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Edited Transcript of FPRX earnings conference call or presentation 8-May-19 8:30pm GMT

Q1 2019 Five Prime Therapeutics Inc Earnings Call

San Francisco May 17, 2019 (Thomson StreetEvents) -- Edited Transcript of Five Prime Therapeutics Inc earnings conference call or presentation Wednesday, May 8, 2019 at 8:30:00pm GMT

TEXT version of Transcript

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Corporate Participants

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* Aron Marc Knickerbocker

Five Prime Therapeutics, Inc. - President, CEO & Director

* Bryan Irving

Five Prime Therapeutics, Inc. - Executive VP & Chief Scientific Officer

* David V. Smith

Five Prime Therapeutics, Inc. - Executive VP & CFO

* Helen Louise Collins

Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer

* Martin Forrest

Five Prime Therapeutics, Inc. - VP of IR & Corporate Communications

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Conference Call Participants

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* Chris Shibutani

Cowen and Company, LLC, Research Division - MD & Senior Research Analyst

* Maryana Ilya Breitman

Goldman Sachs Group Inc., Research Division - Research Analyst

* Michael Werner Schmidt

Guggenheim Securities, LLC, Research Division - Senior Analyst & Senior MD

* Salveen Jaswal Richter

Goldman Sachs Group Inc., Research Division - VP

* Turner Andrew Kufe

JP Morgan Chase & Co, Research Division - Research Analyst

* Wei Ji Chang

SVB Leerink LLC, Research Division - MD of Emerging Oncology & Senior Research Analyst

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Presentation

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Operator [1]

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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.

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Martin Forrest, Five Prime Therapeutics, Inc. - VP of IR & Corporate Communications [2]

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Thank you, Lee.

Good afternoon, everyone, and 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.

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.

I will now turn the call over to Aron.

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Aron Marc Knickerbocker, Five Prime Therapeutics, Inc. - President, CEO & Director [3]

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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. Helen will provide further details on the biomarker data we are seeing in 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, we'll turn the call to Q&A.

Okay. Let's get started with bema and the FIGHT trial, which is testing bemarituzumab in combination with frontline modified FOLFOX6 chemotherapy in patients with gastric or gastroesophageal junction, or GEJ, cancer, whose tumors overexpress FGFR2b.

What we've recently learned is that greater than 30% of patients screened for enrollment in the FIGHT trial have tested positive for FGFR2b overexpression by IHC alone, which is significantly higher than our original expectations. We had expected 10% of patients to test positive by either IHC and/or ctDNA tests. We also expected that 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 differs from our expectations, we decided to conduct an early futility analysis. Our early screening data suggests 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 tests we're using in the FIGHT trial have undergone appropriate testing to demonstrate their specificity, sensitivity, precision and stability and that the labs performing these assays have been properly trained and monitored. Additionally, the concordance of findings across global central labs suggests there is not a problem with implementation and performance of the 2 tests. In other words, we think that tumors 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 on which we base the FIGHT trial design. This represents an additional unknown because we have limited clinical data from patients who 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 fiscally responsible. In the event that the clinical outcomes at the time of the futility analysis do 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 1 in 3 gastric cancer patients rather than our initial planning and assumption of approximately 1 in 10 patients.

We will come back to the FIGHT trial later in the call during Helen's clinical update, so I'll 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 Ia/Ib 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 ESMO meeting in October. We expect to present monotherapy safety data for all patients in the FPA150 Phase I trial, along with preliminary monotherapy efficacy activity data. We also expect to present preliminary safety data from the Phase I 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 in enrollment this year. BMS-986258, a fully human monoclonal antibody targeting TIM-3, an immune checkpoint receptor, continues to progress in a Phase I/II 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 CD80-Fc fusion protein on our last call, and I'm 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 strong leader of our research organization and a top-notch scientist who is uniformly admired at 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 commence an executive search for a Head of Research.

With that, I'll now turn the call over to Helen.

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [4]

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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 real time, review the number of patients prescreened and their rate of 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 had anticipated approximately 10% of the patients screened would 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 3x higher than what we predicted. On the other hand, for the trial 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 of their 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 enroll into the FIGHT trial fall into 1 of 3 subgroups: their tumor tests positive, their blood tests positive or both their tumor and blood test 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 tumor IHC test 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 DMC did not recommend any changes to the trial design.

