Cognition Therapeutics, Inc.

Hello, and thank you for standing by. At this time, I would like to welcome you to the Cognition Therapeutics second quarter 2024 earnings call. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question and answer session. If you would like to ask a question during this time, simply press star followed by the number one on your telephone keypad. If you would like to withdraw your question, press star one again. I would now like to turn the conference over to Tom Johnson. Please go ahead.

Thank you, operator, and good morning, everyone. Welcome to the Cognition Therapeutics second quarter 2024 results conference call. With me today are Lisa Ricciardi, President and Chief Executive Officer, John Doyle, Chief Financial Officer, and Tony Coggiano, Chief Medical Officer. This morning, the company issued a press release detailing its financial results for the second quarter and first half of the 2024 fiscal year. We encourage everyone to read this morning's press release, as well as Cognition's quarterly report on Form 10-Q, annual report on Form 10-K, and periodic reports on Form 8-K, which are now filed with the SEC and available on our website. In addition, this conference call is being webcast through the company's website and will be archived for 30 days. Please note that certain information discussed on the call today is covered by the safe harbor provisions of the Private Securities Litigation Reform Act. We caution listeners that during this call, management will be making forward-looking statements. Actual results could differ materially from those stated or implied by these forward-looking statements due to risks and uncertainties associated with the company's business. These forward-looking statements are qualified by cautionary statements contained in the cognition press release and SEC filings, including its quarterly report on firmware 10Q and previous filings. This conference call contains time-sensitive information, which is accurate only of the date of this live broadcast. Cognition undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call. With that, I would like to hand the call over to Lisa Ricciardi. Lisa?

