Kristin Williams - Investor Relations Jeffrey Albers - Chief Executive Officer Anthony Boral - Chief Medical Officer Michael Landsittel - Vice President of Finance.

Michael King - JMP Securities Eric Schmidt - Cowen and Company David Nierengarten - Wedbush PacGrow Lifes Siences Terence Flynn - Goldman, Sachs & Co..

Good day, ladies and gentlemen, and welcome to the Blueprint Medicines Corporation Q2 2016 Earnings Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session, and instructions will follow at that time.

[Operator Instructions] I would now like to introduce your host of 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 announcement and 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 Investor section of our website at www.blueprintmedicines.com.

Today on our call, Jeff Albers, CEO, will discuss Blueprint Medicines' businesses 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 candidate, preclinical and clinical plans and development timelines, the scope or timing of clinical data or proof-of-concept for our drug candidate, 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 Factor 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 dates. We specifically disclaim any obligations 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 and good morning, everyone. We continue to operating exciting time of Blueprint Medicines as we focused on our mission of seeking to improve the life of patients with genomically defined diseases.

The second half of 2016 is line up to be an eventual period will also post for significant inflection point anticipated across our clinical and this discovery phase pipeline. As I mentioned on our call in May, our primary goal of the company is to develop transformative highly selective and potent kinase inhibitors for patients.

To achieve this goal we remain focus on executing on four fronts. First, 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 activities and broaden our research efforts. So, to the first point we focus on our clinical activities.

We are pleased with the continued advancement of our ongoing Phase I clinical trials of BLU-BLU-285 and patients with gastrointestinal stromal tumor and patients with systemic mastocytosis and in our ongoing Phase I trial of BLU-BLU-BLU-554 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 escalations portion of each trial by year-end. Andy will spend few minutes this morning walking through the diseases we are focused on in the trials as well as the Phase I escalation designing objectives.

Our second objective focus is on our continued platform advancement. In addition to clinical programs we are committed to broadening our pre-clinical and discovery stage efforts to both internal efforts and strategic collaboration. We look forward to filing individual drug application for BLU-667 our RET program by year-end.

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 mutation. RET kinase fusion and mutation have emerged as an important driver in a wide variety of cancers and we believe represent as a substantial opportunity as a target.

The under RET program we are also on-track to achieve our stated goal of publicly disclosing an additional discovery phase program at or prior to our next earnings call. Our collaboration programs 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 immunokinases 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 post pre-clinical milestone within the program and we expect to tame in, 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 continue to refine our operating assumptions and exercise discipline in managing our expenses and portfolio drug candidates.

Based on current operating plans, we now expected that our cash will be sufficient to enable us to fund our operations in 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 formally 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 toward preliminary data read out 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 [grab] (Ph) highly selective potent therapies against new and difficult to drive 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-BLU-285 our highly selective and potent inhibitor of Exon 17 mutant KIT, and D842V Mutant PDGFR-alpha. As you know, BLU-BLU-285 is currently being studied in patients with treatment-resistant GIST and advanced systemic mastocytosis.

Just as most common sarcoma of the GI tract, which we estimated affects about 20,000 patients in the U.S., EU5 and Japan. More than 90% of GIST is driven by KIT gene activation and about 5% is driven by PDGFR-alpha gene activation. Therapy for unrespectable KIT driven GISTs has improved dramatically since the approval of the imatinib in 2001.

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

Our Pase I GIST study is designed with a three plus [indiscernible] dose escalation part followed by an expansion part.

During the escalation part, we include 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 therapeutic with the 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 meetings by the end of 2016. I anticipate that we will have a good understanding of the safety profile and pharmacokinetic of BLU-BLU-285 across a range of doses.

This information would 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 service early makers of BLU-BLU-285 activity.

We also expect to show preliminary assessments response based on imaging scanned in some patients. Naturally, patients on the higher dose levels will be non-study the least amount of time. We will start with the expansion part of the study after we established the recommended dose.

With the expansion part of the study, we will choose larger dose 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-BLU-285 in advanced SM.

systemic mastocytosis is a disease of mast cell, patients primarily receive supportive care into ameliorating many symptoms of organ infiltration by the mast cells including Rash, fatigue, weight loss, abdominal pain and bronchospasm [Indiscernible] life threatening.

In addition, the patients with advanced SM who are enrolling in our Phase I studies 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 in [small joint] (Ph) disease.