In going through the reasons we might be seeing this higher prevalence, the first thing we reviewed are the diagnostic tests. And as Aron already mentioned, we're confident that the diagnostic tests themselves are performing as designed and that 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 found more than twice the frequency of FGFR2b overexpression in the frontline setting compared to what they found in a larger cohort of tumor samples of unknown line of therapy and stage which were used to develop the IHC assay. These data provide further confidence that the overexpression prevalence is higher than 10% in the frontline setting.

So 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 bema to chemo, a change in the proportion of the subgroups enrolled could either make it more or less likely that we achieve our end point.

Let me take a minute to explain what we're seeing and what it means by using an analogy that you're all familiar with: The use of PDL-1 and tumor mutational biomarkers in lung cancer.

If you were 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 1 of 3 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 3 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. There's data to -- that supports the benefit of bema in the other 2 subgroups enrolling in this trial but much less of it.

We continue to think that the use of bema in 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 KEYNOTE-062, the large frontline trial of KEYTRUDA in PDL-1 selected patients with 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 discussed the addition of a futility analysis with our independent DMC, and they're in agreement with the concept. As stated with Aron's remarks, we expect this futility analysis to read out 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 I study for FPA150 has been accepted for poster presentation at ASCO, and our clinical teams are preparing to make 2 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 in a solid tumor -- in any solid tumor, excuse me, and some preliminary data at doses of 3 and 10 milligrams per kilogram from the exploratory cohort of B7-H4-positive patients.

You'll recall that we will be testing the combination of the anti-PD-1 drug, KEYTRUDA, with FPA150 in patients with B7-H4 overexpressing ovarian cancer based on the preclinical 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 employs a novel approach to co-stimulate T-cells through CD28 that acts in conjunction with a T-cell receptor stimulation in the presence of antigen. FPT155 is an exciting approach to target CD28 without superagonism, which may enhance the immune response to tumors that are unresponsive to first-generation immuno-oncology therapies. Accordingly, FPT155 has the potential for activity against a broad spectrum of tumor types. We're making good progress in the dose escalation, and we plan to present preliminary safety data at SITC in late November.

Finally, turning to our partner programs. Cabiralizumab is our antibody that inhibits CSF1R and has been shown to block the activation and survival of tumor-associated macrophages. Our partner, BMS, has advanced development of cabira in pancreatic cancer into a global randomized Phase II trial with 160 planned patients, which is ongoing. Additionally, they continue to add to their list of investigator-sponsored 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 I and II trial is ongoing.

I'll now turn the call over to David.

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David V. Smith, Five Prime Therapeutics, Inc. - Executive VP & CFO [5]

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Thank you, Helen. The complete details of our financial results for the quarter can be found in 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 expected 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 over last year's first quarter revenue of $32.5 million, which included a $25 million milestone that we earned upon like the 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 costs as a result of our reduction in force 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.

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Questions and Answers

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Operator [1]

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(Operator Instructions) And your first question is from Chris Shibutani from Cowen.

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Chris Shibutani, Cowen and Company, LLC, Research Division - MD & Senior Research Analyst [2]

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Great. Appreciated the careful explanation and the analysis. Helen, if I can ask, when we think about what the implication of this are and what a decision tree would be like, if you take it just a little bit further, for instance, if the futility analysis shows that one of the subgroups would need to enroll further, is that the way to think about how you amend the trial in terms of sizing? And can you confirm that in terms of variables that would -- we do not deleverage would be things such as dosing or other key factors for the way the trial is currently being run?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [3]

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Yes. Yes. I think, again, Chris, it's very early in the trial. So you can imagine, the -- but from the beginning, we just want -- every piece of data we can look at, we look at, right? 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 ToGA, the HER2, there is some concern that if -- you could have amplification without expression, 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, right? 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 confounding that we are using ctDNA instead of FISH, but we're confident again in our assay. So I know that, that doesn't directly answer your question, but I'm afraid that's the information that we have, right?

So in terms of the futility, I -- again, the short answer has to be it depends, right? If we have a small proportion of, I'm going to call, amplified-only patients and they're getting a huge benefit, well, then maybe the trial isn't infeasible to make it larger. If we're getting lots of benefit from patients as long as they're just amplified, then you could see how the trial can be smaller. I -- again, I think it's going to depend, right? Too early to tell.

