Hordenine

Hordenine at a Glance

Hordenine is a simple phenethylamine alkaloid — tyramine with two methyl groups on the nitrogen. It forms during barley germination, which is why it survives malting and turns up in beer at a few milligrams per litre ^{4Reference 4Sommer T et al. · 2019In vitroMonitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitroView study →}, and it occurs as a minor amine in mescaline-bearing cacti, in canary grass, and in night-blooming cereus. It is sold as a stimulant ingredient in pre-workout and “fat-burner” products.

The evidence that matters most about it is a route comparison in horses. Given 2.0 mg/kg by rapid intravenous injection, hordenine produced a flehmen response and defecation within sixty seconds, respiratory rates up about 250%, heart rates roughly double resting values, and sweating — all of it gone within thirty minutes. Given the same 2.0 mg/kg by mouth, it produced no change in heart rate, respiratory rate, body temperature or behaviour ^{1Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →}.

Human data point the same way for a different reason. Hordenine is a genuine dopamine D2 receptor agonist in vitro, with a K_i of 13 µM ^{5Reference 5Sommer T et al. · 2017In vitroIdentification of the beer component hordenine as food-derived dopamine D2 receptor agonist by virtual screening a 3D compound database — in vitroView study →}; after drinking beer, free hordenine peaks in plasma at 12–17 nanomolar ^{3Reference 3Sommer T et al. · 2020Clinical trialAbsorption, biokinetics, and metabolism of the dopamine D2 receptor agonist hordenine (N,N-dimethyltyramine) after beer consumption in humans — human volunteersView study →}. That is roughly a thousand-fold short.

The Horse Experiment

Hordenine was studied in horses for a regulatory reason rather than a therapeutic one: it appears in post-race urine samples, because racehorses eat sprouting barley and canary grass, and a positive test needed interpreting. The result is the cleanest route-comparison anyone has published for this molecule.

Ten horses were given 2.0 mg/kg intravenously. The effects were immediate and unambiguous — flehmen and defecation inside a minute, substantial respiratory distress, respiratory rate up around 250%, heart rate roughly doubled, and sweating shortly after injection, with body temperature unaffected. They were transient: the animals appeared normal within thirty minutes, and when tested in a variable-interval responding apparatus half an hour later showed neither residual stimulation nor depression. Plasma peaked near 1.0 µg/mL and fell biexponentially, with an α-phase half-life of about 3 minutes and a β-phase half-life of about 35 minutes ^{1Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →}.

Animals given the same dose orally showed nothing — no change in heart rate, respiratory rate, basal body temperature or behaviour ^{1Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →}.

A German pharmacology group reached the same conclusion from the other direction. Studying hordenine in rats and dogs, they characterised it as an indirectly acting adrenergic agent that releases noradrenaline from stores — positively inotropic, raising systolic and diastolic pressure and peripheral blood flow, inhibiting gut movement, and having no effect on the psychomotor behaviour of mice. Every effect was short-lived and required doses far above anything achievable from feed, and their conclusion was that a measurable improvement in racehorse performance is “quite improbable” ^{2Reference 2Hapke HJ · 1995AnimalPharmacological effects of hordenine — animal modelView study →}.

This is the argument the supplement market has to answer. A compound sold for its stimulant effect, in an oral capsule, whose only controlled oral-versus-injected comparison found the oral route inert.

The Dose Gap

The modern case for hordenine is not the sympathomimetic one but a dopaminergic one, and it fails on the same arithmetic.

Hordenine was found by virtual screening of a food-compound database and confirmed in radioligand and functional assays: it activates D2 receptor G-protein signalling with about 76% of dopamine’s ligand efficacy and a K_i of 13 µM, while antagonising D2-mediated β-arrestin recruitment — making it a functionally selective, or biased, agonist ^{5Reference 5Sommer T et al. · 2017In vitroIdentification of the beer component hordenine as food-derived dopamine D2 receptor agonist by virtual screening a 3D compound database — in vitroView study →}. Its precursor N-methyltyramine binds with similar affinity (K_i 31.3 µM) and the same bias, and both are released continuously from barley malt during mashing and survive fermentation into the finished beer at 1.05–6.32 and 0.59–4.61 mg/L respectively ^{4Reference 4Sommer T et al. · 2019In vitroMonitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitroView study →}.

