Blueprint Medicines Corp (BPMC) 2017 Q1 法說會逐字稿

Good morning. My name is James and I will be your conference operator today. At this time, I would like to welcome everyone to Blueprint Medicines' first-quarter 2017 financial and operating results conference call. (Operator Instructions). Kristin Hodous, you may begin your conference.

Thank you, operator. Good morning. This is Kristin Hodous of Blueprint Medicines and welcome to Blueprint Medicines' first-quarter 2017 financial and operating results conference call.

This morning, we issued a press release, which outlines the topics that we plan to discuss today. The release is available in the investors section of our website at www.blueprintmedicines.com.

Today, on our call, Jeff Albers, Chief Executive Officer, will discuss Blueprint Medicines' first-quarter 2017 business highlights and review our recent clinical updates and Mike Landsittel, Vice President of Finance, will review our first-quarter financial results. We will then open the call for your questions. Andy Boral, our Chief Medical Officer, will also be available for Q&A.

Before we get started, I would like to remind everyone that statements we make on this call will include forward-looking statements. Actual events and 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 Annual Report on Form 10-K 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. Now here is our CEO, Jeff Albers.

Thanks, Kristin and good morning, everyone. 2017 has been a busy year for Blueprint Medicines so far and I am happy to share recent progress as we work to build a broad pipeline of transformative medicines for patients with cancer and other rare diseases.

In the first quarter, we continued to advance our two lead therapeutic candidates, BLU-285 and BLU-554, in the clinic. In addition, with the initiation of a Phase 1 trial of BLU-667 in RET-altered cancers, we now have three wholly-owned therapeutic candidates in the clinic with the potential to address at least six distinct patient populations with significant medical need.

We also recently raised $215 million in a successful follow-on offering in April. The proceeds further strengthen our balance sheet and enable us to expand and accelerate our clinical programs. All of these activities contribute to the four areas of focus for 2017 that I introduced on our last call.

Our first area of focus for the year is to progress our Phase 1 clinical trials of BLU-285 and BLU-554 toward key data disclosures later this year. Today, we are pleased to announce that the first of these dates will come on June 5 at the 2017 ASCO annual meeting where we will present updated data during an oral session from our BLU-285 trial in patients with gastrointestinal stromal tumors or GIST.

In the first quarter, we announced that we initiated the expansion phase of the study and therefore, the data at ASCO will include results from the entire dose-escalation portion of the trial, including safety data and assessments to clinical activity, as well as early safety and clinical data from the dose-expansion portion of the trial for a subset of patients with sufficient follow-up.

As we have disclosed earlier this year, it's our intention to create a natural cadence of data disclosures at major medical conferences over the course of the year. To this end, we expect to provide updated data from our ongoing trials of BLU-554 in hepatocellular carcinoma and BLU-285 in advanced systemic mastocytosis by year-end.

In April, we delivered three oral presentations on the discovery in pre-clinical development of BLU-285 and BLU-554 at the AACR annual meeting and at the American Chemical Society meeting. While both therapeutic candidates emerged from our discovery processes, they came from two different avenues. BLU-285 was a direct hit from our proprietary compound library and BLU-554 came from our rational design approach.

Once the initial scaffolds were identified, we then refined both compounds through extensive medicinal chemistry work. Altogether, these presentations offered us an opportunity to reflect on the power of the Blueprint Medicines platform and our tremendous progress over the last six years. We are extremely proud of how far we have come and the rapid achievement of clinical proof of concept for these programs and believe it's a testament to the commitment and capabilities of our scientists.

Directly related to the continued clinical progress, our second area of focus for 2017 is to further define the long-term clinical and regulatory path for BLU-285 and BLU-554. Across the two BLU-285 study and the BLU-554 study, we are actively evaluating a range of options for expedited development based on the encouraging preliminary datasets we reported last year.

As mentioned on prior calls, additional clinical data over the course of this year will help us to define the path for each program. Today, however, I wanted to highlight our efforts to advance BLU-285 in GIST.

Currently, we are in the process of seeking feedback from regulatory authorities to help us evaluate options for potential expedited development in PDGFRalpha-driven GIST and KIT-driven GIST, two distinct patient populations.

