Good morning. My name is Stephanie and I will be your conference operator today. At this time, I'd like to welcome everyone to the Biogen First Quarter 2015 Earnings Conference Call. All lines have been placed on mute to prevent any background noise. After the speakers' remarks, there will be a question-and-answer session. Please limit yourself to one question to allow time for others in queue to ask a question. I'll now like to turn the call over to Mr. Ben Strain, Associate Director, Investor Relations. You may begin your conference.

Thank you and welcome to Biogen's First Quarter 2015 Earnings Conference Call. Before we begin, I encourage everyone to go to the Investor section of biogen.com to find the press release and the related financial tables, including a reconciliation of the non-GAAP financial measures that we'll discuss today. Our GAAP financials are provided in Tables 1 and 2. Table 3 includes a reconciliation of our GAAP to non-GAAP financial results. We believe non-GAAP financial results better represent the ongoing economics of our business and reflect how we manage the business internally. We have also posted slides on the website that follow the discussion related to this call. I would like to point out that we'll be making forward-looking statements which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties and our actual results may differ materially. I encourage everyone to consult our SEC filings for additional detail. On today's call, I'm joined by our Chief Executive Officer, Dr. George Scangos; Dr. Doug Williams, EVP of Research and Development; Tony Kingsley, EVP of Global Commercial Operations; and our CFO, Paul Clancy. Now, I'll turn the call over to George. George A. Scangos, Ph.D. - Chief Executive Officer & Director: Okay. Thank you, Ben, and good morning, everyone, and thanks for joining us today. Biogen had a mixed start to 2015. We made good progress on our pipeline but our commercial results were not as strong as we'd hoped. Although we achieved 20% revenue growth and 55% non-GAAP EPS growth compared to the same quarter last year, we'd expected to do even better. We saw moderating patient uptake of our oral MS therapy TECFIDERA in the U.S. and Germany. And like other companies, we had foreign exchange headwinds. Our MS franchise continued to gain…

Thanks, Doug. Let me start with the MS franchise. We continue to believe that our portfolio of products is a source of strength in the marketplace with the leading oral agent, the leading high-efficacy agent and two well-positioned interferon options. In the U.S., we believe we continue to capture roughly half of all newly-diagnosed and switch patients within our franchise in Q1. As we've said in prior calls, with the launch of TECFIDERA in 2013 in the U.S. and 2014 in Europe, we saw a period where both market growth and switching dynamics were well above historical averages, and TECFIDERA really drove this. And we expected a natural moderation in these rates through 2014 and into 2015. We believe this is occurring as expected, but also believe that the Tech safety (10:45) event in October further dampened market growth and switch rates in Q1. So in this broader market context, TECFIDERA continued to add patients this quarter but at an overall slower rate. In the U.S., our internal market research suggests that physician intent to prescribe may be improving. We believe these data indicate that we are assisting physicians in putting the updated label into context. In Europe, we saw robust uptake in patient capture in the quarter in the U.K. as well as in newly launched markets such as Italy and Spain. In Germany, the product saw similar headwinds as in the U.S., but for Europe as a whole we saw a nice growth in patients in the quarter. Finally, in markets where we have launched PLEGRIDY, we believe the uptake of that product has also dampened TECFIDERA patient growth by taking some interferon switches that could have gone to TECFIDERA. But obviously for Biogen overall, this is a positive and, again, speaks to the strength of our franchise…

Your first question comes from the line of Geoffrey Porges of Bernstein. Your line is open. Geoffrey C. Porges - Sanford C. Bernstein & Co. LLC: Thank you very much for the question, and perhaps we start off with TECFIDERA. You highlighted the case of PML last year in your comments, but of course there was the other case written up though it was with a different form of MS, not TECFIDERA, this year. And first of all, do you think that that will have any impact on the outlook in the future for TECFIDERA? And secondly, I'd just be curious as to what advice you're now giving physicians with respect to patients who are JCV positive. Do you think the case this year alters the sentiment you had after last year's case, where, of course, the patient was heavily pretreated and lymphopenic. Thanks.

