Renee Leck - Senior Manager, Investor Relations for Agios David Schenkein - CEO Chris Bowden - Chief Medical Officer Andrew Hirsch - Chief Financial Officer

Eric Schmidt - Cowen and Company Anupam Rama - JPMorgan Michael Schmidt - Leerink Partners

Good morning, and welcome to Agios' Second Quarter 2017 Conference Call. At this time, all participants are in a listen-only mode. There will be a question-and-answer session at the end. Please be advised that this call is being recorded at Agios' request. I would now like to turn the conference over to Renee Leck, Senior Manager, Investor Relations for Agios.

Thanks, Shannon. Good morning everyone and welcome to Agios' second quarter 2017 conference call. You access slides for today’s call by going to the Investors section of our website, agios.com. With me on the call today are Dr. David Schenkein, our Chief Executive Officer, who will review business updates and key milestone for 2017, Dr. Chris Bowden, our Chief Medical Officer, who will provide an update on our clinical development activities and Andrew Hirsch, our Chief Financial Officer, who will summarize Agios second quarter 2017 financial results. Before we begin, I’d like to remind everyone that statements we make on this call will include forward-looking statements. Actual results and results could differ materially from those expressed or implied by any forward-looking statements as a result of various risks, uncertainties and other factors, including those set forth in the Risk Factors section of our most recent Annual Report on Form 10-K filed with the SEC and any other filings that we may make with the SEC. In addition, any forward-looking statements made on this call represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. We specifically disclaim any obligation to update or revise any forward-looking statements. With that, I'll turn the call over to David.

Thanks, Renee. Good morning everybody, and thanks for joining us today. We've had a tremendous first half of the year across the business and today I'd like to start by highlighting the recent FDA approval of our first precision medicine. As you know, last week IDHIFA was granted approval for patients with relapse refractory AML and an IVH-2 mutation. This approval is significant for several reasons. The FDA granted IDHIFA full approval given the clear demonstration of clinical benefit. This approach validates our precision medicine approach. IDHIFA went from the lab to U.S. approval in less than eight years against a target we discovered with a compound we created in-house on clinical data from a single arm Phase 1, 2 trial. Additionally, our first approvable demonstrates our ability to translate our expertise in cellular metabolism to important medicines for patients. Before I continue, let me thank all of the Agios employees, our colleagues at Celgene, the team at the FDA and all the patients and their doctors who participated in our clinical trials that made this achievement possible. The most important impact of this approval is that IDHIFA is now available to patients with an IVH-2 mutation who desperately need new treatment options. To me, as haematologist, this means patients I've been treating for decades with limited treatment options now have a targeted oral therapy to treat their specific leukemia. That's an incredible transformation in the AML treatment paradigm. Our hope is that IDHIFA will not only help patients who need it today, but also serve as a foundational shift in treating this devastating disease with the precision medicine. IDHIFA will hopefully be the first of many new medicines that we will deliver for patients. Celgene who is the commercial lead for IDHIFA has been a terrific partner throughout this process since we signed our original partnership agreement in 2010. The Agios sales force and medical science liaison’s are currently in the field alongside their Celgene colleagues. We'd like to thank Celgene for ensuring that IDHIFA was available on the same day as approval. Chris will speak to the recent progress with our wholly owned IVH-1 mutant inhibitor ivosidenib, which will follow a similar regulatory strategy. Now, turning to PK deficiency program. We have completed global regulatory discussions and are on track to initiate two pivotal trials for AG-348 in the first half of 2018. One trial will be conducted in non-transfusion dependent patients and one in patients who are regularly transfused. Pivotal development of AG-348 is an important next step for our PK deficiency program as we work to deliver the first potential disease altering therapy for this serious disease. Chris will walk you through key aspects of both clinical trials. Turning to our research engine. We are on track to submit an IND AG-270 for potential treatment of MTAP-deleted tumors by the end of this year. This will be the sixth IND to come from the Agios research labs since they opened in 2009. We also continue to invest in the research engine that produced IDHIFA and our robots precision medicine pipeline. This is an exciting time for Agios as we celebrate our first product approval and now turn our attention to developing the next truly important medicines for patients. I'll now turn it over to Chris to discuss our clinical activities.

