Renee Leck – Senior Manager, Investor Relations and Public Relations David Schenkein – Chief Executive Officer Chris Bowden – Chief Medical Officer Glenn Goddard – Senior Vice President-Finance Scott Biller – Chief Scientific Officer.

Eric Joseph – J P Morgan Eric Schmidt – Cowen and Company Kennen MacKay – Credit Suisse Terence Flynn – Goldman Sachs John Newman – Canaccord.

Good morning and welcome to Agios’ Fourth Quarter and Year End 2015 Conference Call. At this time all participants are in a listen-only mode. There will be a question-and-answer session at the end of the call. Please be advised that this call is being recorded at Agios request.

I would now like to turn the call over to Renee Leck, Senior Manager, Investor and Public Relations of Agios..

Thanks, Triya. Good morning everyone and welcome to Agios’ fourth quarter and year end 2015 conference call. You can listen to a live webcast with slides or a replay of today’s call by going to the Investors and Media section of our website, agios.com. With me today on the call are Dr.

David Schenkein, our Chief Executive Officer, who will highlight our 2015 progress, 2016 corporate priorities and new announcements; Dr.

Chris Bowden, our Chief Medical Officer, who will discuss our clinical development activities; Glenn Goddard, our Senior Vice President of Finance, who will summarize Agios’ fourth quarter and year-end 2015 financial results, and provide 2016 guidance; and Dr. Scott Biller, our Chief Scientific Officer, who will be joining the call 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 the purposes of the Safe Harbor provisions 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 is 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’ll turn the call over to David..

Thank, Renee, and good morning everybody and thanks for joining us today.

I’d like to open the call by highlighting the tremendous progress at Agios in 2015, where we executed against all of the milestones we set out to achieve, including the rapid advancement of our IDH inhibitors into late-stage clinical development, and the launch of our first Phase 3 study, presentation of the first data in solid tumors for AG-120, and advancing our fifth molecule and second PKR activator, AG-519, into the clinic; a special thank you to all of our employees for making the year such a success.

Looking forward, Agios is in a strong position as a business to execute on our 2016 priorities and reach important milestones, which I’ll touch on before turning the call over to Chris for more detail. As you know, our PKR activator program has the potential to deliver the first disease modifying therapy for patients with pyruvate kinase deficiency.

We’re announcing today that we plan to submit early data from both of our wholly-owned PKR activators, AG-348 and AG-519, for presentation at the European Hematology Association Meeting in June.

We continue to work with the PK deficiency community to better understand the impact of this rare debilitating disease as we aim to provide patients with a meaningful treatment option.

Moving to our IDH programs, our work in this space has driven by a clear long-term goal to one day provide a therapy for every patient who has an IDH mutation, regardless of their tumor type or stage of disease.

We remain committed to a development strategy of speed and breadth for AML and the other hematologic malignancies, as we set out to help patients, who are waiting for more effective and tolerable treatment options.

In relapsed/refractory AML, we’re conducting a set of trials that includes two important 125 patient expansion cohorts for AG-221 and AG-120, both of which are expected to complete enrollment in the second half of 2016.

Our Phase 3 study for AG-221 is ongoing with additional frontline and combination studies for both molecules planned and already underway. Developing our IDH inhibitors, the solid tumor remains a priority, based on our encouraging early Phase 1 data and the potential to help a large number of people with cancer.

Today, we announced that we plan to present data from our AG-120 expansion study in low-grade glioma in the second half of 2016, as well as start a Phase 2 trial in cholangiocarcinoma.

With the heart and soul of Agios is strongly rooted in our research abilities, we’re pleased to be presenting pre-clinical findings on our new program focused on MTAP deleted cancers at the Tumor Metabolism Keystone Symposia later this month.

MTAP is a metabolic gene that is deleted in approximately 15% of all cancers, which represents close to 75,000 new patients per year in the United States alone, across a wide-range of cancer types. As I discussed during my J.P.

