Hello, ladies and gentlemen. Thank you for standing by, and welcome to the Athira Pharma conference call. At this time, all participants are in a listen-only mode. Following the presentation, there will be a question-and-answer session. Please be advised that today's conference call may be recorded. I would now like to hand the conference call over to Julie Rathbun, Head of Investor and Public Relations with Athira. Please go ahead. Thank you, Operator. Good morning, and welcome to the Athira Pharma conference call to discuss the transformative transactions announced in this morning's press release. Joining us today are Dr. Mark Litton, President and CEO; Dr. Javier San Martin, Chief Medical Officer; Dr. Kevin Church, Chief Scientific Officer; Robert Reninger, Chief Financial Officer; and Dr. David Portman, Founder and CEO of Sermonix. Athira issued a press release earlier this morning detailing the content of today's call. A copy can be found on the investors' page of Athira's corporate website. Next slide, please. I want to remind callers that the information discussed in the call today is covered under the Safe Harbor Provisions of the Private Securities Litigation Reform Act. I caution listeners that management will be making forward-looking statements that are based upon management's current beliefs and expectations relating to future events impacting the company and our future clinical development activities, financial condition, or operating performance. Actual results could differ materially from those stated or implied by our forward-looking statements due to our risks and uncertainties associated with the business, including but not limited to those described in today's press release, our slide deck, and in our SEC filings. These forward-looking statements are qualified in their entirety by the cautionary statements contained in today's press release and in our SEC filings. The content of this conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, December 18th, 2025. The company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call and webcast, except as required by law. As a reminder, this conference call and webcast are being recorded and archived. We'll begin the call with prepared remarks and then open the line for your questions. I'll now turn the call over to Dr. Mark Litton. Mark, next slide, please. Thank you, Julie, and thank you all for joining us this morning to discuss the exciting and transformative news for Athira. In short, we announced the acquisition of rights to develop and commercialize an innovative phase III clinical development program for lasofoxifene as a potential treatment for metastatic breast cancer that diversifies our pipeline with a late-stage program. By securing rights to this late-stage program while also advancing ATH-1105 for ALS, we are building a pipeline that we believe has the potential to change lives and create enduring value. To better reflect this transformation, we plan on rebranding Athira in a manner which embodies our commitment to leadership, resilience, and innovation, qualities that define our expanded mission to deliver transformative therapies for patients battling diseases that need better treatment options. Next slide, please. But before I jump into our discussion, I want to take a moment to discuss the exceptional team at Athira, without whom this transaction would not have been possible. This exciting opportunity came to Athira due to the strength of this team and its deep collective expertise built on decades of experience in drug development, regulatory strategy, and commercialization. Importantly, we attracted blue-chip investors who strongly support this transaction based on their evaluation of the underlying clinical and commercial opportunity of this program and their confidence in this leadership team's ability to drive the company's next chapter with clarity, urgency, and excellence. So before we begin, I'm going to have our CMO, Dr. Javier San Martin, our CSO, Dr. Kevin Church, and the founder and CEO of Sermonix, Dr. David Portman, introduce themselves. Many of you know me already as I've been Athira's President and CEO for four years, and before that, I led Athira's strategy and business development as Chief Operating Officer. Prior to Athira, I was with Alder Biopharmaceuticals for more than 14 years, where I was a co-founder and Chief Business Officer before its acquisition by Lundbeck. It was here that I first worked with Javier, which is a good transition for me to introduce our Chief Medical Officer, Dr. Javier San Martin. Over to you, Javier. Thank you, Mark, and good morning, everyone. I joined Athira about a year and a half ago as Chief Medical Officer. Prior to Athira, I was the CMO at Arrowhead Pharmaceuticals for four years. Before that, I spent six years working at Ultragenyx, where I led the development of Crysvita, an antibody targeting FGF23 for a rare disease called XLH. Prior to that, I was Senior Vice President of Clinical Development