Five Prime Therapeutics Inc
Q3 2015 Earnings Call Transcript

Published: 5 Nov 2015

[Operator:]

Welcome to the Five Prime Therapeutics Incorporated 2015 Q3 Quarterly Earnings Conference Call. [Operator Instructions]. I would like to introduce your host for today's conference, Mr. Aron Knickerbocker, Five Prime's Chief Business Officer. You may begin, sir

[Aron Knickerbocker:]

Good afternoon and thanks for joining us as we discuss Five Prime's financial and operational results for the third quarter of 2015. We will begin today's call with opening remarks from Rusty Williams, Chief Executive Officer; Julie Hambleton, our Chief Medical Officer is traveling so Bob Sikorski, Vice President of Global Clinical Development will take you through the status of our clinical programs. I will cover our research programs and collaborations and then Marc Belsky, our Chief Financial Officer will review the financials. Following those prepared remarks we will host the Q&A session. During today's call, Rusty will begin with introductory remarks on our progress during the second quarter. Julie will then give an update on our clinical programs. I will provide an update on our immuno-oncology research programs. And then Marc will discuss our financial results. Finally, we'll conclude the call with a Q&A session. Our team is coming in from two locations today so bear with us if things aren't quite as seamless as usual. I need to remind everyone that today's conference call will include forward looking statements under the Private Security 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 Factor 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'll now turn the call over to Rusty.

[Rusty Williams:]

Thanks, Aron. There has been lot of interest in the deal we've done recently with BMS on FPA008 so I would like to make a few comments about that. This program we feel is another validation of our discovery platform and it also shows our ability to take something from target discovery through research, anti-body generation, clinical trials and value creation. I'd like to tell you the story just for a couple of minutes about how this project went, how it got started, a few years ago we wanted to find the most important pathway for regulating macrophages in humans. Now I remember when a Five Prime scientist excitedly showed me the results of the screen in which he had checked also secreted proteins for their ability to activate macrophages and there was one that stood out and it's efficacy and selectivity and that was Interleukin 34 that was the discovery of that cytokine. We then used our platform to quickly find its receptor, we made anti-bodies to the receptor because we knew that receptor seemed to be the key for regulating macrophages, we show that to the antibodies block macrophages in animal models of cancer and other diseases. And we got it into the clinic and show that it reduces macrophages in humans. So why do we do this transaction with Bristol Myers Squibb now? First of all Bristol Myers Squibb is an ideal partner for us. They're clearly a leader in immune-oncology and we have a good relationship with them having done two collaborative efforts with them in the past. Also Opdivo is an ideal agent to combine FPA008 and we have done preclinical experiments that showed us that this combination was a very good one. It's a fast moving landscape. This program, this collaboration or this transaction with BMS allows us to broaden and accelerate the program. I think it increases the probability of success. We're now competing with large efforts testing these two pathways and I think that now will continue to be extremely competitive. Another point is that in our discussions with BMS the economics did become worth doing it now. So we decided to proceed. We did achieve a key feature that we wanted from the beginning and that is our ability to continue development work on FPA008 so we're continuing the current trials, combination without Opdivo, we're also continuing to develop the drug in PVNS Pigmented Villonodular Synovitis and we also have the ability to combine FPA008 with other agents in our oncology pipeline in the future. So on the one hand our day to day operations haven't changed. We have three clinical candidates each of each of which has made progress in Q2 but on the other hand. This does represent an unprecedented opportunity for us to take the company to a new level. BMS is yield another validation for a platform as I said before. It also shows the power of our development group to move things through early phase of clinical trials. It leaves us in a good position to find another 008 like opportunity and it gives us resources that position us to have a significant impact in this field. So with that I'd like to turn the discussion over to Bob Sikorski.

[Bob Sikorski:]