Morgan Healthcare Conference Presentation, this is the first in our next wave of research programs and we’re really excited to initiate pre-clinical development activities this year. People and culture are central to our future. So, I’m excited to welcome Steve Hoerter to our team, as Chief Commercial Officer.

Steve has more than 20 years of extensive experience in this sector, most recently as Executive Vice President and Chief Commercial Officer at Clovis. I also had the opportunity to work with Steve at Genentech and Roche, where he held several senior commercial roles.

He will be a terrific addition to the team as we build the late-stage development and commercial capabilities needed to become a sustainable long-term company. I also want to take a moment to acknowledge and thank Perry Karsen, who will be stepping down from our board on March 1 following his retirement from Celgene.

Perry has been a tremendous board member and we wish him the best. And with that, I’ll turn the call over the Chris, so he can review our clinical updates..

Thanks, David. Looking back over 2015, I’m very pleased with the extensive dataset we presented for our IDH and PKR programs in 2015. Several important catalysts will build on this momentum over the course of 2016. As David mentioned, our IDH program and relapsed/refractory AML is rapidly advancing.

We have now presented data on over 300 people with IDH mutant positive hematologic malignancies treated with AG-221 or AG-120. The single agent activity for these agents is compelling, based on the overall response rates, durability and the favorable safety profiles seen with once daily oral dosing.

With our drugs unique mechanism of action, we are looking to change the treatment paradigm for AML through the use of a long-term differentiation therapy. As a once a day oral therapy both agents induce durable complete and partial remissions in relapsed/refractory patients that have been unsuccessfully treated with two or more prior therapies.

For some patients with stable disease, we see evidence of improvements in blood counts, which may have important clinical implications for reductions in infection and bleeding, areas where AML patients are particularly vulnerable.

The outcomes we are seeing with our drugs results in the mechanism based differentiation of the malignant blast cells and effective distinct from the non-specific effect of chemotherapy, which also carry a considerable toxicity. The dose escalation component of both studies is now closed.

And consistent with our speed and breadth strategy, we are focused on enrolling the 125 patient expansion cohorts by the end of this year. The AG-221 Phase 3 identified study and relapsed/refractory AML, sponsored by Celgene, is enrolling patients with overall survival as the primary end point.

For AG-120, we’ll be initiating a Phase 3 study in the frontline setting in the second half of this year. As part of our efforts to move swiftly and broadly into the frontline setting, we have two combination trials for newly-diagnosed IDH mutant positive AML patients.

For AML patients eligible for intensive chemotherapy, a Phase 1b combination study of either AG-221 or AG-120 with standard induction and consolidation chemotherapy is enrolling.

For AML patients not eligible for intensive chemotherapy, a Phase 1/2 combination study of either AG-221 or AG-120 with VIDAZA, azacitidine, is planned for the first quarter of 2016.

Based on promising early data at ASH that shows 7 out of 14 myelodysplastic syndrome patients achieving an objective response, we plan to open an AG-221 expansion arm for high-risk patients this year.

Moving to solid tumors, this is an unchartered area of biology with our drugs’ unique mechanism of action, but when we are committed to exploring further in the year ahead. A major focus is in low-grade glioma, where approximately 80% of tumors harbor the IDH1 mutation. The clinical context for patients is really important here.

Low-grade glioma is often associated with the prognosis measured in years, however most patients ultimately die of their disease. A majority of patients are also diagnosed at a young age in many states of likelihood of impaired cognitive function that results from tumor re-growth and intervention such as surgery, cytotoxic therapy and radiation.

We are developing our IDH inhibitors in glioma with the intent to alter the natural history of the disease and delay or eliminate the need for additional therapies.

Against that backdrop, the Phase 1 dose escalation data we presented for AG-120 and solid tumors and glioma, last November, gave us important early data showing that AG-120 is well tolerated in a broad set of solid tumor and glioma patients.

