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The research rationale for a selective NNMT inhibitor is to interrupt exactly that diversion, so the cell keeps more of its NAD+ pool and can run its mitochondrial machinery again

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intact GH Notes for Investigators: Studied for adipose-tissue signaling without broad GHIGF axis activation

TB-500s biological activity is mediated primarily through binding of the LKKTETQ actin-binding motif to G-actin and sequestering actin monomers, regulating actin polymerisation dynamics, and activating downstream signalling through the PI3K/Akt pathway that promotes cell survival, migration, and proliferation in multiple cell types relevant to tissue repair including endothelial cells, fibroblasts, keratinocytes, and myocytes

However, the short answer is no, they are not the same