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Tiratricol (TRIAC)

Also known as: TRIAC, Triiodothyroacetic acid, Teatrois, Téatrois, Emcitate

2
1 · Natty510 · Enhanced

Lower numbers = closer to natural. Higher numbers = more enhanced.

Why this rating?

Tiratricol (TRIAC) is a thyroid-hormone analogue that potently suppresses pituitary TSH, about 18x more potently than T3 itself (Menegay, Juge & Burger 1989, PMID 2588936), but its thyromimetic action is "dissociated," meaning that central (pituitary) potency does not translate into the peripheral tissue/metabolic-rate effect that actually drives fat loss. In a controlled trial, obese subjects on a 1200kcal/day diet plus 2.8mg/day of TRIAC for 2 months lost no more weight than diet-only controls, and heart rate was unchanged (Beck-Peccoz et al. 1988, PMID 3361080); in healthy volunteers, 1.7-3.4mg/day left resting/basal metabolic rate unchanged versus a clear increase with thyroxine (Bracco et al. 1993, PMID 8325946). It is not anabolic and does not affect testosterone or muscle building, and unlike T3 it lacks controlled evidence of a real peripheral fat-loss or performance edge. The main verified effect is central thyroid-axis suppression, not a physique-enhancing one. Rated 2, in line with compounds that carry real hormonal/health risk but little demonstrated muscle- or physique-enhancing benefit.

Overview

A thyroid-hormone analogue (triiodothyroacetic acid) that is an analogue of a naturally circulating metabolite of T3. It acts as a thyroid-hormone receptor agonist and, unlike T3/T4, can enter cells independently of the MCT8 transporter, which is why it is used to treat MCT8 deficiency (Allan-Herndon-Dudley syndrome). It has also been used for thyroid-hormone resistance syndrome and, in France, as adjuvant thyroid-cancer therapy. Separately, it has been widely (and improperly) marketed as a weight-loss aid on the strength of its thyroid-receptor agonism, prompting FDA/Health Canada regulatory warnings, but controlled trials found its central (pituitary TSH-suppressing) potency does not reliably translate into the peripheral, metabolic-rate-raising effect that would actually drive fat loss, so the marketed benefit is scientifically shaky even before weighing the thyrotoxic risk.

Important Warnings

  • •Controlled trials found no extra weight loss and no metabolic-rate increase versus diet/placebo at doses that fully suppress TSH. The fat-burner premise itself is not well supported
  • •Unsupervised/excess dosing (the dietary-supplement context regulators warned against) has caused documented thyrotoxicosis, avoid with any cardiovascular disease
  • •Suppresses the thyroid axis (TSH) far more potently than T3. Taper, do not stop abruptly, and monitor thyroid function
  • •FDA and Health Canada warned (1999-2000) against weight-loss supplements containing tiratricol; suspended in Brazil (2003)
  • •Not approved in the US or Canada; medical use requires specialist supervision
  • •No validated recreational fat-loss dose exists

Purpose & Use Cases

MCT8 Deficiency (Allan-Herndon-Dudley Syndrome)

Its approved use (Emcitate, EU 2025): treats the peripheral thyrotoxicosis of MCT8 deficiency by entering cells independently of the missing MCT8 transporter and restoring thyroid signaling.

Thyroid-Hormone Resistance Syndrome

Used to treat resistance to thyroid hormone: a TR-beta agonist that can act where normal thyroid signaling is impaired.

Adjuvant Thyroid-Cancer Therapy (France)

Used to suppress TSH as part of thyroid-cancer management.

Marketed (Improperly) as a Fat Burner

Sold in weight-loss supplements on the assumption that thyroid-receptor agonism raises metabolic rate the way T3 does, a use that drew FDA and Health Canada warnings due to thyrotoxic risk. Controlled trials undercut the premise itself: 2.8mg/day for 2 months produced no extra weight loss versus diet alone in obese subjects (Beck-Peccoz et al. 1988), because TRIAC's potent central TSH suppression does not reliably carry over into peripheral fat-burning.

Benefits

  • Powerful thyroid-hormone-receptor agonism at the pituitary (TSH suppression roughly 18x more potent than T3)
  • Enters cells independently of MCT8 (the basis of its approved MCT8-deficiency use)
  • Established medical role in MCT8 deficiency and thyroid-hormone resistance
  • Suppresses TSH (useful in thyroid-cancer management)

Good to Know

A T3 metabolite analogue that bypasses MCT8

Tiratricol (TRIAC) is an analogue of a naturally circulating T3 metabolite and acts on the thyroid-hormone receptor much like T3, but it can enter cells without the MCT8 transporter that T3/T4 depend on. That single property is why it is the approved treatment (Emcitate, EU 2025) for MCT8 deficiency, where thyroid hormone otherwise cannot get into cells.

