Good morning, and welcome to the Cardiol Therapeutics Archer phase webcast conference call. All participants will be in a listen-only mode. Later, you will have the opportunity to ask questions during the question-and-answer session. Please note, today's call is being recorded. I will stand by should you need any assistance. It is now my pleasure to turn the conference over to David Elsley, President and Chief Executive Officer of Cardiol Therapeutics. David, you may begin. Thank you, and good morning, everyone. It is my great pleasure to welcome you to this important corporate and clinical update on our Global ARCHER trial in acute myocarditis. Before we begin, I would like to point out that the company's ARCHER data press release covering the ARCHER results presented this past Saturday at the annual meeting of the European Society of Cardiology Working Group on Myocardial and Pericardial Disease in Trieste, Italy, is now available on our website at cardiolrx.com. Also, the slides shown on this webcast will be posted on our website following today's presentation. I would like to remind the audience that during this call, we will be making forward-looking statements within the meaning of applicable securities laws. Forward-looking statement information is based on current expectations and assumptions and is subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied. I am pleased to share this update today with our Chief Medical Officer and Head of R&D, Dr. Andrew Hamer, who will lead the presentation of the Archer results. We are also honored to be joined by two thought leaders from the myocarditis research community who are key members of the Archer study leadership and steering committee: Dr. Dennis McNamara, Professor of Medicine at the University of Pittsburgh, Director of the Center for Heart Failure Research at UPMC, and Chair of the Archer trial, and Dr. Leslie Cooper, Chair of the Department of Cardiovascular Medicine at Mayo Clinic in Florida and Co-Chair of the Archer Steering Committee. Their decades of clinical and scientific experience have been vital in contributing to the success of the ARCHER program, and we thank them for their leadership. Our agenda for today's update call is as follows: Dr. Hamer will present the key results and clinical insights from ARCHER. We will then hear additional perspectives from Dr. McNamara and Dr. Cooper on the ARCHER findings and future directions. A question-and-answer session will then follow and conclude the call. For those who may be new to our story, Cardiol Therapeutics is a late-stage clinical development company dedicated to advancing novel therapies for inflammatory heart disease. Our work focuses on the intersection of inflammasome activation, inflammation, and fibrosis, biological pathways that play a central role in heart conditions such as acute myocarditis, recurrent pericarditis, and heart failure. Our lead drug candidate, Cardiol Rx, is positioned to offer a differentiated therapeutic profile with the potential to address important unmet needs in cardiac medicine. We are privileged to collaborate with leading cardiovascular research centers from around the world, and the caliber of these centers of excellence is reflected in the quality and the design and execution of our clinical programs. These collaborations also underpin our broader clinical strategy and position us well for the future. As we look ahead, the next 6 to 12 months will bring important clinical updates and corporate inflection points for our company that we believe will be of great interest as we advance our mission to bring innovation to the treatment of inflammatory heart disease. Our development pipeline includes two late-stage clinical programs: the pivotal phase III MAVERICK trial and the phase II global ARCHER trial, which are evaluating Cardiol Rx, our lead small molecule oral drug candidate, which is a pharmaceutically manufactured oral solution of high-concentration cannabidiol, and CRD38, our next-generation subcutaneous formulation, both novel therapies targeting inflammasome activation in inflammatory heart disease. The pivotal phase III MAVERICK trial builds on strong phase II results showing that Cardiol Rx delivered rapid, durable symptom relief and reduced markers of inflammation, and resulted in considerably fewer recurrence events per year, all with excellent tolerability and safety profile. These findings supported the FDA's decision to grant orphan drug designation for Cardiol Rx for the treatment of pericarditis, which encompasses the recurrent pericarditis segment. The key findings from Archer, which you will hear about today, show what we believe to be the first demonstration of impact on heart structure in myocarditis and also provide a critical translational bridge to our CRD38 program, which has demonstrated robust impacts on cardiac function, hypertrophy, inflammation, and mitochondrial health in several preclinical models of inflammatory heart disease, including heart failure. Recent data published in the Journal of the American College of Cardiology