The AtlasAmino acidsAromatic
TyrosineTyr · Y
Phenylalanine with one oxygen added, and the raw material for dopamine, adrenaline, thyroid hormone and the pigment in skin.
Molecule · Tyr · 13 heavy atoms
Tyrosine
C9H11NO3181.19 g/mol
Phenylalanine with one oxygen added, and the raw material for dopamine, adrenaline, thyroid hormone and the pigment in skin.
Built fromthe charted ones open their own entry
- Codes
- Tyr · Y
- Formula
- C9H11NO3
- Molar mass
- 181.19 g/mol
- Systematic name
- (2S)-2-amino-3-(4-hydroxyphenyl)propanoic acid
- Side chain
- 4-Hydroxybenzyl: a phenol ring on one carbon; aromatic, weakly polar, ionizes only above pH 10.
- Class
- Aromatic
- In the diet
- Conditionally essential
- Carbon skeleton
- Glucogenic and ketogenic
- pKa
- α-COOH 2.20 · α-NH3+ 9.11 · side chain 10.07
- Isoelectric point
- pH 5.66
- Hydropathy
- -1.3 (Kyte–Doolittle)
- Codons
UAUUAC- Main transporters
- SLC7A5 (LAT1, with CD98), SLC6A19 (B0AT1)
pKa and isoelectric point: Nelson and Cox, Lehninger Principles of Biochemistry, table of amino acid properties (free amino acid, 25 °C). Hydropathy: Kyte and Doolittle, J Mol Biol 1982. Essentiality: Reeds, J Nutr 2000. Formula and mass computed from the structure.
In brief
What it is
Phenylalanine with a hydroxyl group on the far end of its ring, a phenol. The body makes it from phenylalanine, so it is needed in the diet only when that conversion fails 1,2.
Why it matters
It is the starting point for the catecholamines, dopamine, noradrenaline and adrenaline, through tyrosine hydroxylase; for the thyroid hormones, built on tyrosines in thyroglobulin; and for melanin 3,4,5. Phosphorylating tyrosine on proteins is also one of the cell’s main signaling switches 6.
Where it runs short
In phenylketonuria tyrosine can no longer be made from phenylalanine, so it becomes essential and has to be supplied 2,7.
Where it turns
When its breakdown is blocked, tyrosine or its products accumulate: liver failure in tyrosinemia type I, eye and skin lesions in type II, and dark pigment in cartilage in alkaptonuria 8,9,10.
Every disease on this page is a blockage at one step of a single pathway.
The molecule
Tyrosine is phenylalanine with a hydroxyl group at the far end of the ring, which makes the ring a phenol. The hydroxyl gives a protein a site for a hydrogen bond, for iodine and for phosphate, all three of which the body uses 4,6.
The phenol is a very weak acid. Its pKa is about 10, so at the pH of blood it is uncharged and tyrosine counts as an aromatic, slightly polar amino acid rather than a charged one.
Move across the chart to read the charge at any pH.
Computed from its pKa values (α-carboxyl 2.20, α-amino 9.11, side chain 10.07) by the Henderson–Hasselbalch equation, for the free amino acid in water at 25 °C. Inside a folded protein the same groups can shift by a unit or more. The faint lines are the other amino acids.
Kyte–Doolittle hydropathy index: positive values avoid water and tend to be buried inside a folded protein, negative values sit on its surface. Each letter is an amino acid; choose one to open it.
| 1st ↓ 2nd → | U | C | A | G | 3rd |
|---|---|---|---|---|---|
| U | UUUPhe | UCUSer | UAUTyr | UGUCys | U |
| UUCPhe | UCCSer | UACTyr | UGCCys | C | |
| UUALeu | UCASer | UAAStop | UGAStop | A | |
| UUGLeu | UCGSer | UAGStop | UGGTrp | G | |
| C | CUULeu | CCUPro | CAUHis | CGUArg | U |
| CUCLeu | CCCPro | CACHis | CGCArg | C | |
| CUALeu | CCAPro | CAAGln | CGAArg | A | |
| CUGLeu | CCGPro | CAGGln | CGGArg | G | |
| A | AUUIle | ACUThr | AAUAsn | AGUSer | U |
| AUCIle | ACCThr | AACAsn | AGCSer | C | |
| AUAIle | ACAThr | AAALys | AGAArg | A | |
| AUGMet | ACGThr | AAGLys | AGGArg | G | |
| G | GUUVal | GCUAla | GAUAsp | GGUGly | U |
| GUCVal | GCCAla | GACAsp | GGCGly | C | |
| GUAVal | GCAAla | GAAGlu | GGAGly | A | |
| GUGVal | GCGAla | GAGGlu | GGGGly | G |
Where it comes from
The body makes tyrosine from phenylalanine, in one step, by phenylalanine hydroxylase with tetrahydrobiopterin as cofactor 2,11. That makes it conditionally essential: dispensable in a normal diet, essential in phenylketonuria 7.