Then the exposure was measured. Four volunteers drank beer supplying 0.075 mg hordenine per kilogram of body weight. Maximum plasma concentrations of free hordenine were 12.0–17.3 nM, reached within the first hour; phase-II metabolism was dominated first by sulfation and later by glucuronidation; plasma half-lives were 52.7–66.4 minutes for the free compound; and 9.9% of the ingested dose appeared in urine within 24 hours. The authors’ own conclusion is the honest one: the levels observed “seem too low to provoke direct interaction with the dopamine D2 receptor” ^{3Reference 3Sommer T et al. · 2020Clinical trialAbsorption, biokinetics, and metabolism of the dopamine D2 receptor agonist hordenine (N,N-dimethyltyramine) after beer consumption in humans — human volunteersView study →}.

	Value
D2 receptor Ki in vitro 5Reference 5Sommer T et al. · 2017In vitroIdentification of the beer component hordenine as food-derived dopamine D2 receptor agonist by virtual screening a 3D compound database — in vitroView study →	13 µM
Peak free plasma after beer 3Reference 3Sommer T et al. · 2020Clinical trialAbsorption, biokinetics, and metabolism of the dopamine D2 receptor agonist hordenine (N,N-dimethyltyramine) after beer consumption in humans — human volunteersView study →	0.012–0.017 µM
Ratio	roughly 1,000-fold short

Absorption is not the barrier — hordenine plainly gets into the blood, and it is a selective substrate for MAO-B rather than the MAO-A that predominates in intestinal epithelium, so gut monoamine oxidase does not destroy it on the way through ^{8Reference 8Barwell CJ et al. · 1989In vitroDeamination of hordenine by monoamine oxidase and its action on vasa deferentia of the rat — in vitroView study →}. The barrier is arithmetic: the concentration that reaches a receptor from any realistic oral intake is orders of magnitude below the concentration the receptor needs.

Why It Turns Up in Drug Tests

Hordenine has a second life in forensic toxicology that has nothing to do with whether it works. It cross-reacts with opiate immunoassays: tested against a range of ELISA and RIA kits, it reacted most strongly with the morphine kit and least with the etorphine and buprenorphine kits, and it also interfered with thin-layer chromatography of oxymorphone, hydromorphone and apomorphine. The paper naming the problem also names the sources — beer in people, canary grass or barley in horses — and developed GC-MS and HPLC methods to tell hordenine apart from the opiates it mimics on a screen ^{9Reference 9Singh AK et al. · 1992In vitroScreening and confirmation of drugs in urine: interference of hordenine with the immunoassays and thin layer chromatography methods — in vitroView study →}.

So a person who drank beer, or a horse that grazed the wrong pasture, can produce a false-positive opiate screen. Of everything known about hordenine, this is the finding most likely to matter to someone in practice.

What It's Used For

The literature is larger than the molecule deserves, and almost all of it uses routes or concentrations the exposure data above rule out.

Evidence by IndicationStrength of support · Beta

01Sympathomimetic / stimulantShaky22%Two animal pharmacology studies, both finding the effect injection-only and dose-limited ^{1,2Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →Reference 2Hapke HJ · 1995AnimalPharmacological effects of hordenine — animal modelView study →}

02Dopamine D2 signallingShaky20%Well-characterised in-vitro agonism, undercut by measured human exposure ^{3,5Reference 3Sommer T et al. · 2020Clinical trialAbsorption, biokinetics, and metabolism of the dopamine D2 receptor agonist hordenine (N,N-dimethyltyramine) after beer consumption in humans — human volunteersView study →Reference 5Sommer T et al. · 2017In vitroIdentification of the beer component hordenine as food-derived dopamine D2 receptor agonist by virtual screening a 3D compound database — in vitroView study →}

03Alcohol-use and motor behaviour in rodentsShaky18%Two 2023 mouse and nematode studies at 40–50 mg/kg by injection ^{6,7Reference 6Li H et al. · 2023AnimalHordenine improves Parkinsonian-like motor deficits in mice and nematodes by activating dopamine D2 receptor-mediated signaling — animal modelView study →Reference 7Li Y et al. · 2023AnimalThe beer component hordenine inhibits alcohol addiction-associated behaviours in mice — animal modelView study →}

04Antibacterial / quorum-sensing inhibitionShaky12%One in-vitro study at milligram-per-millilitre concentrations ^{10Reference 10Zhou JW et al. · 2018In vitroHordenine: a novel quorum sensing inhibitor and antibiofilm agent against Pseudomonas aeruginosa — in vitroView study →}

