Five Prime Therapeutics Inc
Q3 2016 Earnings Call Transcript

Published: 4 Nov 2016

[Operator:]

Good day, ladies and gentlemen and welcome to the Five Prime Therapeutics Incorporated Third Quarter 2016 Earnings Conference Call. As a reminder, this conference maybe recorded. I'd now like to introduce your host for today's conference, Miss Heather Rowe, Senior Director Investor Relations and Corporate Communications. You may begin.

[Heather Rowe:]

Good afternoon and thank you for joining us. On behalf of Five Prime, I'd like to welcome everyone to our conference call to discuss financial and operational results for the third quarter 2016. We issued a press release this afternoon and also posted slides to accompany this presentation. The slides can be found under the Investor Relations section of our website, under Events and Presentation. Joining me today are Dr. Rusty Williams, Chief Executive Officer; Mr. Aaron Knickerbocker, Chief Business Officer; Dr. Robert Sikorski, Chief Medical 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:]

Thank you Heather. Good afternoon, and thank to each of you for joining us today. As we review our third quarter results, I am really pleased to update you on the progress of our clinical and pre-clinical programs all of which are on track. For those viewing the slides an overview of the program can be seen on slide 3. I'd like to start with the biralizumab, which is the new name for FPA008, for simplicity, I'll refer to it as Cabira. Cabira is our CSF1 receptor antibody that it blocks immune-suppressors tumor-associated macrophages. We and our partner Bristol Myer Squibb are studying Cabira in combination with the PD1 checkpoint inhibitor OPDIVO in multiple tumor settings. We learned a lot about those things from the Phase 1a portion of the trial and building on this momentum, in October we initiated the large Phase 1b extension portion to trial, how to select the Cabira dose in multiple tumor type and setting. Five Prime continues to run the trial and we are pleased with the enrollment progress even if it's early stage. In addition to this immuno-oncology trial were on track for their Phase 2 trial of Cabira and orphan disease Pigmented Villonodular Synovitis or PVNS. In short we are pleased with the progress made in both Cabira trial and we'll collaborate the PMS [ph] to determine the most appropriate venue in which we report data. Next, I’d like to turn to FPA144. This is our isoform selective antibody in development as a targeted immunotherapy for tumors that overexpress the B slight variance of FGF receptor 2. 144 is highly selective for this slight variance and we use our proprietary immunohistochemistry assay to identify patients. This tumor is overexpress FGF receptor 2b We engineered F144 to have inherent antibody dependent cell-mediated cytotoxicity or ADCC. We believe that 144 ability to recruit NK cell followed by a robust recruitment of CD8 T cells into the tumor, we will promote tumor cell killing by converting the tumor from a non-inflamed state into an inflamed state. At ASCO this year, we reported data from our ongoing Phase 1 trial, the encouraging findings confidence to add new gastric and bladder cancer cohorts to this trial during the quarter, filed [ph] with more detail from this cohort shortly. In addition to the current mono therapy trial we are planning combination trials to allow advance that of 144 in the earlier lines of therapy. We are also planning a mono therapy trial in Japan for there is a large population to gastric cancer of patient. To retain global development commercialize to 144. Last a word about our financials. Our cash balance at the end of the third quarter was approximately $440 million, which is in keeping with our previous guidance. Now, I'll turn the call over to Bob to give us some more detailed assay on our clinical program.

[Robert Sikorski:]

