Greetings, and thank you for joining the conference call this morning to introduce the proposed merger agreement between AlloVir and Kalaris Therapeutics. I would like to remind everyone that today's call is being recorded and will be made available for replay via webcast only. Instructions are included in today's press release and in the investor section of AlloVir's website. I would like to turn the call over to Corey Davis from LifeSci Advisors Investor Relations to start the call. Thank you. Please go ahead. Thank you, Operator. Before we begin today's call, I'd like to remind everyone that this discussion and the accompanying presentation will contain forward-looking statements based upon the current expectations of AlloVir and Kalaris, which include but are not limited to statements regarding the expected timing, completion effects, and potential benefits of the transaction, and our future expectations, plans, and prospects for the combined company. Such statements represent management's judgment and intention as of today and involve assumptions, risks, and uncertainties. This slide, titled Disclaimer, provides an overview of these forward-looking statements and the risks and uncertainties that could cause actual outcomes and results to differ materially from those contemplated in these forward-looking statements. Please refer to the slides shown here for more details on this important information. AlloVir and Kalaris undertake no obligation to update or revise any forward-looking statements except as required by law. Further, AlloVir intends to file a registration statement and accompanying proxy statement and prospectus with the SEC relating to the proposed merger. Please be advised to read, when available, the proxy statement and prospectus and other relevant documents filed with the SEC, as these will contain important information about AlloVir, Kalaris, and the transaction. Once available, these documents can be obtained from the SEC at SEC.gov or on AlloVir's website. I'd now like to turn the call over to David Hallal, Chairman of AlloVir, to begin today's conference. Thank you, Corey, and good morning, everyone. Joining me on today's call are Andrew Oxtoby, Chief Executive Officer of Kalaris Therapeutics, and Dr. Matthew Feinsod, Medical Lead of Kalaris Therapeutics. As you likely saw, AlloVir and Kalaris issued a joint press release this morning announcing the signing of our definitive agreement, and AlloVir filed a Form 8-K, which we encourage you to read for more information. I'm pleased to be able to share more details with you about the agreement today. Upon completion of the merger, pre-merger AlloVir stockholders are expected to own approximately 25.05% of the combined company, and pre-merger Kalaris stockholders are expected to own approximately 74.95% of the combined pro forma company. Upon closing, the combined company is expected to have approximately $100 million in cash, which is expected to be sufficient to fund operations through 2026. The merger is expected to close in the first quarter of 2025, and at that time, the company is expected to be renamed Kalaris Therapeutics, remaining on the Nasdaq and trading under a new ticker symbol, KLRS. Before turning the call over to Andrew and Matthew to discuss Kalaris and the highly innovative lead anti-VEGF therapeutic candidate, TH103, I would like to express how delighted I am that we are entering into this definitive agreement with Kalaris. The boards and management teams at each organization truly believe in the synergies that this transaction creates. Collectively, we believe this merger represents the best interests of the stockholders of both AlloVir and Kalaris, with the opportunity to create significant value for patients and shareholders. The combined company will have a strong cash position, which will enable us to advance a potentially transformative clinical stage asset through multiple data readouts over the next few years. I am also thrilled to be joining our experienced management team and board with expertise in building and leading ophthalmic and retina-focused biotech companies from discovery, development, and commercialization. In fact, I had the pleasure of working with many of the founders and leaders of Kalaris nearly 20 years ago when together we brought the world's first anti-VEGF therapy, Macugen, to the market in 2004, and can personally vouch for the remarkable life-changing benefits that have been delivered to a generation of patients living with neovascular age-related macular degeneration, diabetic macular edema, and retinal vein occlusion. Therapies which target VEGF have revolutionized the treatment of many of the most feared and prevalent retinal diseases that have led to significantly improved vision outcomes for millions of patients around the world. We believe that Kalaris's lead asset, TH103, designed by the world's most decorated scientist in this space, Dr. Napoleon Ferrara, has the potential to transform the treatment paradigm yet again. TH103 was designed to bring meaningful innovation and benefits over existing therapies in a growing $14 billion global market, and we are excited to be a part of this transformational merger to accelerate its continued development. With that said, it is my pleasure to introduce Andrew Oxtoby, Chief Executive Officer of Kalaris Therapeutics. Andrew has over two decades of experience in the pharmaceutical and biotech industries and has held a variety of leadership roles across multiple therapeutic areas during his career. Prior to joining Kalaris as CEO in March of this year, Andrew was the Chief Commercial Officer of Chinook Therapeutics and has also held multiple executive leadership roles at both Aimune Therapeutics and Eli Lilly. I am very much looking forward to working closely with Andrew and will now turn the call over to