Five Prime Therapeutics Inc
Q3 2017 Earnings Call Transcript

Published: 7 Nov 2017

[Operator:]

Good day, ladies and gentlemen and welcome to the Third Quarter 2017 Earnings Call for Five Prime Therapeutics. As a reminder, this conference call maybe recorded. I'd now like to introduce your host for today's conference call, Mr. Derek Cole. You may begin.

[Derek Cole:]

Good afternoon and thank you for joining us. I'd like to welcome everyone to our conference call to discuss results for the third quarter of 2017. We issued a press release this afternoon and also posted slides that accompany this presentation. The slides can be found under the Investor Relations section of our web site, under Events and Presentation. Joining me today are Dr. Rusty Williams, Chief Executive Officer; Dr. Helen Collins, Chief Medical Officer; Mr. Aron Knickerbocker, Chief Operating Officer; and Mr. Marc Belsky, 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 Rusty.

[Rusty Williams:]

Thanks Derek. Good afternoon everyone, and thank you for joining us today. As I’m sure you all saw two weeks ago, that our COO Aron Knickerbocker will succeed me as CEO on January 1st. This transition is something I discussed with the board for a while and I wanted to ensure that it took place at a time of strength for the company which is squarely [Ph] we are. I’ll become Executive Chairman; Chair our Scientific Advisory Board and I’ll lead a small innovation group working on a new approach to Immuno-Oncology entitled “Five Prime”. This is a bitter sweet moment for me as this is the last earnings call I’ll lead for Five Prime, but this transition was my idea in the first place and I couldn’t be more pleased with the board’s decision to appoint Aaron as CEO. The board did an extensive search and considered a number of highly qualified candidates including Aaron, but it became clear that his oncology experience, strategic thinking and leadership skills stood out, and these will be critical as Five Prime grows and advances its pipeline. Aaron has already been instrumental in the design and execution of our corporate strategy, whether it be clinical, operation or financial. And importantly, he has remained fully committed to communicating and delivering value for our shareholders through effective pipeline growth and the valuable collaborations we’ve established with leading pharmaceutical companies. We’ve built a truly exceptional management team and I have full confidence in them and our programs as this transition takes place. Aaron will say a few words later about Five Prime picture for 2018, but for now, let me turn back to our programs shown on slide three and the impressive progress we’ve made during the third quarter of 2017 highlighted on slide four. I’ll start with Cabiralizumab our CSF1 receptor antibody that blocks immunosuppressive macrophages. We and our partner, BMS are studying Cabira in combination with the PD-1 checkpoint inhibitor OPDIVO in seven different tumor settings. We have completed enrolment in most of the Phase 1b cohorts and expect the remaining cohorts to fully enrol before the end of the year. More importantly, the first data from this trial is scheduled to be presented in the late breaking oral presentation at the Society for Immunotherapy of Cancer meeting on Saturday November, 11. We’ll share preliminary safety, pharmokokinetic and phamaco dynamic data as well as initial efficacy from one of the expansion cohorts that enrolled quickly. I should also say that the data presentations at SITC are [Indiscernible] so we’ll not be able to provide any clarification or additional information today, but you’ll hear more at the conference. We will host a conference call and webcast with the investor community shortly after the Cabira presentation on Saturday. The details for this call will be announced shortly and that event will include Dr. Zev Wainberg from UCLA, the investigator who will present the data. So you just have to stay tuned for November 11 for more details. We are also studying Cabira in the phase 1/2 trial in the chronic joint disease, pigmented villonodular synovitis or PVNS. We reported initial data at ASCO in June showing clinical benefit from Cabira monotherapy in patients with PVNS. We are preparing to enrol additional patients in the phase 2 portion of the trial to refine the dosing schedule so that we can optimized the therapeutic index of Cabira in this chronic disease setting. We expect the data from these additional patients will allow us to make a decision regarding the initiation of a pivotal trial with an optimal regimen for Cabira and PVNS. We’ve also been very active in advancing our FPA144 development program during the third quarter. FPA144 is our targeted immuno-therapy candidate for gastric and bladder tumors that over express the B splice variant of FGF receptor 2. We’ve now concluded enrolment in the gastric cancer extension cohorts in our ongoing phase 1 clinical trial of FPA 144 monotherapy in anticipation of the start of the phase 1/3 trial which we’ve named the fight trial. This trial will explore the combination of FPA 144 with front line chemotherapy in patients with metastatic gastric cancer and cancer of the gastro oesophageal junction. Phase 1 safety lead-in portion of the trial which we expect to initiate before the end of the year will support the start of Phase 3 portion of the trial which is planned for mid-2018. This randomized controlled phase 3 trial is intended to serve as a global registrational study in patients whose tumors over-express FGF receptor 2b or have FGF receptor 2 gene amplification. In a minute, Helen will provide you more details including our plans to partner this program in China. Turning to bladder cancer, we continue to enrol patients in the phase 1 cohort testing FPA 144 as a treatment for patients with metastatic bladder cancer whose tumors over express FGF receptor 2b. We’ll present an analysis of FGFR2b expression in baseline immune signature and archival tumor samples from patients with bladder cancer and a post rate [Ph] city on Friday November 10. Again, the post rate embargoes so we won’t be able to provide further details on it today. Lastly, I just like to touch briefly on the significant progress we are making with our preclinical immune-oncology pipeline. We now have two promising candidates that we expect to enter the clinic over the next year. In December, we plan to file the IND for the first candidate, FPA 150 that is shown on slide five. This antibody the B7-H4 is designed to inhibitory T-Cell checkpoint pathway and to enhance killing of B7-H4 expressing tumors by ADCC. B7-H4 is frequently over expressed in breast, ovarian, endometrial and other cancers. We’ve presented data in an oral poster at ESMO in September that suggested that FPA 150 has the potential to be an effective therapeutic by improving SI [ph] tumor immune responses in patients with cancer. At the triple meeting in October, we presented the first pre clinical data on our other pre-IND candidate FPT 155 shown on slide six. FPT 155 a CD80-Fc fusion protein is an immune modulator that can stimulate T-cell through three clinical pathways. First, CTLA4 blockade, second CD28 Agonism without super agonism and PD-L1 Blockade. The poster feature work in preclinical models suggesting that FPT 155 has the potential to be a potent T-Cell co-stimulator through the pathway that antigen presenting cells normally use. It has strong pre-clinical anti tumor activity and appears to have synergy when combined with anti-PD1 therapy. We remain on track for IND application or FPT 155 in mid-2018. Also during the quarter, we are really fortunate to add Dr. Bryan Irving to our team as Senior Vice President of Research leading our discovery in research efforts. I’ve known and respected Bryan for years. He has developed a deep knowledge of immune-oncology from his industry and academic experience. His scientific acumen, passion for innovation and strong management skills make him a standout for this important role at Five Prime or a discovery platform continues to yield new and interesting targets to fuel our future pipeline. With that, I’ll now turn the call over to Dr. Helen Collins to discuss our clinical programs in more detail.