Thank you, Rusty. First I will briefly talk about the Cabira IO clinical trial in cancer patients. As Rusty mentioned, we have made notable progress in this trial, that is studying Cabira in combination with the anti PD1 antibody OPDIVO. Recent highlights from the program can be found in Slide 4. The trial design can be found in Slide 5. Initiated the IO trial in September of last year. During Phase 1a we and BMS evaluated safety, pharmacokinetics and biomarkers in patients receiving escalated doses of Cabira, as mono therapy and in combination with the approved 3 milligrams per kilogram dose of OPDIVO. Note that selected cohorts in the Phase 1a portion of the trial are design to continue enrolling in parallel with those in 1b. We recently achieved an important milestone, with the initiation of the Phase 1b portion of the trial. We're now evaluating the safety preliminary efficacy in biomarkers and patients receiving a fine dose of Cabira combination with OPDIVO in selected advance solid tumors. The pre-designed 1b cohort, include non-small cell lung cancer, squamous cell carcinoma of the head and neck, pancreatic cancer glioblastoma, renal cell carcinoma, and ovarian cancer. We see clinical activity in any of these cohorts we can advance that setting for the next phase independently in the rest of the trial. As you may have seen BMS recently reported positive data in head and neck cancer, turning to the growing number of indications where OPDIVO has demonstrated positive data more randomize pivotal trial. If OPDIVO is approved in this indication, so we would now have three setting in our current trial where OPDIVO has regulatory approval, non-small cell lung cancer, renal cell carcinoma in head and neck cancer. These setting represent relatively straight forward regulatory pass for Cabira, as a combination regiment with OPDIVO. In under IO trial we are actively study Cabira in patients with PVNS. You can see this on slide six. There is strong scientific rational for Cabira as the therapy in this disease. PVNS converse are driven by the local secretion of CSF 1, to activate the CSF 1 receptor on monocytes and macrophages. Cabira was designed to blast that specific binding and activation. The tumor in PVNS patients is typically located in joints such as the mini [indiscernible] wrist. This can produce high morbidity due to local cartilage and bone destruction. Slide 7 illustrates us trial design. We are currently in the Phase 2 portion of the ongoing trial, which we are validating response rate, pain and range of motion in approximately 30 PVNS patients. I'll now turn to 144. Slide 8 shows an overview of the program. We are currently studying 144 in the Phase 1 trial that focuses on gastric and bladder cancer. 144 is an antibody that specifically target FGFR2b, which can be over expressed in tumors. We think this cytotoxicity could avoid toxicities associated with less selective antibodies with small molecules that block FGF receptors more broadly. In addition, FT portion of the molecule is AC copulated allowing it to bind with high affinity in T-cells and to recruit them into the tumor. Importantly, we’ve shown that in pre-clinical model that one 144 3d tumors also become infiltrated CDA T-cells, this conversion of the tumor from a non-inflamed state to inflamed state, which is an important goal of immunotherapy As shown in slide nine, we are currently in part 2 of the trial where we are dosing patients with 15 milligrams per kilogram of 144 every two weeks. Worldwide there are about 1.5 million cases of gastric cancer, approximately 5% or close to 80,000 of those patients I believe to a highly overexpressed FGFR2b due to an amplification of the FGFR2b. These patients are being asses in the IHC high cohort of the current trial. There are additional patients who have lower levels of FGFR2b expression were being assessed in the IHC low and moderate cohort. In the recent ASCO meeting, we were pleased to announce early data from Phase 1 trial, from a Phase 2 perceptive, which showed that 144 didn’t reach maximum tolerated dose and had no dose-limiting toxicities. The efficacy data can be seen in slide 10. As of the April 1 data cutoff three of the nine enrolled gastric cancer patients with high levels of FGFR2b achieved and confirmed faster response. From the dose escalation we also started the patient with bladder cancer. We achieved a complete response. Those patients had a moderate amount of FGFR2b over expression, as a result we added a bladder cancer cohort in the trial and also added additional cohorts to assess gastric cancer patients with lower levels of FGFR2b over expression. In summary for 144, we’re pleased with the early data from this targeted immunotherapy, plan to look at future combination studies. Finally, I will conclude with a few remarks about FP-1039, an FGF ligand trap, as shown on slide 11. FP-1039 is currently being combined with frontline cisplatin pemetrexed in the Phase 1b trial as first line therapy in patients with malignant mesothelioma. [Indiscernible] has recently retained all rights to FP-1039 from GSK continues to conduct the ongoing study. GSK concluded enrollment in June and patient still remain on study. Decisions on any future development of FP-1039 in mesothelioma will be based on overall safety, response rate and durability, as well as, other considerations such as drug supply and manufacturing. In summary, we’ve made significant progress in our development efforts across all of our clinical trials. We look forward to providing future updates. I will now turn the call over to Marc to review our financials.