Demonstrated encouraging signs of prolonged stable disease and low grade glioma, demonstrated evidence that 2HG was lowered in the brain for some glioma patients as measured by magnetic resonance spectroscopy and these findings were paired with signs of tumor volume was decreasing based on MRI volumetric assessments in some patients.

These observations in the first ever group of low-grade glioma patients treated with AG-120 enabled us to move forward and hone our investigations for the expansion phase. In low-grade glioma, we are enrolling 25 patients with at least six months of prior scans in order to continue to measure and assess volumetric changes.

We will be presenting this data in the second half of the year. We believe these data will be crucially important for a path forward in the disease where we are setting out to define new ways of measuring patient outcomes beyond the current RANO and RECIST criteria.

Our efforts coincide with the ongoing activities and the larger neuro-oncology community around new imaging endpoints for brain tumors.

Outside of glioma, we are enrolling three additional AG-120 expansion cohorts of 25 patients each in second line cholangiocarcinoma, high-grade metastatic chondrosarcoma and solid tumor patients with an IDH mutation not eligible for cohorts 1 through 3.

A randomized Phase 2 study of AG-120 and IDH1 mutant positive cholangiocarcinoma is also planned for the second half of 2016.

For AG-881, which is a brain-penetrant, pan-IDH mutant inhibitor, we are also enrolling Phase 1 dose escalation and expansion trials in both heme malignancies and solid tumors and we’ll keep you updated as these trials progress. Now turning to our rare genetic disease program.

Starting with AG-348, we are enrolling a Phase 2 trial in adult transfusion independent patients with PK deficiency known as DRIVE PK. We believe this is the best population of pyruvate kinase deficiency patients in which to establish proof-of-concepts.

And if we are successful, we plan to expand our efforts to treat the entire spectrum of the disease, including children and adolescents. As a reminder, DRIVE PK is a global open-label, multi-center, randomized study that includes two arms with 25 patients each, receiving 50 milligrams or 300 milligrams of AG-348 twice daily for at least six months.

We have several key objectives for this first in-patient study understanding the safety and tolerability of AG-348 associated with long-term dosing, using pharmacokinetics and pharmacodynamics to confirm activation as a PKR pathway in patients, assessing changes in hemoglobin levels and other hematologic parameters, early assessments of the correlation between clinical outcomes and mutational background, and evaluating routine clinical and laboratory safety findings, including sex hormones to understand the clinical significance of AG-348’s aromatase inhibition.

Transfusion-independent men and women with the hemoglobin of less than 12 grams per deciliter qualify for this study. Routine laboratory and clinical assessments are conducted weekly for the first few weeks, extending to every three to four weeks until week 24. Safety is continuously monitored while patients are on study.

The presentation we are preparing for the EHA meeting will be early data from 10 to 15 patients in this ongoing trial. For AG-519, we will be submitting preclinical and clinical data to EHA from the Phase 1 study in healthy volunteers that is an integrated single ascending dose and multiple ascending dose trial.

As a reminder, AG-519 is a potent, highly selective and orally bioavailable PKR activator that has no activity against the aromatase enzyme pre-clinical. As part of good drug development, this program provides clinical development optionality for our PK activator portfolio.

With the Phase 1 – healthy volunteers study of – AG-519 running in parallel, excuse me, would DRIVE PK for AG-348, a late-stage development path for PK activator program will be determined as the clinical data matures.

As we announced at R&D Day, the unique mechanism of action of our PKR activators gives us the opportunities to evaluate other hemolytic anemia and we plan to announce our path forward in beta-thalassemia in the second half of this year. Our understanding of pyruvate kinase deficiency continues to evolve.

However, with the help of the ongoing Natural History Study, run by Boston Children’s Hospital, which is enrolled over 200 patients, we are making inroads in understanding disease severity. The clinical spectrum can range from mild to severe and is associated with a range of factors beyond transfusion status.