Yeah, thanks, Geoff. It's Tony. We just spent much of this week in talking to physicians and understanding what their perspective is. Just to highlight, between the Tech event and the BML (23:21) report late last year, what they're seeing is more hesitancy among patients. We talked about market growth as one of the issues in switch rates. Not clear that the physicians, at least that I talked to which was the anecdotal, had a dramatically different perspective themselves, but they see some hesitance in the conversations that they're having with patients. I think it's a little early to tell what the kind of impression result or perception result from the recent New England Journal articles will be. But, Doug, maybe you want to comment on... Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Sure. Geoff, I think the simple answer to your question is that it's our assessment that there's no real change in the benefit/risk profile in the drug for patients with MS. So, it's pretty much status quo at the moment.

Your next question comes from the line of Mark Schoenebaum of Evercore ISI. Your line is open.

Hey, guys. Thanks so much for taking the question. I just maybe turn the conversation to Alzheimer's, and I'm sure a lot of the other analysts will. But, hey, Doug, I just love – I know you addressed some of this or others did at AAN, but maybe just talk a little bit about some of the concerns. I mean obviously most of us think the data are good, but on the concern side is, number one, that the placebo group may have deteriorated more quickly than one would expect in this population; and number two, the risk that some of – at least the caregivers were unblinded to the status given the instance of ARIA. And then also, along the lines of, on Alzheimer's, is ARIA a clinical problem? Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Okay, that's three questions.

No, no, no. It's one question. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: I'm keeping track here. So, let's take the first one, the placebo group and did they behave as expected. It's our view that based on the natural history studies that, yes, they did. And remember that this was a slightly different population in that they were all PET amyloid confirmed. So we had a population that was perhaps slightly different than what the sort of full spectrum in the natural history studies would look like, and I think maybe that's where some of the perception issue comes from. But this was an enriched population of patients based on the fact that they were all amyloid-imaged prior to entering the study. So, that's the first question. The unblinding issue, I'm glad you asked that question because I've heard that several times now. And we feel very confident that that was not an issue in the study for a variety of reasons. Probably the most important is that we anticipated this in the sense that we were aware of other studies with other antibodies where ARIA had been observed. And so as we design the study, we wanted to be sure that we put the appropriate safeguards in place so that this would not be an issue. So we segregated the raters who were looking at the CDR endpoint and the MMSE endpoint, and neither of those raters were the treating physicians. So, they were completely separate from the assessors of clinical results including ARIA. So, we anticipated this. We put the safeguards in place upfront. And I think that that was an important study design aspect. The other piece of information I think is relevant here – if you don't buy that argument, then the…

Your next question comes from the line of Eric Schmidt with Cowen & Company. Your line is open. Eric T. Schmidt - Cowen & Co. LLC: Thanks for the question. Doug, just sticking with Alzheimer's, there's also been some concern out there around the six milligram dose cohort that didn't perform as well, at least at 26 weeks. Do you share that concern? And if we don't see improvement at AAIC in the one-year data for the six milligram dose cohort, what could explain lower performance for that arm? Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Our assessment is that the six milligram dose is actually, given the small cohort size, within the range that we would have expected to see. From an amyloid-reduction perspective, it sort of sits in between the 3 milligram and 10 milligram dose at the 26-week timeframe. So, I think we feel pretty comfortable that that dose cohort is behaving roughly in line with what we would have expected based on the other cohorts in the study at that time point. So, no, we don't have concerns that that particular cohort represents an outlier in any way. Eric T. Schmidt - Cowen & Co. LLC: Cognition as well? Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Well, cognition, I think, again, the real end point or the real question mark will be at the 54-week time point. So, I'm not sure we really saw anything convincing at 26 weeks. The data was within the noise, I think, at 26 weeks. It's at 54 weeks that I think the important data point will emerge.

