Lora Pike - Senior Director, IR and PR David Schenkein - CEO Chris Bowden- Chief Medical Officer Glenn Goddard - SVP, Finance Scott Biller - Chief Scientific Officer.

Christopher Mortko – Citigroup Yatin Suneja – Cowen & Company Carter Gould – JP Morgan Terence Flynn – Goldman Sachs Gena Wang – Leerink Partners.

Good day ladies and gentlemen, and welcome to the Q2 2014 Agios Pharmaceuticals 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 our host for today’s conference, Ms.

Lora Pike, Senior Director Investor Relations and Public Relations. You may begin..

Thank you, Amanda. Good morning, everyone, and welcome to Agios’ second quarter 2014 conference call. You can listen to our live webcast with slides by going to the Investors and Media section of our website, agios.com. With me on the call today with prepared remarks are, Dr.

David Schenkein, our Chief Executive Officer who will review second quarter accomplishments and provide strategic perspective for remainder of the year; Dr.

Chris Bowden, our Chief Medical Officer, who will review progress to date in all three of our clinical programs and expected milestones; and Glenn Goddard, our Senior Vice President, Finance who will summarize Agios’ second quarter 2014 financial results. Scott Biller, our Chief Scientific Officer is also here today and will join us for Q&A.

Before we begin, I would like to remind you that today’s discussion will include statements about the company’s future expectations, plans and prospects that constitute forward-looking statements for purposes of the Safe Harbor provision under the Private Securities Litigation Reform Act of 1995.

Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in the Risk Factors section of our annual report on Form 10-K, which in on file with the SEC.

In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so even if our views change.

With that, I will turn the call over to David..

Thanks, Lora. Good morning, everybody and thank you for joining us on our call today. Before I begin, I would like to introduce everyone to Dr. Chris Bowden. We are thrilled to have Chris join the Agios team.

Chris joins us from the Genentech Roche organization, where he most recently served as a Vice President in their oncology product development franchise. This is Chris’s first investor conference call and we look forward to having you meet him in the future meetings. Today, I will review and provide context for our pipeline accomplishments.

Specifically I’ll summarize how our progress reflects our commitment to precision medicine and bringing novel first-in-class medicines rapidly to patients with serious diseases. I would also like to review these accomplishments in the context of the strategic direction of our business.

It’s fair to say that we’ve had an exceptional first half of the year, and our second quarter was particularly important as we made great progress in all three of our pipeline programs.

In cancer metabolism, the major goals for Agios in 2014 have been the clinical advancement of two drug candidates, AG-221 and AG-120, being developed in collaboration with Celgene.

In the rare genetic disorders’ metabolism portfolio, the major goal in 2014 has been to determine in healthy volunteers the safety pharmacokinetics and pharmacodynamic profile of AG-348, our novel targeted medicine for pyruvate kinase deficiency.

On the business side, we strengthened our financial position through a public offering of our common stock and are well positioned to support our current development plans. Chris will review the specific clinical progress that we are making later in his prepared remarks, but I would like to quickly highlight our achievements.

In April and again in June, we announced Phase 1 data from our lead drug candidate AG-221 an IDH2-mutant inhibitor that showed both proof of mechanism and promising clinical activity as a single agent in patients with IDH2-mutant positive relapsed and refractory acute myelogenous leukemia and myelodysplastic syndrome.

Specifically, the data provided strong signs of durable clinical activity of AG-221 and excellent safety profile and the potential for once-daily dosing regimen.

As our clinical experience accumulates with AG-221, our confidence is growing that targeting IDH-mutations have the potential to improve, in a meaningful way, the treatment of advanced hematologic malignancies, including relapsed or refractory AML.

The Phase 1 data support the initiation of four expansion cohorts in patients with hematologic malignancies which are on track to begin in the second half of this year and the potential for an accelerated development path. It’s gratifying for us to see that our preclinical hypothesis translates so well to patients.

Also for AG-221, in the second quarter we received Orphan Drug Designation in AML and we achieved an important milestone when Celgene exercised its option early to this medicine based on the data presented to date.

We have strong support from Celgene in advancing this program and our partnership is well aligned to shape the global development and registration strategy. Now turning to AG-120, we are well underway in two ongoing Phase 1 clinical trials in patients with an IDH1 mutation; one in advanced hematologic malignancies and one in advanced solid tumors.

