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Carnitine shuttle substrate · β-oxidation carrier
Also known as Levocarnitine · L-(−)-carnitine
The endogenous quaternary ammonium compound that carries long-chain fatty acids into the mitochondrion for oxidation. Supplied as a lyophilized powder for research purposes only.
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Tested lot by lot at ≥99% purity. The Janoshik certificate for your lot is emailed with the order.
Everything Valtrax Research ships is bench material for in-vitro work. None of it is a drug, a supplement, a cosmetic, or a medical device, and none of it is intended for human or animal use, ingestion, or administration. Placing an order is your confirmation that you are a qualified researcher buying for lawful research, under every Canadian law and regulation that applies to you.
Not a peptide. L-carnitine is a small zwitterionic quaternary ammonium compound, and its job in the cell is transport: long-chain fatty acids cannot cross the inner mitochondrial membrane as their CoA thioesters, so they are handed to carnitine first. That single constraint is why the molecule sits at the entrance to β-oxidation.
Worth naming what this is not — acetyl-L-carnitine. ALCAR carries an acetyl group and is studied largely for what that group does in the central nervous system. This vial is the free levo form, the carrier itself.
The question is almost always substrate flux: how fast a given cell moves long-chain fatty acids into the mitochondrion and oxidizes them, and what changes when that shuttle is loaded, blocked, or genetically removed. Skeletal muscle and cardiac tissue are the classical systems; cancer, immune, and stem-cell models are where the recent work sits.
The mechanism is a three-part shuttle. Carnitine palmitoyltransferase 1, on the outer mitochondrial membrane, transfers a long-chain acyl group from CoA onto carnitine; a translocase carries the resulting acylcarnitine across the inner membrane; CPT2 hands the acyl group back to CoA in the matrix, where β-oxidation takes it. CPT1 is the rate-limiting step, which is why so much fatty-acid-oxidation work is really CPT1 work.
Studies read the system through oxidation flux, acylcarnitine profiles, and muscle bioenergetics. The same shuttle keeps reappearing outside metabolism proper — in cancer cell biology, immune-cell fate, and stem-cell function — because whichever cell you are looking at, this is how it burns fat.
Carnitine was worked out as a metabolic carrier across the mid-twentieth century, and by the early 1980s the reviews had settled its role: Bremer’s account of carnitine metabolism and function, and Hoppel’s treatment of carnitine and carnitine palmitoyltransferase in fatty-acid oxidation and ketosis, are the reference points the field still cites.
The modern literature is less about the carrier and more about the enzymes that use it. CPT1 and CPT2 turned into targets and readouts in their own right, and carnitine became the reagent you need to study them.
Bremer, J. (1983). Carnitine--metabolism and functions.
PubMedHoppel, CL. (1982). Carnitine and carnitine palmitoyltransferase in fatty acid oxidation and ketosis.
PubMedQu, Q. et al. (2016). Fatty acid oxidation and carnitine palmitoyltransferase I: emerging therapeutic targets in cancer.
PubMedGnoni, A. et al. (2020). Carnitine in Human Muscle Bioenergetics: Can Carnitine Supplementation Improve Physical Exercise?
PubMedPereyra, AS. et al. (2024). Loss of mitochondria long-chain fatty acid oxidation impairs skeletal muscle contractility by disrupting myofibril structure and calcium homeostasis.
PubMedEvery lot is checked independently by Janoshik for identity, purity, and net content; that certificate is included with the order.
Janoshik Analytical, a laboratory Valtrax does not own, runs the testing — identity by mass spectrometry, purity by RP-HPLC at ≥99%. The certificate covering the lot you receive is also emailed with your order.
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