at Alder Biopharmaceuticals, which, as Mark mentioned, is where our professional paths first crossed. Prior to that, I spent six years working for Amgen, where I led the development of Prolia and also took romosozumab, or Evenity, to the end of phase II clinical development. My first foray into the industry was at Lilly, where, interestingly enough, the first drug I ever worked with was raloxifene, a second-generation SERM. Before I moved to the U.S. in the late 1990s, I was an internal medicine and critical care physician in Argentina. With that overview of my background, let me turn the call over to Kevin Church, our Chief Scientific Officer. Kevin. Thanks, Javier. I'm Kevin Church, Chief Scientific Officer of Athira. I'm a molecular biologist by training with more than 15 years in the industry, nine of which have been with Athira. I've helped to develop our internal pipeline, including our phase II ATH-1105 program for ALS, and I've been working in neuroscience with a focus on neurotrophic factors for the last nine years. In addition to my work in neuroscience, I have a background in cancer biology as well. In fact, my PhD work was on novel therapeutics targeting the growth of solid tumors, so the addition of an oncology program is very interesting and exciting for me. Now, let me turn the call over to Dr. Portman. David? Thanks, Kevin. Good morning, everyone. I'm Dr. David Portman, Founder and CEO of Sermonix. I spent the first 20 years of my career in clinical research practice, where I became an expert in SERM biology and women's health. I was involved in numerous FDA-approved development programs, including those for the SERMs bazedoxifene and ospemifene. I was an advisor to Pfizer during the early non-oncology development of lasofoxifene and the principal investigator for their phase II and III programs in osteoporosis, menopause, and breast cancer prevention. When lasofoxifene became available through Ligand, we in-licensed Ligand's rights to the drug and advanced its development for the potential treatment of metastatic breast cancer with ESR1 mutations. We are now in a pivotal phase III clinical trial. Looking ahead, I'm excited to be working with Athira, confident that Mark and the team share our commitment to innovation and patient impact. Together, I believe we have the expertise and resources to advance the clinical development of lasofoxifene as a potential new treatment option for the many patients battling metastatic breast cancer. With that, I'll turn the call back over to Mark. Next slide, please. Today marks an exciting milestone for our company. We are leveraging the strength of this team, the addition of lasofoxifene, and our ALS phase II program, ATH-1105. This positions us to deliver meaningful data readouts across both programs, expected in 2027, which is central to our investment thesis and long-term growth strategy. On today's call, we'll walk through both programs in detail, starting with lasofoxifene and then ATH-1105. Next slide, please. As Athira takes this exciting step forward, I want to begin by expressing just how energized we are as a leadership team to welcome lasofoxifene into our portfolio and to partner with the innovators who have advanced it to this pivotal stage. This is truly a transformational moment for our company and, more importantly, for patients. Metastatic breast cancer, particularly ER-positive HER2-negative disease, remains the most common breast cancer subtype, representing about 70% of all breast cancer cases. Within this population, resistance driven by ESR1 mutations is both common and clinically challenging, and the medical need is only increasing. The global metastatic ER-positive HER2-negative market is expected to grow from $10.9 billion in 2025 to more than $15.9 billion by 2029, driven by the expansion of combination treatments, biomarker-driven targeted therapies, and demand for better endocrine options. These data underscore not only the scale of the opportunity but the urgency for therapies that can meaningfully change the treatment paradigm. That's exactly why we're so enthusiastic about bringing lasofoxifene into Athira. As you will hear in greater detail shortly, lasofoxifene has demonstrated compelling signals of clinical activity, including double-digit months, progression-free survival in combination therapy in phase II, and a differentiated mechanism designed to overcome the very resistance that limits current endocrine agents. Its tissue-selective pharmacology and strong combinability profile position it uniquely within a landscape that is rapidly shifting towards precision, durability, and improved patient experience. This program is also an incredible strategic fit for Athira. Advancing a phase III asset of this caliber builds on the deep regulatory and development expertise within our team and our experience navigating complex, pivotal, and registration-enabling programs. We firmly believe we are the right company to carry this therapy through the next stages