Thanks, David. I'll start with our recent progress in pyruvate kinase deficiency and then I will move to our IDH programs. Through our work with DRIVE PK in the Natural History Studies we have learned a great deal about pyruvate kinase deficiency as a disease and the potential benefit of AG-348 for patient. These learning’s coupled with input we have gathered from regulators, disease experts and patients have shaped to design two global pivotal trials to evaluate AG-348 in adults with a pyruvate kinase deficiency. I will start by reviewing the design for the trial in non-transfusion dependent patients. This is a randomized placebo controlled trial with a 1 to 1 randomization that will enrol approximately 80 to 100 patients. We have set the hemoglobin eligibility in this trial at 10 grams per deciliter or lower to clearly demonstrate the efficacy of AG-348 in patients with more severe anemia. Based on learning from DRIVE PK, we will enrol patients with a higher likelihood of response based on their genotype. For that reason, patients with two non- missense mutations and those homozygous for the R479H mutation will not be eligible. R479H is a missense mutation and in DRIVE PK none of the five patients who are homozygous for this mutation respond. Approximately 80% of patients with pyruvate kinase deficiency have at least one missense mutation according to data published with the Natural History Study. In order to identify their optimal does, all patience will start with a three month dose titration phase, followed by three months on their optimal dose. Patients who started 5 milligrams of AG-348 or placebo twice daily and will have the flexibility to titrate up to 20 milligrams or 50 milligrams twice daily to find their optimal dose. At month six patients will be un-blinded for analysis of the primary endpoint, which will be the proportion of patients who achieve at least a one 1.5 gram per deciliter increase in hemoglobin sustained over multiple visits. After six months patients on placebo will be able to cross over to receive AG-348 in an extension period. The randomized crossover trial design enables us to accomplish three main goals, one, to demonstrate a significant treatment effective AG-348 on the primary endpoint of hemoglobin increase. Two, to clearly delineate the safety of AG-348 versus a placebo control, and finally, to utilize a patient reported outcome tool developed specifically for pyruvate kinase deficiency. This tool will measure the effective treatment with AG-348 on disease symptoms and their impact on patients lives compared to placebo. So the minority of patients who are regularly transfused, we plan to initiate a pivotal single arm trial of approximately 20 adult patients who have received a minimum of six transfusions over a one year period. This trial will use the same genotype eligibility criteria as a non-transfusion dependent trial and will also have the same dose titration phase. The primary endpoint of the study will be reduction in transfusion burden over a six month period compared to the patient's historical transfusion record. We are now working on global operational preparations and patient recruitment for both studies to initiate in the first half of 2018. The DRIVE PK study continues to be a valuable source of data and we plan to present data on all 52 patients to the American Society of Hematology annual meeting in December. Now let me turn to our IDH programs. Utilizing an adaptive trial design idea, IDHIFA was approved in less than four years from entering the clinic on the basis of a single arm Phase 1, 2 trial. This is a compelling proof point for our speed and breadth strategy in AML On the yields of disapproval, our NDA team is incorporating learning’s from the IDHIFA process into our ivosidenib submission which is on track for the end of the year. We submitted data from the ivosidenib Phase 1 trial that makes up the core of our NDA package to ASH for presentation in December. This will also be the first time we present data from the dose expansion cohorts. Beyond relapse/refractory AML we continue to work to secure a set of labels in the frontline setting. In the second quarter, we initiated AGILE, our Phase 3 study combining ivosidenib and VIDAZA in newly diagnosed AML patients with an IDH1 mutation who are not candidates for intensive chemotherapy. AGILE was a global study set to enrol approximately 400 patients with a primary endpoint of overall survival. We expect to complete enrolment in 2021. Early data from the Phase 1 trial combining 7+3 with ivosidenib or IDHIFA have been submitted for presentation at ASH. We expect the data to focus primarily on safety and tolerability with a preliminary look at efficacy. In AML, our IDH inhibitors act by releasing the block on cellular differentiation. For our work in solid tumors, we are continuing our efforts to understand how this mechanism could translate to clinical benefit for patients with a variety of tumor types. Thus far, we are encouraged by the level of disease control seen in our Phase 1 study with ivosidenib and at ASCO in June we presented the first data from the Phase 1 expansion cohort and advanced cholangiocarcinoma. Cholangiocarcinoma is a devastating disease where we believe we can have a meaningful impact changing tumor biology and delaying tumor growth with a targeted well tolerated oral medicine. There are few affected and no approved therapies in cholangiocarcinoma and a medium progression free survival in the second line setting is short. Data at ASCO demonstrated durable stable disease signal consistent with ivosidenib’s mechanism of action and a highly encouraging first look at Landmark progression free survival. Ivosidenib continues to be well tolerated with a favourable safety profile. ClarIDHy, our Phase 3 trial and its indication continues to open new sites in the US, Europe and Asia. We expect to complete enrolment in 2019 to support global registration. I'm now going to hand the call over to Andrew to cover our financials.