Severe jaundice and anemia can require intensive medical support for infants. This can be followed by a lifetime of extreme fatigue that limits participation in normal day-to-day activities.

The latest Natural History Study data presented at ASH in December, presented a range of severity for the disorder and identified important characteristics such as iron overload, which was found even in patients with no history of regular transfusions. Iron overload is associated with liver fibrosis, endocrinological abnormalities and cardiac events.

New findings from the Natural History Study will be presented in the second half of the year and we look forward to sharing more about this program in the coming months. I’m now going to turn the call over to Glenn to review our financials..

Thanks, Chris. Agios is well-capitalized as we advance multiple programs in the late-stage clinical development and expand our research pipeline. As David noted, we achieved all of our corporate goals and milestones for 2015 and are in a strong position as we enter 2016.

With five clinical stage medicines advancing, $376 million in cash and a great partnership with Celgene, we believe we are in a strong position to build a sustainable multi-product company. Today, we are providing guidance that we expect to end 2016 with more than $180 million of cash, cash equivalents, and marketable securities.

We expect this cash position give us runway until late 2017. The anticipated year-end 2016 cash position does not include any additional program specific milestone payments.

Moving to financial results for the fourth quarter and the full year 2015, our cash, cash equivalents and marketable securities, as of December 31, 2015, were $376 million, compared to $467 million as of December 31, 2014.

The decrease was driven by cash used to fund operating activities of $161.8 million, which was offset by funding of $64.7 million received from Celgene during 2015. As a reminder, Celgene is responsible for all development costs for AG-221, an approximately 50% of the development costs for AG-120 and AG-881.

In January 2016, we received a $25 million milestone payment for the first patient dose in the Phase 3 identified trials of AG-221. We’re also eligible to receive $50 million of milestone payments relate to late-stage clinical development milestones for AG-120.

Collaboration revenue was $59.1 million for the year ended December 31, 2015, compared to $65.4 million for the prior year. The decrease is mainly due to certain AG-221 reimbursable development cost being recognized net of research and development expenses during 2015.

Research and development expenses were $141.8 million for the year ended December 31, 2015, compared to $100.4 million for the prior year. The increase was mainly due to increased investment in our lead investigational medicine as they advanced into late-stage development, along with early development costs for both AG-881 and AG-519.

General and administration expenses were $36 million for the year ended December 31, 2015, compared to $19.1 million for the prior year. The increase was largely related to increased headcount, stock-based compensation and other professional expenses. With that, I’ll turn the call back over to David..

Thanks, Glenn. We’ve made extraordinary progress over the last seven years, creating five novel investigational medicines that have the potential to impact patients’ lives in a profound way. We’re truly excited to bring that same level of passion to our work in 2016.

As we continue to build the organization and we’re also focused on responsibly managing the business by investing in people and groundbreaking science with the highest probability of success, and continuing to focus on creating value and doing what’s right for patients and shareholders. I want to thank you for your time today.

I’m going to end by showing our 2016 milestones and as you can see we’re going to be pretty busy. As always, we want to thank all the patients and their caregivers, the nurses and doctors, who participated in our clinical trials, and of course, all of our employees and shareholders for their continued support.

And with that, we’ll now open the call up to questions, back to you operator..

Thank you. [Operator Instructions] And our first question comes from the line of Anupam Rama of J P Morgan. Your line is now open. Please check your mute button..

Can you hear me? Hi, guys. This is Eric in for Anupam Rama this morning. Thanks for taking my questions. Just a quick one from us coming away from ASH, the actual dates for 221 and 120. Just wondering if you have plans to pursue PDUFA [indiscernible] molecule and what’s gaining factors might be there. Thanks..

Yes, thanks, Eric. Thanks for your question. So as you know, we don’t comment on any regulatory interactions that we have other than, as you know we’re obviously very excited by the data that we’ve seen to date and also have a terrific relationship with the FDA on all of our programs, but we don’t comment on any specific interactions we have..

