RESEARCH MONOGRAPH · KDC-MN-291

Tiratricol (TRIAC)

May 9, 2026 Kodiac biolabs Research Revised May 30, 2026 3 min read

Our opinion on this compound

69/100

The TR-beta-selective T3 metabolite with a genuinely interesting MCT8 rescue story, niche but mechanistically clean

TRIAC (3,3',5-triiodothyroacetic acid) is what you get when you deaminate and oxidatively decarboxylate the alanine side chain of T3. So it's an endogenous T3 metabolite that retains thyroid hormone receptor binding but shows a meaningful preference for TR-beta over TR-alpha. That receptor selectivity is the whole pharmacological story and it's why TRIAC has gotten a second life as an orphan drug.

The interesting clinical work in the last decade is the Allan-Herndon-Dudley syndrome research. AHDS is caused by mutations in MCT8, the thyroid hormone transporter that gets T3 into neurons. The kids have profound neurological impairment from inadequate brain T3 even though their serum thyroid hormones can look elevated. TRIAC enters the brain via a different transport mechanism (it doesn't need MCT8) and can partially rescue the central hypothyroidism. The Triesence/Emcitate trials (the Visser/Friesema groups in the Netherlands) are genuinely interesting work, and the regulatory approval pathway for the indication is moving.

What we like: clean receptor pharmacology, TR-beta selectivity that partly avoids cardiac TR-alpha activation, and a niche-but-real clinical indication where the mechanism actually maps to the clinical effect. The MCT8-independent transport story is one of the more elegant pieces of thyroid pharmacology in recent memory.

What we dont love is how TRIAC has historically been marketed as a weight-loss compound on the back of its thyromimetic activity. That's a misuse of the pharmacology and the cardiac and bone effects of supraphysiologic TR-beta stimulation are real even with the beta-selectivity. The receptor selectivity reduces the cardiac TR-alpha activation, it doesnt eliminate downstream metabolic effects of excess thyroid signaling.

Mechanistically distinct from T3 in the practical sense: shorter half-life, different transporter dependence, and a different tissue distribution profile because the brain penetration is genuinely different. So TRIAC research isnt redundant with T3 research, theyre adjacent.

Sourcing is okay. TRIAC is a small molecule, well-characterized, available pharma-grade as Téatrois (in some European markets) and research-grade from a smaller list of suppliers. The molecule is stable, HPLC purity is easy to verify, and the failure modes are minor.

Evidence: 70
Mechanism: 88
Reliability: 75
Safety: 60
Sourcing: 70
Value: 65
Signal: 60
Staying power: 65

Plain-language summary Intrigue 55 / 100

Tiratricol (TRIAC) is a natural T3 metabolite that retains thyroid receptor activity but with a preference for the TR-beta subtype over TR-alpha. That selectivity matters because TR-alpha drives the cardiac effects of thyroid hormone, while TR-beta dominates in liver and pituitary. The result is a drug that suppresses TSH and affects metabolism without proportionally raising heart rate. Approved in France, Mexico, and other markets for resistance to thyroid hormone (Refetoff syndrome), a rare condition where TR-beta is mutant and unresponsive. Off-label use for fat loss in bodybuilding has caused fatalities from cardiac arrhythmia and severe TSH suppression and is strongly discouraged. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

T3 metabolite (3,3',5-triiodothyroacetic acid)

A naturally occurring T3 metabolite with thyroid-receptor activity; used in resistance to thyroid hormone syndrome and (off-label) for fat loss.

Abstract

Tiratricol (TRIAC, 3,3',5-triiodothyroacetic acid; CAS 51-24-1; molecular formula C14H9I3O4; molecular weight 621.93) is a natural T3 metabolite formed by deamination and oxidative decarboxylation of T3. The compound retains thyroid hormone receptor activity with TR-beta selectivity (approximately 2- to 4-fold over TR-alpha). Approved in France, Mexico, and other markets for resistance to thyroid hormone syndrome (Refetoff syndrome), where the TR-beta selectivity allows TR-beta target tissue (pituitary, liver) effects without the cardiac TR-alpha hyperthyroid effects. Off-label use in obesity and as an athletic fat-loss compound has been documented; the FDA has issued warnings against unapproved supplement products containing tiratricol owing to severe thyrotoxic adverse events at supratherapeutic doses. Plasma half-life is approximately 7 hours, shorter than T4 but longer than T3. Used as a reference TR-beta-selective thyromimetic in research.

Mechanism of action

T3 metabolite with TR-beta-selective thyroid hormone receptor activity. Approximately 2- to 4-fold TR-beta over TR-alpha selectivity.

Reported research dose ranges

Clinical (resistance to thyroid hormone) 350 to 2800 mcg in the published literature. Off-label fat loss (not recommended) 0.5 to 3 mg. Rodent studies 0.05 to 0.5 mg/kg.

References

Beck-Peccoz P, Persani L. Thyrotropin-secreting pituitary adenomas. Endocr Rev 1996.
Sherman SI, Ladenson PW. Organ-specific effects of tiratricol: a thyroid hormone analog with hepatic, not pituitary, superagonist effect. J Clin Endocrinol Metab 1992.
Cohen-Lehman J, et al. Effects of amiodarone therapy on thyroid function. Nat Rev Endocrinol 2010.

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KDC-MN-291

The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

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Tiratricol (TRIAC)

Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

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Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

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