of development and towards commercialization, and we continue building a pipeline that spans late-stage oncology and neuroscience. Lasofoxifene represents exactly the kind of high-impact innovation that aligns with our mission and our strengths. But the real story of lasofoxifene began many years before Athira's involvement, with the vision, persistence, and scientific rigor of the team at Sermonix. Few people understand lasofoxifene, ESR1 biology, and the unmet needs of metastatic breast cancer patients better than its founder. So, with that, it's my pleasure to turn the call over to Dr. David Portman, the physician, scientist, and innovator who has championed lasofoxifene from its earliest days. David will walk you through the compelling clinical data to date and outline where the phase III program is heading, including our regulatory strategy and development timelines. David, next slide. Thank you for that kind introduction, Mark. Lasofoxifene is a well-characterized small molecule with extensive prior non-oncology clinical development, though it has never been commercialized. This makes it a new chemical entity with potential best-in-class combinability, a feature that is often critical in metastatic breast cancer, where treatment increasingly relies on combination therapy due to tumor complexity at progression. While lasofoxifene demonstrated an 83% reduction in new-onset primary wild-type estrogen receptor-positive breast cancer in the osteoporosis setting, our focus is on patients with ER-positive HER2-negative breast cancer who have developed ESR1 mutations. Unlike currently approved therapies that degrade the estrogen receptor, lasofoxifene modulates the receptor, providing tissue selectivity and sparing healthy estrogen receptors in critical tissues such as bone and urogenital tissue. When lasofoxifene was originally developed for the treatment of osteoporosis, its activity against emergent ESR1 mutations was unknown. These mutations commonly arise after first-line endocrine and CDK4/6 therapy. Our phase II ELAINE-2 combination trial demonstrated potential best-in-class progression-free survival, achieving 13 months of PFS, something that had not previously been seen with monotherapy but has recently been validated as an approach in the phase III evERA and EMBER-3 trials. We are currently enrolling a phase III registrational trial to validate this for the lasofoxifene and abemaciclib combination. Next slide, please. ESR1 mutations represent a major mechanism of resistance in second-line treatment for endocrine-dependent breast cancers, the largest breast cancer population. These mutations occur in more than 40% of patients in this setting, creating a significant global market opportunity. These mutations evolve under selective pressure from aromatase inhibitors and other endocrine therapies. In response, an estrogen receptor gene mutation leads to a constitutively active ligand-independent receptor conformation, rendering current endocrine therapies inadequate and creating a clear need for novel approaches. Next slide, please. Conventionally, the most recent approach has been to degrade or eliminate these receptors, but as a women's health physician caring for patients for more than 20 years, I can tell you that complete receptor degradation or blockade often leads to significant tolerability and quality-of-life challenges. Our hypothesis was that lasofoxifene, as a modulator, could inactivate the receptor and breast estrogen receptors without eliminating all estrogen receptor activity in other important estrogen receptor-dependent tissues. Co-crystallography provides confirmatory evidence of this. Lasofoxifene fits into the mutated receptor pocket, locking it into an antagonist conformation in breast cancer cells while retaining agonist properties in tissues like bone and vaginal tissue without evidence of endometrial hyperplasia or cancer risk like tamoxifen. This differentiates lasofoxifene from current degraders, aromatase inhibitors, and earlier-generation SERMs. Next slide, please. An unexpected and important finding was lasofoxifene's relative potency against ESR1-mutated cell lines. As you can see in the middle figure, in vitro data show lasofoxifene maintained potency regardless of ESR1 mutation status, unlike fulvestrant on the left, which exhibited a significant 1 to 2 log shifts in potency, making it more challenging to get sufficient injectable fulvestrant on board. Likewise, on the far right, lasofoxifene also outperformed both approved and investigational SERDs and other estrogen receptor antagonists with a 4 to 40-fold greater potency against mutated receptors. With this potency, this could allow effective dosing of lasofoxifene without pushing limits that can lead to toxicities such as bradycardia, GI issues, and ocular complications, none of which we've seen to date in our program. Next slide, please. Once we observed this in vitro activity, we advanced to MCF7 ESR1-mutated xenograft models, focusing