Okay, great. Thanks..

Thank you. And our next question comes from the line of Eric Schmidt of Cowen and Company. Your line is now open..

Thanks for taking my questions. Maybe on the DRIVE PK study, David and Chris, I think you both called out the early nature of the data and I think Chris remarked we might see 10 or 15 patients’ worth of information.

Will those patients see follow-up for the full six months and will the presentation also include hematologic parameters on those patients?.

Eric, thanks your question. I’ll have Chris tackle that one..

Yes, so the study is open and continuing to enroll. So the patients that we present data on will have varying levels of follow-up. And we’ll be able to provide that – we’ll provide that data at the time of the presentation..

And we’ll see it at least for some patients’ hematologic parameters?.

Yes. The primary objectives of the trial around are safety and tolerability and then there are a number of important secondary objectives, which include changes in hemoglobin, hematocrit as well as other components..

And then a question on the pivotal development for 120 and AML, I think you mentioned for the first time just earlier this year that your intention was to do a frontline trial in that setting.

Can you talk about sort of why the different strategies for 120 versus 221 where you’re going only after third-plus line patients?.

Yes, Eric, it’s Chris here. So we consider a range of options and thinking about clinical development a both of the compounds in AML.

And as we were thinking about what types of trials would have the most impact for patients and the biggest impact in terms of global regulatory impact while certainly the second and third-line patients are high unmet medical meeting that’s why we’re doing a lot of work there.

Taking a look at everything and thinking about the breadth of our program, we’ve decided that the first trial – our randomized trial in the Phase 3 trial in the first-line setting for AG-120 is the right way to go in AML at this point.

We haven’t decided further details around what types of populations that would be in nor the study design, but in terms of thinking through everything and working with our partner, Celgene, that’s the direction that we’re confident with right now..

Would you be – I mean, if that trial is going to start in the second half, Chris, would you be in position to do a combination study with induction chemo or would that be too rushed to timeline?.

Well, I think the details of what the study will look like are going to be forthcoming once we iron those things out.

But there’s certainly a number of different ways you can think of the trial, whether it is in combination or as a single agent and there are ways you can design a trial to be able to get those answers as you’re getting ready to – as you have those things incorporate into the trial design itself..

Okay. And then Glenn noted there’s another $50 million in late-stage milestones associated with 120’s development.

I don’t think any of these are included in the guidance, but would you potentially be eligible for $50 million payment upon start of that pivotal trial?.

So, Eric, David is here. There are two milestones. One is a $25 million milestone for the start of Phase 3, so if the 120 Phase 3 starts in this year, we’ll get a $25 million milestone. And there’s a second $25 million milestone for the last patient enrolled in the expansion cohort of AG-120..

So that could also be this year, David?.

That’s correct. Our guidance, as you know, is to complete enrollment for both expansion cohorts for 221 and 120 by the second – in the second half of year..

But neither of the $25 million payments are included in the $180 million cash balance by year-end?.

Yes. Hey, Eric. This is Glenn. Yes, that’s correct..

Okay, thanks guys..

Thank you..

Thank you. And our next question comes from Kennen MacKay of Credit Suisse. Your line is now open..

Hi, thanks for taking my question. So I’ve been pretty excited about the combination of IDH inhibitors on top of cytotoxic agents.

Can you talk a little bit about when we might see data from the Phase 1b of 120 and 221 on top of chemo in relapsed/refractory AML?.

Yes, thanks, Kennen. So, as you know, those studies started pretty late in the year and the VIDAZA study will be starting in the first quarter, so it’s a little bit too early to commit.

Obviously, we’re really excited about those trials because, as you know, it fits into our speed and breadth, so that we can eventually, one day, get a broad set of labels. So we can’t yet commit to when you’ll see data, but they’re going fine. The VIDAZA one will start shortly and we’ll get that data out as quickly as we can.

