Okay, thanks Antonio. If you didn't hear that, my name is Andrew Booth. I'm the CFO at AbCellera. Happy to spend a half an hour here and walk you through AbCellera and the company. Just the standard legal disclaimer. I loved Ken's comment earlier today. I'm planning on making forward-looking statements, so you should check our SEC submissions for a full set of risks. Okay, I'll give a brief recap of the company and how we got to where we are here. The company was originally spun out of Carl Hansen's lab at UBC. Carl is our Founding CEO. For the first eight or so years of the company's existence, we were really focused on rebuilding the front end of drug discovery, focused on therapeutic antibodies using latest technology. We took that investment and those capabilities to market in a partnership model where we would work with big pharma partners and some small and medium-cap biotech companies on the targets of their choice and come up with these therapeutic antibody candidates. We would maintain a position in those molecules through downstream participation, really through milestones and royalties. That was very successful for us for about eight years or so, and very capital efficient. We managed to not raise very much money at all, keep the cap table quite tight, and mostly, we got to work on the toughest problems that were out there in the industry. The Regenerons, the Lillys of the world, they don't bring you the easy stuff that they can do themselves. They bring you the very, very hard stuff where we have a technical angle on why we might be able to crack those problems. It was through that work that we really honed our ability to invest and to build best-in-world antibody discovery capabilities. Around 2020, we did our first significant private raise, and also we're the discovery engine behind Eli Lilly's antibodies against COVID. Those antibodies went into about 2.5 million patients, estimated to save tens of thousands of lives, which is an amazing thing to be able to say. You can work your entire career in biotech and not have that kind of patient impact, so I think it's a real note of pride for everyone in the company. The business model that we used, we had a royalty on those molecules, and it filled up our balance sheet with probably about $1 billion worth of cash that really put us in an excellent position to continue to invest in the platform and the capabilities. That, coupled with the raise from our IPO and some attractive funding and financing from the Canadian government, has helped us to complete building out these best-in-world capabilities from target all the way through discovery, development, translational sciences, process development, cell line development, and now GMP manufacturing. We have our own GMP manufacturing facility where we will be manufacturing all of our therapeutic antibodies from going forward. We are working on, and with that full balance sheet and those capabilities, we've turned from doing a focused on the partnership model and doing development for others, to focusing on our own internal pipeline and doing development and advancing those molecules on our own. That said, the partnership business was very successful. We've worked on over 100 therapeutic antibody programs. This has accumulated a very large position of royalty downstream participation through milestones and royalties, which is very difficult for the market to understand. I think it's very early. I think we get precisely zero value for this on the market because there's nothing in there that is in late-stage development advanced by some of our partners because it's still a very early-stage portfolio. There are 16 or 17 molecules that are in the clinic where we have downstream participation, but it's still very difficult to try and value. We have resigned ourselves to not talking about it so much because it's so difficult to understand. Although I do believe that over time, that portfolio will develop, and we'll continue to report on the progress it's made. Where we really are focused is turning that best-in-world capability to our own problems, as I mentioned, and own programs. We really focus on the difficult targets, so difficult to find therapeutic antibodies. Think ion channels and GPCRs. These are complex membrane protein targets. Very little of the protein is expressed on the surface of the cell, making it very difficult to find an antibody against. We think that's a competitive differentiation that we have. We also have multi-specific capabilities as well as, we would say, best-in-world capabilities at kind of next generation ADCs. Very importantly, we are indication agnostic. When we are looking for targets and indications that are best suited to our capabilities, we don't close the aperture even further by picking a disease area of focus. It would be too restrictive. Instead, we look where can we address a certain problem with our capabilities and play to our strengths. Now, in pursuing that, we have over 20 programs in discovery. It's always a balance of capital allocation of how much do you focus on the pipeline and how much do you focus on those lead assets. How big does that pipeline need to be to produce some steady flow of assets that are going to be moving into the clinic and keeping the capabilities of the clinical development team busy? We do that at about one-two programs a year advancing into the clinic, would probably be the right, is how we've thought about sizing that portfolio. We, of course, aren't solving for that number, it's got to be a good program that we really believe in the science, and I'll walk through