Good afternoon from the 31st annual Credit Suisse Healthcare Conference. My name is Geoffrey Weiner. I'm from the U.S. Biotech team. It's my pleasure to introduce Sutro Biopharma and CEO Bill Newell. After the presentation, we'll go into a short Q&A session if time allows. Thank you for joining us today, and with that, you have the floor.
Thank you, Jeff, and thank you, Credit Suisse, for having us here today. It's my pleasure to be presenting Sutro Biopharma to you. In the course of my presentation today, I will be making some forward-looking statements. This slide tells you everything you need to know about the qualifications behind those forward-looking statements. For those of you who are unfamiliar with Sutro Biopharma, let me give you a broad overview. We have the world's only platform that produces large molecules in a cell-free protein synthesis manner. This is sometimes known as in vitro transcription and translation. The basic principles behind this approach were elucidated almost 50 years ago, but they were never reduced to practice until Sutro was founded in 2003.
Over the almost 20 years since founding, we've continued to perfect the system so that the technology is one that takes advantage of high science. It is industrialized from a research capacity standpoint, and it is robust in terms of its integration from research into the actual production of the molecules in our own cGMP manufacturing facility. It is transferable to other CDMO facilities for the production of the molecules. What do we do differently? Instead of using a cell to be the vehicle for producing the large molecule, and we focus predominantly on antibody-drug conjugates, but I'll talk about other applications, including a very exciting application in the vaccine field, pioneered by our spin-out Vaxcyte. We use our technology in a way different than others do.
Most people who produce antibody-drug conjugates use CHO cells to actually make the antibody, and then they have to do a conjugation chemistry to try to attach the linker and the warhead in a relatively heterogeneous fashion. We thought that was not the way to go about developing molecules, and so our technology allows us to think differently. What we've been able to do is we take a specially engineered E. coli cell line. We grow it up. We break the cells apart, just as you might do with a CHO cell when you wanted to pull out the protein of interest, and then we pull out the ribosomal machinery that does in vitro transcription and translation. With that, we call that an extract. With that extract, we can then run a protein synthesis reaction in less than 24 hours.
We can make many variants of molecules in a way that no one else has the technological capability to do so. Why do we have partnerships with Merck, with Bristol Myers Squibb, with EMD Serono, and with Astellas? We have partnerships with all of those companies because they know that we are uniquely enabling them to achieve best-in-class molecules that have high interest for them. I'll talk a little bit about those collaborations in a minute. We also realized that our technology was capable of not just making antibody-drug conjugates, but other different modalities, and so we ended up spinning out a company. Originally, it was called SutroVax. Today, it's called Vaxcyte. It's publicly traded. Vaxcyte has been using our technology in order to make the next-generation pneumococcal conjugate vaccine.
It's a 24-valent vaccine, meaning it helps protect against 24 different types of pneumonia that you might be exposed to. They've also been developing a vaccine they call VAX-XP, which now will go beyond 24 to 31 different serotypes that will be protected against. This is a great application of our platform technology, and one of the questions that people were asking us about is, "Well, if you're the only ones in the world, how do we know that it works?" The answer is now being revealed. We have data for our STRO-002 ovarian cancer drug that was released earlier this year, and I will share that with you, giving the first signs that the technology platform that we have actually produces best-in-class molecules. Vaxcyte turned over a card in the last few weeks where they showed tremendous results with their 24-valent pneumococcal conjugate vaccine.
In that case, it is non-inferior to all 20 serotypes of that are in Prevnar 20 and better than the other 4 serotypes that are covered by Pneumovax. This was a significant accomplishment for them, and they are well on their way to becoming the company that we envisioned they would be when we spun them out in 2013. We have a strong relationship with them. Their product candidates would not exist but for our technology platform, and we provide them with the extract and the reagents that allow them to make the molecule. As a consequence of that, we have a 4% royalty on each and every product that they make.
