Agios Pharmaceuticals, Inc. (AGIO) Q1 2016 Earnings Report, Transcript and Summary

Good morning and welcome to the Agios’ First Quarter 2016 Conference Call. [Operator Instructions] 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, Antoine. Good morning, everyone, and welcome to Agios’s first-quarter 2016 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 on the call today with prepared remarks are Dr. David Schenkein, our Chief Executive Officer, who will highlight our 2016 progress, corporate priorities and new announcement; Dr. Chris Bowden, our Chief Medical Officer, who will discuss our clinical development activities; and Glenn Goddard, our Senior Vice President of Finance, who will summarize Agios’ first-quarter 2016 financial results. Dr. Scott Biller, our Chief Scientific Officer, will also be joining 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 will turn the call over to David.

Thanks, Renee. Good morning, everybody, and thanks for joining us today. I’d like to begin with today’s new announcements that highlight the tremendous progress we are making in advancing our portfolio of five investigational medicines and executing against our 2016 key priorities, which are driving the IDH portfolio into late stage development, determining the clinical activity of our PKR activators and advancing our research pipeline. Beginning with our PKR activator program, we are extremely pleased that a total of five abstracts have been accepted for presentation at EHA in June, including the first data from our Phase 2 DRIVE PK study for AG-348 in pyruvate kinase deficiency and the first data from the Phase 1 healthy volunteer study in AG-519. These trials and our partnerships with the broader PK deficiency community will be crucially important to better understand the impact of this rare, debilitating disease on the lives of patients. Ultimately, our goal is to deliver the first disease-modifying therapy for children and adults with pyruvate kinase deficiency. I’m also very pleased to announce that AG-221 has received orphan drug designation in Europe and has completed enrollment in the Phase 2 refractory relapsed AML expansion cohort ahead of schedule. The AG-120 cohort continues to enroll and is expected to complete by the end of 2016. We and Celgene are pushing ahead aggressively to get our IDH therapies to waiting patients as quickly as possible. Our work in this space is driven by a clear goal – to one day provide the therapy for every patient who has an IDH mutation, regardless of their tumor type or stage of disease. And Chris will speak further about the trials that make up our speed and breadth strategy in both hematological malignancies and solid tumors. Pushing our boundaries in research has always a priority for the organization, and I am proud to congratulate Scott’s team for their publication on MTAP deleted cancers in cell reports last 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. This pathway represents the first in our next wave of research programs, and we are excited to initiate preclinical development activities later this year. Finally, as you know, we recently extended the time period allotted for the completion of our 2010 research agreement with Celgene to June 1. We will update you in the near future, once these discussions have been completed. And with that I will turn the call over to Chris so he can review our clinical updates.

