Joining today. My name is Dan Faga. I'm representing AnaptysBio as the CEO. The presentation I'm about to walk through contains forward-looking statements. You can find more details on our website. AnaptysBio is a company focused on producing antibodies that drive towards immune cell modulation. We target cells that are exacerbated in autoimmune diseases in a way that's fast multipliers from what you would see in normal health controls. We have three clinical stage programs. Our lead program, ResNomab, is a PD-1 depleter and agonist. We have two trials. One we just read out positive results in arthritis in a 424-patient trial. We'll spend a lot of time on that upcoming. We have a second trial that is in process in ulcerative colitis, and that reads out in the next six months the initial top-line results. Our second programs that are also in clinical development, AMV033, CD122 antagonist. This is in phase I healthy volunteers right now. We are pursuing a phase IB indication. We're going to have a lot more to say about this. We're going to have an R&D/IR event in the back half of the year. The third program that just initiated in phase IA in healthy volunteers is AMV101, which is a BDCA2 modulator. Right now, there's a competing program in SLE in phase III, as well as in CLE. We are a more potent version of that program. We just initiated the trials, and that'll move over into the phase IB portion later in the back half of the year. We have exciting three programs that are moving forward. We have a research platform that sits underneath this engine. The company has been in business for over 20 years. What's great about a company that's been around this long is we have had multiple successes. We now have royalties that are coming in now and future ones upcoming from three different drugs: Gemprali, which is a PD-1 antagonist being sold by GSK; Cobalamab, which is in phase three development, also by GSK; and Imsudolamab, which we outlicensed to a company called Vanda. They're filing a BLA on that drug in a form of psoriasis in the back half of this year. We have $383 million in cash coming into this quarter. We are able to tap future royalties for development over time. We have cash guidance through year 2027. Let's get into ResNomab and why we're so excited about the markets that we're playing in. RA and UC are two of the biggest markets that you can pursue in the autoimmune environment. There's a lot of similarities, but a couple of key differences here. RA is a $10 billion mature market. What I mean by mature is there's multiple classes of biologics that patients consistently switch through. In UC, we see that emerging: a second, third, fourth-line, branded class switch. What's different here is in UC, you have branded biologics in the first line. In RA, we see a biogenic market that's maturing. Why is this different? In UC, as a biotech company, you can run a phase three trial and launch into that second, third, fourth line and be competitive. The similarities here is what's intriguing and why we're developing both indications. They're grossly underwhelming in terms of what happens in terms of the response rates out six months to a year and beyond. One-third to one-half of patients lose response. You're losing response off of pretty low remission rates to begin with. That's the opportunity. With ResNomab, the hypothesis here is we're resetting homeostasis of disease. This is a PD-1 depleter and agonist. In these diseases, and specifically RA, which is the data that we just reported, over 80% of the T cells in the site of inflammation in the tissue, the synovium, are PD-1 expressing. This is the pathologic driving cell of this disease. We are wiping those out. They're exacerbated in a way that if we can reduce their function, you could bring the system back in a homeostatic state to look like more of a healthy control, which is about 5% of PD-1 high-expressing T cells at any given time. That's what we actually just showed happens with this drug. The results of this 424-patient trial, we have a best-in-disease profile. Profile is the key word here. It's not just JAK-like efficacy in the short term, where you have fast speed and magnitude that's comparable to a JAK in the first three months. At a six-month point, we're seeing rates upwards of 70% of patients in low disease activity and 20% in clinical remission. That's in bioexperienced patients, patients that have already progressed on things like Humira. The second component of profile is we have a safe and tolerable drug. In our trial, greater than 95% of patients continued on through the trial and did not discontinue. Less than 2% of patients discontinued due to AE. That's a lot lower than what you'd expect to see with any other biologic class. Our induction administration is monthly dosing. It's monthly dosing through the first six months. What we've seen here is a durable profile. We have a high rate of patients, very high