Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of 3,5-Diiodo-L-thyronine (3,5-T2) and Cardarine (GW-501516) — 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.
Cardarine (GW-501516) is a synthetic small-molecule PPARδ agonist — not a SARM and not a peptide, despite gray-market marketing that groups it with SARMs. Developed by GSK and taken into human lipid trials, its clinical development was discontinued around 2007 after rodent carcinogenicity findings. It has no regulatory approval anywhere, is WADA-prohibited at all times, and is sold only as a gray-market research chemical.
3,5-Diiodo-L-thyronine (3,5-T2)
Cardarine (GW-501516)
Category
Legal Status
Mechanism
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
3,5-Diiodo-L-thyronine (3,5-T2)
No pricing data yet.
Check 3,5-Diiodo-L-thyronine (3,5-T2) prices →Cardarine (GW-501516)
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
Cardarine (GW-501516)
2
COAs
99.7%
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
Completed GSK-sponsored human trials in low-HDL/dyslipidemia subjects (2.5–10 mg/day, 12 weeks) improved lipids (HDL-C +16.9%, triglycerides −16.9%, LDL −7.3%; Sprecher et al., 2012). GSK halted development around 2007 after a 2-year rodent carcinogenicity study reported tumors across multiple organs; a 2019 mouse study found GW-501516 accelerated colitis-associated colorectal cancer. A published human case report documented severe rhabdomyolysis and hepatotoxicity from self-administration. Never approved for any indication; not a peptide.
Key references
3,5-Diiodo-L-thyronine (3,5-T2) and Cardarine (GW-501516) 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
Disclosed Labs