particularly on the most challenging and aggressive Y537S variant. In these studies, lasofoxifene demonstrated a marked reduction in both tumor weight and metastatic burden, whether administered as monotherapy or in combination with a CDK4/6 inhibitor compared to fulvestrant. Coupled with its optimized pharmaceutical profile, including a six-day half-life, excellent bioavailability, favorable volume of distribution, no drug-drug interactions across 23 phase I studies, and its anticipated potency and tolerability as a next-generation SERM, we were confident in moving lasofoxifene into clinical development for patients with advanced breast cancer. Next slide, please. All of these insights informed our ELAINE clinical program. We were able to move directly into phase II, leveraging data from 40 prior phase I through III trials that characterized lasofoxifene's pharmaceutical and safety profile in depth. ELAINE-1 was a head-to-head signal-seeking study versus fulvestrant. ELAINE-2 was an open-label study combining lasofoxifene with abemaciclib, a strategic choice given abemaciclib's unique properties and Lilly's support in supplying the drug for both the phase II and our ongoing phase III registrational trial. Next slide, please. Indeed, ELAINE-1 results confirmed what we had set out to demonstrate: that a modulator, as compared to a degrader, can deliver meaningful anti-tumor activity in ESR1-mutated breast cancer. This was critical to challenging the conventional thinking that these receptors must be degraded. In ELAINE-1, in patients after progression on aromatase inhibitor and CDK4/6 inhibitors with ESR1 mutations, lasofoxifene achieved a median PFS of 5.6 months, numerically superior to fulvestrant at 3.7 months, with clear separation in the Kaplan-Meier curves. As seen in other monotherapy trials like EMERALD, EMBER-3, and VERITAC-2, there is a rapid drop-off after the first two scans, leading to single-digit PFS of 5.6 months. While lasofoxifene monotherapy shows activity, patients deserve better, and the goal for therapy should be to achieve double-digit months of PFS in the second-line setting. Importantly, lasofoxifene demonstrated excellent target engagement in ELAINE-1. On the far-right lower corner, you can see good clearance or decrease of all ESR1 mutation variants, particularly Y537S, the notoriously difficult-to-treat alteration. Achieving this without degrading the receptor underscores lasofoxifene's unique advantages. Next slide, please. Lasofoxifene's potential as an endocrine partner of choice became even more evident in ELAINE-2, where we combined lasofoxifene with abemaciclib. These patients had progressed on prior CDK4/6 inhibitors and aromatase inhibitors, most after two or three lines of prior therapy. Despite this heavily pretreated population, we observed a median PFS approaching 13 months and an objective response rate of 56%. This was unexpected and compelling, given re-challenging with CDK4/6 inhibitors after progression was still an evolving concept, but our combination therapy looked like a promising strategy for these difficult-to-treat patients. Based on clinical and preclinical results, we believe our combination could potentially offer patients double-digit months of PFS and could offer best-in-class disease control with favorable tolerability. Next slide, please. The central challenge in the second-line ESR1 mutation setting is achieving progression-free survival beyond the six-month median ceiling observed with both traditional and novel endocrine monotherapies in pivotal trials. As shown on the left side of this figure, recent phase III studies with agents such as elacestrant and giredestrant have demonstrated only modest single-agent efficacy. While lasofoxifene monotherapy is competitive with these degraders, we believe patients deserve better outcomes. The comparator we are using in ELAINE-3, fulvestrant plus abemaciclib, achieved a median PFS of six months in prior studies, and the opportunity to break past this ceiling and achieve double-digit months of PFS emerges particularly when targeted therapies are combined with improved endocrine agents, as seen in trials like evERA and EMBER-3. Based on our compelling ELAINE-2 data, we believe that lasofoxifene and abemaciclib combination can deliver this level of benefit for patients in the second line setting over fulvestrant and abemaciclib. Next slide, please. This all informs the ELAINE-3 registrational trial of lasofoxifene and abemaciclib compared to fulvestrant and abemaciclib. This was discussed extensively with the FDA at our end of phase II meeting, and the currently enrolling ELAINE -3 trial focuses on an enriched population, patients with all ESR1-mutated breast cancer, because all comer designs that include wild-type can potentially dilute efficacy for novel endocrine approaches in the second-line setting. Eligible patients are pre- or postmenopausal women or men who have progressed after an aromatase inhibitor and either palbociclib or ribociclib