I am very excited to introduce this next speaker, the CEO of Jade Biosciences, Tom Frohlich. Many thanks for hosting. I did want to just take a moment actually to thank the team at Bloom Burton. This is actually one of my favorite conferences of the entire year. It really is just an amazing opportunity just to see everyone come together in the Canadian ecosystem, see what a thriving ecosystem it is, actually, and also just see lots of friends and colleagues, which is a really nice event. Thank you very much. It's appreciated. As mentioned, I'm Tom Frohlich. I'm the CEO at Jade Biosciences. It's my privilege to present a company overview on behalf of the team. We are a public company, so I will be making forward-looking statements. Please do look at our SEC filings for more details. Who are we at Jade? We are a pretty young company. We are actually officially just formed in June of 2024. We're nearing our second birthday. We're still like a little toddler, I would say. I'm very pleased by the progress that we've made in that short period of time. We're completely dedicated to developing best-in-class therapeutics for autoimmune diseases. We've managed to move so quickly because we have access to three products in our pipeline that we have access to from a company called Paragon. That's a company in Boston that's really expert in developing, discovering antibodies, and they have a particular knack for finding extremely potent, high-affinity binding molecules. They also have expertise around half-life extension technology. With that combination, we really do have this ability to have very deep blockage of the target that we're going after, but also do it for an extended interval. There's multiple benefits of that, but the two main ones are, one, with that deeper coverage throughout the entire dosing interval, we hope to maximize the clinical activity that's available to that target, so really have deep suppression for the extended period. Of course, by having this long dose interval, you do minimize burden for patients, and really have the most convenient possible treatment with the fewest injections for these antibodies. That's the theme that we really drive through across all of our three targets that we have, and really looking at biologically validated targets as well, where there is an asset that's either further ahead in the clinic or maybe even commercial, where we know this target will provide a good benefit-risk profile for patients, but where we can, through that deeper target inhibition and that prolonged dose activity, to really be able to have a differentiated molecule. Our lead program is JADE 101. It's an anti-APRIL targeting antibody, really initially in development for IgA nephropathy. This is a large area. Blocking APRIL really does seem to be the best approach because it has disease-modifying ability, where you are decreasing that pathogenic driver of disease, have large reductions in proteinuria, and really able to stabilize kidney function over time. We think with JADE 101, with its high potency and half-life extension, we do have a clear shot at becoming the best-in-class therapeutic for that disease. That agent is currently in a phase I trial currently. We are aiming to have data presented this quarter on that healthy volunteer data. It's particularly exciting for us actually, because we're very fortunate in IgA nephropathy, where it's a very biomarker-rich indication, where you can see in healthy volunteers, are you impacting the biomarkers that have a direct read-through to the clinical activity? With this molecule, we hope to have the highest level of clinical activity and also do that with the longest possible dose interval. We're aiming for no more frequently than one injection every eight weeks. We're going to report out that data this quarter. Should be an exciting time. Should be able to quite fully characterize the product to allow us to move very quickly into patients and into later-stage development. We have disclosed that we're aiming to start a phase II around the middle of this year and generate data on that in 2027 in patients. Also, that data isn't necessarily gating for us to start a pivotal trial. We do think that we will have fully characterized the product through phase I with those biomarkers to really tell us what is the dose and the dose interval that we need to take forward into patients and allow us to move very quickly into a later-stage trial. We will be looking to see how quickly we can do that as well in that first program. We do have a second program that's nearing the clinic as well, JADE 201. This is a different mechanism. This targets the BAFF receptor, which is a B-cell depleting mechanism. It really can have very broad applicability across a number of different autoimmune diseases. Think about CD20s or CD19s that can be applied to a number of different areas. Things like rituximab, anywhere with that standard of care, this could be an agent that has benefits over that with the mechanism and the long duration of action. That agent is actually going into the clinic this quarter as well. We're initially going into patients with rheumatoid arthritis, really to