rate of patients in low disease activity, then off of drug at least eight weeks. We are out towards month eight and nine are durable. It looks like we will have an extended dosing regimen when you get out beyond that six-month period. That looks like it is Q8 weeks. It is not because of things like half-life extension. We are actually modifying this disease. In order to have inflammation return, it is going to take a long time for the T cell activity to reamplify. We have a huge body of evidence and translational data, objective biomarker data that supports why we are seeing deep responses that are long-term in duration. As a feature of this trial, we also believe we did not see the maximum response rate. You had to achieve these high-order endpoints within three months to stand this trial out through six months where we reported the overall response rates. Patients who were seeing dramatic benefit were not able to actually finish the trial due to trial design based on the regulatory requirements. We'll show you some data in upcoming slides, but the rates that we're showing can only be better, we believe, in phase three trials. Here are our ACR20 response curves. A lot of data on the page. The salmon, blue, and green curves are our three doses. Two of them are monthly. One is every other week. What we're doing here is not trying to promote ACR20. It's a regulatory endpoint for phase three. We had deep responses on ACR20, which is really symptomatic and early clinical improvement. Patients feel better. What we're showing here in orange is Rinvoq's phase 2B control trial. The light orange line is Rinvoq placebo. It looks exactly like ours. The darker orange line is Rinvoq actual responses overlaps with us. We separate at a month, no different than Rinvoq does. We're also highlighting another fact we'll come back to here is that in phase three, you have the opportunity to run all-active head-to-head comparator trials. This is shown in the burgundy or maroon color. There's a benefit to patients when you start in a trial and you know that you are on an active drug. Here's one example of that. It's 15 percentage points better for Rinvoq in the active comparator versus when they were placebo-controlled. We didn't have that advantage in the first three months. We were placebo-controlled. When you get out beyond week 12 and you get week 14, when you're in an all-active period for us, those lines converge. We have a nice gradual slope from week 0 through to week 14 in our trial. You see us matching where Rinvoq is at 14 weeks. What this says overall is the vast majority of patients in on our drug are showing a response and staying on drug. This is the objective biomarker CRP. It's actually the same result. I'm not going to spend a lot of time on this slide, but we have a pretty dramatic and very fast impact on CRP. What's interesting here is we are at the top of the immune cascade hitting T cells. You have to go way down through to see an impact on the biomarker of CRP. The JAKs hit the cytokines. You expect something fast. IL-6 antagonist hits the cytokines, that specific cytokine, which is right upstream from CRP. We're doing just as quick from the top. This is objective. There's no bias in these results. We look jack-like. All right. I mentioned earlier in our trial, you had to hit low disease activity on the CDAI scale to continue on from three months to six months. The average patient on a scale of 0 to 76, the average patient in the trial had a mean of 38, a median of 36. You had to go from there to 10 to stay in our trial from month three to month six. Low disease activity is disease control. This is an endpoint typically looked at around six months and beyond. This was a gate for us to hit at three months. What does this mean? If you went from 38 to 10, which is the definition cutoff of low disease activity in that three months, you have to stay in the trial for another three months and six months of overall treatment. If you went from 38 to 11, you were removed from the trial. That's exceptional benefit, but you weren't able to stay in the trial. We'll come back to this point. Here we're breaking down the 318 patients that received ResNomab in the trial. The green line are responders for LDA by week 12. The dark blue line are responders by week 14. The patients in that collective set, that's about 70% of the patients that touch ResNomab, they hit that low disease activity level early at three months. Again, fast response for us. What is more impressive here is the continuity from week 12 and 14 out through week 28, the active treatment period. That is a straight flat line on the median of patients who stay in disease control. You see some dotted lines beyond that. That is now up to three months off drug. Those responses are stable. Going back to what I said earlier, that is monthly treatment for six months. It looks like we have stability off drug or durability of outcomes off