I don't think people really appreciate the value of that, but believe me, when the company was spun out, and we saw the potential, I knew that the value of a 4% royalty for the sort of vaccines that they were gonna go after would be extremely important to our investors in the long run. I wanna congratulate Vaxcyte on the success that they've had. That's one example of where the technology has demonstrated itself. In another, this will be discussed more at ASH, in a very rare form of pediatric AML that is caused by an oncogenic fusion, the abstract that was just released indicates that in 16 pediatric patients, these are infants and toddlers who had been relapsed from treatment or refractory to treatment.
We achieved 7 complete remissions in treating these kids on a compassionate use basis. 6 of those were MRD-negative. That's stunning results for this very devastating form of pediatric AML, and the drug was well-tolerated. There are two instances there, and if you need a third, we'll talk about STRO-002 and STRO-003 in a moment. This next slide really lists our pipeline. When you ask, is the pipeline, is the platform technology prolific? I think you would have to conclude from this slide that in fact it is. Beginning in 2018, we or our partners have since that time point, put 6 product candidates into clinical development, and all of those product candidates are still in clinical development today.
Our lead program, STRO-002, folate receptor alpha-targeting antibody-drug conjugate, is one I will talk a lot more about today, so please bear with me. I'm gonna jump past that one in a second. Our second proprietary asset, STRO-001, is for B-cell malignancies. Namely, we are going after multiple myeloma and non-Hodgkin's lymphoma. That molecule has been in development, in phase I development for a while, and I'm pleased that our partner, BioNova, has an open IND, and they will be pursuing the development of this molecule in the Greater China market. We're going to be leveraging their development expertise, their development infrastructure to really further elucidate the value of STRO-001. We have a tremendous relationship with Bristol Myers Squibb on a very exciting molecule, CC-99712.
For those of you who are familiar with the BCMA space, there's been a lot of promise for multiple myeloma patients for these new and emerging BCMA therapies. There are CAR Ts, there are bispecifics, and there is an ADC. The bispecifics and the CAR Ts really are limited to settings in which you can have very significant supportive care, like an academic medical center. They're not practical for use in a normal community oncology setting where these patients are mostly treated. A well-behaved antibody drug conjugate, however, is such a therapy that can really be a dominant force in the multiple myeloma landscape, and Bristol understands this. The primary competitor for this molecule today is a drug developed by GSK, and that drug, while it got accelerated approval, has substantial ocular toxicity that really limits the therapeutic benefit of that drug.
Most recently, they failed a confirmatory trial, and so the landscape is wide open for our BCMA ADC to move forward and become best in class. Bristol is pursuing this aggressively, both as a monotherapy and in combination with their own proprietary gamma-secretase inhibitor. You'll see on this slide a relationship with Merck. It's an IL-2 derivative molecule that we created in collaboration with them, and they are advancing it both as monotherapy and in combination with Keytruda. It is not a me-too of something because many of the things that have been trying to be used in combination with checkpoint inhibitors have failed. This is a molecule designed by us and Merck using our technology, and it gives them exclusively the type of molecule they wanted to take into the clinic. We're waiting on that.
We also used our technology to develop a bispecific antibody drug conjugate, where we took the bispecific approach that many do, although we've got a unique one enabled by our partner, EMD Serono, and we added a drug conjugate to it in appropriate places. Now we're pursuing that. It's a MUC1/EGFR bispecific ADC. We're pursuing that in solid tumors. They are in control of that development plan, and we're excited and looking forward to data from them in that program as well. We also have our next up-and-coming asset, STRO-003. It's a ROR1-targeting antibody drug conjugate. ROR1 has shown great promise in hematologic malignancies. Others have been demonstrating good clinical outcomes in that form of cancer.