further validates CRD38's potential, and Archer now offers clinical proof of concept that reinforces it as we accelerate IND-enabling work to advance this exciting next-generation drug candidate into clinical development. I'm also pleased to report that patient recruitment in the ongoing Maverick pivotal phase III program is progressing on schedule and continues to accelerate across leading pericardial disease research centers in the United States, with prominent international centers preparing to join the trial imminently. MAVERICK is supported by an international steering committee of thought leaders in pericardial disease who collaborated with us on the design of this important study and are overseeing its execution. Now, before I turn the call over to Dr. Hamer, just a few brief remarks on the ARCHER trial. Like MAVERICK, ARCHER was an international study of comparable size and scope, making it one of the largest company-sponsored clinical programs in acute myocarditis in many years. This landmark trial enrolled 109 patients across 34 leading myocarditis research centers in the United States, Canada, France, Israel, and Brazil. ARCHER was also designed in collaboration with an international steering committee of leading experts in myocarditis and heart failure who played a central role in shaping the program and overseeing the execution of this important study. With that, I am now pleased to turn the call over to Dr. Andrew Hamer to take us through the exciting results from the ARCHER trial. Thank you, David. Good morning, everyone. First, I want to take a moment to thank the entire Cardiol Therapeutics team for the tremendous effort that went into making this important trial such a success. I also want to extend our gratitude to our external investigators, the clinical trial site staff, and our CROs. Your teamwork and dedication are greatly appreciated. I would especially like to thank the patients who volunteered to participate in the ARCHER trial. At Cardiol, we're developing novel therapies aimed at modulating inflammasome-mediated signaling pathways, which play a central role in the overproduction of pro-inflammatory mediators implicated in the development and progression of inflammatory heart diseases. The NLRP3 inflammasome is an intracellular multiprotein complex. It is a central mediator of the inflammatory injury to tissue injury and inflammation triggered by viral infection, tissue damage, or other stresses, making it an important therapeutic target. The NLRP3 inflammasome is formed and activated in various cardiac pathologies, including acute myocardial infarction or a heart attack, cardiac dysfunction and remodeling, heart failure, cardiotoxicity, pericarditis, and myocarditis. It is important to note that this activation in acute myocarditis can lead to heart failure and arrhythmias through persistent inflammation, edema, and subsequent scar formation. Cannabidiol, the active pharmaceutical ingredient in our lead oral drug candidate Cardiol Rx and in our early-stage subcutaneous formulation CRD38, attenuates the activation of inflammatory and cell death pathways in the heart, including NLRP3 activation. By downregulating activation of NLRP3 signaling pathways, Cardiol Rx and CRD38 represent novel therapeutic approaches to target inflammation in heart diseases. The cardioprotective effects of cannabidiol have been shown across multiple preclinical models of inflammatory heart disease. One of the most relevant examples, especially in the context of the ARCHER findings, is the 2025 Journal of the American College of Cardiology publication demonstrating cannabidiol's ability to prevent cardiac hypertrophy and fibrosis while preserving myocardial infarction. Also of importance is an earlier study in a preclinical model of myosin-induced myocarditis, where cannabidiol was shown to protect against immune-mediated changes in inflammation and cardiac structure. Taken together with other preclinical studies in models of pericarditis and heart failure, these findings are helping to shape the understanding and interpretation of the ARCHER results. The results of the trial were presented this past Saturday by Dr. Leslie Cooper at the annual meeting of the European Society of Cardiology Working Group on Myocardial and Pericardial Disease in Trieste, Italy. We're also pleased to announce that the journal ESC Heart Failure has just accepted the manuscript for publication, and we expect that it will be published later this week or early next week. The ARCHER trial was a phase II multi-center, randomized, double-blind, placebo-controlled trial designed to evaluate the safety, tolerability, and efficacy of Cardiol Rx on cardiac magnetic resonance imaging endpoints known to predict prognosis in an acute myocarditis population. The study enrolled 109 patients at 34 centers. Patients were diagnosed with acute myocarditis that included clinical criteria such as symptoms of chest pain, arrhythmia, shortness of breath, and/or a history of viral-like illness, and myocarditis was confirmed on cardiac MRI. Cardiac