Brilliant. Thank you all. Great to see so many people here. My name's Ben Jackson from the Jefferies European Biopharma team. My job here today is just to introduce Andrew Obenshain, CEO of Inventiva, to the stage to talk to you a little bit about the story, and go from there. Look, I'll hand it over to you, and if there's time at the end, potentially Q&A. I'm not sure. We'll see. Handing over to you. Good to hear from you. Thank you. All right. Good afternoon. Good evening, everyone. I am here to talk about Inventiva and lanifibranor. Inventiva is a one-product company, and lanifibranor is our lead asset. First of all, I'll make some forward-looking statements today. Before I go into the story of lanifibranor, and I'm going to give a background on the commercial side of it, on the history of it, on the clinical data. I actually want to talk about the company a little bit. Inventiva is a French company, based in Dijon. It's been around for about 14 years. It's gone through a recent large amount of change. This is a company that was started at phase III shortly after COVID, and started to run into financial trouble during the execution out of that phase III. This has always been a wonderful asset, but had a struggling company around it. A number of investors came in in October of 2024 to recapitalize the company and to put in a pipe financing of €348 million. That's coming in in three tranches. The first two tranches have already come in. The third comes in with data. This was NEA, Samsara, BVF, a number of other prominent investors. We have one of those investors in the room today, as well. To really kickstart the company back up at that point. Now, the investors had two criteria for the company. Number one was to get rid of all the other assets except for lanifibranor. The second was they brought in Mark Pruzanski as the Board Chair, and Mark was previously the CEO of Intercept and has a lot of experience. From that moment on, the management team has really gone through a reboot, starting with the clinical and regulatory side. Jason Campagna was brought on as the Chief Medical O fficer. He was the former CMO of Intercept. Martine Zimmermann was brought on as Chief Regulatory Officer or the Head of Regulatory. She was previously at Ipsen. Excuse me, forgetting the name for a second. Ipsen as the Head of Regulatory and got a PPAR approved through the FDA. The two of them have incredibly relevant experience. I came on shortly afterwards, my background is as a public company CEO in commercializing assets. I've taken a number of assets from phase III into commercial, we've brought in some commercial expertise with Nazira Amra. We've entirely rebooted the G&A side of the house with a new CFO, new head of legal, and a new head of HR, all of which have significant experience scaling organizations from phase III to commercial. We've wrapped this wonderful product in a very mature team, and along the way, done a number of financings to strengthen the balance sheet, push out some the debt maturity, among other balance sheet and capital structure cleanup. We just announced one yesterday, which I'm not going to go into today. Just suffice to say, we have very good cash runway, and strong management at this point. lanifibranor is expected. We're going to read out in Q4 the top-line data of our phase III. We do anticipate filing with the FDA in the first half of 2027, and then launching this product in the first half of 2028. As those of you familiar with the MASH market know, this is a market that is very underdiagnosed, and also growing extremely rapidly. Currently, let me start by saying this disease is staged by F1, F2, F3, F4. You know F4 is cirrhosis, in other words. The target population that we're going after is the stages of F2 and F3. That's the same patients that Madrigal targets with Rezdiffra. Currently in the U.S., there's about 375,000 patients that have F2 or F3 MASH and are under the treatment of a physician, usually a GI or hepatologist, although occasionally an endocrinologist as well. This market is growing incredibly rapidly. It is growing well over 10% per year. By the time we launch, we anticipate these numbers will be much, much higher. Now, in that market, when you're a second entry into a market, we'll be the second oral coming into the MASH market. Our anticipation is that for those F2 and F3 patients, almost all of them will have tried, be on, or soon try a GLP-1. FGF21s will also be coming to the market relatively soon. We anticipate that those will stay in the F4 space. Really, this will be a competition between Rezdiffra and lanifibranor for F2 and F3 patients adding an oral on top of a GLP-1. There are certain places where we think we have a very, very natural fit. When I go through the clinical profile more, I'll talk about more on why, but the patient population where we think we will be chosen almost every single time is that F3 patient with type 2 diabetes. Why? If a physician is looking at an F3 patient, they know that patient has risk of moving to cirrhosis. We have shown a fibrosis in our phase II/b. We showed fibrosis reduction of 18%, that was at six months, versus Rezdiffra