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Chris Shibutani, Cowen and Company, LLC, Research Division - MD & Senior Research Analyst [4]

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And when I think about the trajectory of how you thought about this asset and developing it clinically, I think a few years back, it was originally aimed at more later line of patients and FIGHT was designed to address more frontline. And so in the event that we get to a scenario where futility analysis indicates it's not feasible or prudent to be moving and -- or continuing with the top line setting, do you a path based upon what you're learning and what you know to still continue pursuing additional clinical development with bema but in later lines of therapy?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [5]

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

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Chris Shibutani, Cowen and Company, LLC, Research Division - MD & Senior Research Analyst [6]

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Got it. And this is a program that's partnered with Zai Lab. They recently hosted an analyst meeting. I don't think that there was any commentary in regards to this. Should we count on the communication and decision-making primarily coming from you guys or to -- any update on this?

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Aron Marc Knickerbocker, Five Prime Therapeutics, Inc. - President, CEO & Director [7]

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Well, Chris, it's Aron. We are in close communication with Zai. They're fully aware of this. They're onboard with this plan as well. We are the global study sponsor worldwide, but we do so in coordination with Zai.

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [8]

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

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Operator [9]

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Your next question is from Michael Schmidt from Guggenheim.

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Michael Werner Schmidt, Guggenheim Securities, LLC, Research Division - Senior Analyst & Senior MD [10]

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Maybe a couple 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?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [11]

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So it's early on in the trial. It is primarily -- the enrollment that we're looking at is based on a few countries. So that is the 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.

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Michael Werner Schmidt, Guggenheim Securities, LLC, Research Division - Senior Analyst & Senior MD [12]

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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 3 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.

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [13]

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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 designed this trial, we didn't just use our Phase I. So we used the mechanism of action. We used our preclinical data. We used our Phase I clinical data. We used 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 that, the confidence that we have of the, I'm going to call them, the 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?

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Michael Werner Schmidt, Guggenheim Securities, LLC, Research Division - Senior Analyst & Senior MD [14]

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And -- yes. Yes. Understood. And then maybe just if you could maybe share some of the -- along the lines of Chris' question, I guess, the futility analysis. Are there any metrics that you could disclose?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [15]

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Yes. Well, so this information is hot off the press. And so our first thing was to make a decision about what to do with it, and that's to get the futility analysis in. We needed to discuss that with our DMC, and so we're working through 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 planned for the early 2020. But the details, we haven't made public.

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Michael Werner Schmidt, Guggenheim Securities, LLC, Research Division - Senior Analyst & Senior MD [16]

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Yes. And then maybe just one 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 may have been treated at higher doses, so I was curious if there might be anything we could glean on early signs of efficacy as well at ASCO.

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [17]

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Yes. I think it's the timing of the data. So happily, this trial -- this dose escalation went extremely quickly. As you know, in less than 9 months, we went through 7, 8 cohorts. And so those higher-dose patients were just dosed at the beginning -- in 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.

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Operator [18]

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And your next question is from Jonathan Chang from SVB Leerink.

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Wei Ji Chang, SVB Leerink LLC, Research Division - MD of Emerging Oncology & Senior Research Analyst [19]

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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'm trying to get a sense of how confident are you that the 30% number is more representative than the 10% number originally expected.

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [20]

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

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Wei Ji Chang, SVB Leerink LLC, Research Division - MD of Emerging Oncology & Senior Research Analyst [21]

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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 add more color to that? What do we know about the mechanism here?

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Aron Marc Knickerbocker, Five Prime Therapeutics, Inc. - President, CEO & Director [22]

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So...

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [23]

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Well, you may go.

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Aron Marc Knickerbocker, Five Prime Therapeutics, Inc. - President, CEO & Director [24]

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Yes. Thanks, Jonathan. We have some data, but, to Helen's earlier point, it's limited. Some clinical and some preclinical data showing activity in tumors that do not have gene amplification with -- that have the target overexpressed. But it's not the preponderance data that we have. And so that's why these proportionality matters come up.

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [25]

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Yes. And again, I'll go back to the confidence that you have. The more data you have, the more confident you are. And so it's 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, Gilead's trial has failed. The Merck's trial failed. You're right about the time we started in the safety lead-in. The ramu 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.

