AOD-9604: A Tiny Piece of Growth Hormone with a Specific Job

AOD-9604 has an unusual development history compared to most peptides on a research catalog. It was deliberately engineered in the 1990s at Monash University in Australia as a “lipolytic fragment” — a piece of human growth hormone selected for the part of the molecule thought to mediate fat metabolism without the rest of the molecule’s growth-related activity. The therapeutic ambition didn’t pan out at scale, but the molecule remained relevant in research. This page summarizes that work, the verification we run on each lot, and the practical handling notes.

We are a research-supply operation, not a clinical lab. Everything below is intended for licensed research use only.

What AOD-9604 actually is

AOD-9604 is a synthetic 16-amino-acid peptide corresponding to residues 177-191 of human growth hormone, with an additional N-terminal tyrosine added for radiolabeling and stability purposes. The sequence is Tyr-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe. The two cysteines form a disulfide bridge between positions 7 and 14 — the same bridge that exists in the parent hGH molecule.

That bridge matters for handling: any reducing agent in the matrix will break it and turn AOD-9604 into a different, linear molecule with different properties. Molecular weight intact is around 1,815 g/mol.

How we verify our AOD-9604 batches

Disulfide-bridged peptides need a more careful verification than bridge-free peptides because the chromatogram for the linear (reduced) form runs at a different retention time than the bridged (oxidized) form, and a synthesis run with poor oxidation control will produce a mixture. We run every lot through Analytical Formulations, Inc.0% by area) and a mass-spec identity check that confirms the bridged form specifically — calculated [M+H]+ of 1,816 Da, with the linear form running at +2 Da.

The lab report is retained on file and posted to the AOD-9604 product page. We have rejected two lots in the past year on the bridged/linear mixture profile, where the supplier’s COA reported the named peptide as ≥99% but the chromatogram showed material under both peaks.

Reconstitution protocol we use in-house

AOD-9604 needs slightly more deliberate handling than bridge-free peptides:

Bring the vial to room temperature for 15-20 minutes.

Use bacteriostatic water (0.9% benzyl alcohol). Avoid any matrix containing reducing agents (DTT, β-mercaptoethanol, TCEP) — these will break the disulfide bridge and generate the linear form.

Add water down the inside wall of the vial. Swirl gently for 30-45 seconds.

Hold for 5 minutes before drawing. The bridge is intact in the lyophilized form and the reconstitution step itself does not threaten it under standard conditions.

A 5 mg vial reconstituted to 2 mL gives 2.5 mg/mL. Mark the reconstitution date on the cap.

Stability — what we observe in our cold-chain

Reconstituted AOD-9604 holds for 14-21 days at 2-8°C in our hands, slightly shorter than bridge-free peptides at the same nominal conditions. The disulfide bridge is the rate-limiting stability feature — slow oxidation/reduction equilibrium gradually shifts the population over weeks at refrigerator temperature.

We publish a 14-day usable window on the product page. For research designs that need longer hold, aliquot and freeze at -20°C — the bridge is most stable in the frozen state. The lyophilized form is the most stable state of all and is what the published shelf life is anchored to.

What the published research actually says

The original characterization came out of Monash. The most-cited animal-model paper on the lipolytic activity of the GH (177-191) fragment is from Heffernan and colleagues, Endocrinology, 2001, on chronic dosing in obese mice. The development program at Metabolic Pharmaceuticals (the Australian biotech that took the molecule into clinical trials in the 2000s) generated additional preclinical and Phase 2 human data that did not advance to broad regulatory approval.

Human evidence is structurally weaker than the animal-model evidence — the Phase 2 trials in obesity did not produce the magnitude of weight-loss effect that would have supported continued development. The molecule has subsequently been used in research and in some compounding-pharmacy contexts, but the strongest claim that can be cleanly made from the published literature is mechanism-level rather than outcome-level. Researchers planning extrapolation should treat that gap honestly.

Common questions from researchers

Does AOD-9604 cause growth-hormone effects? The intent of the engineering was the opposite — to keep the lipolytic activity of the (177-191) fragment without the somatogenic activity of the full molecule. Whether that separation is clean in practice is part of what the research literature has investigated, with mixed answers depending on the model system.

Is the powder white or off-white? White to off-white. A yellow tinge is not normal and should be flagged.

Does it tolerate freeze-thaw? A small number of cycles. We aliquot to single-use volumes if repeated draws are anticipated.

Why is the dose so much higher than other peptides on the catalog? The active fragment is a small piece of a larger native molecule, and the receptor-binding affinity reflects that. The molar dosing required to achieve the effects characterized in the rodent literature is correspondingly higher than for, say, BPC-157.

Related compounds we test

For researchers in the growth-hormone-axis literature: Tesamorelin operates upstream — it stimulates GH release rather than mimicking a fragment of GH itself. CJC-1295 and Sermorelin are also in the GH-releasing-hormone axis. Each runs through the same independent verification at Analytical Formulations, Inc.