In the PDGFRalpha group, preliminary data showed strong clinical activity for BLU-285 at all dose levels. We believe these results may enable an expedited path to approval in this population based on expansion of the ongoing single arm trial.

In the KIT group, BLU-285 showed evidence of clinical activity at higher dose levels; thus indicating a potential dose response. These results are encouraging because patients were generally heavily pretreated and enrolled with highly refractory disease.

Additional data from the ongoing expansion part of the trial will inform the optimal registration strategy, which we believe could include either an expedited path or as discussed on our last earnings call moving from the ongoing study directly into a randomized Phase 3 trial.

To prepare for either scenario, we are moving forward with plans to initiate the randomized Phase 3 trial, which could serve as a confirmatory or initial registration trial depending on the chosen approval path. We expect the trial to run in parallel with the ongoing Phase 1 expansion potentially offering an opportunity to incrementally reduce the time differential between the two scenarios. Currently, we are actively exploring trial design options with clinical experts and we look forward to updating you on our plans in the coming months.

Our third area of focus is to continue to focus on maximizing the value of our scientific platform. We are proud of our diverse and growing pipeline, which we believe is differentiated for our Company of our age and size. However, the true power of the platform and the opportunity it offers to consistently advance innovative compounds into our development pipeline comes with a responsibility to carefully manage the portfolio.

We regularly evaluate the scientific and financial rigor of each program and opportunity with the goal of making efficient and well-informed go/no go decisions. In fact, as we often note, we've halted more programs at Blueprint Medicines than we've progressed through this disciplined portfolio management process.

The output then is that we believe we have advanced the most exciting programs into the clinic and this now includes our newest therapeutic candidate, BLU-667. BLU-667 is particularly promising to us because it was specifically designed to not only target RET mutation infusions, but it also addresses predicted resistance mutations. This profile may offer patients more profound and durable responses over the long term.

Earlier this year, the first patient was dosed with BLU-667 in a Phase 1 trial that includes patients with non-small cell lung cancer, medullary thyroid cancer and other solid tumors with a RET alteration. The initiation of this trial achieves an important 2017 goal and we look forward to sharing data next year.

Finally, our fourth strategic priority is business development, which we also view as a key portfolio management tool. We continue to actively evaluate a range of collaboration opportunities across the pipeline. Given our strong financial position, we will only explore such collaborations if we believe the partner will allow a program to exceed our internal threshold of additional speed and geographic reach.

To that end, our emphasis is on identifying partners who can help us move one of our more advanced therapeutic candidates more quickly towards approval and into the hands of patients and physicians worldwide.

Together, our continued focus on these four areas creates the potential for an event-filled year and we are off to a strong start. With one the initiation of our BLU-667 clinical study; two, the acceptance of our data from the BLU-285 GIST study for an oral presentation at ASCO; and three, a successful financing that affords us flexibility to execute against our plan.

We anticipate a range of additional important milestones in 2017, including new data from each of our BLU-285 and BLU-554 clinical programs, along with updates on our clinical and regulatory plans. Now I'm going to turn it over to Mike Landsittel to review our financial results for the quarter.

Thanks, Jeff. Blueprint Medicines continues to operate from a very strong financial position. As Jeff mentioned, the end of the first quarter was highlighted by our successful follow-on offering, which closed in early April. The offering resulted in net proceeds of approximately $215 million, which will enable us to continue to expand our clinical development activities for our lead programs.

As of March 31, 2017, we had cash, cash equivalents and investments totaling $236.3 million as compared to $268.2 million as of December 31, 2016. Our cash, cash equivalents and investments as of March 31 exclude the net proceeds from our follow-on offering, which we received in April. After giving effect to the offering, we would have had cash of approximately $450 million as of March 31.

Based on our current plans, we expect that our cash, cash equivalents and investments, including the net proceeds received from the April offering, but excluding any potential option fees and milestone payments under our existing collaborations, will be sufficient to enable us to fund our operating expenses and capital expenditure requirements into the second half of 2019. Importantly, we believe this will allow us to reach numerous potential data readouts and inflection points across our portfolio.

