J.P. Morgan Healthcare Conference. My name is Matt Bannon. I'm a healthcare banker here at JPM. I'm really excited to be setting the stage for our next presenting company, Sutro Biopharma. Presenting on behalf of Sutro, we have CEO, Bill Newell.
Thank you, Matt, thank you to J.P. Morgan for giving us the opportunity to help you all close out the conference this year. I'm Bill Newell. I'm the CEO of Sutro Biopharma. As you might imagine, in my discussions today with you, we're gonna make some forward-looking statements, and our legal team appreciates it if you would pay attention to this slide because it indicates things that you need to know about those forward-looking statements. When I first came to Sutro in 2009, I was the 19th employee. We had a novel proprietary cell-free protein synthesis platform. It was unique, and it was a long way away from being where we are today. Today, we have six programs using our technology that are in clinical development and a number more that are on the way.
Cell-free protein synthesis is a unique way of making molecules that are homogeneous so that you can understand structure-activity relationship in a way that is unprecedented in the biological therapeutic field. We have been working on this technology since 2003 when the company was formed, and we today have a GMP manufacturing facility. This is high science. It is industrialized and roboticized for research purposes. It is integrated from research all the way through to manufacturing. And we are really excited that we're now starting to see data in people that prove that we have the opportunity to create best-in-class molecules. Ordinarily, I would start out talking about our exciting programs, but I'm actually going to give a shout-out to a company we spun out. It used to be called SutroVax. Today, it's called Vaxcyte. They had some amazing data using our technology.
We supply them extract and reagents. They produced a 24 valent pneumococcal conjugate vaccine that had outstanding phase I, II data. We're thrilled that they were able to use our technology to create such an important next-generation vaccine candidate to protect against pneumonia in a way that no other molecule does today. We still own a number of shares of Vaxcyte, and we have a 4% royalty on every product that they produce. I'll talk a little bit more about them in a minute. Now I'm gonna go to our platform. We now have established the opportunity for a best-in-class ovarian cancer therapy. This is our molecule. We used to call it STRO-002, but now I'm gonna talk to you about it as Luvelta. It targets folate receptor alpha, a very well-validated target for ovarian cancer patients.
We have important and definitive dose expansion data that I will be sharing with you as we go through the course of our conversation today. It is proprietary. We have all of the rights except the rights in Greater China, which we've partnered with our partner, Tasly. I'm very excited that we're now on the cusp of being able to demonstrate that we can really benefit women who have a really awful disease in ovarian cancer. Importantly, we also have the opportunity to benefit with the same molecule, a pediatric patient population that has a devastating form of AML, and I'll talk briefly about that as well. You will see here a number of partnered programs as well. Bristol Myers Squibb, Merck, Astellas, EMD Serono.
These are all fundamentally broad and important relationships where these companies came to us to ask us to do something that they were unable to do given all of their research prowess. I'm excited to say that for Bristol, we have a BCMA ADC that is in clinical development with them. With Merck, we have an IL-2 derivative in clinical development with them. With EMD Serono, we have a MUC1- EGFR bispecific antibody drug conjugate in clinical development with them. With Astellas, we have a very exciting immunostimulatory ADC research collaboration that I will talk more about in a little bit. We ended last year with a bang. We did a little deal with our company, Vaxcyte, the former, our spin-out.
One of the things that we had always said to our partners, whether it's Vaxcyte, Merck, Bristol, whomever, the secret to our ability to deliver these best-in-class molecules lies in the cell-free protein synthesis technology that we have. And we do not license that technology out. The ability to make that extract that is the core to that technology we keep as a proprietary asset for us, much the way that Coca-Cola keeps Coke® syrup as a proprietary formula for them. Our friends at Vaxcyte made a compelling case to us that as they look forward to a really substantial commercial opportunity, they should make certain that their supply chain has security.