MRI, or CMR as we'll refer to it, was obtained in all subjects at study entry and 12 weeks post-randomization. Patients were randomized one-to-one to either Cardiol Rx or placebo. The key efficacy endpoints were changes in CMR measurements at 12 weeks, including myocardial tissue characteristics assessed by changes in extracellular volume, or ECV, intracellular volume, or ICV, and left ventricular mass, or LV mass. Left ventricular function was assessed by changes in global longitudinal strain, or GLS, and left ventricular ejection fraction, or LVEF. Heart chamber volumes were assessed by changes in left atrial end-systolic volume, or LAESV, left ventricular end-diastolic volume, or LVEDV, and left ventricular end-systolic volume, or LVESV. All CMRs were analyzed in a blinded manner at a single core lab. Safety parameters consisted of the number of adverse events and serious adverse events. Baseline demographics were well matched, as shown here, with key demographics well balanced between treatment arms. Chest pain was the most common presenting symptom occurring in 94% of study participants. Viral-like illness was reported in over 70% of participants, and shortness of breath was reported by over 40% of participants. An elevated troponin level was present in almost all patients at greater than 94%. Patients recruited into ARCHER had predominantly intact left ventricular function, as reflected by left ventricular ejection fraction of approximately 60% in both groups. Although not shown on this slide, it should also be noted that 95% of patients enrolled in the study were hospitalized for the indexed myocarditis event, with median hospital stays of five days in both groups. Now we turn to the exciting new results that were presented at the ESC meeting. ARCHER demonstrated meaningful biologic activity despite, as previously reported, the trial not reaching statistical significance for the two primary endpoints. First, there was a notable reduction of 3.7 ml in the primary endpoint of extracellular volume, as shown on the left. Extracellular volume reflects inflammation and fibrosis within the extracellular matrix of the myocardium. Further, there was a 5.6 ml reduction in intracellular volume, as shown on the right panel of the slide. Intracellular volume reflects the size of the myocardial cell compartment, providing insight into cellular swelling and edema. Improvements in both ECV and ICV are consistent with a reduction in myocardial inflammation and fibrotic remodeling, and together create reduction in left ventricular mass. That brings us to the newly presented results from the ARCHER trial that we are especially excited to highlight: the reduction in left ventricular mass, particularly at magnitude. Cardiol Rx produced a significant reduction in LV mass, just over 9 grams compared to placebo, which is clearly demonstrated in this plot showing the change at 12 weeks. The importance, the relationship, and the relevance of these CMR parameters, ICV, ECV, and LV mass, is summarized on the next slide. As I mentioned, LV mass directly relates to the combination of ECV and ICV, and an increase in LV mass makes the heart muscle thicker and stiffer, limiting its ability to relax and fill properly. Archer has shown that Cardiol Rx improves all three CMR parameters. The clinical relevance of these reductions needs to be highlighted. In the case of heart failure with preserved ejection fraction, the increase in LV mass results in diastolic dysfunction and is associated with an increased risk of mortality and morbidity. Indeed, interventions that decrease LV mass are known to improve clinical outcomes. The significance of Cardiol Rx's impact on LV mass becomes even more compelling when the magnitude of LV mass reduction observed in Archer is viewed alongside reductions achieved by widely prescribed therapies, which are highlighted in the following slide. The 9.2 gram reduction in left ventricular mass achieved with Cardiol Rx in Archer is quite striking. Its magnitude is similar to that seen with several blockbuster therapies for obesity, hypertension, and heart failure, treatments that are proven to improve long-term survival and reduce major cardiac events. Seeing this degree of structural cardiac improvement in just three months and in myocarditis patients who were neither obese nor hypertensive underscores the key significance of the finding. The LV mass reduction in Archer indicates a meaningful resolution of cardiac inflammation, a central pathologic driver of the progression of heart disease. In addition to the ECV, ICV, and LV mass changes favoring Cardiol Rx over placebo, active therapy also demonstrated directional improvements in imaging parameters that measure left ventricular and left atrial chamber volumes that are also consistent with reverse cardiac remodeling, reduced filling pressures, and better control of underlying cardiac condition. In summary, the results of Archer provide compelling biologic evidence that treatment with Cardiol Rx results in meaningful structural recovery in the hearts of patients