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Five Prime Therapeutics, Inc. (NASDAQ:FPRX)

Q2 2014 Earnings Conference Call

August 5, 2014 05:00 pm ET

Executives

Rusty Williams – President & Chief Executive Officer

Julie Hambleton – Senior Vice President & Chief Medical Officer

Marc Belsky – Senior Vice President & Chief Financial Officer

Aron Knickerbocker – Senior Vice President & Chief Business Officer

Brian Wong – Vice President, Research & Head of Cancer Immunotherapy

Analysts

Eun Yang – Jefferies

Shin Kang – Wells Fargo

Bret Holley – Guggenheim

Nick Abbott – BMO Capital Markets

Operator

Good day, ladies and gentlemen, and welcome to the Five Prime Therapeutics, Inc. 2014 Q2 Quarterly Earnings Call. (Operator instructions.) As a reminder, today’s conference is being recorded. I would now like to turn the call over to Five Prime’s Chief Business Officer, Mr. Aaon Knickerbocker. Sir, you may begin.

Aron Knickerbocker

Good afternoon and thank you for joining us. On behalf of Five Prime Therapeutics I’d like to welcome everyone to our conference call to discuss financial and operational results for Q2 2014. Joining me today are Dr. Rusty Williams, Chief Executive Officer; Dr. Julie Hambleton, Chief Medical Officer; and Mr. Marc Belsky, Chief Financial Officer, as well as Brian Wong, Head of Cancer Immunotherapy Research.

During today’s call Rusty will begin with introductory remarks on our progress during Q2. Julie will then give you an update on our clinical programs. I will provide an update on our research collaborations and then Marc will discuss our financial results. We will conclude the call with a Q&A session.

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.

And with that I’ll now turn the call over to Rusty.

Rusty Williams

Thanks, Aron. Good afternoon, everyone. We appreciate you dialing in for this call. So far 2014 has been a very productive year for Five Prime. During the quarter we made considerable progress in each of our programs and we’re on target to achieve a number of important milestones by year-end.

We and GSK are really enthusiastic about the continued advancement of the Phase 1B clinical for FP-1039, an FGF ligand trap. GSK is very actively moving all three arms of the trial forward and has now began enrolling mesothelioma patients in Arm C of the study. We’re looking forward to initial dose escalation results later this year in patients with squamous non-small cell lung cancer who have an FGFR gene application in their tumors.

In the Phase 1 trial of FPA008, this is our anti-CSF1 receptor antibody, we’ve now completed dosing in healthy volunteers. We plan to report data, including the effects of our drug on biomarkers from this part of the trial during Q4. We also expect dosing in rheumatoid arthritis patients will begin by the end of the year. Additionally we’re excited about the prospects for a second therapeutic indication for FPA008 and we plan to disclose this indication by year-end. Julie will tell you more about this.

FPA144, and remember, this is FGF receptor 2b antibody for gastric cancer – we’re making great headway with our plans to initiate a Phase 1 clinical trial before the end of the year. Lastly, on the immuno-oncology research front, we continue to make progress in our checkpoint inhibitor collaboration with Bristol-Myers Squibb as well as in our internal cancer immunotherapy program.

Now I’d like to turn the call over to Julie Hambleton, our Chief Medical Officer, and she’ll give you a more in-depth update on our clinical programs.

Julie Hambleton

Thank you, Rusty, and good afternoon everyone. Let me start with an update on FP-1039. As Rusty mentioned earlier, GSK is enrolling patients in all three arms of the Phase 1b trial with FP-1039. Since our last earnings call GSK initiated enrollment in Arm C of the trial in patients with mesothelioma, a tumor associated with exceptionally high levels of the FGF2 ligand. Arms A and B continue to enroll patients with newly diagnosed or recurrent squamous non-small cell lung cancer whose tumors have amplification of the FGF receptor 1 gene.

GSK also recently elected to open additional clinical sites, including sites that specialize in the treatment of mesothelioma. We anticipate having initial results from the dose escalation portion in non-small cell lung cancer patients by the end of 2014.

At the [AFTA] meeting in June, several companies reported clinical data with their small molecule tyrosine kinase inhibitors that target the FGF receptor pathway. Preliminarily their data were encouraging given the responses seen in FGF receptor 1 amplified tumors; however dosing was limited due to multiple toxicities and poor tolerability. We continue to believe that the selectivity of FP-1039 will avoid many of these toxicities, thus enabling full pathway inhibition in combination with chemotherapy.