Thanks, David. I won’t be covering all of our programs and trials in detail on this call but wanted first to spend some time on our PKR activators with the announcement that all five of our abstracts have been accepted for presentation at EHA next month. Our two PKR activators, AG-348 and AG-519, are in development for the treatment of pyruvate kinase deficiency, a rare genetic disease where mutations in the PKR enzyme cause hemolytic anemia and associated morbidities. The clinical spectrum of pyruvate kinase deficiency is associated with a range of factors beyond transfusion status. Severe jaundice and anemia can require intensive medical support for some patients. In addition, many patients undergo splenectomy in an effort to control hemolysis. This can be followed by a lifetime of extreme fatigue that limits participation in normal day to day activities. Iron overload is another potential complication. It can be found even in patients with no history of regular transfusions. Iron overload is associated with liver fibrosis, endocrinological abnormalities and cardiac events. Our understanding of pyruvate kinase deficiency continues to evolve with the help of the ongoing natural history study run by Boston Children’s Hospital. This study has enrolled over 200 patients and we expect to present new data in the second half of the year. Our first PKR activator, AG-348, is enrolling in a global Phase 2 trial in adult transfusion-independent patients with pyruvate kinase deficiency. This trial is known as DRIVE PK. DRIVE PK is an open-label, randomized study that includes two arms of up to 25 patients each, receiving 50 or 300 milligrams twice daily for at least six months. Transfusion-independent men and women with a hemoglobin of less than 12 milligrams 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. At EHA we will be presenting initial data on the first 15 to 20 patients in this ongoing trial. Our goal for this presentation is to begin to address some of the key objectives we’ve laid out for this first-in-patient study – one, understanding the safety and tolerability of AG-348 with long-term dosing; two, confirming exposure of the drug and activation of the PKR pathway in patients; three, assessing changes in hemoglobin levels and other hematologic parameters; four, early assessment of the correlation between clinical effects and mutational background; and, finally, evaluating routine clinical and laboratory safety findings including sex hormones to understand the potential clinical significance of AG-348 aromatase inhibition. As a reminder, patients in this ongoing trial will have varying amounts of follow-up at the time of the EHA presentation. In the separate abstract, preclinical data for AG-348 in beta thalassemia will also be shown at EHA. , we will be presenting preclinical and clinical data from three abstracts at EHA including the Phase 1 single-ascending dose and multiple-ascending dose trials. Since this trial is still ongoing, we plan to present data from the completed single-ascending dose study in addition to some of the multiple-ascending dose data. As a reminder, AG-519 exhibits no preclinical aromatase inhibition. At EHA the initial data from both DRIVE PK and AG-519 will be presented and we look forward to continuing to study the impact that our PKR activators could have on people with pyruvate kinase deficiency. The activation of wild type and mutant pyruvate kinase enzyme by our PKR activators has the potential to help patients with a broad range of hemolytic anemias beyond pyruvate kinase deficiency. We will continue to explore opportunities that expand the utility of these molecules. Moving to our IDH inhibitors, we remain committed to a development strategy of speed and breadth for AML and other hematologic malignancies as we work to give patients who are waiting for more effective and tolerable therapies’ better options. In relapsed/refractory AML we are conducting a set of trials that include two important expansion cohorts for AG-221 and AG-120. And as David mentioned today we announce that AG-221, the expansion cohorts, has completed enrollment. Our Phase 3 identified study for AG-221 in relapsed/refractory AML is ongoing with additional frontline and combination studies for both molecules planned or already underway. In March Celgene initiated a Phase 1-2 frontline combination study of AG-221 or AG-120 with Vidaza in AML. Together with our ongoing Phase 1B frontline combination study of AG-221 or AG-120 with standard of care, intensive chemotherapy, known as 7+3, these trials position us for broad clinical development of our IDH inhibitor in newly diagnosed patients. With our drug’s unique mechanism of action we are looking to change the treatment paradigm for IDH mutant AML, using a long-term differentiation therapy that is distinct from the end targeted effects of chemotherapy, which also carry considerable toxicity. We have now reported on over 300 people with IDH mutant-positive hematologic malignancies treated with AG-221 or AG-120 in our clinical trials. The single-agent activity for these investigational medicines in AML is compelling, based on the overall response rates, durability and the favorable safety profile seen with once-daily oral dosing. Developing our IDH inhibitors in solid tumors remains a priority based on the potential to help a large number of patients in the early encouraging Phase 1 dose escalation data we presented last year. This is a new area of biology with our drug’s unique mechanism of action but one we are committed to exploring further with our ongoing and planned trials. The data we presented at last year’s ACR-NCI-EORTC meeting demonstrated that AG-120 is well-tolerated in a broad set of solid tumor and glioma patients. It demonstrated encouraging signs of prolonged stable disease in low-grade glioma as well as chondrosarcoma in intrahepatic cholangiocarcinoma and demonstrated evidence that 2HG was lower in the brain for some glioma patients, as measured by magnetic resonance spectroscopy. These observations were paired with signs that tumor volume was decreasing, based on MRI volumetric assessments in some glioma patients. And these findings helped shape our ongoing expansion phase, which includes four 25-patient cohorts in low-grade glioma with at least six months of prior stand [ph] second line cholangiocarcinoma, high-grade metastatic chondrosarcoma and a final cohort of solid tumor patients with IDH1 mutations not eligible for cohorts one through three. We remain on track to present data from our AG-120 expansion study in low-grade glioma and initiate a randomized Phase 2 study in IDH1 mutant positive cholangiocarcinoma in the second half of 2016. For AG-881, which is a brain penetrate pan-IDH mutant inhibitor, we are enrolling Phase 1 dose escalation and expansion trials in both heme malignancies and solid tumors. We will keep you updated as these trials progress. 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 late stage clinical development, expand our research pipeline and build global, sustainable multiproduct company. Moving to the financial results for the first quarter of 2016, our cash, cash equivalents and marketable securities as of March 31, 2016 are $356 million compared to $376 million as of December 31, 2015. The decrease was driven by cash used to fund operating activities of $54.1 million, which was offset by funding of $35.1 million received from Celgene during the first quarter. Collaboration revenue was $31.3 million for the quarter ended March 31, 2016, compared to $34.2 million for the same period in 2015. In January 2016 we recognized the $25 million milestone payment for the first patient dosed in the Phase 3 IDHENTIFY study of AG-221. Research and development expenses were $44 million for the quarter ended March 31, 2016, compared to $32.4 million for the same period in 2015. The increase was mainly due to increased investment in our lead investigational medicines as they advanced into late stage development along with early development costs for both AG-881 and AG-519. Under our collaboration agreements, Celgene is responsible for all development costs for AG-221 and approximately 50% of the development costs for AG-120 and AG-881. General and administration expenses were $10.8 million for the quarter ended March 31, 2016, compared to $7 million for the same period in 2015. The increase was largely due to increased headcount and other professional expenses to support growing operations. And with that I will turn the call back over to David.