It silences your thyroid far more than it burns fat

TRIAC suppresses pituitary TSH about 18x more potently than T3 (Menegay, Juge & Burger 1989), which is why even modest doses crush your own thyroid hormone production. But its action is "dissociated", that central potency does not carry over to the peripheral tissue effect that actually drives fat loss. In obese subjects on a 1200kcal/day diet, adding 2.8mg/day of TRIAC for 2 months produced no extra weight loss versus diet alone, and heart rate stayed flat (Beck-Peccoz et al. 1988); in healthy volunteers, 1.7-3.4mg/day left resting/basal metabolic rate unchanged, unlike an equivalent dose of thyroxine (Bracco et al. 1993). It is not a reliable substitute for T3 as a cutting aid.

The fat-loss use is exactly what regulators warned against

Despite the weak controlled-trial evidence for peripheral fat loss, tiratricol has been widely marketed as a weight-loss aid on thyroid-hormone-agonist grounds. The FDA and Health Canada issued public warnings in 1999-2000 against dietary supplements containing it, and Brazil suspended it in 2003, a documented 2002 case report describes an OTC user developing thyrotoxicosis (nervousness, tremor, insomnia, suppressed TSH, elevated T3) that resolved on stopping the supplement (Bauer et al. 2002).

It suppresses your thyroid axis

As a thyroid-hormone-receptor agonist it suppresses pituitary TSH by negative feedback, an effect deliberately used in thyroid-cancer management and RTH. In a fat-loss context that means it blunts your own thyroid signaling, so it should be tapered, not stopped cold, and used only with thyroid-function monitoring. This is a thyroid-axis issue, distinct from the testosterone/PCT question.

Not anabolic and not WADA-banned

Tiratricol works through thyroid signaling, not muscle-building or performance pathways. As a thyroid-hormone analogue it is not on the WADA Prohibited List (consistent with thyroid hormones), but that is not a safety endorsement. The cardiac and thyroid-axis risks are real.

Dosage Guidelines

Experience LevelDosage Range
Beginner0 – 0 mcg/day
Intermediate350 – 1400 mcg/day
Advanced1400 – 3400 mcg/day
Frequency
Medically: dispersible tablets 1-3 times daily, individually titrated (short ~6-6.5h half-life favors split dosing). Human dose-ranging/PK studies used single daily oral doses.
Typical Cycle Length
4 – 8 weeks
Notes

There is no validated or medically endorsed recreational fat-loss protocol, no dose shown here should be read as a recommendation. The figures above are anchored to real published human dosing, not invented: the MCT8-deficiency trial (Groeneweg et al. 2019, PMID 31377265) started patients at 350mcg/day, titrating in 350mcg increments to a mean final dose of ~38.3mcg/kg bodyweight (range 6.4-84.3mcg/kg); TRIAC dose-response/PK testing used 350, 700, 1400 and 2800mcg oral doses (Menegay et al. 1989); and controlled trials in obese and healthy euthyroid adults used 2.8mg/day (Beck-Peccoz et al. 1988) and 1.7-3.4mg/day (Bracco et al. 1993) respectively. In its approved (Emcitate) use it is given as dispersible tablets 1-3 times daily (dispersed in water or via feeding tube/syringe), starting by body weight and increased gradually roughly every 2 weeks based on serum T3 levels under specialist supervision. Unsupervised/self-dosing carries real thyrotoxic and thyroid-axis risk (see Bauer et al. 2002 case report) and, per the controlled obesity trial above, is not established to actually accelerate fat loss.

Half-Life

6h22min ± 29min after a single 1050mcg oral/IV dose (Menegay, Juge & Burger 1989, PMID 2588936); much shorter than T3's ~1 day, which is why clinical dosing is split 1-3x/day.

Side Effects

Thyrotoxicosis from Unsupervised/Excess Dosing

uncommon
Severity
3/5

Nuanced picture: in its pivotal, supervised MCT8-deficiency trial, heart rate, blood pressure and premature atrial contractions actually improved on treatment (P=0.01, P=0.0037 respectively, Groeneweg et al. 2019, PMID 31377265), because it lowers the patient's own pathologically elevated T3. But unsupervised/excessive dosing (the dietary-supplement context the FDA and Health Canada warned against) can cause real thyrotoxicosis in a normal-thyroid person, a documented case report describes an 87-year-old on an OTC tiratricol supplement developing nervousness, tremor, insomnia and fatigue with suppressed TSH and elevated T3, resolving after stopping (Bauer et al. 2002, PMID 12059130).

