Oligomannate: Chinese Pharmaceutical Miracle


In November 2019, China’s pharma regulator (NMPA) granted marketing approval to the Oligomannate (sodium oligomannate), also known as Nine Phase One (九期一®), a new drug indicated to treat mild-to-moderate Alzheimer’s disease.

The critical importance of the novelty, developed by local Shanghai Green Valley Pharmaceuticals, is that the drug was the first in the past more than a decade and a half, which managed to testify some improvement in cognitive function in patients with this neurodegenerative disease.

The current pharmacological armamentarium for fighting Alzheimer’s has a meager assortment of drugs that focus only on maintenance therapy for dementia. Acetylcholinesterase inhibitors such as tacrine, rivastigmine, galantamine, and donepezil, as well as the NMDA receptor antagonist memantine, all have very little symptomatic effectiveness. None of the drugs slow down or stop the progression of Alzheimer’s.

Many pharmaceutical companies, including most of the Big Pharma players with almost unlimited resources, have attempted to beat dementia. Countless experimental molecules have failed, hundreds of billions of dollars have gone down the drain, and patients’ hopes have remained in vain.

Sodium oligomannate.


Clinical Performance of Oligomannate in Treatment of Alzheimer’s Disease

Regulatory approval came from the NCT02293915 phase 3 clinical trial (randomized, double-blind, placebo-controlled, multicenter), which examined the safety and effectiveness of sodium oligomannate among Chinese patients (n=818) aged 50–85 years with mild to moderate Alzheimer’s disease (overall score on the Mini-Mental State Exam [MMSE] ranging from 11 to 26).

Among the inclusion criteria confirmed on brain MRI was atrophy of the medial temporal lobe ≥ 2 on the visual assessment scale, the degree of white matter lesion < 3 on the Fazekas scale, no more than two foci of lacunar infarction and their absence in vital areas such as the thalamus, hippocampus, the entorhinal cortex, periorbital area, the cortex, and other subcortical gray matter nuclei.

For 36 weeks, participants received Oligomannate twice daily at a dose of 450 mg or placebo. The primary endpoint treatment efficacy was a change in cognitive function as measured by the 12-item version of the Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS-Cog-12) at the end of the study.

The experimental drug group demonstrated a statistically significant improvement in cognitive function compared with the placebo group: the average difference was −2.54 points (p<0.0001). Simultaneously, the difference was observed starting from the 4th week of therapy, steadily persisted until the end of the trial. Improvement was independent of either the baseline cognitive ability score or the presence or absence of the ε4 allele of the apolipoprotein E (APOE) gene.

There was a statistically non-significant trend toward improvement on the Clinician’s Interview-Based Impression of Change with caregiver’s input (CIBIC+) [p=0.059].

No statistically significant improvements were found on criteria such as the Alzheimer’s Disease Cooperative Study — Activities of Daily Living inventory (ADCS-ADL), the Neuropsychiatric Inventory (NPI), and glucose metabolism in the bilateral temporoparietal cortex according to 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET).

The safety profile of sodium oligomannate did not differ from that of the control group. No cases of vasogenic cerebral edema (ARIA-E), common with amyloid beta targeting, were reported.


Oligomannate for Treatment of Alzheimer’s Disease: Details of Clinical Trial

The full results of the NCT02293915 phase 3 clinical trial examining the safety and efficacy of sodium oligomannate for treating Alzheimer’s disease were published in March 2021.

After 36 weeks, the unadjusted difference in ADAS-Cog-12 score between the experimental treatment and placebo groups was −2.54 points. The mean modeled difference was −2.15 points (95% CI: 3.07 to −1.23; p<0.0001).

The administration of sodium oligomannate had a healing effect regardless of the severity of Alzheimer’s disease. Thus, the adjusted ADAS-Cog-12 score difference in the patient subgroups with MMSE scores of 11–14, 15–19, and 20–26 (the higher the MMSE score, the less impaired the cognitive abilities) was −4.20 (95% CI: −6.28 to −2.12), −3.00 (95% CI: −4.57 to −1.43), and −1.59 (95% CI: −2.35 to −0.83) [p<0.0001, p=0.0003, and p<0.0001].