So, they were willing to offer us a deal that equates to about $157.5 million in order to have the right to acquire, extract knowledge so that they could make it for their products. We thought long and hard about it and decided that we would do that. It's structured in a way that gives us twenty-two and a half million dollars initially, then the remainder would be paid over time. Importantly, if they were to be acquired, a number of those payments would accelerate, the option exercise period would shorten, and if it were exercised, we would receive $120 million on exercise. We started this year, earlier this week, by presenting our dose expansion data, which I'm very excited about. We'll talk about that in a minute.
We are on the path to starting a pivotal phase II, III registration-directed study. We call this study REFRαME. I will just detail that for you in a moment. I mentioned the acute myeloid leukemia opportunity for us. I'll pause here for a second. If you had a chance to go to ASH, you would have heard about this application of our drug in this CBFA2T3-GLIS2 rare phenotype. Through some work done in collaboration with Fred Hutch, we were in a position to understand that folate receptor alpha is highly overexpressed for patients who suffer from this very serious form of AML. It is highly refractory to current AML therapies. These children who are identified at the ages of six months to two or three years have a very poor prognosis. They blow through current and conventional AML therapy quite quickly.
We were asked if we would give compassionate use of our drug to these families, and we did. We had 17 patients who were treated with our drug. Of those 17 patients, we had eight complete remissions, and these are patients who are relapsed and refractory to prior therapies. Of those eight, seven were MRD negative. There was no residual disease detectable. That's an important breakthrough. We're excited about it, and we're gonna be talking with FDA about how we can advance that in a rational, small clinical development program that could make this the first approval for STRO-002 in the United States. Of course, we're also looking at ways to expand the market opportunity for STRO-002. We're studying STRO-002 in ovarian cancer. Now I'll shift to Luvelta, so I get used to saying that.
We gonna study, we are studying L uvelta in combination therapy with bevacizumab, and we're looking to move forward with Luvelta in non-small cell lung cancer once we have an appropriate methodology for identifying the right subset of patients with non-small cell lung cancer for whom this therapy is most appropriate. We have our own other proprietary assets that are moving forward. I wanna talk a little bit about our ROR1 ADC later today, but it is in IND-enabling studies as we speak, and we look forward to having it enter the clinic in the first quarter of 2024. Here's the full name of STRO-002, Luveltamab- tazevibulin. I'm gonna refer to it as Luvelta as we move forward. I don't need to tell this audience that ovarian cancer needs newer and better therapies. You know that.
We set out on this journey back in 2017 or so because we felt like the approach that was being taken to address ovarian cancer was a misguided approach. Molecules that were in clinical development at that point in time were insufficient to demonstrate safety and efficacy in a manner that these women really need. We moved forward in a very unique fashion to develop a better molecule. We thought the target was good. Folate Receptor Alpha is now well-validated, and we thought we could design a better molecule. This is a targeted antibody that has a drug-to-antibody ratio of four. We use what was then really sound linker. It's a cleavable linker, a Val-Cit-cathepsin B cleavable linker. We had a hemiasterlin warhead, which is a tubulin inhibitor.
Our research team designed this molecule with precision. They designed it to be more potent than other therapies that were in clinical development at that time. They designed it in a way to minimize the bystander effect. Once the molecule had done its job, it was cleared quickly. We thought that was going to contribute to a better therapeutic window and a better safety profile for patients who were suffering from ovarian cancer. When that molecule was ready for clinical development in 2019, we started with a dose escalation cohort. We started to see activity at 2.9 mgs per kg.
We studied it all the way up to 6.4 mgs per kg and understood the profile of that molecule to be one that while it was effective, even at the higher doses, the tolerability profile was not what we were interested in. We then started a dose expansion cohort of two more intermediate doses, 5.2 MIGS/kg and 4.3 MIGS/kg . We had three objectives when we started the dose expansion study, and we had reported on the dose expansion data about a year ago on an interim basis. Objective one, what's the right patient population for this molecule?
