Welcome to Virtual Investor Conferences. My name is John Vigliotti, and on behalf of OTC Markets, as well as our co-host, Zacks Small-Cap Research, we're very pleased you joined us for our next live presentation from Cognition Therapeutics. Please note you can submit questions for the presenter in the box to the left of the slides and give view of companies' availability for one-on-one meetings through the Schedule Meetings tab found on the conference platform. At this point, I'm very pleased to welcome Lisa Ricciardi. She's the Chief Executive Officer of Cognition Therapeutics, trades on NASDAQ under the symbol CGTX. Welcome, Lisa.
John, thank you. Appreciate being here with all of you this morning. I'm the President and CEO of Cognition Therapeutics, and I am so pleased to tell you about our work. Let me tell you first about our company. We started in 2007 as scientists, neuroscientists, and a chemist. They set out specifically to identify drugs that would target a particular part of Alzheimer's disease, and that they did. Over the years, we've received over $200 million in grant funding. Now, what I can tell you about the scientists and neurologists is they began what has become a company that is very lean. We have less than 30 people in our organization. We have been incredibly capital efficient, and you will see that when I take you through all the work that's been accomplished. Another thing I'd like you to think about is we have very significant catalysts ahead.
We just read out Alzheimer's disease data, and several weeks later, we had additional data. I will show you both of those things. We are particularly pleased because this information will help us with our phase III program that we're now in the process of designing and discussing. We will be discussing it with the FDA. A second catalyst for us is the completion of another trial that will take place by the end of the year. If you look at your calendar, you know that's fast approaching. In December, we believe we'll have another trial to read out. After that, we go to an end of phase II meeting with the FDA. So, a lot happening at Cognition Therapeutics. I would like to point to you our forward-looking statements. You can find in our Ks and Qs all the information about the risks in our company.
We completed a public offering in October 2021. Overview of the company: We work in three disease areas right now. Within Alzheimer's disease, we are studying both early patients as well as patients that have mild to moderate disease. We are also studying another neurodegenerative disease condition called Lewy body dementia. And last, we're running a program, a phase II study in geographic atrophy secondary to dry AMD. We'll touch on all of these things. Let me begin with big news from the summer. Our phase II study of patients with mild to moderate Alzheimer's disease is called SHINE. The SHINE study description is here. As you can see, it's a three-arm study: two doses of drug, one dose of placebo. One thing I want to point your attention to is all patients had a confirmed diagnosis of Alzheimer's disease.
It's important to know who you're treating and to bring rigor to the study, and that we did. Patient populations reflected here. Largely, what we're talking about are women who are Caucasian, approximately 72 years old. Their MMSE score, as you see here at 21, indicates that they were somewhat towards the moderate, mild to moderate end of the disease, and 60% of these people were carriers of the APOE4 gene, which you may know gives a much higher propensity for disease. Now, let's talk about the results. Right here up front, you see the subhead: 39% slowing of cognitive decline in patients who were treated with drug in this trial. I'd like to show you the data now. Let's look here: ADAS-Cog-11 and the MMSE. ADAS-Cog-11 and 13 are very standard treatment rating scales for Alzheimer's disease.
MMSE stands for Mini-Mental State Examination, another way of categorizing the degree of cognitive deficits in your patient population. So, on the left, the MMSE. This was our primary endpoint. And to be clear, we took our 100 and our 300 milligram patients and combined them. We also have this data separately, but this was the predetermined endpoint. Placebo patients are here in gray. And as you see, placebo patients unfortunately continue the process of their neurodegeneration over the six months, whereas patients on drug, as you see here at the end of six months, had a 39% slowing of disease progression. On the right-hand side, on another version of looking at efficacy, we saw a 70% slowing, a gap between those patients on placebo and those patients on active drug. Additionally, we looked at the ADAS-Cog-13. We had multiple measures in this trial.
And again, no surprise, a 39% slowing on this separate scale measuring cognition, and last on a score called the cognitive composite, a 70% scale. Now, let me be clear about something. The actual percentages matter less to us than the fact that consistently, no matter how we looked at this data, patients on drug did better than patients on placebo over the six-month course of study. I would also tell you that these findings are very consistent with what has been published by both Eisai in their trials with Leqembi, as well as with Lilly's trials on a drug called Kisunla. These monoclonal antibodies most recently approved showed very similar levels of efficacy. The difference for us, this is an oral once-a-day drug. Patients in our studies do not require imaging or other forms of surveillance because we do not impact plaque being removed from brain vessels.