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Wei Ji Chang, SVB Leerink LLC, Research Division - MD of Emerging Oncology & Senior Research Analyst [26]

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Got it. And...

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Aron Marc Knickerbocker, Five Prime Therapeutics, Inc. - President, CEO & Director [27]

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This decision and our announcement today really reflect our desire to be number one, transparent; and number two, to demonstrate good fiscal discipline. But we also still think the drug merits clinical investigation, and we think that it's appropriate to take this early look with the futility analysis.

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Wei Ji Chang, SVB Leerink LLC, Research Division - MD of Emerging Oncology & Senior Research Analyst [28]

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Got it. Just one last question, if I may, on the cabira PT-cell study recently added on clinicaltrials.gov. Can you talk about the rationale for this OPDIVO combination study? And what do we know about the role of CSF1R in PT-cell?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [29]

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Well, let me -- this is, again, a study that's being done at University of Michigan, right, and BMS is supporting it. So although we -- this is a partnership, it's -- we're not directly involved in any way. I am aware of data looking at CSF1 expression. It's not so much macrophages, but on some of the stem cells, in some of these subtypes of lymphoma, I would speak to Bryan, if you have any specific knowledge of why they're picking the peripheral T-cell, yes.

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Bryan Irving, Five Prime Therapeutics, Inc. - Executive VP & Chief Scientific Officer [30]

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No, I'm surprised by the -- there could be strong rationale. I'm just not aware of it.

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [31]

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Yes. Yes.

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Operator [32]

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Your next question is from Salveen Richter from Goldman Sachs.

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Maryana Ilya Breitman, Goldman Sachs Group Inc., Research Division - Research Analyst [33]

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

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [34]

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

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Maryana Ilya Breitman, Goldman Sachs Group Inc., Research Division - Research Analyst [35]

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Got it. And also, I also wanted to understand a little bit. And so how different are the patients that you're enrolling right now or have enrolled already? How different are they from the ones that you were looking at prior?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [36]

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So again, the -- there are different -- the difference between our FIGHT trial, the Phase III trial, and our Phase I is that in the Phase I, that was late-line patients. So those were patients that had 3 or 4 therapies, right? And they were patients who were getting monotherapy, not getting added to chemotherapy. And again, it was -- and 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 were. So when we designed this trial, again knowing that -- how the drug works, that it requires overexpression, we allowed patients who are either overexpressing or overexpressing and amplified or amplification. And again, the amplification, we're testing by ctDNA, not by FISH.

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Maryana Ilya Breitman, Goldman Sachs Group Inc., Research Division - Research Analyst [37]

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Got it. And then for the -- I -- there is a lot of people who are looking at FGFR right now, and it's colon cancer. And I think like this is actually much more sort of a wider phenomenon that you are seeing. And some people are trying to go into combinations. Are you guys considering any combinations? Or you just want to get this done and figure out what to do next?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [38]

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Well, I think this is where we had our -- done our single-agent study and where we've seen our efficacy, and it's clearly an unmet need. So our idea was to start with this. But you're right, there are other diseases where FGFR2 is important. And certainly, those could be of interest as well. I think it goes back to Chris Shibutani's question that we are hoping that the data from this informs not just frontline gastric cancer but other potential indications for this. And I agree with you. I think it's -- there are other people that are being successful looking at FGFR inhibition and other tumors such as recently the [peripheral] bladder cancer, right? Slightly different mechanism. But it does speak to why we think this is a driver of tumors and why we still believe that our study is a good study and should proceed.

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Operator [39]

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Your next question is from Steve Seedhouse from Raymond James.

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Unidentified Analyst, [40]

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This is [Brian Dashmere] on for Steve Seedhouse at Raymond James. My questions are regarding the bema and the futility analysis. Can you give us any more detail on the explanation for the discrepancy and why there were so many IHC positives but ctDNA-negative patients? And if the trial is successful, would you move forward with just IHC as the companion diagnostic?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [41]

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So again, one of the things is that we do think the patient populations are different, right? So in the frontline, we do truly believe more patients overexpress FGFR2b than they do in the late line. And the reason we believe that is because we are seeing that in the patients that we screen and also because, as we discussed, our IHC partner has gone and found a cohort of patients who matched as closely as possible the patients who were 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 sort of supports that concept. I think we've also wondered, I'll be honest, about our ctDNA test because you -- as you may know, there are some recent published data that suggests when you have patients who have -- okay, back up. 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 tumor 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 dataset ever in frontline gastric cancer patients. There is no other larger dataset.