As you know, given the unique mechanism of action and the excellent safety profile we’ve seen to date, we have no anticipated issues around combination, but that’s why we’re doing the trials..

Got it. And then earlier in the year, you had commented that you had secured a companion diagnostic partner.

Do you have any sense of when you might be able to announce who that is?.

So, we haven’t. I mean, we have a partner secured and we’re confident that, that’s not a rate-limiting step should we be successful on our timeline of obtaining approval because we do expect to have a companion agnostic in the label. Obviously, this is in collaboration with Celgene.

And so there’s no immediate plan to disclose who that partner is, but I can guarantee you that you and the rest of the community will be confident we’ve chosen a high-quality competent partner to take us all the way through label-enabling studies..

Okay, I got it. Thank you. And I guess a final question for Glenn here. Just regarding the milestones, you talked a little bit about 120.

Are there additional milestones we should be thinking about for 221 or additional milestones for 120 associated with solid tumors that we should be modeling at? Just trying to get a little more granularity here – or 881, for that matter? Excuse me..

Sure, yes, great question. So I think for AG-221 and AG-120, remember, each one of those programs are eligible to receive up to $120 million of milestones each. And if you think of them in a cascade the first $25 million in that cascade of $120 million is this Phase 3 initiation milestone.

And then the second bucket of milestones are related to approval and regulatory and they totaled $70 million. And then the last milestone in that sequence is $25 million threshold related milestones. So – and then for AG-881, there is $70 million of milestones that are very much focused on approval and regulatory milestones.

So you could see over the next several years, well, all three programs with these milestone payments coming in providing a good source of capital to the Company to keep driving these things in an aggressive way..

Got it. Okay. Thank you very much for taking the questions..

Thank you. And our next question comes from Terence Flynn of Goldman Sachs. Your line is now open..

Hi, thanks for taking my question and apology for the background noise.

Just wondering first, guys, on 519, it was a little unclear to me, but have you completed both the SAD and MAD work here? Is that still ongoing? And then the second part of that question is, have you already made a decision about moving this drug into a Phase 2 trial in PKD patients?.

Yes, so Terence, those studies are ongoing. But we do anticipate having data to present at EHA and submitting an abstract. And so, we’re obviously looking forward to presenting that data. We haven’t made a commitment yet.

As you know, we have stated that we think that when we see the totality of the data from the DRIVE PK study and the single ascending dose and multiple ascending dose trial for AG-519, we will have the information that we need to make decisions about which molecule moves forward to potentially the next stage of development.

And so, we believe we’ll have that information hopefully in 2016, but can’t really commit to an absolute timeline on that yet..

Okay. Thanks and then just one additional question on the PKD program. So I know you guys have talked about before, there are over 200 mutations here. Would you expect differential activity for 348 and 519 across the mutation? And then are you going to have any of the genotype data for the patients in DRIVE PK at EHA? Thanks..

Terence, it is Chris here. Our plan is to have as much of that genotype data for the patients that we can get our hands on. That’s a protocol-specified assessment so we’re looking forward to looking at that and presenting it.

And then one of the reasons why we want to do the study is to understand what – how outcomes might be correlated with that mutational background. Certainly, we’ve done a lot of preclinical work on the more common mutation types.

We haven’t studied all of them and we’ve shown that the drug at least in the preclinical studies and Scott can certainly talk to further detail that we were encouraged by the activity that we’ve seen..

Yes, I think the other aspect, Terence, as you know from the slide that we showed. That’s one of the reasons that Chris designed the study as a global study, so we could get a broad range of mutational backgrounds. And we also have stratifications to make sure that we don’t get clusters of the same genotype in either of the two arms..

Okay and then have you guys talked about, just if you think about the preclinical data for 348 versus 519 across the mutation? Are they very similar or are there some differences that could be important?.

