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This inhibition preserves cellular NAD+ levels by reducing their consumption, simultaneously increasing GLUT4 transporter expression and activating sirtuin 1, known as the "longevity gene." The compound exhibits high membrane permeability and selectivity without affecting related methyltransferases or NAD+ salvage pathway enzymes, creating targeted metabolic effects while maintaining cellular safety

Since vascular growth is not only up-regulated but also accompanied by significant changes in their architecture (i.e., abnormal vasculature, disorganization, etc.) and function [129,130], a tumor burdened with those vessels may eventually be resistant to various therapeutic methods, including systemic treatment in the form of chemotherapy or radiotherapy [131]

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