For this session, Garry Neil, CEO of Avalo Therapeutics, a clinical-stage biotechnology company developing therapies for immune-mediated inflammatory diseases. Garry? Thank you, Ahmed, and good morning. Thank you everybody for joining us. Avalo is building a company around a simple mission, developing innovative therapies for important inflammatory diseases where patients still need better options. Our lead program, abdakibart, is a highly potent and specific inhibitor of IL-1 beta, and we believe the data generated to date position it to be potentially an important new therapy for HS. I will refer you to our forward-looking statements on our SEC filings for the relevant disclosures. This slide caps the Avalo investment thesis. We are focused on significant inflammatory diseases, beginning with HS, a rapidly growing market we project could exceed $10 billion globally by 2035. Abdakibart has generated positive phase II data with what we believe would be a highly competitive combination of efficacy, safety, and monthly dosing. Behind it is AVTX-010, our next-generation long-acting IL-1 beta antibody, and importantly, following our May financing, we believe we have the capital to execute through the anticipated phase III top-line readout. We have deliberately built a very experienced team. Collectively, this group has more than 220 years in biotech and pharmaceutical development, regulatory affairs, manufacturing, commercialization, and corporate strategy. We built Avalo to remain relatively lean, but with the capabilities required to take abdakibart through phase III while simultaneously building the next generation of the pipeline. Let me now turn to abdakibart, why we believe it has the potential to establish a new standard of treatment in HS. There are four things to remember about abdakibart. First, it selectively and potently inhibits IL-1 beta, which we believe is a really important biology, critical biology in HS. Second, LOTUS, the LOTUS trial demonstrated compelling and consistent efficacy, including a 43% combined HiSCR75 response. Third, we have a favorable safety profile across nearly 500 patients studied to date. Fourth, we have the potential for a very simple monthly dosing regimen beginning essentially from treatment initiation, and going forward. It will be a consistent four-week dosing regimen that nobody else can match today. We think that overall profile is highly competitive. Let us look at the HS market opportunity. HS is particularly attractive because this is both a large market and a rapidly growing one in the I&I space. We project approximately 18% annual market growth through 2032 and a global therapeutics market again exceeding $10 billion by 2035. Yet HS remains considerably less penetrated than psoriasis or atopic dermatitis or almost any other disease in dermatology. Diagnosis is increasing, time to diagnosis is decreasing, biologic treatment is expanding, and newer agents are being rapidly adopted. We believe we are developing abdakibart into a market that should be substantially larger at launch than it is today, but still growing rapidly. It is important to understand just how devastating HS can be. What begins with follicular blockage and rupture progresses through chronic inflammation to nodules, abscesses, draining tunnels, and ultimately permanent tissue destruction and scarring. These lesions frequently occur in very sensitive anatomical locations, so it is not simply a skin disease. It can be painful, disfiguring, and profoundly disruptive to patients' lives. Despite recent therapeutic advances, substantial unmet need remains. Across current biologics, only a minority of moderate to severe patients achieve HiSCR75, and physicians tell us that the burden extends well beyond inflammatory lesion counts to pain, draining fistulas, odor, and recurrent flares that can dominate patients' lives. The opportunity is therefore not simply to introduce another biologic. It is to meaningfully increase the population of patients who achieve deeper disease control and to simplify their treatment regimen. Our interest in IL-1 beta begins with the biology, like everything else we do. IL-1 beta is markedly elevated in HS lesions, and it sits upstream of the major inflammatory effectors, including IL-17 and TNF. It therefore provides an opportunity to intervene relatively high and early in the inflammatory cascade. Importantly, there is also clinical evidence supporting IL-1 inhibition in HS. We have seen other anecdotal as well as clinical studies demonstrating the proof of clinical concept in this mechanism. Abdakibart gives us a highly potent and very specific selective way of further addressing that biology. We believe specificity matters. In HS tissue, IL-1 beta is elevated, whereas IL-1 alpha, for example, does not show the same pattern. Prior clinical experience targeting IL-1 alpha has not demonstrated compelling efficacy. In fact, it has not demonstrated any efficacy at all. Taken together, the biology and the clinical evidence support our strategy of selectively targeting IL-1 beta rather than broadly targeting the IL-1 pathway. In fact, there are potential disadvantages, both in terms of safety and removing drug away, or driving drug away from the target when you address IL-1 alpha simultaneously. Here is our LOTUS phase II-B study. This was a 253-patient randomized placebo-controlled phase II study in moderate to severe HS. We tested two regimens, 150 mg every two weeks and 300 mg every four weeks, each with a loading dose. Importantly, we enrolled a representative and relatively difficult-to-treat population, including both biologic naive and biologic-experienced patients. The primary endpoint was HiSCR75 at week 16. The treatment groups were well-balanced, and this was a meaning affected HS population, as you can see. Mean AN count was approximately 14, and over 40% had early stage 3 disease, with more than 1/3 having received a previous biologic therapy. That context is important when interpreting the efficacy results that follow. This is the key data from the LOTUS trial. The study met its primary endpoint with both doses independently. HiSCR75 was 25.6% for placebo, versus 42.2% and 42.9% with abdakibart. That translates into approximately a 17-point treatment difference for both regimens, with statistically very robustly statistically significant results. The consistency across two independently randomized dose groups gives us additional confidence in the underlying treatment effect. Cross-trial comparisons obviously have important limitations, and these are not head-to-head studies. With that qualification, I'd like to point out that the absolute HiSCR75 responses that we observed with abdakibart in LOTUS compare very favorably with both currently