[Marc Belsky:]

Thank you, Bob. The full details of our financial results can be found in the press release issued this afternoon, as well as Slide 12 and 13. As Rusty said, we have a strong balance sheet. Our cash, cash equivalents and marketable securities totaled $440.7 million as of September 30, 2016. Net loss for the third quarter of 2016 was $19.4 million or $0.72 per basic and diluted share compared to net loss of $24 million or $0.93 per basic and diluted share for the quarter 2015. Collaboration revenue for the third quarter of 2016 was $6.7 million up from $5.9 million in the third quarter of 2015. This was primarily due to revenue recognized under the October 2015 Cabira license agreement with BMS. Recall, BMS is reimbursing us for expenses relating to our Cabira IO trial. Research and development expenses for the third quarter of 2016 were $23.9 million compared to $24.7 million in the third quarter of 2015. Last year in the third quarter, the company recorded an $8 million in license expense, adjusted for this expense, research and development expenses increased $7.2 million, primarily related advancing the FPA 144 clinical trial. Preclinical development and immuno oncology research program. General and administrative expenses for the third quarter of 2016 were $9.1 million compared to $5.2 million in the third quarter of 2015. This increase was primarily due to increases in payroll and stock-based compensation expenses. Today Five Prime filed a new self-registration statement on form S-3 with the Securities and Exchange Commission as the matter of good housekeeping and even through our fire self-registration filed in May 2015. Looking ahead we continue to expect earlier 2016 net cash used from operating activities to be less than a $120 million comprising less than $90 million used in operations and less than $30 million used for tax payment. We estimate ending 2016 with more than $400 million in cash, cash equivalents and marketable security. I’ll now turn the call back to Rusty for closing remarks.

[Rusty Williams:]

Thanks Mark. For those of you following me along, let’s move to slide 14. We have a really special R&D in turn and we’re excited about how it’s generating a lot of new immuno-oncology targets and candidates through our pipeline. At the beginning of 2016 we undertook our most ambitious immuno-oncology meaning efforts to-date, this included six large screens, we did two-functional cell based screen of our entire library of 5700 extra cellular proteins, supplying the key modulators or T-rig and T effector cell. These screens are similar to the ones we did and successfully identify CSF 1 receptor as a key regulator of macrophages leading to our Cabira program. We also conducted in vivo screen of approximately 700 immune related extra cellular protein in three separate tumor model and lastly we just completed an unprecedented immunome by immunome screen. Let me just put the scale of this screening effort and the output in content. In our immunome by immunome screen we created a roadmap defining interactions of 700 key proteins from the surfaces of various immune cells and measured the interactions of these 700 proteins against each other. We did display representing nearly a million [indiscernible] our comprehensive library and our screening platform were crucial for enabling the unprecedented scale of these experiment through this screen we identified nearly every zone, immuno-oncology target interactions including the PD 1, CTLI4 and get a fast ways as well as others. This validates the effort. But importantly we also discovered multiple new tuck-in interactions that we’re now prioritizing as immuno-oncology drugs target. Separately we’re actively working on numerous targets identified in our Treg and T Effector cell on multiple screens as well as in our vivo screen to advance the most promising immuno-oncology targets and validation. And our expectation is these discoveries will translate into multiple therapeutics both in campaign for getting into 2017. Now on the preclinical front. We continue to advance multiple immuno-oncology program and have initiated IND enabling activities for three therapeutics candidate including our [indiscernible] agonist antibody, a T-cell modulator and an additional multi-functional immune modulator. We intend to share further details on these three pre-clinical programs and our screenings efforts during our R&D day in New York on December 8. We remain committed to our goal of filing at least one IND for a new therapeutic protein each year for the foreseeable future to getting in 2017. Now finally I’ll draw your attention to slide 15 which highlights our recent and anticipated milestone. As I just mentioned we’re especially pleased that we have advanced three of our research programs into an IND enabling activity and I’ll remind you this exceeded our stated goal to advance two programs by the year end. I'm incredibly pleased with our momentum beyond the notable progress we’ve made with our clinical pipeline and so we’re also excited about the wave of immuno-oncology programs that are advancing in course IND. And finally we’re opening the call up for questions. I’d like to extend my appreciation for our Five Prime employees as well as many patients and investigators involved in our clinical trials. I’ll now open it up for questions.