him. Andrew? Thank you, David, and sincere thanks to the entire management team and board at AlloVir for your enthusiastic support of Kalaris and our development program. We at Kalaris are thrilled to be a part of this merger, and I personally look forward to working together to further the development of our lead asset, TH103. With TH103, we truly believe we have the opportunity to potentially bring something remarkable to the treatment of retinal disease. Our molecule is a fusion protein which targets vascular endothelial growth factor, or VEGF, which is the primary mediator and target of pathologic angiogenesis and exudation in retinal vascular disease. As David mentioned, anti-VEGF therapies have become the standard of care for the treatment of multiple vascular and exudative diseases since their introduction over 20 years ago, and we're energized by the prospect of developing a novel intravitreal agent against a validated target which has the potential to provide a meaningful advance over existing treatment options. The molecule was developed by Dr. Napoleon Ferrara, the distinguished professor of ophthalmology and pathology in the UC San Diego School of Medicine, and an acknowledged pioneer in the field of VEGF. Dr. Ferrara co-founded Kalaris along with Dr. Srini Akkaraju and Dr. Mike Dybbs from Samsara BioCapital, as well as Dr. Samir Patel, who himself has a long and successful history in the development and commercialization of therapies in the field of ophthalmology and retinal disease, with executive leadership roles at Ophthotech and Eyetech. TH103 has demonstrated increased anti-VEGF activity, as well as sustained retention in the retina in head-to-head preclinical studies versus aflibercept, and shortly, I'll be turning the presentation over to the Kalaris medical lead, Dr. Matt Feinsod, to provide further details on these data, as well as an overview of our Phase I clinical program that recently began enrolling patients. Before I do that, I'd like to spend a minute or two discussing the current market for anti-VEGF therapies and explain why patients need a new therapeutic option. Today, the global market for branded anti-VEGF agents used to treat prevalent retinal diseases such as neovascular age-related macular degeneration, or wet AMD, diabetic macular edema, or DME, and retinal vein occlusion, or RVO, stands at approximately $14 billion. As you can see, there continues to be a large proportion of off-label use of compounded bevacizumab to treat these diseases. And yet, even with that dynamic, as well as the potential launches of new therapies against less established targets in the coming years, the market for branded VEGF agents is projected to grow to approximately $18 billion by 2029. The use of anti-VEGF therapies will continue to make a huge difference in the lives of patients all over the globe, yet still an unmet need persists for a treatment option that could potentially deliver even better patient outcomes. This slide illustrates the need to develop further advances in therapy to treat these diseases. The chart on the left from a registrational clinical trial is representative of what has been seen consistently across all agents over the last 20 years, where visual acuity is initially improved from baseline to a certain level, and then that level of improvement is maintained by patients over time in the controlled setting of a clinical study. On the right is a chart from a study looking at the outcomes for patients who receive the same drug in a real-world setting. This is one example of a phenomenon which has been seen consistently in this class of therapies, specifically that real-world patient outcomes over time have broadly not been able to replicate registrational clinical study results, with most of this being attributed to suboptimal compliance related to the burden of frequent clinic visits. Patient response to all anti-VEGF agents is heterogeneous and unpredictable, necessitating frequent in-person visits to the clinic, both for clinical assessment as well as for the injections themselves. Patients are often elderly and require further assistance from a family member or caregiver to make appointments, which can lead to inconsistent adherence to therapy regimens and inevitably a decline in patient vision. Extending the interval between injections and therefore clinic visits could help to relieve this treatment burden. A novel therapeutic that could potentially deliver greater anti-VEGF activity and be sequestered longer in the retina could provide a clinically meaningful advance over the current treatment options available by helping to address this issue. Before I turn the presentation over to Matt to take you through the details of TH103, I would be remiss if I didn't further acknowledge the role that our co-founder and board member, Dr. Napoleon Ferrara has played in the invention and development of the molecule. Matthew is truly a pioneer in the world of medicine and drug development, having originally discovered and isolated the VEGF signaling protein and its various isoforms. He's also behind two of the most successful and foundational anti-VEGF therapies ever developed in Avastin and Lucentis during his time at Genentech. Recognizing the treatment burden associated with currently available therapies, Matthew and his colleagues sought to discover and design a novel long-acting VEGF inhibitor which could potentially extend treatment duration, reduce treatment burden, improve patient compliance, and deliver better patient outcomes as a result. This molecule became TH103. We at Kalaris feel privileged to be a part of steering Matthew's most recent innovation in this field through a clinical development program and towards commercialization, where it has the potential to make a meaningful difference in the lives of patients suffering from retinal