Requirements for the two aromatic amino acids are set together, at 25 mg per kilogram a day 12.
Conditionally essentialMade from phenylalanine by phenylalanine hydroxylase, so not needed in the diet unless that enzyme fails; requirements are set for the two together, 25 mg per kilogram a day 2,12. In adult men given a fixed phenylalanine intake, the tyrosine requirement was about 6 mg/kg a day 1.
How much
With phenylalanine, 25 mg per kilogram a day for adults 12.
In the bottle · fermentedCommercial tyrosine is made by fermentation in engineered Escherichia coli or Corynebacterium glutamicum through the shikimate pathway 13. The product is identical to the tyrosine in food.
What the body does with it
Tyrosine hydroxylase turns tyrosine into L-DOPA, which is decarboxylated to dopamine; in some cells dopamine is hydroxylated to noradrenaline and that is methylated to adrenaline 14. Most catecholamine breakdown happens inside the same cells that make them, as transmitter leaks from storage vesicles into the cytoplasm, and the adrenal medulla is the largest source of the metanephrines measured to detect a phaeochromocytoma 14.
In the thyroid, tyrosine is not used free. Tyrosine residues within thyroglobulin are iodinated and coupled while still part of that protein, and the hormones are cut out of it afterwards 4. Mutations in the thyroglobulin gene are a cause of congenital hypothyroidism 4.
In melanocytes, tyrosinase oxidizes tyrosine in the first and rate-limiting step of melanin synthesis; defects in the gene cause the commonest form of oculocutaneous albinism 5.
There is a fourth role, and it is the plainest one: tyrosine has to be loaded onto its transfer RNA before any protein containing it can be made, and when that step is weak, tyrosine itself becomes the limiting reagent. Biallelic variants in YARS1 cripple tyrosyl-tRNA synthetase and impair neurological development, growth, liver function and blood counts. Nine children were given tyrosine, seven of them with a high-protein diet: cooperation, endurance and motor skills improved in eight of nine, two made significant progress in active language, weight gain improved in six of nine, vomiting stopped in all, and blood counts improved in four of nine. The reason is measurable in their own cells — in three fibroblast lines homozygous for p.(Arg367Trp), enzyme activity at the physiological blood tyrosine concentration was 0%, 6% and 24% of control, and rose to almost normal when tyrosine was raised fivefold 15. A dose-dependent rescue of a specific enzyme, not a tonic. The same logic has now been extended to the DOMINANT YARS1 variants that cause a form of Charcot-Marie-Tooth neuropathy, which has no disease-modifying treatment: expressing G41R, D81I and E196Q in a humanized yeast model produced a dominant-negative growth defect, worse at higher temperature, and tyrosine supplementation significantly rescued it across all three 16.
In three sentences each
The rate-limiting step for catecholamines
Tyrosine hydroxylase converts tyrosine to L-DOPA, the step that sets how fast dopamine, noradrenaline and adrenaline are made; children who lack it have too little of all three in the brain 2,3.
Iodinated in thyroglobulin
The thyroid iodinates tyrosine residues on thyroglobulin to make mono- and diiodotyrosine; two diiodotyrosines couple to make T4, and a mono- with a diiodotyrosine makes T3 4.
A phosphate switch
In 1980 the cancer-causing protein of Rous sarcoma virus was found to add phosphate to tyrosine, a kind of protein kinase no one had seen before; tyrosine phosphorylation is now known as a central signal for growth 6.
How it is made, moved and broken down
Tyrosine’s breakdown runs through five enzymes in the liver. Each has its own disease, which is what makes the pathway so well known: tyrosine aminotransferase (tyrosinemia type II), 4-hydroxyphenylpyruvate dioxygenase (the target of nitisinone), homogentisate dioxygenase (alkaptonuria) and fumarylacetoacetate hydrolase (tyrosinemia type I) 8,9,10,17. The last step yields fumarate and acetoacetate 18.
Carbon skeleton · glucogenic and ketogenicBroken down to fumarate, which can make glucose, and acetoacetate, a ketone body 18.
- Tyrosine
- Tyrosine hydroxylaseTH · BH4, iron
- L-DOPA
- Aromatic L-amino acid decarboxylaseDDC · vitamin B6
- Dopamine
- Dopamine β-hydroxylaseDBH · vitamin C, copper
- Noradrenaline
- Phenylethanolamine N-methyltransferasePNMT · SAM
- Adrenaline
- Tyrosine
- Tyrosine aminotransferaseTAT · vitamin B6
- 4-Hydroxyphenylpyruvate
- 4-Hydroxyphenylpyruvate dioxygenaseHPD · iron, O₂
- Homogentisate
- Homogentisate 1,2-dioxygenaseHGD · iron, O₂
- Maleylacetoacetate
- Maleylacetoacetate isomeraseGSTZ1 · glutathione
- Fumarylacetoacetate
- Fumarylacetoacetate hydrolaseFAH
- Fumarate + acetoacetate
- Tyrosines in thyroglobulin
- Thyroid peroxidaseTPO · iodide
- MIT and DIT
- Thyroid peroxidase (coupling)TPO
- T4, or T3
Where it matters most
- Brain
- Dopamine and noradrenaline neurons; tyrosine hydroxylase deficiency causes an infantile movement disorder treatable with L-DOPA 3.