I would now like to provide you with an update on our Phase 1 clinical trial for FPA008, an anti-CSF1 receptor antibody. We have now completed testing multiple ascending doses in FPA008 in healthy volunteers. We remain on track to report preliminary pharmacokinetic, safety, and biomarker data in Q4. We are encouraged because we see signs of biomarker modulation that support our mechanistic hypotheses.

Also before year-end we expect to begin dosing FPA008 in patients with moderate to severe rheumatoid arthritis who are receiving methotrexate. We plan to test FPA008 versus placebo in a blinded fashion in these RA patients. Clinical and radiographic endpoints, such as clinical signs and symptoms and magnetic resonance imaging, will be incorporated in this part of the trial.

Lastly for FPA008, by the end of this year we plan to announce a second indication for clinical development. Because FPA008 is an antibody that blocks the proliferation of monocytes in macrophages as well as the generation of cytokines we are looking at cancer settings and inflammatory disorders in which monocyte-lineage cells play a pivotal role. Among the indications we are evaluating are cancer; pigmented villonodular synovitis, which is also known as PVNS; and fibrotic diseases.

At the AASCO 2014 Meeting other companies introduced two important therapeutic concepts involving the CSF1 receptor pathway. The first was the potential therapeutic benefits of combining an anti-CSF1 receptor antibody with a checkpoint inhibitor in patients with cancer. This concept of combining a checkpoint inhibitor with an anti-CSF1 receptor antibody was further supported by the DeNardo Group in an article just published last week in the journal Cancer Research.

The second concept from AASCO was targeting this pathway in PVNS, which is a rare joint tumor driven by CSF1 receptor activation. We have been actively exploring these concepts as we evaluate additional indications for FPA008.

Now let’s turn to our third product candidate, FPA144, which we are developing for gastric cancer patients with FGF receptor 2b overexpression. Five Prime engineered this monoclonal antibody to have enhanced ADCC. During Q2 we completed GMP manufacturing of the drug substance, finished substantially all of the 13-week GLP toxicology studies, and selected a central lab partner for molecular diagnostic tests that will be used in this trial.

We are on track to submit an IND and initiate a global Phase 1 trial by year-end. This trial will first enroll unselective patients with solid tumors and will subsequently enroll selective gastric cancer patients with FGF receptor 2b protein overexpression or FGF receptor 2 gene amplification in their tumors. We plan to evaluate FPA144 initially as a monotherapy in gastro cancer which may enable an accelerated development path.

At this point I’d like to turn the call over to Aron to discuss our research collaborations.

Aron Knickerbocker

Thank you, Julie. We continue to make great strides in our research collaborations behind the scenes. In terms of updates we’re pleased to report that subsequent to the end of Q2 we selected a cancer immunotherapy target for an antibody generation campaign, now getting underway with Adimab. Adimab will use its proprietary discovery and optimization platform to identify fully human antibodies for the undisclosed checkpoint targets selected by Five Prime.

This is an important milestone for our internal cancer immunotherapy program and we continue to expand our team and efforts at Five Prime to pursue opportunities in this promising area of oncology.

At this point I’ll turn the call over to Marc to discuss our financials.

Marc Belsky

Thank you, Aron. In Q2 2014 Five Prime had a net loss of $9.9 million or $0.46 per basic and diluted share compared to a net loss of $7.3 million or $5.82 per basic and diluted share for Q2 2013.

Collaboration revenue was $5.0 million for Q2 2014 compared to $3.5 million for Q2 2013. This increase was primarily due to $1.9 million of revenue recognized under the checkpoint inhibitor collaboration with BMS; a $0.3 million increase in revenue recognized under the fibrosis CNS collaboration with UCB; and a $0.2 million increase in revenue recognized under the respiratory diseases collaboration with GSK – all of which were offset by a $0.9 million decrease in revenue from the now-concluded research terms in the muscle diseases collaboration with GSK.