how we think about that. It has led to what now are two clinical programs in the clinic, and two that are right behind it expected to go in the clinic sometime in next year or about a year from now. It's quite exciting to be able to say a year ago when I presented at Bloom Burton, we were a preclinical company. Now we are a clinical company with a significantly de-risking readout happening in Q3, and I'll start talking about that shortly. As well as next year, we could have as many as four, maybe even five molecules in the clinic. We're really well on our way, and if you missed it on the first slide, and I didn't talk about it, that is still with a very enviable liquidity position of about $700 million in available liquidity. We have the capital to keep advancing this pipeline forward. I'm going to focus for quite some time now on ABCL635. It's our lead asset, and the one that has this significant de-risking readout in the third quarter. ABCL635 is a first-in-class antibody against a GPCR target called neurokinin 3 receptor, which is implicated in hot flashes, most commonly in menopausal women. This is a very attractive target and a large unmet medical need. I'm going to walk you through, just very briefly, the framework we use to assess all targets and use ABCL635 as an example of why did we move forward with ABCL635, what was it about it that made us invest the capital to put this forward into clinical development. We look at these in a framework with really these four kind of metrics. First is, do we believe in the science? In the case of NK3R, the science has been well-validated by two small molecules that have recently received approval, one from Astellas called fezolinetant, and one for Bayer called elinzanetant. I may refer to them as fezo and eli just for going forward. These have validated that this pathway and that this works. Those are small molecules. A risk that we had with developing an antibody is can we engage that target with a large molecule and an antibody? I'll go into the science in a couple of pages and just let you know also how we think about that and what risk really remains. We also look at the commercial opportunity. This is a very large unmet medical need, where women, particularly after the Women's Health Initiative in the early 2000s, kind of removed hormone replacement therapy, which is a very good therapy from a generation of women. There are really very few alternatives. We actually see the removal of the boxed warning on hormone replacement therapy as a good thing, raising the awareness of treatments that are available for hot flashes. I'll break down the size of this market, but we believe there's about a $6 billion TAM available for non-hormonal options for the treatment of hot flashes in menopausal women. Here, our differentiation thesis comes from the fact that the two small molecules have got a safety signal, specifically requiring liver monitoring and liver toxicity, and in the case of fezo, a boxed warning. Still, fezo actually achieves $300 million in its second year of sales, even with required liver monitoring and a boxed warning. We have an opportunity to be a first-in-class antibody with a cleaner safety signal, and we would argue preferred administration with a target product profile of a once-monthly subcutaneous injection with an auto-injector. I'll talk about that as well a little bit more. Finally, do we like the clinical development path? Can we outlay not too much capital to get to dispositive clinical data? That is where we are at right now with our phase II readout scheduled for the third quarter, and I'll talk in a second about what exactly we expect to see. First of all, in this market, the market size and the unmet medical need. If you look at menopause in the United States, there are about 12 million women at any point in time suffering moderate to severe hot flashes. Hot flashes last for seven-10 years. About half of those women will seek out treatment, so about 6 million women. What's important there is, there is a contraindication for menopausal hormone therapy or hormone replacement therapy, as it's previously been known. It is an excellent treatment. It is not very expensive. It resolves not only the symptom of hot flashes, but there are other health benefits to taking hormone replacement therapy, and it is a great first line for women suffering from these symptoms. The fact is that there are about 12% of women who are contraindicated, either because of risks of history of cancer, cardiovascular disease, or family history of cancer, cardiovascular disease, or start HRT and cannot tolerate it and have to discontinue taking hormones after about six months. The combined total of those two kind of hard and soft contraindications or tolerability is about 20% of the market. On the 6 million who are suffering moderate to severe hot flashes and seek treatment, that's 1.2 million women in the United States. The small molecules have priced at a $5,000 kind of net price annually, and so that's a $6 billion TAM. As I mentioned, in their second year, Astellas, going after that, validating that there is a market, even with liver monitoring requirement and the toxicity, the boxed warning, they are going to do $300 million in their second year, and they are calling for over $1 billion-$1.7 billion in peak sales. That is in the face of competition from Bayer, who just last year received their approval for their small molecule, which also requires liver monitoring and has a warning for somnolence, and who are also calling a similar peak sales number. Both of those tying to the $6 billion total