Blueprint Medicines Corp (BPMC) 2016 Q2 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the Blueprint Medicines Corporation Q2 2016 Earnings Conference Call.

(Operator Instructions)

I would now like to introduce your host for today's conference, Ms. Kristin Williams with Blueprint Medicines. Ma'am, please go ahead.

Thank you, operator. Good morning and welcome to the Blueprint Medicines second quarter 2016 financial and operating results conference call. This morning, we issued a press release which outlines the topics that we plan to discus today. The release is available in the Investors section of our website at www.blueprintmedicines.com.

Today on our call, Jeff Albers, CEO, will discuss Blueprint Medicines' business and corporate highlights. Andy Boral, CMO, will discuss clinical updates. And Mike Landsittel, Vice President of Finance, will review our second quarter financial results.

We will then open the call for your questions.

Before we begin, I would like to briefly remind everyone that statements we make on this conference call will include forward-looking statements. These may include statements about our strategy, business plans and focus, the potential success of our drug candidates, preclinical and clinical plans and development time lines, the scope or timing of clinical data or proof-of-concept for our drug candidates, and financial projections. Actual events or results could differ materially from those expressed or implied by any forward-looking statements as a result of various risks, uncertainties, and other factors, including those set forth in the Risk Factors section of our most recent quarterly report on Form 10-Q filed with the SEC and any other filings that we may make with the SEC.

In addition, any forward-looking statements made on this call represent our views only as of today, and should not be relied upon as representing our views as of any subsequent date. We specifically disclaim any obligation to update or revise any forward-looking statements, whether as a result of new information, future events, or otherwise.

With that, let me pass the call over to Jeff. Jeff?

Thanks, Kristin. Good morning, everyone. We continue to operate in an exciting time at Blueprint Medicines as we focus on our mission of seeking to improve the lives of patients with genomically defined diseases. The second half of 2016 is lined up to be an eventful period with multiple significant inflection points anticipated across our clinical and discovery phase pipeline.

As I mentioned on our call in May, our primary goal as a company is to develop transformative highly selective and potent kinase inhibitors for patients. To achieve this goal, we remain focused on executing on four fronts -- first, to continue to progress and expand our clinical trials; second is to maximize the value of our kinase platform; third is to deliver value from a strong financial position; and fourth is to build the team and a culture to support our growing clinical pipeline, expand our business development activity, and broaden our research efforts.

So, to the first point, focus on our clinical activities. We are pleased with the continued advancement of our ongoing Phase 1 clinical trials of BLU-285 in patients with gastrointestinal stromal tumors and patients with systemic mastocytosis, and in our ongoing Phase 1 trial of BLU-554 in patients with hepatocellular carcinoma. Enrollment in all three trials continues to progress well, and we remain on-track to share preliminary data from the dose escalation portion of each study by yearend. Andy will spend a few minutes this morning walking through the diseases we're focused on in these trials as well as the Phase 1 escalation design and objectives.

Our second objective focuses on our continued platform advancement. In addition to clinical programs, we are committed to broadening our pre-clinical and discovery stage efforts through both internal efforts and strategic collaborations. We look forward to filing a New Drug Application for BLU-667, our RET program, by yearend.

At the AACR meeting in April, our scientist presented pre-clinical data demonstrating activity in several RET-altered cell lines including those with predicted resistant mutations. RET kinase fusions and mutations have emerged as an important driver in a wide variety of cancers, and we believe represent a substantial opportunity as a target. Beyond our RET program, we're also on-track to achieve our stated goal of publicly disclosing an additional discovery stage program at or prior to our next earnings call.

For our collaboration programs, we remain pleased with the progress of our programs partnered with Roche and Alexion. As a reminder, the Roche collaboration enables us to accelerate and expand our efforts in the field of cancer immunotherapy by focusing on up to five immunokinase targets. And the Alexion collaboration targets the kinase that is the driver of a rare genetic disease. Notably, under the collaboration with Alexion, we recently achieved the pre-clinical milestone of $1 million, our fourth pre-clinical milestone within the program, and we expect payment in the third quarter this year.

