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TB-500 operates systemically as a **cytoskeleton remodeler**: its primary function is G-actin monomer sequestration (active N-terminal Ac-Ser-Asp-Lys-Pro), its cleaved AcSDKP sequence is an **autonomous angiogenic factor**, it upregulates laminin-5 and matrix metalloproteinases (MMPs), and mobilizes mesenchymal progenitor cells
Pathway-Level Toxicology Considerations: NAD + , SAM, and Methylation Balance The research rationale for NNMT inhibition is connected to the biochemical role of NNMT in nicotinamide methylation and SAM consumption
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