- Adrenal medulla
- Makes adrenaline and is the largest source of circulating metanephrines 14.
- Thyroid
- Builds T4 and T3 on the tyrosines of thyroglobulin 4.
- Skin, hair and eyes
- Melanocytes make melanin from tyrosine through tyrosinase 5.
- Liver
- Breaks tyrosine down; failure of the last step causes liver failure and cancer risk in tyrosinemia type I 8.
When it goes wrong
Inherited
Tyrosinemia type I
FAH · autosomal recessive
Liver failure with kidney and nerve involvement and a long-term risk of liver cancer 8. Nitisinone, which blocks the pathway upstream so the toxic products are never made, brought succinylacetone down to the detection limit in the first five patients treated, reported in 1992; identified early and treated, most infants stay well 8,17. How it is actually managed still varies. A 2025 survey of 32 metabolic centers in 16 European countries found consistency on some points and wide variation in the frequency and method of follow-up, in nitisinone dosing and in the target biochemical ranges; compared with the same exercise in 2014, more patients are now found by newborn screening, nitisinone doses are LOWER, and the field's attention has moved from mainly hepatic outcomes to hepatic and neurocognitive outcomes together 22. The attempt to get rid of the diet is also live: an engineered probiotic designed to consume tyrosine in the gut reduced neonatal death and acute liver injury in FAH-deficient mice, improved chronic liver lesions when combined with nitisinone, carried over to FAH-deficient rabbits, and rapidly metabolized labeled tyrosine given by mouth to minipigs, with no significant adverse effects, no systemic spread and no damaging disruption of the resident microbiota in mice or pigs 23. Three species and no patients.
How it is foundSuccinylacetone in the newborn blood spot, then in plasma and urine 8.
Inherited
Tyrosinemia type II (Richner–Hanhart syndrome)
TAT · autosomal recessive
Very rare. Painful thickening of the skin of the palms and soles, a keratitis that can be mistaken for herpes, and sometimes mild developmental delay; treated by restricting protein 9.
How it is foundPlasma tyrosine and TAT sequencing 9.
Inherited
Alkaptonuria
HGD · autosomal recessive
Ultra-rare. Homogentisic acid accumulates and from the third decade deposits as a bluish-black pigment in cartilage and connective tissue, ochronosis, with destructive arthritis of the spine and large joints 10,24. Nitisinone lowered urinary homogentisic acid by 99.7% in the SONIA 2 trial and in June 2025 became the first treatment approved by the FDA for the disease 25,26. The side effect of that success has not been solved by the obvious means. NMR profiling of plasma and urine from 12 patients before and after three months of nitisinone confirmed the fall in urinary homogentisate alongside a substantial RISE in plasma tyrosine, with the urinary metabolites upstream of the blocked enzyme accumulating as expected. Comparing 10 mg once daily with 10 mg every other day, 4-hydroxyphenylpyruvate was the only metabolite that differed significantly between the regimens — plasma tyrosine stayed elevated on both, which the authors say underscores the limitations of current dosing strategies for controlling nitisinone-induced hypertyrosinemia 27. Spacing the dose out does not fix it, and the ocular risk is what the hypertyrosinemia matters for.
How it is foundUrine homogentisic acid; HGD genetic testing 10,25.
Inherited
Tyrosine hydroxylase deficiency
TH · autosomal recessive
Fewer than 40 cases had been reported by 2010. An infantile movement disorder, or in its severe form a neonatal encephalopathy, from too little dopamine and noradrenaline in the brain; L-DOPA treats it 3.
How it is foundLow homovanillic acid and MHPG with normal 5-HIAA in cerebrospinal fluid; TH sequencing 3.
Inherited
Oculocutaneous albinism type 1
TYR · autosomal recessive
Loss of tyrosinase, the first enzyme of melanin synthesis; the commonest form of albinism in people of European ancestry, though a quarter or more of cases remain genetically unexplained 5.
How it is foundGenetic testing of TYR 5.