And with respect to our financial position or our third area of focus, we ended the second quarter with $172.6 million cash and cash equivalents. As our clinical efforts have ramped up, we've continued to refine our operating assumptions and exercise discipline in managing our expenses and portfolio drug candidates. Based on our current operating plans, we now expect that our cash will be sufficient to enable us to fund our operations into the early 2018. Maintaining a robust financial position is critical to our corporate strategy as it allows us to manage our portfolio decisions from a position of strength and affords us meaningful flexibility as we learn more about our ongoing programs in the months ahead.

And finally, our fourth area of focus is the growth of our team. In April, we announced the appointment of Dr. Lynn Seely to our Board of Director. Dr. Seely is currently the CEO of Myovant Sciences and was formerly Chief Medical Officer of Medivation. She has extensive experience building a clinical organization and executing a successful oncology product launch. And we are thrilled to add her expertise to the board.

So the wrap up, we look forward to keeping you updated as we move towards preliminary data readouts for our first three clinical trials. We believe that this data will help demonstrate the strength of our platform and ability of our scientist to craft highly selective potent therapies against new and difficult to drug targets.

With that, I'll turn the call over to Andy to dive a bit further into our clinical program. Andy?

Thanks Jeff. So I would like to walk you through our pre-clinical trials starting with BLU-285, our highly selective and potent inhibitor of Exon 17 mutant KIT, and D842V mutant PDGFR-alpha. As you know, BLU-285 is currently being studied in patients with treatment-resistant GIST and in advanced systemic mastocytosis.

GIST is the most common sarcoma of the GI tract, which we estimate affects about 20,000 patients in the U.S., EU5, and Japan. More than 80% of GIST is driven by KIT gene activation and about 5% is driven by PDGFR-alpha gene activation.

Therapy for unresectable KIT driven GIST has improved dramatically since the approval of imatinib in 2001. However, unresectable GIST remains a fatal disease. Following progression on imatinib, response rate to sunitinib and regorafenib are less than 10%, and PFS is less than six months.

KIT Exon 17 mutants occur in more than 90% of KIT-driven disease following treatment with at least two kinase inhibitors resulting in broad resistance to available therapies. Importantly, PGDFR-alpha-driven disease is resistant to all available kinase inhibitors at the time of diagnosis.

Our Phase 1 GIST study is designed with a three-plus-three dose escalation part followed by an expansion part. During the escalation part, we included patients with tumors that are known to have D842 mutation in PDGFR-alpha or patients with Exon 17 mutant KIT, which we identified clinically by progression following therapy with imatinib and at least one other kinase inhibitor.

The trial began enrolling patients in the fourth quarter of last year, and we expect to share preliminary data from the dose escalation part of the trial at the medical meeting by the end of 2016. I anticipate that we will have a good understanding of the safety profile and pharmacokinetics of 285 across a range of doses. This information will be important as we plan for an expansion part of the study and for subsequent studies such as combinations and studies in earlier lines of therapy. We will also share data for pharmacodynamic measures of PDGFR-alpha in KIT allele burden in blood, which may serve as early markers of BLU-285 activity.

We also expect to show preliminary assessments of response based on imaging scans in some patients. Naturally, patients on higher dose levels will be on study the least amount of time.

We will start with the expansion part of the study after we establish the recommended dose. With the expansion part of the study, we will treat larger groups of patients with PDGFR-alpha and KIT driven GIST at the recommended dose and be able to better assess response rate and duration.