disease all over the world. With that, I'd like to introduce Dr. Matthew Feinsod, the medical lead for Kalaris. Dr. Feinsod is a board-certified ophthalmologist who has played key roles in a number of private and public biotech companies, including Eyetech and Imagen Biotech, from early-stage development through commercialization in the retina space. Matt has also served as medical officer in the ophthalmology division of the U.S. Food and Drug Administration, and he's going to be discussing the design of TH103, TH103's preclinical data, and the design and goals of our Phase I clinical trial, which is currently enrolling treatment-naive patients in wet AMD. I will now turn the call over to Matt. Matt. Thank you, Andrew. To reinforce Andrew's words, while 20 years of anti-VEGF therapies have transformed patient outcomes for the better, many patients experience suboptimal visual acuity outcomes because it can be challenging for both themselves and their caregivers to adhere to a frequent clinic visit regimen over many years. This onerous regimen has prompted retina specialists to find ways to stretch the visit intervals and has led some patients to delay or even skip their appointments. Recognizing this major unmet need for a differentiated anti-VEGF to meaningfully address these issues, Dr. Ferrara and his colleagues endeavored to engineer a truly long-acting biologic drug with increased anti-VEGF activity. How? By harnessing two molecular attributes intrinsic to native VEGF receptor 1: its high affinity for binding VEGF and its high affinity for binding macromolecules called heparan sulfate proteoglycans, or HSPGs, which are ubiquitous in the eye and can potentially serve as molecular anchors to retain a drug in ocular tissues. From the VEGF receptor 1 backbone, Dr. Ferrara isolated key molecular domains that contribute to these high affinities and fused them to an IgG Fc to create the Kalaris lead asset, a next-generation fully humanized fusion protein VEGF decoy receptor, TH103. What are these key domains? By way of background, depicted here are two of the body's native VEGF receptors called VEGF receptors 1 on the left in blue and 2 on the bottom right in red, each with seven extracellular domains. Importantly, each receptor has differing biologic functions, and there is agreement that VEGF binds to VEGF receptor 1 with substantially higher affinity than it binds VEGF receptor 2. First, drawing your attention to the left illustration, Dr. Ferrara isolated domains 2 and 3 from native VEGF receptor 1 and, as mentioned, fused them to an IgG Fc to create the Kalaris decoy VEGF receptor, TH103. That is, TH103 is derived from domains 2 and 3, both from VEGF receptor 1. In contrast to the right, the current market-leading agent, aflibercept, while also a decoy VEGF receptor sharing some structural similarity with TH103, has a salient molecular difference. It pairs domain 2 of VEGF receptor 1 with domain 3 derived from VEGF receptor 2, shown in red. This salient distinction is the basis for TH103's unique potential advantages. Why? Let's go to the next slide. Because domain 2 of VEGF receptor 1 is primarily responsible for high affinity VEGF binding, and domain 3 on the left has been shown to enhance VEGF binding and to potentially increase drug retention in the eye. How? Domain 3 has high affinity for HSPGs. HSPGs are negatively charged macromolecules present in the extracellular matrix and cell membranes throughout the body, including the retina. Positively charged residues in domain 3 of VEGF receptor 1 adhere to the negatively charged HSPGs, resulting in intraocular tissue deposition. In contrast, as seen on the right, domain 3 from VEGF receptor 2 has lower affinity for HSPG, serving to minimize tissue sequestration. This might be desirable for systemic indications, such as its original indication in oncology, but not for a long-acting retinal therapy. To test these hypotheses, Dr. Ferrara conducted a series of in vitro and in vivo preclinical experiments head-to-head against market leader aflibercept. To begin, in this in vitro experiment, VEGF was introduced to bovine choroidal endothelial cells to stimulate cell proliferation. This model was selected because in neovascular AMD, human choroidal endothelial cells proliferate during pathologic angiogenesis. On these graphs, percent inhibition is on the y-axis and drug concentration on the x-axis. In the left graph, you can see that TH103 inhibited cell proliferation 100% at concentrations greater than one nanomolar, whereas in the right graph, aflibercept inhibited proliferation by not more than 80%, even at the highest tested concentrations. Next, to test TH103 activity in vivo, Dr. Ferrara used the rodent laser-induced choroidal neovascularization model shown on the next slide. This rodent model is the most widely used to study the effects of anti-VEGF agents in inhibiting CNV. While not a direct model of AMD disease, in this experiment, a laser was applied to stimulate growth of CNV lesions, as shown in fluorescent green, on the mouse retina one day after either TH103 or aflibercept was injected. The size of the CNV lesions was measured one week after laser in order to assess the comparative effects of the two agents in preventing CNV growth. As shown in the bar chart, where the y-axis is the CNV size and the x-axis lists each tested agent, the mean CNV size after TH103 was lower compared with equimolar concentrations of aflibercept. Furthermore, note that TH103 performed favorably even when compared to a 10-fold higher concentration of aflibercept. Now let's turn to TH103's second potential advantage: prolonged duration of action. Before reviewing the experimental data, it is helpful to visualize that HSPGs are ubiquitous in the retina, and the left panel shows the adult retina in cross-section, where green represents the