These effects are thought to involve modulation of VEGFR2 activity, FAK-paxillin signaling, and nitric oxide pathways
The limitation of conventional treatment alone is that it relies entirely on the bodys natural healing rate without augmentation
Until such trials are completed, the compound remains experimental
In mouse models of highfat dietinduced liver steatosis, it significantly inhibits hepatic NNMT activity, reduces NAM methylation, increases NAD+ and SAM levels, enhances mitochondrial fatty acid oxidation, reduces hepatic triglyceride and lipid accumulation, lowers lipotoxicity markers (e.g., malondialdehyde, transaminases), improves hepatocellular injury, and reverses steatosis
They serve different purposes, and only a licensed clinician can determine which option is appropriate for your specific situation