Introduce our next presenter. Please join me in welcoming David Crean, Chief Business Officer of MediciNova, a clinical-stage biopharmaceutical company developing novel therapeutics for diseases with high unmet medical needs, including neurodegeneration and metabolic indications. David, all yours. Thank you, Lander, for the kind introduction, and we thank our viewers for joining us today. As Lander said, my name is David Crean, Chief Business Officer for MediciNova. Dr. Yuichi Iwaki will also be joining us today, and also in New York next month. I want to start with the investment case on MediciNova. It is a biopharmaceutical company, as Lander mentioned. We are approaching two clinical readouts this year in 2026, with a balance sheet to reach those catalysts, and additional programs being advanced substantially through outside funding. Before we get started, would like to draw your attention that we will be making some forward-looking statements. Please refer to our SEC filings for any risks and uncertainties. We operate with a relatively lean senior team. Dr. Iwaki founded MediciNova and serves as our President and CEO. Dr. Matsuda is our Chief Medical Officer, Jason Kruger, our CFO, and I lead business development, IR, public relations, and communications. That operating structure is very important when we start getting later on in our discussion about the amount of clinical activity that we have ongoing in support relative to our cash burn. You can see here our board then adds on finance, investment, legal, and medical experience. Let me move directly to the investment case. The investment case for MediciNova really comes down to four points. First, MN-166, or ibudilast, which is our core program. It is our core value driver in ALS. Enrollment, importantly, is complete in the 234-patient registrational trial called COMBAT-ALS. It is a phase II-B/III clinical study, and importantly, top line is expected by the end of this year. Secondly, we have another clinical catalyst ahead of that, MN-001, and that is in a phase II study in patients with hypertriglyceridemia, type 2 diabetes, and NAFLD, or fatty liver disease. Enrollment is importantly also complete in that, and top line is expected in the third quarter of this year, so September. Third is our balance sheet. We reported $25.4 million on the balance sheet at the end of Q2. Historically, we have been operating our burn at approximately $12 million- $13 million annually. We have no debt, no warrants, and our expectation is that the current cash reaches the key clinical data milestones this year. Fourth, we have additional clinical programs being funded externally through government and academic collaborations, which really creates some optionality. Bottom line, our investors do not have to underwrite the entire pipeline. The near-term story is much simpler. You have two clinical readouts. You have cash intended to get us through those readouts, and externally funded optionality behind them. Let's get to our unique model, and this is really how we deploy capital. As I mentioned, ALS is our core focus. It is internally funded, and it is our principal value driver and has the clearest near-term regulatory and commercial pathway. Outside of that core, we have programs in dyslipidemia, NAFLD or MASH, oncology, acute lung injury, where development is partner funded or grant driven. I want to be precise about the phrase that we are using, operationally de-risk, because we are talking about and operating in a financing model. We are not suggesting that clinical risk has disappeared. COMBAT-ALS still remains a binary clinical event until we have the data. So what we have done is to reduce the amount of shareholder capital required to maintain exposure to multiple programs. You can see here our pipeline. There are multiple programs on this slide, but for the current investment horizon, let's just really focus on two. The upper one, which is COMBAT-ALS, as I mentioned, enrollment is complete, and top line is expected in the fourth quarter of this year. At the bottom is MN-001, and that is the cardiometabolic program with top line expected in the third quarter. Behind those are the ALS Expanded Access Program, or EAP. You also have degenerative cervical myelopathy, chemotherapy-induced peripheral neuropathy, and glioblastoma neural oncology. Those programs really create additional shots on goal, but the immediate valuation discussion should be driven primarily by the two upcoming readouts, as I mentioned. This is an important part of our capital deployment, our capitally efficient argument. These partner programs are funded by government agencies and conducted by academic investigators in the U.S., in the U.K., Australia, and Canada. The deck that you see here today really reflects MediciNova retaining the regulatory pathway, very importantly, and it has retained exclusive commercialization rights upon any trial completion. So I would really treat these programs as upside optionality rather than something investors need to be putting into the base valuation today. Let's just really move on to what we consider the most important part of the company's presentation, that is MN-166 in ALS. You can see, as I mentioned, MN-166 or ibudilast is importantly a CNS penetrant, small molecule. The molecule has both oral and intravenous formulations, but what I would tell you that in the COMBAT-ALS trial, we are studying the oral formulation. It acts through several mechanisms relevant to neural inflammation, including inhibition of MIF, multiple phosphodiesterases, you can see there, and TLR4. The intended clinical effects are reduction of neuroinflammation and neuroprotection. That is a multi-targeted profile that really matters because ALS is not a single pathway disease. That brings us to really the biological rationale for using MN-166 in ALS. You can see here the rationale has really three components. As I mentioned, neuroinflammation reduction, you have MIF, PDE, and TLR4 inhibition, and that can reduce pro-inflammatory signaling and attenuate glial cell activation. Secondly, you have that neuroprotection. By reducing the inflammation-supporting protein clearance, the objective is to protect motor neuron function. Then third is really, excuse