[Operator:]

[Operator Instructions] Our first question comes from the line of Robyn Karnauskas with Citigroup. Your line is open.

[Unidentified Analyst:]

Yes thanks this is Mohit for Robyn. Thanks for taking my question. So congrats on the progress. So quick question on the combination approach for FDA 144 you just alluded to, so in terms of combination combining this with any other agent how are you thinking about do you think the chemo approach makes more sense for combination or do you think a checkpoint approach. And follow up question is like do you think that we know that checkpoint is working gastric cancer in terms of responses. Do you think that the patient where have checkpoint response are same as the patient at FGFR2b and FGFR2b does would work? Thank you.

[Rusty Williams:]

Yeah thanks Mohit. So the question is on combos chemo versus checkpoint inhibitors and then the kind of follow up question on the checkpoint inhibitor for say. There are compelling rationales for combinations both with chemo and with checkpoint inhibitors and we've reported preclinical data showing at least that activity is not synergy and both these not a combination. So there is a good rationale for both. And so we're interested in both of these combinations, we haven't given guidance on the specific of what we've planned but we will do that in a relatively near future. I'll let Bob cover the question of checkpoint inhibitors, if there is anything else do you like to say Bob or.

[Robert Sikorski:]

Yeah great question. We've shown as you seeing preclinically that 144 drives in preclinical model the expression of PDL-1 at the same time interrogating T-Cell that’s in triggering obviously it's preclinical models. But that provides very strong scientific link between PDL-1 blockade perhaps and FTF and 144. So that's there is a scientific connections. I think your point to your questions was do they overlap in clinic in terms of who response or who doesn't response to PD-1 inhibitor and we're actively doing biopsies on our patients to tight them for the PDL-1 status when we're looking at there right now. So there is overall summary is those two combinations with chemotherapy and PD-1 inhibitor are I think what we mean by combinations.

[Mohit:]

Great thank you.

[Operator:]

Thank you. Our next question comes from the line of Kennan MacKay from Credit Suisse. Your line is open.

[Unidentified Analyst:]

Hi this is Dua [ph] on for Kennan. So just the first question, any update on interactions with regulatory authorities regarding a potential accelerated approval or potentially registration or trial for 144 in gastric cancer.

[Rusty Williams:]

We haven’t given any specific guess on our interaction with regulatory agencies. So fine to say that we are interested in discussing with the FDA the best path forward. And so we'll be doing that and after at some point with growth initiative.

[Unidentified Analyst:]

Okay. And then any update on when we might be able to expect combo data with the ongoing Cabira and OPDIVO trials.

[Rusty William:]

So Cabira, we have three to sort of look at it as three events 1a the 1b which is the largest part of the trial and in aggregate those are up to 280 patients and for immuno-oncology and the PVNS. We will have data in 2017 for Cabira and so I will be looking into 2017 for some data possibly on any of those areas.

[Unidentified Analyst:]

Got you. And just a last question. With upcoming preclinical data in your GITR, how should we expect to be thinking about clinical development here, like what are some initial indications you would expect to go with this asset?

[Rusty William:]

Yeah so there are a lot of people interested in GITR. As you remember the way we came to GITR as a target was through our in vivo screen showing that a GITR agonist was a powerful suppressor of tumor growth. And when we compare it to a lot of other proteins in that screen. Our special take on GITR is we have a multivalent antibody. And so GITR was clustering to get a molecule. Now which tumors that's best to do in, is an important aspect of any of the GITR programs including ours. And we this is the matter of intense deliberation internally based on [indiscernible] findings and we haven't disclosed yet which indications but this is something really important for us to focus on in best what we are doing. And so we are on track with the GITR program, we remain on track and enthusiastic about it.