Inherited
YARS1 deficiency
YARS1 · autosomal recessive (and dominant forms)
Biallelic variants cripple tyrosyl-tRNA synthetase, the enzyme that loads tyrosine onto its transfer RNA, with impaired neurological development, poor growth, liver dysfunction and abnormal blood counts. Nine children given tyrosine, seven with a high-protein diet, improved in cooperation, endurance and motor skills (8 of 9), weight gain (6 of 9) and blood counts (4 of 9), and vomiting stopped in all of them; the authors advocate therapeutic trials on the cost-risk-benefit ratio 15. Separately, DOMINANT YARS1 variants cause a form of Charcot-Marie-Tooth neuropathy, and tyrosine supplementation rescued the growth defect those variants produce in a humanized yeast model — proof of concept that impaired tyrosine utilization drives the dominant disease too 16. This is the one place on this page where supplementing tyrosine is a rational treatment rather than a claim.
How it is foundYARS1 sequencing; aminoacylation activity in patient fibroblasts shows the dose-dependence 15.
How it is measured
Tyrosine is measured with phenylalanine in plasma and dried blood spots, and the two sample types differ: in one comparison plasma tyrosine read about 6 µmol/L higher than the spot 28. For the tyrosine disorders the more useful markers are the ones downstream, succinylacetone and homogentisic acid 8,25. For succinylacetone the analytical problem is not the diagnosis. Untreated tyrosinemia type 1 raises it several thousand-fold above normal, so traditional methods catch most cases; what matters is the NANOMOLAR range — monitoring patients on nitisinone, finding attenuated or atypical forms, and confirming or refuting a positive newborn screen. A reference laboratory moving from gas chromatography-mass spectrometry to triple-quadrupole GC-MS/MS reached a limit of quantitation of 1 nmol/L on smaller samples with fewer processing steps, which also lets maleylacetoacetate isomerase deficiency be told apart from tyrosinemia type 1 29.
Tyrosine's biggest imaging use is as a tracer, and the one randomized test of steering treatment by it is negative. O-(2-[18F]fluoroethyl)-L-tyrosine PET is more specific than contrast-enhanced MRI for diagnosing recurrent glioblastoma, so 200 patients across 15 German centers were randomized to have their re-irradiation target drawn from the PET or from the MRI. Median progression-free survival was 4.0 months with the PET against 4.9 with the MRI (adjusted hazard ratio 1.14, 95% CI 0.85 to 1.52), with grade 3–4 radionecrosis in 8% and 7%. The conclusion is that the PET-based delineation did not produce a significant clinical benefit and that contrast-enhanced MRI remains the preferred method 30. A more specific test is not automatically a better plan.
Outside the inherited disorders, a raised plasma tyrosine is an ordinary metabolic marker whose meaning depends on where it was measured. In a Japanese community cohort of 12,461 adults with 354 new cases over a median 4.3 years, tyrosine was one of 14 metabolites positively associated with incident type 2 diabetes — but when the authors asked which metabolites MEDIATE the path from polygenic risk to disease, the seven that did were 3-hydroxyisobutyric acid, 2-aminobutyric acid, 2-ketoisocaproic acid, 2-hydroxybutyric acid, leucine, glycine and glucose. Tyrosine was not among them 31. And in a Chilean population-based cohort of 1,738 adults, where branched-chain amino acids and alanine tracked prevalent diabetes and histidine, glycine and glutamine ran inversely, tyrosine does not appear among the significant associations at all, with only isoleucine reaching significance for incident disease 32. The aromatic-amino-acid biomarker story is built largely on European and Asian cohorts, and it does not travel unchanged.
- Newborn tyrosine and succinylacetoneBoth are measured in the heel-prick blood spot 33.Succinylacetone is the better screen for tyrosinemia type I than tyrosine itself 8.Tyrosine is often raised for a while in healthy newborns, especially preterm babies, so it needs separate cut-offs; measuring succinylacetone at the same time distinguishes the transient rise from the disease 33.
- Plasma tyrosine on nitisinoneMonitored in everyone taking nitisinone, which blocks the pathway below tyrosine 8,34.In alkaptonuria trials, nitisinone raised plasma tyrosine by about 700 µmol/L on average 34.The long-term consequences of that rise remain uncertain 10.
- Urine homogentisic acidThe diagnostic and treatment marker for alkaptonuria 25.Fell by 99.7% at 12 months on nitisinone in a randomized trial 25.
Food, supplements and the evidence
Establishedreplicated in people, for a named outcome
Uncertainsmall, short, mixed, surrogate or preclinical
- Tyrosine for thinking under acute stress. Small crossover trials found benefits on working memory and vigilance during cold, noise, hypoxia or a night without sleep, lasting a few hours, at doses of 100 to 300 mg per kilogram 35,36,37,38,39. Two recent trials mark the edges of that. In the heat — the stressor those earlier trials did not use — 150 mg/kg did nothing: in eight trained footballers cycling 92 minutes of high-intensity intervals at 32 °C, peak power, soccer-specific decision-making, cognitive appraisal and affective state were all the same as on placebo 40. Under MENTAL fatigue, which is the stressor the supplement market now sells it for, 300 mg/kg did something: twelve cyclists made mentally fatigued by an hour of Stroop task lasted about 16% longer to exhaustion (459.9 against 398.7 seconds, p = 0.008) with a shallower rise in perceived exertion and no change in oxygen consumption or heart rate, in a study its own authors call preliminary and in need of confirmation in larger samples 41. Eight people and twelve people, pointing opposite ways, is the current state of this literature.
