Five Prime Therapeutics (FPRX) Q1 2019 Earnings Call Transcript

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Five Prime Therapeutics (NASDAQ: FPRX)
Q1 2019 Earnings Call
May. 08, 2019, 4:30 p.m. ET

Contents:

  • Prepared Remarks
  • Questions and Answers
  • Call Participants

Prepared Remarks:


Operator

Welcome to the Five Prime Therapeutics first-quarter 2019 earnings call. As a reminder, this conference call is being recorded. I'd like now to introduce your host for today's conference, Martin Forrest, vice president, investor relations and corporate communications. You may begin your conference.

Martin Forrest -- Vice President, Investor Relations and Corporate Communications

Thank you, Lee. Good afternoon, everyone thank you for joining us today. A press release with the company's first-quarter financial results was issued earlier today, and can be found on our company website. And joining me today are Aron Knickerbocker, chief executive officer; Dr.

Helen Collins, chief medical officer; and David Smith, chief financial officer. Today's conference call will include forward-looking statements under the private securities litigation reform act of 1995, including statements regarding our research and development programs and financial outlook. Actual results may differ from those indicated by these forward-looking statements due to numerous factors, including those discussed in the Risk Factors section of our SEC filings. Our expectations and assumptions could change, while we may elect to update these forward-looking statements in the future, we specifically disclaim any obligation to do so even if our views change.

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I will now turn the call over to Aron.

Aron Knickerbocker -- Chief Executive Officer

Thanks, Martin. Good afternoon, and thanks for joining us today to review our progress and achievements during the first quarter of the year. On our call today I'll recap the highlights for the quarter, including our decision to add an early futility analysis to the FIGHT trial. Aron will provide further details on the biomarker data we are seeing the FIGHT trial, as well as provide an update on our other clinical programs.

David will review financial results for the first quarter, along with cash guidance for 2019. And after that, I'll turn the call to Q&A. OK. Let's get started with bema and the FIGHT trial, which is testing bemarituzumab in combination with frontline modified modified FOLFOX-6 chemotherapy and patients with gastric or junction or gastroesophageal junction, or GEJ cancer, whose tumor is overexpressed FGFR2b.

What we've recently learned is a greater than 30% of patients screened for enrollment in the FIGHT trial and tested positive through FGFR2b overexpression or IHC alone, which is significantly higher than our original expectations. We are expected 10% of patients to test positive by either IHC and or ctDNA test. We also expect that the patients who tested positive for FGFR2b overexpression by IHC alone would represent a minority of the patients enrolled in the FIGHT trial, but these patients represent the vast majority of biomarker positive patients in the FIGHT trial. Because the composition of the patient population we have enrolled, difference from our expectations, we decided to conduct an early futility analysis.

Our early screening data suggest that the FIGHT trial may be enrolling a greater proportion of patients whose tumors are overexpressing FGFR2b due to a reason other than gene amplification. After a comprehensive and ongoing review, we're confident that both the IHC and ctDNA test we're using in the FIGHT trial have undergone appropriate testing to demonstrate their specificity, sensitivity, precision and stability, and as the labs performing these assays have been properly trained and monitored. Additionally, the concordance of finding the cross global central labs suggest there is not a problem with implementation and performance of the In other words, we think the tumor is testing positive by IHC, are truly overexpressing FGFR2b, and the tumors testing negative by ctDNA blood samples are truly negative for the presence of extra copies of the FGFR2 gene in the blood. While all patients being enrolled in FIGHT may benefit from bema, it appears that the patients we are enrolling are different than the patient population in the late-line trial and which we base the FIGHT trial design.

This represents an additional unknown because we have limited clinical data from patients overexpress FGFR2b in the absence of gene amplification. In light of biomarker screening results, we've made the decision to conduct an early futility analysis, which we expect to occur in the first half of 2020. We believe this is both clinically and physically responsible. In the event of the clinical outcomes at the time of the futility analysis support continuing the FIGHT trial, then we believe that the addressable patient population for bemarituzumab may be significantly larger than the original estimate of 10% of advanced gastric and GEJ cancer cases.

Based on current figures for biomarker positivity, it would be conceivable that bema may be appropriate for approximately one in three gastric cancer patients, rather than our initial planning and assumption of approximately one in 10 patients. We will come back to the FIGHT trial later in the call during Helen's clinical update. So I'd now briefly recap other highlights from the quarter. In March, we participated in the new drugs on the horizon oral session at AACR and delivered a podium presentation on FPT155, our first-in-class CD80-Fc fusion protein.