Thank, Rusty and good afternoon everyone. Obviously the third quarter was an important one for FPA008 so let me begin there. As you recall this is our therapeutic anti-body designed to inhibit the CSF1 receptor a signaling molecule required for the activation and the survival of certain monocytes in macrophages. I will recap the status of the three clinical trials that Five Prime is currently executing and then give you a sense of how our development collaboration will be with BMS work going forward. In September Five Prime initiated the dosing of solid tumor patients in our new Phase 1a, 1b trial. The purpose here is to explore the potential of FPA008 as an immuno-oncology agent both as monotherapy and in combination with an anti-PD1 agent. During Phase 1a we’re evaluating safety, pharmacokinetic and pharmacodynamics changes with escalating doses of FPA008 alone and in combination with the approved 3 milligram per kilogram every two week regimen of Opdivo. Approximately 30 patients with advanced cancers are expected to be enrolled during Phase 1a, in Phase 1b we'll evaluate the safety, tolerability and primary efficacy of a selected dose of FPA008 in combination with up Opdivo in approximately 240 patients across eight tumor settings. In September we disclosed two important new cohort of non-small cell lung cancer and melanoma patients who demonstrate resistance to anti-PD1 therapy. We looked for the ability of FPA008 to reverse this resistance. We have a robust translational component in this trial. And are obtaining tumor biopsies before treatment and after one month on treatment in all patients enrolled in the Phase 1a portion. We will also obtain biopsies in the selected subset of patients enrolled in the Phase 1b portion of the trial. This will allow us to analyze the immune cell and overall changes within the tumor microenvironment. We intend to use this knowledge to guide the development of FPA008. The details of this trial were recently featured in the trial in progress presentation at the International Cancer Immunotherapy Conference in September in New York. We expect to complete the Phase 1a dose escalation portion and expand into Phase 1b in early 2016. Turning next to PVNS, we began dosing patients with FPA008 in July in our Phase 1/2 trial. Five Prime will continue independent development of PVNS under the BMS agreement. PVNS is a locally aggressive tumor of the synovium or expression of CSF1 recruit's macrophages that form a tumor mass. The incidence of PVNS is rare but the prevalence is greater as patients typically live decades with their disease. PVNS patients experience a high level of joint morbidity and have no approved treatment options after surgery. During the Phase 1 dose escalation part of the trial we are assessing safety pharmacodynamics and imaging of the joints to determine the dose for expansion. During the Phase 2 expansion, we will evaluate tumor response rate and duration and measures of pain and joint function in approximately 30 patients. We plan to complete dose escalation and move into dose expansion in early 2016. Our third FPA008 trial is the initial Phase 1 study which is now enrolling a final cohort of rheumatoid arthritis patients receiving methotrexate. We’re evaluating safety, and biomarker changes following two or three administrations at three doses levels. Biomarker, safety and PK data from these [indiscernible] patients are informing the ongoing development of FPA008 across all indications. We report data from these RA patients in a poster presentation at the American College of Rheumatology meeting on November 10. As we've noted previously we no longer intend to proceed to a randomize component in rheumatoid arthritis. Neither we or BMS are planning any additional trials RA [indiscernible] trials at this time and we will instead focus our efforts on the development of FPA008 in immune-oncology and PVNS. Future development of FPA008 will expand to involve efforts from both Five Prime and BMS, the BMS development efforts will focus on immuno-oncology initially in combination with Opdivo and potentially in combination with other BMS agents. The Five Prime development effort will focus on PVNS and may in the future include combinations with our oncology assets or those of BMS. We also have the ability to develop FPA008 in non-oncology indications that are not added to the BMS formal development plan. We will continue to work collaboratively with BMS through the framework of a joint development committee. Here we will coordinate FPA008 clinical activities and discuss the scope and responsibilities of the plan trials. Prior to our initiation of a new trial, BMS has the option to add the new trial to its formal development plan. Aron will provide additional details on this shortly. Switching now the FDA144 we are developing this iso-form 80CC enhanced anti-body as a targeted therapy for tumors that overexpressed. FGF Receptor 2b. In our ongoing trial we are enrolling patients with a variety of solid tumors including gastric cancer during the Phase 1a dose escalation portion. We expect to complete this by the end of the year. We will then select the dose and transition to part two of the trial which will enroll gastric cancer patients whose tumors overexpressed FGF Receptor 2b. We're seeking opportunities to present data from the Phase 1a portion at a clinical meeting ideally in early 2016, with positive results FPA144 may have an opportunity for rapid development path given the targeted population and the poor prognosis and lack of treatment options for these patients. Turning to FP1039 or FGF ligand trap, GSK Phase 1b trial is still underway in patients with newly diagnosed or recurrent FGFR1 gene amplified squeamishness non-small cell lung cancer and malignant chloromesothelioma. FT1039 is being administered combination with standard of care chemotherapy in each of the three study arms initial safety and efficacy data from this trial were featured in an oral presentation at the World Conference on lung cancer in September. We are pleased with the data that we've seen thus far particularly in the first line setting in squeamishness non-small cell lung cancer and the study is ongoing. I'll now turn the call over to Aron to cover our collaboration's and discovery programs.

