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Head-to-head comparison of 3,5-Diiodo-L-thyronine (3,5-T2) and BAM15 — mechanism, side effects, legal status, and pricing.
3,5-Diiodo-L-thyronine (3,5-T2) is a non-peptide endogenous iodothyronine produced by deiodination of T3 and T4. It is not an approved drug and has no registered human clinical trials as a study intervention. The only direct human-administration data come from a single 2-person case report. WADA/anti-doping status for 3,5-T2 specifically is unconfirmed; a 2019 secondary source suggested thyroid hormones as a class were not prohibited, but no current primary WADA citation was found.
BAM15 is a synthetic small-molecule mitochondrial uncoupler (protonophore) — not a peptide — studied preclinically for obesity and metabolic disease as a potentially safer alternative to DNP. It has never been tested in humans, has no regulatory approval, and was added to the WADA Prohibited List as an AMPK activator. It is sold as a gray-market research chemical.
3,5-Diiodo-L-thyronine (3,5-T2)
BAM15
Category
Legal Status
Mechanism
Side Effects
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3,5-Diiodo-L-thyronine (3,5-T2)
No pricing data yet.
Check 3,5-Diiodo-L-thyronine (3,5-T2) prices →BAM15
COA corpus from Disclosed Labs — independently tested batches only.
3,5-Diiodo-L-thyronine (3,5-T2)
2
COAs
97.4%
Avg purity
2
Labs
BAM15
3
COAs
99.1%
Avg purity
1
Labs
No approved human drug or registered interventional clinical trial exists. The only direct human-administration data are from a single 2-person case report: oral 3,5-T2 (~5 μg/kg body weight) for 28 days reportedly raised resting metabolic rate by ~15% and lowered body weight by ~4 kg, with no significant changes in principal clinical parameters and no observed side effects. Endogenous 3,5-T2 has been measured in healthy human serum (~0.22–0.33 nM) and as a metabolite in liothyronine (T3) pharmacokinetic trials. Preclinical rodent studies show 3,5-T2 rapidly increases resting metabolic rate (faster than T3), reduces adiposity in high-fat-diet models by increasing fat oxidation, stimulates liver and skeletal muscle mitochondrial bioenergetics, and activates AMPK in skeletal muscle. One rat regimen (25 μg/100g BW, 4 weeks) showed no HPT-axis suppression or cardiac hypertrophy at that specific dose/duration; however, one mouse model (unsaturated-fat diet) showed no improvement in NAFLD or insulin sensitivity.
Key references
In diet-induced obese mice, BAM15 reduced fat mass and improved insulin sensitivity without changing food intake or lean mass (Nature Communications 2020); other mouse work shows benefit in diabetes, and in sepsis/acute kidney injury. Rodent PK is ~67% oral bioavailability with a ~1.7 h half-life; there is no human PK, safety, or dosing data. Not approved; not a peptide.
3,5-Diiodo-L-thyronine (3,5-T2) and BAM15 are both in the Metabolic category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Contraindications
Lab Testing