Mitigation

Cardiac and thyroid-function monitoring for any use outside supervised clinical titration; avoid in anyone with cardiovascular disease. A beta-blocker may be used medically for symptomatic tachycardia.

Thyroid-Axis Suppression

common
Severity
3/5

By acting on the thyroid-hormone receptor it suppresses pituitary TSH via negative feedback roughly 18x more potently than T3 (Menegay et al. 1989), blunting the natural thyroid axis (this TSH suppression is deliberately exploited in thyroid-cancer therapy and RTH).

Mitigation

Use only under specialist supervision with thyroid-function monitoring; do not stop abruptly.

Sweating / Irritability / Anxiety / Nightmares

common
Severity
2/5

Per the EMA product information, up to 1 in 10 patients experience excessive sweating (hyperhidrosis), irritability, anxiety and nightmares, classic thyroid-overactivity symptoms, usually worst at treatment start or dose increases and improving within days. In the pivotal trial, "transiently increased perspiration or irritability" were the only treatment-related adverse events, occurring in 6 of 45 patients (13%) (Groeneweg et al. 2019).

Mitigation

Slow titration; dose reduction if severe.

Diarrhea

common
Severity
2/5

GI disturbance listed among the common (up to 1 in 10) side effects in the EMA product information for Emcitate.

Mitigation

Usually transient; stay hydrated.

General Mitigation Strategies

Tiratricol is a genuine thyroid-hormone-receptor agonist whose main verified risk is thyroid-axis suppression, with thyrotoxicosis (tachycardia, raised blood pressure, atrial ectopy, tremor, insomnia) a real but dose/context-dependent risk. Supervised clinical trials actually showed cardiac parameters improving, while unsupervised over-the-counter use has produced documented thyrotoxicosis. In medicine it is titrated slowly to T3 levels with cardiac and thyroid-function monitoring. Used as an unmonitored fat burner it is both risky and, per the controlled obesity trial, not established to work, the FDA and Health Canada specifically warned against weight-loss supplements containing it. Avoid entirely if you have cardiovascular disease. This is a thyroid-axis drug: no SERM/PCT is relevant; recovery depends on the thyroid axis restarting after TSH suppression.

Post Cycle Therapy (PCT)

✓PCT Not Required

Does not affect the HPT (testosterone) axis, so no traditional PCT applies. It does suppress the hypothalamic-pituitary-THYROID axis via TSH suppression. Taper rather than stop abruptly and allow thyroid recovery, under monitoring.

How It Works

Once inside cells, tiratricol activates the thyroid-hormone receptor in a similar way to endogenous T3, driving thyroid-hormone-mediated gene transcription. Its key clinical distinction is that it can enter cells independently of the monocarboxylate transporter 8 (MCT8) that T3 and T4 rely on, so in MCT8 deficiency, where thyroid hormone cannot reach cells normally, tiratricol restores thyroid signaling in the periphery. As a thyroid-hormone-receptor agonist it powerfully suppresses pituitary TSH by negative feedback, roughly 18x more potently than T3 (Menegay et al. 1989): which is the basis of its adjuvant use in thyroid cancer and RTH. However, its action is "dissociated": that central potency is not matched by an equivalent peripheral (metabolic-rate) effect at tolerable doses. Controlled human trials found no increase in resting/basal metabolic rate at 1.7-3.4mg/day in healthy volunteers (Bracco et al. 1993) and no extra weight loss versus diet alone at 2.8mg/day in obese subjects (Beck-Peccoz et al. 1988): the opposite of what T3 produces at comparable thyromimetic doses.

Fundamentals

Reference on the practices relevant to Tiratricol (TRIAC): how they are done and where they go wrong. Not a recommendation to use it.

Bloodwork: what to measure and when→

The markers that matter here

Warning signs & when to seek care→

When to stop and get help

WADA Status

✓Not Prohibited by WADA

Tiratricol is a thyroid-hormone analogue; thyroid hormones are not on the WADA Prohibited List (consistent with T3/T4). As a substance not approved in many jurisdictions, athletes in tested sport should verify the current list and non-approved-substance rules before any use.

References

Last updated: July 18, 2026