Five Prime Therapeutics, Inc. (FPRX) CEO Aron Knickerbocker on Q2 2019 Results - Earnings Call Transcript

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Five Prime Therapeutics, Inc. (NASDAQ:FPRX)

Q2 2019 Earnings Conference Call

August 00, 2019 04:30 PM ET

Company Participants

Martin Forrest - VP of IR & Corporate Communications

Aron Knickerbocker - CEO

Dr. Helen Collins - CMO

David Smith - CFO

Conference Call Participants

Jonathan Chang - SVB Leerink

Timor Vanicus - Raymond James

Charles Xu - Guggenheim Securities

Chris Shibutani - Cowen

Tony Butler - Roth Capital Partners

Maryana Breitman - Goldman Sachs

Eric Joseph - JP Morgan

Nick Abbott - Wells Fargo

Operator

Welcome to the Five Prime Therapeutics Second 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.

Martin Forrest

Thank you, Sarah. Good afternoon, everyone, and thank you for joining us. A press release with the Company's second 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.

Aron Knickerbocker

Thanks, Martin. Good afternoon and thanks for joining us today to review our progress and achievements during the second quarter and preview upcoming milestones. I'm pleased to say that all clinical programs are on track and we’re entering in a period where upcoming data events will allow us to make disciplined data driven decisions to prioritize pipeline investments.

For the Five Prime controlled assets, our current priorities are; one, bemarituzumab in the FIGHT trial; two, advancing the most promising FPA150 opportunities; and three, safety and dose finding for FPT155. Okay let me start by recapping why we remained confident about bema's potential to be an important new medicine for patients with gastro cancer. Bema is the targeted agent that binds specifically to FGFR2b, which is a protein that is frequently over expressed in gastric cancer and is associated with pour prognosis.

The bema Phase 1 study demonstrated clear monotherapy activity and heavily pretreated gastric and gastrpesphageal junction cancer patients. For patients in the monotherapy Phase 1 study who achieved the trough plasma concentration that the dosing regimen used in FIGHT also achieved, the monotherapy objective response rate was an impressive 31% and the disease control rate was 84% that was without chemotherapy.

Now, we’re combining bema with modified FOLFOX6 chemotherapy in the FIGHT trial, which we know to be additive in efficacy and FGFR2b over expressing tumor models, no overlapping toxicities were identified from the safety lead into the FIGHT trial and validated molecular diagnostic tests have been developed through reliably identified patients who potentially will derive benefit from bema and standard of care chemotherapy.

Additionally, a relevant analog Herceptin has proven the targeted therapies work in gastric cancer and the ToGA trial that resulted in Herceptin’s approval for use as a front therapy in combination with chemotherapy was quite similar in design and power to the FIGHT trial. Herceptin also works that binding to a surface protein over expressed on gastric cancer cells much the same way that bema binds to FGFR2b and Herceptin relies on ADCC as one of its mechanisms of action. However unlike bema, Herceptin is not believed to have much monotherapy activity in gastric cancer.

With respect to the clinical operations in the FIGHT trial, we are pleased that the enrollment continues ahead of plan and we are disclosing today that we have reached the milestone in dosing the first patient in Japan, which has a large population of patients with gastric cancer. While we remained confident about bema, we plan to conduct an early futility analysis in the FIGT trial that Helen would discuss further. This is consistent with our emphasis on portfolio prioritization, and given the higher than expected enrollment rate, we will pause enrollment in the FIGHT trial with sufficient patients have been enrolled to support the plan futility analysis.

We expect that pause and enrollment to occur during the fourth quarter of 2019. This pause will conserve resources while we generate data from the bema, FPA150 and FPT155 programs to make data driven decisions to prioritize pipeline investments. Assuming we have futility analysis in FIGHT, we will have adequate bema drug supply to resume enrollment promptly. As a reminder, if we move forward, we believe one in three gastric cancer patients will be eligible for treatment with bema, which represents a substantial increase in the bema commercial opportunity in the United States, Europe and Asia regions versus our reasonable expectations. Altogether, we continue to be excited about the potential for bema to be an important new medicine for patients with gastric cancer.

Turning to FPA150, ESMO has accepted our abstract and we will present data at the upcoming Annual Meeting in September. We expect to present data from the monotherapy Phase 1b expansion cohorts at the 20 milligram per kilogram dose in patients with breast, ovarian and endometrial cancers over expressing B7-H4. While monotherapy data will be the focus at ESMO, we believe based on preclinical data that FPA150 holds significant potential in combination with other checkpoint inhibitors or chemotherapy agents.

On that front we're approaching completion of the safety lead-in for the combination of FPA150 with Keytruda and expect to open the ovarian expansion cohort later this month. If we identify efficacy in the breast or endometrial monotherapy cohorts, we may also begin additional chemo and/or checkpoint combination studies in those indications.