[Helen Collins:]

Well thank you Rusty. I will briefly review the status of our clinical programs, starting with the Cabiralizumab on slide seven. The IO Phase 1a/1b trial in patients with advanced cancer and recent program highlights are shown on slide eight and nine. We initiated phase 1b a little over a year ago and expect to complete enrolment in all pre specified cohorts by the end of this year. As Rusty mentioned, initial data from this trial were accepted for late breaking oral presentation at SITC where we will share preliminary data on safety, PK and PD as well as initial efficacy from one cohort that it completed enrolment at the time of the data cut off. We plan to review these data and the Cabira IO program in more detail during the conference call and webcast that will follow the presentation. We are pleased with the overall momentum of this program as well as our collaboration with BMS. I’d also like to review the rationale behind the combination of Cabira and OPDIVO as well as the chosen trial design. This trial targets tumors that have high levels of tumor associated macrophages or TAMS. The hypothesis is that combining Cabira and macrophage inhibitor with OPDIVO the checkpoint inhibitor will be effective in tumor where macrophages have an immune inhibitory effect in the tumor micro environment. The tumor type we are evaluating in the trial fall into three categories; first tumors where OPDIVO is already approved, such as non-small cell lung cancer, renal cell, and head/neck cancer. The second in tumors that are resistant or have become resistant to checkpoint inhibitors, such as previously treated non-small cell lung cancer. And the third, tumors where checkpoint inhibitors aren't approved, such as pancreatic, ovarian, and glioblastoma. We believe the bar is lower in these latter two categories, where the unmet clinical need is greater and any evidence of efficacy could be very meaningful to these patients. Moving onto PVNS with slides 10 and 11, I’ll discuss our phase 2 Cabira monotherapy trial in more detail. PVNS is a rare joined disease in which tumor mass is composed of normal macrophages that accumulate because abnormal synovial cells secrete high levels of CSF1. The trial is assessing tumor shrinkage, tolerability, safety and patient reported outcomes. Pain control and functional improvement are top priority for these patients who could currently have no approved therapeutic options. In our Q2 call, I described the initial data we reported at ASCO this year showing that Cabira provided clinical benefit in patients with PVNS. You may recall that most patients enrolled at the 4 milligram per kilogram dose experienced tumor reduction and five out of 11 patients had already a graphic response. Importantly, both radiographic responders and non-responders demonstrated an improvement in the composite clinical outcomes assessment of pain, Synovitis, range of motion and function. While there were no dose of linked [Ph] toxicity that doses up the 4 milligram per kilogram every two weeks, some patients were -- at discontinued treatment due to tolerability. Based on PK, PD and clinical data from our current trials, we believe we can reduce the discontinuation rate within every four week dosing schedule that could be further adjusted at the physician’s discretion. We are preparing to enrol upto 30 additional patients in order to evaluate the new dosing regimen and to refine our clinical outcomes assessment. We hope the data generated in 2018 from these additional patients will drive our decision making on a pivotal trial and help us optimize the design. I’ll turn now to FPA144 which is on slide 12 and 13. This is our antibody that specifically targets the FGFR2b splice variant. Both FGFR2b proteins over expression and FGFR2 gene amplification are associated with poor prognosis and gastric cancer. Our results to date suggest that the specificity of FPA144 avoids the toxicity seen with less selective FGFR2 small molecule therapeutics. As Rusty alluded to we have expanded the FPA144 development program throughout 2017. We have concluded [Ph] a moment in the gastric cancer cohorts and our initial phase 1 monotherapy trial and are now preparing to initiate the Phase 1/3 frontline study of FPA144 combined with chemotherapy in patients with cancer. This is the study that we are calling the fight study. Other targeted therapies in gastric cancer such as Herceptin and Cyramza have demonstrated greater benefit with combined chemotherapy and similarly our preclinical data suggests 144 should also be added when combined with chemotherapy. The planned design of this trial is shown on slide 14. Before year end we expect to begin the phase 1 safety lead-in portion of the trial which will serve to support the randomized control phase 3 portion of the trial which is expected to initiate in 2018. The Phase 3 trial will compare the addition of FPA144 to standard of care FOLFOX6 Chemotherapy versus FOLFOX6 and placebo as a frontline therapy for patients with metastatic gastric or gastro oesophageal junction cancer whose tumors over express FGFR2b or have FGFR2 gene amplification. We plan to use tissue immunohistochemistry and circulating tumor DNA from blood samples to identity the estimated 10% of patients with gastric cancer that we believe would be study eligible. The trials designed to serve the global registrational trial and will have a primary endpoint of overall survival. In parallel to our Phase 3 preparations we continue to enrol patients in a Phase 1 safety trial of FPA144 monotherapy in unselected patients with gastric cancer in Japan where the incidence of gastric cancer is high. Completion of this Phase 1 trial should enable us to include Japanese patients in the planned global phase 3 trials I just mentioned. Additionally, we are taking the necessary steps to include patients from China in the Phase 3 trial since the prevalence of gastric cancer is higher in China than in any other country in the world. Our business development team is actively exploring the potential China focus collaboration for FPA144 which we believe would allow us to increase the speed of the moment and the global pivotal trial and reduce our share of the trial cost. We also continue to enrol patients with bladder cancer and the expansion cohort of our Phase 1 trial and FPA144 as shown on slide 15. As Rusty mentioned, we will present a related poster at SITC this Friday exploring FGFR2b Expression and Baseline Immune Signature in Urothelial tumors which may further inform our development of FPA144 on bladder cancer. Finally, I’d like to briefly touch on FP-1039 shown on slide 16. As a ligand trap FP-1039 binds to and neutralizes a subset of FGF ligand such as FGF2. Data from the Phase 1b trial evaluating FP-1039 with front-line pemetrexed and cisplatin in patients with untreated, unresectable mesothelioma were presented in an oral session at ESMO in September. FP-1039 was well tolerated and the majority of patients across all dose levels experienced tumor reduction. We are – to look for a partner to move the FP-1039 program forward, since we have a handful with the progression of the Cabira program and the FPA144 program as well as the tow novel molecules advancing into the clinic over the next 12 months. I’ll now turn the call over to Mark to discuss our financials.