Research and development expenses were $11.9 million for Q2 2014 compared to $8.6 million for the same period in 2013. This increase was primarily due to an increase of $3.3 million relating to advancing the FPA144 program toward a Phase 1 clinical trial including $1.5 million of milestone costs under Five Prime’s exclusive license agreement with Galaxy Biotech LLC. There was also a $1.0 million increase in research costs related to our cancer immunotherapy program and a concurrent decrease of $1.1 million in costs related to the FPA008 program due to manufacturing costs incurred during Q2 2013.

General and administrative expenses were $3.0 million in Q2 2014 compared to $2.4 million for the same period of 2013. This increase was primarily due to public company related expenses.

Cash, cash equivalents and marketable securities as of June 30, 2014, were $140.6 million compared to $75.7 million as of year-end 2013. This increase was primarily the result of Five Prime’s public offering of common stock in February which raised gross proceeds of $43.1 million and the $21.0 million received from BMS’ purchase of common stock in March.

We continue to expect full-year 2014 net cash used in operating activities to be less than $30 million and to end 2014 with more than $100 million in cash, cash equivalents and marketable securities. We expect to have cash to fund operations for more than two years which does not include any additional collaboration agreement which we may enter into nor receiving any future milestone payments. This provides us run rates and several value inflection points for our key programs.

And with that I’ll turn the call back over to Russ.

Rusty Williams

Thanks, Marc. I’m excited about the progress we’re making on all of our programs and we look forward as a team to delivering on our anticipated milestones during the remainder of the year. Operator, we can now open the call for some questions.

Question-and-Answer Session

Operator

Thank you. (Operator instructions.) And our first question comes from the line of Eun Yang from Jefferies. Your line is now open.

Eun Yang – Jefferies

Thank you. So a question on 1039, so the Arm C for mesothelioma… [technical difficulties]

Rusty Williams

Hi Eun, it’s Rusty. You’re breaking up at least on our end. We heard the beginning but not the rest of your question.

Eun Yang – Jefferies

The question is 1039 in Arm C with the mesothelioma, are you selecting patients with the FGFR1 amplification?

Rusty Williams

So the question is in Arm C are we selecting for FGFR1 amplification? The short answer to that is no. This is a different arm, so the first two Arms A and B have FGFR1 amplifications. I’ll let Julie outline the patient population involved in Arm C.

Julie Hambleton

Thanks, Rusty. Eun, the mesothelioma hypothesis is generally focused on the fact that mesothelioma is a cell that has the highest expression of FGF2 compared to all the cancers that have been surveyed predominantly in cancer cell line encyclopedias. Additionally both GSK and Five Prime have nonclinical data in xenograft where 1039 has single-agent activity directed against mesothelioma in these non-clinical xenograft models. So with that we are taking all comers, patients with malignant pleural mesothelioma. We are collecting tumor samples and retroactively we will look at FGF2 levels and FGFR1 amplification. There may be a small subset of tumors with receptor amplification.

Eun Yang – Jefferies

Okay.

Rusty Willams

Great. Eun, does that answer your question?

Eun Yang – Jefferies

Sure, yeah. And then also you said that the dose escalation portion of the Phase 1B study data that we are expecting by the end of this year, how many patients will that be?

Julie Hambleton

At the current time we really aren’t providing guidance or any predictions of the number of patients. At a minimum we are in Arms A and B looking at three dose levels. This is the standard three plus three Phase 1 design, so depending on whether we experience or observe any dose-limiting toxicities or need to explore some intermediate dose levels, that would determine the number of patients. So it’s hard to predict during the dose escalation component of a Phase 1.

Eun Yang – Jefferies

Thanks. And the last question is on cancer immunotherapy – so now that Adimab is in the process of identifying antibody [derivatives] to this undisclosed target, how long will they take to identify the antibody against the target?

Rusty Williams

So the question is how long will it take Adimab to produce a candidate therapeutic antibody for the collaboration?

Eun Yang – Jefferies

Yes.

Rusty Williams

One of the reasons we picked Adimab was because of the quality of their antibodies, the general characteristics of the antibodies in terms of affinity and also because of their speed. So I’ll let Aron who set up this arrangement with them, I’ll let him speak to that.

Aron Knickerbocker

Hi, Eun. In contrast to other older technologies such as hybridoma technologies, the Adimab yeast-based approach is much quicker but we can’t say precisely how long it will take for them to generate the leads for us. But typically these campaigns are on the order of three to six months.

Eun Yang – Jefferies

Okay. Then do you think that you can actually file an IND next year or do you need some animal study data before you file an IND?