Our Phase 1a/1b abstract for FPA150, our first-in-class B7-H4 antibody, has been accepted for a poster presentation at the upcoming ASCO annual meeting. We remain on track to make a second data presentation on FPA150 at the ASMO meeting in October. We expect to present monotherapy safety data throughout patients in the FPA150 Phase 1 trial, along with preliminary monotherapy efficacy activity data. We also expect to present preliminary safety data from the Phase 1 combination of FPA150 and KEYTRUDA.

We are also on track to present preliminary Phase Ia dose escalation data for FPT155 at the SITC conference in November. We're pleased with the progress of our fully partnered programs as well. The BMS-sponsored randomized controlled Phase II trial of cabira and OPDIVO in second line pancreatic cancer is currently enrolling and we expect to see the trial complete enrollment this year. BMS-986258, a fully human monoclonal antibody targeting TIM-3 immune checkpoint receptor continues to progress in a Phase 1/2 trial and is now being studied in combination with OPDIVO -- Bryan Irving, our chief scientific officer, provided an in-depth update on our first-in-class CDA CD80-Fc fusion protein on our last call.

And I am sad to announce that Bryan has resigned to pursue a new opportunity with a privately held biotech company working on novel technologies in the cancer immunotherapy space. We're disappointed to see Bryan leave Five Prime, but we wish him much success in his new venture. Bryan is a valued member of the Five Prime executive team, a stronger of our research organization and a topnotch scientist to his uniformly admired Five Prime and within the wider community of corporate and academic partners. Bryan has built a strong research organization and its responsibilities have been reassigned to senior leaders of the research organization on an interim basis.

We plan to promptly comment an executive search for a Head of Research. With that, I'll now turn the call over to Helen.

Helen Collins -- Chief Medical Officer

Thank you, Aron. I'd like to build on Aron's comments about the FIGHT trial, then move on to an update of the pipeline. The FIGHT trial has been enrolling well as a result of support from our investigators, great execution by our clinical team and also due to the higher prevalence of FGFR2b positive patients that we predicted. As a reminder, the FIGHT trial is a double-blind placebo-controlled trial, so we remain blinded to outcomes, and it is a biomarker driven trial based on tumors expressing FGFR2b.

And therefore, we are able to, in realtime, review the number of patients prescreened and thei rates are testing positive by either the tissue IHC test or by the blood ctDNA test. It's very early in the trial, and at this point, we anticipated approximately 10% of the patients screened will be biomarker positive. Instead, we're observing greater than 30% of the patients are biomarker positive. On the one hand, the addressable population for bema might be three-times higher than what we predicted.

On the other hand, for the trials to be successful, it depends on the relative level of benefit of each of the subgroups enrolling in the trial. And as the proportions are different than what we predicted, we think it's prudent to add an earlier look at the data by adding futility analysis. So let me walk you through some of the details of what we're seeing. First, I'll review how patients qualify for enrollment in the FIGHT trial.

Patients qualified by either having a biopsy other tumor, test positive for overexpression of FGFR2b using IHC or immunohistochemical staining, or by having a blood sample test positive for amplification of the FGFR2 gene using ctDNA or circulating tumor DNA. Accordingly, the patients who enrolled into the FIGHT trial fall into one of three subgroups. Their tumor test is positive. Their are blood test is positive, or both their tumor and blood test is positive.

The FIGHT trial is the first large-scale global trial screening patients in the frontline gastric cancer setting for FGFR2b. And based on what we've seen so far, over 30% of patients are screening positive for FGFR2b overexpression in their tumor and most are doing this on the basis of the humor IHC just alone. We have predicted that significantly more patients would have both their tumor and their blood test positive. This difference between what we predicted and what we're observing is important, because we based our trial design upon historical data where most of the patients tumors tested positive for both FGFR2b overexpression and FGFR2 gene amplification.

I must point out that there is no concern that any patient has enrolled in the trial incorrectly. In fact, we just had our first independent data monitoring committee meeting, and they are aware of the biomarker screening results. The DMC, of course, reviews unblinded data, and they determine that the overall risk benefit of the trial for patients continues to be in favor of proceeding with the trial as is. The BMC did not recommend any changes to the trial design.

