L-Carnitine (Levocarnitine)

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What Is L-Carnitine?

L-Carnitine (levocarnitine) is a small, water-soluble, quaternary-ammonium amino-acid derivative with the molecular formula C₇H₁₅NEE₃ and molecular weight 161.20 g/mol. It is not a peptide — it is a single-residue zwitterionic molecule derived metabolically from the amino acids L-lysine and L-methionine through a multistep biosynthetic pathway distributed across kidney, liver, and brain. Only the (3R) enantiomer (the L-form / levo form / levocarnitine) is biologically active; the (3S) enantiomer (D-carnitine) is inactive and is now well-documented to interfere with the L-form’s transport, which is why pharmaceutical-grade material is supplied as the enantiomerically pure L-form rather than as racemic DL-carnitine.

The molecule’s central physiological function is to serve as the obligate carrier for transporting long-chain fatty acids (C₁₂+) across the otherwise-impermeable mitochondrial inner membrane, where they are subsequently broken down by β-oxidation to acetyl-CoA, the substrate for the citric acid cycle and ATP synthesis. The transport machinery — carnitine palmitoyltransferase I (CPT-I) on the outer mitochondrial membrane, the carnitine/acylcarnitine translocase (CACT) across the inner membrane, and carnitine palmitoyltransferase II (CPT-II) on the matrix side — converts free fatty acids into acylcarnitines, ferries them across the bilayer, and releases them again as acyl-CoAs for oxidation. L-Carnitine is therefore the rate-limiting metabolite for fat oxidation in tissues with high oxidative demand: skeletal muscle, cardiac muscle, and liver.

L-Carnitine is also a high-affinity buffer of the cellular acyl-CoA / free-CoA ratio. By accepting acyl groups onto its hydroxyl side chain, L-carnitine maintains the intracellular pool of free CoA that other CoA-dependent enzymes (pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, fatty-acid β-oxidation) require to function. Carnitine deficiency therefore produces effects beyond fat oxidation alone — propagating into pyruvate handling, TCA-cycle flux, and overall mitochondrial bioenergetic balance.

L-Carnitine has FDA approval (under the name levocarnitine) for human therapeutic use in primary and secondary carnitine deficiency (oral and IV formulations) and is widely used in research contexts that examine mitochondrial bioenergetics, fat oxidation, insulin sensitivity, cardiovascular function, neuroprotection, exercise physiology, and sperm motility. The research-grade L-Carnitine sold here is supplied uitsluitend voor laboratoriumonderzoek and is not intended for human or veterinary administration without appropriate regulatory authorisation.

Mechanism of Action — Mitochondrial Long-Chain Fatty-Acid Transport

L-Carnitine’s central mechanism is documented across several decades of mitochondrial biochemistry research:

• Carnitine palmitoyltransferase I (CPT-I) — outer mitochondrial membrane — Long-chain fatty acids first activate to long-chain acyl-CoA in the cytoplasm. CPT-I, embedded in the outer mitochondrial membrane, transfers the acyl group from CoA onto L-carnitine’s hydroxyl, generating long-chain acylcarnitine. This is the committed and most heavily regulated step of mitochondrial fat oxidation — CPT-I is allosterically inhibited by malonyl-CoA (the product of acetyl-CoA carboxylase in fed-state lipogenic metabolism), which is how insulin / glucagon and the AMPK system gate fat oxidation against fat synthesis.
• Carnitine/acylcarnitine translocase (CACT) — inner mitochondrial membrane — Long-chain acylcarnitine generated by CPT-I cannot diffuse across the inner mitochondrial membrane. CACT, an antiporter, exchanges cytosolic acylcarnitine for matrix free carnitine in a 1:1 stoichiometry, delivering acylcarnitine into the matrix and recycling carnitine for further rounds of CPT-I.
• Carnitine palmitoyltransferase II (CPT-II) — inner mitochondrial membrane, matrix-facing — In the matrix, CPT-II reverses the CPT-I reaction: it transfers the acyl group from carnitine back onto matrix CoA, regenerating long-chain acyl-CoA, which can now enter β-oxidation. The free carnitine released is returned across the membrane via CACT for another transport cycle.
• Acyl-CoA / free-CoA ratio buffering and metabolic flexibility — Beyond the long-chain shuttle, L-carnitine accepts short- and medium-chain acyl groups (acetylcarnitine, propionylcarnitine) and acts as a high-capacity buffer of the intracellular acyl-CoA / free-CoA ratio. This maintains free CoA for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and β-oxidation. Acetylcarnitine generation also serves as the mechanism by which excess acetyl-CoA — from fasting, ketogenesis, exercise — can be safely buffered and exported across the mitochondrial membrane.