Now, let me turn to BLU-285 in advanced SM. Systemic mastocytosis is a disease of mast cell. Patients primarily receive supportive care aimed at ameliorating the many symptoms of organ infiltration by mast cells including rash, fatigue, weight loss, abdominal pain, and bronchospasm that can be life-threatening. In addition, the patients with advanced SM who are enrolling in our Phase 1 study have an expected survival of only three to five-years. In the U.S., EU5, and Japan, we estimate there are approximately 20,000 SM patients with approximately 4,300 of them having advanced and smoldering disease. We estimate that Exon 17 mutant KIT drugs is used in about 95% of these patients.

BLU-285 has the potential to be a transformative medicine for advanced SM patients for D816V mutation with no approved therapeutic options. The Phase 1 trial in advanced SM is designed similarly to the GIST trial with the dose escalation part followed by the expansion part. The trial began enrolling in the first quarter of this year. Given the late start, the number of patients and duration of therapy for each patient will be less than for the GIST trial when we share data.

Similar to the GIST trial, we anticipate that these preliminary data will include safety tolerability, and pharmacokinetics. We also plan to share initial assessments of clinical activity with a focus on serum tryptase levels, a measure of overall mast cell burden. Another important measure of response is reduction of bone marrow infiltration. We do monitor patients on study with bone marrow biopsies, but they can't be done frequently, so we will only have bone marrow data on a few patients when we share data this year.

Our third clinical trials for BLU-554, which is being developed for patients to the advance advanced hepatocellular carcinoma that's dependent on abnormal activation of the FGFR4 pathway.

HCC reminds me of lung cancer 15 years ago, there were no targeted therapies and no rational participation selection. Sorafenib is the only approved drug with response rate of less than 5%, and the median survival remains less than a year. We estimate that up to 30% of HCC patients may demonstrate abnormal FGFR4 pathway activation and could potentially benefit from an effective FGFR4 inhibitor. This represents approximately 24,000 patients in the U.S., EU5, and Japan, and substantially more in other Asian markets.

So similar to our BLU-285 studies, the BLU-554 HCC trial is designed for the dose escalation part followed by an expansion part. During the dose escalation part, FGFR4 pathway activation is not required for enrollment. However, tumors are tested retrospectively for pathway activation. We are developing a companion diagnostic in collaboration with Ventana, and can now use that test to prospectively evaluate patients for FGFR4 pathway activation.

The trial began enrolling patients in the fourth quarter of last year, and we expect to share preliminary data from the dose escalation part of this study at a medical meeting in the fourth quarter of this year. We anticipate that we will have a good understanding of safety profile in pharmacokinetics of BLU-554 across a range of doses. In order to distinguish BLU-554 from the growing number of non-selective FGFR inhibitors, it's also important to show that BLU-554 effectively inhibits FGFR4 activity as tolerable doses.

To do this, we monitor several pharmacodynamic markers that can measured easily in blood, we expect that we will have sufficient PD data later this year to assess whether or not BLU-554 affectively inhibits FGFR4. We will also share any available assessments of clinical activity based on tumor imaging and measurements of the tumor marker alpha-fetoprotein in blood. However, these data will be limited because we don't select patients for FGFR4 pathway activation during the escalation part.

We will begin the expansion part of the study after we establish the recommended dose of BLU-554. Through expansion, we will prospectively select patients for FGFR4 pathway activation and have the opportunity to evaluate antitumor activity in a larger group of patients across a range of FGF19 expression.

Finally, we have planned to file an IND for our RET inhibitor BLU-667 by the end of 2016. Activating mutations in RET, including gene fusions endpoint mutations, have recently emerged as important drivers in the variety of cancers. These include non-small cell lung cancer, medullary and papillary thyroid cancer, as well as other cancers.

BLU-667 potently inhibits the wild-type RET kinase found in gene fusions, RET-bearing activating mutations and kinase domain, and RET kinase domain mutations predicted to provide resistance to other RET inhibitors. With this profile, BLU-667 has the potential to be active against all RET driven cancers including those in the progressed following other RET inhibitors. We look forward to evaluating BLU-667 in patients.