[Unidentified Analyst:]

Okay. Great. Thank you so much.

[Operator:]

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

[Jim Birchenough:]

Hi guys, congratulation on the progress. Couple of questions, first question, just on the Phase 1a Cabira to the extent of those things still continuing, should we assume that you are seeing some evidence of activity and is there any plans to further dose escalate in the mono therapy arm and then I've got a follow-up.

[Rusty William:]

So, thanks Jim. The main purpose of the 1a plus was cyclical for the specific settings then 1b. And so, we have done that, we have given guidance all along that when we got to point which we can think of those we would be moving into in to 1d. And so that I better leave it that we are not at this point in time discussing activity and 1a or 1b to that matter. So wish I could get into that overview but really would have that now.

[Jim Birchenough:]

That’s fine and when you think about the target inflations for the Phase 1b, could you maybe take us through obviously this working more in terms of a threshold for efficacy across a bit in different indications what are you looking to see that would for moving forward?

[Rusty William:]

Yeah I let Bob, to talk about that.

[Robert Sikorski:]

Yes, let’s talk about that. Good question I haven’t turn to slide five, we provided an overview of this slide of the trial architecture might have to have there is a reference. So, when we go to 1b we have series of define cohort that range from lung cancer that’s PD-1 Naïve, lung cancer that PD-1 resistant or refectory, pancreatic [indiscernible] each of those different cohorts has the different bar, largely driven by the previously known activity of the PD-1 Inhibitors in that setting, that’s how we look at it. So, for instance, if you look at lung cancer that’s Naïve inspected about the 20% response rate and many of the PD-1 Inhibitors in the setting we are in. No matter where in the setting that exactly the setting where our OPDIVO through. So, let's use an example should be double that response rate, that would be interested but we have 20% response rate we know that sort of in the ballpark of the background as the drug itself.

[Rusty William:]

That can give a sense of how we are thinking about it. Lung cancer that’s PD-1 existing is a different story there is no background in the PD-1 Inhibitor. So any response becomes meaningful. I know that I think book India when you look at something like pancreatic cancers it’s not allow the PD-1 data released on that, We would expect that just from our discussion what people are involved in in pancreatic trial that is market sessions with people involving and things we have tie up about a 10% to 20% maximum response rate. So the bar is very low to signal there. And I think the same could probably be set for a varying degree of [indiscernible]. Does that give you a sense of that?

[Robert Sikorski:]

And I would like to ad is that tough cohorts on that side is mono therapy. And of course that’s any responses in the mono therapy settings can we have some specific indications in mind. So any response there would be meaningful.

[Rusty William:]

Good [indiscernible] and also just some of the offsets about 1a. I can clarify little bit we are continuing 1a looking in one of the NDN combination and the same combination as the rest of those defined cohorts. We did that for a few reasons, one sales moving very quickly, we didn’t want to create cohorts for all of these define setting so we created this open ended cohorts where we can final in patient that either or interesting to us from our existing trials or interesting because the field we learned a lot or interest into that for other reasons so, and mono-therapy is one of those cohorts.

[Jim Birchenough:]

And can if you allow me maybe, one final question. Rusty just on when you think about the exercise that just gone through and screening the whole immunome and element 700 guys 700 interactions. Is there front screen particular that you take particularly informative as due to product activity how does CSF 1 will stand out. There is a lot of thoughts, looking at anti PD 1 across XYZ and we off about question why don’t we think the CSF 1R will be so good the honest biological rationale there is something about these screens that you saw in particular instructive?