Mechanisms

Pharmacokinetics

Better characterised than the pharmacology, and the reason the pharmacology does not translate. In four volunteers drinking beer at 0.075 mg hordenine/kg body weight, free hordenine peaked at 12.0–17.3 nM within the first hour. Phase-II metabolism was first dominated by sulfation, later by glucuronidation; plasma half-lives were 52.7–66.4 minutes for free hordenine and roughly 60–80 minutes longer for the sulfate and glucuronide. Urinary excretion peaked at 2–3.5 hours and accounted for 9.9% of the ingested dose over 24 hours ^{3Reference 3Sommer T et al. · 2020Clinical trialAbsorption, biokinetics, and metabolism of the dopamine D2 receptor agonist hordenine (N,N-dimethyltyramine) after beer consumption in humans — human volunteersView study →}.

Two mechanistic points fill in the picture. Hordenine is a highly selective substrate for liver MAO-B (K_m 479 µM, V_max 128 nmol/mg protein/h) and is not deaminated by the MAO-A of intestinal epithelium — the enzyme that destroys dietary tyramine — so dietary hordenine is expected to be absorbed rather than degraded in the gut ^{8Reference 8Barwell CJ et al. · 1989In vitroDeamination of hordenine by monoamine oxidase and its action on vasa deferentia of the rat — in vitroView study →}. And in horses, intravenous hordenine cleared with an α half-life of ~3 minutes and a β half-life of ~35 minutes, with total urinary hordenine peaking near 400 µg/mL and back to background by 24 hours ^{1Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →}.

So the compound is absorbed, cleared quickly, conjugated efficiently — and never present at a concentration close to any of its measured targets.

Clinical Trials

There are no clinical trials of hordenine for any indication. Human exposure is dietary (beer, malt products) and through unregulated supplements, neither of which has been studied for effect.

Last checked: September 2026.

Isolate vs. Plant Studies

Nearly everything here is isolate work: purified hordenine, injected into horses, rats, dogs and mice, or applied to receptors and bacteria ^{1,2,5,6,7,8,10Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →Reference 2Hapke HJ · 1995AnimalPharmacological effects of hordenine — animal modelView study →Reference 5Sommer T et al. · 2017In vitroIdentification of the beer component hordenine as food-derived dopamine D2 receptor agonist by virtual screening a 3D compound database — in vitroView study →Reference 6Li H et al. · 2023AnimalHordenine improves Parkinsonian-like motor deficits in mice and nematodes by activating dopamine D2 receptor-mediated signaling — animal modelView study →Reference 7Li Y et al. · 2023AnimalThe beer component hordenine inhibits alcohol addiction-associated behaviours in mice — animal modelView study →Reference 8Barwell CJ et al. · 1989In vitroDeamination of hordenine by monoamine oxidase and its action on vasa deferentia of the rat — in vitroView study →Reference 10Zhou JW et al. · 2018In vitroHordenine: a novel quorum sensing inhibitor and antibiofilm agent against Pseudomonas aeruginosa — in vitroView study →}. The one genuinely food-based human study is the beer biokinetic trial ^{3Reference 3Sommer T et al. · 2020Clinical trialAbsorption, biokinetics, and metabolism of the dopamine D2 receptor agonist hordenine (N,N-dimethyltyramine) after beer consumption in humans — human volunteersView study →}, and its result is the negative one.

The plant side barely exists. Night-blooming cereus carries hordenine alongside tyramine and N-methyltyramine, and the 1999 European veterinary review of that plant judged the amine concentrations too low to exert pharmacological effects — the herb is used as a drop-dose tincture, which makes the amine content smaller still ^{11Reference 11Committee for Veterinary Medicinal Produ · 1999ReviewSelenicereus grandiflorus summary report (EMEA/MRL/601/99-Final) — regulatory monographView study →}. Barley and beer deliver a few milligrams, quantified ^{4Reference 4Sommer T et al. · 2019In vitroMonitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitroView study →}. Peyote and San Pedro contain it as a minor companion to mescaline, and nothing attributes any part of their effect to it.

The pattern is consistent across every source: hordenine is present, measurable, and present in amounts too small to do what the isolate does.