We are pleased with the enrollment progress of these trials to-date, which we believe have been driven by the strength of data we have presented for AG-221 and the medical community’s excitement around the IDH targets. At this time we plan to report data from these studies at medical conferences in 2015.

If our progress with AG-120 advances more rapidly and we are able to present the data earlier we will update our expectations. Our hope is that AG-221 and AG-120 could change the paradigm for treating IDH-mutant positive hematologic and solid cancers from conventional chemotherapy to that of a targeted precision medicine approach.

Now the progress we achieved recently for our drug candidate AG-348, the novel activator of pyruvate kinase-R for the treatment of pyruvate kinase deficiency. We are pleased to announce today that we completed the single ascending dose escalation study in healthy volunteers and met the primary endpoint.

The multiple ascending dose escalation trial in healthy volunteers while still dose escalating has also met its primary endpoint which was to determine a safe and pharmacodynamically active dose of AG-348. We are now aggressively planning to initiate a study in patients with pyruvate kinase deficiency by early 2015.

We also submitted an abstract of the healthy volunteer studies to the American Society of Hematology Annual Meeting in December. Before I turn the call over to Chris, I’d like to highlight that in our efforts to continue to educate the medical and investor communities on our programs, and we are planning to host an investor meeting in October.

The goal of the meeting will be to discuss our programs in more detail and to share information on the severity, prevalence and treatment options for the diseases that our three lead programs are targeting. We will provide more information on the event in the coming weeks. In closing, I would like to reflect on the past year.

We are thrilled to have met every milestone to date that we set at the beginning of the year and are well positioned to achieve the remaining ones. The rapid progress in advancements we are making, continue to move us closer to our vision of making a difference in patients’ lives.

We are beginning to validate our disruptive approach to targeting cancer and rare genetic diseases and we will continue to set a high bar of using precision medicine, meaning that every molecule we bring in to the clinic will have a set of predicted biomarkers to identify the right patients.

We look forward to a strong finish in 2014 and paving the way for a productive 2015. Finally, our progress would not be possible without the courageous patients who enroll in our studies and the doctors and nurses who care for them. We thank you all. I will now turn the call over to Chris..

Thanks David. I am pleased to join Agios at such an exciting time for the company defined by numerous clinical advancements across our pipeline. Turning first to AG-221, our selective, potent inhibitor of IDH2 mutation.

This drug candidate has a highly novel mechanism of action and in early Phase 1 has shown decreasing levels of the biomarker 2HG and the normalization of cell counts by promoting natural cell differentiation, which has not occurred with chemotherapy.

During the second quarter, we presented early Phase 1 data for AG-221 at two medical meetings in the U.S. and Europe, which provided us the opportunity to expand awareness of this drug candidate globally.

We’ve discussed these data in some detail over the past few months, so today I will review the key takeaways from the data presented at EHA and the clinical programs we are conducting going forward.

As I review the data it is important to remember, as David has said many times before, the data presented at AACR and EHA represents snapshot in time for an ongoing Phase 1 trial and are not final. Now turning to the EHA presentation. We used the May 23, 2014 cut-off date for evaluation of data.

We observed impressive durable clinical activity of AG-221 in patients with relapsed and refractory acute myelogenous leukemia. As of the day of cut-off, we had enrolled 35 patients in six different cohorts ranging in doses of 30 milligram to 100 milligram twice-daily and 100 milligrams to 150 milligrams once-daily.

Key objectives for the Phase 1 trial are to generate safety and efficacy data to support the selection of the optimum dose for Phase 2 and beyond. The data showed objective responses in 14 of 25 evaluable patients on AG-221. An additional five patients had stable disease.

Of the 10 patients who were non-evaluable for responses, seven died due to the severity of their disease during the first few weeks of treatment and could not be evaluated for response to AG-221. This is consistent with other clinical trials conducted in very ill relapsed and refractory AML patients.

Three additional patients have not yet reached the efficacy assessment time point at the time of the data cut. In six patients who achieved the complete remission, CR, evidence of durability was observed up to four months in duration. No responding patients had progressed while on therapy.

AG-221 also showed favorable drug exposure and pharmacokinetics at all doses tested with substantial reduction in plasma levels of the oncometabolite 2HG. Safety data showed that AG-221 was well tolerated with the majority of adverse events reported as mild to moderate, and there were no discontinuations in AG-221 due to adverse events.