addressable market that I mentioned to you. Let me talk just briefly about what this mechanism is. Actually the NK3R is expressed on the KNDy neurons in the hypothalamus, and importantly, it's in the infundibular nucleus. Why that's important is it's near the blood-brain barrier at this fenestrated part of the blood-brain barrier. The role of these KNDy neurons is to sense hormone levels in the blood. They have access to the systemic circulation, which made us feel good about the ability to hit them with an antibody. A big risk we had was, can we actually engage this target? Nobody has ever engaged this part of the brain before with an antibody. It is a GPCR target, as I mentioned, and that is something we tried to de-risk in our phase I, which I'll get to. The signaling here is that in a normal reproductive state, these KNDy neurons and the firing of these KNDy neurons are sort of regulated with a balance of estrogen that is in the system. As women start going through menopause and estrogen is depleted, this signaling goes out of whack. It is part of a feedback loop producing these hormones, and mediating GnRH in the hormone system in the absence of estrogen, these neurons basically are over-firing, and they cast projections inside the blood-brain barrier to the preoptic nucleus, where the thermal regulatory center is within the brain, this imbalance causes these hot flashes. Essentially, our solution to this is ABCL 635, which is an antibody antagonist, so suppressing that signal in order to keep this balance in check, and therefore a subsequent reduction in hot flashes. That is the science behind this, and it has been quite well-validated by the two small molecules that are out there. As I've mentioned these before, fezo and eli, when they were approved, they are both daily oral treatments, and they both have these side effects and safety signals, which we are not expecting to have as a monoclonal antibody, a fully humanized monoclonal antibody or human monoclonal antibody. What is our target product profile is really to provide another option for the treatment of moderate to severe hot flashes, with reduced toxicity and side effects without the somnolence. Elinzanetant is actually a dual-acting NK1R and NK3R molecule, and the NK1R actually causes somnolence, sleepiness, or drowsiness. We're not expecting to have either the liver toxicity or the somnolence in a monoclonal antibody, and we're also expecting to have differentiation from dosing flexibility. When we surveyed a number of women with the question, "With the same efficacy and safety, would you prefer a monthly injection, self-administered with an autoinjector to a daily oral?" Over half of the women preferred the monthly injectable. When you segmented that to those with experience with autoinjectors, it's over 75%, so 75%-80%. With the prevalence of GLP-1s and the autoinjectors, we expect actually that trend to continue, so that the preference would be, we think having for same efficacy and safety, there would still be a preference for a once monthly versus the daily oral. I think importantly, we do see an opportunity for differentiation on efficacy as well. Although our target product profile is the same efficacy, no safety signal, and improved administration. There's reason to believe, if you look at the clinical trials data from fezo specifically, that they left efficacy on the table because of the liver signal that they had, where we're not expected to be dose limited by a safety signal. Again, the target product profile of what you're expecting to see in the phase II data, which will be announced towards the end of Q3, is up in front. The same efficacy, although we do see that there's an opportunity for greater, but if we have the same efficacy, we have a clean safety signal, and we do hit the requirements for a single 2-mL autoinjector, we think this is a blockbuster drug, even in the face of the competition that is out there. Until recently, we had as well planned to disclose the preclinical data, the phase I data, and the phase II data all at the same time. We have been talking to a number of investors, making sure they understand what we're doing at AbCellera, make sure they understand this drug, make sure that they understand what the readout could potentially say, and it's been very frustrating to talk around our safety and biomarker data. We recently made the decision, and actually press released about it yesterday, that we will be disclosing the preclinical data and the phase I data, so safety, PK/PD at our earnings call on May 11th. That will be the first time we have disclosed this data. I think the main reason for holding our cards close to our chest is that it's a very competitive world out there, and it's one thing to say you have a great molecule, and it's another thing to show the data. That said, I'm quite certain that the result of seeing the data will be that people will say, "Well, with that data, I'm not surprised that you moved forward quickly to phase II," which of course is exactly what we did, and it is a relatively straightforward phase II to run. It is a double-blind, placebo-controlled trial in about 80 patients who are experiencing moderate to severe hot flashes. And with clinically relevant data endpoints, specifically reduction in frequency and severity, that are registrational endpoints. It'll be a very de-risking, and it's adequately powered to make sure that if we see the efficacy signal, that we have confidence in that efficacy in the data. I'm very proud to say that the phase I and phase II trials are being run exclusively in Canada, which