Yes, Terence, this is Scott. We’ve looked at across the same set of common mutations and they both performed very comparably so based on the preclinical data, it’s difficult to distinguish but I think the truth will be told in the clinic..

Okay, thanks a lot..

Thanks, Terence..

[Operator Instructions] Our next question comes from John Newman of Canaccord. Your line is now open..

Hi, guys, thanks for taking the question. I’m just curious with the work that you’re doing in low-grade glioma for 120, what do you hope to learn from that particular study? Is there thinking here that there’s a specific subset of gliomas that you’d like to focus on going forward? Thanks..

Yes, it is Chris here. What we are trying to do – what we are looking to do in glioma is expand on some of the early findings that we presented in that Phase 1 presentation that Dr. Berger stated at the Triple meeting in November, where we saw but changes in 2HG by MRS.

We saw some changes in tumor volume that were associated with drops in 2HG and that looked like it could give us more information than just looking at simple bi-dimensional measurements. And that was in particularly in the set of low-grade glioma patients.

So what we’re – the reason why we’ve made some pretty specific eligibility criteria for this expansion cohort is we want to build on those early observations that was seen in a couple of patients and now the important thing for us is to now expand and see – get some further nuance around those observations in low grade glioma patients who have an IDH1 mutation frequency of about 80%.

So when we see that data, I think that will really help us understand what we observed in the Phase 1 and what the next steps might be.

The other thing I highlighted in my comments is that this aspect of volumetric imaging as a way of understanding what’s happening with patient tumors, especially in low-grade gliomas, which are somewhat slower growing than glioblastoma is that this is something that the neuro-oncology community is developing as well.

So that’s important that we are collaborating with them as we move forward in this area where there’s just not a lot of good therapy for these patients..

Okay, great. And then the cholangiocarcinoma study that you mentioned, how many patients will you look to enroll there and for the primary endpoint, will you be looking just directly at survival? Thanks..

Yes, so we have not disclosed details around that trial at this juncture and we look forward to doing that. At this point, it is randomized Phase 2 study.

We think it is important to have a control on which to do some of those comparisons when – and when we select the endpoints and other details around the study, we’re going to be happy to share that with you..

Okay, great, thank you..

Thank you. And our next question comes from Kennen MacKay of Credit Suisse. Your line is now open..

Hi, thanks for taking my follow-up. A quick one for Chris on the upcoming data in the DRIVE PK study.

I was wondering if you could sort of help us think about what might be a meaningful change in hemoglobin on some of the hematologic parameters in the PKD population? And if there’s anything from the collaboration with Boston Children’s that can maybe help us understand what’s clinically meaningful here?.

Yes, so, we’ve talked about this from the context of what these doctors do with patients who have chronic anemias that are symptomatic? And in general, patients get transfused one to two units of blood and we see their hemoglobins go up by 1 gram to 2 grams. And in general, from a qualitative perspective patients tend to feel better.

So, we think that’s the range that we think can certainly be associated with clinical benefit with AG-348. Other parameters, I think we’ll have to see what they look like and how – what the totality of data looks like, not just from hemoglobin, but what about other measures of hemolysis.

And we’re going to be looking at some data around what’s happening with iron and some other outcome measures. So, it is going to be a lot of different things that we need to look at, but we look – we think around 1 gram to 2 grams could be associated with clinical benefits..

Got it. Thanks so much, Chris. I really appreciate it..

Thank you. And at this time, I’m showing no further participants in the queue. I would like to turn the call back to management for closing remarks..

Again, I’d like to thank everybody for participating in the call today and once, a shout out to all of our employees, who put their heart and soul every day and making Agios a special place to work and in focusing on trying to help as many patients as possible. So with that, we’ll end today’s call and look forward to seeing you again at a later date.

Thank you everybody..

Ladies and gentlemen, thank you for your participation on today’s conference. This concludes your program. You may now disconnect. Everyone have a great day..