[Rusty Williams:]

So the way we look at the screen and immuno oncology is how they read on each other that for the data in the aggregate. So let me just clarify what I mean. |That it indicates of the Treg screen and if get here in the Treg screen to functional screen everybody wants to get Treg consumers. If we get a hit the tails as there is a pathway there. And we also get that again for example an in vivo screen modulating tumor growth that tells us a lot. So we kind of look at the data in aggregate that's the big power of our platform as we can look all of these things compare them to each other in multiple screens. Now where are those prices. Prices are actually in almost every screen so the Treg screen has given us a lot of new information about regulation of those cells and hence has the effective T-cell screen. By Immunome screen, the screen has been sort of a struggling as set of results because there is a lot of new information about interaction about in the immune system and of course we're interest in both that are particularly important in cancer. So that's given us some really nice surprises. That you mention combination or what the combined risk with PD-1 pathway blockers. We are in the midst of screen right now in vivo, in which we are combining every one of those immunome proteins actually more than the 700 and we're including additional ones in combination with the PD-1 blocker. So that specifically addresses the issue you just brought up, what is the best thing to use in combination with the PD-1 blocker to get enhanced activity. And so we'll be discussing that screen, we're not going to give away the forum as R&D data will get the enough information so that we will able to see how that progressing. And then the third part of your question was about CSF1R in particular. There are a lot of preclinical data already out there about why the one block CSF1R in combination with Checkpoint inhibitors. And those are in some our slides at the preliminary deck and in our website and in publications. And so we haven't really gone back to we look at that as there are so many data out there on that both in the preclinical data or when you block [indiscernible] or you remove them. You remove all of those inhibitory signals from them you increased CD-8 cells, you increase the ratio of CD-8 Treg cells. And you have synergies and shrinking tumors. And those data I think work a lot more than screening data actually. And then in humans we know for fact that we can reduce the macro based cells and that the disciplined receptor blockage removed reduces them. So I think there are a lot of data suggesting why that's the good pathway to block. But the first including and our field will it's important for our field to feel the clinical data and 2017 will be an important year for that and all the companies working in this field I think. So the way we look at the screen and immune-oncology is how they read on each other that for the data in the agreement. So let me just clarify what I mean. And it indicates of the - screen and if get a hit - screen the functional screen everyone wants to get - consumers. If we get a hit the tails as there is a pathway there. And we also get that again for an example an in vivo screen modulating tumor growth that tells us a lot. So we in two weeks kind of look at the data in aggregate and that's the big power of our platform as we can look all of these things compare them to each other in multiple screens. Now where are those prices. - are actually in almost every screen so the - screen has given us a lot of new information about regulation of those cells and hence has the effective T-cell screen. By Immuno on screen, the screen has been sort of a startling as set of results because there is a lot of new information about interaction from the immune system and of course we're at - in those that are particularly important in cancer. So that's given us some really nice surprises. That you mention combination or what the combined risk with PD-1 pathway walk us. We are in the midst of screening right now in vivo, in which we are combining every one of those immuno-proteins actually more than the 700 and we're including additional ones in combination with the PD-1 blocker. So that specifically addresses the issue you just brought up, what is the best thing to use in combination with the PD-1 blocker to get enhanced activity. And so we'll be discussing that screen, we're not going to give - as R&D data will get the enough information so that we will able to see how that progresses. And then the third part of your question was about CSF1R in particular. There are a lot of preclinical data already out there about why the one block CSF1R in combination with Check point inhibitors. And those are in some our slides at the preliminary deck and in our website and in publications. And so we have a really gone back to we look at that as there are so many data out there on that both in the preclinical data or when you block - or you remove them. You remove all of those inhibitory signals from them you increased CD-8 cells, you increase the ratio of CD-8 - cells. And you have synergies and shrinking tumors. And those data I think working a lot more than screening data actually. And then in humans we know for fact that we can reduce the macro-- cells and that the disciplined receptor blockage removed reduces --. So I think there are a lot of data suggesting why that's the good pathway to block. But the first including and our field will it's important for our field to feel the clinical data and 2017 will be an important year for that and all the companies working in this field I think.

[Jim Birchenough:]

Great thanks for the all the answers.

[Operator:]

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

[Ian Somaiya:]

Thanks. Just wanted to ask about the two additional pre-clinical candidates that are now moving forward. Are they unique to Five Prime or are there other companies pursuing those. And how should we think about sort of the development strategy for in all three of your, I guess, new clinical compounds in the IR area. Should we assume you pursuing independent development. What point would you consider partnership. Just I want to get your longer term view on those assets.

