An H.C. Wainwright Associate. We're confident we're going to be able to provide value to you with over 600 companies presenting at this conference in multiple sector tracks dedicated to life sciences, cryptocurrency, blockchain, and fintech, technology, media, and telecommunications, clean tech, metals and mining, and growth. Please join us for one-on-one meetings, corporate presentations, and panels that will be available live and streaming on September ninth through eleventh. With that said, have a productive and enjoyable day, and I'd like to introduce our first presenter. I'd like to welcome Lisa Ricciardi, who is President and CEO of Cognition Therapeutics, a clinical-stage neuroscience company, which specializes in oral medications designed to treat neurodegenerative and neuro-ophthalmic disorders. Lisa?
Thank you, Abby. Thank you. But let me first thank the Wainwright team for including us in this conference. Today, I'll discuss our clinical programs, highlighting our most recent trial results. At Cognition, our work is based on targeting amyloid beta oligomers and neurodegenerative conditions, including Alzheimer's disease, dementia with Lewy bodies, as well as geographic atrophy subject to age-related dry AMD. We believe that our drug acts as a neuroprotective agent through its mechanism of action. Please see our forward-looking statements. I'm going to get rid of this build and get right to the story. You are all most certainly aware of the challenges of developing treatments for Alzheimer's disease, or as I will say throughout this presentation, AD. For decades, the scientific and clinical focus has been on targeting amyloid beta plaques. The results? Promising work, many publications, good trials, and few drugs.
By contrast, we believe that the amyloid oligomer hypothesis is core to the future of AD drug development. There is strong scientific evidence for this understanding of AD biology and much clinical evidence supporting the role of oligomers as the most toxic form of the amyloid protein. Now, our lead asset is referred to as CT-1812. It is an oral small molecule. It potently antagonizes and directly targets amyloid beta oligomers via a unique mechanism of action that is preventing the binding and causing the displacement of oligomers from their binding sites. In preclinical models, our drug completely reverses cognitive decline in animal models. CT-1812 is currently in a phase II study for early to mild Alzheimer's disease and recently completed a study in mild to moderate Alzheimer's disease. As I said earlier, we're also studying two additional indications. Let's get started.
At the recent AAIC conference in Philadelphia last month, we presented the results of our proof of concept study called the SHINE Trial. This is a study in patients with mild to moderate Alzheimer's disease. Highlights from this study included a slowing of cognitive decline by 39%, as measured by the ADAS-Cog 11. In addition, all functional and clinical cognitive measures trended in favor of CT-1812, with multiple endpoints being significant. We saw an excellent safety profile and believe the data, taken as a whole, supports advancing our drug into the next phase of the development. All data from this trial is now available on our website. What you see here is one of the posters we presented at the conference, and that is also available on our website. Now, I'll turn briefly to some of the highlights of this study.
In the SHINE trial, 153 participants from 30 sites around the world were randomized to receive 100 or 300 milligrams of placebo... Excuse me, 100 or 300 milligrams of drug or placebo. All patients were adults with confirmed AD pathology via PET imaging or through CSF measures of amyloid or tau. Patients were required to have an MMSE score between 18 and 26, and they were allowed to be on a stable regimen of acetylcholinesterase inhibitors or memantine. Now, as a proof of concept study, the primary objectives were safety and tolerability. Additional exploratory measures included the ADAS-Cog 11, 13, MMSE, and cognitive composite. The trial population was evenly balanced across all three arms.
The majority of participants were female, Caucasian, seventy-two years of age, approximately, with an MMSE score of twenty-one point three seven, and 60% of the participants carried the APOE4 gene. Now, in this trial, the primary analysis was designated as the pooled one hundred and three hundred milligram dose groups versus placebo. In addition, we've captured the separate results of each dose group. As you can see here on the left, placebo-treated patients, and that is the gray line, continued to worsen throughout the study. By contrast, in those treated with CT-1812, there is an overall slowing of disease progression and an overall 39% slowing of cognitive decline relative to placebo. On the right, you can see the MMSE scale, where the findings were similar.
Patients on drug showed early benefit in the pooled group, that's the dark blue line, compared to placebo, and the placebo group worsened over time. With regard to the ADAS-Cog13 and cognitive composite scales, we saw similar results. Not surprisingly, the ADAS-Cog13 profile looks similar to the ADAS-Cog11 results, with an overall effect of, again, approximately 39% slowing of disease compared to the placebo groups. In the cognitive composite groups, we saw a result closer to 50% of cognitive decline impacted by the drug over placebo. Now let's turn briefly to a summary of the safety and tolerability findings in this trial. CT-1812 demonstrated a favorable safety and tolerability profile, with most treatment emergent adverse events being mild or moderate in severity.
There was a similar percentage of adverse events in the treated and placebo groups, no discontinuations due to adverse events in the 100-milligram dose group, and finally, most of the discontinuations were in the 300 milligram group, and all reportable liver enzyme elevations were in the 300 milligram group. Now, let's look at these exploratory endpoints as a whole. We believe CT-1812 demonstrated a consistent positive improvement compared with placebo across multiple endpoints of cognition, the ADAS-Cog11, 13, MMSE, and cognitive composite. Another important point from these data is the magnitude of effect. When you look at the rate of decline, as reflected in this chart showing CT-1812 compared to placebo, you observe a large and consistent change across most of the clinical measures.
