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Home: Disease Management: Treatment
Drugs In Clinical Trials

Important Notice: The Forum does not endorse any medical product or therapy. ALL medications and supplements should be taken ONLY under the supervision of a physician, due to the possibility of side-effects, drug interactions, etc.

Name: Nicotinamide
Other Names: Enduramide™, Niacinamide, Nicotinic acid amide, Vitamin B3
Therapeutic Applications: Mild to moderate Alzheimer Disease
Therapy Types: Small molecule, vitamin
Mechanisms: competitive inhibitor of the sirtuins or class III NAD+ dependent HDACs
Development Status: investigational in U.S.
FDA Phase: Phase II/IIa/IIb
Primary Medical Role: Nicotinamide is a water-soluble vitamin that is converted into niacin in vivo. Niacin is an essential component to form nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), coenzymes involved in redox reactions in all living cells.
Role in Alzheimer's Disease: In transgenic mouse models of Alzheimer's Disease (Green et al 2008), nicotinamide has been shown to restore cognition in water maze tests and improves contextual learning, preventing fear memory deficits. Nicotinamide did not reduce plaque deposition or reduce either soluble or insoluble Ab in 3xTg AD mice, but did decrease tau pathology and selectively reduced Thr231 phosphorylated tau, known to inhibit microtubule polymerization. Nicotinamide was also shown in this study to inhibit sirtuin deacetylase and increases microtubule stability. Also see Alzforum News.
Notes: A Phase I/II clinical trial testing Nicotinamide/Enduramide (extended-release niacinamide), located at UC Irvine School of Medicine, is currently recruiting participants. See NCT00580931.

This entry was updated November 16, 2010.


References

Green KN, Steffan JS, Martinez-Coria H, Sun X, Schreiber SS, Thompson LM, LaFerla FM. Nicotinamide restores cognition in Alzheimer's disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau. J Neurosci. 2008 Nov 5;28(45):11500-10. POW Link and Comments


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