Pyridorin: Treating An Underlying Cause of Diabetic Nephropathy

Studies found slowing of disease progression in target population

PYRIDORIN® (pyridoxamine dihydrochloride) is a novel small molecule drug candidate with a chemical structure similar to, but distinct from, vitamin B6 (pyridoxine). Unlike vitamin B6, pyridoxamine is regulated as an investigational drug candidate by the U.S. Food and Drug Administration.

The compound has a distinct structure and is comprised of a pyridine ring containing hydroxyl, methyl, aminomethyl, hydroxymethyl and phenol substituent groups. The phenol at position 3 and the aminomethyl group at the 4th position of its ring give pyridoxamine a variety of unique inhibitory activities against pathogenic oxidative chemistries. These inhibitory activities reduce the formation of advanced glycation endpoint products, or AGEs, which are known to damage protein structure and their function and lead to vascular injury. Microvascular injury is the fundamental cause of diabetic nephropathy.

Pyridorin performs several key inhibitory actions against pathogenic oxidative chemistries, which include:

  • Scavenging activity toward free radical and carbonyl compounds that form during the breakdown of sugars and lipids that can lead to AGE formation;
  • Redox metal binding activity, which inhibits the oxidation of Amadori intermediates to AGEs.

A variety of completed preclinical studies in animal models of diabetes demonstrate that treatment with Pyridorin improves kidney histology and slows the progression of diabetic nephropathy. Completed Phase 2 clinical studies indicate that Pyridorin therapy slows the progression of nephropathy in diabetic patients with mild and moderate kidney disease and those with advanced disease on an established regimen of standard of care.