Treatment of Alzheimer’s disease with sodium oligomannate demonstrated a consistent therapeutic effect on ADAS-Cog-12 score, according to the breakdown of patients into other subgroups:

  • Presence of APOE-ε4 allele: −2.40 (95% CI: −3.37 to −1.43)
  • Absence of APOE-ε4 allele: −2.67 (95% CI: −3.74 to −1.60)
  • Age ≤ 65 years: −2.55 (95% CI: −3.73 to −1.37)
  • Age > 65 years: −2.48 (95% CI: −3.36 to −1.60)
  • Male gender: −2.94 (95% CI: −3.96 to −1.92)
  • Female gender: −2.13 (95% CI: −3.11 to −1.15)
  • Above-average education: −2.37 (95% CI: −3.12 to −1.62)
  • Secondary education: −3.29 (95% CI: −5.18 to −1.40).

Although changes in secondary endpoints, such as CIBIC+, ADCS-ADL, and NPI, did not show a statistically significant difference between the sodium oligomannate and placebo groups, there was a correlated trend with the severity of Alzheimer’s disease in favor of improving these measures. Simultaneously, the subgroup of patients with an MMSE score of 11–14 showed a statistically significant difference from the control group on the NPI score: effect size of 1.3 (p=0.017).

According to the researchers, the CIBIC+, ADCS-ADL, and NPI, which reflect global cognitive function, daily activity ability, and behavioral symptoms, respectively, may not have improved during treatment for several reasons. First, the limited sample size of patients in the clinical trial. Second, the relatively short duration of the trial. Third, cultural differences may have distorted the sensitivity and validity of assessing disease progression and pharmacological treatment effects because the scales in question are too universal to be unconditionally applied to the entire human population.

Again, the unusually strong response in the placebo group is probably due to the high proportion of patients with mild Alzheimer’s, as well as the excellent patient care in this clinical trial and the high expectations of treatment by the participants and their caregivers. Similar strong placebo effects have been observed in other studies conducted in China, which is related, as already mentioned, due to significant cultural differences between the Western and East Asian worlds. For example, in developed Western countries, the elderly usually live separately from their relatives, and therefore, even minor cognitive impairments are mirrored by serious disruptions to independent daily activities. In contrast, in China, Japan, Korea, and Taiwan, the elderly almost always receive more than strong support from relatives, so the assessment of their cognitive abilities is often blurred.


Which Patients With Alzheimer’s Disease Could Benefit From Oligomannate?

Based on the available data, it is safe to say that the therapeutic effects of Oligomannate exceed those of approved drugs, including the aforementioned donepezil.

It should be understood that cognitive decline in Alzheimer’s disease is divided into seven stages. Oligomannate has been tested in patients with the disease up to and including stage 4, which is manifested by difficulty performing simple arithmetic operations, poor short-term memory (e.g., impossible to remember what was eaten for breakfast), inability to manage finances and pay bills, and forgetting details from life.

If Alzheimer’s disease progresses further, Oligomannate is unlikely to “fix” brain neurodegeneration that has progressed to the point where the patient is already faced with inability to self-care in everyday life.

Oligomannate is not recommended as a prophylactic drug for elderly patients without any signs and symptoms of Alzheimer’s because it is not known whether it has a preventive effect.


How Exactly Does Oligomannate Works?

Despite the enormous efforts of the world pharmaceutical industry, which has already tested more than 320 medical compounds in an attempt to find an effective therapy for Alzheimer’s disease, all attempts ended in failure, disappointing patients, doctors, and investors. In most cases, pharmaceutical companies have tried prove the amyloid hypothesis, believing that removing neurotoxic extracellular deposits of amyloid beta from the brain will have the proper therapeutic effect. Green Valley has staked its claim on a decidedly different theory.

Studies on animals and humans have indicated a dynamic interaction between the microbiota (communities of commensal, symbiotic, and pathogenic microorganisms) of the gut and the body’s immune system. Dysbacteriosis of the intestinal microbiota as an imbalance can compromise the host’s immune responses and contribute to the development of various inflammatory diseases. In the case of Alzheimer’s, evidence has been found that disturbances in the diversity of microorganisms inhabiting the gut lead to microglial-mediated neuroinflammation and amyloidosis.