approved biologic therapies and several investigational agents that also done large trials. We therefore believe the LOTUS efficacy results supports advancing abdakibart into phase III and gives us the potential for a highly competitive efficacy profile. The result is very consistent when you look at HiSCR50 responses were 59% and 64.3% for the two abdakibart regimens, and 40% for placebo. Both treatment arms were highly statistically significantly better than placebo. The combined response was 61.7%, and this remains the FDA approval standard. The treatment effect isn't dependent on a single threshold of clinical response. Again, we see consistent evidence of activity across measures. Here's the cross-trial comparison of HiSCR50, and again, recognizing all the limitations I mentioned before. Abdakibart produced strong absolute response rates relative to the published experience with approved and investigational therapies. Our goal in phase III is to now reproduce this efficacy in a larger registrational program while preserving the favorable safety and the convenient dosing profile. Another encouraging feature is the onset of activity and the consistency of response and improvement of response over time. Separation from placebo was evident as early as week four, particularly with the 300 mg monthly dosing regimen, and the treatment effect continued to develop through week 16. For a chronic and burdensome disease like HS, both the magnitude and the timing of the response ultimately matter a great deal to patients and physicians. There's also an important result commercially. Abdakibart demonstrated activity in both biologically naive and biologically experienced patients. In the 300 mg monthly group, HiSCR75 was actually very similar across those populations. That suggests abdakibart may potentially have utility both earlier in the treatment regimen and in patients who've already received other advanced therapy. Very suitable for first-line therapy as well as in patients who may be refractory or intolerant of the drug. Again, we were very encouraged by the consistency of response across secondary endpoints. We saw statistically significant or numerically favorable results where we didn't have sufficient statistical power across every measure of disease severity, draining tunnels, flares, inflammatory lesion counts, and deeper HiSCR90 responses. Pain was more variable and did not reach statistical significance, although the 300 mg arm showed a numerical improvement. Overall, we view the secondary endpoints as highly supportive of a broad and internally consistent clinical effect, again, increasing our confidence for being able to reproduce these data in phase III. The safety profile is another important part of the potential differentiation. Overall adverse event and serious adverse event rates were similar to placebo as you see here. We observed no neutropenia, serious infections, opportunistic infections, major cardiovascular events, malignancies, tuberculosis, et cetera, in LOTUS. While the safety database will obviously expand substantially in phase III, the profile observed to date is reassuring and consistent with the established safety experience of selective IL-1 beta inhibition. This is going to be extremely important to patients and to dermatologists. Convenience may provide another meaningful differential. Our intended regimen is a single loading dose, followed by 300 mg every four weeks as a single injection. We also intend that to be with an auto-injector. That means only four doses during the first 16 weeks, and approximately 13 doses in the entire first year. Several current and investigational competitors require substantially more intensive induction or maintenance schedules. For example, eltrekibart is being dosed weekly in their induction phase. If phase III confirms the LOTUS profile, we believe monthly dosing from the outset could be a very attractive option for patients and physicians. Abdakibart establishes the clinical foundation. AVTX-010, which is our next generation, represents that next generation of our IL-1 beta strategy. AVTX-010 is an engineered anti-IL-1 beta antibody designed for an extended dosing interval. We see it as both a potential follow-on to abdakibart in HS, and importantly, as a molecule that could allow us to expand IL-1 beta inhibition into additional immune-mediated inflammatory diseases, especially where less frequent dosing would be highly desirable. We are pursuing a streamlined development path, and we currently plan to submit the IND in the first half of 2027. This was all internally engineered, by the way. Let me finish now with the milestones ahead because we are entering a particularly important period of execution for Avalo. We have established a strong record of delivering against milestones we have set. From the AlmataBio transaction through IND activation, LOTUS enrollment, the positive phase II readout, and we are on track for the milestones ahead as well. The next steps are equally important. We expect our end of phase II regulatory discussions in the second half of this year, followed in the first half by initiation of the phase III HS program and the IND for AVTX-010, and again, we are making great progress towards those milestones. Our opportunity extends beyond HS. IL-1 biology has clinical validation across a surprisingly broad range of diseases, including auto-inflammatory disorders, arthritis, and even cardiovascular disease. There is also mechanistic and clinical rationale in areas that are very interesting to us, such as crystal-induced arthropathies, which afflicts a large number of patients in the U.S. and around the world, and other inflammatory diseases. We are actively evaluating where the combination of biology, unmet need, and commercial opportunity would justify additional investment. I will leave you with five points. We are addressing a large and rapidly growing HS market. Abdakibart has produced compelling phase II efficacy with a favorable safety profile and potentially differentiated monthly dosing. We have a next-generation molecule in AVTX-010 that can extend the franchise. We have major value-creating milestones beginning with phase III and the AVTX-010 IND in the first half of 2027. And with $472 million of cash and investments at the end of June, we have the capital to execute through anticipated Phase III top-line data. In closing, this is Avalo today, a company with validated clinical data, a major phase III opportunity with a differentiated product ahead of us, a growing IL-1 beta franchise, the capital and the team to execute. Thank you, and I look forward to any questions you might have. Thank you, Garry, for that fantastic presentation. We do have a few minutes for questions if anyone has any.