is a first in Canada. It was part of the work that we did with the government of Canada and the government of British Columbia to advance a portfolio of products through discovery, development, and phase I clinical trials, and in the case of ABCL635, also phase II clinical trials. We're very excited and looking forward to this readout. In addition to ABCL635, we also have a data readout on ABCL575, which is very briefly, ABCL575 is an OX40 ligand, very similar to Sanofi's amlitelimab. Sanofi has had a somewhat disappointing readout with the amlitelimab recently. There's been some safety signals. Our plan with this molecule was that we really do believe in the upstream science of the OX40 ligand blockade in autoimmunity. Our thesis was that if amlitelimab's data reads out, that this will be a very attractive class, and it was our intent to partner this molecule. Our intent right now is to still complete the phase I and see if there are partnering opportunities, but a lot of that depends on amlitelimab's readout, and we'll probably wait and see. We don't at this time have any intention to advance that through phase II. I've talked about this already, in terms of what you can expect later this year. With a slight change onto this slide is that recently we've announced that we're going to release the phase I data in a few weeks' time, and then the phase II data will be released at the end of Q3. Just to round it out, we have ABCL635 in hot flashes for menopausal women. If successful, we would also move forward with additional indications in hot flashes associated with cancer treatment, specifically breast cancer and prostate cancer, with the same mechanism. Patients receiving androgen deprivation therapy also experience hot flashes. This would be effective, potentially, in those patients, providing some relief for those patients, too. We have ABCL688 in autoimmunity and ABCL386 in oncology, both in IND-enabling studies where we intend to bring them into the clinic in 2027. We have another molecule hot off the heel right behind that, with a stretch goal of also bringing that into the clinic in 2027. From a year ago being a preclinical company, sometime next year, we could have five clinical assets, including a pivotal trial, because if successful with ABCL635, we'd move it quickly into a registrational trial that would start in 2027. With that, I've left three minutes if there's any questions, and hopefully that was an adequate review. Yeah. Go ahead. Congrats on the internal clinical development. Question, two compounds both show liver tox. What's the mechanism? What's going on? Yeah, the belief there is it's related to how those molecules are getting processed in the liver. Small molecules, of course, are metabolized in the liver, and it's not believed to be an on-target effect. The NK3R does have some expression in the gastrointestinal, so there are some minor GI issues which have not been material. The toxicity is from how those molecules and their scaffolds are processed in the liver. We will release the safety data that we saw in phase I as well on the May 11th, and we feel very good about the safety signal, and of course, we're monitoring potential liver toxicity very closely. Thanks. Any other questions? Over here. There was a question. Hi. Thanks for taking my question. Given the promising safety profile that you're able to achieve in phase I, congrats by the way, have you put any thought into perhaps a head-to-head trial against a competitor for pivotal trial? Of course, we've thought about it. No, have we made any decisions regarding that? We don't want to get too far ahead of ourselves. We'll wait to see what the phase I or the phase II data says and how strong that signal may be. I didn't talk about specifically the biomarker data that we'd be looking at, but we do believe we will have very strong and sustained target engagement. The half-life of the small molecules is on the order of hours, and there's once daily dosage. You would expect some fluctuations of this mechanism throughout the day. We're not expecting that in a monoclonal antibody where the half-life is on the order of weeks. You would get this sustained targeted engagement. How does that translate into efficacy? We don't know yet. That's the data we're going to get. Depending on how strong that signal is, and it'll help influence how do we design that trial and whether we're going to do it versus placebo or whether we would do a head-to-head. Just to make sure, I just want to state the remaining risk. Like in the phase I data, we were measuring the biomarker. Actually, the biomarker happens to be testosterone, the same in males. If you inhibit this same pathway, it drives down testosterone, and you can measure that very reliably. Of course, testosterone reduction is not reduction in frequency and severity. It was significantly de-risking in terms of can we engage the target in the infundibular nucleus? We feel very strongly about that. What remains unknown is that sufficient to drive down the hot flashes. NK3R is also expressed in the preoptic nucleus, and where the small molecules presumably can get there, we are not expecting that our large molecule will get there. This, we don't think that's necessary in order to get the clinical impact we are looking for, but it still remains a risk that we're going to retire in the phase II. Depending on how that works, and there is some risk there, if it's a very, very strong signal, versus not, we'll have to think about whether it's versus placebo or a head-to-head. Any other questions? I think we're at time. Thanks, Antonia.