[Marc Belsky:]

Thank you, Helen. The full details of our financial results can be found in the press release issued this afternoon, as well as slides 17 and 18. On September 30, 2017 we had approximately $321 million in cash, cash equivalents and marketable securities. Net loss for the third quarter of 2017 was $43.3 million or $1.54 per basic and diluted share, compared to a net loss of $19.4 million or $0.72 per basic and diluted share for the third quarter of 2016, collaboration revenue for the third quarter of 2017 increased by $1.6 million to $8.3 million as compared to the third quarter of 2016. This increase was primarily due to revenue recognized under the 2015 Cabira collaboration agreement with BMS, under which Five Prime is reimbursed for the expenses from the Cabira Immuno-Oncology trial. Research and development expenses for the third quarter of 2017 increased by $18.8 million to $42.7 million as compared to the third quarter of 2016, this increase was primarily related to FPA144 development and advancing the FPA150 and FPT155 program towards IND application. General and administrative expense for the third quarter of 2017 increased by $600,000 to $9.7 million as compared to the third quarter of 2016, this increase was primarily due to accruing rent for the lease on our new corporate office which we plan to move into in December, 2017. Looking ahead, we continue expect full year 2017 net cash use from operating activities to be less than a $120 million. The company estimates ending 2017 with slightly less than $300 million in cash, cash equivalents and marketable securities. I will now turn the call to Aron to discuss our plan and expectations for 2018.

[Aron Knickerbocker:]

Thanks, Marc and thank you Rusty for your kind opening words. And I’m honored to be chosen to lead Five Prime as we look to the future in our next phase of the growth. The extraordinary potential of Five Prime highlighting our platform, our programs and our people, and is fair amount that we’re making most of each. In terms of our corporate culture, we must continues to cultivate the spirit of renovation, collaboration and commitment to scientific and clinical excellence that has benefit heart of Five Prime since Rusty founded the company. So, if I look ahead to 2018 my top priorities include ensuring a smooth leadership transition as I assume the role of CEO and Rusty, transition to Executive Chairman and that we maintain the significant momentum we are building in our development programs. To that point, I’d like to highlight the important news flow in milestones we anticipate during 2018 seen on slide 19. With all of the cohorts in our Cabira OPDIVO® Phase 1B study enrolled by the end of 2017, we expect further data to emerge in the study during the second half of 2018. However the content, timing and forms for data presentation will depend on how quickly the data mature. We continue to evaluate Cabira monotherapy in PVNS and explore flexibility every four-week dose in schedule. We hope the Phase 2 data generated in 2018 only form a decision in the second half of the year regarding a potential pivotal trial. Moving to FPA144, the Phase 1 safety portion is our Phase 1/3 chemo combination trial in first line gastric cancer is scheduled to begin before the end of 2017. If all goes well we expect to transition to the global randomized Phase 3 portion of the trial in mid 2018 beside in the U.S., Europe and Asia including Japan and China. Additionally we look forward to adding two new first-in-class clinical programs to our pipeline over the next year. We plan to file the IND for B7-H4 antibody FPA150 next month. So we anticipate we could begin enrollment in dosing in Phase 1 trial in the first half of 2018. We are also on track to file an IND for our CD80-Fc program, FPT155 in mid 2018 and plan to begin a Phase 1 trial during the second half of the year. As a science focused company we are committed sharing result of our research and development at scientific and clinical conferences and our 2018 publication planning is on going. And keeping with our practice we expect to submit data to various meetings and conferences, and hope to share further details as the year unfolds. Overall, we’re building toward a very exciting in 2018 developing robust portfolio of novel immuno-oncology therapeutic adding two new candidates, the mechanism to our clinical pipeline and new initiation of Five Prime’s pivotal trial with FPA144. I look forward to working together with our board, the management team and all of our employees as we strive to bring promising protein therapies to patients with cancer. I’ll now turn the call back to Rusty for closing remarks.