Turning now to our P&L, collaboration revenues were $5.8 million for the first quarter of 2017 compared to $6.8 million for the first quarter of 2016. This decrease was primarily due to the recognition of a milestone in the first quarter of 2016, as well as lower reimbursable R&D expenses in our collaboration with Alexion based on the timing of certain R&D activities.

Research and development expenses were $28.5 million for the first quarter of 2017 compared to $17.6 million for the same period in the prior year. The increase in R&D spending was primarily driven by increased clinical and manufacturing expenses associated with advancing our ongoing clinical trials, as well as increased personnel-related expenses, which include stock-based compensation expense.

G&A expenses were $5.6 million for the first quarter of 2017 compared to $4.6 million for the first quarter of 2016. The increase in G&A spending is primarily due to increased personnel-related expenses, which again also includes stock-based compensation expense.

Net loss for the first quarter was $28 million or $0.84 per share compared to a net loss of $15.5 million or $0.57 per share for the same period in the prior year.

So as we have highlighted on this call, we continue to be very excited about the opportunities ahead of us in 2017 and believe that we are well-positioned financially to execute on our goals.

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

(Operator Instructions). Eric Schmidt, Cowen and Company.

Congrats, Blueprint team, on the progress. Jeff, it sounds like you are having some productive early discussions with the FDA and other regulators around 285 in GIST. What do you need on your end to bring those discussions to conclusion? Do you think you have enough data from the Phase 1 and early expansion cohort studies or are you still waiting for more data either in PDGFR or c-KIT-driven GIST?

So we always think about -- when you say to a conclusion -- we always think about our dialogue with regulatory agencies as a continuum and it is an ongoing discussion and so nothing in our hands today changes that.

As we noted, we think the data we shared particularly around the PDGFRalpha subset was particularly compelling and as we have guided to previously, we would seek to have a face-to-face meeting over the first half of this year.

What we haven't said or what is certainly our practice is that when we have that type of feedback, we will look to find a forum to share the specific feedback. So we are not at that point yet, but we certainly would be looking to provide an update very soon.

Okay. And maybe in terms of the upcoming ASCO presentation, I guess can Andy tell us roughly how many more patients we might see in either the two GIST cohorts at ASCO?

Thanks for the question. So the study continues to enroll well and we are adding sites to prepare for the expansion part -- or continued expansion part of the study, I should say, but we really do want to keep the whole data set intact and present it at once at ASCO and Dr. Heinrich will present the current update of the enrollment, as well as the latest antitumor activity and safety data both on the escalation part of the study and on the expansion part of the study for patients who have had sufficient follow-up.

I think we saw 36 patients at EORTC and 28 of them were valuable, Andy. Is it going to be meaningfully more than that that?

We continue to enroll at a similar pace, so I think it will be enough more than that to have a more complete story to tell.

The way I think about that, as a matter of course, we will take the same approach this year with all of our data updates that we did last year, which is we obviously have a certain amount of data when we submit the abstract, but we will look to do a data cut closer to the time of the conference to include as much additional data as possible when we share that at the time.

Great. Thanks, guys.

Terence Flynn, Goldman Sachs.

Hi. This is Cameron on for Terence. Thank you for taking our question. Maybe just one on BLU-285 for SM. Can you provide any update on the expansion portion of the trial? Can you tell us what dose or doses will be explored and then how many patients are you targeting for enrollment? Thank you.

I will take that. So the ongoing Phase 1 study in mastocytosis is on track and as we said in the release, we expect to initiate the expansion part of the study soon. We have now dosed up to the MTD defined in the GIST study and we don't plan to go higher than that. However, we are still evaluating the top dose levels to determine the actual specific recommended dose for part 2 of the study.

The study design is outlined in clinicaltrials.gov. In the expansion part, we have three groups, the aggressive mastocytosis, the aggressive with the -- excuse me -- advanced mastocytosis, advanced with another heme disorder and mast cell leukemia. And that part of the study includes about 35 patients.

Okay. Thank you.

Chris Raymond, Raymond James.