[Aron Knickerbocker:]

Thank you, Bob. I begin by recapping the terms of our new exclusive worldwide license and collaboration agreement with BMS or FPA008, the agreement is subject to review under the heart Hart-Scott-Rodino Antitrust Improvements Act and will become effective once clearance is received which we expect by the end of this month. In addition to the $350 million upfront payment from the PVNS Five Prime will be eligible to receive development and regulatory milestone payments for each anti-CSF1 receptor anti-body product as follows. Up to $505 million for combinations with Opdivo, up to $542.5 million for oncology combination therapies with one or more BMS or Five Prime products at least one of which is not Opdivo. And up to $340 million for therapeutic uses in PVNS and non-oncology indications. BMS will be responsible for manufacturing and global commercialization. We would receive tiered royalty percentages ranging from the high teens to the low 20s in world-wide net sales. If we exercise our U.S. co-promotion option we would be entitled to an additional low single digit percentage royalty on net sales in the U.S. As Bob alluded to earlier Five Prime retains the ability to continue independent development of FPA008 in certain areas potentially all the way to approval. Prior to the initiation of a new study by Five Prime BMS will have the opportunity to add the development path to their formal development plan. If they do so they will be responsible for development costs and milestone payments. So let me give you some examples of how this might work. If we were pursuing an additional FPA008 combination with Opdivo in a Five Prime funded trial in a tumor type outside of BMS formal development plan, BMS can subsequently add this development path to their plan. If they do BMS would reimburse us for the development costs we incurred and would fund further development and would make payments associated with milestones that they achieve going forward. In this example if BMS had not chosen to add this development path to their formal plan and we took the combination all the way to approval, BMS would reimburse our development costs at a premium. In either case upon approval. Five Prime would receive payment for all past milestones achieved by Five Prime during it's independent development. Now PVNS is a special exception in terms of the milestones BMS will be responsible for making payments to Five Prime as milestones are achieved regardless of whether PVNS is added to PVNS format development plan or not. Moving on now from BMS agreement to our new GITR program. In July we expanded our early immuno-oncology pipeline by in-licensing novel multivalent anti-bodies Inhibrx, target [indiscernible] receptor or GITR. Our proprietary platform had identified GITR as one of the most potent immune cell activators in blocking, tumor growth. The addition of this P-Cell agonistic also fit for their strategy to develop combinations of immuno-oncology agents that work through complementary pathways. We believe these multivalent antibodies gap holds are well differentiated bringing the desired property stop to my safety, efficacy and combined ability with other therapies. As well as the ability to activate GITR independent of Fc binding. We’re enthusiastic about this program and are targeting an IND in 2017. We also signed a new agreement in October which will expand our internal anti-body capabilities. We have obtained a license from open monoclonal technology or OMT to assess their mono and bi-specific anti-body platforms and antibody repertoire sequencing technology. These platforms are designed to deliver human antibodies with high affinity, specificity, expression, sailability and stability. This enhanced to our internal anybody capabilities and expertise further strengthens our ability to rapidly move from immuno-oncology targets we identify to antibodies for clinical development. In fact this agreement as well as our in-licensing of the GITR program are examples of how we are actively complementing our internal efforts with opportunities that broaden our capabilities and pipeline particularly in immuno-oncology. Finally I will provide two quick updates about our ongoing discovery collaborations. In September. GSK exercised it's option to reserve specific targets discovered by Five Prime under the respiratory disease research collaboration between the companies. This triggered a $300,000 payment to Five Prime. Also in September UCB exercised its options to reserve certain targets discovered by Five Prine under the discovery collaboration between the companies in the area of fibrosis related inflammatory diseases. This triggered a $140,000 in payments that were received in the third quarter. I will hand the call over to Marc now to discuss our financials.