The maximum tolerated dose has not been reached. We have submitted additional data from the ongoing one Phase 1 trial for presentation at ASH, the 2014 American Society of Hematology Annual Meeting.

If the abstract is accepted we hope to provide data on more patients as well as additional information on the patients included in our previously reported data. As for next steps, we will continue to enroll patients in Phase 1 study in order to gather additional clinical data and to determine the NTD.

However, determining NTD is not a gaiting factor to initiate the expansion cohort, as we believe the data we have generated to date will allow us to select the best dose and schedule in time to open the four expansion cohorts in the second half of the year. In June, we announced the design of this planned expansion cohorts.

To review the cohorts include; cohort 1, relapsed or refractory AML patients who are not likely candidates for transplant based on age or prior transplant; cohort 2, relapsed or refractory AML patients under age 60; cohort 3, untreated AML patients who declined standard of care chemotherapy due to age or comorbid medical issues; and cohort 4, patients with other IDH2-mutant positive hematologic malignancies, for example, lymphoma, myelodysplastic syndrome or multiple myeloma.

Primary objective of the expansion cohorts is to provide additional information on the safety, tolerability and clinical activity of AG-221 and to evaluate AG-221 in more homogenous patient population.

These expansion cohorts will also provide the information needed to design and accelerate the late stage development plan and will form an important part of the discussions with global regulatory authorities regarding the registration pathway for AG-221.

Beyond the expansion cohorts we are also committed to realizing the full potential of AG-221 in a wide range of additional IDH2-mutant positive hematological and solid cancer indications with our partner, Celgene. We are preparing to initiate a Phase 1 study in advanced IDH2-mutant positive solid tumors in the second half of 2014.

Turning now to our other cancer metabolism drug candidate, AG-120. AG-120 is an orally available selective, potent inhibitor of the mutated IDH1 protein. We have two Phase 1 clinical trials underway with an early development plan that is similar in scope to that of AG-221. These trials were initiated in the spring of this year.

The Phase 1 clinical trials for AG-120, one in advance solid tumors and one in hematologic malignancies, will only enroll patients whose cancer carry an IDH1 mutation. The dose escalation phase is in progress and will be followed by multiple disease specific expansion cohorts once the appropriate Phase 2 dose has been established.

Now for the remainder of my time, I will focus on AG-348. For those new to this program, AG-348 is our lead candidate for the treatment of pyruvate kinase deficiency, a rare genetic disorder that causes severe and chronic hemolytic anemia.

This disease results from mutations in red cell pyruvate kinase, also called PKR, a critical enzyme in the glycolysis pathway. Glycolysis provides the sole source of energy for the red blood cell and is required for red cell survival.

These patients currently have no disease alternate treatment available and only have supportive care with transfusions and splenectomy as options.

We announced today that the single ascending dose Phase 1 study in healthy volunteers is complete and met its protocol defined primary end of assessing the safety and tolerability of single ascending doses of AG-348. Excellent safety profile seen in the SAD study allowed for the initiation of the multiple ascending dose study.

This MAD study is still ongoing and has also met its primary end point, which is identification of a safe and pharmacodynamically effective dosing schedule for AG-348 to be used in subsequent clinical studies in patients with pyruvate kinase deficiency.

The SAD and MAD studies in healthy volunteers provide the foundation for launching a clinical program in patients with pyruvate kinase deficiency by providing important information about the safety of AG-348 and important pharmacokinetic and pharmacodynamic information based on the AG-348 effects observed on wild type PKR enzyme in the healthy volunteers.

The design of subsequent trials in patients with pyruvate kinase deficiency will be guided by the totality of the safety, pharmacokinetics and pharmacodynamic data obtained in healthy volunteers. These results increase our confidence that we could observe clinical activity in patients with PK deficiency.

The next steps for AG-348 clinical program are to complete the MAD Phase 1 study, compile the data from the SAD and MAD studies, and work with global regulatory authorities to facilitate the initiation of a Phase 2 trial in patients with pyruvate kinase deficiency by early 2015.

We also plan to present the data from the volunteer studies at ASH later this year, pending acceptance of abstract, of course. In summary, our expanding clinical development effort has established a great momentum and we look forward to building on this momentum for both our cancer metabolism and rare genetic disorders of metabolism programs.

With that I will now turn the call over to Glenn..