see what kind of a signal that we can get there in terms of safety, PK/PD, really understand those dynamics of B-cell depletion. RA is a very intriguing indication for this mechanism, but it might not actually necessarily rise to the top of our priority indications. As mentioned, it can really be used anywhere rituximab is used. Also, we're following in the footsteps, as I mentioned, our approach is to go after biologically validated targets. Novartis actually has an agent targeting BAFF-R, and they're currently in 6 different phase IIIs across different autoimmune indications. We will be able to see how those read out over the next year or so, and really be able to understand where can we differentiate from that product, have a best-in-class approach in one of those indications, or potentially go into a different indication where Novartis didn't go for strategic or pipeline prioritization reasons, to really be able to have a first-in-class approach as well. A very exciting program where we aim to have some data on that in 2027 as well. We have a third program, not disclosed, similar playbook. We're not disclosing it mainly for competitive reasons, just because we have noticed as soon as you disclose a target, lots of other people pop out. We will disclose that as we get closer to the clinic, currently on track to be in the clinic in the first half of 2027. This is all underpinned by a very strong team. In that short time that we've been around, we've actually managed to pull together a very capable development team. A lot of people I formerly worked with at Chinook Therapeutics are now part of Jade. We have the capabilities to really move products into clinic quickly, but then also get them deep into the clinic through to approval. Of course, we also went public last year, so that's why I had to have that slide with the forward-looking statements. We managed to raise a significant amount of money, so we're well-financed. We have closed last year with $336 million, and that should fund our operations across these three programs through multiple inflection points into the first half of 2028. Going to spend a little bit more time just describing JADE 101, and why we're so excited by this opportunity. First of all, IgA nephropathy is a significant commercial opportunity. It is a kidney disease that patients are typically diagnosed in their 20s and 30s and have very few other comorbidities, but have a really high lifetime risk of disease progression. We were formerly actually quoting that we think this is roughly a $10 billion-plus branded opportunity in the U.S. alone. Recent developments actually have a lot of people thinking this is potentially a much larger commercial opportunity. A lot of that is actually driven by the success from Otsuka with a drug called sibeprenlimab that was approved at the end of last year. There's two things that really have driven that larger market size. One, they were approved with a very broad indication statement. All other drugs that were previously approved for IgA nephropathy had a cutoff where you had to be above a certain proteinuria level, which is associated with severity and disease progression. Sibeprenlimab was actually approved with a very broad label that really says that any patient at high risk of progression should be treated. Much larger patient population that is applicable. Then the other thing they did is they priced sort of at the higher end of the range that people were expecting. They priced it at $30,000 per vial, and they're dosed once every four weeks. $390,000 a year in the U.S. Really opened that up to be quite a large market opportunity. Room for multiple entrants to be successful in this disease area. We believe within that large market opportunity that the selective anti-APRILs, which JADE 101 is part of that group, are going to be the dominant class. They do, as I mentioned, have the ability to take away that pathogenic driver of disease. Also they have very high reductions in proteinuria, and have shown in shorter trials to stabilize kidney function, and to do that all with a very good tolerability and safety profile. We believe that is going to become the dominant class. Within the anti-APRILs, we do believe, though, that JADE has the opportunity to have a very straight line to being the best in class. As mentioned, JADE 101 is extremely potent, has the ability to completely suppress APRIL through the entire dose interval, and to do that with a very long dose interval. We're aiming, as mentioned, no more than one injection every eight weeks, which we believe is going to be very convenient for patients. We should be able to prove all this very efficiently. As mentioned, our phase I is reading out this quarter, we will be able to characterize the dose and the dose interval, plus the relative efficacy of the drug based off that healthy volunteer data, and give us a very straight line path forward to registration. The current pathway for IgA nephropathy drugs to get registered is actually based on a surrogate biomarker, there's a very efficient pathway to the market. A very attractive indication for JADE to be working in. Very quickly, just on the market