... Ready to go?
Talking a lot today.
Yeah. All right. Thank you, sir.
Appreciate you. Thank you.
All right, we'll do that again. So, thanks, everyone, for joining the next Fireside here. My name is Derek Archilla. I'm with Wells Fargo. We're very excited to have AnaptysBio here. We got the CEO, Dan Faga. Dan, great to have you here.
Thank you very much. Good to see you.
All right. Well, let's get started. Maybe, you know, kind of just level set us here. You know, it's been a busy year already. Maybe just kind of, you know, give us kind of the high-level view, and then ultimately, what to expect for the remainder of the year, and we'll dig into the Q&A.
Perfect. So, good morning, afternoon, everybody, wherever we're at, at this point. You know, I agree. There's a lot happening in the company. I think defining the first half of the year was arthritis data for our lead program, rosnilimab, which is a selective and potent depleter of pathogenic T cells. We had positive three-month data in February. We had even more impressive six-month data in June, and in August, we announced the trial was completed, and we had stable off-drug data through nine months. We have a second trial that had been enrolling in the background. We've also announced it's fully enrolled, and that's in ulcerative colitis. We have initial top-line three-month data coming up in Q4 of this year. Two other drugs in clinical development. We have a CD122 antagonist.
We started phase 1a development October of last year. We're well through that. Psoriatic disease will be the initial phase 1b program. This is for ANB033. Sure we'll dive into it.
Mm-hmm.
ANB101 is a BDCA2 modulator. That's in phase 1a as well. We're well capitalized through year-end 2027, approximately just under $300 million coming into this quarter, and we have a massive, substantial royalty asset in Gemperli from GSK, which I hope we can talk a little bit about as well.
Sure. Awesome.
A lot going on, a lot coming up. Lots to talk about.
Yeah, so thanks, Dan, for that intro. So maybe to start, just in terms of, you know, the upcoming data set in ulcerative colitis, you know, what gets you really confident in terms of, you know, rosnilimab's MOA here in this specific indication? And then we can kind of go through some of the trial details, but, you know, just kind of biologically, what gets you excited?
Yeah. When we... I'll hit a little bit in arthritis first, 'cause I think it-
Sure
It sets a tone for why we're excited about colitis. In all these autoimmune diseases, you don't see disease modification too often with the types of therapies that are out in the commercial market. What we observed in arthritis, and we were able to design our colitis trial to maximize the outcomes here, what we saw in arthritis was deepening responses over time, particularly between month three and month six. So patients who hit low disease activity, we saw conversions into ACR70s and clinical remissions at six months. What I mentioned earlier is, with disease modification, translationally, we are depleting greater than 90% of the pathogenic T cells in the periphery at all of our doses. Within the synovium, we're depleting 90% of those same pathogenic T cells at the mid and the high dose.
We saw a dose response there translationally. A lot of that probably has to do with having enough drug to penetrate into the synovium, 'cause the potency was clear. It's there if we can access the target. What's happening is then off the drug, we're seeing a very slow return towards baseline. From those 90% depletion points in the blood, we are still more than 50% three months off of drug. That data we made public in June, or partial data we made public in June. But importantly here, we're seeing consistency then of the stability off drug through at least 12 weeks. Then anecdotally, we've heard reports from different KOLs of remissions, well over a year off of drug. We're getting stable responses if you can get to remission.
It's a different disease than colitis, but we're able to do in the colitis trial, unlike in the arthritis trial, two different divisions of the FDA. The colitis trial is a one-year efficacy trial. It's a six-month treat-through design. There's two active doses, a low Q4-week dose, a high Q2-week dose, and placebo. The two active doses treat through six months. Then at six months, assuming you're at a relatively low bar symptomatic response, we want patients to stay on drug if they want to. You move into a maintenance phase of Q8-week dosing. We are looking to drive to maximum clinical remissions at six months. That was the design from two and a half years ago when we hypothesized how this drug can work and what could be different in the marketplace. Now, the placebo, there is a crossover at three months.