We believe this molecule can benefit all women who have platinum-resistant ovarian cancer. It will benefit some more than others. We wanted to identify those women who would receive the most benefit from our molecule. The second thing we wanted to do was we wanted to understand, at these intermediate doses, what was the right dose that had the most benefit for patients and had the best safety profile? The third thing we wanted to do is make sure that we completely understood the safety profile. Many molecules, particularly ADCs, contribute to ocular toxicity. We hadn't seen that in our dose escalation. We wanted to ensure that for women who were treated on a regular basis that we thought were the best, most optimal therapeutic doses, we were not seeing ocular toxicity. We designed this trial to bring in 44 patients.
They were randomized between 5.2 MIGS/kg and 4.3 MIGS/ kg. And we thought about the cutoff. Is there an enrichment strategy that makes the most sense? There are various ways that one can look at the expression of folate receptor alpha. Some companies use what's called a pS2+ scoring algorithm. That's a scoring algorithm that is used to identify the highest of the high expressers, about 35% of the overall platinum-resistant ovarian cancer population. We had seen activity in patients who are not the highest of the high expressers during dose escalation. So we looked at a different scoring algorithm, one called a tumor proportion score. It's a pretty simple algorithm. Using an IHC assay, in fact, the same one that been advanced into regulatory approval by one of our competitors.
You look at the percentage of cells on a slide that's stained positive for the target over the total number of cells that are in that slide., and y ou have a score. It's gonna be it could be zero or one, it could be 100, but somewhere in 0-100 is what the score is. We felt that we had understood from the interim data that the Tumor Proportion Score correlating with above 25% produced the best outcome for this patient population. You'll see me demonstrating why we've now concluded that that is in fact right, and we're gonna talk about those patients who are folate receptor alpha selected, meaning their Tumor Proportion Score is greater than 25%. The other thing we did was we decided that one of the safety signals that we had seen was neutropenia.
This is transient, generally goes away within a week to 10 days. It is asymptomatic to the patient. Very few cases of febrile neutropenia, still something that could potentially pose a safety risk. We began to study the higher dose, 5.2 MIGS/ kg, in 15 patients with a prophylactic approach to managing the neutropenia using pegfilgrastim. I'll talk about the outcome there, not to bury the headline, we've got a way to manage neutropenia dramatically down. Let's get into the data for Luvelta. I said originally that what we wanted to do was identify the right patient population, and in fact, we have.
You look in the middle panel, you will see that patients who have a TPS, tumor proportion score, of less than or equal to 25% in the light yellow shading, have a response rate of only 11%. If you look just to the left, there's a gray panel that reflects all patients who are folate receptor alpha selected and have a tumor proportion score greater than 25%, irrespective of which dose they were given. That ORR is 37.5%. We have a median duration of response of 5.5 months, which is very clinically relevant and meaningful, and we have a median PFS in that group of 6.1 months. Again, much more relevant and clinically significant than standard of care therapy that would be available to these women.
So now we know for certain that a Tumor Proportion Score above 25% gives us the right patient population. We've answered that question. Next question, what's the right dose? If you look at the far right panel, what you will see is that at the starting dose of 5.2 MIGS/ kg, 43.8% of patients achieved a partial response that was confirmed. They had a 5.4-month median duration of response and an impressive 6.6-month progression-free survival. If you were at 4.3 MIGS/ kg, you did well too. You had a 31.3% response rate, which is comparable to our competitor's response rate in their minor population is 35% or so of the platinum-resistant cancer patient population. We had a duration of response that is impressive in the number 13.
We think it's probably not 13, but nonetheless that's a good starting point for it, and it has a median PFS, again, in the six-month range, 6.1 months. It looks like 5.2 milligrams per kilogram is a better dose. You do see higher neutropenia levels that are grade 3 or grade 4. We'll talk about how we manage those, as I alluded to previously. If you wonder as to whether these stats were driven by patients who are higher expressers, you see in the middle category that regardless of dose, starting dose level, if you had a TPS greater than 75%, you had a 40% response rate. That's a pretty good response rate. If you were between 25% and 75%, you had a 33.3% response rate, also quite respectable, and this is irrespective of dose.
