All right, I think we'll get started here with the next fireside. So my name is Derek Archila. I'm one of the Wells Fargo biotech analysts. Our next discussion is with Sutro Biopharma. From the company, we have William Newell, CEO, as well as Jane Chung, President and Chief Operating Officer. Nice to see you.
Thanks for having us.
Yeah.
All right.
Glad to be here.
Maybe, Bill, you want to just start at a high level, you know, what you guys are working on and kind of the genesis of the company, and then we can kind of get a little bit more specific with the questions in terms of some of the upcoming milestones and catalysts.
That's great. You know, I, I started as CEO of Sutro in 2009 . I was the nineteenth employee. Here we are in 2024 , and we're going to tell you a story about a platform technology that is unparalleled in our industry, and a utilization of that platform technology to offer patients both more and less. And we'll unpack why I say more and less, as we talk about what we're doing at Sutro. Effectively, today, we are a late-stage clinical company working in oncology. Our lead program is a antibody drug conjugate targeting folate receptor alpha. We call it Luvelta for shorthand. It's luveltamab tazevibulin. And the thing that we're excited about it is that we believe it can deliver more therapy, more efficacy to more patients than existing therapies, and less toxicity at the same time.
So that molecule is in pivotal trials now for registration in ovarian cancer, and we've started a trial in a rare form of AML. It's a pediatric AML that we'll talk a little bit more about, as well as a non-small cell lung cancer cohort that we've opened up as well. So it's really got the potential to be a pipeline and a product, as the phrase goes, and we're very excited about that. And if that were all we had, that'd be enough for many companies. But we also have the ability to make next-generation antibody-drug conjugates using the latest technologies in terms of linkers and warheads. So our next molecule, moving to the clinic next year, is what we call STRO-004. It is a tissue factor-targeting antibody-drug conjugate.
It's got a beta-glucuronidase linker as well as an exatecan warhead and a DAR of eight. So that is where the industry in general is going, although we think you can't just follow the industry, you actually have to lead the industry. So we have other molecules beyond tissue factor ADC using that technology, and importantly, we're pioneering the next generation of ADCs. We call them immunostimulatory ADCs, where in one molecule, homogeneously, you have an immunostimulatory agent and a cytotoxic payload. So the cytotoxic payload kills the cells as they stress.
The immunostimulatory agent tells the immune system, "You need to pay attention here and go and clean up the work that's there." And if it works as well as it did in mice, you'll have effectively an immune response that will allow you to fight off the cancer as it tries to mutate and grow again after the chemotherapy is no longer active. We have two programs with Astellas there. And last but not least, a bunch of years ago, we spun off a company called Vaxcyte today, which had some dramatic results with our technology platform applied to a 31- valent pneumococcal conjugate vaccine. That is our technology that allows them to make that molecule. Brilliant result in terms of their most recent dataset. Kudos to them, but we're really thrilled that the technology lives in various forms and has lots of applications in our industry.
Excellent. Awesome. Well, I wanted to ask first about, you know, you have some upcoming data at ESMO, so literally, like, in a week or so-
Yep
... you know, for Luvelta plus bevacizumab. And, I just want to kind of maybe you can tee it up for us, what should we expect in that dataset? And in terms of, like, number of patients and, you know, a level of, I don't know if you're going to have, like, the duration of therapy, like, how long these patients have been on. But, just, you know, give us some of the specifics that we can, you know, get teed up here for.
Great. Jane's going to answer that. So, thanks.
Sure, go ahead.
Happy to. So we shared some early data on this bev combo back in January when we held an investor Luvelta forum. And the combination showed a promising, encouraging overall response rates for an all-comer strategy. So irrespective of folate receptor alpha expression levels, we were able to show about a 35% overall response rate. I think in addition, we were able to see that patients who were less heavily treated had an increased response rate of about 50%, and we saw about a PFS benefit, about eight to nine months. So we think that these are really encouraging data. We will be able to share an update on that cohort at ESMO, and more to come on sort of the overall efficacy by the preferred dose as well as longer follow-up.
I mean, how should we be thinking about that compared to Mirv + Bev? And like, you know, again, is this really an apples to apples, or, or what would you kind of say in terms of like, you know, the context between-
Yeah
... what, you know, they've shown in what type of patients versus what you'll have?