We estimate that Exon 17 Mutant KIT drugs is used in about 95% of this patients. BLU-BLU-285 has the potential to be a transformative medicine for advance SM mutations for D816V mutation with nil approved therapy [indiscernible].

The Phase I trial in advanced SM is designed similarly to the GIST trial for the dose escalation part followed by the expansion part. The trial begin enrolling in the first quarter of this year given a late start to number of patients and duration of therapy for each patients 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 effectiveness of clinical activities 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 of BLU-BLU-BLU-554, which is being developed for patients to the advance advanced hepatocellular carcinoma that dependant on abnormal activation of the FGFR4 pathway. HCC reminds me of one cancer 15-years ago, there were no targeted therapies and no rational participation collection.

Sorafenib is the only approved drug, with response rate of less than 5% and the medium survival remains less than a year. We estimate it 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-BLU-285 studies the BLU-BLU-BLU-554 HCC trials 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 retrospectively 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 understandings of safety profile in pharmacokinetics of BLU-BLU-BLU-554 plus a range of doses.

In order to distinguish BLU-BLU-BLU-554 from the growing number of non-selective FGFR inhibitors. It’s also important to show that BLU-BLU-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 [CT] (Ph) data later this year to assess whether or not BLU-BLU-BLU-554 affectively inhibits FGFR4.

We will also share any available sessions 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 established the recommended dose of BLU-BLU-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 inhibit 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 for wild type RET kinase down in gene fusion, RET bearing activating mutations and kinase domain and RET kinase domain mutations predicted to provide resistance to other inhibitors.

With this profile, BLU-667 has the potential to be active against all RET fusion cancers including those in the progress [indiscernible] 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 report the data from our clinical trials in GIST, SM, and HCC and to file and IND for BLU-667 in RET driven diseases. So with that, I will pass to Mike to review our financial results for the quarter..

Thanks, Andy. In Blueprint continues to operate from a physician 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 a $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 increase R&D activity and 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-BLU-285 and BLU-BLU-BLU-554 in the clinical trials. Increased preclinical expenses associated with advancing BLU-667 and towards our goal on IND filing by the end of this year.

Continuing to build our platform and advancer discovery pipeline, and increased personnel expense. 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 increase 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 investments balance, will be at least 120 million as of December 31st 2016.

In addition, as Jeff mentioned earlier we continue to exercise disciplined 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 equivalent 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..

Thank you. [Operator Instructions] Our first question comes from Mike King from JMP Securities. Your line is now open..

Couple of quick questions Andy, 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-BLU-BLU-554 too, but the BLU-BLU-285, if you have reached the doses that which you expect to get clinical activity in both GIST and SM and I guess the same question would stand for BLU-BLU-BLU-554 as well?.

Mike, its Andy. Thanks for the question. So, maybe I'll just shuffle back at the end of the of our first quarter we announce that we had ongoing to fiscal ward above the GIST study and the HCC study and since then we've made good progress guys have maintained on track and so we continue to escalate.

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

Okay. I have a quick question on BLU-667 as well and just wondering with regards 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 I/II trials, but also potentially for registration.

Do you think the FDA is in place where it would be comfortable with - a study of that was focused on the translocation rather than at least the pathology of the tumor..

Yes, Andy again speaking. So I think that’s a pretty fast in the regulatory question. Certainly we haven’t yet really revised our registration strategy for BLU-667, but I think a nice thing about RET is that offers actually both opportunities.

There are specific diseases particular lung cancer and thyroid cancer, where you can both do target and these focused development, which would kind of allow more traditional oncology down in approach.

But of course even based on some work done originally at Blueprint, we know that RET fusion do appear a low frequencies across the broad range of tumors and we certainly do want to figure out how to get us those patients on both figure out the works in those diseases and ultimately expand into those diseases from a registration perspective.

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

Okay thanks for that. And then just one more quick one if I may, you have any thoughts about where we might see potentially the first target arrives that in the Roche I mean what kind is program, thank you..

Sure this is Jeff. With regard to the timing of this closing one of the Roche target so what we have said is we have initiated two of the programs, out of the five programs and we anticipate that will initiate of third in a 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, would 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 there some kind of pre-clinical proof of concept before you would announce? You think you will announce anything together with them?.

Our wholly owned programs we usually announce the program that will disclose later this year, and we are moving towards close to the development candidate, so 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 have got over a year to figured that out at least..

Thanks for taken the questions..

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

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 think maybe [Indiscernible] that kind of correlates what might be needed in terms of allele burden reduction in order to see response?.

So, Eric yes. It's pretty the same question.

