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Flavin mononucleotide (FMN), also called riboflavin-5'-phosphate, is a coenzyme made from riboflavin (vitamin B2) that helps enzymes carry out electron-transfer reactions. It acts as the working partner, or prosthetic group, for a range of oxidoreductase enzymes, and it is the form in which riboflavin is first activated inside the body. FMN is also used as an orange-red food coloring.
- supports Complex I and ATP production
- pre-activated form of B2
- supports fat and energy metabolism
- aids antioxidant regeneration
Overview
Flavin mononucleotide, or FMN, is a flavin coenzyme derived from riboflavin, the B vitamin also called vitamin B2, and it is known by the chemical name riboflavin-5'-phosphate [1][2]. It consists of the flavin ring system attached to a ribitol sugar chain that ends in a phosphate group, and it is the principal form in which riboflavin is held and used within cells and tissues [1]. FMN is produced when the enzyme riboflavin kinase adds a phosphate to riboflavin; this same molecule is also the intermediate from which the other main flavin coenzyme, flavin adenine dinucleotide (FAD), is subsequently built [1].
As a coenzyme, FMN serves as the prosthetic group of numerous oxidoreductase enzymes, the proteins that catalyze biological oxidation and reduction [1]. A prominent example is NADH dehydrogenase, known as Complex I of the mitochondrial respiratory chain, where FMN receives electrons from NADH at the very start of the electron transport chain [1]. Enzymes such as dihydropyrimidine dehydrogenase likewise use FMN alongside FAD and iron-sulfur clusters to relay electrons [3]. Roughly a sixth of human flavoproteins depend on FMN, while most of the remainder use FAD [1].
Beyond its metabolic role, FMN has practical applications. It is used as a food additive that supplies an orange-red color, designated in Europe as E101a, and it dissolves in water more readily than riboflavin itself [1]. Because it is a natural derivative of an essential vitamin, FMN is not a drug in the ordinary sense; its ultimate source is dietary riboflavin, and a shortage of that vitamin reduces the supply of both FMN and FAD, undermining the many enzymes that require them [2].
Mechanism
FMN functions as a redox cofactor, the chemical group that enables its host enzyme to move electrons [1]. Like other flavins it can shift between an oxidized form (FMN), a one-electron semiquinone, and a fully reduced form (FMNH2), and this capacity to accept and release either one or two electrons is what makes it versatile in enzyme catalysis [1]. In Complex I of the electron transport chain, FMN takes up electrons from NADH and passes them onward toward the iron-sulfur clusters of the respiratory chain, an early step in the process that ultimately produces ATP [1]. FMN also serves as the light-sensitive component of certain blue-light photoreceptor proteins and acts as the working cofactor in a variety of other oxidoreductase enzymes [1][3].
receptor fingerprint
NADH dehydrogenase (Complex I)cofactor
Riboflavin/FAD conversionintermediate
Glutathione systemcofactor
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
Like other B2 forms, FMN is water soluble and very safe, with excess excreted in urine (turning it bright yellow). No meaningful toxicity is established at typical doses. High-dose isolated FMN has limited specific study.
Interactionsdocumented pairs only, not exhaustive
FMN is the phosphorylated form of riboflavin, and its interactions are best understood at the level of the vitamin as a whole. They are minor.
The best characterized involves drugs that block flavokinase, the enzyme converting riboflavin to FMN. Chlorpromazine, imipramine and amitriptyline all inhibit it, and in rats chronic chlorpromazine lowered tissue FMN and FAD and more than doubled urinary riboflavin excretion, despite a diet containing many times the recommended intake. Whether long term phenothiazine or tricyclic use produces a clinically meaningful riboflavin deficit in people has not been settled, but it is a plausible reason for a higher requirement.
Probenecid slows both gastrointestinal absorption and renal secretion of riboflavin, shifting its pharmacokinetics without obviously changing status. Anticholinergics slow transit and modestly increase absorption, since uptake is saturable and confined to the proximal small intestine.
Riboflavin does not inhibit or induce cytochrome P450 enzymes, and no interaction of consequence has been reported at supplemental doses.
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Subjective profileweighing the evidence above
A valid activated form of vitamin B2; useful but rarely worth a big premium over plain riboflavin for most people.
Resources
This entry is here for reference.
Research
- 2013first citedThe human flavoproteome
- 2023most recentCauses and Clinical Sequelae of Riboflavin Deficiency
- 1.The human flavoproteome
- 2.Causes and Clinical Sequelae of Riboflavin Deficiency
- 3.Mammalian dihydropyrimidine dehydrogenase.
3 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
How is FMN different from riboflavin?
FMN is riboflavin with a phosphate added, making it the already-activated form. The body normally makes FMN from riboflavin anyway.
Is FMN the same as the NMN longevity supplement?
No. FMN is a flavin (vitamin B2 derived). NMN is a nicotinamide compound tied to NAD+. Different molecules despite similar acronyms.
Do I need FMN specifically?
Usually not. Plain riboflavin converts to FMN readily. FMN is an option if you prefer the activated form.
Will it turn my urine yellow?
Yes, that is normal and harmless; it is just the excess flavin being excreted.
Notes and cautions
- Not used as a conventional drug
- Comes from dietary riboflavin, which is well tolerated
- Any excess riboflavin is cleared in the urine and can brighten its color
- No established toxicity at normal dietary levels