Rusty Williams

Well, I’d love to be able to assign a date to tell you when we’ll be able to file an IND on this antibody and some of our other programs, too. It’s just too early for us to make such a prediction. But we’ll move it as quickly as we can of course, and we’d love to be in a position to be able to disclose more to you about this program but at the moment I think it’s in the company’s and shareholders’ best interests for us to just move it as fast as possible and remain silent about the specifics.

Eun Yang – Jefferies

Once the antibody is produced will you disclose the target? That’s my last question, thank you.

Rusty Williams

Thanks, Eun. I’m not sure when we’ll be ready to disclose the target. Our cancer immunotherapy program in general, we have a number of targets in that program that are of course not disclosed. I know it’s kind of frustrating for our investors and analysts that we don’t disclose the nature of those, especially the novel targets but we think again that this is a competitive area and we just, we need to move as quickly as we can, follow the patents as robustly as we can. And we will make some disclosures.

We don’t plan to be mum forever on this and as soon as we can we’ll make some disclosures about some of these specific targets. It’s just not the best time right now in terms of the competitive landscape. Our patents will begin to publish on some of these new targets during the next year and so we’ll be more forthcoming about some of these things during that period of time.

Eun Yang – Jefferies

Thank you.

Operator

Thank you. And our next question comes from the line of Brian Abrahams of Wells Fargo. Your line is now open.

Shin Kang – Wells Fargo

Hi, this is Shin calling in for Brian, thanks for taking the questions. I have a couple of questions on 008 in cancer. If you were to move the program into cancer indications what are some of the gating factors in starting the trial? Would you need any additional tox or dose finding studies? And do you anticipate this indication to be a monotherapy approach or a combination, and have you had any discussions with BMS regarding potentially doing a combination study with their checkpoint inhibitors?

Rusty Williams

Hi, Shin. So in general we’ve done a Phase 1 trial in healthy volunteers and that gives us a good safety database, and we’ll continue to get safety data as Phase 1 progresses. In terms of how we, so in terms of tox, I think we have a good understanding now and we’ll increase our database in terms of tox, and I think we’ll be in pretty good shape on that. Of course any trial we do in combination there’ll be a toxicity component of that, and I’ll let Julie elaborate on that in just a second.

Just in terms of, you asked the question would we use this agent as a single agent in cancer – of course, as Julie mentioned in PVNS which is a kind of tumor, it’s not as malignant as some cancers, it could be used as a single agent. However, I think the big opportunity that people see for this pathway as Julie mentioned both in AASCO and in publications now is in combination with checkpoint inhibitors. And there’s some pretty compelling rationale for that that these myeloid cells in the tumor are suppressing the immune system, and so if you sort of give it a double whammy by blocking the myeloid suppressive effect and block the checkpoints there’s a very compelling rationale for that.

So that’s in the literature and we’re paying close attention to that, and doing our own experiments and getting KOL input. And you know, if we do this in combination with a checkpoint inhibitor we’ll have to, we’ll work with whoever is the best partner for that. And of course BMS is on the list, we’d be crazy not to consider them but we’d work with whoever we’d pair best with. Does that answer your question, Shin?

Shin Kang – Wells Fargo

Yes, yes. Lastly, I don’t know if you mentioned this before, could you remind us when you expect to have the top line data from the mesothelioma arm of the 1039?

Julie Hambleton

The Arm C of the Phase 1b trial actually just opened and started enrolling, so we have not yet fully predicted when we will be reading out data. We have gotten a lot of enthusiasm from investigators which is one of the main reasons why GSK is opening up additional sites with mesothelioma expertise but we still are in that so-called “slow” part of the trial where we’re doing the dose escalation and following subjects for dose limiting toxicities. So we haven’t provided guidance yet and we’ll do so as soon as we have a better idea of the enrollment rate in this arm.

Shin Kang – Wells Fargo

Great, thank you very much.

Rusty Williams

Just to recap this question and follow up on Eun’s, the Arm C, just to be clear about it as Julie said is to test a different patient population. These are patients, these tumors have high FGF ligand concentrations. So we view this as a big addition to the overall program because we’re testing two separate hypotheses involving the FGF pathway – Arms A and B testing the hypothesis that amplified FGF receptor 1 drives tumor cells proliferation and survival; and Arm C that ligand overexpression drives tumor cell growth and survival as well as androgenesis.