So as you can see we are keeping busy in making nice progress as we continue to grow and advance our pipeline. In the coming months, we look forward to reporting data from our clinical trials in GIST, SM, and HCC, and to file an IND for BLU-667 in RET-driven diseases.

So, with that, I will pass it to Mike to review our financial results for the quarter.

Thanks, Andy. Blueprint continues to operate from a position of financial strength as we advance our lead programs and discovery platform forward. In this morning's press release, we reported cash, cash equivalents, and investments totaling $172.6 million as of June 30, 2016, compared to a $162.7 million as of December 31, 2015. This increase was primarily due to the $45 million upfront payment received in March 2016 under our cancer immunotherapy collaboration with Roche, offset by cash used in operating activities.

Collaboration revenues for the second quarter of 2016 were $7.1 million, compared to $2.7 million in the same period in 2015. This increase was due to increased R&D activity in our collaboration with Alexion and the amortization of the upfront payment from our new collaboration with Roche.

Research and development expenditures for the second quarter of 2016 were $21.3 million, compared to $11.2 million for the same period in 2015. This increase was primarily attributable to increased manufacturing and clinical expenses associated with advancing BLU-285 and BLU-554 into clinical trials; increased preclinical expenses associated with advancing BLU-667 towards our goal of an IND filing by the end of this year; continuing to build our platform and advance our discovery pipeline; and increased personnel related expenses.

General and administrative expenses for the second quarter of 2016 were $4.7 million, compared to $3.8 million for the same period in 2015. The increase was primarily due to increased professional fees. Net loss for the second quarter of 2016 was $18.9 million, or $0.70 per share, compared to a net loss of $13 million or $0.81 per share for the same period in 2015.

Finally, as we mentioned on our first quarter earnings call in May, we expect our cash, cash equivalents, and investment balance, will be at least 120 million as of December 31st 2016. In addition, as Jeff mentioned earlier, we continue to exercise discipline in managing our operating expenses and portfolio of drug candidates. As a result, based on our current operating plans, we now expect that our existing cash, cash equivalents, and investments will be sufficient to enable us to fund our operating expenses and capital expenditure requirements into early 2018.

With that, we would now like to open up the call for your questions. Operator?

(Operator Instructions) Our first question comes from Mike King from JMP Securities. Your line is now open.

Good morning, guys. Thanks for taking the question and congrats on all the progress throughout the year. A couple of quick questions, Andy. I just wanted to better understand. I know you guys have been going through fairly regimented dose escalation process. So I'm just wondering on BLU-285, well, I guess it holds for BLU-554, too, but the BLU-285, if you have reached the doses at which you expect to get clinical activity in both GIST and SM, and I guess the same question would stand for BLU-554 as well?

Mike, this is Andy. Thanks for the question. So, maybe I'll just circle back. At the end of the, of our first quarter, we announced that we had -- we're enrolling the fifth cohort of both the GIST study and the HCC study. And since then, we've made good progress. Studies have maintained on track, and so we've continued to escalate.

Based on what we -- based on where we are, we would expect that we are well in the active range for both BLU-285 and BLU-554. And certainly that will be an important part of the data that we would share at end of the year.

Okay.

Is there another part, I'm sorry?

No, no, that was it. I had a quick question on BLU-667 as well. And I'm just wondering with regard to the relative uncommon nature of RET fusions and resistant mutants, just wondering if you guys are contemplating a basket approach, not just for your Phase 1 and 2 trials, but also potentially for registration. Do you think the FDA is in place where it would be comfortable with a study that was focused on the translocation rather than the pathology of the tumor?

Yes, Andy, again, speaking. So, yes, I think that's a pretty fascinating regulatory question. Certainly we haven't yet really devised our registration strategy for BLU-667, but I think a nice thing about RET is that it offers actually both opportunities. There are specific diseases, particularly lung cancer and thyroid cancer, where you can both do target and disease-focused development, which is kind of a lot more traditional oncology development approach. But, of course, even based on some work done originally at Blueprint, we know that RET fusions do appear at low frequencies across the broad range of tumors. And we certainly do want to figure out how to get us those patients, and both figure out if the drug works in those diseases and ultimately expand into those diseases from a registration perspective.