Turning to FPT155, enrollment is proceeding according to plan in the dose escalation portion of the Phase 1 trial with fixed dose level cohorts enrolled and dose escalation continuing. We have submitted an abstract to present dose escalation safety and pharmacokinetic data from this program at SITC at November. For our partner programs, completion of enrollment in the randomized Phase 2 trial of cabira and OPDIVO in second line pancreatic cancer is imminent and we expect BMS to have actionable data by next year.

BMS is a trial sponsor and will determine when it's appropriate to disclose data and next steps for this program. And finally, BMS-986258, a fully human antibody targeting TIM-3, an immune checkpoint receptor, continues to advance in a Phase 1/2 clinical trial and is now being studied by BMS in combination with OPDIVO. As I mentioned earlier, we are preparing for several upcoming data events that will allow us to make disciplined data driven decisions to prioritize pipeline investments.

And with that, I'll turn the call over now to Dr. Helen.

Dr. Helen Collins

Thank you, Aron. Let's begin with bema. Building on Aron's earlier comments, the reason to add an early futility analysis to the FIGHT trial is to ensure the trial is adequately powered to detect an overall survival benefit at full enrolment. I'd like to remind you the FIGHT trial is a double-blind placebo-controlled trial which means we don't see the unblinded data. There is an independent DMC, which does review the unblinded data and at our last meeting with them, they recommended continuation of a trial without modification.

The trial continues to enroll very well and we continue to see globally a prevalence of FGFR2b in the frontline setting of over 30%. In light of rapid enrollment and our desire to manage our resources wisely, we're planning to pause the enrollment in the FIGHT trial during the fourth quarter. We estimate that by the fourth quarter, we will enroll approximately 25% of the total plan patients, which should be sufficient to generate the number of events needed to conduct a futility analysis in the first half of 2020. The utility analysis is a crucial de-risking event for the FIGHT trial, as once we know the outcome of this analysis, we will be able to make a data-driven decision to either resume enrollment and then trial will discontinue.

Bema is a well tolerated, target monoclonal antibody with demonstrated single agent entity, being used in a biomarker selected patient population. And we remain, optimistic about the potential for bema to improve the survival of patients in frontline FGFR2b over expressing gastric cancer.

Moving on the FPA150 which is our first-in-class B7-H4 antibody, this antibody is designed to target tumor cells through two mechanisms of action, by enhancing killing of B7-H4 over expressing tumors to enhance ADCC and by blocking B7-H4 from sending an inhibitory signal to CD8 T cell.

We plan to present preliminary data as ESMO from approximately 30 patients preselected for B7-H4 over expression across the ovarian, breast and endometrial monotherapy expansion cohorts. This will be early data as most of these patients who had a single scan and only handful would have on study long enough to have had the second scan. We also anticipate having safety data from the first four patients enrolled in the combination of cohort of Keytruda and FPA150.

Our preclinical data for FPA150 demonstrate same synergy with anti-PD-1 additivity with chemo and modest activity as a single agent. For this reason, we believe the ultimate development path for FPA150 will be at the component of combination regimen, similar to how other monoclonal antibodies directed to solid tumor targets are used. For example, Herceptin and Perjeta are used in combination with chemotherapy.

In May, we initiated the combination dosing and a B7-H4 selected ovarian cohort with full doses of both FPA150 and Keytruda. We anticipate completing the safety lead-in and opening the Keytruda combination expansion later this month, which should generate efficacy data to make a go-no-go decision in 2020 for the FPA150 Keytruda combination in ovarian cancer.

Turning to FPT155, the dose escalation is proceeding according to plans and we expect to present the first available safety and pharmacokinetic for the initial dose escalation cohort at SITC November. As you recall, an antibody that activates T-cell through CD28 resulted in superagonism and severe cytokine release syndrome.

By contrast, preclinical data demonstrate with FPT155 requires co-stimulation for T-cell activation and therefore should not trigger superagonism. So reporting early safety, tolerability and lack of syndrome at early dose levels will support the key differentiating feature of FPT155.

Aron has already provided you an update on the partner programs, so I will now turn the call to our CFO, David Smith.

David Smith

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 and on our company website. We ended Q2 with a strong balance sheet. Cash, cash equivalents and marketable securities totaled $214.1 million on June 30, 2019 compare to $237 million on March 31, 2019. 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 $34.4 million or $0.99 per basic per basic and diluted share. This was flat with the prior year. Collaboration and license revenue was $3.3 million for the quarter. This is a decrease from last year second quarter revenue of $7.6 million and was expected. It is primarily related to lower collaboration revenues from Bristol-Myers Squibb as a result of the completion of the research term under the immuno-oncology discovery collaboration in March 2019.