The pharmacokinetic profile of orally-administered L-carnitine is unusual: oral bioavailability is low (~15%) due to active intestinal saturation, with the remaining 85% subject to extensive bacterial degradation in the colon (yielding TMA and TMAO — a finding that has attracted attention in cardiovascular research). Intravenous and intramuscular research routes achieve much higher plasma levels and bypass the gut-microbial degradation pathway entirely, which is why pharmacological research protocols commonly use parenteral administration despite the convenience of oral dosing.

Published Research Applications

L-Carnitine is used in laboratory research contexts that investigate:

• Mitochondrial function and bioenergetics — Seahorse / Oroboros respirometry, mitochondrial membrane potential, ATP generation rate, fatty-acid-oxidation rate in primary hepatocyte, skeletal-muscle, and cardiomyocyte cultures
• Fat oxidation and metabolic flexibility — switching between glucose and fat oxidation in skeletal muscle and liver; insulin-resistance reversal models; obese-rodent and DIO study cohorts
• Insulin sensitivity research — improvement in skeletal-muscle insulin sensitivity in models of metabolic syndrome and type 2 diabetes preclinical research; mechanistic dissection of the L-carnitine / acyl-CoA buffering / pyruvate handling axis
• Cardiovascular research — angina, heart failure, ischemia-reperfusion injury, cardiomyopathy (in particular doxorubicin-induced cardiotoxicity and primary carnitine-deficiency cardiomyopathy); TMA/TMAO microbiome-axis cardiovascular research
• Neuroprotection research — Alzheimer-disease in-vitro models (acetylcarnitine specifically), Parkinson-disease models, peripheral diabetic neuropathy preclinical models, autism-spectrum research where carnitine deficiency has been implicated
• Sperm motility and male fertility research — epididymal acquisition of motility, mitochondrial energetics of sperm flagellar beat, antioxidant protection of spermatozoa; one of the most-studied compounds in male-fertility research
• Exercise physiology and endurance research — substrate utilisation during prolonged exercise, glycogen sparing, post-exercise recovery; research interest in carnitine loading protocols and insulin co-administration to overcome muscle-uptake saturation
• Chronic kidney disease / haemodialysis research — carnitine deficiency is common in dialysis-dependent end-stage renal disease patients and L-carnitine has FDA approval for this indication; preclinical research continues on dialysis-related cardiomyopathy and muscle weakness

For broader context on mitochondrial and metabolic-axis research compounds in this catalogue, see NAD⁺ (oxidised dinucleotide coenzyme, central electron-transport substrate), SS-31 (Elamipretide) (mitochondrial-targeted cardiolipin-binding peptide), and MOTS-c (mitochondrial-derived metabolic-regulator peptide). Browse the full research peptides & compounds catalog voor gerelateerde verbindingen.

Beschikbare sterktes en concentraties

MedsBase stocks L-Carnitine in two lyophilized vial sizes calibrated to typical research protocol lengths. Each strength is available in 10-vial or 20-vial pack formats:

Both strengths are the same chemical form (lyophilized levocarnitine zwitterion, ≥99% HPLC purity). Vial doses are deliberately much larger than the peptide range (5–20 mg) because L-carnitine is a small molecule used at gram-level doses — a 600 mg or 1200 mg vial corresponds roughly to a single intravenous research dose in rodent or large-animal protocols. Researchers should determine specific dose ranges from peer-reviewed literature appropriate to the protocol.

How It Compares — L-Carnitine vs NAD⁺

L-Carnitine and NAD⁺ are the two non-peptide mitochondrial / metabolic research compounds in this catalogue, and they target completely different layers of mitochondrial bioenergetics. L-Carnitine sits on the fuel side — it transports long-chain fatty acids into the matrix for β-oxidation. NAD⁺ sits on the electron-transport side — it is the obligate electron acceptor for β-oxidation, glycolysis, and the TCA cycle, regenerated by Complex I of the electron transport chain. The two compounds are mechanistically complementary, and research protocols sometimes combine them to probe upstream-substrate vs downstream-electron-flux contributions to mitochondrial output.

For research focused on long-chain fatty-acid oxidation, cardiovascular metabolic function, insulin sensitivity, or sperm motility, L-Carnitine is the canonical reference compound. For research focused on sirtuin biology, longevity-axis biochemistry, or NAD-dependent redox regulation, NAD⁺ is the more targeted tool. See also SS-31 (Elamipretide) for cardiolipin / inner-membrane-targeted mitochondrial research and MOTS-c for mitochondrial-derived peptide-signalling research.

Opslag en Reconstituering

Voor reconstituering: store lyophilized vials refrigerated at 2–8 °C in original packaging for short-term working stock. For long-term storage, freeze unopened vials at −20 °C. Lyophilized L-Carnitine is stable under refrigeration for up to 36 months and at −20 °C for up to 60 months — substantially more stable than most lyophilized peptides because the small-molecule structure has no amide bonds or disulfide bridges to hydrolyse. The compound is, however, hygroscopic, so reseal vials promptly after each withdrawal and avoid prolonged exposure to ambient humidity.