Then going to the reasons we might be seeing this higher prevalence, the first thing we reviewed are diagnostic tests. And as Aron already mentioned, we're confident the diagnostic tests themselves are performing as designed and at these IHC positive tumors truly are positive for FGFR2b overexpression. This means that the most likely explanation for the observation is due to differences in the population of frontline versus late line gastric cancer. Supporting this hypothesis, our IHC partner recently evaluated a subset of commercially sourced gastric cancer samples and sound more than twice the frequency of FGFR2b overexpression in the frontline setting compared to what they found in the larger cohort of tumor samples of unknown line of therapy and stage, which were used to develop the IHC assay.

These data provides further confidence at the overexpression prevalence is higher than 10% in the frontline setting. For the question raised by this new data is from a trial design and statistical perspective. Assuming different subgroups of patients may benefit different amounts from the addition of beam to chemo, a change in the proportion of the subgroups enrolled could either make it more or less likely that we achieve our endpoint. Let me take a minute to explain what we're seeing and what it means for using an analogy that you're all familiar with, the use of PDL-1 and tumor mutational burden markers in lung cancer.

If you're going to design a lung cancer trial today, testing the efficacy of a PD-1 antibody, you would select patients based on their tumors testing positive for PDL-1. You likely would also select patients based on their tumor's mutational burden or the TMB status. If you did this, you would enroll patients whose tumor falls into one of three subgroups, those that are PDL-1 positive, those that have high tumor mutational burden, and those that are both PDL-1 positive and have high tumor mutational burden. And although you're confident that all three of these subgroups have the potential to benefit from your drug, the relative benefit in each subgroup is likely to be different.

Additionally, you know a lot about the expected benefit in patients based on their PDL-1 status, but you know less about the benefit of TMB status since most of that data comes from retrospective studies. Nonetheless, you make an estimation of enrollment of each subgroup and an estimation of the benefit you expect to see in each subgroup and size your trial accordingly. If you make the right estimations, your trial should be sized properly. So bringing this analogy back to the FIGHT trial, the majority of data we based our trial design on was on patients who tested positive for both FGFR2b overexpression and FGFR2 gene amplification.

Those data that supports the benefit of bema and the other two subgroups enrolling in this trial, but much less other. We continue to think that the use of bema and frontline FGFR2b overexpressing gastric cancer has the potential for success because it's demonstrated single-agent activity should not have overlapping toxicity with chemotherapy and literature suggesting FGFR2b overexpression is a poor prognostic factor, and we remain confident that all patients qualifying for this trial have the potential to benefit from bema. We all know gastric cancer is a tough cancer to treat. Many drugs have failed and the most recent was the announcement of the failure 062, the large frontline trial of Keytruda in end PDL-1 selected patients for gastric cancer.

Merck's announcement also underscores the wisdom of adding this futility analysis. We already had an interim analysis included in this trial, but we think it's prudent that we have an earlier evaluation. Doing so, we'll add some reassurance that the trial is less likely to miss its final end point. We discuss the addition of a futility analysis with our independent DMC, and they're in agreement with the concept.

As stated with the Aron's remark, we expect this futility analysis to readout in the first half of 2020. And like any futility analysis, the outcome will lead to a recommendation to continue the trial as is, stop the trial or amend the trial. Moving on to FPA150, which is our first-in-class B7-H4 antibody. This antibody is designed to target tumor cells through 2 mechanisms of action: By blocking B7-H4 from sending an inhibitory signal to CD8 T cells and by enhancing killing a B7-H4 overexpressing tumors through enhanced ADCC.

B7-H4 is frequently overexpressed in breast, ovarian and endometrial cancers. We're pleased that our Phase 1 study for FPA150 has been accepted for poster presentation at ASCO, and our clinical teams are preparing to make two FPA150 data disclosures this year. The first at ASCO and the second at ESMO. The data presentation at ASCO will be the first time that we will be reporting clinical data from this program and will include safety and PK data from the dose escalation of the solid tumor -- in any solid tumor, excuse me, and some preliminary data at doses of three and 10 milligrams.per kilogram from the expiratory cohort of B7-H4 positive patients.

You'll recall that we will be testing the combination of a anti-PD1 drug Keytruda with FPA150 in patients with the B7-H4 overexpressing ovarian cancer based on the pre-clinical data supporting synergistic activity of the combination of PD-1 and B7-H4 antibodies. We've recently opened this on for screening and expect to enroll our first patient in the Keytruda FPA150 combination this month. Later in the year at ESMO, we plan to present preliminary data from the monotherapy expansion cohorts at the full 20-milligram per kilogram dose and available safety data from the Keytruda combination. Turning to FPT155.