- Reviews conclude it may help only when catecholamines are temporarily depleted, with a weak recommendation at most for cognition under stress and none for physical performance 42,43.
- Whether the doses used in those trials are safe to repeat, which nobody had asked. The first four-week dose-ranging safety trial gave 30 healthy men graded daily doses up to 4 g, each dose for four weeks with washout: no clinically meaningful or statistically significant dose-related abnormality in hematological, biochemical or electrolyte measures, no serious adverse events, mild-to-moderate events no more common than on placebo, and fasting plasma tyrosine rising only modestly and only at 4 g a day. The authors set 4 g/day as the no-observed-adverse-effect level under those conditions 44. Note the arithmetic: 4 g is the tested ceiling, and the cognition trials this page cites used 100 to 300 mg per kilogram — 7 to 21 g for a 70 kg adult, at doses nobody has given for four weeks. Three of that trial's four authors work for an amino acid manufacturer, which makes the ceiling they report more notable rather than less.
Sold asthe claim on the label, against the evidence
- “Tyrosine for everyday focus and energy.” The positive trials were under acute stress, cold, noise, sleep loss; there is no good evidence it improves an unstressed brain 42,43.
- “Tyrosine stacked with something else.” In 24 professional footballers given a single dose in a four-condition crossover, L-carnosine improved anaerobic power and agility, L-tyrosine mainly improved cognitive performance, and the combination reportedly raised peak power by about 17% and mean power by 16%, cut sprint and agility times by 7 to 13%, and shortened incongruent Stroop reaction time by about 15%, with lower perceived exertion and no difference in blood lactate 45. Gains of that size from one acute dose in 24 athletes are a reason to wait for independent replication, not a reason to buy the stack; the unchanged lactate is the detail to notice.
- And one stack exists only as a diagram. A 2026 review proposes betaine, tyrosine and Cordyceps as an integrated “mitochondrial-methylation-neurotransmitter” model for athletes, older adults and people with metabolic dysfunction — and contains no trial of the combination, closing instead with the statement that mechanistic and clinical investigations are still essential to substantiate the approach 46. The mechanism is the product.
What is strange about it
Nitisinone began as a weed killer. Chemists working from leptospermone, a natural herbicide, made a family of triketones; one of them, NTBC, damaged the corneas of rats and dogs because it blocked tyrosine breakdown, and that same action turned it into the treatment for tyrosinemia type I 17,47. The story has a third act, and then a fourth. Blood-feeding insects die when they ingest inhibitors of 4-hydroxyphenylpyruvate dioxygenase, and of four β-triketone herbicides screened on treated glass, ONLY nitisinone killed blood-fed Anopheles gambiae on tarsal contact — mesotrione, sulcotrione and tembotrione did not. It was equally lethal to pyrethroid-susceptible mosquitoes and to strains carrying multiple resistance mechanisms, across Anopheles, Culex and Aedes, by targeting blood digestion rather than any currently classified insecticide target — which makes the orphan drug for a tyrosine disorder a candidate for treated bednets 48. Then the fourth act: at the concentration that kills Anopheles, sand flies — the vector of visceral leishmaniasis — showed no difference in survival from controls over 14 days, indicating no insecticidal effect at that dose and a species-specific tolerance 49. The herbicide-to-drug-to-insecticide line does not extend to every blood-feeding insect, and the people who looked published the negative result.
Alkaptonuria was the disease Archibald Garrod used in 1902 to propose “chemical individuality,” the idea of inborn errors of metabolism; the urine darkens on standing because homogentisic acid oxidizes 10,50.
Before nitisinone, the only effective treatment for tyrosinemia type I was a liver transplant 17.
Where it connects
Topics on the map
On the map
A star in Conditional amino acids, one of 14. Precursor to dopamine, noradrenaline and thyroid hormone. The trials that find an effect are almost all under acute stress — cold, noise, sleep loss.
Sources
50 sources, numbered as they are cited. Every one was checked against PubMed or its publisher before it was cited here; the note under each says what it shows and what it does not.
- 1Roberts SA, Thorpe JM, Ball RO, Pencharz PB. Tyrosine requirement of healthy men receiving a fixed phenylalanine intake determined by using indicator amino acid oxidation.doi:10.1093/ajcn/73.2.276 · PMID 11157324
Six men; mean tyrosine requirement 6.0 mg/kg/day, safe 7.0.
- 2Fitzpatrick PF. Structural insights into the regulation of aromatic amino acid hydroxylation.doi:10.1016/j.sbi.2015.07.004 · PMID 26241318
PAH, TH and TPH and how each is regulated.