Green Valley’s scientists suggested that since carbohydrates (in the form of mono- or oligosaccharides) are the main source of nutrients for bacteria, it is possible to modulate the microbiota, shifting the microbial population in the right direction, by delivering special therapeutic carbohydrate compounds into the body. In this scenario, oral sodium oligomannate (sodium oligomannurarate, GV-971) is a mixture of acidic linear oligosaccharides (with degrees of polymerization ranging from dimers to decamers and an average molecular weight of maximum 1 kDa) derived from marine brown algae Ecklonia kurome. Generally, the original idea came from the observation that older persons who regularly eat seaweed are relatively rarely affected by Alzheimer’s.

Chemical structure of sodium oligomannate.

The results show very elegantly in mouse models with amyloid beta amyloidosis how it is gut microbiota dysbiosis, that leads to altered amino acid metabolism and peripheral adaptive immunity, contributes to Alzheimer’s disease progression. Increased levels of phenylalanine and isoleucine increase the diversity of plasma type 1 helper T cells (Th1), which, by proliferating, differentiating, and infiltrating the brain parenchyma, promote neuroinflammation (by increasing the number of proinflammatory cytotoxic M1 microglia) and directly contribute to the pathogenesis of Alzheimer’s, manifested by deposits of amyloid beta and neurofibrillary tangles. The administration of sodium oligomannate reconstitutes the gut microbiota and limits the contribution of altered peripheral immunity to the pathogenesis of Alzheimer’s.

Some sodium oligomannate also penetrate the blood-brain barrier through transporters, including Type 1 glucose transporter (GLUT1), which binds to multiple subregions of amyloid beta to directly inhibit amyloid beta fibril formation and destabilizes the preformed fibrils into nontoxic monomers.

In humans, sodium oligomannate, by eliminating gut microbiota dysbiosis, suppresses, it is believed, abnormally high activity of gut microflora metabolites, modulates peripheral and central inflammation, reduces amyloid beta deposition and tau protein hyperphosphorylation, and reverses cognitive impairment. However, the exact mechanism of action of the drug remains unclear — although near 2000 patients with Alzheimer’s disease participated in all of its clinical trials.


Oligomannate and Alzheimer’s Disease: Near Future

In late December 2019, Oligomannate went on sale in China at a price of 3580 yuan ($516) for a one-month course of treatment, which requires taking 3 capsules of the drug at 150 mg each twice a day (900 mg total).

The therapy is priced at about twice the cost of acetylcholinesterase inhibitors.

From the beginning of December 2021, the purchase of the drug by Chinese patients is subsidized by the government and covered by insurance, so the monthly out-of-pocket cost for Oligomannate treatment will be the less than 600 yuan ($91).

Oligomannate has received conditional approval: the National Medical Products Administration (NMPA), a Chinese equivalent of the U.S. Food and Drug Administration (FDA), has been allowed to issue a favorable verdict for drugs still under research if they have a “predictable” clinical value for life-threatening conditions for which no effective treatment exists or is offered by global pharmaceutical companies but at prices unaffordable to most people. Long-term safety and efficacy (through postmarketing clinical trials) must be confirmed for Oligomannate to be fully approved. The respective validation is organized in the 96-week NCT05058040 and NCT05181475 phase 4 clinical trials.

The development of sodium oligomannate, conducted by China’s Shanghai Green Valley Pharmaceuticals in collaboration with the Ocean University of China and the Shanghai Institute of Materia Medica of the Chinese Academy of Sciences, took 22 years. Geng Meiyu, Ph.D. (sixth from right), made the main contribution to the invention. Jin Liwang/Xinhua/Getty Images.

Green Valley intends to offer Oligomannate to all patients worldwide and has therefore scheduled the launch of a GREEN MEMORY phase 3 pivotal international clinical trial in early 2020 to enroll patients with Alzheimer’s residing in the United States, Europe, and Asia. At the same time, data will be collected on certain biomarkers of this neurodegenerative disease, which will help to thoroughly clarify the mechanism of action of Oligomannate in the human body. Then, by the way, there will be an opportunity to rationally design an updated version of the drug with an enhanced targeting effect.