at 12% at 12 months. Stronger fibrosis control, you need the fibrosis control in order to stop that patient moving into F4. The driver of this disease is diabetes. If you have diabetes, you progress faster because an unhealthy metabolism leads to an unhealthy liver. PPARs have been known as diabetes drugs in the past. We have HbA1c control, we can actually address the diabetes as well. In that segment, we think we win every single time. By extension, we think we do very well in the F2 segment and diabetes because of the diabetes control and in the F3 non-diabetes segment due to the fibrosis control. Where Rezdiffra likely retains a foothold is in that F2 non-diabetic patient population, where there's not the driver of diabetes, and there's not the same risk of that patient going to F4 overnight. However, if we do better than that 18% in our phase III trial, we think that segment is up for grabs as well. Let me actually move to more the clinical side and give actually a little bit of a history lesson here on the development of this therapy, because this was a rationally designed molecule from the very beginning. This is not an accidental discovery. There, the Fournier was the French pharmaceutical company that developed TRICOR fenofibrate, which was a PPAR as well, but for lowering triglycerides. That same team set out to design a new PPAR, a pan-PPAR, that really reduced the liabilities of past PPARs. There's PPAR alphas, gammas, deltas, and actually had a pan-PPAR effect. They had two observations. Number one, that if you bind too tightly, if you bind at the nanomolar level, it leads to toxicity, especially on PPAR gamma. You want to actually bind at the micromolar level. As one of the biologists said, you want to tickle the receptors, not bind them tightly. Second thing is you want balanced activity across all three because they're networked. If you hit one more than others, it can actually lead to side effects. They designed a PPAR that was a non-TZD, so not like Actos and Avandia, which were TZDs. A non-TZD binding at a different part of the pocket, was balanced across the isoforms, and bound at the micromolar level. That was lanifibranor. The hypothesis was that you would get rid of some of the side effects, especially of the alphas and the deltas and the gammas as well. They went into animal models, mice, for two years, then non-human primates for 12 months, and showed an absence of the class-defining toxicities of alpha and delta, the cardiac toxicity, the renal toxicity, skeletal muscle toxicity, and some of the bladder cancer findings that were in some of the PPARs as well. I swear I did not know about the Abivax cancer stuff from yesterday when I put up that. This is a new slide, the no carcinogenic findings. It has nothing to do with that. It has to do with the bladder cancer from that rosiglitazone. This was a very clean tox profile pre-clinically. The company said, "Okay, let's go and take a look at this clinically." What they expected to see for MASH, when you went into MASH, was that you would both impact the liver and the whole body. On the liver, these three isoforms acted differently on different symptoms of MASH. You would be able to reduce steatosis, inflammation, fibrosis, and actually improve some of the vasculature health. The whole body, you'd be able to reduce HbA1c, fasting glucose, actually increase HDL, and lower triglycerides. They ran a phase II/b milestone, our phase II/b trial. This was a trial of 247 patients, three arms, an 800 mg dose of lanifibranor, and a 1,200 mg dose of lanifibranor once daily. They ran it for 24 weeks. It was a biopsy trial, so biopsy the patients at the very beginning and at the very end. This included F1, F2, and F3 patients and showed that yes, indeed, there was a very good effect clinically on MASH. There was an 18% effect size overall in the improvement of fibrosis with no worsening of MASH, and a 24% effect size on the dual endpoint, which will be our primary in the phase III, on fibrosis improvement and MASH resolution. Really strong clinical results in the phase IIb. This was supported also by the biomarkers. Not only histological findings, but biomarker findings as well. Those biomarkers applied both intrahepatically, you saw a reduction in steatosis markers, a reduction in steatohepatitis markers, a reduction in fibrosis markers, but also extrahepatic benefits as expected. Lowered fasting insulin, lowering HbA1c, some good cardiovascular markers, too. I'll just point out, there's been quite a bit of hype around adiponectin as well, this is some of the strongest reductions in adiponectin seen in clinical trials. With that, the company decided to move into a phase III. As we designed that phase III, there's some slight differences in that phase III than phase II. One of them is that there's no F1 patients. It's F2 and F3 only. As we were designing the phase III clinical trial, I say we, I wasn't there at the time, but the company was designing the phase III clinical trial. They chose an endpoint that was a resolution of MASH and improvement in fibrosis, because the placebo rate in that group is much lower. It's a much lower placebo rate. In