Thanks, Glenn. Looking at the milestones ahead of us, 2016 is set up to be a busy and exciting year. We’re off to a strong start as we continue to develop medicines that have the potential to impact patients’ lives in a profound way. As Agios continues to grow, we are also mindful of responsibly managing the business by investing in groundbreaking science with the highest probability of success and hiring great people. Keeping the patient at the center of everything we do ultimately creates value for everyone in the Agios community. As always, I want to thank all Agios employees for their dedication and great work and all the patients who participated in our clinical trials. I want to thank all of you for your continued support, and we will see you at EHA. And with that I will now turn the call over to the operator for questions.

Thank you. [Operator Instructions] Our first question comes from Kennen MacKay from Credit Suisse. Your line is open.

So it sounds like maybe we are going to see actually a few more PKD patients at EHA than we were really expecting with the 15 to 20. Has that trial been enrolling maybe a little bit faster than you had anticipated? And could you also maybe comment on what kind of durations we might see at EHA?

I’m going to ask Chris to, obviously, handle that question for you.

Enrollment for DRIVE PK is on track and the trial is open. It’s a global study, and so what the presentation will include will be patients who are at varying durations of treatment. As I stated in my remarks, it’s a randomized trial where patients get two different doses of drug and they could be treated for up to six months and then there’s an extension phase. So, given that the study is still open, you will see varying durations of follow-up. And we will try to be specific in terms of where that’s pertinent in presenting the data.

Got you. Okay, thank you. And then maybe just one quick follow-up for David – I was wondering if you could just help us understand what kind of options are on the table as you and Celgene are negotiating the collaboration agreement. Could we see another equity investment from Celgene here?

So remember that this extension is the wrapping up of the 2010 research agreement. And so, what this deals with are the handful of assets that were not early enough to come back to Agios free, totally owned, or late enough for Celgene to have an option to license. And that’s why we are looking at whether or not there’s an alternate mechanism that may be better than the one that was specified in the original 2010 contract. So that’s really only what this deals with. And obviously, we will update you as soon as that is available. We are working with them on that now.

Great. Thanks for taking my questions and look forward to the data at EHA.

Next we have a question from the line of Eric Schmidt from Cowen and Company.

David, I see in the press release that you refer to the cohort expansion study for AG-221 in advanced AML as crucial to bringing this drug potentially to patients. Can we interpret crucial as necessary and sufficient?

We’ve always said that these expansion cohorts are very important data for patients, for physicians and for us and, potentially, for regulators. But our goal obviously is to do all the trials that we need to bring as quickly as we can these molecules to the market. I can’t specify whether one aspect is more crucial than another. Obviously, the Phase 3 studies that are either initiated or planned are going to be really, really important. But we do think this data is very important, as we’ve said in the past.

Okay. In terms of the EHA presentation, I know the abstracts are coming out on the 19th. Will they have substantive data? And do you plan to call or some sort of a press release around those abstracts?

We always do what we call a curtain raiser and let people know where the abstracts are going to be. Obviously, given the proximity of the abstract posting and the meeting itself to where we are today, we can’t really comment on a lot of specifics that may be in the abstracts, so – that we expect to present. But as you know, these abstracts are always written well in advance. And so anything that is in the abstract will certainly be updated at the actual meeting.

So we shouldn’t expect 15 to 20 patients in the abstract?

I think that’s a fair assumption.

Okay. And then last question from me, just in terms, again, of the PKD development plan – have you had enough discussion with the FDA to have a sense of what might be required in a primary endpoint pivotal trial?