me. Sorry. Third is autophagy, and the work that is supporting our MN-166 suggests an effect on the clearance of TDP-43 protein aggregates, which are tightly and highly relevant to ALS pathology. We are not relying upon one receptor or one molecular pathway. We have a multi-targeted mechanism addressing several components of ALS biology. Our mechanism alone does not create value. What matters is whether it is going to translate into a clinical effect for the benefit of patients. Our first ALS study gave us a signal to pursue that question in a larger trial, and you can see here in our phase II-A responder signal in our first trial, this was our first clinical efficacy signal that we saw. It was a phase II-A study enrolling 51 patients. They were relatively long duration ALS patients with ALS history of approximately five years, and they were also on riluzole, standard of care. Patients received 60 mg per day of MN-166 or given placebo for six months, followed by an open label extension. What interested us as well as clinicians was the responder pattern. On the ALSFRS, defined here as stable or improved from baseline, the responder rate was 21.2% on MN-166 versus 12.5% on placebo. For the quality of life, it was 51% versus 25%. Manual muscle testing was 33% versus 25% on placebo. I want to be careful about these data. This was a 51-patient trial, phase II-A study. It was not designed to really establish definitive efficacy. What we saw, though, was a directional responder signal across function, across quality of life, and muscle strength. That signal, together with the biological rationale and the support of our investigators, really supported us moving into the larger registrational COMBAT-ALS study. You can see here that the commercial opportunity is relatively straightforward. There is approximately 30,000 people with ALS in the U.S., and average life expectancy remaining roughly two to five years from diagnosis. Treatment options, however, remain limited, and with the withdrawal of Amylyx's drug, RELYVRIO, it reinforces really the standard that matters here, a new therapy that has to demonstrate meaningful clinical benefit. You can see very large global market estimated at more than $2 billion. For us, market size is really secondary. If COMBAT-ALS demonstrate meaningful benefit on function and survival in a broad sporadic ALS population, then the commercial opportunity really follows from the data. Here is our ongoing COMBAT phase II/III-B ALS study called COMBAT. It is the pivotal study in this presentation. It is a randomized, placebo-controlled, double-blind phase II-B/III study conducted across multiple centers in the U.S. and Canada. Patients were randomized one-to-one to MN-166 or placebo. The dose was 100 mg per day. The double-blind treatment was 12 months, followed by a six-month open label extension. The plan size going into it was 234, but we ultimately randomized 234, and enrollment was completed in September of last year in 2025. Importantly, these are early-stage ALS patients. The protocol requires disease onset within 18 months. The primary endpoint is the combined assessment of functionality and survival. It combines a change in ALSFRS at month 12 with survival time through a global rank analysis. This is an important endpoint in ALS because it does not look just at functionality in isolation, it incorporates both functional progression and mortality. The secondary measures include muscle strength, also quality of life, responder analysis, survival, safety and tolerability. Compared with the original phase II-A study that I showed you prior to this COMBAT study, it is much larger, uses the 100 mg dose, and enrolls patients earlier in the disease course of ALS and evaluates them through a full year of double-blind treatment, so very important. Recruitment risk is now behind us, which is great. The issue is no longer whether we can enroll the study. The issue is what the data is going to show at the end of the year. Top line, as I mentioned, is expected by the end of this year. You can see here, this slide gives you some context on who we actually enrolled. Mean age is approximately 61 years of age. Mean ALSFRS at screening was around 40, and the mean progression rate at screening is approximately 0.6 points per month, and the mean disease history from first symptom is approximately 12 and a half months. Just under 54% of patients were receiving edaravone at baseline. As I mentioned, they are on standard of care. The trial therefore enrolled an early-stage patient population, but one with measurable disease progression and meaningful use of background therapy. These are the baseline characteristics that are certainly going to matter when we interpret the magnitude and consistency of any treatment effect in the final data readout at the end of the year. You see here the competitive differentiation. I apologize, it is a busy slide, but I would really reduce it down to three points. First, MN-166 is intended for a broad ALS population. It is not restricted to a small genetically defined subset. Secondly, it is an oral approach and very excited about this relative to a number of the companies that are coming into it. Certainly a very large market opportunity, and we have the data that is expected to come out at the end of the year. I wanted to get to a point on the and we also have an additional study to support our registrational trial, although it is a separately funded study. It is an expanded access program. It was funded by the government to the tune of $22 million. We are currently doing this study through the Mayo Clinic down in Jacksonville. It is a multi-center study, 20 centers, open label, and importantly, it is in late stage ALS patients. We are running this at a 60 mg dose, and in June of this year, we achieved our target enrollment of 200 patients. As I mentioned, it is a treatment duration of six months. From a primary endpoint standpoint, we are collecting plasma neurofilament light and also looking at ALSFRS. Importantly, as I mentioned, we achieved our target patient enrollment in June of this year. Now let us move on to our second asset, MN-001. You can see here it is an oral small molecule, and it has several mechanisms, including