Research and development expenses were $29.4 million for the second quarter of 2019 compared to $33.4 million in the second quarter of 2018. This decrease was primarily related to lower compensation cost as well as lower manufacturing cost related to FPT155 drug production and lower diagnostics cost related to the FIGHT trial. These cost reductions were partially offset by higher CRO costs that were related to strong patient enrollment and the opening of new clinical trial sites.

G&A expenses totaled $9.7 million which were essentially 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 a $148 million to a $153 million in cash, cash equivalents and marketable securities. In closing, we have the resources that will take us not just through, but beyond go-no-go decisions for the FIGHT trial, FTA150 and FPG155.

Now I’ll turn the call back to the operator for Q&A.

Question-and-Answer Session

Operator

Thank you. [Operator Instructions] Our first question comes from the line of Jonathan Chang with SVB Leerink. Your line is now open.

Jonathan Chang

First question, can you provide more color on the rational for pausing in moment in the FIGHT trial when you've enrolled enough patients to support the futility analysis?

Dr. Helen Collins

Yes, hi, Jonathan. This is Helen. Yes, absolutely, I mean I think we -- at the last quarter call, we talked about adding futility based on seeing such a high number of patients qualifying for the trial and wanting to make sure that while we thought all patients have a scientific rationale to benefit from bema. Obviously, we need to make sure that the trial is powered such that, that when we may complete enrollment, we will be -- the trial will be successful.

So, and at that point, we were a little bit vague as to when it would happen because we didn’t -- we were still ramping up sites in Europe, and really we haven't had any events yet. So, now we feel like we’re on a point where we know when we want that futility and when that futility can occur. And then again because enrollment so quick, we think it’s prudent for our company that we end up pausing enrollment, observing, reading the futility, and them resuming enrollment, presuming that we pass. So, I think it’s really a matter -- maybe Aron, you’d like to add to this about also all of our -- the rest of our portfolio.

Aron Knickerbocker

Yes, that is the -- the other element here is fiscal discipline we’re exercising with respect to the portfolio and I think once we see whether this event becomes a de-risking event as we pass and we would be in a position to rapidly resume enrollment. We have drug supply ready to go and I think we have investigator enthusiasm so we passed futility.

Dr. Helen Collins

Yes, you could imagine Jonathan, the patients you've enrolled said, after Q4 until you read out the futility, are going to contribute to the futility. So, of course, yes, it'd be nice to have those patients while we resume, but everything, the trials open at essentially all the sites we want to be open and so enrolling for a quickly and we feel confident that we can resume things quickly.

Jonathan Chang

And second question, can you provide more granularity on how enrollment in the FIGHT space progress versus you initial projections? As I've heard you correctly, you've indicated 25% enrollment in the fourth quarter. How does that compare to your initial part?

Dr. Helen Collins

Yes, we didn't ever give exact projections publicly about our enrollments. We made analogy to the ToGA trial. You may recall that where if you go back and look at the ToGA trial, which is now you know 8 to 10 years ago that it took them 36 months to enroll a trial that was fairly similarly sized. And of course, there's a lot more competition out there. But then we also have access to China to partnership. So that was kind of a vague guidance that we gave previously. And I decided that we're ahead of that schedule.

Operator

Thank you. Our next question comes from the line of Steve Seedhouse with Raymond James. Your line is now open.

Timor Vanicus

This is Timor Vanicus on for Steve Seedhouse. So, we have a couple questions about bema. So, in terms of this potential futility analysis, have you settled on the hazard ratio threshold that will be used? And could you talk about some of the factors? And how you will be choosing that that ratio?

Dr. Helen Collins

This is again Helen. I can start with that and Aron can jump in. So, we haven't said what it is, this is obviously -- we have a recommendation that will be making to our DMC, but there is a conversation that that has to occur there. What we do definitely want to do and plan to do and there should not be an issue and doing is making sure that that hazard ratio is less than one. So sometimes you may see trials designed where an early futility, the hazard ratio is set at one and essentially what they're trying to do is very early on, just make sure that drug isn't worse than placebo. We're not concerned about that, right. What we really want to do is make sure that we're on track my show benefits, so -- and to make sure that this trial, again with its 540, 550 or so planed patients is powered to achieve its endpoint. So Aron, you want to add to that?

Aron Knickerbocker

No, I think that answers it. Thanks Helen.

Timor Vanicus

Okay, thanks. And next question, I guess, could you talk a little bit more about the process that informs about the enrolled patient characteristics in this bema trial? I mean, it sounds like you have a pre-specified plan. And it sounded like you had another check-in recently. And could you talk about the proportion of Asian population that you see now versus what you saw in the first 100 patients, I believe it was 100 patients that you look at originally?