and have an ESR1 mutation detected. With PFS as the primary endpoint and key secondary endpoints including overall survival, overall response rates, and quality-of-life patient-reported outcomes, we believe lasofoxifene's tissue selective profile can deliver meaningful tolerability benefits alongside strong combination efficacy and that new entrants have an opportunity to achieve commercial success in a multi-billion-dollar category if they deliver competitive efficacy while offering superior tolerability. We're now more than halfway enrolled and expect the top-line data readout in mid-2027. Working with an experienced global CRO and a team with deep expertise, we believe our timelines are achievable, and we have an opportunity to bring this promising medicine to patients expeditiously. Next slide, please. Lasofoxifene's unique tissue selectivity is expected to deliver a real quality-of-life advantage. Even in metastatic patients in the ELAINE-1 study, we evaluated improvements in urogenital symptoms, a common and burdensome issue for most breast cancer patients. Using a validated patient-reported outcome measure, patients on lasofoxifene reported significant improvements in vaginal and vulvar dryness and pain, consistent with prior phase III findings in healthy postmenopausal women. Addressing these symptoms could make a meaningful difference for patients, and we anticipate that lasofoxifene may help mitigate these common adverse effects in breast cancer care. In ELAINE -3, our patient-reported outcome assessments include domains specifically focused on vaginal and sexual health, where we aim to confirm these encouraging results. Next slide, please. In addition to lasofoxifene's unique urogenital health benefits driven by its SERM tissue selectivity, extensive data from the earlier osteoporosis program highlights its bone-sparing properties. As shown here, lasofoxifene significantly reduced both vertebral and nonvertebral fractures, an outcome not demonstrated by other SERMs and likely reflective of the potency of this next-generation agent. Further, lasofoxifene improved LDL cholesterol and reduced coronary heart disease events, while also lowering the incidence of new-onset breast cancer in a large prevention study. These findings underscore lasofoxifene's ability to act as an estrogen agonist in critical tissues while serving as a potent antagonist in the breast, delivering a unique and clinically meaningful profile. Next slide, please. As we've discussed, monotherapies in the second-line ESR1 setting only get you so far. Several new agents, such as elacestrant and imlunestrant, were approved for this indication, yet all hit the six-month median PFS ceiling. Recent data have further validated that combination approaches with novel endocrine agents can deliver superior outcomes, and we're proud to be among the few companies focused on this strategy as a registrational path. ELAINE-3 is now more than 50% enrolled, and we believe this trial provides us with the opportunity to bring the only pure SERM to market for this patient population. Importantly, ELAINE-2 demonstrated a median PFS of 13 months for lasofoxifene combined with abemaciclib in a heavily pretreated population. Our goal is to achieve double-digit months of progression-free survival in the second-line setting and deliver a potential best-in-class, well-tolerated option for patients facing this challenging disease. Next slide, please. Among the two registrational programs evaluating abemaciclib sequencing in this population, lasofoxifene stands out for its excellent tolerability profile, without observed drug-drug interactions, QT prolongation, bradycardia, or ocular toxicities that have challenged other estrogen receptor degrading agents. Combined with anticipated progression-free survival and overall response rates based on ELAINE-2, we believe lasofoxifene can play an important role in this setting. Importantly, given abemaciclib's known association with diarrhea, we were pleased to see no increase in higher-grade diarrhea in ELAINE-2, a key management challenge for patients and physicians. By contrast, imlunestrant has diarrhea as a monotherapy side effect, and grade 3 diarrhea was observed in EMBER -3. Next slide, please. In second-line breast cancer, the choice of endocrine backbone is critical because it drives long-term safety, tolerability, and adherence when combined with CDK4/6 inhibitors. Lasofoxifene offers a favorable tolerability profile with no observed stacking toxicities, such as diarrhea, and provides additional quality-of-life benefits. Unlike oral SERDs, which are still maturing in their chronic safety data and may have impact on healthy tissues, lasofoxifene brings decades of SERM safety experience. With the potential to deliver durable efficacy, minimize long-term risk, and improve patient quality of life, we believe lasofoxifene is well-positioned to become the next backbone endocrine therapy. The long duration of therapy underscores the importance