This is our first-in-class CD80-Fc fusion protein, which employees a novel approach to costimulate T-cells sales through CD28, but as in conjunction with the T cell receptor stimulation in the presence of antigen. FPT155 is an exciting approach to target CD28 without superagonism, which may enhance the nume reponse to tumors that are unresponsive to first-generation immuno-oncology therapies. Accordingly, FPT155 has a potential for activity against a broad spectrum of tumor types. We're making good progress in the dose escalation, and we plan to present primary safety data at in late November.

Finally, turning to our partner programs. Cabiralizumab is our antibody that inhibit CSF1R to and has been shown to block the activation and survival of tumor-associated macrophages. Our partner BMS has advanced development of cabira and pancreatic cancer into a global randomized Phase 2 trial with 160 planned patient, which is ongoing. Additionally, they continue to add to their list of investigator-sponsor trials in a variety of combination therapies and tumor types having just posted another IST in peripheral T-cell lymphoma this past week.

You will also recall that we have another partner program with BMS targeting TIM-3 and their Phase 1 and 2 trial is ongoing. I'll now turn the call over to David.

David Smith -- Chief Financial Officer

Thank you, Helen. The complete details of our financial results for the quarter can be found on the press release that we issued earlier this afternoon. We ended Q1 with a strong balance sheet, cash, cash equivalents and marketable securities totaled 270 -- $237 million on March 31, 2019, compared to $270.1 million on December 31, 2018. This expect a decrease over the prior quarter reflects operating and other expenses during the quarter that exceeded revenues.

The net loss for the quarter was $35.4 million or $1.02 per basic and diluted share. Collaboration and license revenue was $5.3 million for the quarter. This is a decrease of last year's first quarter revenue of $32.5 million, which included a $25 million milestone that we earned upon like a cabira collaboration agreement -- under the cabira collaboration agreement on BMS's initiation of its Phase II clinical trial testing cabiralizumab in combination with nivolumab with and without chemotherapy in second-line pancreatic cancer. Research and development expenses were $31.8 million in the first quarter of 2019 compared to $43.6 million in the first quarter of 2018, a decrease of $11.8 million or 27%.

This decrease was primarily related to companion diagnostic expense incurred in the first quarter of 2018 with no corresponding expense in the first quarter of 2019 and lower compensation cost as a result of our reduction, enforce along with lower clinical trial expenses that were partially offset by higher manufacturing costs related to our FPA150 program. G&A expenses totaled $10.5 million, which were flat year over year. Looking ahead, we continue to expect full year 2019 net cash used in operating activities to be in the range of $117 million to $122 million. We estimate ending 2019 with approximately $148 million to $153 million in cash, cash equivalents and marketable securities.Now I'll turn the call back to the operator for Q&A.

Questions & Answers:


Operator

[Operator instructions] And your first question is from Chris Shibutani from Cowen. Your line is now open.

Chris Shibutani -- Cowen and Company -- Analyst

Hey, thanks very much. I appreciated the careful explanation and the analysis. Helen, if I can ask when we think about what the implication of this are and what is addition tree would be like. If you think like a bit further different then if the futility analysis shows that one of the groups need to enroll further, is that a way to think about how you've in this file in terms of sizing? And can you confirm that in terms of variable that would be not leverage such as dosing or other key factors for the way that trial was being run?

Helen Collins -- Chief Medical Officer

Yeah. I think, again, Chris, it's very early in the trial. So you can imagine -- from the beginning, we just watched every piece of data we can look at we look at, right? So I think the group ironically that we were most concerned about because I know you've been following this from the beginning were patients that were -- that we identified just by amplification because as you know, at least with the toga, the HER2, there is some concern that if you could have amplification without expressions, right? So in some ways, it's good to see that the disparity, if you will, is happening from patients who are overexpressing because that's how our drug works. Our drug works on the cell surface.

But at the same time, again, all I can do is say what we know and what we know is in our late line trial. We had purposely enrolled patients who had both overexpression and amplification and what we're seeing here is mostly overexpression. We do have the added compounding that we are using ctDNA instead of but we're confident again in our assay. So I know that doesn't directly answer your question, but I'm afraid that's the information that we have, right? So in terms of the design -- the futility, I mean, again, the short answer has to be it depends, right? If we have a small proportion, I'm going to call an amplified only patients and they're getting a huge benefit, then maybe the trial is infeasible to make it larger, a forbidding -- lots of benefits from patients as long as they're just amplified.

