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(2000) Heffernan, Jiang, Thorburn, and Ng evaluated the metabolic effects of orally administered AOD-9604 in rodent models and the lipolytic activity of the compound on isolated human adipose tissue ex vivo
(2) NNMT catalyzes the N-methylation of nicotinamide using SAM as a methyl donor, consuming both substrates in the process
AOD-9604 operates independently of GH receptors and doesn't engage the broader GH signaling cascade that produces IGF-1 elevation
By inhibiting NNMT, 5-Amino-1MQ may spare nicotinamide for NAD+ synthesis via the salvage pathway, thereby activating SIRT1 (Sirtuin 1) pathways associated with mitochondrial biogenesis, fat oxidation, and metabolic flexibility [3]
National Library of Medicine (PubMed)