the phase II, we saw a 24% effect size across F1, F2, and F3. If you actually remove the F1 patients, you see that that effect size actually remains pretty close to the same, gets a little bit better, as a matter of fact. In fact, if you look at just the diabetes patients, that effect size is, again, extremely strong. We went into a phase III trial that went out to measure the resolution of MASH and fibrosis improvement of at least 1 stage. That's the left-hand side where it's showing the 24%. Our phase II data compared very well with other agents. I'm not going to go through this eye chart. It'll be on our website. It's one of my favorite things, to compare all the trials together. Just suffice to say, if you look at that middle column there, that is fibrosis improvement by one stage with no worsening of MASH. It's the endpoint that a lot of people have used. It's an endpoint doctors think about. That's the 18% effect size that I was talking about with lanifibranor. It's what we think if we duplicate that in the phase III, that we have an extremely successful drug. The safety profile in the phase II as well was consistent with what we would have expected from a PPAR gamma. What you don't see in this side effect table is the PPAR alpha and delta side effects. It's really a moderated PPAR gamma. The hallmark of the gammas is some weight gain due to fluid retention. About 50% of patients didn't gain weight, about 30% had a weight gain of 5% or more. The weight gain was not associated with any difference in efficacy. It was not correlated with efficacy at all. It did coincide with broad metabolic improvement. We looked at adiponectin lipids, liver enzymes, histology. The drug worked equally as well in patients that gained weight versus not. The phase III trial was a trial of, we've enrolled 1,000 patients. It is an 18-month trial, biopsy trial again, biopsy at the beginning, biopsy at the end. Again, two doses, 800 mg, 1,200 mg, oral once daily. There's an exploratory cohort, so patients that screen fail with F1 or F4 are put into an exploratory cohort of about 400 patients. The primary endpoint is these patients having both MASH resolution and one-stage fibrosis improvement. I will note that in the phase II, there was no GLP-1s because GLP-1s weren't around at the time. The GLP-1s were around for the phase III, patients under a stable dose of a GLP-1 for at least three months were allowed into the trial. The population in this phase III trial is remarkably consistent with the phase IIb. I'll point out a few differences. First of all, type 2 diabetes. We enrolled more in the U.S. than in the phase III than we did in the phase II, there was more of a diabetic patient population. As I pointed out before, there's really no difference in outcomes from our phase II, whether the patients were diabetic or not. We don't think that will make much of a difference. Diabetes actually tracks with stage of disease. If you have diabetes, you tend to be more severe, and that's why you see the F3s being a little bit higher in the phase III than the phase II. I pointed out that there was more GLP-1s. 14% of the patients actually entered the trial on a stable dose of GLP-1. There was more SGLT2. There was 10% of the patients entered on SGLT2 into the phase III versus close to zero in the phase II. We are anticipating that readout in Q4. One of the things that we will also do in Q4 is start to investigate lanifibranor in an outcomes trial. We will be receiving, if approved, it will be under a conditional approval due to the fibrosis biomarker, so we will have to do an outcomes trial. We thought a lot about how to design that trial to make sure that we can generate outcomes. When you're doing an F4 study, you want to make sure the patients are sick enough that they can actually have outcomes, but not so sick that you can't treat them. Those two things come together nicely with patients who have portal hypertension. Patients with portal hypertension tend to move to outcomes more quickly because they have a stiffening vasculature in the liver. The blood starts to back up, and that's when you can get these varices in the esophagus and bleeds. We have pre-clinical data that shows that lanifibranor actually has the potential to address that portal hypertension. We are planning to study lanifibranor in this population. We will start that trial before we file the NDA for lanifibranor. The next steps here, Q4 is the big quarter. We will expect top-line results then. We're planning to start that confirmatory trial in the first half of 2027, and also then file in the first half of 2027 as well, with a potential launch in 2028. We have a cash runway now all the way through to Q1 2028, when we include both the debt financing that we just did and the third tranche of financing from the October 2024 financing as well. We have a very healthy cash balance, healthy runway, and now a strong management team wrapped around this product. We're looking forward to getting the company ready to transition from the clinical stage into the commercial stage in 2028. Looking forward to bringing you guys all updates, hopefully very shortly. Thank you