It all stays blinded. If placebo patients are not in symptomatic response at three months, they would cross over to the high dose. So at six months, we'll have four arms. We'll have this three-month arm at the high dose, we'll have the six-month arm at the high dose, six-month at low, and some residual placebo. I don't know how many people will have not crossed over and still be in this trial at six months on placebo, but it's technically four arms blinded through six months. So we designed a trial to maximize the biology here for what we could see. We do have a three-month read coming up in Q4. We need to know the drug is doing something and works.
Yep.
But it's a six-month TPP, so we talk more about that.
Yeah. So I mean, well, let's talk about and flesh out, like, what are the expectations around that three-month update, and ultimately, you know, there's some advantages. I know you're, you know, the higher doses, which you haven't necessarily disclosed, but, like, in terms of, like, well, relative to RA, like, I guess, what is your expectation to what we see at three months? And then obviously, the six-month data seems like that's probably the more, you know, important data in terms of seeing the depth of response that you want to see.
Yeah. They're both important in different ways... but the six-month data is the TPP.
Yep.
Let me give some context when you think about the comps that exist out there in the space. Clinical remissions for Skyrizi, the IL-23p19s, or even the TL1As. Clinical remission, not response, but remission at 12 weeks in bio-naive patients on an absolute basis is plus or minus 30%. For bio-experienced patients, they're in the high teens. On a blended basis, somewhere in the mid-twenties. Those are the two biologic classes that with Skyrizi, you're penetrating frontline.
Mm-hmm.
TL1As, you know, presumably will be on the market and get utilized in second, third-line context. That's an interesting bar, but the TPP that we think matters here is what's happening to these patients through six months in a year? We spend a lot of time with R&D folks, you know, with big pharma at conferences and whatnot, but you go talk to these commercial folks at the big pharma companies. They want drugs that patients are going to stay on for a year-
Mm-hmm.
not used for three or four months and then lose response. What are the facts here with these trials to date? A third to half of patients lose response between three months and a year. So what does that imply? If 25% are in remission at three months, we're talking low mid-teens on an ITT basis at a year.
Mm-hmm.
Said another way, that's 85% of patients, somewhere between three months and a year, need another drug class. There aren't enough drug classes in UC today, unlike in RA, where you cycle for four lines of biologics. That's still emerging in UC, which is why this is so attractive. So I've been really pushing hard here on trying to educate what is a phase II design that de-risks phase III differentiation? That's why we ran this design, that's why we pushed so much that the six-month readout for clinical remissions or even endoscopic remissions are going to show, do we have a differentiated drug over time? So in the three-month readout that's coming in Q4, we need to know our drug works. Our primary endpoint is change in MMS versus placebo. We'll show the c...
The key secondaries that you're used to seeing, clinical response, clinical remission, but the other important thing is how tolerable is this drug?
Mm-hmm.
And are patients staying on through month six? Because in a commercial setting, you don't get scoped at three months. You have a discussion with your doctor if you have colitis, "Do you feel better?" You're feeling better, staying on the drug, you get scoped at six months. That's the reality of this. So we need to be in the game at three months, in and around these other biologic classes, and we're trying to drive for better remission data over time that's stable. The RA data helps de-risk it.
Mm-hmm.
The biologies of these diseases are similar. If it works in UC, and we're depleting out these cells in the tissue, in the lamina propria, as well as in the periphery, we should have the same long-lasting PD effect. It's a hypothesis, but it... That was the hypothesis coming in, we saw that in RA play out.
Mm-hmm. I mean, does depletion occur faster in UC versus in the joints in RA, or is it kind of about the same?
We don't know.
You don't know.
In our phase I in healthy volunteers, now you're dealing with smaller substrate, but it was the first read, one week in, you had full depletion. The first read in the RA study, which is two weeks in, full depletion. So in the periphery, at any dose, we expect something equivalent.
Yeah.
In RA, you see a two- to threefold increase in TPH cells. TPH cells, peripheral helper T cells, they secrete CXCL13. They recruit immature B cells, which mature into plasma cells, right? So in RA, there's very clear biology on this. There's also correlations of eliminating these cells in UC lead to remissions as well. That's how alpha-4 beta-7s work, that's how S1Ps work. Where I'm going with this is that should still be fast. We are dosing at a higher dose-
Right
... in our high dose in colitis than we did in RA. Right, you have to make adjustments here such that you will get enough drug to the lamina propria, which is the inflamed tissue in the gut in UC. So, you know, to be determined how fast. We had one biopsy in the ileum, which is rare for a smaller cap company to do-
Mm-hmm.