If Green Valley scientifically proves that Oligomannate really works, its business prospects are incredible: at least 50 million people in the world now are affected by dementia, with 60%–70% of its cases being caused precisely by Alzheimer’s disease. By 2050, this disease could affect 150 million patients, as life expectancy increases and the world population ages.

Green Valley will build a new manufacturing facility in Shanghai to meet international pharmaceutical standards. The factory, which will take about three years to build (just in time for the global availability of Oligomannate), will be able to cover the needs of 2 million patients annually.

The main contribution to the invention of sodium oligomannate belongs to the doctor of pharmacology Geng Meiyu. Jin Liwang/Xinhua/Getty Images.




The scheduled international clinical trial (randomized, double-blind) of sodium oligomannate will cover more than 2 thousand patients with mild-to-moderate Alzheimer’s disease and will be conducted in two hundred clinical centers in North America, the European Union, Eastern Europe, and the Asia-Pacific region. The 12- and 6-month trial will end in 2024. Submission of a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) will occur in 2024.

The ten-year investment in the Oligomannate project is estimated to be $3 billion: the costs include both clinical validation and elucidation of the exact mechanism of action, as well as studying the drug in the therapy of other diseases, including Parkinson’s disease and vascular dementia.



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In late April 2020, the FDA granted Green Valley approval to conduct a phase 3 clinical trial of sodium oligomannate consisting of a 12-month double-blind study followed by a 6-month open-label study. The study will complete in 2024. A New Drug Application (NDA) will be submitted by 2025.



In July 2020, Green Valley began construction of the manufacturing site required for large-scale production of sodium oligomannate. The 55,000-square-meter facility will cost 1.2 billion yuan ($183 million) and is expected to be completed in 2024.



In November 2020, Green Valley began enrolling participants in the GREEN MEMORY (NCT04520412) phase 3 (randomized, double-blind, placebo-controlled, multicenter, international) clinical trial that will evaluate the safety and effectiveness of sodium oligomannate among adult (50–85 years old) patients (n=2046) with mild-to-moderate Alzheimer’s disease.

Inclusion criteria: history of cognitive and functional decline over at least 1 year, MMSE scores between 11 and 24 (inclusive) at baseline, brain MRI scan showing the highest possibility of Alzheimer’s disease.

China is expected to recruit 40% of patients for this trial, which will be conducted in 200 clinical sites in 14 countries, with North American and European participants accounting for 30% each. One-fifth of the subjects will be recruited within the next 6 months.

Participants will receive sodium oligomannate or placebo for a 52-week double-blind period, followed by sodium oligomannate alone for a 26-week open period.

Primary endpoints are set by changes in ADAS-Cog-11 and Alzheimer’s Disease Cooperative Study — Clinical Global Impression of Change (ADCS-CGIC) scores. Secondary endpoints included changes in NPI, MMSE, and ADCS-ADL scores, changes in blood levels of amyloid beta and phosphorylated tau protein.

The GREEN MEMORY, which will cost 4 billion yuan ($600 million), should be completed by the end of 2025.



In mid-June 2021, Green Valley reported that features of Oligomannate’s mechanism of action offer hope for its suitability for therapy of other neurodegenerative diseases, including Parkinson’s disease, vascular dementia, neuromyelitis optica spectrum disorder (NMOSD), and amyotrophic lateral sclerosis (ALS).



In mid-January 2022, the FDA granted Green Valley approval to conduct a clinical trial of Oligomannate for treating Parkinson’s disease, which affects at least 10 million people worldwide.

It is believed that the beneficial therapeutic effect of the drug, realized through modulation of brain-gut axis, should also work for other diseases of neurodegenerative nature. According to preclinical studies of Oligomannate in animal models of Parkinson’s, the drug, which regulates imbalances in the gut microbiota, inhibits alpha-synuclein aggregation, reduces alpha-synuclein deposits in the gut and brain, reduces neuroinflammation, protects dopaminergic neurons and improves motor and non-motor symptoms.

