Name: Alzhemed™
Synonyms: Vivimind™, Tramiprosate, NC-531, homotaurine, 3-APS
Chemical Name: 3-amino-1-propanesulfonic acid, 3-aminopropylsulfonic acid
Therapy Type: Dietary Supplement (timeline)
Target Type: Amyloid-Related (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Inactive)
Company: Neurochem, Inc.
Approved for: None


Alzhemed was designed as an anti-amyloid therapy. It is a patented variant of the amino acid taurine, which is reported to inhibit the interaction of Aβ with endogenous glycosaminoglycans and thereby prevent β-sheet formation. This drug originated in a screen for low-molecular-weight molecules that mimic glycosaminoglycans and can therefore antagonize the interaction of Aβ with endogenous glycosaminoglycans. Glycosaminoglycans have been shown to promote Aβ aggregation and plaque stability (Gupta-Bansal et al., 1995) has been proposed to interfere with amyloid fibril formation and deposition into plaques.


In vitro, Alzhemed was shown to preferentially bind soluble Aβ, inhibit Aβ aggregation and fibrillogenesis, and inhibit Aβ neurotoxicity (Gervais et al., 2001, Gervais et al., 2007). Treatment of TgCRND8 transgenic mice with systemic Alzhemed resulted in significant reduction (∼30 percent) in the brain amyloid plaque load (Gervais et al., 2007).


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Research Models Citations

  1. TgCRND8

Paper Citations

  1. . Glycosaminoglycan mimetics: a therapeutic approach to cerebral amyloid angiopathy. Amyloid. 2001 Jul;8 Suppl 1:28-35. PubMed.
  2. . Targeting soluble Abeta peptide with Tramiprosate for the treatment of brain amyloidosis. Neurobiol Aging. 2007 Apr;28(4):537-47. PubMed.
  3. . Proteoglycan-mediated inhibition of A beta proteolysis. A potential cause of senile plaque accumulation. J Biol Chem. 1995 Aug 4;270(31):18666-71. PubMed.

Further Reading

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