Support compounds

Meldonium (Mildronate)

Updated · 20 sources · Editorial policy

Meldonium, sold as Mildronate, is a small synthetic molecule developed at the Latvian Institute of Organic Synthesis in the 1970s. It lowers the body’s supply of L-carnitine, the molecule cells need to burn long-chain fatty acids in mitochondria. In Latvia, Russia and several other former Soviet and Eastern European countries it is used as an “anti-ischemic” drug for angina, heart failure and stroke. It has never been approved in the United States.

Meldonium became widely known in sport. Testing in 2015 found it in 8.7% of urine samples at the Baku European Games, and the World Anti-Doping Agency (WADA) has prohibited it since January 1, 2016. Hundreds of athletes then tested positive, partly because traces of the drug stay in urine for months. Despite its reputation, no well-designed trial has shown that it improves performance in healthy athletes.

This page summarizes what clinical trials, pharmacokinetic studies and anti-doping research report. It is for education only and is not medical advice.

Property Detail
Drug class Metabolic modulator; inhibitor of L-carnitine synthesis and transport
Other names Mildronate, MET-88, THP, Quaterine
Origin Latvian Institute of Organic Synthesis, 1970s; manufacturer JSC Grindeks (Latvia)
Route Oral capsules; intravenous injection
Doses studied in trials 100–3,000 mg/day orally in angina; 500 mg twice daily in several trials; 250–1,000 mg IV in kinetic studies
Plasma half-life ≈5.6–6.6 h after a single IV dose; a very slow terminal phase (≈655 h) explains months-long urine detection
Main mechanism Blocks γ-butyrobetaine hydroxylase and the carnitine transporter OCTN2, lowering L-carnitine
US status Not FDA-approved
WADA status Prohibited at all times, class S4.4.3 (metabolic modulators); non-Specified Substance

What it is

Meldonium’s chemical name is 3-(2,2,2-trimethylhydrazinium)propionate. It has the formula C₆H₁₄N₂O₂ and a molecular weight of 146.19 g/mol (PubChem). The marketed form is the dihydrate (molecular weight 182.22 g/mol) (PubChem).

The molecule is a structural analogue of γ-butyrobetaine (GBB), the last precursor the body converts into L-carnitine. It was first developed as a growth-promoting agent for farm animals before its use in human medicine (Görgens et al., Drug Test Anal 2015). A 2026 review dates its development to 1974 and credits Ivars Kalvins as its inventor (Malm & Svensson, Front Sports Act Living 2026).

How it works

Meldonium has two main known targets (Dambrova et al., Pharmacol Res 2016):

  • γ-butyrobetaine hydroxylase, the enzyme that makes L-carnitine from GBB. Blocking it lowers new carnitine production.
  • OCTN2 (organic cation/carnitine transporter 2), which carries carnitine into cells and lets the kidneys reabsorb it. Blocking it lowers tissue carnitine and increases carnitine loss in urine.

Carnitine shuttles long-chain fatty acids into mitochondria. With less carnitine, cells burn less fat and more glucose. Glucose needs less oxygen per unit of energy (ATP) produced, so the proposed benefit is in tissue short of oxygen, such as heart muscle during ischemia (reduced blood flow) (Malm & Svensson 2026). Much of the detailed mechanistic evidence comes from rodent and cell studies.

The carnitine-lowering effect has been confirmed in people. In healthy volunteers given 500 mg twice daily for 4 weeks, plasma L-carnitine fell by 18% and plasma GBB roughly doubled. Eating meat partly offset the drop in carnitine (Liepinsh et al., J Pharm Pharmacol 2011).

Meldonium is therefore close to the opposite of a carnitine supplement. For the supplement itself, see L-Carnitine and Carnitine.

Pharmacokinetics

Meldonium’s kinetics are unusual: it clears quickly from plasma at first, then lingers in tissues for weeks to months. Human data come mainly from small studies in healthy volunteers:

Study Design Key finding
Peng et al., J Chromatogr B 2010 Single IV doses of 250, 500 and 1,000 mg in healthy Chinese volunteers Half-life 5.56, 6.46 and 6.55 h; peak level and exposure rose in proportion to dose; accumulation with repeated dosing
Zhang et al., Fundam Clin Pharmacol 2013 40 volunteers; oral 250–1,500 mg single doses, then 500 mg three times daily for 13 days Nonlinear kinetics: half-life depended on dose; the drug accumulated with repeated dosing
Forsdahl et al., J Pharm Biomed Anal 2018 6 volunteers; three 250 mg IV injections over 5 days; urine collected for 8 months Three-phase elimination with half-lives of 1.4 h, 9.4 h and 655 h (≈27 days); detectable in urine for 94–162 days
Rabin et al., Drug Test Anal 2019 32 athlete volunteers; 1.0 or 2.0 g/day orally for 3 weeks Several days to reach steady state; elimination over several months after stopping

