Okay. Thank you very much for coming. My name is Andrew Booth. I'm the CFO at AbCellera, and my pleasure to walk you through the company and give you an update as to where we are at with our pipeline. Just a reminder, I'll be making certain forward-looking statements, and please check our SEC materials for all of the risks associated. Just as a quick recap of AbCellera is a company based in Vancouver, Canada, also with offices in Montreal, Canada, and in Sydney, Australia. Founded in 2012 out of our founder and CEO, Carl Hansen's lab from the University of British Columbia. We undertook a mission to focus on technology and rebuild the front end of drug discovery, really focused on therapeutic antibodies. We originally took that business plan to the market in a partnership model where we've worked on over 100 therapeutic antibody programs for our partners, accumulating a portfolio of royalties in those molecules over a period of about 10 years or so. We were also well-known for the work we did during COVID. We were the discovery engine behind Eli Lilly and Company's COVID antibodies and had a royalty on those molecules, which brought in close to $1 billion in non-dilutive funding in order to continue our investment into the platform. In addition, during that time, we've also partnered with the government of Canada, bringing in additional funds to the tune of about CAD 400 million to continue the build-out of our infrastructure and capabilities, as well as advance a portfolio of programs in our own pipeline through all the preclinical work and even into phase I. That recently has been the real focus of the company. Since 2023, we positioned away from the partnership model and more to a focus on our own proprietary pipeline, where we have two molecules in the clinic and another two in IND-enabling activities that are expected to move to the clinic in the near future, and I'll talk about those later in the pitch. Importantly, we are here still in a very strong liquidity position with about CAD 655 million in total liquidity that we are using to advance our pipeline, and that is sufficient liquidity to take us through at least the next three years of pipeline and investments, and also continuing the portfolio of early discovery programs, which will be the source of our own proprietary clinical programs. As I mentioned, for about 10 years or so, we worked in partnership with many different companies, really validating the discovery capabilities that we have. This was a very capital-efficient model for us to build up the capabilities within the company, and as I mentioned off the top, we have a portfolio of royalties. Looking back, perhaps the most valuable contribution to the company that this partnership model brought was working on the toughest of problems brought to us by some of the industry's best. That allowed us to focus and build our capabilities and really focus on somewhere where we believe we have a competitive advantage in discovering antibodies for difficult targets. We would call these our complex membrane protein targets, specifically ion channel and GPCR targets, working on novel modalities, including these multispecifics and what we would call next generation ADCs. Importantly, as we try to discover or try to determine where do we point this capability, we look at indications across different therapeutic areas. As we say, if we're already focusing on these difficult targets, the ion channels and GPCRs, or areas where our competitive advantage would give us a unique ability to find therapeutic antibodies, it doesn't make sense to further close the aperture on a specific therapeutic area. At the moment, especially in the preclinical work and in the early clinical work, we are indication agnostic. Looking at where our current pipeline sits at the moment, we have our lead molecule, which is ABCL635. It is an antibody antagonist against the NK3R, a neurokinin 3 receptor. It is a relevant target in the indication of hot flashes really associated with menopause, and we'll be talking a lot more about that program as I progress through the pitch here. We have a second molecule, which is ABCL575. It is against OX40 ligand. This originally was a molecule that we worked on in partnership with EQRx. EQRx had some challenges to their business model and eventually were bought by Revolution Medicines, and this molecule reverted to us. We have taken it through phase I, and initially, this was a fast follower molecule to Sanofi's amlitelimab, which they purchased off of Chimerix through the acquisition of Chimerix. The bet here was that if successful, this would be a very important pathway, and we looked to partner this if Sanofi had been successful. It's fair to say that the OX40 class of drugs has had a few headwinds in the past year. I think amlitelimab's readout in phase III did not really reproduce the phase II results that they had, and there were some safety signals both from amlitelimab and also rocatinlimab, OX40, that was advanced by Amgen. Our intention here is really to take this through to the end of phase I and then not allocate any more capital on it. We do believe it will be as advertised in terms of a long half-life, suitable for every six-month dosing. We will wait to see if there's any partnering opportunities, but we'll not be continuing that on our own steam. Behind that, we have two molecules, ABCL688, ABCL386. 