Thank you, Tom, and good morning, everyone. We appreciate your participation in Cognition Therapeutics' financial results conference call. Today, our CFO, John Doyle, and I will share prepared remarks on the company's progress and financial performance over the first half of the year, after which we'll take your questions. For Q&A, we'll be joined by our Chief Medical Officer and Head of R&D, Dr. Tony Taggiano. At Cognition Therapeutics, our focus is on the development of innovative, orally available drug candidates targeting age-related degenerative conditions of the CNS and retina. Our clinical programs include multiple Phase II trials for both early and mild to moderate Alzheimer's disease. We are also studying CT1812 in dementia with Lewy bodies and geographic atrophy secondary to dry AMD. Now during today's call, my formal remarks will be on the completed SHINE trial and then on our next study to read out the SHIMR trial. Let's begin with SHINE. Our SHINE study was a Phase II clinical trial proof of concept study of CT1812 in mild to moderate Alzheimer's disease. This was our first proof of concept study. The trial enrolled a total of 153 adults with mild to moderate Alzheimer's disease. Participants were randomized to receive either placebo or oral doses of 100 or 300 milligrams of CT-1812, and there were 51 participants in each arm of the study. Our primary purpose was to assess safety and solubility after six months of daily dosing. We also evaluated multiple cognitive endpoints, including the ATIS-COG-11, ATIS-COG-13, cognitive composite, and the MMSE. Functional improvement scales were included as were biomarker analyses. In this study, participants who were treated with CT1812 for six months showed a consistent trend in slowing cognitive decline Compared to placebo across all cognitive measures, the ATIS-COG 11 and 13 cognitive composite at MMSE. On the most commonly used measures, the ATIS-COG 11 and 13 skills, CT 1812 treated participants showed a 39% slowing of cognitive decline after six months. To put SHINE results into context, The recently approved monoclonal antibodies demonstrated 25% to 30% slowing in an early patient population over 18 months. We were very encouraged by the 39% slowing in six months with a once-daily pill. Now, furthermore, on the ATIS-COG11 and MMSE skills at day 98, the midpoint of the study, In the combined 100 and 300-milligram dose group, p-values of less than 0.05 were observed. Putting the full SHINE data readouts in context in the completed trial, participants on placebo in the intent-to-treat analysis worsened by 2.7 points as measured by ATIS-COG-11. In the pooled 100 and 300 milligram dose group, there was a reduction of 1.66 points or 39% slower loss of cognition than in the placebo group. Said another way, CT1812 rescued about 40% of the cognitive decline that participants could have experienced. In this trial, we used the functional measures of the ADCS-ADL, or Activities of Daily Living, and the ADCS-CIGIC, the Clinical Global Impression of Change. CT1812 demonstrated a slowing of loss of function towards the latter part of the trial. With 150 people enrolled or approximately 50 people per arm, the SHINE trial did not achieve statistical significance on the ATIS-COG-11 scale. However, this is the important part. The multiple measures we assessed show a consistency across time and dose that is positive. It is this consistency that motivates us to look ahead to longer and larger trials. With regard to safety, CT1812 demonstrated a favorable safety and tolerability profile with most treatment adverse events being mild or moderate. The AEs were consistent with previous clinical experience. There was one case of asymptomatic area H and no cases of ARIA-E. At the 300 milligram dose, nine participants experienced treatment emergent LFT increases greater than three times the upper limit of normal. These resolved after cessation of drug without evidence of serious liver injuries. Importantly, there were no LFT elevations observed in the 100 milligram dose. This data is all publicly available on our website. We are continuing to analyze the exploratory CSF biomarker program data. The study showed significant change in neurofilament light, or NFL, and this is a marker of neurodegenerative disease. This occurred at the 300 milligram dose. We believe that this is evidence CT1812 acts as a synaptoprotective agent. Other CSF biomarkers assess including NeuroGrenin, Synaptotagmin, SNAP25, T-Tau, Total Tau, and GFAP. We'll share more in the future as we continue analyzing biomarker data from this trial. Taken in total, we believe these findings provide evidence that the amyloid oligomer antagonism, a new and distinct mechanism for therapeutic intervention, may have a role as a monotherapy or a drug used in combination with approved drugs for the treatment of AD and other dementias. We met our key objectives of assessing safety, tolerability, and cognitive and functional changes. We learned that the 100 milligram dose showed good efficacy and had no incidence of elevated liver enzymes or discontinuations due to AEs. There were no new safety signals in the SHINE trial. We had a strong and consistent trend demonstrating potential efficacy as slowing cognitive decline in patients with mild to moderate disease. we believe the magnitude of effect is consistent with other drugs recently developed and approved. We believe the biomarker data supports the true slowing of neurodegeneration. While in Philadelphia last week at the AAIC conference, we had the opportunity to speak with multiple physicians and PIs from the SHINE trial. They were very supportive of the trial results and particularly the consistency of cognitive changes across the scales. They value the new safety information and profile of the 100 milligram dose group. Consistent with feedback from various investors, RPIs are interested in the next steps in terms of a new trial, duration, dose, patient population, endpoints, and trial size. We also know that pharma groups, having winnowed CNS programs over the years, are now looking to add to their portfolios important CNS drugs. For many, Alzheimer's disease is a top target. We are looking forward to continuing our dialogue with these companies. Our next step is to convene a panel of leading neurologists to review our data, best the findings, and discuss their thinking on next steps in CT1812 drug development. I would like now to turn to the SHIMR study, which is our next data readout. This Phase II trial with CT1812 enrolled 130 people with mild to moderate dementia with gloomy bodies, or DLB. As a reminder, there are an estimated million and a half people in the U.S. affected by DLB, and this disease is the second most common form of dementia. These patients are characterized by dementia, mobility issues, visual and sensory hallucinations, and significant GI issues. There are no currently approved treatment options. From a pathological perspective, more than half of the DLB patients are estimated to both have alpha-synuclein and A-beta oligomers in their brain. We believe that CT1812, with its novel mechanism of action, protecting neurons from the toxicity of both pathogenic proteins, has the potential to treat DLB patients. This is a double-blind, randomized, three-armed study. Patients are randomized one-to-one-to-one with 100 or 300 milligrams of CT1812 or placebo. This study is not powered to show significance. It is designed as a proof of concept study to determine the change in the MOCA, if that is the Montreal Cognitive Assessment Scale, after six months of receiving CT1812 or placebo. This trial is supported by non-diluted funding from the NIH, and the trial is being led by Dr. James Galvin from the University of Miami Miller School of Medicine. We have completed enrollment, and we expect to report top-line results by year-end. We believe the SHIMR trial results will add to the understanding of CT1812's potential for treating neurodegenerative disease. As with AD patients in the SHINE trial, we look forward to providing patients and caregivers an effective, convenient option to slow the progress of DLB. Now, a word about our other two trials. In brief, our start START trial is actively recruiting participants with early Alzheimer's disease. Participants on stable background therapy with licanumab and dinanumab will be allowed to enroll in the trial, and we expect this will allow us to provide real-world evidence of CT1812's potential as monotherapy and in combination with monoclonal antibody treatments. We're also actively enrolling participants in our MAGNIFY study. This is a randomized placebo-controlled phase two study of 240 participants who have dry age-related macular degeneration and measurable geographic atrophy. Over the treatment period, change in lesion size and best corrected visual acuity will be assessed to determine if CT1812 in slow vision loss. During this past year, cognition scientists published multiple manuscripts and made at least nine presentations at medical and scientific conferences. All the publications are available on our website. Importantly, the scientific evidence generated by our team has continued to support our development efforts. providing insights into proteins and biological processes impacted by CT1812 in neurologic and ophthalmology conditions. In closing, in 2024, we have made significant progress advancing CT1812, and we believe this drug has the potential to be an important part of the developing paradigm for dementia treatment. With that, I turn the call over to John Doyle for a review of our results.