This is referred to as ARIA. You've probably heard a lot about it. It's something that is associated with monoclonal antibodies. It is not associated with our drug. So, we believe we have a much simpler and effective offering for patients and their caregivers. Now, one thing we did at the end of the summer is we asked neurologists about these findings. These are the people we talked to. They were academics. They were private practice doctors, folks working in community hospitals. And this here on the right, I call this the bullseye because what they did, what they do, these people, is treat mild, moderate, severe, and early patients. We talked to 51 physicians that see on balance 250 patients apiece, and they see every aspect of this disease.
That to me said these are people who know very well what they're looking for in therapeutic options going forward. Among the questions we asked them was, what was compelling to you about the findings that we showed in our SHINE trial? You can see here on a scale out of 10, the efficacy score in the ADAS-Cog-11 and 13, cognitive composite, MMSE, all of these things were very compelling to the doctors. Here are some verbatims. The efficacy is as good or better than the monoclonal antibodies. Terrific to get these results over six weeks. It was clearly a positive result. We then said, talk to us about the safety profile of our drug. How would you rank the things that are most appealing to you? You see it here: efficacy, safety, tolerability, dosing, and route of administration.
It would be hard to ask for a better profile from a practicing clinician to describe your drug. So, this was a very favorable finding for us at the end of the first set of results from our SHINE trial. As I said at the beginning, when you run a large study, we worked with a CRO, contract research organization, to execute the trial. They provided the results to us in tranches. The biggest set of data is reflected here. We got an additional set of information on safety as well as biomarkers. Those things came later. And what I'm going to show you is what we just received several weeks ago. The data I'm showing you here was presented at a conference in Madrid. It's called CTAD, and the initials stand for Clinical Trials in Alzheimer's Disease. This meeting runs between the U.S. and Europe. It alternates every year.
This is where most clinicians go for updated information about the field. You can see again here in the subhead, the key point: 95% slowing of cognitive decline. This means patients experienced almost no loss of cognition. Now, let me tell you about who these patients were and what we were following. The headline here indicates tau burden. We were looking at the level of tau in patients. Why? Because tau burden, baseline tau levels rather, are a very good indicator of a patient's likelihood of responding to therapy. The measurement of p-tau reflects how much amyloid and tau is in the brain. This is a blood test, a commercially available blood test, and so it's relatively simple to execute. We didn't just come up with this idea. If you see here, TRAILBLAZER, this refers to the Lilly trial. Lilly studied 1,700 patients or more.
They too looked at levels of tau: high, medium, and low. And they found that patients with low tau had the best clinical results. That was true for us as well. We took all our patients, we measured their tau, drew a line in the middle, and said the high ones will separate from the low ones, low levels of tau at baseline. And here is what we learned. Now, on the left is what I showed you from the whole group. This is everybody. On the right are the patients that had median tau, that is below the halfway mark of tau. And what you see is from the beginning to the end of the study, no deterioration in cognition, 95% protection, if you will, relative to patients who were on placebo.
We studied this further by looking at MMSE, patients that had mild disease and patients that had more advanced disease, and what you see are the same things. Blue is the score for treated patients. You can see at the beginning and at the end, their cognitive levels are actually slightly increased, and the same thing with moderate patients, a 97% slowing, so this was a very, very important and compelling finding. Now, let me wrap up talking about this phase two mild-to-moderate study. What we learned is that our drug is safe and well tolerated. We got excellent information about what's the next dose that we want to take forward into trials. We saw similar effects, AE, adverse events in the treated groups and in the placebo groups, so there was nothing distinguishing there.
In all cases, cognitive and functional measures, we saw favoring the results of the treatment arm. As this subhead says right here, we are using this data to determine how it is we move into phase III. Now, I've talked about mild to moderate disease. We actually have in Alzheimer's disease a trial we refer to as START. This study has 540 patients. The treatment for this study, this statement is incorrect. It's actually 18 months. And we are studying two doses of drug. This trial is recruiting at top centers around the country. We look forward to having more information to describe to you about this population. At the very beginning, I said we're looking at multiple disease areas. Another form of neurodegeneration is dementia with Lewy bodies. Let's talk about that.
This is the catalyst that I described at the beginning where we'll be getting data in a matter of weeks. We work with Dr. Jim Galvin. He's probably the world's most comprehensive leader of research in this area. And one thing Jim always says is, this is the most common dementia you've never heard of. Take a look at this chart on the right. These are all forms of dementia in the U.S. You can see the lion's share is Alzheimer's disease. But DLB is right here. And it's slightly bigger than Parkinson's disease or close to it. And yet, I'm sure you all hear much more about Parkinson's, 1.5 million people. Now, what was intriguing to us about this condition is that patients with Lewy body dementia or dementia with Lewy bodies is that they have what's called alpha-synuclein oligomers, toxic proteins.