The kidneys are the main route of excretion (Zhao et al., Drug Res 2016). The long tail is linked to the same transporter it blocks. OCTN2 concentrates meldonium in muscle during long-term use, and it then leaves tissue only slowly. In mice, giving carnitine or GBB during washout sped up elimination, while the diuretic furosemide did not (Liepinsh et al., Basic Clin Pharmacol Toxicol 2017).

Rabin and colleagues found that daily dose, frequency and duration of use were the main factors in how long elimination takes. This long detection window is central to the wave of positive tests in 2016.

Approved medical use

Meldonium is registered in Latvia, Lithuania and several other countries, including Russia, Ukraine, Georgia, Kazakhstan, Azerbaijan, Belarus, Uzbekistan and Moldova. A 2026 review also lists Poland among EU states where it is authorized through national procedures. It is not registered in the United States (Malm & Svensson 2026). In Russia and parts of Eastern Europe and Central Asia it is often available without a prescription.

Its main uses are cardiovascular: angina, heart failure and recovery after myocardial infarction (heart attack) (Dambrova et al. 2016). It has also been studied in neurological and metabolic disease (Schobersberger et al., Br J Sports Med 2017). We could not access an official product label, so this page does not list labeled doses. The dose of 500 mg twice daily was used in the healthy-volunteer carnitine study, was the most effective dose in the main angina trial, and is described as the “recommended” oral dose in a 2016 commentary (Arduini & Zammit, Postgrad Med J 2016).

What the research shows

Reviewers have repeatedly noted that, despite decades of use, there are few rigorous clinical trials of meldonium (Schobersberger et al. 2017). Much of the clinical literature is in Russian or Ukrainian, and many studies are small or uncontrolled.

Stable angina

The largest randomized trial, MILSS I, enrolled 512 patients with stable angina at 72 centers in 4 countries. It was a double-blind, placebo-controlled phase 2 study in which patients added meldonium or placebo to their standard therapy for 12 weeks (Dzerve et al., Medicina 2011). The primary outcome was the change in total exercise time on a bicycle test:

Arm (daily dose) Mean change in exercise time
Placebo −7.1 s
100 mg −2.1 s (not significant vs placebo)
300 mg +11.5 s (not significant vs placebo)
1,000 mg +35.2 s (p = 0.002)
3,000 mg Smaller increase than 1,000 mg

The authors concluded that 500 mg twice daily was the most effective dose. The absolute gain was about half a minute of exercise time, and the trial measured exercise tolerance, not heart attacks or survival.

Acute ischemic stroke

A randomized, double-blind phase 2 trial in China compared IV meldonium (n = 113) with another IV drug, cinepazide (n = 114), in acute ischemic stroke, with aspirin in both groups (Zhu et al., Clin Drug Investig 2013). At 3 months there was no significant difference in disability scores (modified Rankin Scale 0–1: p = 0.52; 0–2: p = 0.07), and serious adverse events were similar. There was no placebo arm, so the trial shows only that the two drugs performed similarly.

Right heart failure

In an open-label study without a control group, 20 patients with right heart failure from pulmonary arterial hypertension took 500 mg twice daily for 30 days (Kigitovica et al., J Clin Med 2025). Six-minute walk distance rose from 352 m to about 399 m (p = 0.021), and quality-of-life and breathlessness scores improved. BNP, a blood marker of heart strain, did not change. Without a placebo group, these results are preliminary.

Athletic performance

There is no good evidence that meldonium improves performance in healthy athletes. A 2026 review found only one placebo-controlled study in healthy athletes (Malm & Svensson 2026):

  • The trial: a Russian-language study of 20 elite biathletes and cross-country skiers over 15 days. Allocation was based on exercise-test results, not randomization, and the meldonium group started with a much higher VO₂max (maximal oxygen uptake).
  • The results: in the reviewers’ reanalysis, the meldonium group’s VO₂max and workload fell by day 15, its mood scores declined compared with placebo, and blood lactate after exercise did not differ.
  • Other studies: an often-cited study of 25 youth ice hockey players had no control group.