[Marc Belsky:]

Thank you, Aron. In the third quarter of 2015 Five Prime had a net loss of 24 million or $0.93 per basic and diluted share compared with a net loss of $7.1 million or $0.33 per basic and diluted share for the third quarter of two 2014. This increase in net loss was primarily related to in licensing, GITR antibodies, advancing the FPA008 development program into additional indications and expanding internal immuno-oncology research and pre-clinical activities. Collaboration and license revenue was $5.9 million for the third quarter of 2015 compared with $6.1 million for the third quarter of 2014. Research and development expenses were $24.7 million for the third quarter of 2015 compared with $9.8 million for the same period in 2014. This increase was primarily related to in-licensing GITR antibodies, advancing the FPA008 development program into additional indications and expanding the company's internal immuno-oncology research and pre-clinical activities. General and administrative expenses were $5.2 million in the third quarter of 2015 compared with $3.4 million for the same period of 2014. This increase was primarily due to increases in personnel related expenses including stock based compensation and facility cost. Cash, cash equivalents and marketable securities totaled $183.4 million on September 30, 2015 compared with a $149.1 million on December 31, 2014. The increase was primarily attributable to Five Prime's January 2015 public offering of common stock offset by cash used in operations. This does not include the $350 million upfront payment from BMS, the company expects to receive under the FPA008 license and collaboration agreement. Five Prime expects to have an excess of $500 million in cash, cash equivalents and marketable securities upon receipt of the $350 million upfront payment from BMS which we anticipate in December following HSR clearance. Five Prime currently anticipates recognizing the $350 million upfront payment from BMS as revenue in the fourth quarter of 2015 and to be able to utilize substantially all of its existing net operating loss carry forwards to partially offset taxable income in 2015. Five Prime continues to expect full year 2015 net cash used in operating activities to be between $65 million and $70 million without giving consideration to the $350 million upfront payment from BMS. And with that I'll turn the call back over to Rusty.

[Rusty Williams:]

Thanks, Marc. As I mentioned earlier this is really been a remarkable quarter for Five Prime and all of our programs. I'm very excited about what the teams at our company have accomplished, very proud of these teams and we intend to leverage the momentum that we have now to fuel our growth and to continue with our strategy to be a leader in immuno-oncology. We're now happy to take your questions so operator can you please open the Q&A session.

[Operator:]

[Operator Instructions]. Your first question comes from Eun Yang from Jefferies.

[Eun Yang:]

So in the combination trial with the anti-PD1 and FPA008 and now you are including two more tumor types anti-PD1 [indiscernible], is there any preclinical data is showing adding anti-CSFR1R to anti-PD1 disease and tumors make the tumors susceptible again?

[Rusty Williams:]

We don’t have preclinical experiments done in that order of treatments. Of course we Bristol and publicly published experiments have shown that the combination is synergistic into [indiscernible] but we don't have preclinical data showing that they order that you just suggested is efficacious you could infer that from those combination studies done simultaneously, that you get a better result. Bob, do you want to add something?

[Bob Sikorski:]

Yes I can add to it. We realize that these are two settings once Opdivo was approved in both melanoma and in lung cancer. It created two essentially new indications, 80% of patients do not initially respond to lung cancer to any of the PD1 agents and in melanoma it's probably 60%. So we thought that was a nice indication that we could have a small trial to see if we could either block the resistance or reverse it. So that's really the opportunity here was to go into -- it is emerging as sort of a new setting.

[Eun Yang:]

And then one another question on PVNS, so Daiichi recently initiated a Phase 3 with their TKI [ph] so whether they are running Phase 3 trials and you are doing Phase 2, do you expect to see some slow than in patient enrollment as you complete patients in this small population?

[Bob Sikorski:]

You're referring to the Daiichi Plexxikon small molecule CSF-1R inhibitor, just a little background here. Two recent papers were published over the summer that are informative both on the Plexxikon compound in PVNS is in New England Journal Paper and Lancet Oncology paper on the [indiscernible] inhibiting antibody in PVNS. So you kind of have an apples to apples comparison of the inhibition by small molecule and inhibition by an antibody with those two papers and what they found was that the Daiichi Plexxikon molecule has about a 52% response rate. Interesting the [indiscernible] antibody was 86% and they had reasonable numbers of subjects to show that that's probably a real effect. So looking that that from a high level we think that approaching this disease with an antibody is more attractive certainly from an efficacy standpoint that data would tell you that and secondly from a safety perspective. We don't have -- we have a very on target antibody, small molecule has some off target effects for fatigue and hair color changes due to [indiscernible]. So it really the two drugs have different product profiles. I think that's one thing to look at and our trials are doing quite well. We're doing we're on track. As we pointed out to dose escalate in just a few cohorts this year and transition rapidly into as we go into next year in the expanded study. And we have had no problems with in rolling that study at all and then we're going to take the data approach to the agency and work with them on the collaboratively on a path forward. Again this is an unmet medical need post-surgery, post-surgery there's nothing available for these patients and we think that having the antibodies is a reasonable approach.

[Operator:]

Our next question comes from Michael Schmidt with Leerink.