Thanks Chris. During the second quarter of 2014, we were pleased to strengthen our balance sheet with the addition of approximately $95 million of net proceeds from our public offering of 2.3 million shares of common stock allowing us to end the quarter with the cash position of $261 million.

We expect that our existing cash as of June 30, 2014, will enable us to fund our operations until mid-2017. And importantly provide us with the runway to drive all of our lead programs beyond proof-of-concept and in to late-stage clinical development. Now moving to our financial results for the second quarter.

As I just referenced, our cash, cash equivalents and investments as of June 30, 2014 were $261 million, compared to 194 million as of December 31, 2013.

The increase was mainly drive by the addition of approximately $95 million from our public offering, the receipt of $20 million from Celgene related to their extension of discovery phase of our collaboration agreement, offset by cash used to fund operating activities as our three lead programs advance in clinical development.

Our collaboration revenue was $8.4 million in second quarter of 2014 compared to $6.3 million in the second quarter of 2013. Collaboration revenue was comprised of the amortization of deferred revenue from payment received in previous periods from Celgene.

The increase in collaboration revenue in the second quarter related to revenue earned on Celgene’s December 2013 election to extend the discovery phase of the collaboration agreement through April of 2015. Research and development expenses were $22.6 million in the second quarter of 2014 compared to $13 million in the second quarter of 2013.

The increase was largely due to increased spending on the ongoing development activities for our three lead programs now in the clinic. As a reminder, Celgene is responsible for all development cost related to our AG-221 program and will reimburse Agios for all development cost incurred for this program.

The first reimbursement payment will be in the form of milestone payment and is expected in the second half of 2014. General and administrative expenses were $4.2 million in second quarter of 2014, compared to $1.8 million in the second quarter of 2013. The increase was largely related to expenses of supporting public company operations.

Also today, we are reiterating our previous guidance that we expect to end 2014 with more than 200 million of cash, cash equivalents and marketable securities. With that I will now turn the call back over to David..

Thanks Glenn and thank you all for joining us today and for your continued interest and support. We are extremely pleased with the significant progress that has been made across all of the areas of Agios during the first half of the year.

We understand that focus and execution will be important to the achievement of the many growth opportunities we have.

The major advancements we are making as a company reflect the quality and commitment of everyone here at Agios to capture the great potential of our programs and the support from patients enrolling in our studies and the doctors and nurses who conduct the trials. We expect the remainder of the year to be highlighted by major clinical advances.

We are looking forward to this and the potential they represent for patients, the company, our employees and shareholders. We look forward to keep you updated on future call. And thank you very much for your continued support. Operator, we’ll now go to questions..

(Operator Instructions). Our first question comes from Christopher Mortko with Citi. Your line is open..

Great. Thank you for taking my question and congratulations on the all the progress. I had a couple of questions.

For AG-348, now that we are getting data earlier than expected, can you comment on what led to the acceleration? And did I hear correctly that you have selected your Phase 2 dose?.

Yeah. So Chris thanks for your questions. I’ll take that. So obviously we are very pleased that we were able to bring in the data earlier than we had anticipated from both the SAD and the MAD studies and submit an abstract to ASH.

As we’ve always said, when we make the decision to move to the next phase of development or present data at a medical meeting, we need to make sure we have enough data that it make sense to present at a meeting. And we believe we have achieved that.

When you conduct these studies you’ll never exactly know how long it’s going to take for them to enroll and to bring all the data together. So were very pleased not only that things came in faster than anticipated but also that we achieved the primary end points in both of those studies.

As Chris mentioned in his comments, we believe now we have the data to be able to move aggressively in to a Phase 2 study in patients with pyruvate kinase deficiency. And to be able to know what doses we should be testing as we start out.

Certainly as we get closer to initiating that trial as we conclude our discussions with the regulatory authorities, we’ll give you a lot more information about the nature of those studies and the design of them. But it’s just a little too early at this point..

Okay.

And can you, I know this is primarily a safety study, but can you share may be little bit about the effect on pyruvate kinase activity that you saw in healthy volunteers?.

Yeah. So Chris as we’ve said before, we are not going to present any data unless it’s at a conference. But it’s important to look at as we mentioned on the call that the primary end point of the MAD study was to determine both a safe and pharmacodynamically active dose.

And as we’ve talked in the past, we have a range of pharmacodynamic end points that Scott and his team have delivered, that allow us to look through the whole glycolytic pathway, both the intermediates and the end product and the activation of the enzyme itself.