of minimizing cumulative toxicity in order to enhance adherence by providing a regimen that patients can tolerate comfortably, ultimately supporting both efficacy and quality of life. Next slide, please. The global breast cancer market is approximately $55 billion, with the U.S. second-line breast cancer segment alone exceeding $5 billion-$6 billion annually and expected to grow as patients live longer with the disease. A substantial portion of these patients harbor ESR1 mutations, and with testing now routine, this represents a significant unmet need and commercial opportunity. With lasofoxifene and abemaciclib's potential for extended treatment duration, combined with lasofoxifene's unique attributes and favorable tolerability profile, we believe that if approved, there is an opportunity for lasofoxifene to achieve peak annual U.S. sales approaching $1 billion. Next slide, please. And beyond our epidemiological assumptions, we believe this opportunity has been commercially validated by Orserdu's performance in this biomarker-driven population. Despite being a modestly effective monotherapy, Orserdu is rapidly approaching annual sales of more than $1 billion, underscoring the significant market potential in this setting. Next slide, please. Lastly, with no drug-drug interactions observed to date and excellent tolerability, lasofoxifene offers the opportunity to combine with other targeted therapies to address additional genomic alterations, such as PIK3CA, as well as wild-type populations, expanding its reach beyond the ESR1 mutation space. Furthermore, lasofoxifene's tissue selective benefits for bone, urogenital health, and lipid profile create a strong rationale for moving into earlier lines of therapy, including adjuvant settings. We believe this could potentially position lasofoxifene as a meaningful option across the entire treatment journey and unlock significant potential within the broader breast cancer market. Next slide, please. In summary, lasofoxifene is an orally administered, well-tolerated, highly combinable therapy with compelling clinical trial results, quality-of-life benefits, and expansion potential. We're excited about its best-in-class potential and thrilled to partner with Athira on advancing this innovative clinical development program. Now, let me turn the call over to Athira's CMO, Javier San Martin, to introduce another exciting and promising program in ALS with ATH-1105. Javier, next slide, please. Thank you, David, and I'll now provide an overview of our ATH-1105 program for the potential treatment of ALS. Next slide, please. As we all know, ALS is a devastating neurodegenerative disease with profound unmet needs. It affects approximately 2,000 patients-25,000 patients globally, including about 33,000 in the U.S. The prognosis after diagnosis is poor, and the treatment landscape is extremely limited, with few options that meaningfully slow disease progression. There is an urgent need for therapies that can preserve motor function, extend survival, and improve quality of life. Our program, ATH-1105, aims to address this need. We're extremely proud of the cutting-edge work coming out of Dr. Church's lab here at Athira, and I'm happy to turn the call over to Kevin to discuss this exciting program and how it might offer hope to patients facing an ALS diagnosis. Next slide, please. Thank you, Javier. So, our compound in development is ATH-1105, an orally available, CNS-penetrant small molecule that positively modulates the hepatocyte growth factor, or HGF, system. HGF, originally identified in hepatocytes, is now recognized as a key neurotrophic factor, critical for maintaining neuronal health and function. In the CNS, glial cells secrete HGF, and its receptor Met is expressed on the surface of neurons and glia. ATH-1105 promotes a stable signaling complex between HGF and Met, significantly increasing Met activation. This activation drives downstream processes that help counteract cellular pathologies associated with ALS. There is strong scientific rationale for targeting HGF modulation in ALS, supported by our own work and that of others. Preclinical models consistently show that enhancing HGF signaling improves motor function and prevents neurodegeneration. Next slide, please. I'll now discuss a few examples of neuroprotective activity of ATH-1105 in preclinical models. As shown here, in patient-derived motor neurons, or iPSCs, from ALS patients differentiated into motor neurons, ATH-1105 demonstrated robust target engagement, significantly increasing Met activation, and improving neuronal survival in vitro. Next slide, please. A key characteristic of ALS is TDP-43 pathology. In vivo, we tested ATH-1105 in a TDP-43 transgenic mouse model, which recapitulates key ALS features, including motor decline and neurodegeneration. Treatment with ATH-1105 preserved motor function over two months and significantly prolonged survival compared to untreated animals. Next slide, please. To understand how ATH-1105 may