[Rusty Williams:]

Thanks Aron. I chose this year to initiate the CEO transition, because I wanted the company to be in position of strength, which is evident in our expanding pipeline, progress in our program, the capabilities of our leadership team and our solid balance sheet. I’m confident in the promise of our portfolio and our platform and an ability of Aaron and the rest of our season team to successfully execute our clinical and corporate strategy. In closing, I’d like to express my appreciation to all our employees for their commitment to Five Prime, and our vision. And also to thank the many patients and investigators who are participating in a clinical trial. I’d also like to thank each of you on the call and our colleagues in the investment community, I’ve learned much from you. I’ve truly enjoyed our interactions and I'm grateful for your support of our programs at Five Prime. Operator, we are ready to open the call for questions.

[Operator:]

Thank you. [Operator Instructions] Our first question comes from the line of Michael Schmidt of Leerink. Your line is now open.

[Michael Schmidt:]

Hey, guys. Thanks for taking my question. Congrats on all the progress. I had one regarding the presentation for Cabiralizumab. And that my question is really is – were Cabiralizumab be included in the abstract that are going to be published tomorrow where late breakers come out at a different time point? And if it's included, how can you comment on how much data would be in abstract and relative to the full presentation at the conference? Thanks,

[Rusty Williams:]

Thanks, Michael. The late breaker abstract are published on December 7, so they are different category from the rest of the abstract. So, we’ll have to wait for SITC publication.

[Michael Schmidt:]

Great. Okay. Thanks for clarifying that. And then, regarding the actual presentation for you, you’re talking about PK, PD and preliminary efficacy data, I guess in this context, I’ll curious to know what of the next steps for the trial with one extension code clearly more mature than some of the others. I guess you will you look at this code in isolation in terms of making determination of next steps together Bristol, will you be waiting until you have more mature from our cohort for determining excess [ph]. Could you just comment on the path forward for Cabiralizumab in combination of the Opdivo? Thanks.

[Rusty Williams:]

Yes. So, each of the cohorts in the Phase 1B and each of the cohorts in this trial of Cabira combination with nivo [ph]. We’ve always said that we consider them and their path independently of each other. So, we and BMS look at it that way. We continue to look at it that way. So, we could move forward in one cohort without having data from all the cohorts available to us, so that we continue on that path.

[Michael Schmidt:]

Okay. And I guess what type of data do you think would be necessary to determine next step. It’s a decision that's made based on say response rates, the duration of responses or their other endpoints are important term the next step for the program.

[Rusty Williams:]

Yes. In immuno-oncology it’s important to not only get responses but to get durable response. And so that’s the way we think about it. These are the important parameters to look at. And we’ll be able to give you a little bit more guidance on that after SITC presentation. As I said, we have some -- we have a webcast after that and reception on Saturday evening. So I will get a little bit more color on that at that point.

[Michael Schmidt:]

Great, thanks. Thanks for the added information. I’ll hop back in the queque.

[Rusty Williams:]

Sure. Thank you, Michael.

[Operator:]

Thank you. Our next question comes from Kennen MacKay of RBC Capital Markets. Your line is now open.

[Kennen MacKay:]

Hi. Thanks for talking the question. Another one on the Cabiralizumab plus OPDIVO combo trail, I was wondering if in that trial you were either prospectively or retrospectively looking at some biomarkers such as MSI high and just sort of clarify, one point around the examination of the patients in this trial. Are these all patients that are high in PSF1R or was that a biomarker use to fetch enrolment? Thank you.

[Helen Collins:]

Hi. So this is Helen Collins. Thank you for that. So, we think biomarkers are important thing to look at in this study, proposition of all the patients were required to have baseline and on treatment biomarker. We have some of that data but we do not have all of data but we do think it’s important for look at. Certainly as far as MSI or MS High and they are some cohorts where that would important, some maybe there’s less known about that but that would be something that we would definitely want to look at if we see responses in particular cohorts. In terms of CSF1 High that is something that we are looking at but it was not a criteria for inclusion.

[Kennen MacKay:]

Okay. Thank you, Helen. And then maybe another one on the movement towards sort of the Phase 1, 3, FPA144 trial, can you maybe talk a little about some of your interactions with the FDA and getting this trial setup and really start to what we need to see from the Phase 1 cohort in order to move forward with the Phase 3 cohort. Is that just safety or is there sort of an efficacy criteria that we’d have to see there as we move forward?

[Helen Collins:]

So, we haven’t given a lot of detail about it or any more than we talked about today, but I can say that the study is designed as a single study, a phase 1, 2 or safety lead in Phase 3. We have had conversations with the FDA. We feel confident that’s a good way to do this trial and really that has to do with – and I think we talk about before the specificity of the FPA144 for that particular slight variant, and data that we represented as the updated at ASCO. There is not any anticipated overlapping toxicity with chemotherapy. So we don’t anticipate there to be a difficulty adding the two, so that’s what made this confident to move and the FDA certainly supported our trial design.