Chris?

We don’t comment on our specific interactions with FDA. And at this point the important pieces are to analyze that first data coming out from DRIVE PK with AG-348, look at our data from AG-519, understand do we have proof of clinical concept with AG-348 in patients with the disease and what it looks like with six months’ dosing. And once we get a really good luck and get a handle on that overall picture, then we can start thinking about how we might take the next steps in development. But it’s really too early to get into details around what would be approvable endpoints in registration trials.

Eric, just to add on that, you’ve heard me say this in the past, that we do have some precedent to work with. And that’s obviously the work that others have done in getting drugs approved for chronic hemolytic anemias. And certainly those will be important in all the ongoing discussions we have had with the agencies.

Okay. Chris, in terms of your hope to get some proof of clinical concept here from the DRIVE PK study, should we be looking at the hemoglobin races that you alluded to in the past of one gram to two gram per deciliter magnitude improvement? Or is there something maybe more on these early clinical effects that you mentioned, as potentially mentioned to various genotypes that we should also be looking for?

Yes, Eric. We think all of that data is potentially important. Those are the things you mentioned, changes in hemoglobin and genotype, outcome type relationships are a really important component. I want to emphasize the primary objective of AG-348 as well, which is to understand the safety and tolerability of the drug. The AG-348 volunteer data that we presented last year at EHA was 14 days of dosing. Now we are getting it to six months. And so that’s a really key part. So as we look at how patients tolerate the drug versus what types of changes we see from an efficacy perspective will be really important in terms of the equation. Overall, one of the things we have been stating when people have been asking us what could be associated with clinical benefit, we tend to talk about the benchmarks of 1 to 2 gram increase in hemoglobin because that’s the type of increase you see when patients get transfused with red blood cells in a standard approach. And if you think about patients with pyruvate kinase deficiency who undergo splenectomy, those who do respond to splenectomy have about 1 to 2 gram increase in hemoglobin. And when you talk to clinicians broadly about – and patients, for that matter – do they feel better after they get transfusions and their hemoglobin goes up by 1 to 2 grams, they tend to say, yes, I feel a little better. So we think that’s a very reasonable benchmark in terms of assessing one of the major efficacy outcomes from DRIVE PK.

Helpful, thank you.

Next we have a question from Yatin Suneja from SunTrust Robinson.

Just following up on Eric’s question on 221, could you maybe talk about what sort of efficacy profile might be appealing to the FDA to get an accelerated approval if you go that way? We know Myotar [ph] was approved on an ORR of around 25%-28%. So is that a good benchmark? And I have a follow-up.

As you know, we really can’t give you out any specific regulatory guidance around the discussions we’ve had, nor have we guided towards accelerated approval. What we’ve always said is that, as Chris mentioned on the call, that we believe the data that we’ve seen to date in over 300 patients with largely relapsed/refractory AML with both 221 and 120 are compelling, given both the safety profile and the efficacy we’ve seen and the unique mechanism of action. This is not chemotherapy. That being said, it’s really hard to benchmark because, as you know, in the last 30 years there has really only been one or two drugs that have been approved in AML. So we are obviously very pleased with the ongoing discussions we’ve had on both sides of the Pond for regulatory agencies but really can’t get into any details about what a benchmark would look like, since every drug is really a little bit different.

So that’s helpful. And then on the PKD programs, what sort of incremental data you would still need before you make a decision to take one of these programs further in clinical development? Do you see a scenario where you might take both of them? Could you maybe just help us understand that?

Ladies and gentlemen, please stand by. The conference will begin again momentarily. You guys are back into the main conference room.

Okay.

Can you connect us with the Q&A?

We are using the cell phone now.

Mr. Suneja, are you still there? Our next question comes from Anupam Rama from JPMorgan.

Congrats on the completion of enrollment of the fifth cohort for 221. Maybe can you talk to us a little bit about the speed of identification of patient enrollment here? And have your views of the prevalence of IDH mutations changed, given the pace of enrollment? And when could we see some data? Thanks.

Yes. First of all, I’m going to apologize to the folks on the phone. We’ve had some technical difficulties with the phone lines, so hopefully you can hear me okay. Look, we are really pleased that the 221 cohort finished up even earlier than expected. 120 is on track. I don’t think we have any updated guidance on the prevalence of the mutation. It has been holding pretty much on track and I wouldn’t interpret anything from that. So we are just really pleased with the way things are going. Obviously, 221 finished a little bit earlier and 120 this on track for by the end of this year.