Then you could see how the trial can be smaller. I mean, again, I think it's going to depend, right? Too early to tell.

Chris Shibutani -- Cowen and Company -- Analyst

And when I think about the trajectory of how you thought about this asset and developing clinically, a few years back was originally aimed at more later line of patients and design to address more frontline. And so in the event of different [Inaudible] futility analysis indicates not feasibly or prudent to be moving in -- continuing with top-line setting, do you see a based on what you're learning and what you know to still continue pursuing additional clinical development with bema in later lines of therapy?

Helen Collins -- Chief Medical Officer

Certainly, potentially, I mean -- and again, it will depend on what the data shows, right? But there are other tumors that also amplify and overexpress FGFR2. So it would agian depend on what the data showed.

Chris Shibutani -- Cowen and Company -- Analyst

Got it. And this is a program that's partnered with by labs and in analyst and I don't think there is any commentary. Should we count on the medication of this making primarily coming from you guys any update on this?

Aron Knickerbocker -- Chief Executive Officer

Well, Chris, this is Aron. We are in close communication with Zai. They're fully aware of this. They are on board with this plan as well.

We are the global study sponsor worldwide, but we do so in coordination with Zai.

Helen Collins -- Chief Medical Officer

I mean -- and one other thing and, again, these are all hypotheses, right? I mean, when you try and think why would you see more overexpression in the front line and less later on. I mean, it's a poor prognostic indicator, could have been that these patients don't make it to late line. And so, but again, these are all hypotheses. So --

Chris Shibutani -- Cowen and Company -- Analyst

Got it. OK. Thank you very much. I'll get back to the queue.

Aron Knickerbocker -- Chief Executive Officer

Thank you, Chris.

Operator

Your next question is from Michael Schmidt from Guggenheim. Your line is now open.

Michael Schmidt -- Guggenheim Securities -- Analyst

Hey, thanks for taking my questions. Maybe a couple of follow-ups on bema. I'm just trying to understand maybe number one. I guess, could you share maybe how many patients have been screened today then whether you've seen any regional differences, for example, in expression pattern?

Helen Collins -- Chief Medical Officer

So you know, it's early on in a trial. It is primarily the enrollment that we're looking at is based on a few countries. So that limitations of the data, that's why we're saying it's early. So it's just too early for us to say whether there's regional differences.

Michael Schmidt -- Guggenheim Securities -- Analyst

Understood. And maybe then on your comment, it sounded like, you did say, you did make some assumptions when powering the study for, I guess, relative efficacy in those three different biomarker subcategories. And just wondering, if you could maybe remind us whether you did actually, in fact, see efficacy differences in either IHC test positive only or DNA amplification or both? And how we should think about relative efficacy contribution in those subgroups maybe?

Helen Collins -- Chief Medical Officer

So no. So that's a great question. So I think it's really more about the confidence of the data. So we most -- when we've designed this trial, we didn't just use our Phase 1, so we used the mechanism of action, we used our preclinical data, we used our Phase 1 clinical data, we used the data in the literatures.

There may be -- there are other people that have looked at FGFR2 expression and amplification. And then we also worked very closely with our diagnostic partners who looked at over 5,000 commercially sourced samples to help us pick our various cutoffs. So -- but based on all of that, the confidence that we have of the, I'm going to call them, a double positive group, that's where most of our data is. So in our case, it's not so much that we think one group is less than the other.

It's just that that's where our data is and that group of patients is smaller. So it's really a confidence issue, not so much that I can tell you there's some relative benefit. Does that help?

Michael Schmidt -- Guggenheim Securities -- Analyst

Yeah, understood. And then maybe, just if you could share us some of along the lines of Chris question, I guess, the futility analysis, are there any metrics that you could disclose?

Helen Collins -- Chief Medical Officer

Yeah. Well so this information is you know, hot off the press. And so our first thing was to make a decision about what to do with it and that's bit futility analysis in. We need to discuss that with our DMC.

And so we're working those those details now. I think everybody is aligned that we want to do this much earlier than we would have been doing our interim analysis. And that right now that's plan for the early 2020. But the details we haven't made public.

Michael Schmidt -- Guggenheim Securities -- Analyst

Yeah. And then maybe just one on, on the upcoming ASCO presentation for FPA150. Just trying to understand, I guess, whether -- I know it's primarily a safety and PK presentation, but just maybe help us understand, it sounds like some patients or a fair amount of patients have been treated at higher doses. So is there might be anything we could gain on early signs of efficacy as well at ASCO?

