mL over 4 hours.
When combined with insulin, reduced plasma ketones from an initial 1,532 μmol/100 mL to 69 μmol/100 mL over 4 hours.
Had no effect on plasma glucose, with levels remaining at ~1,043-1,045 mg/100 mL over 4 hours.
When combined with insulin, reduced plasma glucose from an initial 896 mg/100 mL to 281 mg/100 mL over 4 hours.
-
Animal Model:Sprague-Dawley (male, initial weight ~130 g, weight ~100 g at experiment start, alloxan-induced diabetic ketoacidosis)[1]
-
Dosage:20 mg/mL
-
Administration:i.v.; 10 min infusion
-
Result:Reduced plasma ketone levels from an initial 1,863 μmol/100 mL to 1,254 μmol/100 mL over 2 hours.
When combined with insulin, reduced plasma ketones from an initial 1,754 μmol/100 mL to 717 μmol/100 mL over 2 hours.
Had no effect on plasma glucose, and did not enhance insulin-induced hypoglycemia in awake animals.
Caused an increase in plasma free fatty acid levels, and blunted the insulin-induced fall in free fatty acids.
-
Animal Model:Sprague-Dawley (male, initial weight ~130 g, weight ~100 g at experiment start, alloxan-induced diabetic ketoacidosis)[1]
-
Dosage:20 mg/mL (0.5 mL total)
-
Administration:i.v.; single injection over 2 min
-
Result:Reduced plasma ketone levels at a faster rate than insulin alone.
The combination of (+)-Decanoylcarnitine and insulin produced a greater ketone reduction than either agent alone.
Had no effect on plasma glucose, and did not enhance insulin-induced hypoglycemia.
Did not blunt the insulin-induced fall in free fatty acids.
Chemical Information
-
CAS No. 25518-51-8
-
Molecular Weight 315.45
-
Formula C17H33NO4
-
SMILES
[C@@H](OC(CCCCCCCCC)=O)(C[N+](C)(C)C)CC([O-])=O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
-
ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
-
Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)