[Rusty Williams:]

And with respect to – do we have to achieve an efficacy threshold to move forward? No. Because we feel that we’ve already shown efficacy as monotherapy, and as Helen said we updated up that with a 19% response rate at ASCO. That’s compare in very late line therapy average of fourth line or later and that compares very favorably to monotherapy response rates of other agents that have been or are being developing that stage of gastric cancer. So we feel that we’ve already past that efficacy threshold for knowing that we have an active drug. And so that – the short answer to – of course that long statement is, we don’t have an efficacy thresholds that we need to past. Those are the reasons.

[Kennen MacKay:]

Got it. Thank you, Helen and Rusty. Maybe just one more on PVNS if I concluded in, just on Q4 re-dosing paradigm that you’re moving forward with it at the 4 mgs. Wanted to get your perspective and again maybe sort of coming out of contact to some of the FDA meetings that you have here. Is this really something to you enhance the convenience and sort of commerciality of this drug or is this more to try to mitigate some of the adverse events associated with targeting CSF1R like the periorbital edema? Thank you.

[Rusty Williams:]

Yes. Thanks, Kennen. This all has to do with the disease contact. So PVNS it’s a disease that causes a lot of suffering for many years life long disease once you get it, but doesn’t kill people like metastatic cancer. And so we think of it in terms of it setting and how to develop a regimen and the use for many year in a disease in which the tolerability threshold maybe a little bit different from that metatstic cancer, because the patients are not – they don’t have a life threatening disease. So from that point of view we thought that right now it’s a time to get on optimize regimen that really addresses this patients population with some flexibility so that if the patient lab abnormality for CK or something like that goes high because you’ve inhibited Kupffer cell you can briefly go after drug or reduce the dose to give flexibility to the physician treating the patient to do that kind of thing. A few four-week regimen, we think that you don’t need coverage of the receptor in other words you don’t have full receptor inhibition all the time everyday in order to achieve the clinical benefit because you’re treating cells that are – they’re mutated cells and macrophages are normal macrophages, you're just blocking them. And so, the disease doesn’t get away from you like metastatic cancer. So, we think it's a different disease setting and those ideas in mind that we thought that we could -- if patient get rash or some periorbital edema, since those are reversible with this drug, we feel that this more flexible regimen can help us address the patients needs better in term of therapy.

[Kennen MacKay:]

Okay. Thank you very much.

[Rusty Williams:]

Yes. You’re welcome.

[Kennen MacKay:]

I appreciate it for taking my question.

[Rusty Williams:]

Thank you, Kennen.

[Operator:]

Thank you. Our next question comes from Jim Birchenough of Wells Fargo Securities. Your line is now open.

[Jim Birchenough:]

Hi, guys. Thanks for taking the questions, and congrats on all the progress. I guess the first question maybe starting with PVNS. Should we look at the pexidartinib and why been trial as a frame of reference that what you might need to do in the PVNS pivotal study? And I guess any thoughts on how that might set a bar for you guys, and how do you different Cabira from pexi?

[Helen Collins:]

Yes. This is Helen. I can answer that. I mean, I think certainly we only know what’s been in the public domain about pexidartinib trial, so we know that trial design from clinicaltrial.gov. We know that press release where they’ve said they achieve their response endpoint and that they’re looking at totality of a data. I think that comment aligns with just what Rusty previously said that for the patients, it’s really their functional improvement that matters to them. They don’t care if those cancers that they’re tumor a bit smaller. They care of they could now walk when they couldn’t walk before or they can do the things that they couldn’t do before. So certainly we – our interactions with regulatory with FDA align with that being a very important endpoint and I think that’s the only kind of thoughts we have.

[Rusty Williams:]

Yes. We did note that the pexidartinib study they’ve reported two cases of severe liver toxicity. And so, again, gets back to this point, that in this patient population its not like treating metastatic cancer, and so we don’t have any special insight into pexidartinib data aren’t publicly available, but that’s a – it goes along with our thinking that we really do – we really want to put the effort into developing regimen that we think might be best in class because it addresses the patient’s needs.

[Helen Collins:]

And I can add one thing was just that, what we did notice in terms of and this maybe goes back to the previous question in terms of the dosing regimen is that, patient symptoms as we said responders and non-responders all improved within the first two doses, within the first four week and yet we didn’t see anybody having difficulties discontinuing until beyond the four-week. So that was – first the clinical data that supported this and then it certainly was supported by PK and PD. So…

[Rusty Williams:]

And then final point is that pexidartinib is tyrosine kinase inhibitors and it block kinases other than CSF1 receptor. And they’ve reported side effects that are likely to be related to those off target effect, so that’s another issue for that drug going forward.

[Jim Birchenough:]

And then maybe one other question if you allow on going into SITC, I know you can’t say which of the cohort would be discussed, but Helen you mentioned where there’s a lower bar in pancreatic ovarian and glioblastoma, so maybe so we’re pinpointing one of those. Could let us now what you see is the bar has been set by current standard repair maybe starting with second line pancreatic cancer and maybe give us some context for what you guys think would be good response rate data and good durability?

[Helen Collins:]

Well, I think you’re right. If those three, as well as the resistant non-small cell lung cancer vitamin, so I think we’ve highlight those four or I did when I’m speaking because those are the four groups where PD1 PDL-1 have not been approved, so you could see that essentially any response, certainly anything that was durable would be beneficial or it would be meaningful. In terms of second line pancreatic cancer, I mean, I think the bar is pretty low there even outside of IO therapy, why there’s no reported efficacy to a PD1, PDL-1 along that I’m aware of. And second line chemo therapies not so great. It has I think somewhere I would say like a five months or so survival, three months PFS, but don’t’ quote me on that, I have to go look at up. So, I mean, you thinking about the same way we would be thinking about is what standard – two things, what Standard of Care which [Indiscernible] bar you really want to be better then what’s the best that’s been seen with the PD1 alone, right, so

[Rusty Williams:]

Yes. We thought obviously ask a lot of people and gotten lot of data all the day we can for PD1 responses and all these cohorts but in pancreatic there is no response in that setting to PD1 unless there’s MSI activity and so you have to really think of you’re refocus on MSI’s negative to reach any conclusion.