Thanks, Chris. I'll start by summarizing our second quarter financial results, which you can find in the press release issued this morning. More detail will be included in our 10-Q filing later today. For the second quarter of 2017 we recognized approximately $11 million of collaboration revenue, an increase of approximately $4 million compared to the second quarter of 2016. This year-over-year increase was primarily due to the achievement of deliverables under the Celgene agreement for AG-270, our program focused MTAP-deleted cancers and our metabolic immuno-oncology research efforts. In addition, in the second quarter we recognized approximately $1 million of reimbursement by Celgene for the Agios US co-commercialization effort for IDHIFA. The reimbursement we received from Celgene for IDHIFA commercialization efforts is included in the collaboration revenue line, and the amounts will be broken out in the collaboration agreement section of our SEC filings going forward. Research and development expense during the second quarter of 2017 was approximately $80 million compared to approximately $51 million for the same period in 2016. The growth in R&D expense was primarily driven by increased costs related to the ivosidenib program. There were three main drivers of this increase. NDA submission costs, including the manufacturing of our validation lots, clinical trial activity for the Phase 3 trial AGILE and ClarIDHy studies and the fact that Celgene no longer funds 50% of the program which they did through August 2016. R&D expense also increased compared to the second quarter of 2016 as a result of preparations to initiate the 348 pivotal program in the first half of 2018 and the $3 million upfront payment as part of the Aurigene license agreement signed during the second quarter. General and administrative expenses were approximately $60 million for the second quarter of 2017, an increase of $3 million from 2016, driven by increased headcount and other professional expenses to support our growing commercial infrastructure to the launch of IDHIFA and potential launch of ivosidenib in 2018. Turning to our cash position and runway guidance. We ended the second quarter with cash, cash equivalents and marketable securities of approximately $716 million. In our press release this morning we reiterated our cash guidance with our current runway through at least the end of 2019. Before I close, I would like to note that with the IDHIFA approval last week, we will begin to record royalty revenue as a percentage of net IDHIFA sales. As a reminder, our royalty percentage is low double-digits to mid-teens tiered based on sales levels. And at this point we don’t plan on providing guidance on this line item. With that, I'll turn it over to David to close.

Thanks, Andrew. We've proven our ability to discover novel biology and translate those discoveries into precision medicines in areas of high unmet need. IDHIFA is just a start as we expect to launch ivosidenib in 2018, move AG-348 into pivotal trials, submit a sixth IND for MTAP and continue to fund R&D to support our ability to do this again and again. I want to thank you for your support and hope you enjoy the rest of your summer. And with that, I'll turn the call back over to the operator to take your questions.

Thank you. [Operator Instructions] Our first question comes from Eric Schmidt with Cowen and Company. You may begin.

Thanks. Congrats to the Agios team for all the progress and especially approval of IDHIFA. Maybe for Chris on AG-348 non-transfusion dependent patient trial, just a couple of other details, I think you mentioned that the primary analysis at six months you need to achieve a 1.5 gram per deciliter increase in hemoglobin over multiple visits. Could you just provide a little more color there what multiple means?

Eric. This is David. Thanks for the question. I'm going to turn it over to Chris to go through that with you.

Hey, Eric. Chris here. So you – I just want to get a little – I’ll answer the question from two angles, you started with transfusing dependent and then…

I'm sorry…

You moved in some details around MTD. So let me start with - go with the MTD. So that trial is designed as the primary endpoint which has demonstrated an increase in hemoglobin at 1.5 grams per deciliter. And that will be measured at the six month time period from when patients get randomized to either drug or placebo. We put that trial together based on all the data we've been deriving from DRIVE PK, as well as in my remarks and talked about interacting with regulators, doctors have been working with us, as well as patients to put this study together. So just a real high level to run through it, patients are randomized to 348 versus placebo. They were on active drug or placebo for six months. That the primary endpoint is right out at that point at which time patients get un-blinded and those on placebo can crossover and move into an extension period in patients who are on 348 and who are responding and doing well and also continuing the extension phase.