Yeah. Before I get to Mirv, I think historically, the stage setting has really been established by the AURELIA trial, which was the Bev chemo combination in platinum resistance, which showed about a 26% ORR and a PFS benefit about six months. When we look at the Elahere data, we see about an overall 44% ORR, but mostly driven by the 2+, 75% high, super high expressing patients, and less so by the medium and low, and I think what's differentiating about our results and our data so far, if it can continue to mature and stay and maybe be maintained, is that you could look at even going lower to lower expressers or even no expressers, and this all-comer strategy is highly disruptive in a space where you may not need to even test.
As we think about the life cycle program for Luvelta or luveltamab tazevibulin, our folate receptor ADC. Already eight out of ten women, potentially on a monotherapy, can benefit from this drug, and that's doubling the patient population that Elahere today serves. And so, moving forward, that's an incremental 20% in the platinum-resistant setting. But as we think about earlier lines, and these patients are kind of the same, right? They're just more heavily treated by the time they get to platinum resistant. So these patients, in an earlier line setting, there's much bigger opportunity there. And if you can get an all-comer strategy and disrupt the whole testing paradigm, and actually access 100% of the patients in a maintenance strategy, whether it be first line or second line, that would be very valuable.
Yeah. Okay, so how does the, once you read this out, I mean, how is this going to inform? Are you going to start, you know, a registrational trial with the combo, or like, what, what's kind of next? And,
Yeah.
Obviously, I think you're going to continue to follow these patients, but, you know, again, what's kind of, you know, how are you going to leverage this data?
Yeah. We actually, thanks for asking, because I forgot to mention, we added another additional cohort. The first 17, 18 patients were dose escalation. This next cohort, we expanded in more of an expansion cohort on the preferred or optimized dose, and we'll see more of that data come next year, and then from there, we'll make bigger decisions and more decisions about the earlier line trial.
Perfect. Okay. So anything else in terms of the ESMO, like, data that we should, you know, take away or, you know, we should probably, you know, interpret the... How we should interpret the data?
I think we've covered it.
Okay.
Yeah.
Got it. So going to the phase, you know, the REFRaME trial, I guess, can you just remind us where you are with that in terms of like, you know, next steps and timing? Like, because I think the big thing is like, when are we going to get the data?
Yeah, absolutely. So as you will recall, the FDA has an initiative called Project Optimist, that every company in the cancer field has to now check the box on. And our pivotal trial has two portions to it. The first portion is really designed to address FDA's requirements for Project Optimist. I'll talk about that in a second. The second portion is the pivotal phase, where you actually have your chemotherapy control arm. We started the second portion already. That was started in April, May of this year, and it's going to take a few years for us to reach the patient numbers that are going to be required, both for accelerated approval opportunity as well as for a full approval opportunity.
But let me unpack the first stage, because once you're in the phase where you have a chemo comparator arm, the company is going to be blinded from the data until we get time for the data readout. So, what I can talk about is where we are with part one. So, as I indicated, FDA wanted to make certain that we met their criteria for Project Optimist. And we thought we'd done a lot of work in our earlier development, where we randomized about 44 patients between what we think are the two best doses for patients, both from an efficacy and a tolerability standpoint. That's 5.2 mg/kg and 4.3 mg/kg. Not that much different, dosed once every three weeks.
We had a preference for one, well, but when we talked to FDA about it, they said: You know, really forty-four patients is not enough, even if they were randomly assigned. We'd like to see another fifty patients or so worth of data to make sure that you have got the lowest effective dose, right? You no longer maximum tolerated dose. You have to find that lower, lowest effective dose. And so we've done that. Those patients were recruited in less than a year, and what we indicated to FDA we would do, and they agreed, is we would follow them for a period of time that was agreed with FDA for purposes of doing an exposure-response analysis, which would inform a recommendation on what the dose was that satisfies Project Optimist.
Now, we previously said we expect to have gotten our exposure response analysis concluded and talked to FDA, and decided on what the optimized dose is before the end of the year. In the meantime, until we do that, our pivotal trial has both doses going forward, along with the chemotherapy control arm. So today, a patient who enrolls in our trial has a two to one chance of getting our drug versus chemotherapy. When we have identified the optimized dose and gotten agreement with FDA, we will drop the non-optimized dose arm. Those patients will be followed for safety, but they're not included in the statistical analysis. So we'll take that optimized dose, which we started enrolling patients on in April of this year, and we'll be comparing it against chemotherapy, which we also started at that same point in time.