inhibit disease progression in this model, we explored plasma biomarkers in nerve histology. Here, images of sciatic nerve cross-sections from ATH-1105-treated animals show preserved axonal integrity and myelination, closely resembling wild-type morphology. Untreated animals exhibit severe degeneration. Plasma neurofilament light chain, or NfL, a validated biomarker of neurodegeneration, was markedly reduced with ATH-1105 treatment, further evidence of neuroprotection in this model. Next slide, please. We also explored treatment timing. Early intervention preserved motor and nerve function in the TDP-43 transgenic mouse model, as expected. Importantly, delayed treatment initiated after significant neurodegeneration still altered disease trajectory. Neuromotor function stabilized, and plasma NfL decreased after treatment began, further supporting the neuroprotective activity of ATH-1105, even in advanced disease. Next slide, please. ATH-1105 has completed a phase I SAD-MAD study in healthy volunteers. The molecule was well tolerated, with no dose-limiting toxicities, no serious adverse events, and only mild AEs. PK was favorable, with dose linearity, no accumulation after 10 days of repeat dosing, and strong CNS penetration confirmed by CSF sampling. We achieved target concentrations consistent with preclinical efficacy. Additionally, exploratory biomarker data showed encouraging signs of target engagement in plasma, which we'll discuss briefly. We wanted to explore whether ATH-1105 demonstrates target engagement in humans. We know that Met activation triggers phosphorylation of several downstream proteins, and from our preclinical work, one key target is GSK3 beta. GSK3 beta is a kinase that has been linked to TDP-43 pathology in ALS, potentially contributing to TDP-43 phosphorylation, aggregation, and cytotoxicity. Inhibiting GSK3 beta activity could therefore impact TDP-43 pathology, an effect we've investigated preclinically. The graph in the center shows in vitro data from spinal motor neurons treated with ATH-1105. We observed a significant increase in phosphorylation of GSK3 beta at serine-9, which has been shown to inhibit GSK3 beta activity. This is highly encouraging because it suggests that ATH-1105 can modulate a pathway directly relevant to ALS pathology. Preclinically, we also saw reductions in phosphorylated TDP-43, which we've presented previously. Building on this, we analyzed neuron-derived exosomes, or extracellular vesicles, in the plasma of phase I volunteers. The graph on the right shows a dose-dependent increase in phospho-GSK3 beta at serine-9 with ATH-1105 treatment, consistent with our preclinical findings. This suggests target engagement in humans and biological activity towards an important target in ALS pathology. Now, I'll hand it back to Javier. Next slide, please. Given this exciting clinical and preclinical data, we're working forward to evaluating ATH-1105 in a phase II clinical trial in ALS patients. Planning is underway for the design of a proof-of-concept study to explore effects of ATH-1105 on functional measures, biomarkers, safety, and tolerability in ALS patients. Given the preclinical findings, we're very interested to investigate the effects of ATH-1105 on plasma NfL and explore other key outcome measures, including functional scales, grip strength, and vital capacity. Our aim is to obtain signals of preliminary efficacy to inform a potential future pivotal program. Next slide. In summary, ATH-1105 has demonstrated robust neuroprotection in multiple preclinical models, significant reduction in plasma NfL, and target engagements in mice and humans, all supported by a favorable safety and PK profile. These findings give us confidence that ATH-1105 has the potential to meaningfully impact ALS progression and improve patient outcomes. We're ready to advance into phase II with a proof-of-concept study designed to confirm safety, explore efficacy, and validate the biomarkers that could accelerate development. Beyond ALS, the biology of HGF modulation may open the door to other neurodegenerative conditions, which will create a broader opportunity for this mechanism. This is an exciting moment for the program and for the patients living with ALS, and we look forward to sharing more as we move into the next stage. With that, I'll turn the call back to Mark for closing remarks. Next slide, please. As you've seen from today's presentation, this transaction is not only expanding our pipeline. It is expected to transform our future. Upon closing, we will have two very promising development programs that have the potential to deliver life-changing therapies for patients with metastatic breast cancer and ALS. These are areas of profound unmet need, and we are committed to advancing these programs with focus and rigor. Next slide, please. We are honored to have the backing of some of the most respected biotechnology funds in the industry. Their participation is not only a vote of confidence. It underscores the