[Jim Birchenough:]

Great. Thanks for taking questions.

[Rusty Williams:]

You’re welcome.

[Operator:]

Thank you. Our next question comes from Ian Somaiya of BMO Capital. Your line is now open.

[Ian Somaiya:]

Thank you and congratulations on all the progress and congratulations Rusty there on your new roles?

[Rusty Williams:]

Thank you.

[Ian Somaiya:]

Just following up on SITC, just again given the area of expertise of the investigator present in data, I think we’re in overall quickly reaching the conclusion that we are going to see second line pancreatic cancer data. And what I wanted to just better appreciate was is your goal to be better than a current standard care which is a chemo combination. So would you say comparable or sort of better efficacy, better safety and sort of threshold we should consider when obviously hearing the presentation or is it different than that?

[Rusty Williams:]

Well, we set this trial up with BMS to be a signal seeking trial. And so, that’s – there no control arm, they’re no in the trial, so that we set it up to be signal seeking. And in some cohorts you could interpret a signal in terms of responses, with more meaning than in other cohorts and pancreatic would be one of those cohorts where a signal is easy to discern if you get any kind of any kind of response rate that’s in any durability to it, and so that kind of how we look at it. It wasn’t our goal to compare with Standard and Care, it was just to seek signal and settings where we could attribute the signal to the drug.

[Ian Somaiya:]

Right. And how should we think about sort of the likely next steps, does it make sense to evaluate at first line, because again if you think about second line therapeutic cancer the current standard of Care there is a combination with chemo. And that’s a marketplace I would ideally would want to get away from chemo?

[Rusty Williams:]

Yes. We can’t give any guidance right now on next step. We might give you a little color on that at our event, at our webcast and our event after the SITC presentation.

[Ian Somaiya:]

Okay. And just one last question, I know last earnings call you mentioned the sort of the transfer manufacturing responsibility to Bristol, I was just curious where we are in that process, that’s at all sort of [Indiscernible] limiting step and your ability to moving to maybe larger settings with Cabira?

[Rusty Williams:]

Yes. Thanks for paying attention to that. The transfer went very well. It’s done. No hick-ups, no delays anticipated. Material – as far as we can tell material is not great limiting step at this point.

[Ian Somaiya:]

Okay. And if I can just have one final question, what do you expect your role to be in sort of the further development, future development of Cabira? Just wanting to get a sense for how the responsibilities will be shared with your and your partner?

[Aron Knickerbocker:]

Yes. Hi. It’s Aron. So, you may recall that PVNS is treated somewhat differently in this arrangement. That’s an independent program of Five Prime, so we are conducting those studies, operationalizing them and we’re eligible for milestone payments as the program advances. For subsequent development however in immuno-oncology that would be up to our partners at BMS. That said, we also have the rights if we wish to do additional studies in oncology either with the BMS products or with Five Prime products. And so that’s how it’s available to us as well, but we would expect that most next step in IO would be led by BMS.

[Ian Somaiya:]

Okay. Thank you again, and we are looking forward to Saturday.

[Rusty Williams:]

Thanks.

[Operator:]

Thank you. Our next question comes from Eun Yang of Jefferies. Your line is now open.

[Eun Yang:]

Thank you. I have questions for FPA144, so in this safety leading Phase 1 push [ph] how patients are you planning to enroll and when you’re moving to Phase 3, how many patients are going to be there?

[Rusty Williams:]

Hi. Thanks for the question. I’ll let Helen get into views [ph] on that. On the number of patients in the safety leading [ph] in the number of patients in the Phase 3.

[Helen Collins:]

So, we haven’t said exactly, you could imagine based on my previous response that we don’t think we need for many, and that’s the fact that we’re going to anticipate starting the Phase 1 now and then yet being ready to start moving into Phase 3 in the middle of next year. I should give you some inkling of how we think this will go, but that just closest.

[Rusty Williams:]

So you know it’s a standard those escalation in Phase 1 we, as Helen said, we don’t anticipate any overlap of safety issues with 144 and chemotherapy, because of the data we already have. And so we think – we never to be sure, but we think that’s going to go relatively quickly. No reason to think otherwise. FPA144 head surprisingly in a way, given the fact of what it does, it surprisingly good safety profile and the data we’ve shown so far. Now in the Phase 3 of course we – that’s a different matter. We want – this is a pivotal trial. We help this registrational and so we set it up this power [ph] to show overall survival because we think that’s what gets us towards the finish line on this in a quick as possible manner. In gastric cancer and the setting that we’re in, these patients gastric cancer progress, metastatic gastric cancer unfortunately progress rapidly. And so if you compare OS or other endpoints, does the OS is probably the best way to go, so we probably to see OS and that’s what we plan to do and we think that’s imminently doable. Part of that will be facilitated by our partner in China where a lot of patients with tremendous number of patients with gastric cancer are and so we think that if we get the high-quality partner in China, prevail to enhance the speed of this. So we don't think it's can take an unreasonably long period of time and it will be able to get enough data to show OS. That’s what we hope.