The 36-week phase 2 clinical trial (randomized, double-blind, placebo-controlled, multicenter, international) will enroll 300 patients with early-stage Parkinson’s disease from North America and the Asia-Pacific region and then proceed to an open 36-week phase.


Oligomannate and Alzheimer’s Therapy: Wave of Distrust

The attitude of the global scientific community toward Oligomannate is saturated with obvious skepticism. Experts are understandable since any therapeutic breakthrough in such an impenetrable pathology as Alzheimer’s disease makes one look hard and sternly for a catch. Again, mechanistically (and successfully!) linking the microbiota to neurodegenerative processes is something out of the realm of science fiction.



Sodium oligomannate demonstrated improvement of 2.70 points on the ADAS-Cog-12 scale, and at least 3 points are needed for clinically meaningful results. In addition, the calculations on this scale are characterized by considerable variability, and therefore additional information is needed as to which model was chosen in the case of the drug.



Alzheimer’s is too severe and rapid in its progression to be able to reach a clear divergence from the placebo group in a measly month of treatment. The suddenly large gap with the placebo group between 24 and 36 weeks of therapy is also astonishing.



The efficacy and safety of Oligomannate were tested for nine months, clearly not enough to draw unequivocal conclusions about the long-term benefits of Alzheimer’s therapy. The same donepezil only at the beginning of treatment restrains cognitive deterioration at an acceptable level, then the slope of the curve is essentially no different from that of the placebo.



In the NCT01453569 phase 2 (randomized, double-blind, placebo-controlled, multicenter) clinical trial involving a similar patient population (n=255), the administration of sodium oligomannate in daily doses of 600 or 900 mg for 24 weeks provided very different results than those shown in the registry study.

Thus, there was no statistically significant difference from placebo on the ADAS-Cog-12 score (p=0.886 and p=0.302), although a statistically significant difference in CIBIC+ (p=0.014) was found in the 900-mg dose group. However, the experimental therapy showed itself, first, to improve glucose metabolism in some brain regions and, second, to witness an increase in the concentration of Aβp1–42 in the cerebrospinal fluid, thus reflecting the desired antiaggregant clearance of the neurotoxic amyloid beta.



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The very fact that an innovative drug has appeared to this extent in China, where adherence to international quality standards is still under great question, is a red flag. Not to mention the fact that in 2007, Green Valley was convicted of fraudulent promotion of an anticancer drug on the basis of mushroom Ganoderma lucidum (reishi, lingzhi, ling chih, mushroom of immortality), which is positioned as a panacea for all cancers. Investigations revealed that the drug, which belongs to traditional Chinese medicine and has been widely advertised in newspapers and on television, does not possess the claimed miraculous antitumor and immunomodulatory properties that allowed it to be chosen as a replacement for standard first-line chemotherapy. However, G. lucidum could be administered as an alternative adjunct to conventional treatment in consideration of its potential of enhancing tumor response and stimulating host immunity.

After all, Green Valley made the more than 800 million yuan ($122 million) from G. lucidum sales in a single year alone, when a 200-g package sold for 1590 yuan ($240) and at least three courses of treatment costing 25,000 yuan ($3800) was required.



Geng Meiyu does not seem to be shy about engaging in the practices of manipulating data and fabricating illustrations in articles published in peer-reviewed scientific journals. At any rate, this is evident from the thorough analyses on PubPeer, the anonymous commenting site for scientific publications. However, few scientists do not do this in the name of presenting the results in the best possible way.



The widespread infowar against Geng Meiyu (耿美玉) and her Oligomannate (九期一) was started by Rao Yi (饶毅), a respected Chinese neurobiologist, head of two brain research institutes and president of Capital University of Medicine (CUM), known for his active position on the reform of science and related disciplines.

Beginning in the fall of 2019, Rao Yi spread messages in scientific social media groups that Oligomannate was a fake drug: supposedly it was impossible to treat Alzheimer’s disease by modulating the gut microbiome.