These ileum biopsies. That was at six weeks, and that's where we saw full depletion. That was our one read there. The biopsy will give us the same information at 12 weeks.
Gotcha. And then I guess, so you're making the case that, you know, ultimately, with existing therapies, these patients start to, like, you know, not respond, and by six months, you know, maybe it's cut in half from, like, again, 20, 20-something%. And where you guys, as we've seen in RA, you actually see an increase in response over time, because maybe it's just the MOA, you know, again, the PD effect, or it's just maybe it's a little bit slower build. So is that how we should be thinking about it? It's like you, at six months or even before, you're crossing where the other agents are kind of starting to-
Yeah
You know, fall off.
This is what's not clear. It's not like we worked slowly in RA. I mean, ACR20, we had 80% ACR20 in naive patients and over 60% in experienced patients.
Mm-hmm.
That's a really... I mean, at some point, you can't be better than that. We also saw pretty high LDA-
Mm-hmm
at three-plus months, but still the point holds. It got better over time.
Right. Right, right.
We don't know if the PD is exactly the same in a different disease. The harder part with colitis is, it's binary in that you're getting results at three months and at six months. In RA, you could see a curve.
Mm-hmm.
Maybe the inflection point's at week sixteen.
Yeah.
I don't know when it's going to be, but we'll have two different reads.
Yeah.
So that's what's unclear, and that's why I keep coming back to tolerability, and our patients stay on drug. Because if they're feeling better, they're not going to drop out of these trials, right? And this is a competitive market in terms of development. There's choices for patients. Patients know if they're feeling better, they have a year on this drug. That's a real benefit for a phase II trial to be that long. So the incentives are there, if you're feeling better, to drive to six months and drive to twelve months. But no untolerability, and it's important for this class, because I think there's a lot of potentially even misunderstanding. One, the drug works fast symptomatically in RA. We should see a benefit symptomatically in UC at three months. That's the primary endpoint. That has to happen.
Less than 2% of our patients in the RA trial dropped out due to AE. This is a 424-patient trial. It's a huge trial. One patient dropped out of this trial after three months due to AE, which is grade 2 headache.
Mm-hmm.
It's a highly tolerable agent, so we shouldn't see dropouts here as-
Yeah.
So you drop out for lack of efficacy, and that's why I keep coming back to, we want maximum number of patients at six months.
Gotcha. So maybe you can help frame the benchmarks, what we should see at three months and at six months. Obviously, from a tolerability standpoint, you've kind of already shown that's very good, so, like, you know, we kind of are expecting the same. But, you know, what, what should we be looking for, you know, on the efficacy endpoints?
Yeah, so like I said earlier, we'll read out the primary at three months, which is change in MMS. I'll dive into that in a second. We'll also look at clinical response and clinical remission. The comps for clinical remission are 30% bio-naive, 19%, 18%, 17% bio-experienced for again now IL-23s and TL1As, which are the comps, I think, today-
Yeah. Okay
...that matter the most. We will have a blended average. We enrolled 136 patients in our trial across those three arms. Approximately 50%, 50, were bio-experienced or advanced therapy.
Okay.
Could have been JAKs, it could have been-
Right.
Some of those patients will also be third-line patients as well. There's going to be a mixed bag in here, so a blended rate is the right way to conceptually think about this. We're talking in the mid-twenties to be comparable. I don't think you need to even be that high, because at the end of the day, if you're in range with these biologic classes, what are you looking at six months?
Right.
At that point. So I think that's the guy. The primary endpoint, Arena used this as well, as a smaller cap biotech company to change MMS. There's some nuance differences here that matter. Their inclusion criteria was four to nine on MMS, we're five to nine. What Arena saw was a two-point change on their high dose, a one-and-a-half point change on their, low dose, and a one-point change on placebo. So when you're talking a one to two-point change over three months, even just one point at baseline, more mild patients could make a difference. They were a third or less than a third bio-experience, we're half. So the comps are... The primary endpoint comp is hard. I think the key here is, are you better than placebo? Are you stat sig?