Durability and PFS were strong in both of these cohorts. What do I conclude from all of this? We have a drug. We have a patient population, which by the way represents about 80% of the platinum-resistant ovarian cancer patients, and we now have a way to manage neutropenia, which I'll talk about in a minute. This is the waterfall plot that everybody shows. I'm gonna make a few comments about it. I'm going to start with the fact that regardless of dose, over 80% of patients achieve disease control, and that's what we're looking for. For regulatory approval, we need to see response rates that are substantial, and we have them.
We need to see good durability that's clinically relevant, we have that, we need a safety profile that makes sense given the responses that you're seeing and the durability that you're seeing, we have that. Importantly, though, many women do not achieve a response. Our competitors, case 7 0% of women don't respond. For those women, can you actually give them benefit? The answer is, with Luvelta, we can. So, as you look at this waterfall or this waterfall plot, you will see, as I said, disease control rate of 81.3% across the board. When you look at the patients who responded, and we have a dozen of them in this folate receptor alpha-selected population, you see that there are some significant tumor shrinkage and disease control.
You see by the scores at the bottom of this waterfall plot that it wasn't just the highest of the high who benefited from Luvelta. They are patients not eligible for our competitor's drug in the lighter yellow shading who had strong responses, and yet they would not have been otherwise eligible for therapy beyond chemotherapy. This is the swimmer's plot that people show as well. We've divided the swimmer's plot into two dose groups, the starting growth dose of 5.2 and the next dose of 4.3. The orange dots represent the first onset of a response. What you see in 5.2 is that patients who are going to respond responded at about the six-week mark, which is the end of two cycles.
That's a very rapid response, and for women who've had 1-3 prior regimens, it's impressive to see their disease control that quickly. For patients who started at 4.3, they too achieved responses. It just took longer, about twice as long. It took almost 11 weeks to achieve those responses compared to six for 5.2. For 5.2, we do see faster disease control, and that's something that's exciting for patients and for their physicians. We also see that even though these doses might not be maintained but are subject to dose adjustments as the patient continues with their course of therapy, we are able to maintain those responses, and a number of these responses are long-lived. Importantly, for patients who did not respond, they still achieved substantial disease control for clinically meaningful periods of time, and that translates into our PFS.
As you look at the summary of dose modification data, you can see that there was more dose delay and dose reduction at the 5.2 MIGS/ kg level. This was largely driven by the neutropenia that we were seeing that I've alluded to. Let's talk about Cohort C and what we learned about how to manage neutropenia. We enrolled 15 patients towards the end of last year. We had a data cutoff at December 8, and we had access to about 10 of those 15 patients who had completed a cycle and were continuing with their treatment. They were all started at 5.2 milligrams per kilogram on a Q3W cycle. On day eight after the initial dosing, they were treated prophylactically with pegfilgrastim.
That day was chosen based on the timing of the onset of the neutropenia and really the maximum benefit from the pegfilgrastim within the context of a Q3W cycle. If you looked at the women who were in the dose expansion cohort, you would see that 66% of them had a grade 3 or higher neutropenia score at the first cycle. Using this approach of prophylactic pegfilgrastim, we were able to reduce that dramatically by 85% so that only one in ten had a grade 3 or higher neutropenia score. Dose delays at cycle 2 were meaningfully reduced as well. 76% in the dose expansion cohort at 5.2 mgs per kg experienced a dose delay of about 10 days. That was reduced 60% to a 30% rate.
Our major liability has now been demonstrated to be able to be controlled with a short course of prophylactic pegfilgrastim. What are the other treatment emergent adverse events? This table shows them. We had previously presented a very similar table about a year ago when we presented our safety data at the interim data look. We've talked about neutropenia. Arthralgia, a little bone pain, was the second most common grade 3 event and the second most treatment emergent adverse event leading to dose reduction. As I've indicated, even if you are dose adjusted, you can maintain your disease control and your response can be maintained. There were some other significant grade 3 treatment emergent adverse events that were unrelated to study drug. I will note in particular, there were no meaningful drug-related ocular or lung adverse events.