And Eric, this is David. Just one - you know you were asking about how many visits did they have to have 1.5, we put that language in there to make sure that anybody who's got a blip up, which is uncommon, but does can occur doesn't get counted. We haven't given out some of those gory details yet, we will as the protocol gets ready to start because those are all being finalized now. But it will be on more than one visit to make sure it really captures patients who have a sustained response, which as you know from the DRIVE PK when you have a response it typically is very sustained and doesn't wobble around.

Got it. Thanks. And is the PRO a formal secondary endpoint in the trial?

Yes. We've been developing a tool and we've been in lots of contact with regulatory agencies to get feedback back and forth on that. So that will be a formal endpoint. We think that's going to be important in terms of supporting the additional clinical benefit in patients who respond.

Thanks. Good luck getting that going.

Thanks, Eric.

Thank you. Our next question comes from Anupam Rama with JPMorgan. You may begin.

Thanks for taking the question. On the back of the IDHIFA approval, is the expectation that ivosidenib would also be similarly eligible for a full approval. And is that something you guys will specifically request as part of the NDA submission? And then may be a quick on AG-88, the preclinical data are supposed to be presented at the triple meeting. What should we be looking for in that data set and when can we expect some clinical data from the program? Thanks so much.

Yes. Thanks, Anupam. I'll take the first one and Chris will take the 881 on. So on the ivosidenib it's obviously too early for us to comment on the regulatory interatction. Obviously we were very pleased and gratified along with Celgene to receive full regulatory approval. Quite unusual based on a Phase 1, 2 clinical trial and it really demonstrates the true clinical benefit that patients do achieve with IDHIFA based not only on durable CRs, the transfusion independence and other factors as well. We hope that we see a similar approach from the agency on ivosidenib because as you remember those trials were designed in parallel and have a lot of similarities in terms of both patient population and the input and data that we collected. But it's just too early for us to comment on how we're going to approach them. Other than we do plan to take the same regulatory strategy and we'll give you updates as we go forward. We remain on track to submit that NDA at the end of this year. Let me turn it over to Chris to talk about 881.

Hey, Anupam. How are you doing? We - for the submissions for the preclinical data we’ve just been doing a lot of work with 881 in some of our preclinical models and to provide some additional information on the preclinical profile one of the molecule. So that - that's what will be published at the triple meeting. As far as 881 goes in the clinic, we did state in our press release that we completed the enrolment of the dose escalation phase of the Phase 1 study of 881 and IDH-1 mutant positive glioma. And so now we are working with our partner Celgene in terms of looking at the data from a PK safety perspective and pulling together what the next steps are going to be in terms of bringing that molecule forward. I don't have a clear picture yet of when we will publish some data, clinical data on that, but hope to update you soon on that. And then the other piece that we put in the press releases, we're going to update that cohort data that we showed at the SNO meeting last year for AG-120. So we're looking forward to that. And that pulls together this whole picture in this disease where we have two molecules in development. We see a high unmet need and our decisions about what the next steps are with either both molecules that will really be data driven.

Great. Thanks so much for taking the questions.

Thanks, Anupam.

Thank you. Our next question comes from Michael Schmidt with Leerink Partners. You may begin.

Hey, guys. Good morning and thanks for taking my questions. I had one regarding the IDHIFA label, I thought it was very interesting to see the recommended treatment they’re raising, already six months in patients without disease progressing and I was wondering what percentage of patients you expect to fall into that category? And the I have a follow up/

Yeah. Thanks Michael. This is David. I’ll turn it over to Chris.

Well, the reason why that language was put in is because if you look at the time to complete remission or CR/CRh that generally occurs in a two to three month timeframe. The median time to their first response is 1.9 months and the median time of the best response is CR/CRh is 3.7 months and there's also language in the label that talks about patients who achieve the best response of CR/CRh, 85% or so did so within six months of initiating IDHIFA. So the direction there is for in the absence of florid progression of disease to give the IDHIFA its best chance of working in patients. How many do we think will be actually on the drug for that long? Is not an easy question to answer? But you can bring into play response rates and how long it takes you to declare a response to get some sense of what that will look like. But the direction is much more important in terms of talking to physicians and healthcare providers about how long should I keep treating with IDHIFA in the absence of florid progression. And this language says you should hang in there for at least six months if the patient's doing reasonably well.

