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The program established a favorable safety profile but the Phase IIb endpoint did not differentiate sufficiently from placebo to support continued development for obesity

Interestingly, while antagonism of YIL781 and TAK-779 did not interfere with this effect, the administration of AMD3100, a CXCR4 antagonist, markedly reduced the LC3 II-to-LC3 I ratio in DOX-treated muscle co-administered with GHRP-6, suggesting that CXCR4 signaling plays a crucial role in mediating autophagic responses [2]