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PT-141 acts earlier in that sequence, at the level of central melanocortin receptors, making it the more relevant option when the core issue is drive rather than physical response

Further potentiation of SDF-1 could activate deleterious neurohormonal systems [74, 75], interact unfavorably with concurrently administered beta-adrenergic receptor blockers [71, 76], and promote progenitor cell infiltration, cardiac inflammation and adverse cardiac remodeling [77,78,79]

All findings pertain strictly to laboratory and preclinical research contexts