Shin Kang – Wells Fargo

Thank you.

Rusty Williams

You’re welcome.

Operator

Thank you. And our next question comes from the line of Bret Holley with Guggenheim Securities. Your line is now open.

Bret Holley – Guggenheim

Thanks for taking the questions, I really appreciate it. I’m wondering on Arms A and B of the 1039 trial, I’m just wondering about the levels you’ve been able to dose escalate to. Have you gotten to a point where you feel you’re kind of past the projected therapeutic threshold for 1039 at this point? And I guess what I’m trying to ask is how should I think about the first dataset? I mean is it going to be very low doses where you really wouldn’t expect to see efficacy or is it going to be adequate doses in your view, and how many patients – not exact number of patients, just qualitatively?

Rusty Williams

Hi Bret, thanks for joining us. I think your question is by the end of the year how far along are we going to be and will we be at a therapeutically interpretable dose – is that sort of what you’re getting at?

Bret Holley – Guggenheim

Yep, yep.

Rusty Williams

I’ll let Julie summarize our position on that.

Julie Hambleton

Yeah, hi Bret. So in the Five Prime monotherapy Phase 1 you’ll recall we looked at seven doses over approximately eight cohorts and stopped dosing at the equivalent of 20 [mgs/kg] once weekly. Yet at much lower doses, half of that, we actually saw complete suppression of FGF2 levels – or actually I should correctly say they were non-measurable. So we felt that at 20 mgs/kg we were in far excess of where we needed to be.

For the GSK Phase 1b the initial dose that is being studied is 5 mg/kg and the goal is to dose up to 20 mg/kg, is where we left off in the monotherapy trial. So we believe that we will be choosing a dose that is in that good therapeutic range based on the Phase 1 monotherapy data. ‘

Bret Holley – Guggenheim

And I guess from what you said about the suppression of FGF, I mean even at 5 mg/kg you might expect that you’re having some effect, potentially therapeutic effect. Am I misinterpreting that?

Julie Hambleton

Well, that is certainly something we’re speculating. If you’ll recall in our monotherapy trial we did not enroll selective patients who may be more sensitive to the therapeutic. Now we are looking specifically at FGFR1 amplified tumors but we hope and expect to be above that 5 mg level.

Your earlier question then on number of patients, again this is a three plus three so the idea is three patients at one dose level, follow them for a month looking at dose limiting toxicity; if none then you dose escalate to the next. So it will be on the order of multiples of three by the time we actually have chosen a dose to expand.

Bret Holley – Guggenheim

And sorry, one last question on this: so if you start at 5 mg what’s the next escalation after that, have you said that? I’m just trying to get the increments that you’re going up to 20 mg on.

Julie Hambleton

Yeah, and this is on our ClinicalTrials.gov website. So you can keep me honest here but it’s a starting dose of 5 mg and it goes up to 20 mg, 10 mg is the intermediate cohort but there is provisions to perhaps go to 15 mg if needs be.

Bret Holley – Guggenheim

Okay. So it sounds like it’s going to be a reasonably fulsome dataset at least the initial dataset as far as the therapeutic meaningfulness.

Julie Hambleton

Yes, and I will say that I think what is most important about this aspect of the trial is being able to look at safety in combination with chemotherapy. That is something that we believe the small molecule inhibitors, which are our main competitors cannot do. So we believe that we can combine this therapeutic safely with not only a single chemo but with a chemo doublet, and that’s what Arms A and C will show us.

Bret Holley – Guggenheim

Great, thank you very much, Julie, and thank you, Rusty.

Rusty Williams

Thank you, Bret.

Operator

Thank you. And our next question comes from the line of Nick Abbott with BMO Capital Markets. Your line is now open.

Nick Abbott – BMO Capital Markets

Good afternoon, thanks for taking my question and congrats on the progress. I’ve another follow-up question on 1039: I understand [nominally] by the end of the year we’ll have that dose escalation data. Do you think we’ll be reporting response rate data or just recommended Phase 2 dose and a “We’re moving to Phase 2” kind of press release?

Rusty Williams

Hi, Nick, thanks for calling in. I’m going to let Julie answer that as best we can. You know, we’re still in the mix of this escalation.

