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T2 (3,5-Diiodothyronine)

Also known as: 3,5-Diiodothyronine, 3,5-T2, Diiodothyronine

4
1 · Natty510 · Enhanced

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

Why this rating?

T2 (3,5-diiodothyronine) is a naturally occurring iodothyronine, an active thyroid-hormone metabolite most likely produced from T3 via an as-yet-unidentified enzymatic pathway. Unlike T3, its best-characterized action is rapid and non-genomic: it binds subunit Va of cytochrome c oxidase (complex IV) and relieves ATP's allosteric inhibition of mitochondrial respiration, increasing oxygen consumption and energy expenditure. It is marketed as a "milder, cardiac-sparing" fat burner. Human evidence is extremely thin: a single small 2011 pilot study (Antonelli et al., n=2, placebo-controlled) found continuous 300mcg/day raised resting metabolic rate and cut body weight ~4% over a few weeks with no change in FT3/FT4/TSH and no cardiac side effects, a real but statistically negligible signal, while almost everything else (dose-response, fat-mass, lipid data) is rodent/in-vitro, and it still has genuine thyromimetic effects at the heart and pituitary. Rated 4 as a metabolic-rate enhancer with a plausible but essentially unestablished human effect that works outside anabolic pathways, below T3 (rated 5, more robust human evidence of a genuine metabolic/fat-loss effect), above tiratricol (rated 2, whose larger controlled human trials found no measurable metabolic-rate or weight-loss benefit despite potent TSH suppression), and on par with T4 (also rated 4) as a milder, thinner-evidence thyroid-axis tool.

Overview

An endogenous diiodothyronine thyroid-hormone metabolite (two iodine atoms at the 3 and 5 positions) that is marketed as a fat-loss supplement. Its distinguishing feature versus T3 is a rapid, non-genomic action directly at the mitochondria to raise metabolic rate. In rodents it increases energy expenditure and reduces fat mass without some of the classic thyrotoxic effects seen with T3, but that "cardiac-sparing" profile is contested, and in humans it has only been tested in a single tiny pilot study (n=2), so robust controlled data are essentially lacking.

Important Warnings

  • •Human efficacy/safety evidence is limited to a single 2-subject pilot trial. Treat as experimental
  • •Has real thyromimetic effects at the heart and pituitary despite "cardiac-sparing" marketing
  • •Can suppress TSH and disrupt the thyroid axis
  • •Avoid in anyone with cardiovascular or thyroid disease
  • •No validated human dosing protocol from a large controlled trial exists. The ranges given are community/clinical-blog derived, not clinical prescribing guidance

Purpose & Use Cases

Metabolic Rate Increase

Directly stimulates mitochondrial respiration (via cytochrome c oxidase), raising oxygen consumption and energy expenditure, the basis of its use as a fat burner.

Fat / Lipid Effects (rodent data)

In rats, T2 lowered body weight and fat mass and reduced serum triglycerides and cholesterol. These findings are preclinical, not established in humans.

Claimed "Milder" Thyroid Effect

Marketed as raising metabolism with less thyrotoxic/cardiac impact than T3. This claim is contested and largely untested in people.

Benefits

  • Rapid, non-genomic stimulation of mitochondrial metabolic rate
  • Increases energy expenditure in preclinical models
  • Reduced fat mass and improved lipids in rodent studies
  • Marketed as gentler on the heart/thyroid axis than T3 (unproven in humans)

Good to Know

A thyroid-hormone metabolite that works on the mitochondria

T2 is a naturally occurring diiodothyronine, most likely made from T3. Its signature action is non-genomic: it binds cytochrome c oxidase (complex IV) and removes ATP's brake on respiration, so it raises mitochondrial oxygen use and metabolic rate quickly, a different route from T3's slower, gene-transcription-based effect.

The "cardiac-sparing" claim is contested, not proven

T2 is sold as a metabolism booster that spares the heart and thyroid axis. In rodents it did raise metabolism and cut fat with fewer thyrotoxic signs, but the review evidence notes deleterious cardiac and hypothalamic-pituitary-thyroid effects at higher doses, and T2 does have thyromimetic action at the myocardium and pituitary. Treat "less cardiac than T3" as a marketing claim, not an established fact.

Human evidence is very thin

Almost all of the metabolic and fat-loss data are from rats and cell studies. The only human trial (Antonelli et al. 2011) had just 2 subjects. It found ~4% body-weight loss and a rise in resting metabolic rate at 300mcg/day with no change in thyroid labs, but a sample of 2 cannot establish real-world efficacy or safety, and there is no established human dosing from a larger trial. This is a thyroid-axis compound (not a testosterone/PCT issue), if it suppresses your TSH, no SERM helps; you are relying on the axis to recover.

