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The R311C mutation results in a catastrophic loss-of-function as it destabilises key electrostatic interactions within the catalytic site that are essential for CaMKK2 activity [144]

Ipamorelin : 2nd-generation GHRP, highly selective for GHS-R1a, no significant impact on cortisol or prolactin the current darling of modern protocols GHRP-6 : first generation, potent but triggers marked hunger (ghrelin-like action on the arcuate nucleus) and slight prolactin/cortisol elevation Hexarelin : most potent on acute GH release, but rapid GHS-R1a desensitization after prolonged use and more pronounced cortisol elevation Key point: GHRPs add an amplifying signal that potentiates GHRH, but chronic monotherapy triggers receptor down-regulation

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These effects are mediated by the upregulation of TP53, CASP3 and CASP8 genes and the reduction in BCL-2, NRAS and KRAS genes