- 3Willemsen MA, Verbeek MM, Kamsteeg EJ, et al. Tyrosine hydroxylase deficiency: a treatable disorder of brain catecholamine biosynthesis.doi:10.1093/brain/awq087 · PMID 20430833
36 patients; two phenotypes; L-DOPA treatment.
- 4Citterio CE, Targovnik HM, Arvan P. The role of thyroglobulin in thyroid hormonogenesis.doi:10.1038/s41574-019-0184-8 · PMID 30886364
MIT and DIT on thyroglobulin tyrosines; coupling to T4 and T3.
- 5Lin S, Sanchez-Bretaño A, Leslie JS, et al. Evidence that the Ser192Tyr/Arg402Gln in cis tyrosinase gene haplotype is a disease-causing allele in oculocutaneous albinism type 1B (OCA1B).doi:10.1038/s41525-021-00275-9 · PMID 35027574
Tyrosinase as the rate-limiting enzyme of melanin; OCA1 and its missing heritability.
- 6Hunter T, Sefton BM. Transforming gene product of Rous sarcoma virus phosphorylates tyrosine.doi:10.1073/pnas.77.3.1311 · PMID 6246487
The discovery of tyrosine phosphorylation.
- 7van Spronsen FJ, Blau N, Harding C, et al. Phenylketonuria.doi:10.1038/s41572-021-00267-0 · PMID 34017006
Review of PKU and its treatment.
- 8Chinsky JM, Singh R, Ficicioglu C, et al. Diagnosis and treatment of tyrosinemia type I: a US and Canadian consensus group review and recommendations.doi:10.1038/gim.2017.101 · PMID 28771246
Succinylacetone screening; nitisinone and diet; liver cancer risk.
- 9Bouyacoub Y, Zribi H, Azzouz H, et al. Novel and recurrent mutations in the TAT gene in Tunisian families affected with Richner–Hanhart syndrome.doi:10.1016/j.gene.2013.07.066 · PMID 23954227
Tyrosinemia type II: features and genetics.
- 10Davison AS, Norman BP. Alkaptonuria: past, present and future.doi:10.1016/bs.acc.2023.02.005 · PMID 37268334
Review; uncertainty about the hypertyrosinemia nitisinone causes.
- 11Blau N. Sepiapterin: from sapropterin to next-generation therapy.doi:10.1016/j.ymgme.2026.110110 · PMID 42119485
BH4 as the hydroxylases’ cofactor.
- 12Joint WHO/FAO/UNU Expert Consultation. Protein and amino acid requirements in human nutrition.PMID 18330140
Phenylalanine plus tyrosine, 25 mg/kg/day.
- 13Hirasawa T, Satoh Y, Koma D. Production of aromatic amino acids and their derivatives by Escherichia coli and Corynebacterium glutamicum.doi:10.1007/s11274-025-04264-3 · PMID 39915353
Fermentation through the shikimate pathway.
- 14Eisenhofer G, Kopin IJ, Goldstein DS. Catecholamine metabolism: a contemporary view with implications for physiology and medicine.doi:10.1124/pr.56.3.1 · PMID 15317907
Synthesis and breakdown of catecholamines; the adrenal medulla and metanephrines.
- 15Averdunk L, Konzett K, Mandel H, et al. Tyrosine supplementation with high-protein diet as a therapeutic strategy for YARS1 deficiency.doi:10.1016/j.gim.2025.101682 · PMID 41518087
Nine children, with the enzyme assay in their own fibroblasts to show why the dose matters.
- 16Sun N, Samuels TN, Hoffman K, et al. Tyrosine supplementation rescues a growth defect in a humanized yeast model of YARS1 associated with CMT-DI.doi:10.3390/ijms27167481 · PMID 42653481
The organism is italicised out of the indexed title; the model is humanized yeast. Proof of concept for the DOMINANT disease, which had been the open question.
- 17Lindstedt S, Holme E, Lock EA, et al. Treatment of hereditary tyrosinaemia type I by inhibition of 4-hydroxyphenylpyruvate dioxygenase.doi:10.1016/0140-6736(92)92685-9 · PMID 1383656
Five patients treated with NTBC; liver transplant had been the only treatment.
- 18Han C, Ren C, Zhi T, et al. Disruption of fumarylacetoacetate hydrolase causes spontaneous cell death under short-day conditions in Arabidopsis.doi:10.1104/pp.113.216804 · PMID 23743712
Cited for the last step of tyrosine breakdown, to fumarate and acetoacetate.
- 19Scalise M, Galluccio M, Console L, et al. The human SLC7A5 (LAT1): the intriguing histidine/large neutral amino acid transporter and its relevance to human health.doi:10.3389/fchem.2018.00243 · PMID 29988369
LAT1 at the placenta and blood–brain barrier.
- 20Lu X. The role of large neutral amino acid transporter (LAT1) in cancer.doi:10.2174/1568009619666190802135714 · PMID 31376820
LAT1 carries thyroid hormones and drugs including L-DOPA across the blood–brain barrier.