drug and potentially a Q8 week dosing beyond. Also, what is interesting here is this light blue line. This is a subset of patients who did not get to stay in the trial. They did start with higher disease control. They had dramatic benefit. These are ACR70s. You would never take a patient off trial in real life. You would never take a patient off trial seeing this response in a phase three. These patients had to be removed from the trial due to the protocol constraints. They received a lot of benefit. They are not counted in our response rates moving forward because they're considered discontinuations. When you take all that into account, that dark green, the green and the dark blue line, the subset that were naive, this is shown in the blue bar here versus Rinvoq and Orencia in the first two gray bars for CDAI LDA for ACR50 and ACR70. Our data is better than JAK-like. This is comparing the JAK Rinvoq and Orencia in a phase three all-active head-to-head trial where there's inherently bias in that design inflating their response rates. You could see that pretty clearly on the next slide as well. I think this is the more commercial relevant market. The naive is great because you can compare all these drugs relatively apples to apples before they've had any treatment. Here you're seeing the same endpoint, CDAI LDA on the left, ACR50 in the middle, ACR70 on the right across our three doses in the colors, the low, mid, and high dose in salmon, blue, and green versus these gray bars, Rinvoq in dark gray, Orencia in the moderate gray, and then Orencia's phase three control trial in the third gray bars. The reason we're showing all this is we look JAK-like again versus a very high bar of phase three active comparator trials where there's bias. We're also highlighting again the difference between Orencia, which outperformed itself versus how it does in a phase three trial that's more apples to apples to us. You could see just a pretty dramatic difference because patients know they're on drug or they're not when you look at the Orencia bars. The composite overall here is attractive in a very hard-to-treat population. 29% of our patients actually had JAK experience. They're arguably harder to treat. Again, this excludes those responders who hit response at week 18 that were not allowed to stay in the trial. This excludes last observed carry-forward population. We had eight discontinuations. Seven of them were still in LDA. They were imputed as non-responders here. They've left the trial for various reasons that have nothing to do with AEs. They were all in low disease activity or remission. This is very good data. I mentioned the durable responses. There's a completers analysis. The trial is still technically ongoing in these follow-up periods. For the patients who have gotten out to week 34, 85% of them were still in low disease activity. I think even more impressive is the very small subset who were not. They are not considered flares to kind of round it out. The median CDAI was 13 for the patients who are not in low disease activity. It's three points higher. A big portion of them were under 11. They were near misses. These aren't flares. This is supporting what's at least a Q8 week profile. We have evidence of patients who are now out six months off drug who are still in remission from this treatment. Let's compare it to some of the competitors out there. Lilly had a PD-1 depleter that they discontinued back in November. They ran a phase 2B trial. That data is not published. What we know from their phase 2A trial is that this was a profile that likely was never moving forward. It was exciting at the time. It was initial proof of concept for a first-in-class agent. What you're seeing here is our data head-to-head versus theirs or side by side to theirs. Top left is our CDAI LDA for all the whole population, naive and experienced. You see a spike up through week 14 and a pretty consistent stable outcome through week 28. Again, we're at a ceiling at week 14. You can't be any higher than that. Lilly's phase 2A in the top right has the same trial design. Their peak response at week 14 is lower than our peak response at week 14. When you see them at week 24, you're starting to see a very significant loss of response. They don't have stable outcomes. At week 24, they drop from 55% to 35%. Our week 28 numbers are still higher than their week 14 peak. It's a dramatically different outcome. On the bottom, you could start to see a glimpse as to why. This is the reduction of PD-1 high expressing T cells in the periphery. We are over 90% across doses. The mid and high dose perform better than our low dose. The key point in this slide is Lilly reduces PD-1 high expressing T cells in the periphery by 60%. We reduced by more than 90%. Lilly's leaving a lot of T cells still activated, driving cytokine activity. That's why their response rates aren't as high. That's why they're losing response over