That's an efficient way to accelerate the collection of data. We aside from telling people, okay, this is the dose, that is the optimized dose, I know there's a need or an understanding or a desire to understand, what does that whole 50-patient cohort look like? They're both on active doses. We know that from prior work. Why did you choose this one? And what does that tell us about probability of success for the remainder of the trial? You know, right now, we understand that were we to talk about data that we're seeing, and we don't have all the data yet, but if we were talking about the data we were seeing, that could really create an issue for our ongoing pivotal trial in terms of biasing the trial.
So what we've come to understand is we need to be mum about the data until we've agreed on what the optimized dose is with FDA, and we then have to have a conversation with them to make certain that our talking about that data does not give them concerns about clinical trial integrity. Because the worst thing, worse than, you know, not sharing data, would be to share data and then have FDA make us start the study all over again because they didn't think we properly honored their requirements for clinical trial integrity. We don't think that's going to happen. The best advice we have so far suggests we will be able to talk about the Part One data, but until we actually have that conversation with the regulators, I won't be able to commit to that.
But if we do, it should be around the end of this year that we're in a position to have those conversations with investors.
Got it. Okay.
And the only thing I'd add is that REFRaME has FR alpha embedded in it. People pick that up. We're reframing the opportunity and the benefit for expanded benefit for more patients, right? And I think this trial within a trial design that Bill just spoke to is somewhat new, but it really addresses the new regulations by the FDA with the requirements for Project Optimist, as well as the requirements to have your confirmatory phase III largely enrolled by the time the FDA has to make an action on your data. So this trial within a trial is set up so that you can actually go after an accelerated approval first, and then get the full approval all seamlessly within one trial.
Got you. So basically, you're saying you'll have an FDA, some sort of meeting between now and the end of the year and an update for investors by the end of the year?
You know,
In a perfect world.
In a perfect world with FDA-
With their blessing, we'll be able to share more data.
There you go. All right. Okay.
With FDA holding to timelines, that would be a good thing.
Got it. Okay, perfect. I mean, anything else or any other updates that we should be aware of, you know, coming from, you know, the ovarian, you know, the program or, also, you know, the competitive dynamics here? We can get into that in a second, but just, you know, from you guys, any other newsworthy items that we should expect, you know, by the end of the year?
Well, we spoke to the ESMO data that's likely to come soon on the bev combo, and we completed the expansion cohort in about a month, in a month's time. And this is what happens. You can go fast when you don't have a biomarker approach, right? You don't have to wait for the testing to come back. So, I think we'll be in a position to share more data first half of next year.
Really, the other things are the commencement of the non-small cell lung trial, that we won't have data this year, but we expect to have some data next year.
Okay.
The pediatric AML trial, pivotal trial is ongoing as well. This is a ultra-rare form of leukemia. It affects kids who are diagnosed between the ages of six months and two years, and about 85% of them do not live two years after diagnosis. They get standard chemotherapy to allow them, if they go into remission, to get a stem cell transplant, but frankly, many of them never get to remission, and so they never get stem cell transplant. They are just treated with more chemotherapy. For the ones who do get a stem cell transplant, many of them are not able to maintain that remission. They relapse, and they get chemotherapy, and that's pretty much it.
What we've demonstrated through a compassionate use delivery of the molecule to physicians around the world, and this was data from ASH of last year, that we can get these kids, after a couple of cycles of Luvelta, into complete remission. About 40% get into complete remission, and that then allows them the opportunity for a stem cell transplant. So it's a relatively well-tolerated molecule in them. Principally, one of the things that we do see with Luvelta is some neutropenia.
Right.
These kids are already neutropenic, so you can't, you can't actually give them more neutropenia. They already have it as a result of the course of the disease and the therapies that they have received. So, we're excited about that trial. It only takes about 20 kids to be part of that study. We think we can enroll quickly as they present themselves. We've got a global approach to enrolling them in our study, and it really provides not only hope for the parents and the children who suffer from this form of leukemia, but it provides us with the possibility for a Priority Review Voucher. It allows us to establish our infrastructure for purposes of a faster and more successful launch in the ovarian marketplace, and frankly, it's the right thing to do.
So you'll see more about that, hopefully next year, but we're excited about what we've been able to demonstrate in that indication.
Got it. In terms of, you know, other folate receptor alpha, you know, ADCs that are out there, I mean, obviously, Mirv's approved, and, you know, we saw some movement with, like, ProfoundBio getting acquired.
Mm-hmm.
You know, the promise for you guys is obviously expanding the pie, right? Getting to low expressers. You know, I think Profound and Zymeworks, and everyone's trying to kind of get on the bandwagon, too. So I guess, how do you think, you know, this market evolves, and how do you feel like you're differentiated versus those molecules?