- 21Kleta R, Romeo E, Ristic Z, et al. Mutations in SLC6A19, encoding B0AT1, cause Hartnup disorder.doi:10.1038/ng1405 · PMID 15286787
Neutral amino acid transport in gut and kidney.
- 22Kuypers AM, Das AM, Maiorana A, Heiner-Fokkema MR, van Spronsen FJ. Overview of European practices for management of tyrosinemia type 1: towards European guidelines.doi:10.1002/jimd.70089 · PMID 40965374
32 centers in 16 countries, compared against the same survey in 2014. Two real changes fall out of it.
- 23Gu P, Zhao Y, Hu J, et al. An optimized engineered bacterium for tyrosinemia type 1 therapy: a multi-species preclinical study.doi:10.1016/j.ymthe.2026.05.024 · PMID 42226462
Mice, rabbits and minipigs, with safety and microbiome disruption looked for and not found. No people yet.
- 24Salem KH, Elmoghazy AD. Ochronotic arthropathy: skeletal manifestations and orthopaedic treatment.doi:10.1530/EOR-2023-0112 · PMID 40071956
The skeletal disease of alkaptonuria.
- 25Ranganath LR, Psarelli EE, Arnoux JB, et al. Efficacy and safety of once-daily nitisinone for patients with alkaptonuria (SONIA 2): an international, multicentre, open-label, randomised controlled trial.doi:10.1016/S2213-8587(20)30228-X · PMID 32822600
138 patients; urinary homogentisic acid −99.7% at 12 months.
- 26Chandani HK, Hujjat SFZ, Chandani DK, et al. Harliku (nitisinone): first FDA-approved disease-modifying therapy for alkaptonuria.doi:10.1097/MS9.0000000000004033 · PMID 41377225
Editorial on the June 2025 approval.
- 27Grasso D, Balloni V, Bianchi E, et al. Plasma and urinary NMR metabolic profiling of the phenylalanine-tyrosine pathway in nitisinone-treated alkaptonuria: comparison of two dosing regimens and identification of a candidate pharmacodynamic biomarker.doi:10.1016/j.ymgme.2026.110255 · PMID 42685651
Twelve patients, before and after three months, with the obvious fix for the side effect tested and found wanting.
- 28van Vliet K, van Ginkel WG, van Dam E, et al. Dried blood spot versus venous blood sampling for phenylalanine and tyrosine.doi:10.1186/s13023-020-1343-7 · PMID 32245393
Plasma tyrosine about 6.4 µmol/L above the blood spot.
- 29Cyr D, Maranda B, Waters PJ. Quantitative succinylacetone measurement by gas chromatography-tandem mass spectrometry (GC-MS/MS) facilitates diagnosis, monitoring, and characterization of tyrosinemia type 1 and other hypersuccinylacetonemias.doi:10.1002/jmd2.70078 · PMID 41767123
A reference laboratory describing its own method change, and what the extra sensitivity is actually for.
- 30Grosu AL, Weber WA, Graf E, et al. O-(2-[18F]fluoroethyl)-L-tyrosine-PET-guided versus contrast-enhanced T1-weighted MRI-guided re-irradiation in patients with recurrent glioblastoma (GLIAA/NOA-10 ARO2013-01): a multicentre, open-label, randomised trial.doi:10.1016/S1470-2045(25)00642-4 · PMID 41429128
200 patients across 15 German centers, eight years of recruitment. A randomized test of an imaging strategy, which is rare.
- 31Takase M, Nakaya N, Kogure M, et al. Association of circulating metabolites and polygenic risk score with incident type 2 diabetes: a prospective community-based cohort study.doi:10.1186/s12933-025-02849-8 · PMID 40813662
12,461 adults, 43 metabolites, and a mediation analysis that separates association from pathway.
- 32Huidobro L, Cofre S, Santos JL, et al. Circulating amino acids and Type 2 diabetes in a Latin American population-based cohort.doi:10.1186/s12933-026-03146-8 · PMID 41888767
1,738 Chilean adults, with tyrosine measured and not reported among the significant associations. Most cohorts in this literature are European or Asian.
- 33Lee B, Heo WY, Kim JA, et al. Comprehensive evaluation of the NeoBase 2 non-derivatized MSMS assay and exploration of analytes with significantly different concentrations between term and preterm neonates.doi:10.3343/alm.2023.43.2.153 · PMID 36281509
Preterm cut-offs for tyrosine; succinylacetone separates transient tyrosinemia.
- 34Mayrink FD, Dorneles G, da Silva IM, Areda CA. Efficacy and safety of nitisinone for patients with alkaptonuria: a systematic review with metanalysis.doi:10.1016/j.ymgme.2025.109099 · PMID 40157162
Three studies, 218 patients; tyrosine up by a mean 709 µmol/L.