Not anabolic and not WADA-banned

T2 works on metabolic rate, not muscle-building or performance pathways. As a thyroid hormone it is not on the WADA Prohibited List (consistent with T3/T4). That is not a safety endorsement. The cardiac and thyroid-axis risks are real and the human data are minimal (essentially one 2-subject pilot study).

Dosage Guidelines

Experience LevelDosage Range
Beginner100 – 150 mcg/day
Intermediate150 – 250 mcg/day
Advanced250 – 300 mcg/day
Frequency
Typically once daily; the only human trial (Antonelli et al. 2011) and community/clinical-blog protocols use continuous daily dosing, no formally established optimal split exists.
Typical Cycle Length
6 – 12 weeks
Notes

There is no established human dosing protocol from a large controlled trial. The efficacy and dose-response data reviewed are still predominantly rodent/in-vitro. The only human data are a small 2011 pilot study (Antonelli et al., n=2, placebo-controlled crossover) in which continuous oral T2 at 300mcg/day raised resting metabolic rate and cut body weight by about 4% over several weeks, with no change in FT3/FT4/TSH and no cardiac side effects reported. The ranges above are anchored to non-peer-reviewed community/clinical-blog guidance (not a controlled trial) that treats ~100-200mcg/day as a typical dose and 300mcg/day as an upper ceiling. Doses above that are reported to risk hyperthyroid-type symptoms, and rodent data show cardiac/HPT-axis effects at very high, supraphysiological exposures. That same source states T2 needs ~6 weeks of daily use to reach steady state and is generally used continuously/long-term rather than in short cycles, though there is no safety data for exposures beyond the few-week human pilot trial. Because T2 has real thyromimetic effects at the heart and pituitary, self-dosing carries genuine thyroid-axis and cardiac risk. Treat any use as experimental, and consider monitoring TSH/free T3/free T4 and heart rate.

Side Effects

TSH Suppression / Thyroid-Axis Disruption

uncommon
Severity
3/5

T2 has thyromimetic effects at the pituitary and can suppress TSH release. Exogenous dosing can therefore blunt the natural thyroid axis, as with other thyroid hormones.

Mitigation

Avoid stacking with other thyroid agents; monitor thyroid function (TSH, free T3/T4) if used.

Cardiac (Thyromimetic) Effects

uncommon
Severity
3/5

Despite the "cardiac-sparing" marketing, T2 has agonistic (thyromimetic) effects at myocardial tissue, and some studies report deleterious cardiac and thyroid-axis effects at high doses.

Mitigation

Avoid in anyone with cardiovascular disease; keep any use conservative given the lack of human safety data.

Unknown Human Safety Profile

common
Severity
2/5

The side-effect profile in humans is essentially uncharacterized. The only human trial (Antonelli et al. 2011) enrolled just 2 subjects at 300mcg/day and reported no cardiac or thyroid-lab changes, but a sample of 2 cannot rule out uncommon or dose/duration-dependent effects.

Mitigation

Treat as experimental; the absence of larger trial data is itself a risk.

General Mitigation Strategies

The honest position is that T2 is a thyroid-hormone metabolite with real thyromimetic activity but almost no controlled human data, a single 2-subject pilot study aside. It is not the risk-free "clean" thyroid booster it is marketed as. It can suppress TSH and has myocardial effects. If used at all, avoid combining it with T3/T4 or stimulants, keep doses conservative, and monitor thyroid function and heart rate. Anyone with cardiac or thyroid conditions should avoid it.

Post Cycle Therapy (PCT)

✓PCT Not Required

Does not affect the HPT (testosterone) axis, so no traditional PCT applies. It can, however, suppress the hypothalamic-pituitary-THYROID axis via TSH suppression, if used, taper rather than stop abruptly and allow thyroid function to recover, as with other thyroid agents.

How It Works

T2 (3,5-diiodothyronine) is a naturally occurring diiodothyronine, most probably produced from T3. Its best-characterized effect is non-genomic and mitochondrial: it binds subunit Va of cytochrome c oxidase (complex IV of the electron transport chain) and abolishes the allosteric inhibition of respiration by ATP, producing a rapid stimulation of oxygen consumption (seen at picomolar concentrations, and more rapidly than T3 acts). It also stimulates the thyroid-hormone receptor TR-beta and increases energy expenditure. Because part of its action bypasses nuclear thyroid-receptor gene transcription, it is described as raising metabolic rate quickly; however, it also has thyromimetic (thyroid-hormone-like) effects at myocardial tissue and at the pituitary, where it can suppress TSH release.

Fundamentals

Reference on the practices relevant to T2 (3,5-Diiodothyronine): 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

T2 (3,5-diiodothyronine) is a thyroid hormone and is not listed on the WADA Prohibited List, consistent with T3/T4, which are not prohibited. As a non-approved substance, athletes in tested sport should verify the current list and consider anti-doping rules around non-approved substances before use.

References

Last updated: July 18, 2026