Yeah. So, I mean, we like the fact that it's a validated target with the FR alpha expression. I think, you know, we are closely watching this market evolve with all the potential competitors, but we believe we're in a position to be first to actually serve the lower medium expressing patients. And time, this is a really critical time where we have our global trial set up such that Elahere is not available right now in Europe, and so we can actually recruit for this trial in steady pace to be able to serve and get that broader patient population mix within our trial. I think when you're coming in later, it's going to be really hard to compete for the patients. You're gonna have a different standard of care to compare against.
I think this race to approval matters, and we feel like we're in a good position right now to be first to serve those lower medium expressive patients.
Derek, let me amplify just at one point. I think that may be underappreciated, and that is... If we're successful in getting this medicine approved for patients in the low and medium expression level, whoever is following us has a different standard of care that they're being compared against.
Yeah.
It's not the 12% that's chemotherapy, it's the 30%-
Yeah.
That is Elahere. It's that what we hope will be 30% or more, that is us with Luvelta. So the bar is materially higher, meaning they have to now scrap any plans for competing against chemotherapy, and they have to compete against one or both of us.
How do you think about, you know, efficacy in different levels of expression? Like, how is that going to play a role in your pivotal trial? Obviously, we don't get a sense of that with Mirv, because they're not looking at a range of expression types. So, but I guess, what do we know from your existing data, and I guess, what we've seen maybe preclinically just to understand that?
Yeah. So in our early phase 1 program, we looked at our. It's worth noting that our cutoff threshold is lower at 25%. And despite enrolling patients 25% and higher, we see consistent efficacy in the lower medium expressor group, and the efficacy is not driven by, like, a small number of the high expressors. So that's what's giving us confidence to pursue this much broader label, much broader opportunity. And so we'll see how this all plays out in the phase 3.
And there's a design feature that I think is worth noting, and it's, you know, we're talking earlier about Vaxcyte's great success. It's the same design feature that they use, right? And it's really the ability to make a molecule that is homogeneous, meaning every molecule you're dosing a patient is the same. It is not a mixture of different drug antibody ratios. It is consistent for us as a DAR4. For Vaxcyte, they have a protein carrier, which is got six non-natural amino acids attached to it, and then they conjugate the same way we conjugate our linker and warhead, they conjugate their polysaccharides to it, and that gives them a very specific molecule.
We believe the specificity of the molecule, the design of it, allows us to really reach patients who have lower expression levels, and that's. I mean, you can't. If you don't have much target, you're probably not going to get a lot of benefit. But if you have a certain minimum threshold, then your drug should be active, just as Vaxcyte's vaccine is active in all patients above that threshold. Now, based on our preclinical work and our clinical work, we think that threshold is 25%, but in combination, we might be able to lower it. But the point being, it's the design that gives us the opportunity to know that a patient who expresses between 25% and 50% of the target is going to do as well as a patient who's 50-75% and beyond.
So that's, that's the data that we've seen. We're going to see more of that in this trial.
Got it. Maybe talk about the non-small cell lung cancer opportunity, and obviously, you know, what you're doing there with the trial. I mean, and what percent of patients actually have high expression? You know, kind of go through the
Yeah. So I mean, the design properties are really important, but they need to translate into clinical benefit, and that's what we're seeing in the ovarian cancer studies so far. And I think the differentiating piece for Luvelta and why we believe there's a pipeline and a drug here is because of the activity in this lower expressing patient population. Ovarian cancer expresses folate receptor alpha, upwards of 80%. In lung cancer, about 30%-60% folate receptor alpha expression, so a bit lower. And in our cutoff of TPS greater than 25%, we see about 30% folate receptor alpha expression in the adenocarcinoma non-small cell lung cancer space. And in addition to that, we have some preclinical data on Luvelta as a monotherapy and in combination with a PD-L1 that shows strong activity.
So the rationale is there to pursue lung cancer approach. Even if we were able to get 1%-2% of lung cancer, lung cancer is a huge opportunity because there's so many patients and the incidence numbers are great. So I think it's worth pursuing for Luvelta.
Got it. So we'll get data for that or some early data next year?
So yes, we started the trial, as Bill mentioned. Actually, we started the trial this year, hopefully getting the first patient in later this year, and then we'll have a handful of patients next year that we can take a look at. This is not a registrational trial. It's a phase two safety signal-finding kind of trial. So we have control and access to that data, and we'll be able to take a peek.