So I think we'll do -- I imagine two-pronged approach focusing on the disease-specific areas, lung and thyroid, but certainly working with FDA, potentially EMA, on these broader RET fusion diseases in baskets, I do think we would anticipate looking at basket arms in our studies as well.

Okay, thanks for that. And then just one more quick one, if I may. Do you have any thoughts about when we might see potentially the first target arise at the Roche immunokinase program? Thank you.

Sure. So this is Jeff. With regard to the timing of disclosing one of the Roche targets, so what we have said is we've initiated two of the programs; so there's up to five programs. And we anticipate that will initiate a third later this year or early next year. So from that perspective, we are very much on track.

Then in terms of disclosing. This is a discovery stage collaboration so it's still early days. So we haven't set a timing of when we will disclose but it certainly won't be this year.

Okay, will you at least be willing to say what sort of data or what inflection point you need to get to? Would you need to get to some kind of pre-clinical proof of concept before you would announce, you think you would announce anything together with them?

Yes. So on -- for our wholly owned programs, we usually announce -- the program that will disclose later this year is -- when we are moving towards, close to the development [candidate]. We have that -- we can establish in vitro and in vivo efficacy relationship. We have not decided exactly how we will do that with Roche yet, but I think it would certainly be at that time or later. So we've got over a year to figure that out at least.

Thanks for taking the questions.

Our next question comes from Eric Schmidt with Cowen and Company. Your line is now open.

Thanks for taking my questions as well. And really looking forward to seeing all the data toward yearend. Andy, you mentioned on the BLU-285 that we will see sort of PD markers in terms of the GIST study, I guess, looking at reductions in allele burden. Is there anything in the literature, I'm thinking maybe Gleevec or Sutent or regorafenib, that kind of correlates what might be needed in terms of allele burden reduction in order to see response?

So, Eric, yes, that's pretty interesting question. I think that the short answer in GIST is no, but I think there is an incredibly robust data set in CML with imatinib and nilotinib, and some of the other second and third generation inhibitors suggesting that allele burden certainly in the CML setting correlates very well to long-term outcome if you can drive the allele burden down very low.

In our current studies, really both SM and GIST, I really see the allele burden as, in the short-term, is a pharmacodynamic marker that we convince us that our drug is actually impacting the disease, reducing the disease burden, presumably killing and lysing tumor cells. While I would hope that if we can make be a little -- drive the allele burden very low, it would correlate with durable responses. Actually -- we don't have actually any data confirming that that's true in GIST. We would have to extrapolate from the CML data.

Okay, fair enough. On the safety side -- from a safety standpoint across any of the three trials, has there been any significant AEs or serious adverse events that might qualify for dose limiting toxicities?

So, I'd say the compounds are behaving as expected and maybe I'll kind of back up a bit and say that with any TKIs, the most common kinds of toxicities we would expect are things like GI, nausea, vomiting, diarrhea, liver function -- transaminases being elevated, fatigue. So we would expect those to be, I think, the most common for both compounds like typical TKIs. If we had very -- as we achieve high exposures with BLU-285, if we start to hitting the wild type KIT, we would expect to start to see some, potentially some anemia, thrombocytopenia, evidence of bone marrow suppression.

And maybe I'll just leave it that way. We haven't -- everything has been kind of as expected at this point. And certainly that's an important piece of data that I want to describe in the context of PK pharmacodynamics when we present data at the end of the year in detail.

Okay. And maybe for Jeff. I guess you could be in an enviable position of wanting to move forward three different programs in 2017 across multiple dose expansion cohorts and other cohorts. Just how does a company of your size manage that? And are you thinking business development at this point not licensing some of these opportunities?