The reviewers concluded that the drug’s reputation as a performance enhancer rests mainly on anecdote, mechanism and animal data. Earlier commentators made the same point: restricting fat oxidation may be useful in an ischemic heart, but healthy muscle depends on carnitine for high rates of fat burning (Arduini & Zammit 2016).

About “endurance and recovery” claims. Meldonium is often described as boosting endurance, lowering lactate and speeding recovery. These effects come mostly from rodent experiments and patients with ischemic disease. No published human study has shown improved recovery, anaerobic capacity or maximal performance in healthy athletes (Malm & Svensson 2026).

Side effects and risks

What is known about safety

In the trials above, meldonium was generally well tolerated in the short term. No serious adverse events were reported in the healthy-volunteer kinetic studies (Zhang et al. 2013; Zhao et al. 2016). In the stroke trial, serious adverse events were similar to the comparator drug.

Long-term safety is much less clear. Reviewers note that toxicology studies meeting current international standards are scarce, especially in healthy people. They also point out that meldonium contains a hydrazine-type group, a chemical feature linked to liver injury in some other drugs; whether this matters for meldonium has not been studied adequately (Malm & Svensson 2026).

Carnitine depletion

Lowering carnitine is the drug’s intended effect, but severe carnitine deficiency is harmful. Inherited carnitine deficiency causes low blood sugar, fatigue, seizures and cardiomyopathy (heart muscle disease). Arduini and Zammit argued that standard doses are unlikely to cause such deficiency. They also warned that athletes taking much higher doses could push carnitine toward harmful levels (Arduini & Zammit 2016).

Who should be cautious

Without an accessible official label, we cannot list formal contraindications or interactions. Meldonium is excreted mainly by the kidneys and accumulates with repeated dosing, but we found no published studies of its use in people with reduced kidney function.

Anti-doping history

  • 2015. Meldonium was added to WADA’s Monitoring Program. A Cologne anti-doping laboratory study published that year found it in 182 of 8,320 routine doping-control samples (2.2%), across many sports, with urine concentrations as high as 1,428 µg/mL (Görgens et al. 2015).
  • Baku 2015 European Games. Only 23 of 662 athletes (3.5%) declared using meldonium, but 66 of 762 samples (8.7%) tested positive. Use was found in 15 of 21 sports (Stuart et al., Br J Sports Med 2016).
  • January 1, 2016. Meldonium was added to the WADA Prohibited List (Schobersberger et al. 2017). Tennis player Maria Sharapova was among the hundreds of athletes who had been taking it (Arduini & Zammit 2016).
  • After the ban. Meldonium accounted for 515 adverse analytical findings (positive tests) in 2016, then between 26 and 111 a year from 2017 to 2024. It has consistently ranked first or second among findings in its class (Malm & Svensson 2026).

On the current list, meldonium is named under S4.4.3, metabolic modulators. It is prohibited both in and out of competition and is classed as a non-Specified Substance (WADA 2026 Prohibited List). The same class lists trimetazidine, which reviewers group with meldonium as an inhibitor of fatty-acid oxidation (Malm & Svensson 2026).

Inadvertent exposure through food

A veterinary drug, Emidonol, breaks down into meldonium in livestock. Two pilot studies tested whether food could cause a positive test:

  • Milk. Volunteers who drank milk spiked with meldonium had peak urine levels of 7.5–18.6 ng/mL (Guddat et al., Drug Test Anal 2021).
  • Meat. Volunteers who ate a single portion of cooked meat from Emidonol-treated calves had urine levels of 219–386 ng/mL. For the first 2–14 hours these could exceed WADA’s minimum required reporting level, and meldonium stayed detectable for 24–28 hours (Postnikov & Efimova, Drug Test Anal 2026).

Key takeaways

  • A carnitine blocker, not a stimulant or anabolic. Meldonium lowers L-carnitine by blocking its synthesis and transport, shifting cells from burning fat toward burning glucose.
  • Used for heart disease in parts of Europe, not approved in the US. It is registered in Latvia, Russia and other former Soviet and some EU states, mainly for angina and heart failure.
  • Thin clinical evidence. The largest randomized angina trial found about 35 seconds more exercise time at 1,000 mg/day, with no benefit at lower doses.
  • No proven benefit for healthy athletes. The only placebo-controlled athlete study was small, non-randomized and showed no improvement.
  • Very long detection window. Plasma half-life is about 6 hours, but a slow terminal phase kept meldonium detectable in urine for 94–162 days in one IV study.
  • Prohibited in sport since 2016. WADA lists it under S4.4.3, prohibited at all times, and it remains among the most common positive findings in its class.