Mm-hmm.
Are you numerically better? I think really what everyone's going to then look at are the key secondaries, and importantly, remission rates.
Yeah. Perfect. I guess in terms of, like, let's say, success in UC, how do you start balancing between resources? You know, do you pursue UC? Do you pursue RA?
Yeah.
Do you do both? Do you partner? Like, what, what are the options?
Decision-making in colitis will be off of the TPP, which is at six months.
Okay.
Now, there's theoreticals where you shut your trial down three months if you're inferior, you're hurting patients, there's a safety issue. And just to comment on that for a second, we updated in writing in our August, Q2 report that there's no SAIs of concern on a blinded basis in our colitis trial. I'll say that again right now, as of last week, that still holds. So we're not seeing a safety issue, but these are the reasons you would shut something down. Let's just assume that's low likelihood. The decision-making on colitis will come in twenty twenty-six, should you advance into the next phase, phase III or something that's pivotal. We announced in June, we tried to be very, very clear on this, there's two primary paths forward that we're considering. One was you move forward independently in UC.
The reason we like UC is a growth market where frontline is still branded, second, third, fourth line is still emerging with class switching. And as I walked through earlier, the vast majority of patients are class switching here-
Mm-hmm
... or will be, and the alternative is surgery and so there's a huge opportunity for a new mechanism. You're going to go to a new mechanism before you go to IL-23 plus or the third TL1A and these other things. You're going to try different mechanisms that could give you a different chance for an outcome, and this has been seen in every disease state and then there's the combinations, and I think that's going to be our competition.
Mm-hmm.
That makes a lot of sense. There's not a contracting where you need portfolio sitting here today, because you still branded assets in the front line, where you can go launch into second, third, fourth line independently in the US. So we can do it ourselves. So that's a viable path forward. Alternatively, do you move forward multiple programs. I'm sorry, multiple diseases, RA and UC, and then other phase IIs? And I think people forget this. It's. There's a lot of capital that needs to go into any one of these, plus you want to launch into other diseases that are rational, given success. You ultimately need a partner to do it all.
Mm-hmm.
Ultimately, you need a partner to go launch in Europe and Japan, and everything.
Sure.
Someday, this drug gets partnered, so they're not mutually exclusive. You could start charging forward in UC in phase III and look for a partner and not have to take a deal, right? And there's a whole dynamic there. So I think those have been the primary paths. The criticism is, well, you like your RAD so much, why aren't you moving forward? Incrementally, we think UC is a bigger opportunity independently. If UC does not hit the TPP, there's paths forward in RA. I'm just not sticking my neck out there describing them, and we're definitely not focused on enabling that today-
Mm-hmm
... because then all I'll be doing is pulling it back. And we are in a very good competitive position in RA. And I don't like to sit here and say we're sitting on it, but there's work happening in the background to plan-
Yeah
... obviously, hopefully. But our competitors aren't moving forward in the same mechanism, and there's good reason for it. Their drugs aren't potent. Lilly can't sustain a response. We're seeing the opposite. We have a very different drug. We have a very tolerable profile. I don't know what's going on with Lilly's drug, but they're very different drugs where we have double the potency on depletion, which is driving efficacy. That said, when you look at the RA landscape, bigger picture, there is nothing in phase III right now. There's also not been a new class launched in 13 or 14 years. So while I don't want to sit on it, we're not losing competitive tension... like we would in UC if we didn't move quickly. So it's a very different dynamic.
If Lilly was moving forward in RA, we'd be having a very different discussion right now on what we'd have to do. So we're being, I think, good custodians of capital. We're focused on ROE for investors, and we will move forward where it makes sense, and I'm taking the option value right now to wait for our UC data, which is right around the corner.
Yeah.
to make a decision.
Gotcha. I guess, you know, looking back, you know, obviously, you already have RA data, but when you were looking at both UC and RA, evaluating in terms of like, you know, the biological rationale, which one did you feel stronger about, you know, based on the early data just? Yeah.
It's a hard question to answer because Lilly had proof of concept in RA.
Yeah.
There's no way to sit here and say the probability of success in RA was lower than UC.