Helen Collins -- Chief Medical Officer

Yeah, I think it's a timing of the data. So you know, happily this trial -- this dose escalation went extremely quickly, as you know, less than nine months, we went through seven, eight cohorts. And so those higher dose patients were just dosed at the beginning the first quarter. So we don't have the durability of time on there to be able to have the efficacy.

So that's the issue. So that's why this is safety data. You're right. Some patients are dosed at the higher dose, but we don't have the time on there for us to be able to present any of that data.

Michael Schmidt -- Guggenheim Securities -- Analyst

OK. Great. Thank you. Appreciate it.

Operator

And your next question is from Jonathan Chang from SVB Leerink. Your line is now open.

Jonathan Chang -- SVB Leerink -- Analyst

And just following up on Michael's question on the FIGHT study, can you talk broadly about how large the data set is, given the early stage of the study? And I am trying to get a sense of how confident are you that the 30% number is more representative than the 10% number originally expected?

Helen Collins -- Chief Medical Officer

So we prescreen on the hundreds range and -- but -- and our enrollment is little less than 10%. Small numbers for trial of this size and again, concentrated on a few countries because those are the ones that got nothing going. So it is early.

Jonathan Chang -- SVB Leerink -- Analyst

Got it. And then just second question. You mentioned in the prepared remarks that there could be reasons for greater FGFR2b expression in the absence of gene amplification. Could you had more color to that? I mean, what do we know about the mechanism here?

Aron Knickerbocker -- Chief Executive Officer

So yeah, thanks Jonathan. We have some data that Helen's really is limited. Some clinical and some preclinical data showing activity in tumors that do not have gene amplification with that have the target overexpress. But it's not the proponent data that we have.

So that's why this proportionality matters come up.

Helen Collins -- Chief Medical Officer

Yeah. And again, I'll go back to the confidence you have. The more data I have, the more confident you are. And so if a group that you have a little bit of data on, but still data that it should work, but it's -- then your confidence interval is wider and then that's -- and to be honest, as I also mentioned, I think the continued failures of other frontline trials, so since we started this trial, trial has failed.

Merck's trial failed. They're right about the time we started in the safety lead-in, the frontline trial failed. So I think it also is just a prudent thing to do when you're looking at gastric cancer. It's a tough tumor, right? And so when we say prudent, we think prudent also for the company and the other things that we have in the pipeline.

And --

Jonathan Chang -- SVB Leerink -- Analyst

Got it.

Aron Knickerbocker -- Chief Executive Officer

It is in our announcement today, really reflects our desire to be No. 1, transparent and No.2, to demonstrate good physical discipline, but we also still think the drug clinical investigation, and we think it's appropriate to take this early look with the futility analysis.

Jonathan Chang -- SVB Leerink -- Analyst

Got it. And just one last question if I may on the cabira study recently added on clinicaltrials.gov. Can you talk about the rational for this OPDIVO combination study and what we know about the roll of the CSF1R and PT sale? Thanks.

Helen Collins -- Chief Medical Officer

Well, you know, I mean, this is, again, a study that's being done, University in Michigan, right, and BMS is supporting it. So this is a partnership that we are not directly involved in any way. I am aware of data looking at CSF1 expression, it's also macrophages, but on some of the stem cells in some of these subtypes of lymphoma, and we will speak to Bryan if you have any specific knowledge of why they are picking the peripheral thanks.

Bryan Irving -- Chief Scientific Officer

No, I am surprised by the -- there couldn't be strong rational. I am just now aware of it.

Helen Collins -- Chief Medical Officer

Yeah.

Jonathan Chang -- SVB Leerink -- Analyst

Got it. Thank you.

Operator

Your next question is from Salveen Richter from Goldman Sachs. Your line is now open.

Maryana Breitman -- Goldman Sachs -- Analyst

This is Maryana Breitman for Salveen. I have a quick question, thank you for taking my question. Would the futility analysis change the statistical considerations that are going into the trial design?

Helen Collins -- Chief Medical Officer

No, no, no. So -- and, again, I mean, one thing is, you can imagine for a trial this size, we initially had a lot of discussion about futility analysis. So I think, you know, in some ways, this is just -- it's something we were thinking about but just made the data coming in made that we need to do this. So -- but no, we would not change the statistical analysis.

Maryana Breitman -- Goldman Sachs -- Analyst

Got it. And also, I also -- I wanted to understand a little bit. So how different are the patients issuing volume rates now in the rolled already how different are the ones that you're looking at prior?