- 35Banderet LE, Lieberman HR. Treatment with tyrosine, a neurotransmitter precursor, reduces environmental stress in humans.doi:10.1016/0361-9230(89)90096-8 · PMID 2736402
100 mg/kg; cold and hypoxia; crossover.
- 36Shurtleff D, Thomas JR, Schrot J, et al. Tyrosine reverses a cold-induced working memory deficit in humans.doi:10.1016/0091-3057(94)90299-2 · PMID 8029265
Eight men at 4 °C; no effect at room temperature.
- 37Deijen JB, Orlebeke JF. Effect of tyrosine on cognitive function and blood pressure under stress.doi:10.1016/0361-9230(94)90200-3 · PMID 8293316
Sixteen people; 90 dB noise.
- 38Neri DF, Wiegmann D, Stanny RR, et al. The effects of tyrosine on cognitive performance during extended wakefulness.PMID 7794222
More than 24 hours awake; benefit lasted about three hours.
- 39Mahoney CR, Castellani J, Kramer FM, et al. Tyrosine supplementation mitigates working memory decrements during cold exposure.doi:10.1016/j.physbeh.2007.05.003 · PMID 17585971
Nineteen people in cold water; 300 mg/kg.
- 40Donnan KJ, Williams EL, Stanger N. Tyrosine supplementation is ineffective in facilitating soccer players' physical and cognitive performance during high-intensity intermittent exercise in hot conditions.doi:10.1371/journal.pone.0317486 · PMID 39820592
Eight players, 92 minutes at 32 °C, a commonly used dose. Small, and the stressor the earlier trials did not test.
- 41Solon-Júnior LJF, Boullosa D, Dias CV, de Sousa Fortes L. Effects of L-tyrosine ingestion on endurance performance in mentally fatigued cyclists.doi:10.1002/ejsc.70150 · PMID 41818465
Twelve cyclists, mentally fatigued by an hour of Stroop. The authors call their own findings preliminary.
- 42Jongkees BJ, Hommel B, Kühn S, Colzato LS. Effect of tyrosine supplementation on clinical and healthy populations under stress or cognitive demands: a review.doi:10.1016/j.jpsychires.2015.08.014 · PMID 26424423
Helps only when dopamine and noradrenaline are temporarily depleted.
- 43Attipoe S, Zeno SA, Lee C, et al. Tyrosine for mitigating stress and enhancing performance in healthy adult humans, a rapid evidence assessment of the literature.doi:10.7205/MILMED-D-14-00594 · PMID 26126245
Weak recommendation for cognitive stress; none for physical performance.
- 44Matsumoto H, Miura N, Naito M, Elango R. Evaluation of the safety and tolerability of L-tyrosine supplementation in healthy adult men: a randomized crossover trial.doi:10.3390/nu18122020 · PMID 42356406
30 men, graded doses, four weeks each with washout. Three of the four authors work for Ajinomoto, which manufactures amino acids; the result is a ceiling rather than a selling point, which is worth noting.
- 45Bilgin S, Bozyılan E, Buzdağlı Y, et al. Combined L-carnosine and L-tyrosine supplementation as an ergogenic strategy for physical and cognitive performance under fatigue in professional football players.doi:10.3389/fnut.2026.1868802 · PMID 42676602
24 players, four conditions, one acute dose. The size of the reported effects is the reason to be skeptical, not the reason to be impressed.
- 46Xu C, Cai W, Li J, Ma Y. Skeletal muscle mitochondrial-methylation-neurotransmitter crosstalk: a novel synergistic model of betaine, tyrosine, and Cordyceps for exercise performance in older adults, individuals with metabolic disorders, and healthy populations.doi:10.3389/fnut.2026.1812286 · PMID 42682565
A review of a product that has not been tested. Its own closing sentence says the clinical investigations are still essential.
- 47Lock EA. From weed killer to wonder drug.doi:10.1007/978-3-319-55780-9_16 · PMID 28755195
The herbicide origin of nitisinone.
- 48Stavrou-Dowd ZT, Parsons G, Rose C, et al. The β-triketone, nitisinone, kills insecticide-resistant mosquitoes through cuticular uptake.doi:10.1186/s13071-025-06939-0 · PMID 40745331
Four herbicides screened and only the drug worked, across three mosquito genera including pyrethroid-resistant strains.
- 49Augendre L, Alexandre Farias de Souza L, Costa Ribeiro MCVD, Depaquit J, Martinet JP, Prudhomme J. Evaluating the impact of nitisinone at mosquito-lethal doses on Lutzomyia longipalpis.doi:10.1371/journal.pntd.0013871 · PMID 41525420
A published failure to confirm, at the dose that kills mosquitoes. Sand flies tolerated it.
- 50Garrod AE. The incidence of alkaptonuria: a study in chemical individuality. 1902.PMID 8784780
The founding paper of inborn errors of metabolism.
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