And while we are not giving out any specific data today, the totality of that met the primary end point not only safety. And as we’ve said before, one of the big advantages we had with this program and the one of the reasons we went in to a volunteer study is that we could not only determine safety but pharmacodynamic.

So we really get a good PK PD relationship as we move in to the Phase 2 study in patients which is so critically important..

Great. That’s really helpful. And then just one last question on AG-221. One of the question we get often, I’m sure you do too, is around durability of response. And I know it’s very early so it’s hard to answer that question. But at EHA I believe the median number of cycles was two.

As we get the in to the next updated ASH, where might we be in term so of the median number of the cycles? And how many patients of data can be expected to see based on your estimates?.

Yeah. Chris, thanks. Again we really can’t share any data that sits in the ASH abstract or what’s likely to be there. What I can tell you is that enrollment continues at a very brisk pace, and we are very obviously pleased with the physicians’ excitement about using AG-221. Remember, there are two things to look at.

One is durability of response and we are very pleased with the data we showed at EHA with the patient out four months in response. The other is median duration number of cycles, and that depends on where you are enrolling patients and how many are enrolling. So two different numbers there.

So certainly what you will see, well I anticipate you’ll see at ASH is more patients and so additional new data as well as longer follow up on the patients who been on the study..

Great. Thank you very much..

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

Hi, guys. This is Yatin in for Eric. Thanks for taking my questions and congrats on all the progress. First one with regard to AG-221.

Could you tell us what is the maximum dose that you have used so far? And if there is any DLT that you have experienced?.

Yeah. So maybe I’ll take that. So thanks for your questions. So again we are not giving out any new data beyond what we presented at EHA. What you can hear from our comments is that we had enrolled patients in ranges at EHA from 30 milligrams to 100 milligrams twice-daily and on the once-daily schedule up to 150 milligrams. We’ve not achieved an MTD.

But we are not giving out any new data around either safety or efficacy at this time. We’ll do that at ASH..

Okay. Thanks. And then it looks like the therapeutic window is fairly wide on this molecule. So is there any point at which you are going to call it off and just move to the expansion cohort? Thank you..

Yes, hi. It’s Chris Bowden here. We are interested in exploring and conducting the trial to see if we can determine the MTD. There is certainly as we shown at EHA there are range of possible doses based upon the pharmacokinetic, pharmacodynamic, safety as well as efficacy.

So it is possible that we would declare, we have all the information we need to move on to the expansion cohorts before we achieve the MTD, that’s certainly possible and that was reflected in some of the remarks I made today.

However, when you are in a Phase 1 trial and your first in man study some time having that understanding of the limits and what the maximum tolerated dose is can be very valuable over time..

Thanks guys..

Our next question comes from Geoff Meacham with JP Morgan. Your line is open..

Hello. Good morning. This is Carter on for Geoff. One of the questions we often get on 221 is how you might see transplant being incorporated alongside the drug. Could you imagine patients with durable responses being driven to transplants or should we be thinking about the drug being used until progression? Thank you..

Yeah. Great question. Thanks. So as we’ve always said there was two factors here and this is one of the things we will spend some more time at our investor event in October, spend a little bit more time talking about AML. As you know, AML is primarily disease of the elderly.

And as such, it is estimated only about 10% of AML patients will be eligible for a transplant based on either donor availability or age. Now it is an important component for younger patients. Our hope as the data mature, is that 221 becomes sort of the foundation of therapy for patients with an IDH2 positive hematologic malignancy in a particular AML.

And what that means is that while our study is now relapsed refractory AML and we know that in the elderly patients they won’t be eligible for transplant we could hope that AG-221 will move and we will move aggressively in to earlier lines of therapy even in front line therapy and potentially using it before and after a transplant.

So that we see patients one day getting 221 through-out their entire course of their illness to try and achieve as high degree of response and cure as possible..

Thank you..

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

Hi. Thanks for taking the questions. Just two from me. So the first is, David I was just wondering if you could recap the preclinical data for 120 for us in both solid and liquid tumors? And how that was similar or different to what you saw with 221? And then the second question was on 348.

Just wondering, obviously you guys said you met the primary end point of this study. But just why are you continuing to dose escalate then, is it the same reason why you are continuing to dose escalate with 221? Thanks..