Thanks, Eric. So this is Jeff. I think it's a great question. It's the one that we can, [if I'm honest], as we frame our areas of focus, we have a couple of priorities. One is to continue to advance all these clinical programs. We also want to continue to invest in early stage programs. So we think we have got great value in our platforms, so we want to make sure that we continue to bring new programs forward.

And then we want to do that all in the financially disciplined manner. And so what that does mean is we've constantly got, need to be evaluating the tradeoff between collaboration and more traditional financing the options, and to the very point you just made with three programs moving forward, contemplating global opportunities, the notion that with targeted therapies, there is potential for accelerated path to approval that we will be active later this year and into next year in potential partnering discussions; and using the same criteria that we used with the immunokinase collaboration that we will partner when the economics makes sense, but more importantly, when we think that with a partner, we can do a program or advance the program more effectively than we can on our own.

Thanks and congrats on the progress.

Thanks.

Our next question comes from David Nierengarten from Wedbush Securities. Your line is now open.

Okay, thanks for taking the question. So, given the recent results on Phase 2 results and Phase 3 results for midostaurin in mastocytosis, is there a bar for activity that you are looking for in that study or in your patients, or maybe you could help us with what you are looking for at the early stages to convince you that it's the worth pursuing? Or if you could compare and contrast maybe some of the activity or side effects that you would be looking for to make sure that mastocytosis program is still viable in the face of that competition. Thanks.

This is Andy, I'll take this one. So, yes, so it's been pretty interesting to see the midostaurin data evolve the, of course, what was presented in the journal articles the same, essentially the same data set as was presented by Jason Gotlib at ASH two years ago. So it all existed within the framework of what we were expecting when we designed our program, in fact.

So I think there is two time points that I'd like to try to distinguish in terms of how we think about the data. The first is what would we like to see as we finish escalation and make a decision to initiate the expansion part of the study. And there, really, the focus is very much on having established a tolerable recommended dose that patients can take for several -- for repeated cycles, understanding that the pharmacokinetics supports once-daily dosing as we are we are doing, and then, of course, showing that there is at least pharmacodynamic effects on disease. Of course, to proceed with the Phase -- to the expansion program, we'd love to see anti-tumor activity, but I don't know that that will be absolutely required, but I would expect to.

I think when you are getting more at those, as we get the data from the expansion part of the study with sufficient follow-up, what do we really think we would need for, say, submission or for competitive drug based somewhat we have seen with midostaurin? And so, certainly we would hope we could look better than midostaurin. I think they reported a response rate in the 60-something-percent range without complete responses. So I mean I'd love to see complete response [at this].

I think another -- I don't know that the safety often is the, get you the approval in oncology. But as you have multiple drugs, it is important. I mean I think a really important thing about mastocytosis, even in the advanced setting, but even more so in the smoldering and highly symptomatic indolent setting, is that the patients' main issues are things like GI toxicities, nausea, vomiting, diarrhea, fatigue.

And so, I think a drug that contributes to that kind of stuff is a real problem in that disease. And I think that's one downside of these non-selective kinase inhibitors like midostaurin. Those tend to be the kinds of toxicities that they have. I would hope that by selectively inhibiting KIT, we would have a cleaner profile that way and see less of that; so assuming we have good activity that looks a bit better where the drug would be preferred on the basis of toxicities.

And then maybe a quick follow-up. You don't anticipate or you haven't seen any effects on recruiting with the full results. As you said, they have been around for a bit of time but I'm curious if there's been any effect on patient recruitment?

Yes, I say that on the study -- so the -- our SM study started in the first quarter of this year, and it's been going pretty constantly since then. We have not seen any recent change. I'd say it's been gratifyingly on-track.

Okay, thanks.

Our next question comes from Arlinda Lee from Canaccord. Your line is now open.

Hi, guys. Thanks for taking my question. I had a question about BLU-554 and hepatocellular cancer diagnostic that you guys are developing in parallel. Can you kind of maybe talk a little bit more about the logistics? Is it going to be a biopsy-based sample or a drug sample. What kinds of information might we get in terms of the population or cut off when you talk about the data later this year? Thank you.