Dr. Helen Collins

Yes, I can't off of the top of my head tell you what proportion of patients are China, ex-China Asian, U.S. or European. I can't say that just like we saw back and talk about it in our Q1 call that we are seeing a FGFR2b over expression prevalence in this frontline setting that is similar globally. So there's no difference in the different geographic areas. And then as you may recall, what we talked about at that point was that we are seeing, we had originally designed the trial where patients will be enrolled based on being over expressing FGFR2b on their tumors.

And then as a proxy for that over expression, we had added ctDNA because we were concerned that biopsies might miss patients, and what we're finding is that we are capturing more patients than we actually thought based on just the over expression alone. And again, based on the mechanism of action, this drug that it requires protein on the surface of the cell, this is what we would want to see. So, but it is different than the patient population that we found our late line, Phase I study.

Aron Knickerbocker

I'll just add that the way that the sites have come in terms of the country and site activation serve in East to West pattern. So, the first sites were opened in China and then South Korea, later in North America and most recently in Europe. And so, now we're up to 18 countries with sites open and it's today and most recent is Japan. So, we're in a early days of trial, most of patients would have been coming from South Korea and China, that's now skewing downward as we get more patients entering in North America and Europe is now contributing a number of patients. So, that ratio is going to continue to change as more European patients come into the trial but as we said, this positivity rate is holding at over 30% and seems to be relatively consistent around the globe.

Timor Vanicus

Okay. Thank you. And then I guess, we do have a quick question FPT155. So, in terms of the type of data presentations that you have since, I think for FPA150, you talked about presenting safety data but then obviously also included some efficacy data. Is that kind of per forma we should expect at SITC? Thank you.

Aron Knickerbocker

No, because we were filing along with does escalations with FPA150 at the time of the ASCO presentation. We're still in the midst of dose escalation as I noted earlier today on the call. We are in the sixth dose level, but it's our plan to present whatever is safety and pharmacokinetics and we have from those early levels but we're still continuing dose escalation.

Timor Vanicus

Okay, great. Thank you very much.

Aron Knickerbocker

We do feel it is important to us, as Helen noted, just given the way that this module act, by signal in QCD 28 and acting as a T-cell co-stimulator to show safety and given the history with molecule anybody directed to CD28 which is not safe because it new superagonism. As a result, release syndrome that was very severe, we have nothing at all, pre-clinically. We benchmarked to prepare antibody. So, we are confident about that going into the clinic, but we also recognize that we need to sell versus safe dose in humans. So, we think this is a very important set of data for de-risking practice.

Operator

Thank you. Our next question comes from the line of Michael Schmidt with Guggenheim Securities. Your line is now open.

Charles Xu

Hey, guys. This is Charles Xu on for Michael Schmidt. Thanks for taking the questions and congrats on a quarter. I had a -- let's just start off with a couple of clarifying questions on the bema FIGHT trial. On the FGFR2 positivity, I just kind of wonder if you could provide any incremental detail around the percentage of patients that may have tested positive by ctDNA alone, positive by ctDNA and negative by IHC or positive for both?

Aron Knickerbocker

Yes, we haven't shared that publicly yet. It's -- the ctDNA rate of positivity is consistent with our expectations going in study based on published data and what's been seen previously. So, that's holding up with what's interesting though is the IHC rates in this previous patients is higher than we expected and that is now holding up as well consistently with many more patients now on study.

Charles Xu

Got it, okay. And then next clarifying question for the -- let's was some kind of dose modifications that may have taken place to try to maintain certain levels of our plasma concentrations. I just want to clarify, when this modification occurred and how many Phase 3 patients if any may have received the prior dosing scheme? Thank you.

Aron Knickerbocker

Yes, this to be clear, it wasn’t a modification with the dosing scheme we tested in the safety lead-in and how can I describe the dose levels that were tested there and what we took forward and in the Phase 3 portion.

Dr. Helen Collins

Yes, so I can say in our phase, actually monotherapy Phase 1 patients were dosed every two weeks and you may recall that we did not have any dosing limiting toxicity, so that the dose eventually were chosen based on, obviously efficacy being observed in the single agent, and then also at the dose that we had predicted there'd be efficacy based on new remodels. And so, what we did when we went to our Phase 3 -- excuse me, our safety lead-in a chemotherapy plus bema is, we really what we wanted to do. It hit its target C trough faster and of course you can do that one of two ways. You can either have a higher loading dose on day one or you can add a single dose on day eight. So that patients were treated every two weeks except when they are in their first cycle they also get one extra dose on day eight.

So we chose to do this so the later way demonstrated in that safety lead in that and since the all patients achieved the target trough by day 15 and we think this is important because it’s what we saw retrospectively when we looked at our Phase 1 data it’s only patients achieve that target trough did they actually have efficacy. And I think that’s what Aron you’ve mentioned in the earnings call that we actually look at that sub-group the response rate that’s almost 30% again it’s being retrospective so we think it’s important to hit the target trough we think the monotherapy data supports that and every patient on the Phase 3 trial from the beginning has received this dosing schema.