strength and credibility of this financing and transaction. This $90 million raise speaks volumes about their belief in our vision and our science. This initial funding supports the company through key data readouts and regulatory milestones and provides cash runway into 2028. Furthermore, the inclusion of warrants, which could provide up to an additional $146 million upon exercise, offers a future opportunity to further strengthen our balance sheet. Taken together, these terms reflect the conviction that leading biotech investors have in our team, our platform, and the transformative potential of our programs. Next slide, please. Importantly, the financing better positions us to reach critical data readout across both programs between now and the end of 2027, giving us a clear path to value creation. We are entering this next chapter with conviction. Our strategy is bold, our opportunities are significant, and our team is ready to deliver. Thank you for your continued support and belief in what we are building. Together, we are creating a company that we believe has the power to change the lives and the potential to generate enduring shareholder value. Operator, we are ready to open the call to questions. Certainly. As a reminder, to ask a question, please press star one one on your touch-tone telephone. Certainly. As a reminder, to ask a question, please press star one one on your touch-tone telephone. Again, as a reminder, please press star one one on your touch-tone telephone. And our first question. Our first question will be coming from Douglas McPherson. Your line is open. Hi there. This is Doug. Thanks for taking my call and congrats so much on the next phase for the company. I am curious about the history of the new drug. It looks like it's marketed by Pfizer in a couple of European countries for osteoporosis. Curious about sort of intellectual property. Does Pfizer own it, and it's sort of out-licensed for this breast cancer indication? Just any sort of color on that would be helpful. Great. Thank you, Doug. David, do you want to answer that question? Yeah. Hi, Doug. That's not accurate information. The drug is not commercially available. Pfizer never launched or commercialized it. There may be some misinformation around that on the web, but all rights were returned from Pfizer to Ligand back in 2011. Pfizer did get the drug approved for osteoporosis by EMA, but at the same time had acquired Wyeth at that time with another competing portfolio product. So never launched the drug, and after three years of no commercial launch, market authorization is automatically withdrawn in Europe due to the sunset provision. And once that was withdrawn, Ligand took the rights back. So it's not commercially available anywhere in the world. Gotcha. Thanks so much for that. Yeah. Sorry. That was just the result of a quick Wikipedia search on lasofoxifene. I'll write a letter to the editor. I do appreciate that. And while I have you, curious about the phase III trial. Looks like with PFS as a primary endpoint, it's sort of event-driven. You indicated you're looking for a double-digit PFS, sort of like beating the standard of care and other trials that show about a six-month median PFS. Just any insight on sort of powering? Yeah. Yes. So we did present an updated trial-in-progress poster at San Antonio this past month. The trial is powered to show a hazard ratio of 0.68, which with a roughly three-month delta between the control arm. Historically, fulvestrant abemaciclib, if you look at postMONARCH, has achieved six months of median PFS, and that's been seen in some retrospective cohorts as well. With our 13 months of PFS in a much more heavily pretreated population, we certainly think we can achieve that. But obviously, the randomized trial will confirm that. Gotcha. And that's with 250 patients in each arm? Correct. 250 patients in each arm. Great. And then a little more color, if you are able, about sort of maybe milestones tied to the financing exercise of warrants, sort of royalty payment setups, just sort of any more color on that would be appreciated. Sure. So, essentially, the warrant is triggered on completion of enrollment that we are shooting for to be completed with enrollment the middle of 2026. In terms of color on the license, essentially, there's equity associated with that. There is sort of mid- to lower double-digit royalties associated with that, as well as milestones. Cool. Great. Thanks so much for taking my questions. I had an extensive laundry list of questions, but they were almost all answered during the call and presentation. Really appreciate it. Congrats again. Thanks a lot, Doug. And I would now like to hand the call back to Mark Litton. Thanks. And thank you all again for taking the time to listen to our story. I'd like to wish everybody a happy holiday, and we're really looking forward to meeting with everybody in 2026. Thanks. And this concludes today's conference. Thank you for participating. You may now disconnect.