So another question on BLU-285 in SM, so maybe around the midostaurin approval, so this drug, the label and the data are focused on advanced SM. You guys have indicated an interest in exploring indolent disease and I think some of the data that we have seen with midostaurin is that there is a tolerability issue for sure.

Maybe just talk about the different risk-benefit profiles that you see between indolent and advanced SM and how you see BLU-285 fitting into both -- now that this drug is on the market and maybe if you can give any feedback in terms of enrollment dynamics since that approval and your view there. Thanks.

I will take that. So I want to start by saying that it was really gratifying to us to see a new medicine approved for patients with advanced systemic mastocytosis. Obviously, there's a huge, huge need there.

That being said, we do think that 285 offers a unique selective approach to mastocytosis therapy and that is distinct from the approach taken by midostaurin.

In terms of the indolent aspects of the disease, as we have disclosed at the ASH meeting or Dr. D'Angelo presented at the ASH meeting at the end of last year, we were very encouraged to see evidence of activity at the earliest dose levels with a very well-tolerated safety profile and that is what really gives us a lot of -- has really expanded our interest in a broader range of -- a broader population of mastocytosis, including the indolent population.

We are working now with clinical experts. We will have an advisory meeting in the coming months and we will be planning interactions with health authorities really to design the right clinical trial to evaluate 285 in indolent systemic mastocytosis patients.

Regarding the potential impact or I guess the potential now, the approval just occurred, of midostaurin and enrollment of our study, we don't really expect to see much impact. Midostaurin store and has been available through compassionate use throughout the entire period that our study was running. We see patients who have and have not had prior midostaurin on the study already. So we don't expect it to have any meaningful impact on the conduct of the ongoing study.

Great, thank you.

Mike King, JMP Securities.

Just wanted to follow up with questions on 285 and 544 for that matter. I just generally maybe missed it, but have you stated whether you have reached MTD on either? And specifically on 285, I'm wondering if we should think about MTD being different or driven by, maybe that is a better way to put it, driven by coverage of the various KIT mutations in GIST?

I will take that. So I will start with 285. Yes, we have disclosed that we determined the MTD and the recommended dose for BLU-285 in GIST. That's 400 milligrams once a day and the expansion part of that study is ongoing.

As [Eric Evans] presented at AACR, when you look at biochemical assays, BLU-285 has the potential to inhibit a broad range of activating mutations and resistance mutations in KIT and this raises the possibility that we might have activity across a broader GIST population perhaps in earlier lines of therapy, but I think it's important to keep in mind that there's always a lot of uncertainty when we translate preclinical data to patients.

So while we are encouraged by the emerging clinical and safety data that we have that we are seeing, but we need to complete the expansion part of the study to really understand the breadth of activity across the range of the KIT-driven GIST population.

Do you feel comfortable you've got tolerability to go above 400 milligrams?

No, we have already determined that the doses we explored above 400 milligrams (technical difficulty), so we won't go above 400 milligrams.

And you also had asked about 554, so in 554, we actually did present the -- or disclosed the maximum tolerated dose late last year and that's 600 milligrams once a day and we are expanding that in the HCC expansion cohorts at that dose level. We are still looking at the biomarker positive IHC FGF19 positive subset, an amplified IHC positive subset and completing a negative subset, biomarker negative subset.

To add one additional point there is that we did amend both the HCC trial design and the GIST trial design to allow for a higher number of patients in both of those studies as we moved into the expansion phase.

Right. Okay. I know you have talked about in heavily relapsed or heavily treated GIST that you might do a randomized study against imatinib rechallenge. I don't know if you can give any more color on that, if that's still a part of your thinking on that?

So Mike, our initial plans for Phase 3 development -- well, first, I should really say our -- we are working through them. We've recently had an advisory meeting here at Blueprint to talk to some of the key leaders in the GIST community.

As Jeff mentioned, we are planning regulatory interactions to -- with both the FDA and European health authorities really to map out the most efficient path forward -- regulatory path forward -- in GIST.

As I think we've discussed before, I think our initial Phase 3 interest really focuses on moving into earlier lines of therapy such as potentially a head-to-head versus regorafenib in third-line GIST. We have also contemplated other possibilities in later -- later in disease and I think the outcome of our advisory meetings and our regulatory interactions will really help us to find the most appropriate path forward.