I think our risk of a black box is pretty close to zero for ocular events. What have we got in this drug? We have a drug that has the potential to treat 80% of women who have platinum-resistant ovarian cancer. We've demonstrated best-in-class efficacy at a minimum of 31%, but perhaps as much as 44%. We have a manageable safety profile and even at the higher dose level, which we think is the better dose to move forward, but we'll have to demonstrate that a little bit further. We can control higher grade neutropenia with prophylactic pegfilgrastim. How are we going to move forward? The Luvelta phase II, III clinical trial design is right here. This is a study we're calling REFRαME.
It is an integrated design that is the result of our data set and our conversation with FDA as to our data and our conversation with clinical and regulatory advisors. This is the most cost-effective, most efficient trial design that leads to the most rapid opportunity for both Accelerated Approval and for full approval. We looked at a variety of other trial designs. This one is the best. Some of you have heard of Project Optimus. This is FDA's initiative to make sure that we are no longer following the old cancer treatment paradigm of dose the heck out of the patient, give them as much as they can tolerate, and hope that that does the job. In fact, FDA is of the mind, and they're probably right, that sometimes that's not the optimal way to treat the patient.
So. Qhat they are looking to see is the most tolerable, lowest effective dose. We had done work, as I said, randomizing between 5.2 and 4.3. We know that from that data set, we think 5.2 is the optimal dose to move forward with, but the FDA felt that we should have some additional data to validate that. We will start this study in the second quarter of this year with a lead-in dose selection cohort of 50 patients. 25 will be treated at 5.2 milligrams per kilogram, this time with prophylactic pegfilgrastim on day eight for the first two cycles. Because we know they can be dose reduced safely and continue to respond, we will dose reduce them to 4.3 MIGS/ kg.
The other arm will be a Cohort B of 4.3 milligrams per kilogram, just as we had in the dose expansion cohort. These will be platinum-resistant ovarian cancer patients who have previously been pretreated with bevacizumab, 1- 3 prior lines. This will be our folate receptor alpha selected patient population. When we get to patient 51, we will then convert this study into a Part 2 randomized study. We will continue both Cohort A and Cohort B until we've reached agreement with FDA that following Project Optimus, 1 of these 2 doses is the right dose for us to be studying against standard of care chemotherapy. Patient 51 and forward will be randomized between Cohort A, Cohort B, and standard of care chemotherapy. When we reach the conclusion with FDA, we will drop the arm that is not going to be going forward.
So we'll be down to our selected dose regimen versus standard of care. When we have 110 patients worth of data on the selected Luvelta arm, and that includes the 25 patients that were in Cohort A, we'll have an opportunity to take a look at the data set. There will be a very small adjustment to our alpha as a result of doing that, and we have the opportunity then to file for accelerated approval. FDA suggested that this might be an optimal way to proceed with this next stage of development, and we agree with that. We will be looking at the overall response rate of the Luvelta arm. Of course, the response rates we've demonstrated look much better than standard of care chemotherapy.
We'll be looking at whether the durability of those responses are clinically meaningful, and today we know they are based on the data that we've just generated. Obviously, safety will play a part, and we expect, as I said, to have controlled the highest grades of neutropenia at the higher doses. We will, as I say, continue enrolling until we get to a total of 160 patients in each of the standard of care cohort and the selected cohort. In this case, it will only be those patients who started enrolling at patient 51. The endpoint for full approval will be progression-free survival. This will be powered at an 80% level with a hazard ratio of 0.72.
As I said. We believe this study design is the most efficient, cost-effective study design that we can envision for Luvelta. We're excited to get going in the coming months. So we have a lot of commercial opportunity for this molecule now that we know what the profile of it is. The size of the platinum-resistant ovarian cancer patient population right now is about 4,000 patients per year if you're folate receptor alpha selected. Endometrial cancer has a much more significant incidence. As we continue our study design of that, we're looking forward to really understanding if we can broaden the indication to include endometrial cancer patients. I talked briefly about this CBFA2T3-GLIS2, sometimes called the RAM phenotype. We have Orphan Drug Designation for this application of Luvelta. We also have Rare Pediatric Disease program designation for this molecule, for this patient population.