size, I did mention that these patients are typically diagnosed quite young. They have very few other comorbidities, typically diagnosed in their 20s and 30s, they have a very high lifetime risk of disease progression. The chart on the right-hand side here, you can see those patients stratified by their level of proteinuria. That's the amount of protein that's in the urine, sort of a signal of how leaky or how damaged the kidney is. By cohort trial, you can see here that patients, if they have higher levels of proteinuria over sort of a 10, 15-year period, have a very high lifetime risk of losing their kidneys. You extrapolate that out if you're diagnosed in your 20s, your lifetime risk is extraordinarily high. There's about 170,000 patients in the U.S. that have been diagnosed with IgA nephropathy, several hundred thousand in Europe, and a few million actually in Asia. It is quite a burdensome problem. The KDIGO guidelines, which I'll talk about next, really say that 60%-75% of those patients do need treatment because they do have residual proteinuria levels above a half a gram a day. That's where you can see that if you can get patients down to those very low levels of proteinuria, you actually are minimizing that risk of disease progression and kidney function loss over time. As mentioned, the KDIGO guidelines are very much pushing in the direction. These are the guidelines from the nephrologist on how to treat this indication. Two really key things to point out. One is they are really lowering the targets for proteinuria levels. The goal is to get patients as low as possible. They're saying that you have to get patients to below 0.5 grams a day, and ideally back into clinical remission, so back to below 0.3 grams a day, because that's when you're really minimizing that chance of disease progression. They're also, for the first time, saying that IgA nephropathy needs to be treated like an autoimmune disease. They're categorizing treatments into two different areas. On the one side, they're saying you need to protect local nephron loss by hemodynamic agents, so things like ACE inhibitors or SGLT2s. They're saying you should use those in patients, but you also need to treat the root cause, this pathogenic IgA that's actually causing the disease. That's where the selective anti-APRIL class or the anti-APRIL/BAFFs are going to really move to frontline foundational therapy because they are taking away that pathogenic driver of disease. That's where JADE101 is perfectly positioned. We potentially have the best-in-class agent in terms of potency and the ability to knock down APRIL, to do that for a very long dose interval, and to do that without any unnecessary immunosuppression. I did mention that the two classes of agents that have shown this dramatic decrease in pathogenic IgA are the selective anti-APRILs, or there's these dual APRIL/BAFFs. What we do know is that APRIL is actually driving all of the efficacy in this category. The APRILs or the APRIL/BAFFs. We know that from the disease biology because you can see here on the right-hand side, the pathogenesis of disease is everybody has IgA. It's your antibody that lines your mucosal system. It really prevents bacterial infection in mucosa. For some reason, patients with IgA nephropathy have this missing sugar in their hinge region of the IgA, which causes it to be noticed by the immune system, and you actually get these autoantibodies that form these complexes and deposit on the kidneys. We know that blocking APRIL actually stops plasma cells from producing this IgA and class switching to IgA-producing cells. Conversely though, with BAFF, we have seen things like rituximab used, which is blocking BAFF-type cells with no impact actually on IgA nephropathy, IgA levels, or proteinuria. Actually, even historically, selective BAFF inhibitors were tried, something called blisibimod, with no effect. We really know that APRIL is driving all of the efficacy here. This has been recently confirmed by some phase III. There are more advanced assets out there. I mentioned sibeprenlimab from Otsuka, demonstrated very positive results, a 51% reduction in proteinuria, and that's a selective anti-APRIL. Then there's two recent publications from dual APRIL/BAFFs, so atacicept and povetacicept. You can clearly see that there is no added efficacy from including BAFF. They really are around the same level of proteinuria reduction. You can probably even argue numerically they're a little bit lower than sibeprenlimab. Why do we think that we can win here? We do think the selective anti-APRILs are going to be the most used and preferred class when we come to market. We did see in their phase II, we don't think that sibeprenlimab in Otsuka is actually optimizing their dosing. You can see here a phase II where they used IV body weight-adjusted dosing. They had two, four, and eight milligrams per kilogram. You can see along the top here, they have variable levels of APRIL reduction. Then on the bottom, you can see levels of proteinuria reduction as measured by UPCR. You can see a clear dose effect where at the top dose, they were getting nearly a 63% reduction in UPCR. Then very