Okay. All right, then just speaking of earlier lines, on the PDGFRalpha population, I'm just trying to envision what kind of agent you could randomize against if you were to do a randomized study in treatment-naive PDGFRalpha patients or would they have to at least have failed imatinib before rolling to 285?

So in PDGFRalpha, we remain very encouraged by the preliminary data that we have seen and increasing the data we presented at the end of last year and we do think that that is a situation where there is a very real opportunity for an accelerated approval based on an expanded set of single agent, single arm data. That is a path we will discuss with regulatory authorities.

If we were successful there and achieve an accelerated approval, I think there are a variety of possibilities for a confirmatory study. And those are issues we will discuss with the regulators, but it doesn't necessarily have to be a randomized study just in PDGFRalpha patients. There are I think -- I think that would obviously be a tough [setting] to do and we would have to think about a variety of different options.

Okay. Thanks for taking the questions, guys.

David Nierengarten, Wedbush Securities.

I just had one on 554. We saw at AACR a FGF401 response rate in liver cancer being 8% PR and 52% stable disease, 4.1 median duration. Is that a benchmark to be looking for for 554 when you report out the next set of results? Do you think you need to beat that level or duration of response? How you are thinking about the competitive space there? Thanks.

I will take that. So we were very pleased with the -- it was very preliminary data that we presented at the triple meeting at the end of last year where it was primarily data from the escalation part of the study. At that point, we did have -- I think the key things we found that we were very encouraged by is that we clearly demonstrated that BLU-554 has preferential activity in the biomarker positive, meaning FGF19 positive subset of patients with tumor shrinkage in 5 out of 10 patients at that point in time. And that certainly gave us enthusiasm to continue this study.

In terms of the potential approval pathways for 554 in HCC, we certainly plan to evaluate opportunities for expedited development based on additional data from the ongoing Phase 1 trial, which will primarily now be expanded data from the -- at the maximum tolerated dose and the recommended dose that we are expanding at now.

But I think it's really premature to comment on what the specific parameters would be for an expedited approval pathway. In general, we do see HCC as a classic opportunity for expedited approval. The patients have a very poor prognosis even with the available therapies and I don't think that's really changed even with the approval of regorafenib, but in terms of the specifics, that will be the outcome of discussions with the regulatory authorities.

And then maybe just a quick follow-up on the -- just back to what we saw with FGF401. They saw some responses in both FGF19 negative and positive patients. Your selectivity is just better and you are more likely to see the responses in the overexpressed patients or is there any other product profile differences that you are thinking about?

Yes, so that was very interesting to see the FGF401 data at -- just recently in April I guess it was. We are very convinced from our data that BLU-554 is preferentially active in the biomarker positive population as we have defined, FGFR4 pathway activation measured by FGF19 overexpression using immunohistochemistry. And as I mentioned we did see tumor shrinkage in 5 of 10 biomarker positive patients using those criteria.

Novartis is using a completely different method to select patients. It is RNA-based and the resulting population is almost certainly different, so it makes it pretty hard to compare results between the studies.

Got it. Thanks. Just checking.

(Operator Instructions). Carmen Augustine, Jefferies.

So for BLU-667 in lung cancer with RET fusion, could you speak a bit to the competitive landscape and how you see 667 potentially being differentiated from other kinase inhibitors that have activity against KIT -- sorry -- RET?

I will take that. Thanks very much. So we really think BLU-667 is a very special inhibitor of RET. It is a pretty impressive chemistry feat. We have designed a compound that is a very potent and selective inhibitor of the wild type RET kinase, which is the kinase seen in the fusions that predominate in lung cancer, non-small cell lung cancer and a variety of other -- small fractions of a variety of other tumors.

It also very selectively inhibits the activating mutations that predominate in medullary thyroid cancer and it was also designed to hit some of the key predicted resistance mutations that, based on our data and others, we would expect to be the primary causes of resistance when patients are treated with the nonselective RET inhibitors out there that are currently available and being used.

