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 BAM15 and Sobetirome (GC-1) — mechanism, side effects, legal status, and pricing.
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.
Sobetirome (GC-1) is a non-peptide small-molecule thyromimetic that selectively activates thyroid hormone receptor beta (TRβ) over TRα, designed to lower cholesterol and triglycerides without the cardiac effects of natural thyroid hormone. It completed Phase 1 trials in healthy volunteers for dyslipidemia (discontinued), but has no FDA or EMA approval and no validated human dose for any indication. Planned human trials in X-linked adrenoleukodystrophy were withdrawn before enrollment; all neurological data are preclinical only.
BAM15
Sobetirome (GC-1)
Category
Legal Status
Mechanism
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
BAM15
Sobetirome (GC-1)
COA corpus from Disclosed Labs — independently tested batches only.
BAM15
3
COAs
99.1%
Avg purity
1
Labs
Sobetirome (GC-1)
1
COAs
97.3%
Avg purity
1
Labs
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.
Key references
Human data are limited to Phase 1 trials in healthy volunteers conducted by QuatRx Pharmaceuticals; company press releases (not peer-reviewed) reported LDL-C reductions up to 22% (single-ascending-dose, 1–450 mcg) and 41% (multiple-ascending-dose, 10–100 mcg/day × 14 days) with no significant heart-rate or TSH change. Development for dyslipidemia was discontinued and no Phase 2/3 data exist. Two planned human trials in X-linked adrenoleukodystrophy (NCT01787578, NCT03196765) were withdrawn before enrolling any participants; zero human neurological efficacy data exist. In Abcd1 knockout mice (X-ALD model), intraperitoneal dosing (0.1–1.0 mg/kg/day, 7–28 days) lowered serum and tissue very-long-chain fatty acid (VLCFA) levels; chronic oral dosing (0.4–2.0 mg/kg, 11–18 weeks) modestly reduced brain C26 VLCFA by 13–24% after 12 weeks, though the higher dose caused up to 20% body-weight loss requiring early termination. In experimental autoimmune encephalomyelitis mice, sobetirome reduced clinical disease severity, axonal degeneration, and oligodendrocyte loss versus vehicle controls.
Key references
BAM15 and Sobetirome (GC-1) 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