[Michael Schmidt:]

I just had a bigger picture question. Congrats on the Bristol again, obviously you now have a significant cash balance of over 500 million, can you just give us a sense of strategic priorities in terms of how you leverage this cash going forward to accelerate the pipeline growth?

[Rusty Williams:]

Yes, sure. We can give you of some broad comments now and over the next couple of months by JPMorgan we hope to give you more specific ideas. So there are a few things that we are investing in for sure one is we want to be poised with our FPA144 program pending data to be able to accelerate that program into further indications perhaps and to other territories and so this is an important aspect for us. We also would like to -- we're investing in antibody technology internally. We just recently brought in the OMT technology so that we can make antibodies quickly to our discoveries that come in immuno-oncology target area. So we now have the capability to really move faster with those and to get a better picture of the targets and line them up against each other which ones are our best and then finally we have a unique aspect of our platform. That's reflected in the GITR program that we recently unlicensed, our platform since we check all extracellular proteins all the targets of antibodies, all the extra-cellular domains and ligand traps in the same assays and the same mouse models we check all of them, compare them. We can see known targets were stacked up against targets that are proof products we can see targets that are other people are working on and novel targets all lined up with each other and we see a good opportunity like we did with GITR, then we may pursue that for in-licensing and so we have we're really attentive to that. It's kind of a cross between an internal capability and external in-licensing opportunities and so those are our thoughts now.

[Michael Schmidt:]

And then maybe another one, can you just give us a sense where you’re with your internal efforts in terms of new immune checkpoint discovery and second question you previously guided to Phase 1a data for [indiscernible] for one potentially in early '16 and is that still the case following the Bristol deal? Thank you.

[Rusty Williams:]

So with respect to the internal programs we have some quite interesting findings and we have antibody program just to give you a stage where we are, we have antibody generation programs and antibody selection programs with some of our internal early phase programs and that goes all the way back to early phase of discovery. We do think that in addition to the pre-clinical programs that we have currently. These antibodies programs that some of the targets that we find over the next year will also be quite valuable. Of course those are very early programs and so the issue is that it's often brought up as well we disclose those and we won't prematurely identify those in order to preserve the value especially if they're quite novel. And then the second part of your question Michael, could you repeat that?

[Michael Schmidt:]

In terms of first PD1 combination data for FPA008 are we still looking at that potentially in early 2016?

[Bob Sikorski:]

We’re currently in dose escalation component of that trial. So we just released at a meeting in September the immuno-oncology ACR meeting in New York some designs data on that trial. We have eight cohorts that we’re expanding into in the Phase 1b section but before we get to those expansions we wanted to have three cohorts with different doses of FPA008 and the approved dose of [indiscernible]. And those were ongoing, we also importantly have two cohorts of monotherapy with FPA008 in cancer patients as well that are ongoing currently. Remember we never dosed cancer patients yet as monotherapy so that's really important. All of the Phase 1a part, those five cohorts I just mentioned have pre-imposed biopsies mandated. That means that as we screen patients we do a tumor biopsy and then after we treat them for 30 days we do another biopsy and we're really looking for clues as to how these two drugs work together the tumor level. Changes in cellular infiltrates changes in PDL-1 status etcetera. So that's an important you know if I were to look at it from a high level, the translational aspect of the Phase 1a is an important part and we're likely to share that next year we think. The expansion will start next year and will go generate data as it flows. Remember these are an eight different cohorts, there launched sequentially next year for the expansion in 1b and they will be behave quite independently in terms of our thinking going forward.

[Operator:]

Our next question comes from Christopher Marai with Oppenheimer.

[Christopher Marai:]

So I was actually wondering with respect to FPA144 do you anticipate that you would perhaps do a combo of that in gastro cancer with Nivo given the positive data for that drug [indiscernible] and when might we expect an update there?

[Rusty Williams:]

So we FDA144 is an antibody with enhanced ADCC, and we have shown pre-clinically a remarkable infiltrate of in [indiscernible] cells into the tumors that express FGR Receptor 2b when treated with FDA144. So it is a good idea to think of this as in NK [ph] cell recruiter and it would be rational and important to consider combination with other immuno-oncology approaches and we have been doing experiments along those lines and it's premature for me to disclose the data, but you're thinking the same way we are.

[Christopher Marai:]

Okay and then just on that topic with NK cells because obviously they can be modulated by checkpoints like PD1 access. You know what about lenalidomide, have you thought about any combinations potentially with len just given that it's known to help potentiate those cells?

