L-Carnitine - L-Carnitine (levocarnitine) is an amino-acid derivative that

L-Carnitine

L-Carnitine (levocarnitine) is an amino-acid derivative that transports long-chain fatty acids into the mitochondrion for beta-oxidation.

Mitochondrial
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1 vial · 5000 mg total

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฿950

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For research & laboratory use only. Not for human consumption.

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Half-Life

~17.4 hours (oral single dose); shorter for parenteral administration

Fatty-Acid Transport

Carries long-chain fatty acids into the mitochondrion for beta-oxidation

Mitochondrial Cofactor

Cofactor in mitochondrial ATP-linked pathways

Exertion Models

Studied for muscle damage markers after exertion (Fielding 2018)

Mechanism of Action

L-Carnitine is a quaternary ammonium compound synthesised endogenously from lysine and methionine, mostly in the liver and kidney. Its defining role is the carnitine shuttle, the transport system that moves long-chain fatty acids across the otherwise impermeable inner mitochondrial membrane so they can undergo beta-oxidation. Carnitine palmitoyltransferase I (CPT1) on the outer membrane conjugates acyl groups to carnitine, a translocase carries the acylcarnitine across, and CPT2 releases the fatty acid into the matrix.

Scientific Research

Why Researchers Study L-Carnitine

L-Carnitine (levocarnitine) is the biologically active form of carnitine, a small amino-acid derivative the body makes from lysine and methionine. Its central function is the carnitine shuttle - the only route by which long-chain fatty acids reach the mitochondrial matrix to be burned for energy. Because that shuttle is the rate-limiting step of fat oxidation, carnitine availability is a natural lever for research into fuel selection, energy metabolism and exercise recovery.

Mechanism of Action

Long-chain fatty acids cannot cross the inner mitochondrial membrane on their own. Carnitine palmitoyltransferase I (CPT1) attaches the fatty acyl group to carnitine, carnitine-acylcarnitine translocase (CACT) moves the resulting acylcarnitine across the membrane, and CPT2 hands the acyl group back to CoA inside the matrix for beta-oxidation. Stephens, Constantin-Teodosiu and Greenhaff (2007) showed that free-carnitine availability can become limiting to fat oxidation during higher-intensity submaximal exercise, establishing carnitine as an active regulator of muscle fuel selection rather than a passive carrier.

Beyond transport, carnitine buffers the mitochondrial acetyl-CoA/CoASH ratio by exporting excess acetyl groups as acetylcarnitine, freeing CoA for pyruvate dehydrogenase and the TCA cycle.

Research Context

Wall et al. (2011) demonstrated that muscle total-carnitine content can actually be raised in humans and that doing so shifts fuel use - sparing glycogen at low intensity and improving work output at high intensity. Separately, Fielding et al. (2018) reviewed evidence that carnitine supplementation attenuates markers of exercise-induced muscle damage, free-radical formation and soreness during recovery. Investigational interest therefore spans fat-oxidation models, exercise performance and post-exertion recovery.

Handling & Storage

Supplied as a sterile, ready-to-use 500 mg/ml aqueous solution in a 10 ml vial (5000 mg total) - no reconstitution or bacteriostatic water is required. Store refrigerated at 2-8 °C and protect from light; allow the vial to reach room temperature before drawing. A 500 mg research dose corresponds to 1 ml.

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