with acute myocarditis, demonstrated by significant reduction in left ventricular mass and consistent directional improvements across other key imaging markers of cardiac remodeling. The observed changes in CMR parameters likely result from an attenuation of cardiac inflammation and immune cell infiltration, limitation of fibrosis, and mitigation of hypertrophic signaling. Equally important is that Archer reaffirms the strong safety profile of Cardiol Rx. As in our prior clinical studies, the therapy was well tolerated and adverse event rates comparable to placebo. Taken together, the ARCHER findings mark an important milestone for Cardiol. We are now seeing in patients the same cardiac protective effects that were observed across multiple preclinical models of heart disease. This reinforces our confidence in the ongoing phase III MAVERICK trial and enhances our enthusiasm for the potential of Cardiol Rx and CRD-38 to address a broad range of inflammatory cardiac conditions, including heart failure. I'd now like to turn it back to David. Thank you, Andrew, for sharing the results from the ARCHER trial. I'd now just like to spend a few minutes and turn to the strategic importance of ARCHER for Cardiol. For all the reasons Andrew has described, we believe ARCHER data represents a major advance for our company. The significant reduction in left ventricular mass marks what we believe to be the first demonstration of structural cardiac improvement in patients treated with Cardiol Rx and underscores the clinical relevance of ARCHER findings. We believe the improvements observed across multiple CMR measurements, findings typically associated with myocardial healing, suggest that Cardiol Rx may be exerting a direct biological effect on cardiac tissue and provide an important translational link to the substantial body of preclinical research demonstrating the anti-inflammatory and cardioprotective properties of our novel therapies across numerous models of heart failure and cardiac injury. Taken together, these clinical results and translational insights support a broader development pathway. As the second phase II study to deliver positive proof of concept results in inflammatory heart disease, these findings provide additional support and further strengthen our confidence in the ongoing pivotal MAVERICK phase III trial in recurrent pericarditis. More broadly, the observed effects on inflammation and cardiac structure reinforce the rationale for accelerating the development of our exciting next-generation subcutaneous drug candidate, CRD38, for conditions characterized by edema, fibrosis, and remodeling, including segments of heart failure where inflammation is increasingly recognized as a key driver of disease progression. Furthermore, we believe this novel drug candidate will be of strong interest to large pharmaceutical companies with dominant positions focused on heart failure medicine. I'm now pleased to introduce our guests, Dr. Dennis McNamara and Dr. Leslie Cooper, who are key opinion leaders in inflammatory heart disease. Dr. Dennis McNamara is Professor of Medicine at the University of Pittsburgh and Director of the Center for Heart Failure Research at UPMC, where he is widely recognized as a leading expert in advanced heart failure, myocarditis, and nonischemic cardiomyopathies. He has authored more than 150 peer-reviewed publications and led seminal studies, including investigations of pregnancy-associated cardiomyopathy that have advanced understanding of the mechanisms, genetics, and recovery pathways in cardiomyopathy and myocarditis. Through his leadership at UPMC and his contributions to broader cardiovascular research, Dr. McNamara has played a pivotal role in improving diagnosis, management, and outcomes for patients with complex forms of heart failure and inflammatory disease. Dr. Leslie Cooper, Chair of Department of Cardiology, Chair of Department of Cardiovascular Medicine at Mayo Clinic, is internationally recognized as one of the foremost experts in myocarditis and inflammatory cardiomyopathies with a career spanning groundbreaking research, transformative clinical leadership, and deep commitment to patient advocacy. He has authored more than 130 peer-reviewed publications that have shaped the field's understanding of how inflammation drives cardiac dysfunction and has helped establish modern standards for diagnosing and managing inflammatory heart disease. Dr. Cooper's contributions continue to guide both clinical practice and the development of new therapies. In addition to his leadership roles at Mayo Clinic, he co-founded the Myocarditis Foundation and continues to serve as a board member, advancing public awareness, scientific collaboration, and patient support. I'm now pleased to turn the call over to Dr. McNamara, who will be followed by Dr. Cooper for their insights. David, thank you very much. I'm pleased to discuss this pivotal trial we feel in myocarditis. As you know, myocarditis, unfortunately, is a potential trigger to other problems with heart failure, particularly with