[Rusty Williams:]

Are you talking about with FPA144 and lenalidomide?

[Christopher Marai:]

And thus you know how can it augment that NK cell activity or is that perhaps unnecessary at this point given all that recruitment we’re seeing?

[Rusty Williams:]

Yes. It's a fascinating idea, we would hope that the indications would overlap a little bit more. So again we’re targeting an ISO-form selective once FGFR2B target and so we’re constrained by where that target is expressed obviously. Currently we know it's in gastric cancer at a certain percentage. We know it's expressed through translocations in another tumors and we're very actively pre-clinically sorting out which of those tumor types might be of most interest to us, but again just top of my head don't see us overlapping tumor type with lenalidomide. Interestingly in the setting drugs like CD137 which do increase in K Cell seem attractive as well, they would an interesting partner with us too.

[Christopher Marai:]

And then I guess just one more here. So thank you for clarifying the transaction details I guess it sounds like you're able to combo FPA008 with any of your own internal IO candidate I guess some of that you’ve discussed some of that you’ve licensed and alike. So when might we see the first combination and then what might be the criteria to explore these combinations beyond efficacy data would be -- you would be looking to use these to gain a strategic advantage for instance I think perhaps not as crowded as some others but getting there. Do you think this might provide a strategic advantage in terms of bringing through the clinic?

[Rusty Williams:]

Well first of all we think that the combination -- we don't have a disclosure right now about what's the next combination that we would do with FPA008, just to answer your question directly. But to give some color around our thinking on that. We do think and this was a key thing in our discussions with BMS on this. We do think that the way we look at immuno-oncology approach is that there are several different approaches that when taken simultaneously are likely to give better results than individually. And so we think that having a macrophage inhibitor to combine with either a T cell agonist or with other pathways that we're finding in our discovery platform is a competitive advantage. And so it was important for us to preserve this activity, this ability to use it. And you can see one example of this in a poster we have at the City Meeting in which we've combined FPA008 pre-clinical model with anti-CT40 and so that's an agonist pathway, that just shows and you get synergy so that does show as one example we're not developing anti-CD40 by the way but it was a preclinical experiment, we felt comfortable and disclosing just to tell a straight to point. So we think in summary that having FPA008 or a macrophage inhibitor is still an important pathway for to use in combination with other agents that we develop. And that's why we -- this was such a key issue for us in our discussions with BMS.

[Christopher Marai:]

Remind us that’s completely uninhibited from any sort of financial obligations to BMS if you combine it with any of the other candidates, Correct?

[Aron Knickerbocker:]

Yes, Chris, that’s correct there no financial obligation to BMS. However we do first need to present the idea to BMS and they can decide whether or not to add it to their formal development plan. If they do then there would be financial obligations with respect to funding the development but nothing -- there are no rights that they would receive to our other product.

[Operator:]

Our next question comes from Tony Butler with Guggenheim Securities.

[Tony Butler:]

It's really, back around to GITR and while you'll spend a good bit of '16 I suspect on that lead optimization etcetera. Question is can you provide any thoughts around what you would initially do with GITR and more importantly is it simply, is monotherapy in some tumor type or is it -- are there also thoughts at the same time of pursuing combination therapy? Thanks very much.

[Bob Sikorski:]

Our molecule we think is poised to be one of the best in class. We know that agonizing TNF receptors requires multivalents so our molecule is an antibody like molecule with multivalent, it has lot of interesting properties. We also know like it can work without binding two the FC receptors which is important for some combinations particularly with [indiscernible] where you’re actually removing the Fc receptors by removing monocytes in macrophages. And so our anti-GITR antibody as an agonist is a really attractive molecule now, how did they develop in the clinic? Arguably Merck is far ahead in this field. They had started out with a monotherapy study in advanced in combination with their PD1 inhibitor and they'll provide a bit of a roadmap for I think most people looking through this setting. We would envision a monotherapy experience and combinations with the approved or nearly approvable agents at the time, in general I think that's how we look at.

[Operator:]

[Operator Instructions]. And I'm not showing any further questions at this time I like to turn the call back over to Rusty Williams.

[Rusty Williams:]

Okay, well I would like to thank everybody for joining us today and for your continued support and interest in Five Prime. We look forward to updating you further in our next quarterly call and we're also happy to take calls after this conference call. Thank you.

[Operator:]

Ladies and gentlemen this concludes today's presentation. You now disconnect and have a wonderful day.