Great, thanks so much for taking our questions.

Then there’s a questions from Terence Flynn from Goldman Sachs.

This is Samir Siddhanti on for Terence. In the press release you noted that in the second half of 2016, you plan to outline the clinical development plans for your PKR activators in beta thal. So can we assume that you will definitively forward here and you are waiting to make a decision on either to advance 348 or 519? Or are you waiting for any other inputs to make this decision?

As you know, we were obviously pleased when Scott presented preclinical data originally for the efficacy in the beta thal model at our R&D day last year. And that’s what allowed us to really consider about how to move either of these molecules ahead in beta thal. And I think at this point we remain committed to our guidance that by the end of the year we will give you an update of how we’re thinking about beta thal. But that guidance that had a commitment to start a clinical trial; it was really around giving you how we think about approaching the disease.

Got it, thanks. And just one follow-up for Glenn – on your last call you mentioned that your cash position should give you runway until late 2017. Are there any changes to that guidance or is that still the expectation?

Yes, it’s a great question. So we are not updating the cash guidance today, so that remains in place.

Great, thank you so much.

Our next question is from Seamus Fernandez from Leerink Partners. You may go ahead sir.

This is Marc [ph] in for Seamus this morning. Congratulations on the progress this quarter. So one more on your Phase 2 AG-221 single-arm expansion cohort in relapsed refractory. I think you said you expect to complete the cohort by year end. Am I correct in assuming that this timeframe will allow you to collect a mature OS data set here? And do you plan to wait to have mature OS data before talking to regulators about potentially registration enabling with this data set? And then, second, given the recent approval of Venclexta, venetoclax in CLL and the fact that this agent has clear activity in AML, do you have any plans for testing a combination of one of your IDH inhibitors with venetoclax clinically at any point? Thank you.

Yes. So with regards to the first part of your question, around the completion of the enrollment in AG-221, and our overall goal of completing enrollment to the AG-120 by the end of this year, that would mean that the last patient coming in and certainly overall survival needs to be followed in these patients for some period of time. So we haven’t provided that level of detail in terms of survival follow-up. From the regulatory perspective we don’t comment on our interaction, specific interactions we have with the authorities except to state that when we have important data to discuss with them we bring it forward. And all of the data from efficacy, safety, etc., in terms of thinking what the regulatory pathways are for moving our drugs to getting them to patients as quickly as possible. With regards to venetoclax and other new agents and standard of care agents, both in terms of combining them with our drugs, it’s something that we are certainly thinking about. And I think there’s clear evidence of how we are developing our IDH inhibitors in AML as evidenced by these first combination studies that we’ve done with seven and three [ph] patients who are eligible for intensive chemotherapy and for Vidaza for those who are not. So the new drugs are certainly of interest to us. We just haven’t gotten to a point where we are ready to give formal and detailed statements around what our next development is.

Great, thanks.

[Operator Instructions] Our next question comes from Debjit Chattopadhyay, from Janney.

First, on AG-881, should we assume these patients have already experienced disease progression on prior AG-120 or 221? And in that case, could you explain the mechanistic rationale, why inhibiting IDH after primary progression would still be effective?

So one of the things that we are looking to do in the AG-881 Phase 1 trials is identify the safety, tolerability and pharmacokinetics. Patients could have had stable disease or progressive disease on an IDH inhibitor in order to get on the trial. And so there’s a possibility that they might benefit from the drug, given some of the different profile. The main objective for AG-881 is to demonstrate efficacy and safety profile in this setting.

Then on AG-120 in the frontline setting, the Phase 3 that you alluded to, are these patients going to be ineligible for induction chemo? Or how should we handicap the expectations on overall survival?

Sorry, which trial?

The AG-120, Phase 3.

So – for patients who – what has happened to them, should they have a response – this is an important component of Phase 3 trials in AML, in general. In patients who have an inadequate response to the investigational agent to the control on – and this is true for identifiers – they can certainly go on to transplant. If you look at historically how often that happens in relapsed/refractory trials, is pretty rare.

And I’ll just remind you that we have not given out the trial design yet for that Phase 3, and we will do that as we get closer.

Great. And back to the question regarding the IDH levels – you have noted in the past that in your ongoing study of the expansion cohort studies, patients have had disease progression but the IDH levels have remained suppressed. What does that imply as you move into the frontline settings?

