Thank you. Great. Thank you, Andrew. Great. Thank you, Andrew. Thank you, Ananda. Thank you, H.C. Wainw right, for letting us present today. We are very excited to share a bit about our pipeline, our upcoming milestones, and what we have been working on. Maybe to start, shown here, Maggie, a person living with post-bariatric hypoglycemia. She is also on our patient council, and we really thank her for all of her work in educating us and making sure we are doing everything we can to serve people with PBH. Before I start, we will be making forward-looking statements. For more information on that, I would refer you to this disclaimer, as well as look on our investor relations website for more. At AMYLYX, we have three assets in four ongoing clinical trials. Our lead asset is avexitide. Avexitide is a first-in-class GLP-1 receptor antagonist. It has FDA breakthrough therapy designation, as well as orphan drug designation. We have an ongoing pivotal study in post-bariatric hypoglycemia, which I'll talk about in a little bit. We are targeting completion of recruitment of that study at the end of this year with top-line results in the first half of next year, which, with a positive study, would mean commercialization in 2027. We also have AMX0035, our combination small molecule in two diseases targeting stress and mitochondrial dysfunction. The first is Wolfram syndrome. We just announced last week more positive results from our first trial in people with Wolfram syndrome. Josh will share a little more on that, but we're very excited about the prospects there. We are also testing AMX0035 in progressive supranuclear palsy, which is a devastating neurodegenerative disease, and we will have the readout of our phase II-B portion of the trial next quarter. Last, certainly not least, is AMX0114, which shows our antisense oligonucleotide targeting calpain 2, which is a well-known target in neurodegenerative disease, but this is the first antisense oligo targeting it, and that would be for the treatment of ALS. We have a first-in-patient study ongoing now, and we expect the first cohort data at the end of this year. So many exciting assets and milestones ahead. I'll first be focusing on our lead, which is Avexitide for the potential treatment of post-bariatric hypoglycemia. Post-bariatric hypoglycemia is a condition that affects people in the years following bariatric surgery. Not everyone develops it. It's rare. We estimate about 8% of people with bariatric surgery may develop post-bariatric hypoglycemia. What appears to happen is that the body upregulates the GLP-1 response. The body overproduces GLP-1. Blood levels can be as high as 10x normal. GLP-1 is one of the body's master regulators of insulin and therefore glucose. With this very high level of GLP-1, people experience very precipitous drops in blood glucose. When our bodies do not have enough glucose, our brains stop functioning the way that they are supposed to. The medical term is called neuroglycopenia. We are developing avexitide, which is a GLP-1 receptor antagonist. It blocks endogenous GLP-1 from interacting with the receptor, thereby raising the glucose nadir back to normal levels. I mentioned that PBH is rare. It happens, we estimate, in about 8% of people who get bariatric surgery, but there have been millions of bariatric procedures in just the last decade in the United States alone. Shown here are some of the studies that have been done looking at the population in the years following bariatric surgery who will develop this persistent and symptomatic hypoglycemia. There are very good retrospective and prospective studies. What really characterizes the disease is that they get these very persistent and symptomatic drops in glucose that cause people to have severe bouts of confusion, loss of consciousness, even seizures. As you might imagine, this is a very severe and debilitating condition. We estimate there are about 160,000 people in the United States today who have PBH. Once someone has PBH, it appears to be persistent. In fact, it can even be progressive. We expect the population to only go up. We've also done our own claims-based work looking at medical claims providers, and we get to very similar estimates as what's been shown in the literature. Orphan disease, but large orphan disease. Now, avexitide has been studied in five trials already in people with PBH, three phase I trials and two phase II trials. In each of those trials, what was really dramatically shown was a change in the post-meal glucose nadir. The glucose nadir is the lowest point of someone's glucose. That is where they're in the hypoglycemic range. What I hope you can appreciate is that in each study, very significant increases in the post-prandial glucose nadir and thereby helping with PBH. This is what helped support the FDA breakthrough therapy designation. In the two phase IIs, avexitide cut the rates of level two and level three hypoglycemic events very significantly as well, with the highest dose tested about 53% reduction in level two events and 66% reduction in level three events. Now, level two events are defined as a blood glucose less than 54 mg per dL. That is the range at which people become neuroglycopenic. They become at risk of having these very severe symptoms. Level three is that someone is so significantly incapacitated, they need independent help. They need somebody to rescue them. These are very meaningful events, and these have long been defined by the American Diabetes Association and other groups. Now, as we go into this pivotal study, we will be testing the 90 mg once-daily dose, looking at the composite of level two and level three hypoglycemic events. This is an outcome that FDA has reviewed in our protocol. It is also in FDA guidance when drugs are looking at treating hypoglycemia. Importantly, avexitide was also well tolerated. Looking at AEs, injection site