Helen Collins -- Chief Medical Officer

So -- so again, there are different -- the difference between our FIGHT trial, the Phase 3 trial and our Phase 1 is that in the Phase 1 that would late line patients. So those were patients that had three or four therapies, right? And they were patients who are getting monotherapy, not getting additive chemotherapy. And again, it was frontline versus late line, right? So those are the patients that we looked at in our monotherapy trial. Those patients, in general, the majority of them were both IHC positive and amplified by fish, so not everybody, but most of them are.

So when we designed this trial, again, knowing that how the drug works, that it requires overexpression, we allow patients who are either overexpressing or overexpressing and amplified or amplification. And again, the amplification we're testing by ctDNA not by fish.

Maryana Breitman -- Goldman Sachs -- Analyst

Got it. And then for the I -- because there is a lot of people who are looking at FGFR right now, and it's rolling cancer, and I think this is like actually a much more sort of a wider phenomenon sourcing and something people are trying to going to cover this is are you guys considering a combination that you just wanted to get this done and figure out what to do next?

Got it. Thanks a lot -- thanks a lot for the call.

Aron Knickerbocker -- Chief Executive Officer

Thanks, Maryana.

Operator

Your next question is from Steve Seedhouse from Raymond James. Your line is now open.

Unknown Analyst

Hi, this is Bryan Deschner on for Steve Seedhouse at Raymond James. My questions are, regarding the futility analysis, can you give us any more detail on the expression for the discrepancy? And why there were so many IHC positive, but ctDNA negative patients? And if the trial is as successful, would you move forward with just IHC as the companion diagnostic?

Helen Collins -- Chief Medical Officer

So again, one of the things is that we do think that the patient populations are different, right? So in the front line, we do truly believe more patients overexpress FGFR2b than they do in the late line. And the reason we believe that because we are seeing that the patients that we screen and also because as we discussed our IHC partner has done and found a cohort of patients who match as closely as possible the patients who are enrolling in the trial meaning that they were frontline advanced stage and found more than double the rate that when you look at other groups of FGFR2b. So that's our support that concept. I think we've also wondered, I mean, I'll be honest about our ctDNA test because as you may know, there are some recent published data that suggest when you have patients, who have the backup, the blood ctDNA test relies on shedding of the DNA into the bloodstream from the tumor.

And if a patient has not received any therapy, that shedding appears to be less, because you need dying cells to do that. So it certainly may be that even though the test itself is accurate, you won't see the humor, no shedding into that, you're not going to be picking up that DNA. But, again, the vast, that's not going to make a huge difference and the vast majority of these patients are FGFR2b positive alone. But otherwise, everything is hypothetical, right, we can't, because this is the largest or does it ever in front line, gastric cancer patients.

There is no other large dataset.

Unknown Analyst

And will there be --

Helen Collins -- Chief Medical Officer

And especially with the validated test because we're the first people doing this, we're the the first people to spend the time to make sure that the tests that we're using truly have gone through all of the process development steps that you want for potentially CDx approved. So again, we are confident it is data, but what I can tell you is what it means for whether the study will be more or less likely to be successful. And it's early, very early.

Unknown Analyst

OK. OK. Are there prespecified group analysis baked into look at their by each individual biomarker?

Helen Collins -- Chief Medical Officer

We have some stratification, but you're limited, again, by the number of patients what your stratification. Right now, we have not stratified by biomarkers. So retrospectively, we would expect certainly, you know regulatory agencies all we do that, respectively, there will be all sorts of subgroups, but not perspectively we did, we chose not to stratify based on this.

Unknown Analyst

OK. And then real quickly on FPT155. Do you anticipate any manufacturer ability issues associated with it, specifically regarding stability and in terms of aggregations or proteolytic degradation?

Aron Knickerbocker -- Chief Executive Officer

No, it's not been a problem so far, and we've not been limited by drug supply.

David Smith -- Chief Financial Officer

Or with aggregation problem.

Unknown Analyst

OK.

Helen Collins -- Chief Medical Officer

Yeah, we're pleased with the trial, it's moving along.

Unknown Analyst

Thank you.

Aron Knickerbocker -- Chief Executive Officer

Thank you, Brian.

Operator

Your next question is from Eric Joseph from J.P. Morgan. Your line is now open.