And at the same time, it was particularly designed not to inhibit a variety of other targets that we think are responsible for a lot of the toxicities of the nonselective compounds used to inhibit RET such as VEGF receptor. And so we think that combination really makes it completely different from the available multi-kinase therapies out there, cabozantinib and vandetanib, some of the other broad compounds used to treat lung cancer now and we look forward to testing it in the clinic and proving that clinically.

Great, thanks. And then, in SM, you mentioned additional results would be available later in 2017 and I think you have mentioned in the past that would include response rate data. So would there be response data available from both the escalation and expansion cohorts later this year?

Are you talking about BLU-667?

No, no, SM.

Oh, SM, I'm sorry, BLU-285 in SM. Okay. Yes, so we do plan to update the ongoing study later this year and I would anticipate that would include data certainly from the escalation part of the study and similar to the approach we are taking with BLU-285 in GIST, we would update with data from patients with sufficient follow-up in the expansion part of the study.

Okay, great. Thanks.

Arlinda Lee, Canaccord.

A couple of questions on 285. Can you remind us how many -- on the data that we're going to see at ASH, we will see the complete data set for the dose escalation portion of the trial, is that correct?

I will take that. So BLU-285 in GIST we are talking about now, right? Yes. So we will present the complete data from the escalation part of the study with the understanding that patients continue on study. We don't have a defined endpoint, but we will present the data supporting the choice of the MTD and the recommended dose and we will have substantially more information on both antitumor activity and safety in that population. So that will essentially complete that escalation data set and we will, as I think Jeff had mentioned, we will also present preliminary data from the expansion part of the study on patients that have sufficient follow-up.

In the dose-escalation portion, how many patients are at that 400 milligram dose that you have decided to use for the expansion cohort?

So again I would really like to leave the details for Dr. Heinrich to present. So he will give all the numbers of patients, length of follow-up, etc., but we would rather not get into that in pieces here.

Okay. And then on the randomized Phase 2 that you are planning, can you clarify, is that going to be just for KIT or what are you guys thinking at this point, second line versus third line, only KIT, kit and PDGFR?

In terms of GIST, so, yes, we haven't really talked specifically about a randomized Phase 2 study. I think what we've said at this point is that we are really excited -- based on the data we have in hand -- we are very excited to get moving, get a Phase 3 study in earlier line of therapy started sooner for two reasons.

One, it may be necessary as a confirmatory study following, if we successfully achieve an accelerated approval in the PDGFRalpha subset of GIST, and it may also serve as an initial approval study in GIST depending on the status of PDGFRalpha and of course would give us potentially the opportunity to get into the broader range of KIT-driven patients.

At the moment, as I was saying earlier, we are most interested now looking at third-line GIST compared to regorafenib, but we are also considering other possibilities and we will discuss that further with our clinical advisors and with regulatory authorities.

Maybe I will just add one comment. From a simplistic perspective, the way I think about that is there are two paths forward. What we have done in the first quarter once we hit the recommended part 2 dose is we amended the protocol both in the PDGFRalpha arm and the KIT-driven arm such that we maintain the potential based on the results we see in those subsets to move forward on an expedited path.

In the meantime, if either of those are successful, we knew and know that we would have to have a confirmatory study and what we've tried to do is more aggressively move forward with that study because, in essence, it creates a hedge for us, that it's either the confirmatory study or if we decide that we need more data and there's not an expedited path for either of the two arms, that could then become our registration path. And what we need to close that loop is regulatory feedback, one and then additional data from the expansion arms, two and we will then make that decision later this year.

Okay. Great. And then on the expansion trial of 55 -- or a portion of the trial for 554, you had initially talked about having three different groups. Are you going to enroll equally into each of these three groups or is there a possibility to enroll more in the high FGF19 group?

I will pick that one up. So we are enrolling all three expansion groups, the IHC positive, the amplified, FGF19 amplified and the biomarker negative groups and we have recently -- this should now be on clinicaltrials.gov -- we have recently expanded the IHC positive, so overexpressed group of patients in that study from 15 to 30 because we think that that's, based on our data that we presented earlier -- excuse me -- at the end of last year -- we think that's the group where we have the most opportunity to see activity.

