Name: GV-971
Synonyms: sodium oligomannate, sodium oligo-mannurarate
Therapy Type: Small Molecule (timeline)
Target Type: Amyloid-Related (timeline), Inflammation (timeline)
Condition(s): Alzheimer's Disease
U.S. FDA Status: Alzheimer's Disease (Phase 3)
Status in Select Countries: Approved in China
Company: Shanghai Green Valley Pharmaceuticals


This mixture of acidic oligosaccharides is derived from brown algae. The mechanism of action of the preparation remains unclear. One preclinical study proposed an anti-neuroinflammatory effect via alteration of gut bacteria (Wang et al., 2019). In that study, the gut microflora in 5XFAD and APP/PS1 AD mice facilitated peripheral immune cell entry to the brain, microglia activation, and disease progression. Treatment with GV-971 returned the gut microbial profile to normal and lessened brain immune cell infiltration and inflammations. The drug reportedly also reduced brain Aβ burden, tau hyperphosphorylation, and cognitive deficits in these mice.

Previously, the same group reported that algae-derived acidic oligosaccharides bind and de-aggregate Aβ, and prevent inflammatory responses to amyloid plaques (Hu et al., 2004; Wang et al., 2007).


According to the company, Green Valley completed a Phase 1 study in 112 normal people in 2008, though no information on this trial appears in  

In October 2011, the company launched a Phase 2 trial at multiple sites in China, enrolling 255 people with mild to moderate AD who were not receiving treatment with any other AD drugs. They received 600 or 900 mg of GV-971 per day or placebo for six months. The primary endpoint was the change in ADAS-Cog/12; secondary endpoints include changes on the Clinician’s Impression of Change-plus (CIBIC-plus), activities of daily living (ADL), and neuropsychiatric inventory (NPI). According to results presented at the 2014 CTAD conference, the trial failed to meet its primary endpoint, with no slowing of decline on the ADAS-cog in the treated group. The 900 mg dose did slow decline on the CIBIC-plus compared with placebo (Medscape news).

In April 2014, Green Valley started a Phase 3 trial at 34 sites in China. In the study, 818 people with clinically diagnosed mild to moderate AD were to be randomized to 900 mg drug per day or placebo for nine months. Participants were not allowed to take cholinesterase inhibitors during the study, and no amyloid or tau biomarkers were used. Again, the primary outcome was change on ADAS-Cog; secondary outcomes were the same as in Phase 2, with the addition of FDG-PET. 

As reported at CTAD 2018, this trial reached its primary endpoint, with the treatment group posting higher ADAS-Cog scores than placebo at four, 12, 24 and 36 weeks. There was a trend toward improvement on the CIBIC, but no change in any other secondary outcomes (Nov 2018 conference news). A subgroup analysis suggested the drug effects were larger in people with lower MMSE scores at the start of the trial. GV-971 was well-tolerated. Eighty percent of participants completed the trial, and rates of adverse events were similar between treatment and placebo groups.

On November 2, 2019, Green Valley announced that the drug had received conditional marketing approval in China to improve cognitive function in mild to moderate AD (see press release). The company expects full approval in early 2020, pending the submission of animal safety data (Nov 2019 news and commentary).

Green Valley announced plans to begin an international, multicenter, Phase 3 trial in the U.S., Europe, and China in 2020. 

According to, the investigators completed a second Phase 1 study in China, testing bioavailability of different capsule formulations in healthy adults, and are recruiting for an additional Phase 1 study, also in China, to assess safety and pharmacokinetics of higher doses up to 1,500 mg.

For details, see

Last Updated: 28 Nov 2019


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News Citations

  1. Fits and Starts: Trial Results from the CTAD Conference
  2. China Approves Seaweed Sugar as First New Alzheimer’s Drug in 17 Years

Paper Citations

  1. . Sodium oligomannate therapeutically remodels gut microbiota and suppresses gut bacterial amino acids-shaped neuroinflammation to inhibit Alzheimer's disease progression. Cell Res. 2019 Oct;29(10):787-803. Epub 2019 Sep 6 PubMed.
  2. . Acidic oligosaccharide sugar chain, a marine-derived acidic oligosaccharide, inhibits the cytotoxicity and aggregation of amyloid beta protein. J Pharmacol Sci. 2004 Jun;95(2):248-55. PubMed.
  3. . A marine-derived acidic oligosaccharide sugar chain specifically inhibits neuronal cell injury mediated by beta-amyloid-induced astrocyte activation in vitro. Neurol Res. 2007 Jan;29(1):96-102. PubMed.

External Citations

  1. Medscape news
  2. press release

Further Reading


  1. . The microbiome: A target for Alzheimer disease?. Cell Res. 2019 Oct;29(10):779-780. PubMed.