I don’t think you can really draw much from that. I think what you are – may be referring to, what we are very pleased with was the data we presented last year that in the handful of patients who have progressed on either 120 or 221 their 2HG level, which, as you know, is made by the tumor, is still suppressed. And that tells us that, although the patient has progressed, it’s not because the drug no longer binds the target, which is a common mechanism of resistance in oncology and is clearly not the case here. That in and of itself is very important data. That does open the possibility, and we’ve talked about this before, of this content of treatment in multiple lines, that you essentially theoretically always want to be suppressing this clone. And so if you are starting in the frontline setting, even if the patient would progress at some point, because we are still binding to the target you would want to potentially keep that patient on the drug and add something else. Now, we will need to prove that with clinical trials. And that’s one of the things that’s planned for the future.

And then, one last question – on the 348 and 519 program, the translation from transfusion-independent to transfusion-dependent – what would you think is the threshold for hemoglobin increase? Is that the same 1 to 2 grams per deciliter?

Yes, interesting question. And I just want to point out that for DRIVE PK that definition of transfusion independence was put in there so that we could have individuals, patients who came on the trial, who had not had a prior transfusion so that when we did some of our translational and biomarker studies we didn’t have transfused red cells circulating. People are very interested in this distinction between transfusion-dependent and transfusion-independent. But when we talk to both clinicians as well as patients, that distinction isn’t as clear, because some patients really choose not to have transfusions unless their hemoglobin goes really low, for a number of reasons including some justified concerns around iron overload. Suffice it to say that we think that that 1 to 2 gram per deciliter benchmark that we have been talking about applies to patients who are getting transfused on some sort of regular basis as well as patients who are not getting transfusions.

Thanks for the clarification.

And next we go to the line of John Newman from Canaccord. You may go ahead.

I just wondered, on 348 you are studying different genotypes but it seems that you are also doing work understanding the various groups in terms of severity for the disease. And my question is, after you see the results from the upcoming data at EHA, does it make sense to think that, going forward into a potential pivotal study, you could potentially look at a specific population not only with certain genotypes but also in a way that allows you to select for patients within those genotypes that have a given severity so that you could potentially optimize the patient population?

That’s all possible, John. It’s too early to say what exactly we will do because we’ve got to see the data and think it through. We are going to be talking about 15 to 20 patients with varying levels of follow-up. And as you know, there’s a number of mutations, over 200, of the PKR gene that have been described for this disease. And so that’s going to be – we will need to really take a very careful look at that in terms of understanding associations with genotype and outcomes to our PKR activators. So, while that is one interesting way to proceed, it’s just too early to get – to make definitive – for us to make definitive statements of how we will proceed at this time.

Okay, great. And when you also potentially be able to learn a bit from the EHA data in terms of things like fatigue and just how patients may be feeling on the drug, not just the hemoglobin increases but if they are just starting to feel a bit better?

Yes. Remember that this is a first presentation. And we are so close to the presentation that we have really got to be cautious not to try and delve too much into what you are likely to see or not. Remember, this is a first presentation of an ongoing study. And you are likely to see – we’re certainly collecting a lot of that data. But I’m just not clear yet whether or not we will have all of that data available for you or if that will be a subsequent presentation. So this is just the first presentation.

Okay, great. Thanks, guys.

Next we have a question from the line of Eric Schmidt from Cowen and Company.

Just a quick follow-up on 221 in the cohort expansion study. Now that that is fully enrolled, can you give us a sense of when you expect data?

So we have not given out guidance yet for any actuality AML data for the remainder of the year. We early in the year set the expectation that because these large expansion cohorts are obviously very important data, as I articulated earlier, that we weren’t going to give out any guidance on when to expect to see data. But it’s likely as the year progresses we will give guidance out about what to expect to see in the second half of the year with respect to 221 and 120 at various meetings. But it’s just a little bit too early at this time.

Thank you.

I am showing no further questions at this time. I would now like to turn the call over to Mr. David Schenkein for any closing remarks.

I just want to thank everybody again for all your ongoing support. If there’s anybody listening, obviously, I want to thank all the patients who participate in our clinical trials and thank all of our Agios employees for all of the great work and all of you for your support. Look forward to seeing you at EHA and thank you very much.

Ladies and gentlemen, thank you for participating in today’s conference. This concludes the program. You may all disconnect. Everyone have a great day.