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 AOD-9604 and Sobetirome (GC-1) — mechanism, side effects, legal status, and pricing.
AOD-9604 is a 16-amino-acid synthetic peptide corresponding to the C-terminal fragment of human growth hormone (residues 177-191) with an additional N-terminal tyrosine. Developed by Metabolic Pharmaceuticals (Australia) to isolate a purported 'lipolytic' activity of GH without GH-receptor-mediated growth or diabetogenic effects. AOD-9604 is NOT FDA-approved for any indication; controlled human trials for obesity did not demonstrate clinically meaningful weight loss, and obesity development was terminated in 2007.
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 Planned human trials in X-linked adrenoleukodystrophy were withdrawn before enrollment; all neurological data are preclinical only.
AOD-9604
Sobetirome (GC-1)
Category
Legal Status
Mechanism
Half-life
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
AOD-9604
Sobetirome (GC-1)
COA corpus from Disclosed Labs — independently tested batches only.
AOD-9604
97
COAs
99.5%
Avg purity
16
Labs
Sobetirome (GC-1)
1
COAs
97.3%
Avg purity
1
Labs
Clinical: AOD-9604 went through six randomized, double-blind, placebo-controlled Phase 1/2 trials across approximately 900 subjects (Stier et al., J Endocrinol Metab 2013). These established a safety profile indistinguishable from placebo — no effect on IGF-1, no impairment of glucose tolerance, no anti-AOD-9604 antibodies — but did NOT demonstrate clinically meaningful weight loss. A 24-week Phase 2b trial (~536 obese subjects) failed its primary efficacy endpoint and Metabolic Pharmaceuticals / Calzada terminated obesity development in 2007. Preclinical: Heffernan et al. (Int J Obes 2001, PMID 11673763; Endocrinology 2001, PMID 11713213) reported reduced body-weight gain and increased fat oxidation in obese mice and showed the lipolytic action did not require direct β3-AR agonism (β3-knock-out animals still responded). Ng et al. (Horm Res 2000, PMID 11146367) reported metabolic effects in obese Zucker rats without insulin-sensitivity impairment. Osteoarthritis exploration is limited to preclinical animal work — Kwon & Park (Ann Clin Lab Sci 2015, PMID 26275694) reported intra-articular AOD-9604 plus hyaluronic acid was superior to either alone in a collagenase-induced rabbit OA model; no adequately powered human OA trial has been published. Regulatory: NOT FDA-approved; widely-cited 'FDA GRAS' status has not been confirmed in the FDA GRAS Notice Inventory. PCAC voted AGAINST including AOD-9604 on the 503A Bulks List on December 4, 2024.
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.
AOD-9604 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
Key references
Disclosed Labs