Yeah.
But in a vacuum, there's more preclinical evidence that UC would work-
Yeah
... that we've generated ourselves. We've done our own animal models, where we've induced colitis in mice, and we see that's preventative with our drug, which a lot of other successful classes have done. There is very strong data suggesting that clinical remission in UC is tied to a reduction of TPH cells, peripheral helper T cells in the periphery.
Mm-hmm.
When you look mechanistically at other classes that exist, I was mentioning before, the alpha-4 beta-7s, all they're really doing, their primary mechanism, they could be doing other things, is binding to TPH cells in the blood and preventing their trafficking into tissue. We just showed you in RA, at every single dose, we're depleting more than 90% of them, with a similar elevation in both diseases. The S1Ps prevent the efflux out of the lymph system of these exact same cells that we're depleting in the periphery. TL1As, they're impacting ultimately the macrophages that are responding from effector T-cells that are PD-1 expressing. As long as we're getting drug to the lamina propria, we should have effect on there too.
So there's other mechanisms that work here that we've shown and de-risked in RA that we're having an effect on. I think lastly, we did have a robust translational package in RA, where we showed, through the synovium data, gene expression panels, where we saw reductions in TNF pathways, TREM-1, DAO, IL-23, co-receptor IL, IL-12 receptor beta. We're seeing genes that are reduced that are relevant, and you see that we're seeing reduced in RA patients through the gene expression in the synovium biopsies. So I think there's more anecdotal evidence now, but there's a good body of research that says we should be effective in UC, and then I think the better question is, how competitive are you?
Yeah.
To be addressed.
Gotcha. All right, well, that's great, and obviously, looking forward to that data. Maybe just, you know, shifting gears to, you know, zero three three, and talking about that program. So maybe just kinda highlight, you know, what the program is and what you're working on there.
Yeah. Well, look, this asset could be its own company, and it's a big space, and we'll spend 40 minutes in one-on-ones and never get to the program still. ANB033 is a CD122 antagonist, and what CD122 is, it's a receptor on, generally speaking, activated cells, for CD8s and CD4s, as well as NK cells. And it's a dimeric receptor that blocks IL-15 and IL-2. So the IL-15 class is, I think, showed very compelling data recently in a number of different diseases. Novartis bought a company called Calypso 18 months ago. They've said they're going to announce their phase II strategy this back half of the year. Teva's been advancing their program. They're both, they're both very potent, high-affinity IL-15s. But by blocking CD122, you have a dual mechanism of action.
There are other CD122s out there that have shown interesting proof of concept, including in celiac disease. We've announced that celiac will be our initial phase Ib trial. I said earlier that we initiated the phase Ia in healthies nine, ten months ago. So we do have an IR event coming up in Q4, where we'll be dedicated to this asset. We will walk through the mechanism in a lot more detail relative to IL-15s. We'll talk about differentiation with our program. We haven't shown a lot of data here. We did design against a company called Villaris, which had an academic and an IgG antibody that Incyte bought a couple of years ago, preclinically. It's in a late phase Ib. We know we have a higher affinity asset that has a different epitope in terms of blocking both of those receptors.
That's a bit about the differentiation. We'll show you the data. So there's going to be a lot that's going to come out, in that event that I'll save some of this for.
Sure.
We're really excited about the drug. There's more to do here than just in celiac disease. This was another antibody that was discovered by Anaptys that we're moving forward through the platform.
Gotcha. Again, obviously, there's some proof of concept in celiac, but maybe, you know, I guess why... Is that just more for proof-of-concept modeling, or is it more just like an actual opportunity that you think is interesting?
There's over two million patients in the United States that have celiac. The diagnosis rate continues to escalate. It's over 30% at this point, and there's nothing approved, so when you think about competitive dynamics, there's a lot of interest in this space. There's a reason Amgen, Pfizer, Takeda, Sanofi, Novartis have all focused on this disease, is there's a major market opportunity if you get a drug that works, and like a lot of diseases, the biology has become more known on how to target this disease and show results. Interesting comp that happened recently, and it's a disease that we follow for a number of the autoimmune conditions that we're interested in in our portfolio. This is not for ANB033, but Sjogren's disease. Nothing worked until it did.
