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Structurally, AOD 9604 retains a disulfide-linked cyclic conformation formed by cysteine residues, preserving key features of the native GH region responsible for lipid metabolism signaling

AOD-9604 dosage protocols leverage this synthetic 16aminoacid fragment (TyrhGH 177191) to support lipolysis (fat breakdown) and inhibit lipogenesis (fat storage) without elevating IGF1 levels or causing insulin resistance [1] [2]

In preclinical heart failure models, NNMT enzyme inhibition markedly reduced cardiac 1-MNA (by 77.1%), improved cardiac function, reduced left ventricular hypertrophy and fibrosis, and decreased pro-inflammatory gene expression

These statements have not been evaluated by the FDA