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Key mechanistic features: Selective GHSR-1a agonism Potent GH release without cortisol/ACTH/prolactin elevation Gq/11 Ca signalling Intracellular calcium rise triggers GH exocytosis Pulsatile GH release Preserves physiological GH pulse pattern

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Then literatures reported the Ala177Val mutation has no influence on the kinetic parameters of bacterial MTHFR, but rather reduces enzyme stability and affinity for cofactor, and thus increases the tendency to form inactive enzyme via flavin dissociation, compared to the wild-type enzyme 27

OFarrell M, Almohaileb FI, le Roux CW