Yeah, and Michael I think the other thing that it reflects and that's why we were so pleased with this language is it clearly reflects the agency's recognition of the unique mechanism of action here because you don't typically see this with a cytotoxic chemotherapy, but with an agent that works for differentiation you want to give the drug the ability to have its best response.

Yeah. And the question regarding potential development in frontline treatment of AML, we obviously already initiated the AGILE study in elderly patients, wondering what next steps could be in terms of addressing the younger patient population in combination with 7+3 and what the different considerations could be there in terms of trial design? Thanks.

Well, we've got an ongoing Phase 1 study with 7 and 3 that's built to accept patients with either an IDH-1 mutation in which case they get 7 and 3 plus ivosidenib, and if they were in IDH-2 mutation they get IDHIFA. So we're collaborating with Celgene on that trial and that sets up nicely for the 20% of patients with a AML diagnosis who are going to have an IDH mutation. And we're going to provide - you'll get a look at that data from a safety and some preliminary efficacy data at the ASH meeting. So your question is a very interesting one about what the next steps would be. Clearly, one can think about a randomized trial which is a very simple answer 7 and 3 plus or minus the requisite IDH inhibitor. The end points are numerous and they range from overall survival which has been a pretty standard endpoint unlike they wanted to accomplish and then recently we're starting to see some interest in event free survival as an end point in the frontline AML study. There's a lot of interest in molecular response, so where we’re going to end up with this remains to be seen. But it’s an area of great interest for us and we're starting to get the data together that suggests that we're going to be in a place to do that.

And remember Michael, this is David here, that in the press release we did mention that we've submitted an abstract to ASH for the first look at the 7 and 3 data and on a previous quarterly call we did mention that we've already passed the safety gate. So we know that it was safe to combine either IDHIFA or ivosidenib with full doses of 7 and 3 and then consolidation and you'll see some of that data at ASH this year hopefully.

Okay. Great. Thanks for the added information. Congrats on the IDHIFA approval from me as well.

Thanks, Michael.

Thank you. Our next question comes from Terence Flynn with Goldman Sachs. You may begin.

Hi. This is Cameron on for Terence. Thank you for taking our question. And got congrats on all the progress. First one, 348, can you just give us any update on plans to address the younger PKD patient population? And then second on 881, did you reach the maximum tolerated dose in Phase 1 and can you provide any color on the safety and tolerability profile there? Thank you.

Thanks, Cameron. I'll take the first one on 348 and paediatrics and have Chris walk you through where we are with 881 on MTD et cetera. So on 348 as you know we've always said that our commitment in pyruvate kinase deficiency is to treat all available patients and obviously like with most diseases we're starting in adults as Chris's outlined. But we do feel committed to try and understand how best to treat children with a serious disorder. Obviously we need to wait to see more data on 348s effect on hormones to see whether there is a path forward with 348. Like all of our drug development programs, we have a robust chemistry back up set of programs and if it's deemed its necessary for us to create a molecule that we – is more appropriate for children because it lacks aromatase binding, we're obviously working on that as well. And so we'll be able to decide as we look through those how to select that, but clearly we have a commitment to treat all patients with pyruvate kinase deficiency. So let me turn it over to Chris to talk about 881.

So a lot of work going on there. And as we pointed out that we completed the dose escalation point. We did not reach MTD and we're exploring a number of different doses there and looking at the PK and the safety profile. And what - I don't want to get in the individual details because we're still looking at that data. But certainly look forward to bring it when we've got it ready and have the critical mass of data to present at a meeting.

Okay. Thank you.

Thank you. Our next question comes from Alethia Young with Credit Suisse. You may begin.

Hi. This is Derrick on for Alethia. Thank you for taking the question. Congrats on the progress for the quarter. I guess a couple of quick ones. First for 348, could you elaborate what was the enrolment situation for PKD [ph] Natural History Study, just want to get a sense of how you know, [indiscernible] go for the pivotal studies? And second, wondering, I know it’s depending on the data, but is it a single arm transfusion dependent fellable [ph] on its own or it’s going to be dependent on the other trial? Thank you.