The real promise for this molecule is in solid tumors, and we're aggressively moving this forward to the clinic as our third program proprietary, and we'll be pursuing it in the solid tumor space. I did mention Vaxcyte, so I wanna just say, I hope they continue to have the success that they so richly deserve from all the investment that they've made. Certainly, Sutro and our platform technology are well known in the industry. That's why we have the deals that we have, and that's why Vaxcyte has so many eyes on them at this point in time. Here's a list of our achievements and our milestones this year. We're still working forward to checking all of these boxes, but we've made substantial progress in moving our assets forward.
In particular, we're going to be reporting by the end of this year data on our dose expansion study. It'll be a final analysis or near final analysis of the 44 patients that are in that study. I'll talk more about that in coming slides. We're excited to do the presentation at ASH, where we talk about this pediatric AML opportunity. I think the data will be viewed very favorably by the pediatric oncology community, and we're excited for these patients because getting to a complete remission when you've been relapsed or refractory in this very aggressive form of AML is a sign of hope for their families. Let's talk about our lead asset, STRO-002. This is a site-specific, homogeneously designed antibody-drug conjugate that we profiled against a benchmark that was designed to mimic the properties of another folate receptor antibody-drug conjugate, mirvetuximab, from ImmunoGen.
Preclinically, we wanted to establish that several things matter. One, that a site-specific approach produces a better outcome, a better tolerability, and hopefully no ocular toxicity, that you see with a heterogeneous mixture and certainly is a hallmark of data sets that ImmunoGen has produced to date. Secondly, we wanted something that gave a wide therapeutic window, and as you will see, we started seeing responses at 2.9 mg per kg all the way up through the 6 mg per kg and 6.4 mg per kg dose. We've got a level of responsiveness that allows us to do dose optimization. Three, we wanted to make a molecule that could benefit a larger patient population of platinum-resistant ovarian cancer patients than were presently being served by other drugs in development, and we've delivered on all of these things.
We did a study that started in 2019 with dose escalation, where we tried to understand that therapeutic window. Once we understood that we had activity at 2.9 mg/kg in a very advanced patient population that had not been preselected for any level of folate receptor expression. Some could have a high degree of expression, some could have low to none. We weren't selecting. We saw activity in multiple different categories of patients who had different expression levels, and we wanted to explore that. We did a dose expansion study, which started in January 2021. In that study, we looked at 44 patients, and we completed enrollment of the 44th patient in November of last year.
Looking at those 44 patients, we then divided them between two dose levels on a random basis to try to understand the optimal starting dose, 5.2 versus 4.3, well within the range where we saw activity in dose escalation. We also decided to ask the question, "What's the right patient for our drug?" We collected tissue samples to understand if expression levels correlated with responsiveness. In January of this year, we presented some initial data on 33 of those 44 patients, and I'm pleased to report that we started to see things that were very encouraging in terms of what is our pivotal trial going to look like, what patients should we be including, and how should we be dosing them. This is a little bit of the patient characteristics. Let's get into the data.
We saw substantial number of responses at 5.2 and at 4.3 mg per kg. We also saw good disease control, but it did appear that at the end of the day, based on the interim data that we had, a 5.2 mg per kg starting dose was more likely to lead to a higher response rate. As you see from this slide, we were able to achieve 8 PRs at the 5.2 mg per kg dose range, again, regardless of expression levels, versus 3 at 4.3 mg per kg. Overall, if you look at the two doses combined, we had a very robust 33% response rate based on this interim data.
As I said, it was not only starting dose that we were interested in, but we also wanted to look at the folate receptor alpha expression. Here's a spider plot, by the way, that shows visually what the data suggests notionally, that if you start at 5.2, you have a much faster response, and it gets deeper more quickly than if you start at 4.3. The swimmer plot also shows that you can continue on a dose that is lower than your starting dose and still have an ongoing response. That's encouraging because we wanna optimize the dosing for each patient so that they get a regular treatment every 3 weeks. That's important for maintaining disease control as opposed to having to go off treatment for an extended period of time.