I’ll start with the 348 one, Terence. And thanks for your questions. So clearly we believe we’ve met the end point for 348 in the multiple ascending dose trial. But as you correctly pointed out, we’ll take the opportunity to continue to dose escalate so that we can determine what the MTD and top safety profile was in volunteers.

All of that is just so critical information for us as we determine what those ranges are and obviously the regulatory authorities are interested in that. I’ll ask Scott to sort of review it, at a high level, similarities and differences for 120, 221 pre-clinically..

Sure. Thanks David. Yeah with 120 it’s clearly a very different molecule and a very different target yet it has a very similar pharmacokinetics or exposure in animals, a great properties in general as a drug similar to 221. In animal models we’ve done some work in animal models and seen very similar results.

And probably the best data we have is ex-vivo looking at patient AML data, patient AML samples ex-vivo across a variety of patients where we see a very similar, a relief in the blocker differentiation and moving the blast down in to differentiated cells beyond further down the pathway.

So very, very similar properties, ex-vivo, in-vivo and drug properties..

And Terence, this is David. Remember that both share the common mechanism. I know, you know this that the both enzymes when they are mutated lead to the production of 2HG as Scott mentioned which then blocks differentiation..

Great. Thanks..

Our next question comes from Gena Wang with Leerink Partners. Your line is open..

Hi. Thank you for taking my questions. So I have a few questions on 221. In your high dose cohorts it seems that you enrolled mostly MDS patients.

Will you be or have you been enrolling more AML patients to help access at a higher dose in AML? And for also your continued dose escalation, will you expanding I think Yatin asked before, and I just wanted to ask little bit more.

Will you be expanding BID dosing or QD dosing?.

Yeah. Thanks for your questions. So I think I don’t think I would characterize as we are enrolling more MDS or AML. I mean the majority of the patients on this study have been relapsed refractory AML, and I suspect that will continue given that it’s a more common finding in AML than it is in MDS.

So one needs to be little bit careful with small numbers in some of the cohorts we presented at EHA that will settle out overtime. There is certainly no push to enroll MDS versus AML. We are certainly gratified that we’ve seen some very promising activity in MDS. But I suspect the majority of the patients will have AML.

We’ve not yet committed to whether we’ll use once-daily or twice-daily, when we go in to the expansion cohorts. Obviously we’ve shown at EHA both pharmacokinetic, pharmacodynamic and safety data that looks very promising for daily which would offer convenience factor to patients. But we haven’t made that final determination.

And when we start the expansion cohorts, we’ll let you know that..

Great.

And for the solid tumor, wondering will you be also starting with 30 milligrams as well? And will you also be exploring both BID and QD dosing?.

Yes. So as we’ve done in the past, we’re not going to share any of those details until those studies initiate and then we’ll give you some more granularity on what those studies look like..

Okay. May be one last question.

So wondering when the program continues down the road, will you continue lead trial design all the way to pivotal trial? How much control will be from Celgene?.

Yeah. So we are working very collaboratively with Celgene. They’ve been a great partner from the beginning when we worked with them pre-clinically and now certainly as their clinical group have become engaged with us. It’s similarly very collaborative relationship. We haven’t given out a lot of granularity in terms of who’s exactly doing what.

But I think it’s fair to say that it will be highly collaborative project with both groups, both participating in the design and in the operations of AG-221. And at the moment Agios continues to lead the current study and we’ll discuss that in more detail as new studies start..

Okay. May be one last question on the 348.

Wonder will you be waiting for some data from natural history in order to start 348 next clinical trial?.

No. So as Chris mentioned in his comments, really it’s the totality of the data from the SAD and the MAD studies. And then designing the right study and having the appropriate regulatory conversations.

The natural history study is a very important study, we’re going to learn a lot about pyruvate kinase deficiency over the next several years as this study will continue to follow patients. And certainly that information will be very important but it’s not a gaiting factor to initiate the Phase 2 study..

Great. Thank you..

I am not showing any further questions at this time. I would like to hand the call back to David Schenkein for closing remarks. .

Thanks. I would like to just thank everybody, obviously, who participated in the call today, everybody at Agios for their commitment to help patients and to all of you for your support to help build Agios in to a great company for the future. So I appreciate your support and hope you have a good day..

Thank you for participating in today’s conference. This does conclude the program. You may all disconnect. Everyone have a great day..