Okay. And then I guess given some of the other data that was presented at AACR, I know you talked a little bit about the competitive landscape and how it might not be apples to oranges, but can you maybe talk about, I guess, the emerging landscape with other drugs targeting FGF in HCC and what do you think the bogeys might be or what information do you need to get to those decisions?

I think the only compound with really clinical data that has been presented now is FGF401 from Novartis and I think it looks like an interesting compound. As I was saying earlier, they have taken a very different approach to patient selection and it makes it very hard to compare our results to theirs.

We are very confident that our IHC-based assessment of FGF19 is identifying a pathway-activated population and again, we think our data demonstrate that 554 is preferentially active in that population. I think that using a different approach there, the FGF401 data is likely in a different population.

Really though I think the answer is that over time we just need to see how the clinical data evolve in the clinical trials and so we are pretty much focused on executing our study, understanding how our compound behaves in the amplified patients, in the overexpressed patients and mapping out the most appropriate path to registration for BLU-554. And I think that's really where we are going to focus more than worrying too much about the other compounds.

Okay. Thank you very much.

(Operator Instructions). Mike King, JMP Securities.

I was just wondering if, on 667, if we have any further color or you are attempting to get more detail on the epidemiology of RET? I believe RET is part of the Foundation Medicine panel, but maybe I'm wrong. I am just trying to get a sense of the prevalence of either RET mutations, RET translocations in the broad solid tumor population.

I will start on that. So RET is covered by the Foundation Medicine panel, and I think that is one of the -- that will be over time one of the sources of patients who are known to be RET-activated.

Based on current data, we think that it's in the range of 1% to 2% of non-small cell lung cancer patients and the large majority I think of medullary thyroid cancer patients. It is a -- RET is the driver seen in the congenital syndromes that are associated with medullary thyroid cancer.

It's also identified -- I think fusions more than point mutations as an activator in a smaller fraction of a very broad range of solid tumors. I have seen reports of ranges from, I don't know, 0.1% to 0.5%, something like that. And I think that's really uncertain at this point in time. It will require a lot more data from folks like Foundation Medicine who are screening large numbers of patients to really answer that question.

Mike, I will add one piece to that. With all of our programs, when we are going after a targeted patient population, I think suffice to say that our understanding of the underlying epi data is always evolving, trying to get the best available handle on the number of patients -- if you takes systemic mastocytosis, that's one, for instance, where there isn't a great data set or source to look to. And one of the ways we practically address that is how is our ability to identify these patients in our trials. And one of the things that we found gratifying to date is that, in all four of our trials, we've been able to work with investigators who seem to have those patients and have them in numbers that allow us to enroll each expansion phase or escalation phase quickly. And then as we have moved into the expansion phase, we have seen that accelerate in the two cases where we are now into expansion.

So while that's not a specific number, if I apply that to the RET study, we started as all Phase 1s in the first cohort where we only had one site up and running and now with each subsequent cohort, we are adding sites and finding it easier to identify those patients. So RET is fitting the mold of our prior therapies quite nicely thus far.

Okay. And stupid question, but I would imagine most of these -- are these naive patients or I imagine most patients will be treated with cabozantinib.

In terms of our study, we are pretty early and so we don't have a very good understanding of where it will enroll, but across the field of RET-activated non-small cell lung cancer, actually platinum-based chemotherapy is still standard of care and that would be -- I would expect that almost all of our patients will have received that. I guess we will see in terms of the other multi-targeted inhibitors. As we talk to our investigators, they are not very enthusiastic about using those drugs like cabozantinib.

All right. Thanks, guys.

There are no further questions at this time. I'd like to turn the call back over to you, Mr. Albers.

Thanks, operator. As we look out over the rest of the year with continued enthusiasm, especially with regard to our ongoing clinical trials as we just walked through in some detail during the Q&A, and on behalf of the more than 100 employees at Blueprint Medicines, we want to thank all of you for your support and interest in the Company and we look forward to providing updates with you all again soon. Thanks for your time and have a great day. Bye.

This concludes today's conference call. You may now disconnect.