AOD-9604

Dominikowski A, Rękoś Z, Olejarz M, Szczepanek-Parulska E, Domin R, RuchaŁa M

Frontiers in endocrinology

A 2026 narrative review synthesizing the pharmacology of peptides marketed to modulate the growth hormone-IGF-1 axis, including AOD9604 (described as human growth hormone fragment 176-191), that catalogs structural characteristics and reported pharmacologic effects for this compound class and stratifies the evidence into tiers ranging from regulatory-grade trial data to a near-total absence of controlled human studies for several of the peptides discussed.

Mendias CL, Awan TM

Sports medicine (Auckland, N.Z.)

A 2026 narrative review of approved and unapproved peptides used in sports-medicine and musculoskeletal-research contexts, including AOD-9604, reporting that several of these peptides show favorable outcomes in animal-model studies of tissue and metabolic pathways, while rigorous controlled human data remain scarce across the class.

Cox HD, Smeal SJ, Hughes CM, Cox JE, Eichner D

Drug testing and analysis

A 2014 in vitro study incubated AOD9604 (a synthetic peptide comprising the C-terminal fragment of human growth hormone, residues 177-191, with an added N-terminal tyrosine) in serum and urine to map its metabolic breakdown pathway; the researchers identified six candidate metabolites and found one fragment, sequence CRSVEGSCG, to be markedly more stable than the parent peptide or the other breakdown products.

Heffernan M, Summers RJ, Thorburn A, Ogru E, Gianello R, Jiang WJ, et al.

Endocrinology

A 2001 mechanistic study in obese mice and beta3-adrenergic-receptor (beta3-AR) knockout mice found that chronic intraperitoneal administration of AOD9604 reduced body weight and adiposity in wild-type animals, an effect that correlated with upregulated adipose-tissue beta3-AR mRNA expression; the chronic body-weight and lipolytic-sensitivity effect was absent in beta3-AR knockout mice, while an acute increase in energy expenditure and fat oxidation persisted independent of the beta3-AR pathway.