Reconstitueringsprocedure: inject bacteriostatic water down the side wall of the vial (not directly onto the lyophilized cake). For a 600 mg vial, 3.0 mL of bacteriostatic water yields a 200 mg/mL working concentration; 1.2 mL yields a 500 mg/mL stock. For a 1200 mg vial, 6.0 mL yields a 200 mg/mL working stock; 2.4 mL yields a 500 mg/mL stock. L-Carnitine dissolves very rapidly with gentle swirling — typically within 10–30 seconds — because it is a small zwitterion with no folded structure to disturb. Once reconstituted, store the vial at 2–8 °C and use within 30 days. Protect from light. Discard if cloudiness, particulates, or colour change appears.

Veelgestelde vragen

Is L-Carnitine a peptide?

No. L-Carnitine is a small-molecule quaternary-ammonium amino-acid derivative (MW 161.20 g/mol), niet a peptide. We stock it in our research-peptide catalogue alongside NAD⁺ because it serves a complementary role in mitochondrial / metabolic research and is supplied in the same injectable vial format. The spec table Sequence row is marked “n/a” for this reason.

What is the difference between L-Carnitine and acetyl-L-carnitine (ALCAR)?

Acetyl-L-carnitine is L-carnitine with an acetyl group esterified to the hydroxyl side chain. ALCAR crosses the blood-brain barrier more efficiently and is the form most commonly used in CNS-focused research (Alzheimer-disease, peripheral neuropathy). The base L-carnitine zwitterion that we supply here is the form used in peripheral metabolic research (cardiovascular, skeletal muscle, sperm motility, dialysis-related deficiency). The two compounds interconvert metabolically through carnitine acetyltransferase.

What is the difference between L-Carnitine and racemic DL-carnitine?

Only the L (3R) enantiomer is biologically active. The D (3S) enantiomer is inactive and is now well-documented to interfere with L-form transport, accumulating in tissue and producing weakness and other adverse effects in long-term high-dose contexts. Pharmaceutical-grade levocarnitine (what we supply) is the enantiomerically pure L-form. The racemic DL-form is obsolete and is no longer used in either clinical or rigorous research contexts.

Why is the research dose so much larger than the peptide doses in this catalogue?

L-Carnitine is a small molecule (MW 161) and is used at gram-level doses — the body’s endogenous carnitine pool is approximately 25 g, concentrated in skeletal muscle. Research protocols typically use 100–500 mg/kg in rodent in-vivo work, which translates to hundreds of milligrams to grams per dose. Compare this to research peptides (BPC-157, semaglutide, etc.) where typical doses are 100 µg to 5 mg per administration — three to four orders of magnitude smaller, reflecting the different molecular weights and the different receptor / mechanism scales.

What is the TMA / TMAO question I see in cardiovascular research?

A subset of L-carnitine ingested orally is degraded by gut bacteria to trimethylamine (TMA), which the liver then oxidises to trimethylamine-N-oxide (TMAO). Elevated TMAO levels have been associated in epidemiological research with adverse cardiovascular events, raising a controversy about whether long-term high-dose oral L-carnitine supplementation may be net-beneficial or net-harmful for cardiovascular endpoints. The question is active and unresolved. Parenteral L-carnitine bypasses the gut-microbial degradation pathway and is not subject to this concern.

What does CPT-I inhibition mean in metabolic research?

Carnitine palmitoyltransferase I (CPT-I) is the rate-limiting enzyme for mitochondrial long-chain fatty-acid uptake. Etomoxir is a classical CPT-I inhibitor used to block fat oxidation in research models; it is the pharmacological tool counterpart to the L-carnitine substrate. Research protocols sometimes combine L-carnitine supplementation (substrate side) with CPT-I inhibition (enzymatic side) to dissect substrate-limited vs enzyme-limited fat oxidation in different tissues and conditions.

Can I combine L-Carnitine with NAD⁺ in the same research protocol?

Yes — the two compounds target different layers of mitochondrial bioenergetics (substrate transport vs electron transport), and combination is commonly used in research that aims to probe upstream vs downstream limitations on mitochondrial output. They are chemically stable in solution together. Reconstitute each separately first to establish stability and concentration accuracy, then combine immediately before use rather than co-storing reconstituted vials.

What route of administration is used in published research?

Intravenous and intramuscular routes are most common in pharmacological research because they bypass the low (~15%) oral bioavailability and the gut-microbial TMA/TMAO degradation pathway. Subcutaneous administration is used in some rodent protocols. Oral administration is used in pharmacokinetic and nutritional research where the bioavailability question is itself the research focus.

Meer opties in Peptiden

Gerangschikt op recente bestelvolumes van MedsBase — wat andere klanten in deze categorie kiezen.

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