They also have the same A beta oligomers that are associated with Alzheimer's disease. We have data that tells us our drug is able to displace both of these toxins from where they sit in the brain. And so, we believe we have a particularly appropriate agent to treat these patients. If you're unfamiliar with the condition, I would ask you to look at this, which is, what is it these patients present with? First of all, there is a cognitive impact from the disease. Second, there are a great deal of fluctuations. Caregivers will say there are on days when patients are showtiming, and you wouldn't know anything is wrong. And there are other days where patients have no affect at all. It's not something the patient can control. Visual spatial perception is deeply altered. Hallucinations are a hallmark of this condition.
Perhaps one of the most important things is a very significant interruption of sleep with REM sleep disorders, where patients act out the symptoms of their, or they act out, that is, the reality of what they're experiencing in their dreams. In this trial, we're studying two doses of drug, very similar to what I showed you on the prior trial called SHINE. It is a six-month study. As I just described to you, the symptoms you can see here under assessments, we have measurements for all of these things. We're primarily looking at cognition, but we're also looking at function. The UPDRS is a scale very often seen in Parkinson's disease. These patients with DLB have terrible gait problems and often fall and end up in the emergency room. There are behavioral scores we're looking at to see if sleep improves.
A number of very important findings we anticipate from this trial. Two other things I want to tell you. We applied for and received a $30 million grant to conduct this study. I did not mention to you that in our AD study that I just showed you, we also applied for and received a $30 million grant. We are very pleased about that. The second thing I want to tell you is this study is 130 patients. The prior study was 150. We view these trials as trials that are signal finding. That is, they give us a lot of information about which parameters of disease we impact. And that's shown right here. And that information will allow us to determine how we progress to phase III. Now we've talked about mild to moderate Alzheimer's disease.
We've touched on the fact we have a trial in early disease, and we've also talked about Lewy body dementia. Let me turn to the last program. Again, we are talking about an oral drug. In this case, an oral drug that we believe will get to the back of the eye to prevent the damage to the macula. Patients with dry AMD experience a deterioration of their macula, which can ultimately lead to blindness. Now, take a look at this chart here. These are patients in the U.S. that are considered to have age-related macular degeneration. There are two types of this condition, wet, and that's this blue part here. This is a very established clinical area. Regeneron has a drug called Eylea. Genentech has a drug called Lucentis. There are many established drugs, all of which are injections that have helped this patient population over the years.
Obviously, this is a much larger patient population that have dry AMD. What you see in the U.S., there are two drugs now approved to treat dry AMD. One's called Syfovre. The other one is called Izervae. They are both injectable drugs. Neither drug has been approved for treatment, excuse me, outside of the U.S. Another thing is these drugs work by targeting a pathway called the complement pathway. Our drug has a different mechanism of action, and we believe that our drug may be complementary to this complement pathway. The biggest factor to consider is that our drug is oral. It is not an injectable, and so, we think that may have real benefits for doctors and patients when they contemplate starting on therapy and perhaps adding on other drugs later. All of that has to be proved in the clinic. We are running a study now.
It's called MAGNIFY. It's an 18-month study. It's one dose of drug and placebo. And I will tell you, there is a great deal of enthusiasm, both on the part of patients and research sites to study our drug, CT1812, to determine if this drug can get to the back of the eye and prevent this loss of vision. Now, let me wrap up here. I began by telling you Cognition Therapeutics was founded in 2007 by a scientist and a chemist working together. Over those years, we have developed a very high degree of scientific and clinical foundation to support all the work we do. Our studies here have all been published. I believe our SHINE study is under review. Everything is available on our website. We have worked with highly credible research centers.
And so, we're quite confident as we look ahead, the foundation we have built will allow us to move into phase three to find important treatment options for patients across multiple therapeutic areas. So, in summary, first-in-class drug. I have not talked about A beta oligomer antagonism via the sigma-2 receptor. You can trust me when I tell you, technically, this is how our drug works. We target these oligomers. That's part of the plaque that ends up in the brain. We prevent those oligomers from binding and causing damage, simplest way to say it. I showed you data from multiple cuts of our mild to moderate disease study where we show over and over again, based on multiple measures, strong trends in the treatment of Alzheimer's disease up to patients who showed no progression of their cognitive decline over a six-month period.