importantly, in the middle row here, you can see at that top dose, they had nearly twice as many patients getting into that clinical remission zone, so below 0.3 grams a day, which is the recommended new target from the KDIGO guidelines. Otsuka actually switched from an IV body weight-adjusted dose in phase II into a flat sub Q in phase III. They picked a dose that's closer to their middle dose. They're leaving a little bit of efficacy on the table that we want to try to capture with JADE101. JADE101 is designed to be an ultra-high potency binding antibody with a half-life extension. What we've seen pre-clinically is it is extremely potent. In terms of potency, it's a femtomolar binder to APRIL. It's about 750-fold more potent than sibeprenlimab, about 2,000-fold more potent than zigakibart, which is another selective anti-APRIL, which really can translate into lower doses to get to the same level of inhibition. What we've seen in non-human primates is that this is associated with an extraordinarily long PK. You can see that the half-life of JADE101 is nearly four-fold of sibeprenlimab, and that translates into much larger reductions in IgA in non-human primates, and more sustained over time as well. We're currently proving this out in healthy volunteers. We're currently in a phase I that has 4 dose levels. We will be reading this out, as I mentioned, in Q2 of this year. We will be looking obviously at safety and tolerability, so that'll be extremely important, as well as looking at PK/PD to really understand what is the profile of the drug. As mentioned, we can compare this to the drugs that have gone ahead of us. You never want to be very late to market behind some key competitors that are showing good data. In this case, we can learn a lot from the data that they've shown in the past. What we can see here, it's maybe a bit of a busy slide, but we've mapped out a translational framework to look at the other agents, anti-APRILs or dual APRIL/BAFFs, and to see what level of IgA reductions they get in healthy volunteers with their dose levels. We can see how are we performing compared to that. We really truly believe that if we can get similar levels of IgA reductions in healthy volunteers with a much longer dose interval, once every 8 weeks or fewer, then we'll be in a very good position to positively differentiate from these agents. We're targeting reductions of 55%-ish of IgA in healthy volunteers for that 8-week period. That has been shown to translate those IgA reductions into proteinuria reductions, which is the ultimate approvable endpoint here in IgA nephropathy. A very exciting time for us with JADE101, where we think that we can demonstrate a lot of value over the next short period of time. I won't spend too much time on JADE201, just except to say that it is very positively differentiated from the other agents that are targeting B-cell depletion. It's really designed to try to overcome some of the limitations of other B-cell depleters, like the CD20s or CD19s. The main differentiation there is to get more complete B-cell depletion, which has always been associated with higher levels of clinical activity in autoimmune disease. What we have seen is with CD19 and CD20, when you get a rapid depletion of B cells, you get this compensatory upregulation in BAFF. We're aiming to block that signaling to have more sustained B-cell depletion over time as well. We are looking to mimic the properties of ianalumab. That is the agent that I told you about that's at Novartis, that has shown positive data across a number of different autoimmune diseases and are currently in 6 different phase III indications. We've designed JADE201 to mimic the biological properties of ianalumab, but to overcome the key limitation of a short human half-life through this half-life mutation technology. I won't go through the data, but we have shown similar B-cell depletion and blocking of BAFF signaling, and done that in non-human primates. Also shown a doubling of their half-life in PK as well, to once again have better coverage of the target through the entire dose interval, potentially get higher levels of clinical activity and less frequent dosing for patients, which would be a big benefit. We're just initiating this phase I in rheumatoid arthritis patients, as mentioned, we're picking our lead indications. This could potentially be used across any indication where rituximab is effective. We are looking at indications where Novartis is active. I mentioned they're in those 6 phase IIIs, also looking at some other areas where they haven't gone for strategic reasons. Really broad potential for this agent. Very exciting time. Obviously, we're going from a transition from a company that was just formed in June of 2024, really building the foundations through this core pipeline, bringing the core team together. We're about 70 people now, but building very quickly. We've raised enough financing to move these programs through multiple inflection points. Also just about to transition from being a preclinical company with no data to having multiple data readouts over the next period of time. Thank you very much. Appreciate you spending time listening.