Charles Xu

Got it, that makes sense. And then the last question from me. Shifting gears a bit now to FPA150 the B7-H4 I recall you guys mentioned very briefly earlier on the call that your go-no-go decision may occur in 2020 if you guys snitched the safety lead with the key through the FPA combination just kind of wondering what kind of benchmarks are you thinking about regarding around this go-no-go decision and how much efficacy would you hope to see in terms of continue? Thank you.

Dr. Helen Collins

Again I’ll start with this I mean as you know these are three tumors with a novel section triple negative breast cancer but for ovarian and endometrial and all the rest of breast cancer there are no checkpoint inhibitors approved the single agent activity is maybe anecdotally up to sort of 12%, 15% or less than that so obviously we want to see higher the reason I'm a little bit vague because again it’s always a risk benefit and I think one of the properties we’re seeing about FPA150 is that there’s very little toxicity.

So then I don’t know if Aron really whether there’s a benchmark I think you’ve been talking some - questions so you want to see double what you might expect with the PD1 alone. But again it’s really it’s a whole totality of the data until its tolerated and particularly with drugs that have checkpoint activity, durability of response is obviously really important as well. It’s really more the overall survival in PFS, arguably, at times that can be more important than response rate.

Operator

Thank you. Our next question comes from the line of Chris Shibutani with Cowen. Your line is now open.

Chris Shibutani

Great, thank you very much, apologies. I missed part of the beginning of the call. So hopefully I can raise the topics that haven’t already been addressed. So please do let me know. Looking to see with regard to your thinking around business development, the overall strategy in particular, you had described continued efforts to explore that. How are you feeling about that relative to some of the decisions that you've had to make to sort of narrow your focus a little bit earlier this year? What's your outlook?

Aron Knickerbocker

So business development is an ongoing focus of ours. We have discussions ongoing now that are active spanning multiple assets. We don't provide guidance on those. But we do feel that it will be an important part of our strategy going forward, as it has been historically, as we look to collaborative relationships, access, non-diluted capital, but also other things as well. So that can be broader development programs, combination agents, for example, global manufacturing, and commercial reach. All of those sorts of things are important elements to us as we seek to advance the programs and five prem. So it is an active area for us. We don't guide on any business development activities. But it is core to the strategy for how we intend to advance these programs. And discussions are active.

Chris Shibutani

Right now, I've always thought that the proteomics platforms wouldn't be a valuable asset in terms of figuring out how to further leverage that. During this year, you've also announced previously that your Chief Scientific Officer was moving on to another opportunity, can you update us on the status of your efforts to recruit someone to replace that important role?

Aron Knickerbocker

Yes, so we have hired a search firm and retained search firm, their efforts are ongoing, that they've identified a number of interesting candidates. But in the meantime, we have assigned the duties of the courts incentive foster two very capable Vice Presidents here at Five Prime. So each has responsibility for roughly half of the research organizations, one group focused on discovery in the late stage research programs, the other focused on our biotherapeutics and molecular biology areas. And so, they've risen to the task nicely and none of the programs have really suffered as a result of the departure. And they are still progressing, as we hope but services ongoing and will update you further.

Chris Shibutani

Great, and then you provided some updates on some shifting of the components of your board members. Can you just help us understand what you're thinking about in terms of those decisions that you've made in terms of what the relative distribution and capabilities or insights that you're hoping to gain at this stage for the Company?

Aron Knickerbocker

We strive to have a board that's composed of people with diverse backgrounds, experiences and capabilities. And I think, if you take note of the two recent additions, what you've seen there is we've added in the case of Carol Schafer, who was most recently at Wells Fargo in Equity Capital Markets, somebody who's a very experienced person with respect to capital markets and financing biotech companies. She's also been in an operational role at Lexicon Pharmaceuticals in her past. And so, she brings a lot of depth in terms of financial acumen and awareness of capital markets and has worked with a number of companies like ours and getting them finance to capitalize. So that was the rationale for adding Carol Schafer.

And then, we're also happy to have welcomed Lori Lyons-Williams. She brings a different profile. She is a commercial leader and is currently in that capacity at Dermira in the dermatology space and Allergan before that, and others, other companies as well, but very experienced and capable, commercial leader who's launched important brands, built out commercial groups, and I think real depth and current acumen about how drugs are brought to market, commercialized and reimbursed. So, that's why we have chosen to add those two members to our Board. I think with those additions, we have a well-rounded and diverse Board and they are really intentionally selected, just given the backgrounds and capabilities.

Chris Shibutani

Great, and then last one, and I'll try to laser down to one year asset, it is a partnered asset. But the TIM-3, I noticed in the release, you mentioned that the expected trials size is increased from 380 to 383. What should we take that to mean? And apologies, again, if I've already bought this up.