time. We're not seeing that. We're seeing stable outcomes in and off drug, consistent with the durable efficacy. In the bottom left, you can see off drug, there is a gradual return upwards, but we're far from baseline. Even three months off drug, we're still better than Lilly at their peak. We have a very different drug than Eli Lilly. Some translation data that's also exciting. It's not just in the periphery. You have to be able to hit the synovium pretty hard with your antibody and show the same reductions. Like I mentioned earlier, there's huge T cell activity at the site of inflammation. What you're seeing here in our mid and high dose on the left at baseline, high level of PD-1 high T cells. When we took the biopsies at week six, so pretty fast, you're seeing a complete reduction at the high mid dose. It's greater than 90% reduction of these PD-1 high expressing T cells. There was a dose response, a 100 milligram dose while it was effective in the periphery. For various reasons, did not perform as well at week six. In placebo, you actually saw an increase. This is really good data. J&J, who had the other PD-1 depleter that is in clinical development, they actually put out some translational data a couple of weeks ago in an abstract that we presented at EULAR in a week and a half. We have a much more potent outcome than J&J. J&J is seeing a 40-50% reduction in the synovium of PD-1 high T cells. That is different than 90%. That is reminiscent to the prior slide of where we showed pretty dramatic differences from Eli Lilly. J&J either did not have enough drug or high enough dose. Their drug is not as potent or a combination of both. you cut it, Johnson & Johnson has an inferior outcome when you look at translational data similar to Eli Lilly. I think we have a much more potent asset, which is why we're driving differentiated responses. That's not just in RA. We do think this will have read-through into ulcerative colitis. Some other interesting translational data we're hitting, not obviously the T cell pathways, but we're seeing downstream impact to the B cell activation pathways on these gene expression panels. They're statistically significant for our responders, which are still at a higher multiplier with the non-responders than placebo. We're having an impact on the T cells. We're seeing the impact we were hoping to see on the B cell activation state. Furthermore, various different production pathways were showing you TNF and IL-6 that were interestingly differentiated versus placebo in terms of reductions of the cytokines. We're having the immune cell impact that we were hoping to see. The hypothesis, I think, is holding in what we're seeing with the gene panels of the reductions of cytokines that are relevant, not just in RA, but also similar diseases like colitis. Quick word on safety. This is a disease population where you have dramatic comorbidities for these patients. Most of the drugs that are standard of care have black boxes and exacerbate those comorbidities. Severe infection, MACE, malignancy. This is not uncommon. The only drug that doesn't have a black box is the only other immune cell modulator, which is Orencia. Orencia works by blocking T cell activation. It works slowly. What we do is we're depleting the T cells that are actually activated and overexpressed. The only one on here that doesn't have a black box is Orencia. Our AE profile looks a lot more similar to Orencia than anything else. We look a lot like placebo. What you're seeing on the page here are our full results through the six months. On the left is in the placebo-controlled portion. It's unremarkable. That's a positive. We look very placebo-like. Through 28 weeks, we weren't placebo-controlled. We're showing on a relative basis in adjusted patient years. The key point here is a highly tolerable drug, less than 2% dropout overall. In the second three months, month three, and month six, we had one dropout due to grade moderate headache, which was true with Tylenol. Patients are getting a response. They're staying on this drug. We have a very low rate of serious infections, lower than what you're seeing on these other drugs that are out there on the market. No malignancies. No drug-related SAEs. Couple of points on ulcerative colitis. I showed you some translational data from RA that's really exciting that we do believe reads through into what we should expect to see in colitis. We're showing on the top left on this page, similar to RA in the synovium, in ulcerative colitis and lamina propria, you have an exacerbation of PD-1 high expressing T cells. Top right is an animal model. We're seeing what we would hope to see here in terms of weight substances in mice that are seeing induced colitis. On the bottom, it's interesting. There's a correlation between the reduction of those PD-1 high expressing T cells in the periphery and clinical remission. This is literature, real patients on the bottom left. We're