presence of heparan sulfate and blue represents cell nuclei. As mentioned, the HSPGs serve as molecular binding partners for domain 3 of VEGF receptor 1, thereby potentially increasing TH103 retention in the eye. The following describes Dr. Ferrara's experiments to assess whether TH103 was retained in retinal layers and remained biologically active. In this rabbit model, drug presence is assessed by staining intensity, as measured by immunohistochemistry. To compare retinal retention of drug, staining intensity was measured 14 days after intravitreal administration, and as visible in these retina cross-sections, at 14 days, TH103 showed darker staining compared with aflibercept. Next, to assess whether these data translate to biologic activity at later time points in vivo, Dr. Ferrara repeated the rodent laser-induced CNV model, but with one important experimental change. In order to assess relative duration of action this time, instead of injecting TH103 or aflibercept one day prior to laser, his team injected the agents two weeks prior, as shown in the left panel, to assess durability of effect, i.e., would the drug remain active as measured by CNV area three weeks after administration. As shown in this bar chart, three weeks after administration, TH103 retained its biologic activity compared with equimolar concentration of aflibercept and control, again showing lower mean CNV area. To help visualize these in vivo results, from left to right, representative images from the same experiment show the difference in CNV area three weeks after administration of control, aflibercept, and TH103, with TH103 clearly showing a reduction in CNV area, indicating a preserved biological effect even at this later time point. To summarize, Dr. Ferrara and colleagues have engineered the Kalaris lead asset, TH103, for prolonged duration of action and increased anti-VEGF activity, and favorable preclinical head-to-head experimental data compared with aflibercept support its progression to clinical trials to assess whether these results translate in human disease. As such, Kalaris is actively enrolling a Phase I clinical trial. The Phase I trial is enrolling treatment-naive neovascular AMD patients with initial clinical data anticipated in the third quarter of next year, and Kalaris plans for a natural expansion of TH103 into the other prevalent VEGF-mediated retinal diseases in the future. To provide more detail on the Phase I clinical trial, Phase I objectives include safety, dose finding, pharmacokinetics, and initial pharmacodynamics. The trial is divided into two parts. In part one, we are studying a 20-fold dose range divided into four cohorts of three patients, each receiving a single intravitreal dose. In part two, 12 patients with verified anti-VEGF response and then fluid reemergence after treatment with standard of care aflibercept are to be randomized to one of two doses of TH103 selected from part one. Part two is designed to potentially allow for within-subject data comparisons with aflibercept. As mentioned, initial clinical data from part one are expected in the third quarter of 2025. I will now turn the call back over to Andrew. Thank you, Matt. I'd like to wrap up the presentation by highlighting the current Kalaris management team and members of the board of directors that are expected to be a part of the combined organization moving forward. Working alongside myself as CEO and Matt as the combined company's medical lead, will be Dr. Jeffrey Nau as the Chief Operating Officer, who joined Kalaris in April of this year. Jeff has 20 years of experience working in ophthalmology and was the President and CEO of Oyster Point Pharmaceuticals prior to joining Kalaris, where he guided its corporate evolution from inception through to the company's subsequent acquisition by Viatris. David Hallal, the current Chair of the AlloVir board, will be the Chair of the combined company's board. Dr. Samir Patel has served as the Kalaris Executive Chairman since he co-founded the company along with Dr. Ferrara and the team at Samsara, and with David as the combined company's chair, I'm pleased to share that Samir will become a board member of the combined company. Also expected to join the future board alongside David, Samir, and myself are Dr. Akkaraju and Dr. Dybbs from our founding VC, Samsara, as well as Dr. Tony Adamis, who is the co-founder of both Eyetech and EyeBio after previously serving as the global head of ophthalmology, immunology, metabolism, and infectious disease at Genentech. Two additional board members are also expected to be named to the combined company's board of directors, one to be selected by AlloVir and the other to be mutually agreed upon by the two companies. The proposed merger we are announcing today is expected to close in the first quarter of 2025 and is subject to customary closing conditions, including termination or expiration of applicable antitrust waiting periods and approvals by the stockholders of AlloVir and Kalaris. Following the closing, the combined company expects to have proceeds of approximately $100 million to accelerate the development of TH103, which should be sufficient cash runway to fund operations until Q4 of 2026, including the completion of both parts of our Phase I study, as well as the initiation of a Phase II repeat dose clinical trial of TH103. We expect to be able to share initial data from part one of our Phase I study in the third quarter of 2025 and further data from part two of the study in the first half of 2026. We're excited by the prospect of accelerating our development program and look forward to being able to share these initial clinical data with you. With this, I'd like to thank all of you for your interest in our company, and this concludes the call. Ladies and gentlemen, thank you for joining us. You may now disconnect from.