688 is in autoimmunity and 386 is oncology. We haven't given very many other details about either of those programs. Because it's a competitive world out there, we would rather keep our cards close to our chest as we advance that in preclinical work until we get to the clinic. They are both on track to be in the clinic in 2027. I'll focus a lot of the program today on the NK3R asset. ABCL635 is a first-in-class antibody for the treatment of VMS, also known as hot flashes. It is, as I mentioned earlier, an antibody antagonist against neurokinin 3 receptor. It has come from our GPCR and ion channel work that we've done over the years, I'll get into a little bit of the market and of the biology there. This is potentially a very large market. When we look at menopause and specifically hot flashes associated with menopause, approximately 12 million women, by our estimates in the United States, suffer moderate to severe hot flashes at any moment in time. Approximately 50% of those, or 6 million, seek treatment. Where we are really targeted is on those where hormone replacement therapy is not appropriate. Either they are contraindicated, hard or soft contraindicated, or cannot tolerate hormone replacement therapy. By our estimates, that is about 20% of the population. Just multiplying that through 20% of 6 million women is approximately 1.2 million women. There are two small molecules, one by Astellas and another by Bayer, that have recently received approval. Astellas has, in their second year of sales, had quite a successful launch, we would say, with $300 million being sold in their second year despite some of the drawbacks. The Bayer molecule just recently received approval in late 2025. Both of those molecules are priced at roughly about $5,000 in annual cost for the treatment. Just looking at the 1.2 million women and about $5,000 of net cost, that for us indicates about a $6 billion total addressable market for this class of drugs, really only for those where hormone replacement therapy is not an option. Our thesis here is that women who find themselves in that category will be looking for non-hormonal options for treating one of the largest symptoms associated with menopause, of course, being hot flashes. Just going into a little bit of biology here. What we see is that the pathway that we are looking at here is the NK3R, a neurokinin 3 receptor that are on KNDy neurons in the hypothalamus. A thesis we had early is that the role of these KNDy neurons is to detect hormone levels in the blood. We believe that despite being in the hypothalamus, they're in this part of the hypothalamus called the infundibular nucleus, which has got a fenestrated blood-brain barrier. Because of their role in detecting hormone levels in the blood, we believe that they have access to the systemic circulation and therefore could be targeted by an antibody. The role of Neurokinin 3 here, as I mentioned, is it gets regulated by the presence of estrogen, and then in the absence of estrogen, drives the GnRH pathway through to the production of estrogen to kind of balance this. In the state of menopause, where estrogen has dropped, these NK3R neurons are overstimulated and therefore are driving sort of a feedback loop to produce estrogen. Of course, going through menopause, there is not the production of estrogen, and this feedback loop then causes projections into the preoptic area of the hypothalamus, which then gives signals to the thermoregulatory center within the brain that causes this pulsation of hot flashes. The mechanism that we are looking to engage here with our ABCL-635 is to block that signal to the NK3R pathway, therefore suppressing this kind of pulsating projections that are going and ultimately reducing the hot flashes. This is a well-proven biology, really the leaders here are both Astellas with fezolinetant that is marketed under the brand name of VEOZAH, and Bayer, who has elinzanetant, marketed under the brand name of Lynkuet. These are two small molecules, as I mentioned, that have received approval in the recent past. Fezolinetant, approved in 2023, does have some drawbacks, and specifically, there is required liver monitoring because of a liver signal, and in fact, it has also received a boxed warning since its launch. Despite that, as I mentioned, it has achieved $300 million in its second year of sales. Elinzanetant by Bayer, recently approved just in the fall of last year. They do have required liver monitoring, although not a boxed warning as fezolinetant does. They also have an additional warning associated with somnolence, and that is because this molecule is both an NK1R and NK3R antagonist. It was originally developed for NK1R, which is known to cause some issues with sleep. We are, with ABCL635, just a pure NK3R antagonist, and therefore, we don't expect to have those same side effects. Recently, just on the May 11th earnings call that we had, we disclosed the results of our phase I study, including the trial design of both a SAD portion and a MAD portion. You'll see the trial design here on the page, and I won't go over it in detail, but these slides are available off of our website. We did see a very favorable tolerability profile. You see here some of the events that were seen in the variety of cohorts for the SAD, and you see also the placebo