showing that compared to what we've done in RA on these PD-1 high expressing TPH cells. What you could see in blue in the bottom right panel, at baseline, you see an increase of what you expect in a control of those TPH cells. At week 12, you see a reduction. At week 28, you see a similar, even stronger reduction. Just by working the periphery, we do think we'll be able to drive efficacy in UC. We do think we're dosing high enough in UC. We're dosing higher than RA to get drug into the gut. We should be able to hit those PD-1 expressing T cells there, no different than we did in the synovium in RA patients, which would drive a dual effect in tissue and in the periphery. What are we looking for in the colitis readout, TPP? Similar to what we saw in RA, what these markets need, like I said out of the gate, is patients need to feel better at three months and drive towards remissions. You need a tolerable drug, and you need meaningfully differentiated endoscopic remission out through six months that's stable. Being two or three or four or five percentage points better at three months and then having the patients drop out between month six and month 12 because they lose remission is not changing the treatment landscape. We just showed in RA, we can drive deep remission and control of disease that's stable. That's what's going to be differentiated with products in the future, is to drive higher remission rates through six months and have them be stable off drug. We're looking to be IL-23-like in that first six months and then looking for differentiation in the longer term. Our trial is set up to show that. It's different than what we did in the RA trial. The GI division gave us more liberties here in what we were able to do. We have a treat-through design from three months to month six. We have three-month primary endpoints to change in MMS, just showing symptomatic improvement, improvement on the scopes relative to placebo. We need to be obviously statistically significant there. What we're looking for is peak responses at month six. In our trial, if you've hit response at month six, you could stay on through month 12. We'll be able to see longer-term safety, longer-term efficacy, sustainability of those remissions. I think uniquely for us, we had pre-designed this. We're looking at Q8 week dosing in that month six to month 12 period. We'll be able to look at extended dosing profile. We think the administration profile will be competitive. It's monthly dosing or every other week dosing out of the gate into every other month dosing in the longer term. To date, I announced a couple of days ago when we reported our phase 2B data, we're almost done with the enrollment here in this trial. It's 132 patients, two active doses versus placebo. From blinded surveillance, there's no SAEs of concern, no MACE, no malignancies, no serious infections. Mentioned earlier, ANB033, this is our exciting second program that's in clinical development. It's a CD122 antagonist. What CD122 is, it's a dynamic receptor found on CD8-positive cytotoxic T cells, Temra cells, and NK cells, resident memory T cells. It blocks IL-15 and IL-2. We're moving quickly through the phase 1A. We have subcutaneous dosing. We'll be in the phase 1B in the back half of the year. We're going to have an IR event upcoming in the back half of the year to walk through not just the mechanism of action here, but why we think we're different than the other IL-15s that are in development today, as well as the other CD122s that are in development today. We're really excited about this program, so there's more to come there. Finally, like I mentioned out of the gate, we have a strong capital position, $383 million in cash coming out of the first quarter, but substantial upside from GSK royalties. Said simply, if you take Wall Street consensus curves on what they're modeling for just Gemprali, forget Cobalamab, which is being looked at in combination with Gemprali, forget Imsudolamab. The MPV, at any modest discount rate of Wall Street consensus, is worth more than a market cap. There's a huge amount of capital we could tap into over time for future development of our portfolio. Finally, catalysts that are upcoming. We just presented the RA data. Our colitis data is going to be initially reported out of the top line. All patients through three months, a subset through six months, fourth quarter of this year. We're well on track for that. We have the IR event in 0 through 3. Strategically, we're not moving forward in RA and UC on our own altogether. These are huge markets, big, big opportunities. We're going to get through our colitis data. We have a path forward independently there. We are going to look for a global partnership to move rosnilimab forward in phase three programs in RA and UC and hopefully expand in multiple other indications. With that, if there are any other questions, I'll wrap up. Thank you very much for your time.