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The proposed mechanisms include: Beta-3 adrenergic receptor stimulation: Promoting fat cell breakdown (lipolysis), especially in visceral adipose tissue Inhibition of lipogenesis: Reducing the conversion of carbohydrates into fat No IGF-1 stimulation: Unlike full hGH, neither peptide appears to significantly raise IGF-1 levels in animal studies No effect on blood glucose: Both appear metabolically neutral with regard to insulin sensitivity in most studies The Key Difference: Structure and Stability AOD-9604’s added tyrosine residue and disulfide bridge confer structural changes that affect receptor binding kinetics and metabolic half-life