It's Andy. I'll take this one as well. So the test we are developing now is an immunohistochemistry-based test that we have developed in collaboration with Ventana, who are real experts in developing IHC tests, that looks at tumor tissue, hepatocellular carcinoma of tumor tissue. So, it is a tumor tissue-based test looking at protein expression by immunohistochemistry. We can use archival samples that it looks at paraffin embedded tissues so we can use archival samples that were originally obtained due to biopsies, some patients with that partial resections, and if the patient has no tissue available in the study, they do need to actually have a biopsy. And in the sites we are using, that's really not been limiting. We're in major academic centers and are finding that the patients either have samples available, or if they don't, the docs are happy to get tumor biopsies.

It is true that in HCC, it's probably -- it's pretty unique cancer, and that diagnosis doesn't absolutely require tumor tissue, which is pretty unique to HCC. I really do think that's changing. I think as there are more people developing targeted therapies in HCC, it's becoming much more common to biopsy. People who start to see that with PD-1 inhibitors, like in nivolumab, or they are going to want to start look at PD-L1, et cetera.

So, I actually don't see that as a real obstacle over the coming a couple of years. The action -- was there another piece? I feel like I missed the latter part of your question (multiple speakers) --

Yes. So -- yes, no, you got that part. On maybe we might see at yearend in terms of the data coming out of the tumor tissue, [then kind of] proof of the data --

Yes.

Will we get an idea of what the cut points might be (multiple speakers) --

Yes.

-- have this mutational activation if there's even -- [if there's] archival versus fresh samples and things like that?

Yes, yes. No, so we have done a fair bit of work with historical samples just to establish the frequency of FGF19 expression using the Ventana assay. And that's up to about sort of in the 25 to 30 once -- one quarter to a third range, up to about 30%, we say.

Now, obviously, we will have good handle on what it actually is in our population at the time that we present data and we will share that. We are -- while the escalation part of the study does not require the patients are FGF19 positive, we are getting samples on most, a very large majority of patients, I think it will give you a good understanding of the frequency of FGF19 positivity and pathway activation. And we are obviously going to look at -- we get a range of levels of expression. We will certainly describe that at when we share data. And certainly we would do any correlations amongst activity, be it via protein or radiological activity with level FGF19 expression. But that piece I think it will be pretty exploratory based on the numbers and will really be a focus of the expansion part of the study where we really correlate activity with degrees of expression because we just won't have enough data at the end of the year to say a lot about that.

Okay. Thank you.

(Operator Instructions) Our next question comes from Terence Flynn from Goldman Sachs. Your line is now open.

Hi, thanks for taking the question. I was just wondering, Jeff, if you guys think you will have sufficient data by yearend to make a decision on expansion cohorts for all three of these trials? Or is there a potential situation where you are making decision on some and waiting until next year for additional follow-up data to make that decision? Thanks.

Sure. So I think, at this point, we are confident we will have the information, but keep in mind that these, all three of these trials are continuing to enroll patients, so we are going to be learning a lot between now and the time of that disclosure as well. And as Andy has alluded to, we have not hit, reached a DLT, a recommended Phase 2 dose yet in those studies. So as we move closer, we will constantly evaluate that. But based on how the molecules are behaving to-date, we think we will be well positioned to be making those decisions late this year, early next year.

Thank you. I'm showing no further questions at this time. I would now like to turn the call back over to Jeff Albers, CEO of Blueprint Medicines, for any further remarks.

All right. Thank you, operator. So, in closing, the second quarter was really a quarter focused on clinical and discovery program execution, and all of that then sets us up nicely for a potential exciting second half of the year. The remainder of 2016 has a potential of being a transformative period for Blueprint Medicines. In closing, we appreciate your interest and support, and look forward updating you again as we continue to make progress. And thanks for your time. Bye-bye.

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