[Rusty William:]

Yeah thanks. So first of all with respect to the three programs something along, where we just not talk about that's most secret. The other two programs as far as we know there is nobody in the clinic with those programs like ours. And potentially for one of those programs we don't think anybody is pursuing is at least very far long in development. And it came out of our screen and we never know but other people may come up with the same idea but just came directly from our effort. And so we make sure that going we’re going to be lead on that. And so that we’ll disclose some more about these programs in near future and at our R&D Dat. And then you had the second question on, forgot the second part of the question.

[Ian Somaiya:]

Yes, just I mean how should we think about development of those drug and how far you willing to sort of pursue independent development and when do you consider partnership?

[Rusty Williams:]

Yes, so the key to our strategy, and immuno-oncology is to address multiple T-cell types in the tumor market environment. I think all of us believe that combination therapy is going to be an essential part of going forward and we oppose that in a very rational scientific way to how to do the combination. And that’s why we are taking those that we are and we have the tam, blocker , we have in phase trial, recruiter and just talking about Treg screen TDI screen et cetera. So, we are looking at immuno-oncology as a way to do combination and we want be able to combined but if you remember from our Cabiral deal the CMS we preserve the right to combined Cabira with any agents that we developed in our pipeline. So, going forward we will develop single agent but having the ability to combine agents in our own pipeline with each other I think would be a big advantage for us. Now, whether we do partnerships with other companies other agents and ready to get combinations that we don’t have internally we’ll had to see how that plays out but we are not [indiscernible] for that. We do think that we need to develop our own compound our own agents through to commercialization and that is core to our strategy.

[Ian Somaiya:]

Thanks Rusty.

[Rusty Williams:]

You’re welcome.

[Operator:]

Thank you. Your next question comes from the line of [indiscernible] Guggenheim. Your line is open.

[Unidentified Analyst:]

Hi everyone. So for my first question, in the presentation to ask us on if we are able to detect elevated copy numbers of FPRX for their FPRX inhibitor in respondent, and I was - I know you have been using the screen for adjust special levels but have you seen elevated levels is the question? Outside of the primary consumer and following that have you more potentially moving toward the blood base FGFs and then - sorry to be - I’ll follow up with the different question.

[Rusty Williams:]

Okay. We’ll have, we’ll come back to for your second question after the first one.

[Robert Sikorski:]

Hi Kevin. To answer your question we are very similar with that data but those who aren't after [indiscernible] in the highest amplified DNA you can easily see in the tumor you can easily see in the blood. We without saying too much think that probably accurate we intend in our current file we do have and select blood for circulating tumor DNA and analyzing them.

[Rusty William:]

We think that's potentially important for the future.

[Robert Sikorski:]

So, that server as a complement perhaps to what we are doing as I see. So we wouldn’t rollout that and we will then start in the future. It’s in emerging field we’re trying that and we're measuring that end I see looking at those correlations.

[Rusty William:]

And Kevin, you had another question.

[Unidentified Analyst:]

Yes. Okay, thanks. And secondly you have done the same period for Treg do you have any sense [indiscernible] season future function target seems?

[Rusty William:]

Yes, that’s on our lips. We haven’t done that yet. But that’s we haven’t interest in that. Each of these things we have to you can do screen if then I’m going to do Treg so this is something. But you really have to be careful about to insure that you work on a real Treg and same thing goes for NVSC so I think the challenge with NVSC is to be sure you actually have and NVSC in your screening assay that resembles the NVSC in the tumor and that we're trying to figure out now. We think we did figure that out for Treg.

[Unidentified Analyst:]

Okay. Thanks.

[Operator:]

[Operator Instructions]. Thank you. I’m showing no further questions at this time. I would like to turn the call back over to Rusty Williams Chief Executive Officer for closing remarks.

[Rusty Williams:]

Well thanks each of you for joining us today and also for your support and interest in Five Prime. And we look forward to updating you in the future on calls. Thanks again.

[Operator:]

Ladies and gentlemen thank you again for your participation in today's conference. This is now concludes the program. And you may all disconnect at this time. Everyone have a great day.