Its Role in Plants

In barley, hordenine is not a curiosity but a defence and allelopathic compound, made along with the indole alkaloid gramine and released from roots to suppress competing plants. The two work on membranes: molecular simulation and experiments on artificial bilayers mimicking the plant plasma membrane showed both compounds interacting directly with the lipid phase, with gramine and hordenine differing in how they insert ^{12Reference 12Lebecque S et al. · 2018In vitroInteraction between the barley allelochemical compounds gramine and hordenine and artificial lipid bilayers mimicking the plant plasma membrane — in vitroView study →}. Both are classed as phytotoxic alkaloids persistent enough in soil to matter agriculturally, and soil bacteria capable of degrading them have been characterised ^{13Reference 13Wu Y et al. · 2025In vitroMicrobial degradation of two major phytotoxic alkaloids from barley — in vitroView study →}.

Its accumulation is developmental — it appears during germination and is highest in sprouting grain and malt, which is exactly why malting concentrates it into beer ^{4Reference 4Sommer T et al. · 2019In vitroMonitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitroView study →} and why racehorses grazing sprouting barley excrete it ^{1,9Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →Reference 9Singh AK et al. · 1992In vitroScreening and confirmation of drugs in urine: interference of hordenine with the immunoassays and thin layer chromatography methods — in vitroView study →}.

Prevalence in Nature

Hordenine is named for Hordeum, barley, and barley is its defining source: it forms during germination, is released continuously from malt during mashing, survives fermentation and conditioning intact, and reaches 1.05–6.32 mg/L in commercial beers, with N-methyltyramine at 0.59–4.61 mg/L alongside it. Caramel malts tended to release more than base malts ^{4Reference 4Sommer T et al. · 2019In vitroMonitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitroView study →}.

Beyond the grain it is a widely distributed minor amine. It occurs in the Cactaceae — peyote (Lophophora williamsii) and San Pedro (Echinopsis pachanoi), where it accompanies mescaline — and in night-blooming cereus’s amine fraction alongside tyramine and N-methyltyramine ^{11Reference 11Committee for Veterinary Medicinal Produ · 1999ReviewSelenicereus grandiflorus summary report (EMEA/MRL/601/99-Final) — regulatory monographView study →}. It is a notable constituent of canary grass (Phalaris species), which is how it enters grazing horses ^{9Reference 9Singh AK et al. · 1992In vitroScreening and confirmation of drugs in urine: interference of hordenine with the immunoassays and thin layer chromatography methods — in vitroView study →}, and is reported from bitter orange and a range of other plants.

No source concentrates it. In every plant where it has been measured it is a minor component, which is consistent with the exposure data: dietary hordenine intake is in the low milligram range even for a beer drinker ^{4Reference 4Sommer T et al. · 2019In vitroMonitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitroView study →}.

Discovery & Synthesis

Hordenine takes its name from barley, and has travelled under two other names — anhaline, from its isolation in cactus material, and eremursine. The original isolation reports predate the indexed literature and are not given a date here rather than a guessed one.

Biosynthetically it is tyrosine → tyramine → N-methyltyramine → hordenine, two successive N-methylations of a decarboxylated amino acid; the intermediate N-methyltyramine is itself present in beer at comparable levels ^{4Reference 4Sommer T et al. · 2019In vitroMonitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitroView study →}. Modern manufacture is straightforward: a combined chemoenzymatic route in continuous flow, starting from tyrosine, was published in 2022 as a sustainable synthesis of the natural product ^{14Reference 14Gianolio S et al. · 2022In vitroCombined chemoenzymatic strategy for sustainable continuous synthesis of the natural product hordenine — in vitroView study →}. Commercially, supplement-grade hordenine is a synthetic material sold as the hydrochloride, not a barley extract.

Analytical interest is ongoing, driven by the two contexts that matter — beer composition and supplement quality control — and includes electrochemical ion-transfer voltammetry methods validated on both beer and a bodybuilding supplement ^{15Reference 15Rudnicki K et al. · 2025In vitroDetermination of hordenine in beer samples and bodybuilding supplement at the electrified liquid-liquid interface — in vitroView study →}.

Patents: not yet researched (future patent-loop pass).

Toxicity & Safety

Hordenine keeps a moderate flag. Not because a hazard has been demonstrated at dietary levels — it has not — but because it is marketed as a stimulant at doses nobody has studied, in a product category with documented labelling problems, and because it is an amine with a real monoamine-oxidase interaction rationale.