effects here. We think overall this is a very clean safety profile that we then quickly had moved into and I'll show you some of the biomarker and PK/PD data in a couple of slides. We moved this forward quickly into the phase II. There were a couple of adverse events that we note here, specifically on the headache that was seen in the 900 mg cohort. We do make some elaboration on this because these cohorts were dosed together and kept together in a room, were in a kind of a dormitory-style room with all of the participants together. They were not allowed to enjoy sort of your regular daily pleasures such as coffee, which we also assume also led to some of the headache, particularly in that one cohort. Notably, you'll see there were none of those effects in the 600 mg, although we don't expect that the headache was due to the administration of the dose, but rather to those who were deprived of coffee for a couple of days. Overall, we felt very comfortable with the safety profile, and we looked to the liver signal included in the safety profile. As I mentioned, fezolinetant did have a liver signal here. If we look here at the variety of metrics that we use to detect if we would have any liver signal, you see we're well within or well below the upper range of normal in each of the measurements we had here, confirming our belief that an antibody being not metabolized in the liver would have a clean safety profile for use in this indication. We also looked at what the PK profile is here. Our target product profile is to have a once-monthly subcutaneous injection, and we saw that the PK profile closely matched what our modeling was that supported this administration, and we feel very comfortable with a half-life of about 25 days to support the monthly profile that we were targeting. On the left of this slide, you do notice the similar diagram as I talked about before. Importantly, this mechanism driving the GnRH pathway gave us a nice biomarker that was used by Astellas in the clinical development of fezolinetant, and that is testosterone in healthy males. What we see is that this same pathway, the GnRH pathway, that is the feedback loop for driving estrogen, also in males, drives testosterone. It was believed, and actually fezolinetant provided this nice biomarker and the data which you see on the right, that if you suppress NK3R, that in males, it will also suppress testosterone. Because there is a nice steady level of testosterone in males, you could use this in order to be a measure of target engagement. A risk of entering the phase I for ABCL635 was, can we indeed hit this part of the brain with an antibody? We were able to significantly de-risk that using this biomarker. On the right, you see the fezolinetant data. You see that on the timeframe of one day, they do get the target engagement and a dose-dependent target engagement. The orange line that you see there is close to their clinical dose of 45 mg a day. This is 46 mg that they used in this study. The doses that give deeper target engagement of 90 mg and 180 mg are also labeled on that chart, and we see that there is this dose dependence on target engagement, which is what we were hoping to replicate with our antibody in the phase I trial. Here what you see are the results of that biomarker validating that we, indeed, with ABCL635, do engage the target. What you see on the dark blue line at the bottom is the 900 mg dose. The blue line above that is the 600 mg dose. That's in bold because that's the dose that we're taking forward into our phase II. You see that in comparison to the fezolinetant data, which with their dose, they get a number of hours of coverage, of getting the suppression and engagement of the target to the tune of maybe 40% change in testosterone levels. And our target dose of 600 mg at least as a loading dose, we get stable 60% reduction in testosterone. Making us feel very good that we are do reach the target and most notable here as well, or also notable, is that on the right with the fezolinetant data, which is dosed daily, you see the change in this, with a fairly short half-life, the change in this engagement over the course of that 24-hour period. On the left, because we are intending to dose monthly, you'll see that the timescale is over the course of that month. It takes up to a week in order to get full target engagement, you see sustained target engagement over the course of those four weeks. We saw this in our phase I and felt very good about the ability to engage the target, and on the basis of this, moved quickly into the phase II. As I mentioned, we released this data just a number of weeks ago in our Q1 earnings on May 11th. We also saw the reduced stimulation in other areas, the GnRH pathway, in FSH and LH, both meeting what we would consider to be strong target engagement. Our target product profile here is to have a favorable, at least as good efficacy as the small molecules, a clean safety signal, and preferred dosing of this once-monthly subcutaneous dosing. We are now moving forward into the phase II. Oh, sorry, I thought I had some more information on the phase II there. We're moving forward into the phase II, which is a double-blind, placebo-controlled trial with 80 patients, with 40 patients in the placebo arm and 40 patients in the treatment arm, with four week endpoint and 12 week