Mechanism of Pyridorin™
Pyridorin™ has been shown to inhibit AGE formation and scavenge ROS and toxic carbonyl compounds in extensive in vitro studies. Specifically, Pyridorin™ has been shown to:
- Uniquely inhibit the degradation of glycated proteins to AGEs via the post-Amadori pathway
- Inhibit lipoxidation by trapping lipoxidation intermediates, particularly 1,4-dicarbonyls
- Scavenge glycoaldehyde and dicarbonyls intermediates of carbonyl stress, such as glyoxal and methylglyoxal
- Trap hydroxyl radicals
- Bind redox transition metal ions to interfere with their catalytic role in oxidative reactions
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All of the above processes and reactive compounds have been implicated directly or indirectly in the development of diabetic microvascular disease, which is the basis of diabetic complications. The vitamin B6 compounds pyridoxal phosphate and pyridoxine exhibit little or no activity against these pathogenic oxidative chemistries.
Thus, extensive evidence now exists for the role of advanced glycation end products, ROS, and toxic carbonyls in the development of diabetic complications, including nephropathy. There is also a broad foundation of evidence that Pyridorin™ possesses activity against these oxidative chemistries, and thus a solid scientific rationale exists for the use of Pyridorin™ therapy to slow the progression of diabetic kidney disease. |