reactions, it was quite similar to placebo in the phase II and phase II- B studies. We look forward to now continuing to look at that in the phase III. The goal of the phase III pivotal study is really to try to be as consistent as possible with the phase IIs. The phase IIs showed very strong reductions in level two and level three hypoglycemic events. The phase II trials, probably the key differences, the phase IIs were both 28-day studies, so four weeks. The pivotal study is a 16-week placebo-controlled trial. The key inclusion criteria are first looking at the event rate, so how many level two or level three events someone needs in order to qualify for the study. In the phase IIs, it was two events in two weeks. We are doing three events in three weeks, so same event rate. Notably as well, we are studying in people who have Roux-en-Y gastric bypass, post-bariatric hypoglycemia. While we do not believe that there is a difference in surgery leading to PBH, we believe PBH is PBH. We have the most data in people who had Roux-en-Y gastric bypass and then PBH. That is what we're studying in the trial. As I mentioned, the study is up and running. We dosed our first participant in the study last month, and we're seeking to complete recruitment at the end of the year with top-line results in the first half of next year. We are very excited about the program. PBH is a significant unmet need, 160,000 people and growing. There are no FDA-approved treatments for PBH. Current standard of care is medical nutrition therapy. With a positive study next year that would support commercialization in 2027, and our patents go out through base case 2037, and that is before patent term extension. We are very excited about avexitide as our lead asset. As I mentioned, we have three other ongoing clinical studies. For more on that, I will pass to Josh. Thanks, Justin. Sorry. I'll talk through some of our additional assets that are advancing through the clinic as well. I'm going to start with AMX0035. This is a fixed-dose combination of sodium phenylbutyrate and taurursodiol. We designed this combination therapy based on the idea of mitigating endoplasmic reticulum stress and mitochondrial dysfunction, which have been implicated in a number of diseases. I'll start by talking about Wolfram syndrome. We started working on Wolfram syndrome about eight years ago when a physician contacted us, raising the point that Wolfram syndrome is often considered a prototypical disease of stress. He was quite interested in studying our compounds in it, given the link of the disease to stress. What is Wolfram syndrome? It's a progressive neurodegenerative and endocrine disease. It starts by looking like type 1 diabetes. Patients will present with early onset diabetes, usually in childhood. As the disease progresses, they go on to have blindness, deafness, difficulty swallowing, breathing, walking, and ultimately generally pass away in their early 30s. You can think about it primarily as starting with diabetes, having vision loss, and then a number of other neurodegenerative symptoms. We estimate that there are about 3,000 people living in the United States with the disease. That is really building off of some of the genetic data and prevalence work that has been done in the disease. It is a monogenic disease. It is caused by mutations in the WFS1 gene, which, as I said, is thought to be critical in how the cell resolves endoplasmic reticulum stress. AMX0035 is a combination of sodium phenylbutyrate and taurursodiol. Both of the compounds have been extensively studied in the literature and also by us, showing clear ability to mitigate stress. We also, over those eight years that we've been working in Wolfram, studied quite a number of cell models, including patient-derived cells from people living with Wolfram syndrome, as well as a mouse model of Wolfram syndrome, where we showed highly significant resolution in some of the symptoms that are important in Wolfram syndrome, including preventing the neurons from dying in the neuronal cell models and preventing some of the glycemic and diabetic phenotypes in the mouse model and in patient-derived beta cells as well. That led us into our clinical program. We started with a clinical trial in 12 people living with Wolfram syndrome, open-label study, initial study to get a sense of the biological activity of the drug. What we would expect, given that this is a progressive disease, is for patients to show progression on diabetic outcomes, including C-peptide, hemoglobin A1c, and time in target range by continuous glucose monitoring, as well as visual outcomes, visual acuity being the main one, and also in their general symptoms, which we're assessing with a clinician global impression of change and a patient global impression of change. What we saw instead was actually stabilization or improvement across these outcomes. Probably just to highlight on all of the diabetic outcomes we're looking at, C-peptide being the primary outcome in the study, but also looking at hemoglobin A1c, time in range, we saw improvements over time. Just recently, we presented our 48-week data, and we saw continued improvement. It seemed that the improvements we were seeing at 24 weeks, in many cases, nearly doubled as we went out to 48 weeks. Here is our primary outcome, the mixed meal tolerance test. There is a QR code here to see all the other outcomes of the study. As you can see, we see kind of improvement over time in C-peptide, which is a measure of beta cell function. That moved in lockstep with the other glycemic measures that we were looking at in the study. AMX0035 has been in many, many patients. Safety profile here was consistent with everything we have seen thus far, generally some mild diarrhea, but not much else in terms of safety events. Where do we stand now? We have just released the week 48 data, which we are excited