Unknown Analyst

Hey, this is [Inaudible] on for Eric. Thank you for taking my question. I know you mentioned that around -- greater than 30% of patients were FGFR2 positive. I'm curious if you can quantify specifically what percent was by IHC alone? What percent was amplifiers? And what percent were both?

Helen Collins -- Chief Medical Officer

Well, the reason we haven't done because again, the data is so small. And if you've heard the earlier comment, right now we've enrolled just slightly less than 10%. It's very concentrated in a few countries, and of course, that means a side usually and if you can discover because that is the way these things work. So we just not right now giving these big numbers on purpose, because we don't want to mislead people.

So it's more than 30% of the patients are qualifying and based on one test or the other and by far most of them are the FGFR2b alone. I am -- sorry, it is not just because I couldn't be statistical accuracy on what that dashboard those are with her than what I'm telling you. I'm not going to be at this year, it is just too early.

Unkown Analyst

OK. Understood. And then I'm just kind of curious, maybe not mentioned around 5,000 samples or so that determine to cut us from the samples are there primarily frontline or the later-line patients or some combination of both?

Helen Collins -- Chief Medical Officer

Yeah, when you get these commercial samples, they are, for the most part, completely de-identified. right? So you don't know anything about them. There is appropriately no -- we don't know. And that's why what we did do is, when we started getting these results back, we went back to our IHC partner and said, could you look through those 5,000 plus samples and see if you can call out those that you do know that they are frontline, you do know that they're advanced stage.

And that's where they saw more than double the rate in that subgroup. So more than double the rate of FGFR2b positivity.

Unkown Analyst

OK. Great. And then maybe one last quick one, I was just kind of curious, can you talk about how you validated your assays specifically? And what gives you confidence that you're appropriately measuring FGFR levels?

Helen Collins -- Chief Medical Officer

Well, I think we've announced previously that we work with Ventana. So they're obviously one of the readers, if not the leader in development of IHC test. And they go through a whole series of trying to make sure that the assay, as we said, in a very specific. They do in interim reader testing, different data testing.

You're meeting to make sure that things are reproducible, from the assay point of view and from the reader point of view, I should my biomarker. There's a whole list of things they go through for the standard design control, they met with SEDAR about their plans. So these are -- they've gone through appropriate steps, again, to develop the IUO. So --

Unkown Analyst

OK. Great. Thank you.

Operator

And we have a follow-up question from Salveen Richter from Goldman Sachs. Your line is now open.

Salveen Richter -- Goldman Sachs -- Analyst

I just quickly wanted to ask. There is not going to be any opex exchanges on that, right? I mean, based on the trial [Inaudible]?

Aron Knickerbocker -- Chief Executive Officer

She's asking will there be some operating expense changes?

David Smith -- Chief Financial Officer

No, there will be not any operating expense changes. We've kept our guidance consisted for cash utilization.

Salveen Richter -- Goldman Sachs -- Analyst

Got it. Thank you. Thanks.

Operator

[Operator instructions] I am showing no further question at this time. I would like to turn the conference back to Aron Knickerbocker for closing remarks.

Aron Knickerbocker -- Chief Executive Officer

As I said at the beginning of the call, we and our partners continue to make steady progress in advancing our pipeline, and we're swiftly responding to new information from the Phase 3 FIGHT trial as you've heard today. We remain confident about the science underpinning our pipeline, and we're committed to following disciplined decision-making process. We've cleared hurdles to gauge the ongoing advancements of our pipeline programs,s and to exercise fiscal discipline. With that, I'd like to thank you all for joining us today.

I'd also like to thank the patients and investigators participating in our clinical trials, our Five Prime employees, and our strategic collaborators who all contributed to the continued advancement of our clinical programs. And we look forward to seeing many of you at ASCO and at one of the investor conferences that we will be attending during the month of June. And we look forward to updating you on our future calls. Thank you.

Operator

[Operator signoff]

Duration: 46 minutes

Call participants:

Martin Forrest -- Vice President, Investor Relations and Corporate Communications

Aron Knickerbocker -- Chief Executive Officer

Helen Collins -- Chief Medical Officer

David Smith -- Chief Financial Officer

Chris Shibutani -- Cowen and Company -- Analyst

Michael Schmidt -- Guggenheim Securities -- Analyst

Jonathan Chang -- SVB Leerink -- Analyst

Bryan Irving -- Chief Scientific Officer

Maryana Breitman -- Goldman Sachs -- Analyst

Unknown Analyst

Unkown Analyst

Salveen Richter -- Goldman Sachs -- Analyst



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