In the summer of 2020, Rao Yi appeared in Cell Research, where he is a member of the editorial board, to criticize a Geng Meiyu publication on the mechanism of action of sodium oligomannate that was published in the same journal. According to Rao Yi, Geng Meiyu’s team since 2003 has published 12 articles on sodium oligomannate and related compounds with completely different mechanisms of action, without any hint of modulation of the intestinal microbiome.

Specifically, sodium oligomannate can treat Parkinson’s disease in animal models, can directly bind to amyloid beta peptides; can protect neurons from amyloid beta toxicity; can ameliorate memory loss caused by amyloid beta peptide injection into the brain; can inhibit H2O2 induced neuronal death directly; can attenuate scopolamine induced memory impairment in rats; can act on astrocytes in vitro; can bind to proteins inside neurons.

As Rao Yi suggested, this is simply impossible: sodium oligomannate interacts with too many targets important in treating Alzheimer’s; in biomedicine, it is extremely rare to find drugs with so many targets working together to treat one disease and without associated adverse reactions. Rao Yi also wondered why Geng Meiyu’s publication describing the modulation of brain-gut axis with sodium oligomannate did not include a single reference to the above dozen articles.

In response to the criticism, Geng Meiyu said through Cell Research that the continuous development of science has made it possible to look differently at the mechanism of action of sodium oligomannate, and past publications on the subject have too little to do with the effects of modulation of brain-gut axis to refer to them. Geng Meiyu also cited the anti-diabetic metformin as an example of a drug compound with a multiple mechanism of action involving seemingly completely heterogeneous signaling pathways for implementing glycemic control.

Rao Yi was not satisfied, launching into claims on his blog. The professor was furious. He said that if before Geng Meiyu stated that sodium oligomannate acts on nerve and glial cells of the brain, now she claims that the drug works through the gut microbiome, and it is the latter mechanism of action that is key in treating Alzheimer’s. The question arises, why are the results of preclinical studies based on completely different mechanisms of action of one drug generally not different and not inconsistent with each other?

In January 2021, China’s Ministry of Science and Technology (MOST) notified that it found no fraud in Geng Meiyu’s article on brain-gut axis modulation with sodium oligomannate, except for a minor misuse of images.

As a result, the parties went to court, which ruled in December 2021 that legitimate academic controversy and criticism must be addressed from a medical advancement perspective, and all related issues must be resolved through scientific discussion and debate involving the publication of raw data and repeated experiments. In doing so, the court rejected the claims of plaintiff Geng Meiyu, who accused defendant Rao Yi of damaging her reputation, negatively impacting Green Valley’s business, and misleading the medical community.



Finally, it cannot be ruled out that the Chinese government approved the Oligomannate because of the rapidly escalating trade and technology confrontation with the United States: the Communist bosses were happy to anger the U.S. government one more time.

The tears of joy of Geng Meiyu, who invented a new treatment for Alzheimer’s disease, cannot be faked. CCTV.com.

Alzheimer’s disease is one of the most unacceptable diseases, which places the greatest burden on families and society. I learned about Alzheimer’s in Japan, and after returning to China, I worked a lot on it. But I didn’t expect to necessarily create a drug, I just hoped for some results from active research. And now, there is hope. But it was an incredibly long and difficult road, a road of loneliness and misunderstanding.

Geng Meiyu

In any case, critics of Oligomannate are reminded of the instructive example of artemisinin and its derivatives. The drug compound discovered in the 1970s by Chinese pharmacologist Tu Youyou was initially ridiculed by the Western scientific community. And this is true: to isolate a supereffective antimalarial from sweet wormwood (Artemisia annua) based on the recommendations of an ancient Chinese traditional medicine book is utopian. In 2015, Tu Youyou was awarded the Nobel Prize in Physiology or Medicine.



A 36-week multicenter, randomized, double-blind, placebo-controlled, parallel-group, phase 3 clinical trial of sodium oligomannate for mild-to-moderate Alzheimer’s dementia. Alzheimers Res Ther. 2021 Mar 17;13(1):62. [source]

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. [source]

A phase II randomized trial of sodium oligomannate in Alzheimer’s dementia. Alzheimer’s Res Ther. 2020 Sep 14;12(1):110. [source]

Sodium oligomannate: First approval. Drugs. 2020 Mar;80(4):441-444. [source]

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