Aron Knickerbocker

No, that's fine. We just mentioned it briefly and it's a significant program, it's a Phase 1/2 trial and has multiple components. So initially there was dose escalation with monotherapy anti-TIM-3 and then BMS is combining both with Opdivo as well as recombinant hyaluronidase for potential subcu administration, and I think it signifies continued investment in this program. We are pleased what BMS is doing with the TIM-3. We can't obviously divulge anything confidential about the nature of the trial. So, I have to leave it with that, but we're pleased with their commitment to this program.

Operator

Thank you. Our next question comes from the line of Tony Butler with Roth Capital Partners. Your line is now open.

Tony Butler

Thanks very much. Helen or Aron, just apologies for just sticking with the FIGHT trial, but three really brief questions. When you had a conversation with the sites for how you -- I guess the question is, how did you communicate to them that would have that an arm pause and what's will be around the fourth quarter? And the reason I asked this is because this is actually question two, you asked about the hazard ratio on this call, but I did recall before that you were growing to put the futility, you want to put the futility now and having hazard ratio clearly less than one so there would be clearly some activity, and I wanted to know if that's still the case because importantly would you communicate what that number is back to those sites, once that analysis has occurred importantly because you alluded also to their excitement to re-enroll and I wondered if they make it hand-in-hand? And then the last question is, and you may said forgive me for missing it, is enrollment ramping at all sites, not just ones or two or three but also to new sites which have just opened? Thanks a lot.

Dr. Helen Collins

Thanks. So again, I'll start and Aron will jump in with those things I forget. So, first in terms of the communication of the pause, we're in the process of doing that, that needs to done in conjunction with when we're going public with you. So the investigators won't hear about that till over the 24 hours. We obviously did communicate to them about findings in terms of the prevalence FGFR2b and so that's confident and as you think that's contributed to the fast enrollment and the enthusiasm of the study. In terms of the hazard ratio, you absolutely correct, and I think that is still our intent to have hazard ratio less than one.

I'll remind you that, when you are looking at futility, what you are doing is you are looking at the ability of your trial to demonstrate the benefit of the drug. You are not looking at the drugs benefit per se. So futility, the actual bar is usually not something that's communicated publicly. What is communicated obviously is after our discussion with the DMC is that. We have passed futility and that the trial is appropriately sized and designed to demonstrate the benefits that we think we need to get approval of the drug. So, obviously, the investigators do hear outcomes of DMC. They will hear that the futility has been passed, but they will not know what that bar is.

And then finally I guess it was the question about enrollment. So, yes, we have not seen greater interest or less interest, anywhere. I think as Aron said earlier and I thought it was very nice you said that Aron, we’ve opened sites going from East to West and that’s just more regulatory how long it take to open trials in various countries. But whenever sites have opened, they're enrolling at approximately the same rate. China obviously has more gastric cancer, they’re a bit higher on proportionally for those patients enrolled per site, but otherwise there’s not really a geographic difference in terms of other moments.

Operator

Thank you. Our next question comes from the line of Salveen Richter with Goldman Sachs. Your line is now open.

Maryana Breitman

Yes, hi. Thank you for taking my questions. This is Maryana Breitman on for Salveen. I had a couple on the FTP155 is a monotherapy right now, but it looks like combinations will make sense. Are you thinking about combinations going forward? And what those will be and also in which indications?

Dr. Helen Collins

So for 155 for the CD80-Fc is that, which is in B7-H4 antibody, okay.

Maryana Breitman

Yes.

Aron Knickerbocker

155.

Maryana Breitman

Yes.

Dr. Helen Collins

So, 155, certainly, preclinical data suggest that a combination as we represented that in ACR last year and there was excellent preclinical data to suggest with a combination may work better than single agent. Right, now we’re concentrating on the single agent and so as we said we think it’s really important to show that there’s a therapeutic window here this particular mechanism of the action. So, we're certainly keeping the idea of combination in mind.

Maryana Breitman

So, but do you have any idea for the indications like I mean, right now, it’s a basket trial, but like what are you thinking or you just want to see with the data?

Dr. Helen Collins

We've had lots of conversations about this. I mean I think as we do dose escalation to some extent, it will depend what we see. I mean the mechanism of action obviously what we’re hoping to do is to see a much broader response in then what you feel the CTLA agonist alone for example because we’re doing -- we’re inhibiting that mechanism as well as directly stimulating the T-cell. But at the same time obviously, the tumor has that T-cell there, so we do have some thought about this but we have not made those public.

Maryana Breitman

Got it got it and another one I just wanted to, if you can give some commentary on. We still have expanded the cabira program. It looks like they keep bringing new indications and I was just wondering. What is the dialog about that? And would you ship on them like why I mean what do they see that they keep bringing more indications on that so…?