Julie Hambleton

Yeah, I’ll say our goal is to be able to at least provide guidance around the selection of the dose that’s safe to combine with chemotherapy. Now, we do want to preserve the data and be able to present them at a major scientific meeting so if we can’t meet that goal by the end of the year then that more detailed body of data that you’re looking for would be sometime in 2015 where we would look at a whole host of things including pharmacokinetic safety and preliminary response rate data in that dose escalation portion.

Nick Abbott – BMO Capital Markets

Okay. And just as an allied question I read a paper this morning, an abstract this morning and unfortunately I couldn’t lay my hands on it just before the call but it was suggesting that FGF receptor 1 plays an important role in signaling in lung cancer tissues that are not overexpressing FGF receptor or have some kind of copy number aberration – suggesting that it might still be an important signaling pathway. So my question more broadly is at what point do you say to maybe open up the enrollment criteria for this trial? How compelling, what level of data do you need to see that says well, maybe we don’t need to be so restrictive?

Rusty Williams

Nick, that’s an interesting question. First of all we’re looking at each other – we don’t know the abstract that you’re referring to but we’ll sure look for that. And I think I’d be the first to say that it’s possible that the FGF pathway could be involved in cancer other than through an amplification or overexpression. We do feel however that selecting patients the way we have and selecting mesothelioma, so by selecting for FGFR amplification we’re certainly we think enriched in responsiveness; and our xenograft data led us to that conclusion because the response rate was proportional to the degree of FGF receptor amplification in a number of xenografts.

And by testing it in that context and in mesothelioma, so as Julie said, if you arrayed cancers and looked for the ones that expressed the most FGF ligand that’s been studied, FGF2, mesothelioma would be at the top of the list. But those are the most likely places to start. I think then if we see good responses in these populations then we’d be looking at a broader population. I think it’d be premature right now to expand criteria for looking more broadly but we’ll certainly look for that abstract. Thank you for bringing that up.

Nick Abbott – BMO Capital Markets

My last question is on 008. It looks like you have a choice of perhaps rare disease, potentially fast to market or accelerated strategy; or you have opportunities either in fibrotic disease or cancer where the development is likely to be – and sorry, cancer without saying a checkpoint inhibitor – where development’s likely to be more protracted and more complex. So is this really an either/or or do you think you can do both?

Rusty Williams

Well, we have known for several years that this pathway, that the CFS1 receptor pathway is important in a number of diseases and that macrophages are important in a number of disease settings. And that’s precisely the reason we went into this because there are approved drugs to block macrophages. And when we discovered Interleukin 34 as in our view the best activator of human macrophages, it along with CFS1 – and they both act through this CFS1 receptor – we did that deliberately because we knew that there were multiple disease settings we could study.

Now, having said that, we do have to pick the ones obviously where we think there’s the best chance to get a response and so we can’t do everything. So I think it’s not an either/or but I think it’s a small defined number of indications to pursue where we think, and we’re also as we go along adapting to the literature and to what other people are finding about this pathway. We feel lucky to be poised at this point having completed a healthy volunteer phase of the Phase 1 trial, the healthy volunteer section of that trial, when we have a number of indications that are before us that look very promising.

And so we can’t do everything. We have in our budget to do a second indication – that was one of the rationales for the follow-on offering that we did back in last February. So it’s not as if we’re you know, (inaudible) but we will have to pick and choose. But I think we should cast a broad enough net to give this molecule a good shot because I’m pretty convinced personally just as a scientist and clinician that blocking this pathway will have therapeutic benefit in one disease or another – we just have to pick the right one.

Nick Abbott – BMO Capital Markets

Okay, thank you very much.

Rusty Williams

Sure.

Operator

Thank you. (Operator instructions.) And I’m showing no further questions at this time. I would like to turn the call back over to Mr. Rusty Williams, CEO, for any closing remarks.

Rusty Williams

Okay, well thanks everybody for joining us and for your insightful questions. We really do appreciate your continued interest and your support and we look forward to updating you on our progress next quarter; and we’re happy of course to take any calls in between. So thanks again.

Operator

Ladies and gentlemen, thank you for participating in today’s conference. This does conclude the program and you may all disconnect. Have a great day, everyone.

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Source: Five Prime Therapeutics (FPRX) CEO Rusty Williams on Q2 2014 Results - Earnings Call Transcript

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