Are you only looking at a single dose, or are you looking at a range of what's, you know, different cohorts?
We have disclosed that we are moving forward with the 4.3 mg per kg for the lung cancer. They do have an option to escalate to 5.2 if they are able to tolerate the 4.3. But it's a way for us to... These are heavily treated patients.
Yeah.
and we want to make sure that they have a good experience.
And then maybe to the expanded pipeline beyond Luvelta. You've been talking about, you know, some of the other ADCs you have in development, and you can get to the platform last, but like, you know, just kind of things are coming up, there's new targets, you know, what, what's your focus most going to be on?
Yeah, well, let me talk a little bit about the journey that we've been on.
Sure.
- and then Jane will talk about the specific, opportunities-
Sure.
that we're pursuing beyond Luvelta. So when I started in 2009, I was the 19th employee at Sutro with a platform that you know what it was going to be good for? My job was to help us figure that out. In 2011, we decided ADCs was actually, and vaccines in 2013, were the two sweet spots, but you couldn't do both. So we found a home for our vaccine applications. That's Vaxcyte, and great home, great outcomes for them. And we continue to focus on antibody drug conjugates. And back then, I remember it was said that: Oh, it doesn't matter, homogeneity doesn't matter. Controlled heterogeneity is what we want our ADCs to be.
We said, "No, that's just, that's bad science." You wanna have a single agent, you wanna optimize that agent, and you wanna get the right balance between safety and efficacy. And with a mixture, it's almost impossible to be able to do that. Fast-forward today, everybody talks about homogeneity in terms of ADCs. This heterogeneity thing is long gone. We thought, Hey, we've got a great linker in this new class of linkers. It's a val-cit cathepsin B cleavable linker. Really exciting linker, better than prior linkers. Guess what? There's a newer class of linkers called beta-glucuronidase linkers, that are even more stable and less likely to be cleaved outside of the tumor microenvironment, and really nicely cleaved inside the tumor microenvironment. Okay, so let's go from one linker to the next generation and keep pushing the envelope.
Let's go from warheads, from auristatins and maytansinoids to, you know, now people are using non-tubulin inhibitors. The exatecans are, you know, the one du jour. So we've continued to progress our platform and evolve better linkers, better payloads, better understanding of where to position the linker and the warhead, and a greater opportunity to have a more meaningful patient benefit, where we give them more in terms of efficacy and less in terms of toxicity. So with that, Jane, you wanna dive into '04 and the rest of the pipeline?
Yeah, yeah. I mean, I think, you know, the real differentiation for Sutro is that this platform is really powerful. We've seen it enable the medicines that Vaxcyte is making. And I think the hypothesis when Sutro was formed, 20 years ago, but, you know, you started when you were 12, maybe. But it was all about, can we make a drug, and can we make an ADC? An ADC is very sophisticated with many different elements on how you construct these molecules, or medicines. And I think now we've made several, drug candidates. Now it's about how do you lean into the differentiation of this platform and technology? And now, yes, the new payloads, exatecans, everybody wants them. They're very much in vogue.
We have them as well, and we have several drug candidates, STRO-004, five, six, and seven, that we're working on right now to really dive into the Exatecan ADC, and we are seeing some early PK data that really shows greater exposure. Greater exposure translates to greater response and hopefully a better TI or therapeutic index or window, but beyond that, we're doubling down on the innovation and the differentiation of this platform. This platform allows for specific protein design and engineering that it could enable even the dual payload strategy. You know, I think very few companies would have this sophistication of protein engineering to be able to do dual payloads, and I think that's really kind of the future state.
You know, if you think about double dose, cytotoxins or different cytotoxins, we're already working on an ADC, iADC concept that enables this feature to be done. But if we think about two different, cytotoxins to be added to one molecule and the delivery of that going into patients, it really changes the entire patient experience as well, and it can even change sort of the payer landscape on how we think about these expensive biologics in the future, but I think, you know, this platform enables us to double down on the future of the innovation here, and I think when you think about how to overcome the resistance of single agent or single payload ADCs, you can think about having a dual payload strategy, and that, I think could be very promising for us.
So we'd love to dive more into this, and we will. We're gonna have a research forum sometime this fall, we'll announce it, where we're gonna spend a lot of time unpacking STRO-004, previewing some of the other Exatecan warheads and molecules that we're developing, as well as talking about the platform innovation and where we see the field going. You know, when we started by saying controlled heterogeneity is ridiculous, you want a homogeneous molecule, now that's the industry trend. When we start saying, "Hey, maybe you can get a two-for-one punch in a homogeneous molecule," it's a very hard thing to do. We've demonstrated the ability to do it in terms of making these molecules. We've got good preclinical activity. We've got a partnership with Astellas on two programs that are iADCs.