inhibition of leukotriene and 5-lipoxygenase pathway and PDE3 and 4. The relevant effects for the current program are anti-inflammatory and anti-fibrotic activity, and importantly, its lipid-lowering properties. For the investment case, the mechanism really once again is secondary. What matters is the metabolic signal we saw previously from a number of studies, in fact, seven independent studies, and whether that signal is reproduced in this randomized study that is now approaching readout in September of this year. The prior study enrolled 19 patients with fatty liver disease or NASH, NAFLD, and hypertriglyceridemia. It was an open label study, so I would characterize this as a signal generating study. Across all 19 patients, triglycerides declined approximately 40%. The subgroup that really drove our interest consisted of 10 patients who also had type 2 diabetes. In that subgroup, triglycerides declined almost 51% from baseline, and the reported P value was 0.098. That triglyceride result was not, unfortunately, statistically significant. At the same time, what we saw was HDL-C cholesterol increased by almost 16% in that subgroup with a P value at a significant level. This prior study really gave us substantial triglyceride signal and a statistically significant HDL signal in patients with type 2 diabetes. It's that observation that drove the design of the current study, which I'll show you in a moment, which specifically targets patients with hypertriglyceridemia, type 2 diabetes, and NAFLD or fatty liver. Now the question is whether those findings can be reproduced under randomized placebo-controlled conditions. Here's where we have our ongoing phase II clinical study, which is going to be reading out in September of this year. MN-001 is a randomized one-to-one placebo-controlled double-blind phase II study conducted at U.S. centers. We randomized 40 patients that had hypertriglyceridemia, type 2 diabetes, and NAFLD. Patients received 500 mg per day of MN-001 or a placebo for 24 weeks. There are really two primary assessments shown here. One was a change from baseline in the controlled attenuation parameter, or CAP, measured by FibroScan, and that gives us really a measure relative to hepatic steatosis. The second is a change from baseline in fasting serum triglycerides at week 24. The secondary measures you can see here were safety and the broader lipid profile, including HDL, LDL, and total cholesterol. Importantly, enrollment is complete. We completed enrollment in June of this year, and top line is expected in September of 2026. It's a 40-patient phase II study, not a registrational size trial. What we are looking for is confirmation of the metabolic signal and a result that provides a clear basis for our next development program or potentially a partnering decision. Near-term catalyst. Let me just sum it up, and this is where I want you to keep in mind. You have the nearest catalyst, as I mentioned, MN-001, which we just talked about. Enrollment is complete. Top line remains expected in September of this year. The larger catalyst is the COMBAT-ALS. We randomized 234 patients, completed enrollment in September of 2025, and expect top line by the end of this year. Around all those events, we're planning regulatory discussions and advancing potential partnering discussions across both core and non-core programs. For the principal valuation events, they're those two clinical readouts, and everything else is really, to us, secondary to those clinical catalyst data. Let's just start wrapping it up. Here's our financial overview. This is a financial position that matters because investors should be able to evaluate those clinical readouts without first assuming any immediate financing event. At the end of Q2 2026, as I mentioned, we had $25 million in cash. Our historical annual operating burn has been approximately $12 million-$13 million annually, as I mentioned, and we've been doing that for about five or six year. We have zero debt, no warrants. I may have mentioned this before, but we're dual-listed on Nasdaq and the Tokyo Stock Exchange. The important point for our clinical catalyst is runway. The company's expectation is that the current cash position is sufficient to reach the key ALS milestones. I would not convert that into any specific number of months because the deck does not provide one. But it is important that because the spending's going to depend on the development activity. But importantly, we have potential partnership transactions going on that could extend the runway further, and it's very important that investors need to assume that a partnership transaction may also get us there, and help with that burn. This is central to the setup on our investment thesis. The next major value inflection is expected to come from data, not from a particular financing activity. Let me bring you back to the investment highlight once again. We're certainly looking to try and refine ALS therapeutics with our core value driver. It has both Orphan Drug Designation in the U.S. as well as in Europe, and Fast Track status in the United States. We have multiple shots on goal from non-core, which provides some optionality for partnering. We have a very lean, de-risked operational model, which potentially preserves our cash, which is currently at $25 million. Our key milestones over the next several months, one in September and one at the end of the year. And importantly, our current cash rate extends through the key ALS milestones. With that, what I'd like to do is close where I started. We expect the two clinical catalysts. We have MN-001 phase II all set next month in September, followed by the COMBAT-ALS readout by the year-end. Enrollment is complete on both of those studies, and execution is now focused on delivering on those data. At this point, I would say, Dr. Iwaki and I appreciate your interest in MediciNova, and we thank H.C. Wainwright for the opportunity to present. Awesome. Perfect, David. That was very clear. We're excited for the upcoming top-line readouts. With this, I would like to thank David and MediciNova for what was a very informative presentation. And to all those in the audience who have joined us today, thanks again from the H.C. Wainwright team.