Safety at a Glance

⚠️ Moderate toxicityCardiac caution

• Monoamine oxidase inhibitors. Hordenine is a selective MAO-B substrate that escapes intestinal MAO-A ^{8Reference 8Barwell CJ et al. · 1989In vitroDeamination of hordenine by monoamine oxidase and its action on vasa deferentia of the rat — in vitroView study →}. Someone on an MAOI loses a clearance route for an indirectly acting sympathomimetic — the same mechanism behind the tyramine “cheese reaction”.
• Supplements containing it are unreliably labelled. In a 2025 analysis of twelve sports supplements, none was accurately labelled; hordenine was among the ingredients found in inaccurate quantities, four products carried an undeclared stimulant, and two contained an FDA-prohibited one ^{16Reference 16Cohen PA et al. · 2025ObservationalPresence and quantity of ingredients in sports supplements purportedly containing the orchid Eria jarensis — observationalView study →}.
• Sympathomimetic in principle, at doses no capsule delivers. Injected, it doubles heart rate briefly ^{1Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →}. Whether an oral supplement dose does anything at all is unestablished, and the one matched oral comparison was negative.
• Cross-reacts with opiate immunoassays ^{9Reference 9Singh AK et al. · 1992In vitroScreening and confirmation of drugs in urine: interference of hordenine with the immunoassays and thin layer chromatography methods — in vitroView study →} — a false-positive drug screen is a documented consequence, from beer as well as from supplements.

Full Safety & Interactions Detail

The interaction rationale. Tyramine is dangerous with MAO inhibitors because intestinal and hepatic MAO normally destroy it before it can release noradrenaline systemically. Hordenine’s position is different in detail and similar in consequence: it is a selective substrate for MAO-B, and it is not deaminated by the MAO-A that predominates in intestinal epithelium, so it is absorbed rather than degraded in the gut — the study establishing this concluded that dietary hordenine is therefore “likely to be absorbed and could affect the sympathetic nervous system” through its inhibition of noradrenaline uptake ^{8Reference 8Barwell CJ et al. · 1989In vitroDeamination of hordenine by monoamine oxidase and its action on vasa deferentia of the rat — in vitroView study →}. Combining it with an MAOI, or with other sympathomimetics, is the interaction to avoid; there is no clinical study of that combination.

Cardiovascular. The direct evidence is the horse study: 2.0 mg/kg intravenously roughly doubled heart rate, raised respiratory rate by about 250% and caused substantial respiratory distress, resolving within thirty minutes ^{1Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →}. Nothing comparable has been done orally in any species, and the matched oral arm produced no cardiovascular change ^{1Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →}. People with cardiovascular disease have a reasonable basis for avoiding a stimulant-marketed sympathomimetic with no oral dose–response data at all.

Supplement quality. This is where the practical risk sits, and it is not really about hordenine. Of twelve sports supplements marketed as containing the orchid Eria jarensis, none was accurately labelled; the products contained inaccurate quantities of caffeine (0.1 to 665 mg per serving), theobromine, hordenine, yohimbine, N,N-dimethylphenethylamine and synephrine; nine either listed an undetected ingredient or contained an unlisted stimulant; and two contained 1,4-dimethylamylamine, prohibited by the FDA ^{16Reference 16Cohen PA et al. · 2025ObservationalPresence and quantity of ingredients in sports supplements purportedly containing the orchid Eria jarensis — observationalView study →}. A product sold for its hordenine content is, on that evidence, unlikely to contain what its label says. Hordenine is also discussed in the doping literature among the stimulants commonly stacked into pre-workout and thermogenic formulations ^{17Reference 17Jędrejko K et al. · 2023ReviewUnauthorized ingredients in “nootropic” dietary supplements: a review of the history, pharmacology, prevalence, international regulations, and potential as doping agents — reviewView study →}.

Reproductive. No reproductive or developmental toxicology exists for hordenine in any species.

Scope. There is no repeat-dose toxicity study, no genotoxicity package and no human safety trial. Dietary exposure through beer and malt has a long, uneventful history; that is a record for milligram amounts in a food matrix, not a clearance for concentrated capsules.

Dosage

No dose has been established for any purpose, and unusually there is a positive reason not to expect one to work: in the only controlled comparison of routes, an oral dose that had a large effect intravenously produced no measurable change at all ^{1Reference 1Frank M et al. · 1990AnimalHordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal modelView study →}.

Dietary intake sits in the low milligram range: a litre of beer supplies roughly 1–6 mg ^{4Reference 4Sommer T et al. · 2019In vitroMonitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitroView study →}. Supplement label amounts should be treated as unverified given the analytical findings above ^{16Reference 16Cohen PA et al. · 2025ObservationalPresence and quantity of ingredients in sports supplements purportedly containing the orchid Eria jarensis — observationalView study →}. These are doses studied in research and are not a personal recommendation.