ARIA is unlikely to occur with our drug. As I talked about briefly before, we do not, through the use of our drug, pull plaque out of blood vessels in the brain. That is what causes ARIA, either edema or hemorrhage. This is not associated with the mechanism of our drug. So, that means it's a relief for patients and their families. It also means you're not going for imaging surveillance on a repeated basis. We know that our drug has a well-tolerated safety profile. We potentially could be the first drug to market for Lewy body dementia. All of that has to be seen, and as an oral administration, there's great simplicity in the offer in the treatment option we have for patients and their caregivers. Now, let's talk about our financial position. Our quarterly results went out on Tuesday morning. We have, at present, $22 million in cash.
Of the grant funding, this is just from the NIH, $170 million. Of that, there is a remaining $53 million. And this will help us to complete our START trial. So, that's where we stand on the economics. What I would like to do now is turn to questions that have come in from the Q&A. I see a question here that says, would a patient be able to continue taking other Alzheimer's drugs, such as Aricept, in conjunction with SHINE, the SHINE trial? Excellent question. Yes, the answer is, in that trial, we treated patients on top of their current therapy. And in fact, in the US, we had two-thirds of the patients came into the trial already taking Aricept. So, we were able to show this benefit on top of the drugs they were already taking. Next question. Thank you for the work you're doing.
Are you working with any academic or strategic partners? Excellent question again. Thank you for the question. What I can tell you is that from the day I started leading this company along with our Chief Medical Officer, his name is here, Dr. Tony Caggiano, we have engaged with all of the drug companies that have programs in the neurodegeneration area. Every time we completed a trial, big or small, we would sit down with them and review our data. The goal was, as in many places in business, to build a relationship with scientists and clinicians so that they would understand the quality and the rigor of our work and understand our results. That process continues. Today, we do not have a collaboration. But that doesn't mean there will not be a collaboration at some time in the future. Here's another question.
How will patients that have the lower levels of p-Tau be incorporated into phase 3 plans? Great question. One of the things I talked about is that patients who present with a lower level of p-Tau are patients who are known to respond better to therapy. And you saw that in our results. These patients showed no progression in their disease. Other patients who had high and low p-Tau, when we combined them, they showed a 39% slowing of disease. You'd prefer to be in the first group to have no continuing cognitive decline. Our thought is to look at this patient population and determine how to target them for phase III trials. That study is being developed and worked on with our outside advisors. So, we don't have a protocol today. But we're looking very closely at how we can incorporate this patient population in our studies. Another question.
How about biomarkers? What can you tell us about biomarkers across your trials? Fantastic question. We have published many abstracts and posters about biomarker results from our studies. To be clear, biomarkers are great indications of what is happening in the brain, in the body, that is adjunctive to clinical results. What we have seen in our SHINE study was a significant reduction in a biomarker called NfL, neurofilament light. NfL is widely understood to be a great marker of disease and disease progression. So, impacting that was important. I just showed you data on p-Tau, and we also have data, which we will be putting out shortly in another set of press releases describing other biomarkers that we have looked at. Again, all reinforcing the cognitive impact of our drug in Alzheimer's disease patients. Another question here. Is there potential to reverse disease rather than slow progression?
That's a fantastic question. What I would tell you is that remains the holy grail. We're pretty excited that we're able to show a stopping of disease. This is a chronic process. And remember, people who are diagnosed with Alzheimer's disease have been running around with amyloid in their brains for decades. I bet every one of us listening on this call has a measurable level of amyloid in their brain. It doesn't mean we will get Alzheimer's disease. But it is a long-standing part of our biology. Are we able to improve it? I don't know. That's a fantastic goal. How did diet affect results? Great question. In our clinical trial, however, we did not monitor patients for diet. So, there's nothing that I can comment on. One last question before we wrap. A question is about our patent life.
As I said, our scientists and chemists together started this company and did all the screening work that resulted in the chemical libraries where our patents come from. They are wholly owned by Cognition. We have patents to 2035 with a patent term extension. This is on our primary composition of matter for our Alzheimer's disease study. Patent term extension to 2041. We anticipate other patents. We actually have a very large patent portfolio. We don't often discuss it, but it is a robust portfolio, and we're confident it will give ourselves, or us in conjunction with a partner, the opportunity to commercialize these drugs for a significant period of time. I'll take one more look at questions, and seeing none, what I would say is thank you all. Thank you to the Zacks team, and thank you for the listeners who joined us today.
If you have questions, you will see this information is on our website. Myself, my Chief Medical Officer, and Chief Financial Officer, John Doyle. You can find our contact information here. Thank you all.