Sources

  1. Dambrova M, Makrecka-Kuka M, Vilskersts R, et al. Pharmacological effects of meldonium: biochemical mechanisms and biomarkers of cardiometabolic activity. Pharmacol Res. 2016;113(Pt B):771–780. PubMed.
  2. Malm C, Svensson M. Meldonium and human sport performance: a narrative review evaluating the evidence for ergogenic potential. Front Sports Act Living. 2026;8:1822778. PubMed.
  3. Schobersberger W, Dünnwald T, Gmeiner G, Blank C. Story behind meldonium-from pharmacology to performance enhancement: a narrative review. Br J Sports Med. 2017;51(1):22–25. PubMed.
  4. Görgens C, Guddat S, Dib J, et al. Mildronate (Meldonium) in professional sports - monitoring doping control urine samples using hydrophilic interaction liquid chromatography - high resolution/high accuracy mass spectrometry. Drug Test Anal. 2015;7(11-12):973–979. PubMed.
  5. Liepinsh E, Konrade I, Skapare E, et al. Mildronate treatment alters γ-butyrobetaine and l-carnitine concentrations in healthy volunteers. J Pharm Pharmacol. 2011;63(9):1195–1201. PubMed.
  6. Peng Y, Yang J, Wang Z, et al. Determination of mildronate by LC-MS/MS and its application to a pharmacokinetic study in healthy Chinese volunteers. J Chromatogr B Analyt Technol Biomed Life Sci. 2010;878(5-6):551–556. PubMed.
  7. Zhang J, Cai LJ, Yang J, et al. Nonlinear pharmacokinetic properties of mildronate capsules: a randomized, open-label, single- and multiple-dose study in healthy volunteers. Fundam Clin Pharmacol. 2013;27(1):120–128. PubMed.
  8. Zhao Z, Chen J, Peng W, et al. Single- and multiple-dose pharmacokinetic, safety and tolerability study of mildronate injection in healthy Chinese subjects. Drug Res (Stuttg). 2016;66(5):251–256. PubMed.
  9. Forsdahl G, Jančić-Stojanović B, Anđelković M, et al. Urinary excretion studies of meldonium after multidose parenteral application. J Pharm Biomed Anal. 2018;161:289–295. PubMed.
  10. Rabin O, Uiba V, Miroshnikova Y, et al. Meldonium long-term excretion period and pharmacokinetics in blood and urine of healthy athlete volunteers. Drug Test Anal. 2019;11(4):554–566. PubMed.
  11. Liepinsh E, Makarova E, Sevostjanovs E, et al. Carnitine and γ-butyrobetaine stimulate elimination of meldonium due to competition for OCTN2-mediated transport. Basic Clin Pharmacol Toxicol. 2017;120(5):450–456. PubMed.
  12. Dzerve V; MILSS I Study Group. A dose-dependent improvement in exercise tolerance in patients with stable angina treated with mildronate: a clinical trial “MILSS I”. Medicina (Kaunas). 2011;47(10):544–551. PubMed.
  13. Zhu Y, Zhang G, Zhao J, et al. Efficacy and safety of mildronate for acute ischemic stroke: a randomized, double-blind, active-controlled phase II multicenter trial. Clin Drug Investig. 2013;33(10):755–760. PubMed.
  14. Kigitovica D, Dzirnieks K, Lejnieks A, et al. Meldonium improves functional capacity in patients with right ventricular failure. J Clin Med. 2025;14(21):7787. PubMed.
  15. Arduini A, Zammit VA. A tennis lesson: sharp practice in the science behind the Sharapova case. Postgrad Med J. 2016;92(1090):429–430. PubMed.
  16. Stuart M, Schneider C, Steinbach K. Meldonium use by athletes at the Baku 2015 European Games. Br J Sports Med. 2016;50(11):694–698. PubMed.
  17. Guddat S, Görgens C, Sobolevsky T, Thevis M. Meldonium residues in milk: a possible scenario for inadvertent doping in sports? Drug Test Anal. 2021;13(11-12):1906–1910. PubMed.
  18. Postnikov PV, Efimova YA. HILIC-MS/MS detection of meldonium in meat from Emidonol-treated calves and volunteer urine after consumption: an anti-doping perspective. Drug Test Anal. 2026;18(9):1198–1202. PubMed.
  19. World Anti-Doping Agency. The 2026 Prohibited List: International Standard. In effect January 1, 2026. WADA 2026 Prohibited List.
  20. National Center for Biotechnology Information. PubChem Compound Summary: Meldonium (CID 123868) and meldonium dihydrate (CID 6918082). PubChem; PubChem.