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Research in preclinical models suggests that AOD 9604 may support lipolysis by upregulating beta-3 adrenergic receptor expression and inhibiting new fat cell formation, with human trial data confirming no IGF-1 elevation or glucose disruption [2, 3]

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When these mice were fed a high-fat, high-sugar diet, AKT1 expression resulted in hypertrophy of fast type two muscle fibers, reductions in body weight and subcutaneous fat and normalization of blood glucose levels

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The human body already produces BPC-157 in small amounts inside the gastrointestinal (GI) tract

Further investigation demonstrated that lactate administration in mice induced hepcidin expression, leading to reduced FPN levels