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Compounds › Verified against primary sources

Meldonium (mildronate)

357 articles, 7 registered trials — and a detection window of months

Partially approvedVerified against primary sources

Experimental material. Read before using anything from here.

Nothing on this page is a medical recommendation, prescription or treatment plan. It is an organized translation of protocols circulating in research communities and, where it exists, of what published trials tested. The two are marked differently — and they are not equivalent.

Most of the compounds here have no FDA approval for human use. Several are sold labeled "research use only", which means they have not gone through purity, sterility or dosage controls for human consumption. A community-reported dose is not a validated dose: it is what someone reported having done.

Talk to a licensed health professional before considering any of these compounds. If you already use one and feel anything unexpected, seek care — do not wait for the next routine test.

Specific caution for this compound: The measured urinary detection window reaches 117 days after six days of use, and several months after three weeks. Anyone subject to anti-doping testing should treat it as unavailable, not as something to suspend in advance.

Summary

Cardioprotective agent developed at the Latvian Institute of Organic Synthesis, in Riga, and registered in Latvia and Russia. It is the best-documented compound in this reference's entire Eastern European block: 357 articles, 35 clinical trials and 7 records on ClinicalTrials.gov. It inhibits L-carnitine biosynthesis — not the other way around — shifting cardiac metabolism from fat to glucose. It has been on the WADA Prohibited List since January 1, 2016.

What it is

Meldonium — also mildronate, MET-88 or quaterine — is 3-(2,2,2-trimethylhydrazinium)propionate. It was developed at the Latvian Institute of Organic Synthesis, in Riga, and is sold as a cardioprotective drug in Latvia, Russia and nearby countries.

It is the best-documented compound in this reference's entire block of Eastern European drugs: 357 articles on PubMed, 35 tagged as clinical trials and 7 registered trials on ClinicalTrials.gov — against zero for the Khavinson bioregulator family.

The mechanism is the opposite of what it seems

Many people assume that a compound linked to carnitine serves to increase carnitine. It is the opposite. According to the review by Dambrova and colleagues, meldonium inhibits γ-butyrobetaine hydroxylase, an enzyme of L-carnitine biosynthesis, and also the OCTN2 transporter. The result is a drop in L-carnitine.

The declared logic of the design is exactly that: with less carnitine, ischemic tissue stops accumulating cytotoxic intermediates of fatty acid beta-oxidation — a process that consumes a lot of oxygen — and metabolism shifts to glucose, which yields more ATP per oxygen spent. Long-chain acylcarnitines and TMAO fall along with it.

In the central nervous system the explanation does not hold together, because the brain does not use fatty acids as fuel. The review by Sjakste, Gutcaits and Kalvinsh — the latter the inventor of the compound — proposes a second mechanism, independent of carnitine, via nitric oxide production in the vascular endothelium.

How much evidence exists

Survey conducted on PubMed and ClinicalTrials.gov on September 4, 2026.

Evidence baseQueryResult
PubMedmeldonium OR mildronate357 articles
PubMed(meldonium OR mildronate) AND (Clinical Trial[Publication Type] OR Randomized Controlled Trial[Publication Type])35 articles
ClinicalTrials.govintervention containing meldonium or mildronate7 records

The registered trials

These are the seven. Note that two of them test meldonium combined with Mexidol (ethylmethylhydroxypyridine succinate), under the BRAINMAX brand — the two compounds appear separately in the same import catalog that originated this list.

RecordPhaseConditionNStatus
NCT018310112Acute ischemic stroke — mildronate vs. cinepazide227Completed
NCT018003572Acute ischemic stroke — versus placebo240Unknown status
NCT066489021/2Metastatic renal carcinoma with treatment-related fatigue60Completed in 2024
NCT073049211Omega-3 metabolism — Riga Stradins, Latvia48Completed
NCT056898274Post-COVID asthenia — BRAINMAX, with Mexidol160Completed
NCT059396224Post-COVID asthenia with fMRI — BRAINMAX, with Mexidol30Completed
NCT07568574N/APerformance substances under medical supervision in elite athletes60Enrolling by invitation

The point that decides use: the detection window

Meldonium entered the WADA prohibited list on January 1, 2016, after a year in the 2015 Monitoring Program. In the first months of 2016, anti-doping laboratories reported an abnormal number of samples with high concentrations.