Another way to say this is as follows: Given the rate of progression of the placebo-treated patients, CT-1812 rescued approximately 40% of the decline, depending on which scale you observe. The magnitude of this effect compares favorably to the percent improvement on cognitive measures seen in monoclonal antibodies most recently approved. Lecanemab, shown here, demonstrated between 24% and 26% reduction in cognitive decline. The magnitude of effect was over 1.5 points over an 18-month period. Now in this trial, we learned the 100-milligram dose group did as well or better than the 300-milligram dose group on most clinical assessment. This will become very important as we plan dosing and our trial design for our next phase of study.
One final note, the results of cognitive changes demonstrated by our drug were supported by changes in neurofilament light chain, or NfL, which significantly decreased in treated patients and increased markedly in the placebo population. NfL is a marker of neurodegeneration. To conclude here, we believe the SHINE trial was a successful study and provided important information to guide our advance to the next stage of work. Again, please see our website for access to posters and the full transcript of our presentation at the AAIC. Now, I said earlier, we're studying early AD patients. That study is conducted through this trial, the START trial, another proof of concept study. This trial has 540 patients who are enrolled or being enrolled for an 18-month period of time. Assessments include the CDR Sum of Boxes, the ADAS-Cog13, as well as additional functional measures.
Biomarker data will be collected as well during the course of the study. Now, importantly, in conjunction with our partners, the ACTC or the Alzheimer's Clinical Trial Consortium, we've taken the decision to allow patients on a stable regimen of lecanemab to enter the study. This will provide us with real-world data on combination use of CT-1812 with monoclonal antibodies. Now, as I said at the outset, our clinical program extends beyond Alzheimer's disease. Let's turn now to our work in patients who have dementia with Lewy bodies as well as dry AMD. For those of you not familiar with dementia with Lewy bodies, it is a condition characterized by toxic alpha-synuclein oligomers. There are several clinical conditions with this hallmark feature, and these conditions are collectively referred to as alpha-synucleinopathies. Synucleinopathies include DLB, Parkinson's disease, multisystem atrophy, or MSA, and other conditions.
Taken together, this class of diseases is second in prevalence to AD. With regard to DLB specifically, there are over 1.4 million people in the U.S. who have DLB. Importantly, 50% to 80% of the DLB patient population has not only alpha-synuclein oligomers, but A-beta pathology as well. Core symptoms of this condition are varied, but they include progressive cognitive decline, fluctuation in cognition, with some days being very high, show timing is how it is often referred to, and other days, patients having no affect at all, impaired visual and spatial perception, recurrent hallucinations, and very often, REM sleep disorders. Now, our scientists had previously demonstrated the ability of our drug to prevent the binding of both A-beta oligomers and alpha-synuclein oligomers.
We believe this is part of the reason why we were granted $30 million to run a phase II clinical trial in this population. We refer to this trial as our SHIMMER study. As you have gathered from my review of the symptoms, DLB is a highly heterogeneous population. As a result, our trial involves multiple endpoints, including the MoCA, the MoCA, the Montreal Cognitive Assessment, the MMSE, the Epworth Sleepiness Scale, as well as additional cognitive and functional measures. Now, this trial is not powered for statistical significance. It is a signal-finding study, and we believe it will allow us to determine insights on safety and efficacy that we can use in the additional stages of trial work. SHIMMER is a 120-patient population study. The patients are being followed for six months.
In April, we announced the last patient had been enrolled, and we anticipate data by the end of the year. I'd like to turn finally to the study we're doing of CT-1812 in dry age-related macular degeneration with geographic atrophy. Geographic atrophy is essentially the most advanced form of macular degeneration. With this condition, there is significant central vision loss. You can see the illustration here. Over time, that dark space gets larger and larger, and because this is central vision loss, patients are unable to read, drive, navigate daily life independently. Now, there's an unmet need for this disease because although there are drug treatments available for this condition, they require injections directly into the eye or both eyes, and these injections occur on an ongoing basis. The pathophysiology of disease involves the death of retinal pigment epithelial cells, or RPE cells.
We know that our drug plays an important role in this disease, and we've chosen this indication based on how our drug targets the sigma-2 receptor. We believe it'll be a huge breakthrough to have an oral drug that treats this condition and obviates the need for needles. Our trial in dry AMD is referred to as the MAGNIFY trial. We've enrolled... are enrolling 246 adults, and these patients will be followed for a two-year period of time. Finally, let me turn to our pipeline. I referred earlier to our study in patients that have early to mild disease. That's our START trial, and we are actively recruiting. Our dementia with Lewy bodies trial has completed enrollment. We anticipate this study will read out by year-end.
Finally, as I just mentioned, our dry, age-related macular degeneration study is actively recruiting, and we know that PIs have a great deal of enthusiasm to get patients into the study. I'd like to close with some highlights of CT-1812. We see this drug as an important new addition to the treatment of neurodegenerative disease. We have seen consistent efficacy across Alzheimer's disease study. Based on our mechanism, we don't anticipate ARIA. We believe it may be the first drug, first to market for the treatment of DLB, and potentially the first oral drug for dry AMD. The drug has been well-tolerated, and its profile as an oral administration product means there's no need for IV therapy, which is a key limitation of immunotherapeutics. No surveillance, greater convenience, and access.
Last quarter, we announced we have $28 million in cash, $57 million of grant study to carry these trials forward. Thank you for your attention.
Thank you, Lisa. I wanna thank all of our presenters for taking part in what has been a very productive and informative series of presentations. We appreciate the time and effort that went into preparing them. We are grateful for your flexibility and your presence at our conference this year. Thank you again from the H.C. Wainwright team.