We will be discussing with FDA shortly the registration path. Given the small number of patients who are out there, we expect this to be a very quick clinical trial with an outcome that we think has a good probability of success. We're going to continue to look at non-small cell lung cancer and see if there's a subpatient population for which folate receptor alpha Luvelta is an appropriate therapy, and then we have combination therapy, as I indicated before. You'll see that combination therapy data in the second half of this year. Now, a lot of companies would stop there, but we have a lot more going on, and I want to talk to you a little bit about our emerging research portfolio. The next molecule we're gonna move forward into clinical development is our ROR1-targeting antibody-drug conjugate.
We've learned a lot through the years that we've been working on ADCs. You'll see that we are at the cutting edge of new technologies all the time. We pioneered the view that a homogeneous molecule was gonna be better than a heterogeneous mixture. We made it clear that not all homogeneous molecules were created equal, but it was important that you had the right homogeneous molecule with the right sites of attachment, the right linker, the right payload, the right drug antibody ratio, and STRO-002 demonstrates that in comparison to our competitor's molecule. For STRO-003, we didn't stop and rest on the laurels of what we've done before. We kept inventing. Now we're using what we believe is the newest class of linker that has the most stability until you get into the tumor microenvironment.
It's the β-glucuronidase linker, we're very excited about how much more protective it can be in the context of preventing premature release of the warhead. We're also going beyond the maytansinoid and hemiasterlin warheads that we've used previously, going to the topoisomerase inhibitor class and exatecan warhead. This molecule has performed extremely well pre-clinically. The safety profile is really very nice, if you'd like to learn a lot more about this program, more than I can say today, please go on our website. You will hear Dr. Trevor Hallam, our President of Research and Chief Scientific Officer, in July, give a research forum describing why we're excited to take this molecule into the clinic. There are other precedented molecules that are in clinical development, we're not taking as much target risk as some might want us to by going after a new modality.
The fact that we can take this molecule into the clinic in solid tumors is something that we're really looking forward to in the first part of next year. ADCs are us, is probably a way I might describe Sutro if somebody asked me about it. We have a bispecific ADC in the clinic. We have multiple ADCs that I've talked about already in the clinic, and we're now working with our partner, Astellas, on an immunostimulatory ADC, which I'll talk about briefly. We have a number of really exciting tumor-associated antigen targets that we have in research. We have the ability to mono or bispecific targeting, and we have a number of different conjugation mechanisms, not to mention linkers and warheads. Our toolbox is without parallel in the industry. Why do I say that? Well, let's talk about a new modality, an immunostimulatory antibody drug conjugate.
This has two different mechanisms of action on it. One mechanism, like a traditional antibody-drug conjugate, you have a payload that gives you a cytotoxic benefit and causes immunogenic cell death. And then you also have an immunostimulatory agent, site-specifically attached to allow the immune system to come in and do the mop-up work with the tumor cells that are remaining. Pre-clinically, we've also demonstrated the opportunity in mice for a memory response, which means when you rechallenge those mice, the tumor does not reestablish itself. Again, I refer you to the research forum where Dr. Hallam goes into some exquisite detail about why we think this is the next generation of antibody-drug conjugate development.
For those of you who wonder whether we're able to sustain this company, at the end of the third quarter, we had $287 million worth of cash and a runway into the first half of 2024. When we get to the time where we release our full year-end numbers, we will update cash, we will update runway guidance. For those of you who've been paying attention, we might have done a few things to augment our cash position in the fourth quarter of the year. We own 1.5 million shares, or we did own 1.5 million shares of Vaxcyte. We still have a substantial ownership position in Vaxcyte. I remind you that our 4% royalty has now been substantially de-risked and is the subject of some interest from people who like to acquire royalties.