Yeah. Thanks, Derrick. I’ll handle both of those – those straight forward. So for the enrolment into the Natural History Study, remember that’s not a treatment study, that's a purely short review. So it's certainly less intensive for patients. We are very gratified that over a couple of year period we enrolled over 200 patients and that has now closed for enrolment. I think that tells us there is a growing interest in the PKD community and physicians interested in this disease, remember they've never had anybody try and treat this disease before. I think it's also important to remember that for both the Natural History Study and the DRIVE PK study was a relatively limited number of trial sites that were opened and in the pivotal program we'll have a much higher number of sites around the world. Your second question around regulatory utility of the single arm TD trial independent of the MTD, we obviously can't go into that kind of detail with our regular conversations. I think it's important to recognize that in general the FDA looks at the totality of the data. And so these are two separate trials and as they look at data from – as the trials emerge obviously we'll work with them to understand in different patient populations how to move forward. But it's just - I can't really comment any further on that at this time. But we're very pleased with the regulatory interactions that we've had and very pleased to be moving forward with these two trials to capture all adults with PK deficiency.

Thanks, Maybe I - can I just squeeze one more question. You have dose titration to 50 milligram [ph] I am wondering what is the reason for that?

We are looking at - it in that dose optimization period. The range of doses that patients can be treated is three doses really 5, 20 and 50. And the reason why we’ve capped to 50 is when we looked at the data it would appear that responders are going to be adequately covered, have adequate exposure at a top range of 50 milligrams. And that way we’ll optimize the therapeutic index if you will. So we'll achieve the exposure that we need to achieve in order to capture the responders and not go over that. So that's why we use the term optimal dose.

Okay. Thank you.

Thank you. Our next question comes from Yatin Suneja with SunTrust. You may begin.

Hey, guys. This is David on for Yatin. Congrats on all the progress in the quarter. Separate question on – now that you have approval in US for IDHIFA, maybe could you provide an update on the regulatory strategy in EU? And also I had a question on AG-348 for the non-transfusion dependent trial, the primary endpoint of the trial 1.5 gram for per decilitre hemoglobin, I am curious how you saw at 1.5 as a endpoint as opposed to some other cut off with this due to some reasons or just some type of reasons that you saw? Thanks.

Yeah. Thanks, David. Maybe I’ll handle the first one quickly and then turn it over to Chris to talk about the 348. So we've said previously during the year that in 2017 for both IDHIFA actually and ivosidenib is the year that both Celgene, Agios together and independently depending on the molecule will seek regulatory guidance in Europe to decide whether or not we can potentially file with the existing data packages or whether we need to wait for the Phase 3 used to read out. And so stay tuned as we complete those regulatory interactions we’ll – we and Celgene will let you know where those stand and I'll turn it over to Chris to talk about the primary endpoint selection for the MTD trial.

Thanks, David. So when we were talking about what was an improvement in hemoglobin that we thought could be associated with clinical benefit and DRIVE PK, we talked about a 1 to 2 gram per deciliter increase because that's what's associated with splenectomy and it's in general practice when patients get transfusions they get one to two units of blood which results in a 1 to 2 gram increase and patients generally feel better. So as we looked at the data, we wanted to understand what's the variance in patients who didn't respond, and I'm looking at the data from DRIVE PK, we settled on that 1.5 gram per deciliter cut off because as David alluded to in one of the earlier questions is that occasionally you will see these blips where a patient will go up and they can go up a gram, gram and a half. But in terms of sustained over two or more visits you just don't see that happen. So that's why - that's where we settled with 1.5 grams, we think it will unequivocally show against placebo that 348 and responding patients is resulting in durable responses that are going to result in meaningful clinical benefit.

Great. Thank you so much.

Thank you. I'm showing no further questions at this time. I’d like to turn the call back over David Schenkein for closing remarks.

Yes. I’d like thank everybody for participating today. A very exciting time for us here at Agios and particularly and most importantly for the patients out there who now have a new treatment option with IDHIFA and like to wish everybody a healthy and happy rest of the summer. Thank you very much.

Ladies and gentlemen, this concludes today's conference. Thanks for you participation. Have a wonderful day.