References

1. Frank M, Weckman TJ, Wood T, et al. (1990). Hordenine: pharmacology, pharmacokinetics and behavioural effects in the horse — animal model. Equine Veterinary Journal. https://pubmed.ncbi.nlm.nih.gov/2269269/
2. Hapke HJ, Strathmann W (1995). Pharmacological effects of hordenine — animal model. Deutsche Tierärztliche Wochenschrift. https://pubmed.ncbi.nlm.nih.gov/8582256/
3. Sommer T, Göen T, Budnik N, Pischetsrieder M (2020). Absorption, biokinetics, and metabolism of the dopamine D2 receptor agonist hordenine (N,N-dimethyltyramine) after beer consumption in humans — human volunteers. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/31984737/
4. Sommer T, Dlugash G, Hübner H, Gmeiner P, Pischetsrieder M (2019). Monitoring of the dopamine D2 receptor agonists hordenine and N-methyltyramine during the brewing process and in commercial beer samples — in vitro. Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/30409657/
5. Sommer T, Hübner H, El Kerdawy A, et al. (2017). Identification of the beer component hordenine as food-derived dopamine D2 receptor agonist by virtual screening a 3D compound database — in vitro. Scientific Reports. https://pubmed.ncbi.nlm.nih.gov/28281694/
6. Li H, Gao M, Chen Z, et al. (2023). Hordenine improves Parkinsonian-like motor deficits in mice and nematodes by activating dopamine D2 receptor-mediated signaling — animal model. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/36883794/
7. Li Y, Vogel C, Kalinichenko LS, et al. (2023). The beer component hordenine inhibits alcohol addiction-associated behaviours in mice — animal model. Addiction Biology. https://pubmed.ncbi.nlm.nih.gov/37500485/
8. Barwell CJ, Basma AN, Lafi MA, Leake LD (1989). Deamination of hordenine by monoamine oxidase and its action on vasa deferentia of the rat — in vitro. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/2570842/
9. Singh AK, Granley K, Misrha U, et al. (1992). Screening and confirmation of drugs in urine: interference of hordenine with the immunoassays and thin layer chromatography methods — in vitro. Forensic Science International. https://pubmed.ncbi.nlm.nih.gov/1618458/
10. Zhou JW, Luo HZ, Jiang H, et al. (2018). Hordenine: a novel quorum sensing inhibitor and antibiofilm agent against Pseudomonas aeruginosa — in vitro. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/29353476/
11. Committee for Veterinary Medicinal Products (1999). Selenicereus grandiflorus summary report (EMEA/MRL/601/99-Final) — regulatory monograph. European Agency for the Evaluation of Medicinal Products. https://www.ema.europa.eu/en/documents/mrl-report/selenicereus-grandiflorus-summary-report-committee-veterinary-medicinal-products_en.pdf
12. Lebecque S, Crowet JM, Lins L, et al. (2018). Interaction between the barley allelochemical compounds gramine and hordenine and artificial lipid bilayers mimicking the plant plasma membrane — in vitro. Scientific Reports. https://pubmed.ncbi.nlm.nih.gov/29955111/
13. Wu Y, Li T, Zhou NY (2025). Microbial degradation of two major phytotoxic alkaloids from barley — in vitro. Journal of Hazardous Materials. https://pubmed.ncbi.nlm.nih.gov/40684507/
14. Gianolio S, Roura Padrosa D, Paradisi F (2022). Combined chemoenzymatic strategy for sustainable continuous synthesis of the natural product hordenine — in vitro. Green Chemistry. https://pubmed.ncbi.nlm.nih.gov/36353210/
15. Rudnicki K, Powałka E, Marciniak K, et al. (2025). Determination of hordenine in beer samples and bodybuilding supplement at the electrified liquid-liquid interface — in vitro. Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/40073602/
16. Cohen PA, Abarca R, Sovereign A, Gonzaga MJ, Gerona R (2025). Presence and quantity of ingredients in sports supplements purportedly containing the orchid Eria jarensis — observational. Clinical Toxicology. https://pubmed.ncbi.nlm.nih.gov/40679500/
17. Jędrejko K, Catlin O, Stewart T, et al. (2023). Unauthorized ingredients in “nootropic” dietary supplements: a review of the history, pharmacology, prevalence, international regulations, and potential as doping agents — review. Drug Testing and Analysis. https://pubmed.ncbi.nlm.nih.gov/37357012/

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