We just had two big hits in the last month of phase III data that worked in this disease, and, you know, there's a lot of pushback here, well, celiac, nothing ever works.
Mm-hmm.
You need the right, you need the right drug, and there's been a lot more understanding of the biology here over time. NK cells are an interesting PD marker for CD122 expression. Cells like cytotoxic CD8s, which are very similar to IELs, are expressing a lot of CD122, and they are the primary target in celiac disease that are responsive and upregulated as a result to the processing of gluten. You also see a lot of IL-2 expression. It's a great biomarker, which we are now blocking, right, with our drug. You're seeing that result from CD4s that are involved in the breakdown and response from gluten. So we're targeting different cell types in celiac, two different modes of action, both with our drug.
And so I think we're point on for why this should work here within celiac disease in a way that drugs that formerly would target the breakdown of gluten itself, which you're always trying to play catch up on, you're actually dealing with the autoimmune impact. So there's a lot of good on point biology within the CD4s and CD8s that are expressing CD122 that we're targeting, and you have the biomarker of the impact from not just IL-2 increase, but also the NK cell impact.
Gotcha. So, and the event later this year, I mean, should we expect just the normal healthy volunteer data, or will we see anything from, you know, actual patients?
We are close to initiating the Celiac phase 1b.
Okay.
We will walk through the trial design and what's different about the approach we're taking than, I think, you know, what's been done historically. That's going to be attractive.
Gotcha. And again, at that event, will you kind of outline, you know, potential future indications as well, or, like, other areas, seeing this could be its own company? Or like-
I walked through what we're committing to so far, but there's always upsides-
Okay. Gotcha
... that you potentially get into over time, whether it's at an event or sometime next year. I, I'm using the word, pointedly here, the initial phase 1b.
Gotcha. And then, yeah, also on one-
But it is competitive, so there's a little bit of a dynamic of do we want everyone else-
No
... in the space knowing where we're going until we're there.
Okay. Gotcha. And then your other asset, one oh one, is... That one's got some more kind of, you know, proof of mechanism out there with Biogen's program and things like that. But I guess, where do you find that one finding a role, you know, within the overall portfolio?
Our drug is more potent than Biogen's BDCA2. They had impressive phase 2 data in SLE. They have three phase 3 trials ongoing right now, two in SLE and one CLE. They don't read out until the back end of next year or early 2027 across that full estate across forms of lupus. That's one, I think, from an investor perspective. It gets a lot more exciting.
Mm-hmm.
We'll decide when and how to put out more information to show the potency differentiation. If this works for Biogen in those diseases, we have a better drug. If it doesn't work there, we have to really put some thought into how does it make sense to move forward. We're in the phase 1a right now. We'll have that data available for the right time. We have plans to move forward, but the overall thesis here across this entire portfolio is, we are targeting, overexpressed disease, modulating immune cells that do not exist in these states in healthy. Whether they're TPH cells, which are in very small quantities in healthy tissue, that rosnilimab's targeting, the BDCA2 targets PDCs, they're almost untraceable-
Mm-hmm
... in healthy tissue.
Yeah.
CD122 expression, 25% of T cells express it in healthy, which is dramatically increased in disease, right? We're very specifically targeting the right diseases for different immune cells that are overexpressed in driving the pathogenesis of these diseases. That's the thematic here across all of our programs.
Gotcha. We'll get to Jim Perley, so we can talk about that. I know you're excited about that.
We got a couple minutes.
Yeah, you got a couple of minutes. There's a lot to talk about. So, you know, you have a very good, you know, situation in terms of your cash runway, but also, you know, kind of the royalty, you know, kind of value here as well. So maybe just talk about that in terms of like, you know, the expansion opportunities for Gemperli and how that really impacts you guys, you know, going forward.
Yeah. And so on, on cash balance, we were, you know, just shy of $300 million coming into the back half of this year. We have a $75 million dollar cash milestone that'll come to us from GSK when Jemperli hits $1 billion for the first time in a calendar year. Q2 results were $262 million from GSK sales at Jemperli. That's a run rate that's already north of $1 billion, so we're gonna get that this year.
Yeah.
