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Name: Alzhemed™
Synonyms: Vivimind™, Tramiprosate, NC-531, homotaurine, 3-APS
Chemical Name: 3-amino-1-propanesulfonic acid, 3-aminopropylsulfonic acid
Therapy Type: Supplement, Dietary (timeline)
Target Type: Amyloid-Related (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Discontinued)
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 reported to promote Aβ aggregation and plaque stability (Gupta-Bansal et al., 1995), and Alzhemed has been proposed to interfere with amyloid fibril formation and deposition into plaques.

In vitro, Alzhemed was reported to preferentially bind soluble Aβ, inhibit its aggregation, fibrillogenesis, and neurotoxicity (Gervais et al., 2001Gervais et al., 2007). A decade later, multiple Alzhemed molecules were reported to bind to one Aβ42 monomer and prevent fibrillar seed formation and neuronal toxicity (Kocis et al., 2017). It takes a 1,000-fold molar excess of Alzhemed over Aβ to prevent oligomer formation. In TgCRND8 mice, systemic Alzhemed reduced brain amyloid by 30 percent. In contrast, the drug reportedly promotes abnormal aggregation of tau (Sept 2007 news).

Homotaurine is also a GABA A receptor agonist (Caltagirone et al., 2012).


In a Phase 2 study beginning in 2002, 58 people with mild to moderate AD received 50, 100, or 150 mg Alzhemed or placebo daily for three months. Endpoints included CSF Aβ and tau concentrations, and cognitive measures. Subsequently, 42 participants continued into open-label dosing with 150 mg for 17 months. The drug appeared safe, and reduced CSF Aβ42 after three months (Aisen et al., 2006). In the long-term extension, people with mild AD were reported to have stayed cognitively stable at 20 months (Jan 2007 conference news).

In June 2004, Alzhemed became the first anti-amyloid drug to enter Phase 3. This study enrolled 1,052 people age 50 or older with mild to moderate AD at 67 centers in the U.S. and Canada. They received 100 or 150 mg Alzhemed or placebo daily for 18 months, followed by one year of open-label extension. Primary endpoints were change in the ADAS-Cog and CDR-SB. The trial also tracked brain volume with MRI, and CSF Aβ and tau concentrations. A similar study in Europe began enrolling 930 participants in 2005.

In mid-2007, NeuroChem announced the trial had failed to measure an improvement in cognition in the North American trial (Aug 2007 news). In November 2007, the company stopped the European trial, but continued the open-label extension of the North American trial. Results were subsequently published (Aisen et al., 2011).

After discontinuing clinical development, NeuroChem pivoted to marketing Alzhemed as a nutritional supplement (Nov 2007 conference news). NeuroChem changed its name to Bellus Health and, in 2008, began to sell Alzhemed under the brand name Vivimind™ over the counter in Canada (Oct 2008 news). In 2011, the FDA refused to permit sales of Vivimind™ in the U.S., on the grounds that homotaurine did not qualify as a nutrient (see news).

Nine years later, a subgroup analysis of the Phase 2 and 3 data, including from their open-label extensions, was reported to indicate that the drug had slowed cognitive decline in ApoE4 homozygotes, and perhaps halted decline in those with mild AD (Abushakra et al., 2016Abushakra et al., 2017). In 2013, the U.S. startup Alzheon licensed ALZ-801, a prodrug version of Alzhemed currently in development for Alzheimer’s disease. 

For details on Alzhemed trials, see

Last Updated: 04 Dec 2019


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News Citations

  1. Cold Spring Harbor: A Grab Bag from the Drug Discovery Folks
  2. FDA Deems U.S. Alzhemed Trial Results Inconclusive
  3. Philadelphia: European Trial of Alzhemed Ends, Marketing Morphs to Supplement
  4. Experts Slam Marketing of Tramiprosate (Alzhemed) as Nutraceutical
  5. Alzhemed Tangles with Tau, Too

Therapeutics Citations

  1. ALZ-801

Paper Citations

  1. . A Phase II study targeting amyloid-beta with 3APS in mild-to-moderate Alzheimer disease. Neurology. 2006 Nov 28;67(10):1757-63. PubMed.
  2. . Tramiprosate in mild-to-moderate Alzheimer's disease - a randomized, double-blind, placebo-controlled, multi-centre study (the Alphase Study). Arch Med Sci. 2011 Feb;7(1):102-11. PubMed.
  3. . Clinical Benefits of Tramiprosate in Alzheimer's Disease Are Associated with Higher Number of APOE4 Alleles: The "APOE4 Gene-Dose Effect". J Prev Alzheimers Dis. 2016;3(4):219-228. PubMed.
  4. . Clinical Effects of Tramiprosate in APOE4/4 Homozygous Patients with Mild Alzheimer's Disease Suggest Disease Modification Potential. J Prev Alzheimers Dis. 2017;4(3):149-156. PubMed.
  5. . 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.
  6. . Glycosaminoglycan mimetics: a therapeutic approach to cerebral amyloid angiopathy. Amyloid. 2001 Jul;8 Suppl 1:28-35. PubMed.
  7. . Targeting soluble Abeta peptide with Tramiprosate for the treatment of brain amyloidosis. Neurobiol Aging. 2007 Apr;28(4):537-47. PubMed.
  8. . Elucidating the Aβ42 Anti-Aggregation Mechanism of Action of Tramiprosate in Alzheimer's Disease: Integrating Molecular Analytical Methods, Pharmacokinetic and Clinical Data. CNS Drugs. 2017 Jun;31(6):495-509. PubMed.

External Citations

  1. news

Further Reading


  1. . Effect of tramiprosate in patients with mild-to-moderate Alzheimer's disease: exploratory analyses of the MRI sub-group of the Alphase study. J Nutr Health Aging. 2009 Jun;13(6):550-7. PubMed.
  2. . Domain-specific cognitive effects of tramiprosate in patients with mild to moderate Alzheimer's disease: ADAS-cog subscale results from the Alphase Study. J Nutr Health Aging. 2009 Nov;13(9):808-12. PubMed.