about, continues to show that sustained benefit. We're right now working with the FDA and planning out a phase III program to hopefully advance this drug to patients as quickly as we possibly can. Moving to our next program, progressive supranuclear palsy, also with AMX0035. I'll start with a little background on PSP. PSP is often considered an atypical Parkinson's. It's often seen by movement disorder specialists. What distinguishes it from Parkinson's is that patients do not respond to dopamine therapy. They'll be given dopamine therapy, they're not responding, and then they also have certain cardinal symptoms that make it clear it's PSP. For example, they have trouble looking up and down. They can look side to side, but have more trouble looking up and down. They'll often walk with a pose with abducted arms out to the side. They have particular balance difficulties. The progressiveness of it is distinct as well. Patients will often lose the ability to speak, swallow, breathe, and survival is generally pretty short at six to eight years with PSP. There is estimated to be about 23,000 people in the United States living with PSP. One thing really important to say, and partly why we were so excited to go into PSP with AMX0035, is that PSP is a tauopathy. There is incredibly strong genetic data linking certain variants in tau to the disease. You can also see by PET scan and also in postmortem brain samples, significant deposition of tau in the exact brain regions where you also see progression of the disease. I mentioned this before, but we had run a kind of investigator collaborated study with AMX0035 in Alzheimer's disease, where we saw a highly significant reduction in total tau and phosphorylated tau in the cerebrospinal fluid in a placebo-controlled study. Having got those results, we thought about where were the what might be the purest tauopathy where we might study this drug. PSP came to the top of the list. Where do we stand with that? We have completed recruitment of a phase II- B study in PSP with 139 participants. We are going to have the data from them in Q3 of this year. That will be a full unblinded analysis looking at outcomes, including the PSPRS and several secondary outcomes. We expect we will have about 80% power to detect a 30% effect on the PSPRS. This initial analysis should give us a sense if the drug is having a benefit in this disease. This will also be the go/no-go for us in this program. As a company with four, in our view, exciting programs, if the data is quite strong, it will encourage us to keep investing and keep moving forward. If the data is weaker, we'll reprioritize into our other programs. Lastly, I'll touch on our AMX0114 program. This is our antisense oligonucleotide targeting calpain 2 for the treatment of ALS. I won't spend an immense amount of time on what ALS is, but in very brief, a progressively paralytic disease where people typically pass away in about two years. Why calpain 2? It's been widely recognized in ALS that axonal degeneration is one of the key pathologies. People often describe it as dying back, this idea that neurons disconnect from the muscle and slowly die back, retract to the spinal cord and to the motor cortex for the upper motor neurons. One of the proteins most associated with axonal degeneration is calpain 2. It makes sense as a target in that sense. Additionally, it's been knocked out and it's been studied in various ALS disease models where inhibiting calpain 2 shows a benefit. One other interesting element about calpain 2, neurofilament, has come to a lot of attention as a biomarker in ALS. What's interesting, if you look at the Western blot on the right of the slide, neurofilament is a 68 kilodalton protein. You'll notice in ALS, there's not really a 68 kilodalton band. The neurofilament that we're observing in ALS is a cleaved fragment of neurofilament. One of the things that calpain is known to do is cleave neurofilament into fragments of about this size. One of the hypotheses also that has us quite interested in calpain in ALS is that it may be causing a lot of the neurofilament increase that we see in the disease. We run our calpain ASO in a number of relevant disease models. We've shown knockdown of neurofilament in neurotoxic insult models. We've seen benefit in ALS-specific models, including TDP-43 directed models. All of this has led us into our clinical trial, which is right now recruiting. We have dosed the first patient. This is a randomized placebo-controlled multiple ascending dose study. There's both an active group and a placebo group, and it is in people living with ALS. We expect to have early cohort data by the end of the year, which will include safety and tolerability, but also early signals on biomarkers and otherwise. Maybe lastly, overall for the company, we have cash through all of these milestones. We expect our cash to take us through the end of 2026. Maybe just reviewing through the various milestones. With avexitide, we're actively recruiting. We dosed our first patient last month. We expect to complete recruitment by the end of the year, have data from the phase III pivotal study in the first half of next year, which, if positive, we expect to support the filing for approval in PBH. With AMX0035, we've just reported our 48-week Wolfram data. We're now working towards finalizing the phase III design, which we expect to share before the end of this year. We are also expecting to present data from our randomized controlled trial in PSP in Q3 of this year. Lastly, with AMX0114, we're actively recruiting for the study. We expect to have early cohort data in ALS, which will include safety, also biomarkers by the end of the year. We are quite excited for everything going on in AMYLYX. We focus only on diseases of substantial unmet need, and we believe we have therapies that have the potential to serve these patients. Thank you.