So let's stay tuned and see how that plays out. We've been grateful to be supported by our collaborators, Celgene originally, Bristol, Merck, EMD Serono, Astellas, and have raised over $600 million in non-dilutive capital. We know how to make antibody-drug conjugates. We believe we make best-in-class molecules. We think the data we've generated for Luvelta demonstrates the opportunity to have a best-in-class ovarian cancer molecule as rapidly as possible. We're pleased that we can benefit these children who have this very rare and deadly short-lived form of AML, and we look forward to developing the rest of our pipeline. Bristol has been hard at work with our BCMA ADC. I hope they will say something about it this year. Merck has been hard at work with the IL-2 derivative. I'd like to hear them say something about that this year.
If you and Bristol and you and Merck are listening today, please, let's get the data out there. That's who we are. That's Sutro. We've been at it for a while. I've been privileged to be CEO since 2009, and as I said, being the 19th employee, seeing a pipeline like this, seeing a drug that benefits women, drug that benefits children, it's a great humbling experience for me to lead this company and get to this point in Sutro's history. Stay tuned. We have a lot more to do, and we're excited about the future. Thank you so much for your attention today.
Thanks, Bill.
Oh, sorry, I forgot we have a good team, and they're here too. They make it happen.
We do have time for Q&A. If any folks have questions, you can raise your hand or submit online through the portal. I do have a couple, Bill.
Absolutely.
Just on the new data set, were you surprised that the PFS was a bit higher than the duration of response?
You know, you don't see that very often. I will say we were not surprised. Our dose expansion or sorry, our dose escalation data had a similar signal. What it really means is we've designed a drug where every molecule is competent. And so as long as you have a certain amount of folate receptor alpha expression above 25%, every molecule in the vial can have a disease-modifying effect. And so even if you don't get the benefit of a partial or a complete response, your disease can be controlled. When you look at the swimmer's plot, you see a number of patients who did not have responses who had long-lived disease control, and that long-lived disease control is what translates into the PFS that I was able to share with you.
Got it. Just on Cohort C, I guess at the outset, what were you hoping to see with the addition of it? What should we expect in terms of timing for the full data?
When we did our dose escalation study, Cohort A, most physicians didn't use growth factor to support the patients who had neutropenia. As a matter of fact, about 20% of the time were patients given growth factor, which we thought was curious, and really it was the physician's decision that the patient didn't need it. Even if it was grade 3 or grade 4, it was asymptomatic, and it resolved within 10 days. We felt that growth factor could actually reduce the risk of higher grade neutropenia, and we had to figure out the timing to introduce growth factor. If you introduce it when, at the time point that it is conventionally introduced with chemotherapy, you find that your active catabolite is still in circulation and could blunt the effects of the growth factor.
If you, however, wait until day eight, given the late onset of neutropenia, we thought there was a very good chance that we could control that neutropenia with dosing at that point in time. In fact, the data demonstrated that our hypothesis was correct, and that leads to the current design for the higher dose in the phase II-III REFRαME study.
Got it. Then expectations for timing, and then efficacy relative to Cohort A.
From a timing standpoint, we will start REFRαME in the second quarter of this year. The first 50 patients, you know, it's hard for me to project. We have a number of centers that are still open today. I will remind folks who are remembering back to our historical recruitment rates, our dose expansion Cohort A was enrolled in 11 months, and that was from a dead start. I'm cautiously optimistic that we will easily beat 11 months on the enrollment of the first 50 patients, and then we'll keep enrolling from there on until we have our global sites open, and we will be in Europe and in Asia, as well as in the United States. Until I see some recruitment rates, I'm not gonna be able to guide on the overall length of the trial.
We believe we have, with this data, a lot of investigator enthusiasm and a lot of motivation for people to come on our study.
Got it. We're up on time, maybe any final quick questions? If not, thanks so much, Bill. Thanks everyone for coming. Have a great rest of your conference.