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Unidentified Analyst, [42]

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And will there be -- I think that's...

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [43]

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And especially done with a validated -- oh, and especially done with validated tests, right? Because we're the first people doing this, we're 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 a potentially CDx that's approved. So again, we're very confident in this data. But what I can't 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.

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Unidentified Analyst, [44]

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Okay. Are there prespecified subgroup analysis, they tend to look their response by each individual biomarker?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [45]

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We have some stratification, but you're limited, again, by the number of patients and what your stratification. Right now, we have not stratified by biomarkers. So retrospectively, we would expect certainly regulatory agencies always do that. Retrospectively, they look at all sorts of subgroups but not prospectively. We did -- we chose not to stratify based on this.

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Unidentified Analyst, [46]

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

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Aron Marc Knickerbocker, Five Prime Therapeutics, Inc. - President, CEO & Director [47]

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

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Bryan Irving, Five Prime Therapeutics, Inc. - Executive VP & Chief Scientific Officer [48]

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Or with aggregation problem.

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [49]

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Yes. We're pleased with the trial. It's moving along.

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Operator [50]

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Your next question is from Eric Joseph from JPMorgan.

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Turner Andrew Kufe, JP Morgan Chase & Co, Research Division - Research Analyst [51]

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This is Turner on for Eric. 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?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [52]

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Well, the reason we haven't done that is because, again, the data is so small. So I don't know if you 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 few sites usually in a few countries because that's the way these things work. So we're just not right now giving these vague 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. So I'm sorry, I'm not -- and it's just because there wouldn't be statistical accuracy around what that -- what those are other than what I'm telling you. So I'm not trying to be evasive. It's just too early.

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Turner Andrew Kufe, JP Morgan Chase & Co, Research Division - Research Analyst [53]

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Okay. Understood. And then I'm just kind of curious. Was you internal threshold maybe not high enough? I know you mentioned there were around 5,000 samples or so that determine the cutoffs. From these samples, were they primarily frontline? Or were they later-line patients? Or some combination of both?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [54]

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Yes. 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 -- 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're 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.

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Turner Andrew Kufe, JP Morgan Chase & Co, Research Division - Research Analyst [55]

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Okay. 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 they were appropriately measuring FGFR levels?

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Helen Louise Collins, Five Prime Therapeutics, Inc. - Senior VP & Chief Medical Officer [56]

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Well, I think we've announced previously that we work with Ventana. So they're obviously one of the leaders, if not the leader, in development of IHC tests. And they go through a whole series of trying to make sure that the assay is, as we've said, very specific. They do in inter-reader testing, different day testing, meaning to make sure that things are reproducible both from the assay point of view and from the reader point of view. I should bring our biomarker person. There's a whole list of things they go through for the standard design control. They've met with SEDAR about their plans. So these are -- they've gone through the appropriate steps, again, to develop the IUO. So...

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Operator [57]

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And we have a follow-up question from Salveen Richter from Goldman Sachs.

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Salveen Jaswal Richter, Goldman Sachs Group Inc., Research Division - VP [58]

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I just quickly wanted to ask. There is not going to be any OpEx changes based on that, right? Based on particular contingencies prior?

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Aron Marc Knickerbocker, Five Prime Therapeutics, Inc. - President, CEO & Director [59]

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She's asking, "Will there be operating expense changes?"

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David V. Smith, Five Prime Therapeutics, Inc. - Executive VP & CFO [60]

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No. There will be not any operating expense changes. We've kept our guidance consistent for cash utilization if those [for the year].

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Operator [61]

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(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.

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Aron Marc Knickerbocker, Five Prime Therapeutics, Inc. - President, CEO & Director [62]

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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 III FIGHT trial, as you've heard today. We remain confident about the science underpinning our pipeline, and we're committed to following a disciplined decision-making progress. We have clear hurdles to gauge the ongoing advancement of our pipeline programs 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.

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Operator [63]

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Ladies and gentlemen, this concludes today's conference. Thank you for your participation, and have a wonderful day. You may all disconnect.