We're continuing to innovate because the industry plays a lot of me-toos, and, you know, we wanna make certain that we're carving out great medicines for patients in unmet need, but we're also staying ahead of the rest of the industry. Big Pharma doesn't do these sorts of things. It takes a little company like Sutro to continually innovate and try and push the envelope, then they'll follow, and, you know, we'll see what happens, but for the time being, as long as we can keep pushing the industry ahead, it's gonna be great for patients, and it's gonna be great for Sutro and our investors.
Can you go into that a little bit more detail around iADCs? And just like, in terms of like, what that is and, you know, why it's interesting. And also after that, the collaboration piece-
Yeah.
Like you've been really good at that as well, so maybe you can just kind of lump that in, too.
Thanks. Yeah. So an immunostimulatory ADC is an antibody drug conjugate with one special and important feature, also site-specifically attached so that you can have it in a homogeneous molecule, is an immunostimulatory agent, like a toll-like receptor agonist, like a STING agonist, something like that, that is gonna amplify the immune system. Now, there are some companies that were pursuing things called ISACs. They were not iADCs. ISACs are just an immunostimulatory agent attached to an antibody. They had some issues, and this is a very difficult thing to do from a protein engineering standpoint. What is the right number of cytotoxics? What's the right cytotoxic that you want for this iADC? What's the right immunostimulatory agent? What are the right numbers? Ratio of immunostimulatory agents to cytotoxics, where do you put them on the molecule? Where do you optimize that?
So we've done a lot of work over the last three or four years to try to answer a bunch of those questions. A little over two years ago, we had sufficient data to persuade Astellas to do an almost $100 million dollar upfront deal with us, and it now covers two programs. We've not disclosed the targets yet, but they are moving forward robustly, and we're really pleased with the work that we're doing with Astellas. The whole notion is to preferentially target the iADC to the tumor microenvironment. The cytotoxic gets released and starts to kill the tumor cell. It'd be lovely if ADCs killed every cell, but they don't. And so, you know, you have to recover from the cytotoxic, and then you can be redosed again, and we're continually playing Whack-A-Mole with an iADC.
With an iADC, though, you've got an immunostimulatory molecule that is present in the tumor microenvironment, and it acts as a beacon to the immune system to say, "Hey, there's something here that you need to actually take care of and clean up," and so the ADC gives the initial signal. The beacon is the immunostimulatory agent, and the immune system actually is this one-two punch to get rid of the tumor cells. Now, the interesting thing about this, in preclinical models, we dosed mice that had been given a particular cancer line. We were able to rescue a bunch of those mice, so they did not show any more signs of tumor with the iADC. We let them live. Most people sack them at the end of an experiment like this.
We let them live, and then a month or two later, we rechallenged them with the same tumor cell line. The mice did not get the cancer to regenerate. There was an immunostimulatory effect that was lasting in a memory response. So if we're able to do that in people, it's almost like a personalized, individualized vaccine. Now, I don't claim that, you know, it's gonna be one and done, and you're cancer-free. But imagine if you could have that one, two effect in a very specific, site-specific, homogeneous molecule, and your time between therapies was not three weeks, but three months, six months, and you had this continual response. So that's what we're hoping to do, and we're really pleased with our relationship with Astellas.
We've demonstrated a lot of ability to excite the industry about what we can achieve with the design of our ADCs, iADCs, ADC squared, other things. As long as I've been CEO, partnering has been a core priority for us. Having our own pipeline is very important. Getting to the stage we are with Luvelta is very important, but you need other ideas, and you need other capital, and we've raised, since I joined in 2009, $1 billion. These are not Biobucks numbers. This is money in the bank, $1 billion from our partners through the years. $600 million we've also raised from public and private investors. You don't get $1 billion as a platform company unless you're actually doing something that is of value to the partner and of value to patients. It's just not something that's done.
So we will continually look at ways where we can leverage our technology platform to provide value for patients, to provide additional supplemental capital to us, that we can then use to advance our own internal pipeline. So that's in a business model sense. That's what I think is the right way to build a sustainable company with a leading-edge platform. Great. Well, maybe we'll leave it there. Bill, thanks so much. Okay. Thanks so much, and thank you all for being here. All right, cool. Good to see you.