[Eun Yang:]

So today what’s the expectations for the control arm OS in the trial and then how many months of additional or weeks of additional survival that are you aiming to show?

[Helen Collins:]

Yes. So again, we haven’t said that, I mean, there was certainly a concurrent meta-analysis that supports I think the clinical data that’s in a literature that Standard of Care [Indiscernible] its about 10 to 11 months overall survival. I think as you know we believe that FGFR 2 over expression or FGFR 2 amplification has a worse prognosis, but so…

[Rusty Williams:]

So the control arm is important, because all the data that are available in the literature show that these patients have a worse prognosis has been standard gastric cancer patient. So if anything you might expect the control arm patient to progress even fast then what’s out there for regular gastric cancer patients without the amplification, so that we think is bad for the patient but it may help us in this trial you’ll see.

[Eun Yang:]

Okay. And then there’s a one trial would that [Indiscernible] factory of regulatory submission for the U.S.,EU and Japan or in Japan do you need to do another bridging study?

[Helen Collins:]

Well, right now we have a Phase 1 in Japan, which is monotherapy and we believe that data from that trial will support patients from Japan being able to involve in the global trial.

[Eun Yang:]

With the global trial would it be enough to file an approval in Japan?

[Helen Collins:]

That is our plan.

[Eun Yang:]

Thank you.

[Operator:]

Thank you. Our next question comes from [Indiscernible]. Your line is now open.

[Unidentified Analyst:]

Great. Thanks very much. All the questions have been asked. But congratulations to Aron and Rusty, we appreciate it. And Rusty you can’t hide from us, we’ll continue seek you out.

[Rusty Williams:]

Thank you, Chris. I wouldn’t want to hide.

[Unidentified Analyst:]

So if we put on Rusty, Helen, Aron decoder ring and try to look at the word enrolment completed quickly in the cohort. Is fair to me interpret possibly that this represents an indication for which there is basically no treatment option?

[Rusty Williams:]

Well, there’s tremendous, I hate the product words but there’s a tremendous unmet need. I guess which says the same thing.

[Helen Collins:]

The investigators had believed it.

[Rusty Williams:]

Yes. Tremendous unmet.

[Unidentified Analyst:]

Okay. And then still sticking over to the Cabira plus PD1 trial, the single arm study obviously how should we think about trying to interpret what component of benefit derives from the backbone PD1 versus Cabira? Can you talk about the prospect of biomarker data or how we could really interpret what’s contributing to the benefit?

[Rusty Williams:]

Yes. I think by – it is an indication where there is no response to PD1 then PD1 pathway blockers, then I think any response that the [Indiscernible] is meaningful. And that’s really the cleanest answer for us is to look in the cohort where you could see that. Obviously other cohorts where you see where people have already been on PD1 therapy and it failed, either broken through or failed responses there meaningful and people in the field have interpreted responses in that way, for example, BMS lack [ph] three et cetera, its maybe slightly less clean than an indication where there’s no response to PD1 therapy, but those cohorts are also interesting and you can make interpretation in those. And so that’s kind of the way we look at -- that’s a data in terms of assessing the contribution of Cabira versus Nivo.

[Unidentified Analyst:]

Okay. And then finally at the Analyst meeting I guess our understanding SITC permit—permitting you to represent data from arm. You did say about how fuller data will come in the second half of 2018, but on Saturday evening at your Analyst Meeting might we’ll be able to get additional data from other cohorts beyond just the ones that you’re present in late breaker? Thank you.

[Rusty Williams:]

It has been our plan all along we’re sticking to that plan to present the data at the SITC meeting and the preps to the analyst event afterwards is to be able to get more color to those data than we can in 10 minute presentation. And so we contacts in those data and kind of where we are, so we haven’t had a plan to go beyond that first cohort that we're disclosing because we have more disclosures later and we think we’re going to stick to this one cohort.

[Unidentified Analyst:]

Okay. Great. Thanks you, guys.

[Rusty Williams:]

At medical conference we will disclose in other settings as Aron alluded to, that other cohort data, but this one we’re going to stick to the one because we think that’s what we and BMS agree to do.

[Unidentified Analyst:]

Thank you. You’re welcome.

[Operator:]

Thank you. Our next question comes from Christopher Marai of Nomura Instinet. Your line is now open.

[Christopher Marai:]

Hey. Thanks for taking the questions. Just to touch upon the last one a little bit here. Thinking about how you look to tease out the contribution from [Indiscernible] versus nivo. I mean you’ve been thinking about this relative to next combination, so I just wonder if you could maybe walk us through that little bit obviously SITC report is chemo make a lot of sense. And then secondarily what data may trigger new combination studies. Obviously there may not be a need to fully flush out all the data before you move in the combo studies. So when might we see those? And then secondarily maybe just the benefit in the front line versus FOLFOX that you’d expect to be required to get that across the finish line? Thanks.

[Helen Collins:]

So, maybe I’ll answer the 144 first. I mean, I think we know that this in 10% of the patient population. We believe we’re going to design the study to have both a statistically significant OS endpoint as well as something that’s clinically meaningful, so we don’t think it’s – we are not designing it so that we can show just one week of overall survival benefit if that’s what you mean by some. The – and in terms of the Cabira -- combo again, it’s very dependent on the tumor type and so sorry it’s sound I’m being evasive but I think each tumor type is rest, you said there is no control on each tumor type we’re going to be looking at the specific individual components of or excuse me the individual characteristics of patients prior therapy, biomarkers and I think all of those things are going to go into helping and form how to move forward and that will be somewhat or very much tumor dependent. Go ahead Rusty.