What matters to anyone facing anti-doping testing is not the ban itself, but how long the molecule remains detectable. Two independent studies measured this, and the result is out of the ordinary:

StudyDose testedDetection windowNote
Görgens et al., 2017
German Sport University, Cologne
500 mg, single dose (5 volunteers)up to 65 daysAbove the 10 ng/mL limit of quantification
Görgens et al., 20172 × 500 mg/day for 6 days (5 volunteers)up to 117 daysBiphasic, non-linear and dose-dependent excretion
Rabin et al., 2018
WADA + FMBA (Russia)
1.0 g or 2.0 g/day for 3 weeks (32 volunteers)several monthsSteady state in blood takes days to reach

Practical reading of these numbers

  • Six days of use can yield almost four months of detection. There is no short clearance window for this compound — it is the pharmacokinetic feature that defined the whole case.
  • Excretion is biphasic and non-linear. The concentration drops fast at first and then drags along a long plateau. A low concentration on the test does not prove old use, and it was precisely that ambiguity that WADA had to manage.
  • Anyone subject to anti-doping testing in any federated sport should treat meldonium as unavailable, and not as something to suspend a few weeks in advance.
  • The 2018 study was co-authored by WADA itself — Olivier Rabin is the agency's scientific director — in partnership with the Russian federal agency. It is evidence of unusual quality for a compound of this origin.

Doses used in published human studies

This is not a dose recommendation: it is a record of what was administered in published studies, with the purpose of each. Outside the study context, these numbers do not transfer.

StudyDoseDurationPurpose of the study
Görgens et al., 2017500 mg, oral, single dose1 dayMeasure the detection window
Görgens et al., 20172 × 500 mg/day, oral6 daysMeasure the detection window with repeated dosing
Rabin et al., 20181.0 g/day or 2.0 g/day, oral3 weeksLong-term pharmacokinetics in healthy athletes
Nechaeva and Zheltikova, 2015not specified in the abstract12 weeksEarly post-infarction period, added to standard therapy

What the post-infarction trial found

According to PubMed, the randomized trial by Nechaeva and Zheltikova followed 67 patients aged 40 to 70 after myocardial infarction: 32 on standard therapy for ischemic heart disease and 35 on the same therapy plus mildronate for 12 weeks.

The mildronate group had fewer angina attacks (p = 0.001), fewer extrasystoles (p = 0.002), fewer paroxysmal rhythm disturbances (p = 0.001) and lower mean arterial pressure (p = 0.001). The authors recorded no adverse effects during the period.

The caveat: a Russian article, 67 participants, 12 weeks of follow-up. It is a signal, not a hard endpoint of mortality or reinfarction.

Regulatory status

  • Latvia, Russia and nearby countries: registered as a cardioprotective medicine, with decades of use.
  • Brazil: no registration.
  • United States and European Union: not approved.
  • WADA: prohibited since January 1, 2016, in and out of competition.

What this page does not answer

I did not locate, in an accessible primary source, a consolidated dosing regimen in a package insert that I could reproduce safely. The Latvian or Russian Mildronate package insert is the valid reference — and it is from there, not from here, that a dose should come.

I also did not assess interactions. A compound that alters carnitine metabolism and shifts the heart's energy substrate is not neutral in someone already taking a cardiovascular drug. That is a conversation with a cardiologist, not with a website.

References

This page did not come from the secondary source. Every number was collected by me from the sources listed below, on September 4, 2026, and the query used is stated above.
  1. Dambrova M et al. Pharmacological effects of meldonium: Biochemical mechanisms and biomarkers of cardiometabolic activity. Pharmacol Res. 2016;113(Pt B):771-780. doi:10.1016/j.phrs.2016.01.019
  2. Sjakste N, Gutcaits A, Kalvinsh I. Mildronate: an antiischemic drug for neurological indications. CNS Drug Rev. 2005;11(2):151-68. doi:10.1111/j.1527-3458.2005.tb00267.x
  3. Gorgens C et al. The atypical excretion profile of meldonium: comparison of urinary detection windows after single- and multiple-dose application in healthy volunteers. J Pharm Biomed Anal. 2017;138:175-179. doi:10.1016/j.jpba.2017.02.011
  4. Rabin O et al. Meldonium long-term excretion period and pharmacokinetics in blood and urine of healthy athlete volunteers. Drug Test Anal. 2018;11(4):554-566. doi:10.1002/dta.2521
  5. Nechaeva GI, Zheltikova EN. [Effects of Meldonium in Early Postmyocardial Infarction Period]. Kardiologiia. 2015;55(8):35-42. PMID 26761970
  6. Records consulted on ClinicalTrials.gov: NCT01831011, NCT01800357, NCT06648902, NCT07304921, NCT05689827, NCT05939622, NCT07568574

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