Dr. Helen Collins

Yes our team is doing work some together again BMS is developing the drug now but I think we’re really pleased by the amount of resources that they putting towards the number of trials that the broad indications that they’re looking at and unfortunately I can’t say more than that other than it’s clear that BMS is not winding down their efforts to the contrary so…

Maryana Breitman

Thank you and thanks all for taking the question.

Operator

Thank you. Our next question comes from the line of Eric Joseph of JP Morgan. Your line is now open.

Eric Joseph

Thanks for taking the questions. Just try to clarify on the futility analysis for Right that and it's based strictly on the primary endpoint of overall survival or where we could get opportunity to look at some of the secondary endpoints with PFS or objective response rates. And I guess, secondary, I guess, given the surprising the proportion of high expressers for FGFR2b and the obvious implications is that as a prognostic indicator. Is there any reason to think that FGFR2b would function differently as a therapeutic target by line of therapy?

Dr. Helen Collins

Yes, so I think the easy question is the second one. So no, there's absolutely no reason to think that it would be by line of therapy. I mean, they're clear growth factors that stimulate the cell to divide, and so blocking that growth factor and then the second mechanism of the ADCC that's going to be regardless of line of therapy. In terms of the futility, again, as we said, we have a proposal that we're that will be talking about with our DMC. So we haven't said specifically what will what endpoints will be using or whether it will be a composite.

Eric Joseph

And it was just a strategy clarification question as it relates to FPA150. Is the expectation at this point that the monotherapy program will not be advanced and really going to just go-no-go decision will be based on the data that you're seeing in combination with Keytruda?

Dr. Helen Collins

So I'm really glad you asked that question. So that's absolutely not the case. I think what happened is to us, we were really excited at ASCO, because what we felt that the data represented was just how much how enthusiastic again, the investigators were how easy was to find these patients, how safe the drug was. Our goal at ESMO is some of those same things now that we're going to have approximate, as you said, 30 patients who would dose at the full dose of 20 milligrams per kilogram, and again some early an early sense of the efficacy.

Now, I think we are trying to temper expectations in that we do not expect based on the mechanism of action and our preclinical data that this is something where you're going to see 70% response rate, we do not expect that, we expect what you might see and that's why we use those analogies of like a Herceptin alone or something where it's our drugs projected that are very successful drugs have some single agent activity, but really their greatest benefit has been in combination. And because of the ubiquitous nature of B7-H4 over expression, it's homogeneity, it's lack of expression on normal cells, the lack of roxane toxicity, that is very likely where we'll end up developing these drugs. It also allows you move earlier to line to therapy.

So, we should expect to see some single agent something now, I think what we're trying to do is just make sure don't go out there thinking it's going to be a 70% response.

Aron Knickerbocker

Yes, I'm trying to stay consistent about this point. As we talked about this program since they went into the clinic, which is we do want to see single agent activity, we're demanding that it does not me and the ultimate use will be as a single agent, Herceptin combined with chemotherapy, we think that's again an analogous setup here. So we are not saying no tomorrow therapy activity, and we are also saying that we think that more likely maximization of patients benefit will be in combination.

Eric Joseph

I guess maybe just in setting the stage for ESMO a bit more here. Can you just talk about sort of the distribution of those 30 patients across different histology cohorts that you are occurring here across rest of ovarian and endometrial, and sort of how to think about duration of follow-up as well? Thanks.

Dr. Helen Collins

Well, I think, as we are saying that we have data on about 30 patients who have had one scan. So again it's going to be early, right, and handful and been long enough to have second scan. In terms of the distribution, well, you can imagine breast and ovarian little more common than endometrial. So, it's a bit more of those than their endometrial, but it's not a huge difference between the different arms.

Operator

Thank you. [Operator Instructions] Our next question comes from the line of Jim Birchenough with Wells Fargo. Your line is now open.

Nick Abbott

Good afternoon, it's Nick calling for Jim. And thank you for taking our questions. Just going back to the bema trial, since you've made this discovery of the IHC-positive and now double positive patients, have you screened the literatures to look for instances where this has occurred on the targets? And what's your theory on why this is occurring in these front line patients, but not the chemotherapy-treated patients? And then secondarily, does the futility allow for analysis of both the double positive and the single positive patients? And then I have a follow-up. Thank you.

Dr. Helen Collins

So, I think the first question really, in some ways, it has to do with assay, and then you have to recall that we're in the first company that have a drug that is geared to FGFR2b over expression. There are drugs out there oral tyrosine kinase and inhibitors for FGFR2b mutation, but that's completely different. So, one of the difficulties with looking at literature is, we're the first people to work with Ventana to come with a high quality I/O of essay.

