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Genetic variants that alter the function of a therapeutic receptor are known to influence drug response through several mechanisms

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[4] The result is a GHRH-receptor agonist that survives slightly longer in circulation than the unmodified hormone while still producing the same fundamental action: stimulation of the somatotroph cells of the anterior pituitary to release GH in a pulsatile, physiologic pattern, which in turn raises IGF-1

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