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SYS · ONLINEPASS · 63.0%
Open Assay
Independent Testing / Est. 2026
BATCH04·26·B
PASS63.0%
N27
PeptidesMetabolicL-Carnitine

L-Carnitine

/ Endogenous quaternary ammonium small molecule; mitochondrial fatty-acid transporter cofactor
TIER 2 · TranslationalN = 0 · TESTING PENDINGMW 161.20 g·mol⁻¹

ALIAS · Carnitor (trade) · Levocarnitine · L-Carnitine

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Research use onlyAny dose figures below describe what specific cited studies used, reported factually. Nothing on this page is guidance for human use.READ FIRST →

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§ A · Identity
Primary sequence— sequence not captured —
MW · 161.20CLASS · Endogenous quaternary ammonium small molecule; mitochondrial fatty-acid transporter cofactorCATEGORY · Metabolic

Tier 2 across the broader supplement-and-clinical literature. FDA-approved as Carnitor (levocarnitine, intravenous and oral) for primary and secondary carnitine deficiency, including in haemodialysis. Multiple small RCTs across cardiac (post-MI), exercise, and PCOS contexts, with mixed results; the cardiac-secondary-prevention meta-analysis (DiNicolantonio 2013) reported a mortality signal that has been debated.

§ B · Mechanism of action

L-Carnitine is a non-essential nutrient synthesised endogenously from lysine and methionine; it is the obligate cofactor of the carnitine-acylcarnitine shuttle that transports long-chain fatty acids across the inner mitochondrial membrane for beta-oxidation. Carnitine palmitoyltransferase 1 (CPT1) on the outer mitochondrial membrane esterifies acyl-CoA to acyl-carnitine; CPT2 on the matrix side reverses the step, regenerating acyl-CoA for beta-oxidation. In primary carnitine deficiency, defective OCTN2 transporter function depletes intracellular carnitine and impairs fatty-acid oxidation; oral supplementation restores tissue concentrations.

§ C · Human clinical evidence

Tier 1 within the FDA-approved indication (primary and secondary carnitine deficiency). Tier 2 across cardiac and exercise indications. DiNicolantonio 2013 (Mayo Clin Proc) meta-analysis of post-MI carnitine trials reported reductions in all-cause mortality, ventricular arrhythmia, and angina, although the included trials were heterogeneous and predominantly older. Mingorance 2011 (Crit Rev Food Sci Nutr) reviewed the broader carnitine literature including cardiac, metabolic, and exercise contexts.

§ D · Primary literature
PubMed21490942Mingorance C et al.Critical update for the clinical use of L-carnitine analogs in cardiometabolic disorders · Vascular Health and Risk Management · reviewNarrative review of L-carnitine and its analogs across cardiometabolic indications including ischaemic heart disease, heart failure, and metabolic syndrome; summarised mechanistic basis and clinical-trial heterogeneity.Limitations: Narrative review; does not synthesise outcome data quantitatively.2011
PubMed23597877DiNicolantonio JJ et al.L-carnitine in the secondary prevention of cardiovascular disease: systematic review and meta-analysis · Mayo Clinic Proceedings · meta-analysisMeta-analysis of 13 trials reported reductions in all-cause mortality, ventricular arrhythmia, and angina associated with L-carnitine in the post-myocardial-infarction setting compared with placebo or control.Limitations: Heterogeneous included trials, predominantly older and small; subsequent commentary debated TMAO-pathway and confounding considerations.2013
§ F · Safety signal

Within the FDA-approved indication, well characterised - GI effects (nausea, diarrhoea, abdominal cramping), fishy body odour (from gut-bacterial conversion of carnitine to trimethylamine), and rare seizures in patients with epilepsy. The trimethylamine-N-oxide (TMAO) cardiovascular concern - that high carnitine intake may raise circulating TMAO via gut microbiota and contribute to atherosclerosis - has been raised in observational and mechanistic literature but not resolved in interventional outcome trials.

§ H · Regulatory status

Regulatory status

FDA status:
FDA-approved
Compounding:
Not eligible for compounding (approved, not in shortage)
§ I · Notable gaps and controversies

L-Carnitine occupies two distinct positioning lanes that are often conflated. Within FDA-approved use for primary or secondary carnitine deficiency, the evidence is strong and the regulatory pathway clear. In the much broader supplement market - exercise performance, weight loss, PCOS, general metabolic enhancement - the evidence is mixed, the doses studied vary widely, and the regulatory framing is supplement rather than approved drug. Vendor positioning sometimes implies the FDA-approved indication transfers to the broader use cases; it does not.