This is a visual example of one patient who derives substantial benefit even at the 4.3 mg per kg dose with a 72% reduction in her tumor burden. Clearly, we have an active drug, and the question then is, what's the right starting dose? What's the right patient population? When we looked at scoring algorithms to determine the right patient population, we came to understand that if you look at Tumor Proportion Score, which is used for PD-L1 screening as well, you look at the number of cells on a slide, you count the number of cells on a slide, that's the denominator, and the numerator is the number of cells that stain positive regardless of intensity. So it's a very simple percentage, and it's a simple thing for pathologists to do.
When you look at the TPS scores, what you see is that if your TPS score was above 25%, again, regardless of dose, you had a 40% chance of responding. If your TPS score was 25% or less, that response rate drops down to 12.5%. Clearly, we're seeing a signal that you need to have some minimum threshold in order to optimize the activity as a monotherapy. If you put the two questions we were asking together and say at the higher starting dose of 5.2 mg/kg and at those patients who had a TPS score greater than 25%, what's the response rate? Well, it jumps all the way up to 54%. That's a really encouraging response rate and gives us our first clues that we have a best-in-class opportunity with this molecule.
I should add that the fact that you're looking at patients who have a greater than 25% TPS score will also give you an opportunity now to treat, we believe, 70%-80% of the platinum-resistant ovarian cancer patient population, almost double the patient population that mirvetuximab has available to it. The drug was generally well-tolerated. 85% of the treatment-emergent adverse events were Grade 1 or 2. There is incidence of neutropenia. It is not febrile neutropenia, importantly. Even though it is a significant percentage, it's important to remember that it was asymptomatic to the patient and that it generally resolves within 1 week.
If you were on a 3-week dosing schedule and you were found to be neutropenic before your next dose, you were sent home for a week, come back a week later, you had recovered, and you could go on with your treatment without any significant delay. I think the last thing I wanna say about this is physicians are very used to managing neutropenia. We've been looking at this data, trying to understand in the final data set how we can best manage neutropenia, and I look forward to talking about that as we get to our data set this presentation later this year. Here we know we've got a drug that in all comers at all dose levels delivers 33% efficacy.
When you find the right dose and you find the right intensity of staining, you can jump that number to 54%, and the safety signals are solid. We have a molecule that we're excited to continue to move forward in clinical development. This is our strategy. In order to think about this both as a monotherapy and a combination therapy, we've initiated a study with bevacizumab, and I expect that we'll have data from that study next year to talk about how the combination works. We've also started an endometrial cohort, and I believe we'll have data in that next year as well, and we're looking carefully at non-small cell lung cancer. For us, the question as we present the data is what comes next?
Well, we've had a very important regulatory conversation with FDA, where we understand that our next study could be a registration-directed trial with a potential for accelerated approval. We'll be talking about those FDA discussions as well as our next clinical trial design at the same time that we present our data on the dose expansion trial. We've got an emerging research portfolio. As I mentioned, our next molecule is a ROR1-targeting ADC. We're using a next-generation linker, a beta-glucuronidase linker that we think is really going to be proven in the clinic to be a superior linker in terms of maintaining stability and not allowing it to be cleaved prematurely. You want it cleaved in the tumor microenvironment. We're using a very exciting class of warhead that has been pioneered by Daiichi, the exatecan class of warhead.
This is a DAR 8, and it was designed to have superior clinical performance. A number of the other ROR1 targeting ADCs do not use the most recent linkers and warheads, and we are excited to see how this performs once it gets into the clinic. What we know is that it has good activity even in low expressing tumor models as well as in those models where there is heterogeneous ROR1 antigen expression. What we know is it has a wide safety window, and we're really thrilled to see that you have no impact on white blood cell counts in non-human primates up to 45 mgs per kg. We know that when you compare it to a current linker, a cathepsin B linker, which many people use, you find incidences of pneumonitis in non-human primates at the higher dose levels, and that's certainly a concern.