follow-up. What we are testing here is the frequency and severity of hot flashes reported on the four week timeframe, and importantly, we saw this data in the phase I of target engagement as very de-risking in terms of can we engage the target in the infundibular nucleus. Unfortunately, testosterone is only a measure of target engagement and not a biomarker of hot flashes. The risk that remains is if it is necessary also to suppress NK3R because it is expressed in the preoptic nucleus, which is behind the blood-brain barrier. The current hypothesis is that it is sufficient to engage and suppress NK3R in the infundibular nucleus, which we have shown in our phase I is we can do. If that is indeed the sufficient biology, then we feel very, very good about reading out positively in our phase II. There does remain the open question as to whether it is necessary to also engage the NK3R inside the preoptic nucleus, and that, of course, is the study that we're doing with our phase II. We're moving forward with a 600 mg dose with a target product profile of a 300 mg maintenance dose. Because of the half-life of the molecule, we expect that 600 mg does emulate what the steady state engagement would be of the target at a 300 mg monthly dose. Because of our formulation at 150 mg/mL in a 2 mL standard auto-injector, we would expect to be able to deliver that 300 mg in a single monthly subcutaneous dose. We feel very good about where we stand, and we have a highly de-risking phase II readout coming up in the not-too-distant future. We have indicated that this is going to be in Q3, so within the next few months, we will get this data, and of course, we'll be excited to share it once we have it. Just looking forward at this pipeline and what we're expecting to see here in 2026, then looking forward into 2027, we of course do have this phase I, II of ABCL635, and if positive, we would continue into a phase III study and pivotal trial in 2027. In addition, we would advance ABCL635 for the treatment of VMS in indications of oncology, specifically in breast cancer for any women on tamoxifen. Where you have a medically induced menopause, those patients do suffer from VMS associated with that medically induced menopause and are looking for, of course, non-hormonal treatments in order to deal with some of the symptoms and get symptom relief. In addition, that same pathway, it leads to VMS in those receiving prostate cancer treatment, where one of the most uncomfortable side effects of that treatment is also in hot flashes. We would be moving forward a couple of phase II studies, specifically in VMS, relating to those oncology treatments. As I mentioned off the top, we'll continue our read-out of 575, and we would expect that also in 2026. We will continue the IND-enabling activities of 688 and 386 with the intention to file those INDs and start clinical trials in 2027. We have indicated as well that we would move our next at least one candidate into IND-enabling activities in 2026, with a stretch goal of also bringing that molecule into the clinic in 2027. Importantly, we have a pipeline or funnel of discovery programs behind that that are in some form of discovery and preclinical development with the goal, as we have said for a couple of years, to bring one to two molecules per year into IND-enabling activities and then subsequently into the clinic. The goal there is to continue this cadence of one or two molecules into the clinic over the coming years. As I mentioned off the top, we do have sufficient capital to continue on that trajectory for the foreseeable future and certainly for the next three years of execution on this plan. With that, I have a few minutes left here if there happen to be any questions. What would you be looking for in a phase II to justify? Astellas and Bayer actually have blazed the trail for us here, and what we're looking for is a statistically significant and clinically meaningful reduction in the frequency and severity of hot flashes at the four-week endpoint. Specifically, in terms of the frequency, what we'd be looking for is a reduction of at least two moderate to severe hot flashes per day, and that would be on the order of what the clinical efficacy has been of the approved small molecules. That is off of a baseline where we've been screening really moderate to severe hot flashes with, let's say, similar to VEOZAH and Lynkuet, of about 50 hot flashes a week, so on the order of seven or eight per day. It would be a reduction of about that 20% of those hot flashes, or two per day would be equivalent efficacy of the small molecules. Of course, continuing with the clean safety profile, and we would expect to see additional data. Although the phase I data seems quite reasonable to believe that we will hit our target product profile of a once-monthly subcutaneous injection. We do have reason to believe that VEOZAH left some efficacy on the table because they were dose-limited by toxicity. You can see that from their phase II study. We will see if, given the mechanism of action here and the clean safety profile of an antibody, if we can access some of that efficacy that was left on the table. Really, we think that with equivalent efficacy, the safety profile, and the once-monthly injection, that this is a potential blockbuster drug. Any other questions? Okay. Well, thank you for your time.