I think that the short answer in GIST is no, but I think there is a incredibly robust data set in CML with imatinib and some of the other second and third generation inhibitors suggesting that allele burden certainly in the CML setting correlates very well to our long-term outcome, if you can drive till your role going down very low.

In our current studies really both SM and GIST, I really see the allele burden as in the short-term is pharmacodynamic marker that we convince us that our drug is actually impacting the disease reducing the disease burden, presumably killing and lacing tumor cells.

While I would hope that if we can make drug in allele burden very low it would correlate with durable response, we don’t actually have any data confirming that that's true in GIST. We would have to extrapolate from the CML data..

Thanks, fair enough. And on the safety side I was trying from the safety standpoint across any of those three trials.

Has there have been any significant AEs or serious adverse events that might qualify for dose limiting toxicities?.

So I would 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 functions, transaminase being elevated, fatigue.

So we would expect those to be I think the most common for both compounds like typical TKIs, as we achieve exposures with BLU-285 if we start to hitting the wild type KIT, we would expect to start to see potentially some anemia, thrombocytopenia, evidence of bone marrow suppression.

And maybe I'll just leave it that way, everything has been kind of as expected at this point and certainly that's 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 it could be an enviable position of wanting to move forward three different programs in 2017 across multiple dose expansion cohorts and other cohorts.

Just how does that company of your size manage that 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. 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 program.

So we think 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 constantly 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 would targeted therapies there is potential for accelerated path to approval that we will be active later this year and into next year.

in potential partner in discussion using the same criteria that we used with the immunokinase collaboration that we will partner wind 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..

Hey thank you for taking the question. So given the recent results on Phase II results and Phase III results midostaurin and mastocytosis.

Is there a bar for activity that you are looking for in that study or in your patients, maybe you could help us with what you are looking for at the early stages to convictive 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 was 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 would 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 imitate the expansion part of the study and there really the focus is very much on having established a tolerable recommended dose that patient can take for several - for repeated cycles, understanding that the pharmacokinetics supports once-daily dosing as we are we are doing.

And then I’m of course showing that there is at least pharmacodynamic effects on disease. Of course, to pursue the phase into the expansion of what we love to see anti-tumor activity, but I don’t know that that will be absolutely required, but I would expect to.

I think where you are getting more dose 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 a 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 it reported response rate in the 60% something range without complete responses. So I mean I would love to see complete responses.

I don’t know that the safety often is get you the a proven oncology, but as you have multiple drugs, it is important, I mean I think it's really important about mastocytosis, even in the advanced setting, but even more so in [indiscernible] symptomatic indolent setting.

The patients’ main issues are things like GI, nausea, vomiting, diarrhea, fatigue. And so I think a drug that contributes to that hand 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 the cleaner profile that way and see less of that. So assume 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 better time but I'm curious has there have been any effect on patient recruitment?.

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

Okay, thanks..

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

I have a question about BLU-554 and hepatocellular - 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 base 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..

Its Andy. I'll take this one as well. So the test we are developing now is 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 our archival samples that it looks at paraffin embedded tissues.

These archival samples that were originally obtained due to biopsies, some patients got partial resection and if the patient had 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 are 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 probably it's pretty unique cancer in that diagnosed 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 and in HCC, it's becoming much more common to biopsy, I think one can start to see that with PDL-1 inhibitors like [indiscernible] or they are going to want to start look at PDL-1 et cetera.

So I actually don’t see that as a real obstacle over the coming couple of years. Was there another piece, I feel like I missed the later part of your question cut off....

So on really what we might see at yearend in terms of the data coming out of the tumor tissues Ventana - data. Will we get an idea of what the cut points might be [Indiscernible] archival versus fresh samples and things like that..

Yes, 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 hands on what is actually is in our population at the time that we present data and we will share that. 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 when we share data.

And certainly we would do any correlations amongst activity be it biopsy or protein radiological activity with level FGF19 expression.

But that piece I think it will be pretty exploratory based on the numbers and we will really be 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..

Thank you. [Operator Instructions] our next question comes from Terence Flynn from Goldman Sachs. Your line is now open..

I was just wondering Jeff if you guys think you will have sufficient data by year-end to make a decision on expansion cohorts for all three of these trials or is there a central 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 or [indiscernible] recommended Phase II dose yet in those studies. So as we move closure, 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 decision 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 quarter focused on clinical and discovery program execution, and all of that then sets us up nicely for a potential exciting second half for the year. The remainder of 2016 has a potential of being 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..