[Rusty Williams:]

Hi, Chris. I think you were also asking about combinations of Cabira with other agents. Is that your question?

[Christopher Marai:]

Yes. [Indiscernible] trigger some of those combinations, obviously those data you guys are going to be developing and that could inform those decisions, you may not be to see the full read out.

[Rusty Williams:]

So I’ll have to answer the question broadly. There is good rationale for using Cabira in combination with other agents other than PD-1 pathway blockers. You see Roche doing that with their CSF-1 receptor antibody. They have the cloud; they have started roughly recently combination with anti CD40, T-Cell agonist. Roche also has a trial done with M.D. Anderson and in ovarian cancer looking at Avastin plus chemo plus Bevacizumab CSF-1 receptor antibody, so they have already disclosed what they are doing and there is a good rationale. As you remember in our agreement with BMS we have a right to do our work in Cabira in combination with other agents including those in our pipeline. And that was an important issue that we sit up for in our discussion with BMS at the beginning. And so there is a good rational. We have not disclosed yet and are not prepared to disclose yet what are the combinations that we might consider, but it’s a good rational for it.

[Christopher Marai:]

Great and then just a level of data that you need to start triggering some of those combination studies?

[Rusty Williams:]

Well it’s hard to pin that down, because I think from this probably we’ve earned a lot. We’ve done some biomarker studies in about a third of the patients in the 1b cohort. We’ve learnt a lot from that. And analyzing those data with respect to responses and response from the tumor micro environment with respect to biomarkers will be important for us. Those kind of things might contribute to a design of a product [Ph] in a different combination. And you know we’ve got – learnt a lot about the drug in terms of safety. We think we have based on the markers that we’ve reported we think that we have a sufficient dose and so I think we’ve come a long way in terms of designing in that case a process of threshold, obviously it’s up to the conclusion that the threshold for doing another combination is not that high. We understand the thoughts, we understand the PK, we think we have a lot of information about the dose.

[Christopher Marai:]

Got it. And just in terms of [Indiscernible] types of trials.

[Rusty Williams:]

And we do have pre clinical work by there on going with other combination, so we are working along designs. Analyst Got it. And then I guess just with respect to what could really have started those trials and specifically referring to when you think those might be able to start, obviously you indicated the potential for a pivotal trial, I guess these wouldn’t be pivotal or been in combinations, and so when might we see this? Thank you.

[Rusty Williams:]

Yes, we haven’t given any guidance on that yet. So sorry I can’t really predict that right now. Can’t really give guidance.

[Christopher Marai:]

Sooner or later than the pivotal trial started?

[Rusty Williams:]

I can’t, I can’t. Analyst Got it. Okay, I tried. Thank you for taking my question.

[Rusty Williams:]

I mean that’s one of those questions, that any answer I could give. Might turn against me because if I say it sooner, then it means we are waiting for pivotal trials on time. But I think its later, means we are waiting for combination. We have got a lady freezing, we are in a hurry on everything. So but the – your broad point is a very good one. There is a rational throughout the combination. So get ahead of myself on this.

[Christopher Marai:]

Got it. Thank you.

[Rusty Williams:]

Yes.

[Operator:]

Thank you. Our next question comes from Tony Butler of Guggenheim Securities. Your line is now open.

[Tony Butler:]

Hi, thanks very much. You’ve prioritized 150 over 155, is there a reason for that? And point B, can you and maybe you said this, I’m sorry, I missed it , but can you discuss would you move on 50 onto a basket study? And then finally on CSF1R [Ph] I have to squeeze this in, why you had made a reference to biomarkers, is tumor rotational burden -- and will patients be segregated by tumor or data be segregated by TMB? Thanks very much.

[Rusty Williams:]

So let me start on that Tony, then I’ll let Helen follow in on the last part. Priortization of 150 over 155, we – these are two high priority projects and we started 150 before we started 155, and simply a matter of timing. We’ve both, we’ve been in a big hurry and so both are moving forward and it’s just a matter of which one was ahead. They are high priority, both of them for us. And we like both of them for different reasons. With respect to markers and TMB, let me let Helen...

[Tony Butler:]

...question about a basket trial.

[Rusty Williams:]

Basket trial for B7-H4

[Helen Collins:]

So we thought of quite a few different trial designs, so haven’t spoken exactly about how was the phase 1 trial going to be designed. So I’m....

[Rusty Williams:]

But we do know it’s for a number of tumor – I mean you are thinking the right way on this. We do know that this is over expressed in a number of tumors, so we know you always get to the heart of the matter and so that concept, I think you are on the right track. That’s the thinking, but we haven’t disclosed anything about the basket, that’s premature. So I think you are thinking about that correctly.

[Tony Butler:]

That’s helpful. And the TMB?

[Helen Collins:]

And the TMB, so that is you mean again that would be an obvious thing, so although we haven’t said exactly what biomarkers are looking at, as we know that is something that’s associated and particularly some certain tumor types with responses to nivolumab or PD-1 alone so that is something that we are looking at.

[Tony Butler:]

That was helpful. Thanks.

[Rusty Williams:]

Yes, thank you Tony.

[Operator:]

Thank you. And this does conclude our question and answer session. I would now like to turn the call back over to Rusty Williams for any closing remarks

[Rusty Williams:]

Okay, well thanks each of you for joining us today and for all your support and your good questions. We look forward to updating you on further calls. Thanks again.

[Operator:]

Ladies and gentlemen, thank you for participation in today's conference. This concludes the program. You may now disconnect. Everyone, have a great day.