What we know is the beta-glucuronidase linker with this warhead does not show that toxicity. We're very encouraged by this and looking forward to moving it into the clinic. In addition, in July, we held a research forum where we talked about our exciting portfolio of earlier stage opportunities. If you go on our website, you'll learn more about why we're interested in tissue factor, PTK7, LIV-1, and the other targets that are shown here. Stay tuned. Sutro is a platform technology that continues to deliver best-in-class product candidate opportunities, and we're excited to continue to move forward. Most importantly, this summer, we announced a major collaboration with Astellas in the immunostimulatory ADC field.
We're taking our site-specific homogeneous ADC technology and amping it up one more level by attaching an immunostimulatory agent to it to give the tumor a one-two punch that really involves the immune system as the sweeper, if you will, that's going to take care of whatever remaining antigen is out there. This is an important relationship for Sutro. We got $90 million up front for a three-target deal. They cover our research costs in moving this forward. We have $422 million in milestones per product opportunity. That's about $1.26 billion in total. We have an option to share costs and profits in the U.S. This is an exciting next-generation approach. Only our platform technology enables an approach like this. As I mentioned, we also have a ROR1 targeting ADC. It is also a site-specific molecule.
It is an earlier generation. It relies on a DAR2 in order to be more sparing of the bone marrow as it attacks the B-cell malignancies. We had a good initial study, moving up through dose escalation, and the drug was extremely well-tolerated. We did see some initial responses, including one complete response. I will say this is a competitive landscape, and it's difficult to recruit patients in the United States, so we're thrilled that our partner, BioNova, is going to be continuing to progress this in the clinic, by themselves, and we will be able to access that data. This is a difficult financing market.
Everybody knows that it has been for a while, and we've been able to use the optionality that our platform has conferred on us to have a strong financial footing to continue to pursue the development of STRO-002 and our other molecules. At the end of the quarter, we announced yesterday, we had $287 million in cash. That does not include the value of the shares of Vaxcyte that we have, nor does it take any account of the fact that we have a 4% royalty on each and every product that Vaxcyte makes. I'm quite confident that that 4% royalty will be something of interest to people who are interested in acquiring royalties, but we'll make the right decision about that at the right time for the right value. That's not included in our projections here.
We are projecting runway into the first half of 2024, but there are many other ways that we are pursuing the value that our platform has created to give us that optionality to find ways to finance the company other than going to the capital markets. If you look at our financing history, you'll see that we don't go every year because we don't have to. We've got a great team, very experienced in drug discovery and development, and we're excited to move our company forward in all of the ways that we've talked about today. Thank you for your attention. I appreciate your interest in Sutro, and I'm excited about what we're gonna be talking about at the end of this year, and I'm excited for 2023. With that, Geoffrey, I think we can take questions.
Thank you. So to s tart off with questions. Could you just put the STRO-002 data into the context of what's been seen with other competing ADC programs in ovarian cancer and m aybe what the current clinical standard of care is?
Yeah. I think clinical standard of care for these platinum-resistant ovarian patients is really chemotherapy at this point in time. Chemotherapy has about a 12% response rate. Now, remember I talked about 33% in all comers and 54% when you get the dose and the patient selection strategy right, so we're well above that. The durability is relatively light, even for chemotherapy. It's about three and a half months duration of response. We do not have sufficient durability at the time of the interim data analysis in order to actually present that data. We will be talking about durability for patients who did respond in the dose expansion trial, as well as the median progression-free survival number so that people can understand the full disease control that we've seen in this dose expansion study.
For other agents that are out there, they address a much smaller patient segment than what we're talking about. Whether they will become standard of care or not is still uncertain at this point in time. The fact of the matter is, having a 54% or anything north of 30 is a really good, strong competitive signal, particularly when you don't have ocular toxicity, which can cause treatment delays that are much more significant than what we experience with patients who are treated with STRO-002.
Great. Thank you. With that, it looks like we've come to the end of our session. Thanks again to Sutro and the team for joining us today.
Thank you.