nonischemic cardiomyopathy, where a viral or autoimmune trigger sets off pathologic inflammation and results in the unfortunate deleterious effects of inflammatory heart disease. In Archer, using the MRI, we have clearly shown that you can potentially affect and diminish this pathologic inflammation. It is a unique study and is, I think, probably the first that I can recall to really show an impact and improvement of structural changes with a therapeutic intervention. We are excited about the potential for this to kind of change the trajectory of myocarditis and to improve function in patients. We're also hopeful that in more severe hemodynamically significant myocarditis, we can really affect clinical outcomes. In the future, we certainly would like to see more investigations of this drug to see if we can truly benefit clinical outcomes, and I believe we would, as well as the use of this novel therapy in other potential inflammatory disorders such as heart failure with preserved ejection fraction, where LV mass has previously been shown to be an important factor. Can we, by changing cardiac structure, improve clinical outcomes? I believe that this cannabidiol has a potential therapeutic role in heart failure, and we look forward to seeing this expanded in the future. Let me turn it over then to my colleague, Leslie Cooper, for his remarks and his perspective on the ARCHER trial. Leslie. Dennis, thank you so much. I would echo what you said, that ARCHER really was important. This was the first study with these imaging endpoints that showed clearly benefit and improvement in alignment with the preclinical hypothesis. I would also add to what everyone said that the study was really well done. Our SRO lost no patients to follow up over the entire study. The core reading of the MR was outstanding. I think that it was very well done. Most importantly, at the end of the day, the reduction in LV mass related to a combination of both extracellular and intracellular volume supported the hypothesis that you can remodel the heart with a specific targeted therapy aimed at myocardial inflammation and specifically edema early in the course of myocarditis. For me, this study is exciting. I think that it should be developed further for inflammatory heart conditions. Those could include, of course, myocarditis, which we studied, recurrent pericarditis, as well as the growing problem of checkpoint inhibitor myocarditis, which is the consequence of some cancer therapies. In summary, I'm excited to be a part of this effort and delighted to share with you these positive findings. Thank you. Thanks very much, Dr. McNamara and Dr. Cooper, for sharing your thoughts and insight on ARCHER. I'll now turn it back to the operator to initiate the question and answer period. Thank you. If you would like to ask a question, please press star one on your telephone keypad now. You will be placed into the queue in the order received. In the order your request was received, excuse me. Please be prepared to ask your question when prompted. Once again, if you would like to ask a question, please press star one on your phone now. Our first question comes from Brandon Fox of HC Wainwright. Hi. Thanks for taking my question and congratulations on the data. Maybe just first from me, just given the LV mass reduction and the strength there, and maybe there's a two-part. David, maybe you can answer it and maybe also the CMO can chime in as well. How do you want to see this data evolve as you go into these potential additional indications? Anything more you want to see? Obviously, we want to see it replicated. How do you view the data from ARCHER if it is replicated through larger trials versus perhaps wanting to see anything additional to sort of gain approval and compete? I can just make some brief high-level remarks and then happy for others to add commentary. I think the key benefits of ARCHER is this is really a second proof of concept. It really enhances our confidence in the ongoing pivotal phase III trial, MAVERICK, which is also, as you know, Brandon, an inflammatory cardiac indication focused on recurrent pericarditis. Equally important, though, is we now have read-through and translation from a very large body of experimental evidence with CRD-38, which is our novel state-of-the-art subQ formulation, which has showed remarkable impacts across several models of heart failure and other models of cardiac injury. We now have this translational moment where we've shown the active pharmaceutical ingredient deployed by both Cardiol Rx and now the more next-generation CRD-38 subQ formulation. We now have this translation. Our key area of developmental focus is to accelerate the IND enabling work, which is ongoing now, to speed this next generation into phase I development. That's really the point at which the pharmaceutical industry increases their interest. We are in discussions currently with many members of the international pharmaceutical industry, with particular focus on those dominant in heart failure research. Their key interests lie in heart failure