A year ago, we wouldn't have been talking about this, but what happened in the last year was, in frontline endometrial cancer, GSK got approval for Gemperli in frontline with a survival label. Keytruda doesn't have that. In January of this year, EMA approved it, and we know that without survival in Europe, you don't really have a play. So we have a big leg up there with this asset in endometrial cancer. And they also showed in the last year, forty-something patient trial out of Memorial Sloan Kettering, that they had a 100% ORR in rectal cancer. That, and a breakthrough therapy designation as a result, the pivotal trial will read out in about a year. That's what's driving uptake right now.
And in Europe, just the math that's generic, and I don't have inside information on this, but reimbursement would generally keep coming online now and over the next half back end of the year. So we expect the growth already is from endometrial. We have probably some synergy here with rectal cancer that's happening in the background. Europe should be coming online. There's a lot of growth left to come.
Mm-hmm.
They had 17%, 18%, 19% quarter over quarter growth over the last few quarters just from this ramp, and we don't expect that to slow down in any real way. You could argue that you could exit the year $1.3-$1.4 billion run rate. Why does this matter? Every $1 billion a year, we get $80 million in royalty. If they did $2 billion in a year, it's $240 million of royalty. GSK is guiding on monotherapy indications alone to $2.5 billion of peak sales. The guidance is as of June, so it's been said by them multiple times over time, but recently. Again, monotherapy indications. Wall Street consensus is at $1.7 billion. Last year, Wall Street consensus was at $1.3 billion, so it's moving in the right direction.
But the challenge for an investor at GSK, this is not a top ten product. Their earnings leverage that GSK has is relatively low since our royalty stack increases so much. So it's not what's in focus from its consensus. But if you take consensus from June at a 10% discount rate back to today, pay off a non-recourse capped monetization that we had done with Sagard, the residual value is worth way more than our market cap. There's a massive amount of value here, and that is a backward-looking forecast. If you do a bottoms-up your own work, this is a much bigger number. If you believe GSK's guidance on an asset that Wall Street doesn't focus on, I don't know why they'd stick their neck out there any otherwise, this is a very, very big opportunity for us. It serves as a valuation backstop.
You know, we had also, will you just spend the money on rosnilimab? We just talked about this. Rosnilimab is going to be a very prudently focused, return on equity-driven approach that we can partner at some time moving forward, and I think we could finance in various different ways. We have a huge royalty here that's going to accrue value over time to us, and we're really excited about it.
Gotcha. And then maybe last question, just in terms of like, you know, I followed AnaptysBio 1.0, and this is AnaptysBio 2.0. But I think the consistent thing here is, you know, we've seen very high quality antibodies come out of this platform, you know, consistently. I guess, you know, how do you think about the platform value, and is there anything else that you can do there or you want to do there, whether internally, externally with that platform?
I don't think I've been asked this question in two to three years. I'm trying to get people... 22 program came out of our platform. The BDCA2, we licensed in, and it was potent. We had a differentiation thesis. The company we licensed it from wasn't focused on autoimmune disease. We took it out of an IND-enabling state. We had to retool something on the process development. That's a big part of the platform that I think gets underappreciated. There aren't many companies out there anymore that have antibody platforms, but it's not just discovery. I think more importantly, it's the translational research and the process development that you can optimize assets, and you could also then use to diligence other programs that are at stages that are before where big pharma would focus.
We have a differentiated edge on how we're thinking about where the spaces are moving. That's been the value of the platform to me and Anaptys two point O, to use your terminology. But look, we have to show that these things work. Like, Gemperli is a great program. We had a drug called imsidolimab, which is a best-in-class IL-36 receptor antagonist, which was developed historically in a lot of places, but the one that made the most sense was GPP. We outlicensed this drug. That was late, it was late to the game. That was the issue from Anaptys one point O, but we outlicensed to Vanda. They're filing a BLA this year. We have a nice royalty that I'll come in on that. We're excited about rosnilimab, we're excited about ANB033, and, and we'll go from there.
So it's a little bit of stepping stones right now, but if we can get folks to value ANB033, that's a big win.
Awesome. All right. Well, Dan, we'll leave it there. Thank you so much.
Thank you very much.
Good to see you.