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The specific vulnerability of tumor cells leveraging the aberrant NADPH-synthesis pathways can be exploited to induce cell death under various cellular stresses

(Eur J Endocrinol 1998) reported that ipamorelin stimulated GH release from anterior pituitary somatotrophs via GHSR-1a (Gq/11PLCIP pathway) at doses up to 200-fold its GH-effective dose without significantly elevating ACTH, cortisol, FSH, LH, prolactin, or TSH above GHRH-stimulated controls in rats