medicine. That is why we're excited to push this new drug forward and ultimately partner with them for its development in broader areas, with Cardiol staying focused on the key areas of the orphan designation programs, which is recurrent pericarditis and myocarditis. Thanks, David. Caelos, anything to add in terms of sort of what you would like to see in future development? Dennis or Leslie, do you have any comments about what you'd like to see in future developments? Dennis speaking, I certainly would like to see whether cannabidiol can make a difference in those patients who present with hemodynamically significant myocarditis, the patients who present with LV dysfunction. As you know, we did not reach the primary endpoint of global longitudinal strain, in part because LV function was relatively preserved. Looking in the smaller fraction of patients that had LV dysfunction, there appeared to be at least a trend towards significant improvements. I would hope that cannabidiol could make a difference for these patients. These were intermediate risk patients hospitalized with troponin elevations for the most part, but for the most part had preserved LV function. I think cannabidiol could make a difference for more severe patients. I hope to see that in one way or another looked at in the future. Yeah. Dennis, that's exactly right. The sicker patients who are at higher risk would be a great next target. I'd say the recurrent pericarditis group is really important, relatively easily identified as well. Then the checkpoint inhibitor group, which is variable in its severity, but has striking adverse events that are both arrhythmic as well as heart failure events, which can happen very suddenly in the course of advanced cancer. Of course, that's a particular situation where you don't want to immunosuppress people a lot because they have cancer. That would be, again, a place where cannabidiol, which did not have any safety signal, might play an adjunctive or primary role. Thank you very much. Congrats again, David, to you and the team. Great. Thank you, Brandon. Our next question comes from Jared Holz of Mizuho Group. Good morning. Thanks for taking the question. Appreciate it, guys. Two quick things. One, can you talk a little bit more to the market size when you kind of look at the data and what the impact might be when you look at the patient population? Obviously, there's a lot of estimates that have to go into that, but just big picture. Secondly, next steps from here, what the phase III trial might look like, how much larger, what the timing would be. Just want to kind of get a little bit more detail on what the go-forward plan is. Thank you. Sure. With respect to market size, as you know, Jared, even the IL-1 blockers, they're approaching, I think they're exceeding $600 million in annual sales in the US, and with many anticipated to see that grow to $1 billion by 2027, 2028. With respect to our lead program, recurrent pericarditis, we anticipate a marketplace that approaches those sales volumes by that time frame. With respect to heart failure, that is order of magnitude larger in terms of market size. Heart failure is an epidemic. It is one of the largest medical challenges facing modern medicine and very costly in the tens of billions of annual care in terms of hospitalization and a high impact on mortality and morbidity. With respect to our next development steps, our primary focus is on continuing with the execution of the pivotal phase 3 Maverick trial, which is our definitive assessment of the role of our lead drug candidate in recurrent pericarditis that is tracking on schedule and indeed accelerating. We will speak with all of our advisors with respect to potential next steps to further the findings with respect to myocarditis potentially, which could include pursuit of a second orphan drug designation. Thirdly, our real area of next focus is accelerating what we believe will be a once-monthly subQ formulation of our lead drug candidate for heart failure. That is in the stage of completing the IND enabling work and preparing to enter clinical development. That is really the stage at which we would look to partner that asset because it is being addressed to this vast market of chronic inflammation associated with segments of the heart failure market, most likely heart failure with preserved ejection fraction. Really appreciate it. Thank you. As a reminder, if you would like to ask a question, please press star one on your phone now. This concludes our question and answer session. I would like to turn the webcast conference call back over to our host, David Elsley, for any closing remarks. Thank you. Thank you, Robert. Thank you, everyone, for joining our Archer update and for your interest in our work at Cardiol Therapeutics. We look forward to keeping you up to date on our progress as we continue to advance the development of novel therapies for patients affected by inflammatory heart disease. Thank you. This concludes today's webcast conference call. Thank you for attending. You may now disconnect.