So, if you've gone through literature, you'll find variations and over expression depending on what essay there you think from a lower, I would say, 7% up to 60% to 80%, probably those 60% to 80% is because the assay is probably not very good. So, even our 30% that was falling into what you might see out there, if you hut around.

In terms of your second question which has to do with the futility. So again, a futility is again really something that we are choosing to do right, which is why it's not -- you don't have to pre-specify that in a protocol because again what we are trying to do is, is to make sure the trials designed appropriately. Certainly, the DMC will have the information about patients whether they're IHC positive, ctDNA positive or both.

But, again, we haven't disclosed how we're going to ask them to look at that. So, yes, I'm being reminded, but our goal again is for the purpose of the trial that because the inclusion criteria either one ctDNA or IHC, but that would still be how this trials designed right now. So, but you want to speak in to whether or not the outcome of the futility could be some change in the trial design or size.

Nick Abbott

Yes, yes.

Aron Knickerbocker

And then going back to your earlier question, on literature data, we've dug into the findings from the ToGA trial which again is a Phase 3 study of Herceptin for chemo versus placebo plus chemo. There you can see that it was over expression that predicted the survival benefit from Herceptin not gene application. So, in patients that were lower of expressers, there were no benefits, so there I see one for instance, there was no hazard ratio benefit seen even if their gene amplified.

But in the patients who were IC2 or 3 status whether or not they were amplified in this case by FISH, there was a significant benefit and the hazard ratio was 0.65. Again, we think that’s a relevant analog and makes a lot of sense for an antibody that works on the cell surface and block growth factors and in cases in NK cells. It shouldn’t matter so much whether there is multiple copies of the gene as long as the target is there, and you can prevent the growth factors signaling the in case NK cells. So that seems to be what happened with Herceptin and the ToGA trial. We think that instructive and germane for the FIGHT trial as well.

Nick Abbott

It’s very hepful. Thanks Aron. And then moving to FPA150, the patient characteristics of these expansion patients that we see at ESMO, are they different enough from those are involved in this dose escalation and really bio-marked positive patients and I fully acknowledge that the doses that you are testing in those patients blow the 20 milligrams that we should expect the data to be different at that coming up from ASCO?

Dr. Helen Collins

See right, the main difference is going to be the dose. I mean again ASCO had a portion of patients who are B7-H4 positive and a proportion that were negative and only a couple that had, that were in a dose level we might we expected to see something for B7-H4 positive. So I think there’s going to be a larger number of those patients obviously 30. But again early, so I think the hardest thing is going to be, how do you judge the patients who have stable disease when they believe one scan, right? Is it going to be stable disease onto the way to PR or stable disease onto way to a progressive disease? And it'll be too early for those patients, right?

Nick Abbott

Okay, but stable disease at least by getting some benefits that one of thing, but just that how low.

Aron Knickerbocker

Right.

Dr. Helen Collins

Yes.

Nick Abbott

And then can you remind me of roughly, how many patients you want to enroll in each of these cohorts? And whether it you're employing a Simon two-stage design?

Dr. Helen Collins

Yes, we have a Simon two-stage design, so -- and up to 30 is how the cohorts are written right now.

Nick Abbott

And then a last one for me on 155, mean, given the nature of this target, I'm assuming that the dose that you had to start out was very much below at therapeutic dose. You're at a dose level of six now. How many doses levels have you planned? Or maybe another way to ask the question is. When do you get to a dose level where the pharmacodynamics that you're seeing is similar to what you’ve needed to see in preclinical models?

Dr. Helen Collins

Yes, I mean, obviously, you have to have that to go into the clinic, right. And that is a big discussion you have with regulatory agency because that determines to some extent where you start. So -- and I realized I am avoiding at your question because we haven't made that public. So, you know, we're getting close, maybe we're there, we get close, maybe we'll there in a little while, but yes,

Operator

Thank you. This concludes today’s question-and-answer session. I would now like to turn the call back to Aron Knickerbocker for closing remarks.

Aron Knickerbocker

Thanks. As I said at the beginning of the call, all of our clinical programs are on track, and just to restate the near term priorities, those are. One, bemarituzumab and the Fight trial; two, advantaging the most promising FPA150 opportunities; then three, safety and dose finding for FPT155.

And as I mentioned, we're committed to making data driven decisions and also exercising tight fiscal discipline. We've got the resources to act on data from the FIGHT futility analysis, FPA150 study, and the ongoing trial with FPT155 and beyond.

So with that, I'd like to thank you all for joining us today. I'd also like to thank the patients and the investigators who participated in our clinical trials, our Five Prime employees and our strategic collaborator who all contributed to the continued advance number of programs. Thank you very much.

Operator

Ladies and gentlemen, thank you for participating in today's conference. This does conclude today's program. You may all disconnect. Everyone have a great day.

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