Your next question comes from the line of Chris Raymond with Robert Baird & Company. Your line is open Chris J. Raymond - Robert W. Baird & Co., Inc. (Broker): Hey, thanks. Just curious on anti-LINGO. You had some data obviously this week, and just curious, your reaction, at the highest 100 mg/kg dose, obviously you're getting into some sizable drug product on a per dose basis when you think about a 70 kilogram patient. I'm just wondering how you think about dosing with that kind of dose level and then potential cost of goods. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Yeah, let me just sort of frame, the purpose of the study was really a proof of biology study. I think we're not, at the moment, planning to go into acute optic neuritis as an indication per se. But we thought it was an elegant way to assess whether or not we could demonstrate remyelination in man. The 100 mg/kg dose was simply chosen because we were only planning to do a single dose cohort and we chose the top dose that we had looked at in the single ascending dose safety study. So, we wanted to make sure we had adequate drug onboard to see a treatment effect if there was going to be one. And I think we're encouraged now by the fact that we've seen through two different measures of VEP and also looking at the percentage of patients that actually returned to a latency level that looks like normal, which is roughly 2x in the treated group versus the placebo group, that in fact we're convinced that there's remyelination that translates to a benefit in terms of improved latency. So, 100 mg/kg was chosen just as a dose that we could give to make sure we had adequate drug onboard. But we don't believe that that will be the dose. And in fact, the Phase II study that's underway, SYNERGY, is exploring a whole range of doses to allow us to pick the minimum effective dose to take forward hopefully into Phase III studies.

Your next question comes from the line of Matt Roden with UBS. Your line is open.

Great. Thanks very much for taking the question. At AAN, there seemed to be some talk at the BIIB037 poster an about both IV and subcutaneous administrations of BIIB037. Can you give us a sense for whether or not we can see a subcutaneous emerge either in the Phase III later this year or maybe further dosing work in a sort of Phase I level as you go forward? Obviously, it'd be attractive to have a subcutaneous formulation if you had it. Just wondering if you'd give us some update there. Thanks. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Yeah, I think that you should anticipate that the Phase III study will be given by the same route of administration as the Phase Ib. But you are correct. We're already beginning to think about the benefits to patients of developing a subcutaneous formulation, so I think that that's something that will be in the offing but not likely incorporated into the Phase III program. But it is a patient convenience issue that we're thinking about already.

If you'd be able to take that forward, would you have to run a bridging study or you wouldn't have to run in a separate Phase III, just a bridging should be fine, if you could advance that? Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: I think it's likely to be a bridging study. That would be our assumption at this point. But obviously, that would require confirmation with the regulators.

Your next question comes from the line of Geoff Meacham with Barclays. Your line is open.

Hi. Good morning, guys. Thanks for taking the question. Doug, another one for you. In Alzheimer's, it looks like you have a very good idea of the Phase III design. So, is this final meeting with the FDA for sign-off or are there any additional design issues in play? And then, can you give us any perspective on what treatment effect you're looking for or maybe what we should use as a historical benchmark for CDR at 18 months? Thanks. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Well, yeah, I think the design is not final until it's final. I'm not trying to be cute. But obviously, we're still in active discussion with the regulators. I think we feel like we've really nailed down a lot of the key issues, most of which I have delineated for you in the script a bit earlier. There are, obviously, a few remaining issues that we need to tie down and make sure that we're coordinated with regulatory agencies around the world. So, we want to conduct a program that would support registration in a very broad sense geographically. And then in terms of the treatment effect, again, this is the first time that anyone with an amyloid antibody has seen a treatment effect of this magnitude. I think our goal is to attempt to replicate the Phase Ib data at least at a high level. The specifics around the treatment effect that will be acceptable for registration, I'm not prepared to discuss that at this point. I think once we've finalized all of our negotiations with regulators, we'll have more to say about the study design and get into a bit more details once we begin enrollment.

Your next question comes from the line of Terence Flynn with Goldman Sachs. Your line is open. Terence C. Flynn - Goldman Sachs & Co.: Hi. Thanks for taking the question. Maybe just one with respect to the gross-to-net in the quarter on TECFIDERA. Just wondering if you can give us any more color about the delta there versus your expectations. And then, should we expect that that's going to continue over the balance of the year? It was a little unclear from your comments. Thank you. Paul J. Clancy - Chief Financial Officer & Executive Vice President: Yeah, thanks, Terence. This is Paul. Yeah, we saw the gross-to-net drift upward versus the last four quarters. We had anticipated for a full year coming into 2015 that we'd have a little bit of upward pressure on gross-to-net just as we continued to penetrate managed care contracts. Q1 drifted up for two reasons. The normal Q1 donut hole, et al., and we also just had a adjustment made in the managed care accounts. That resulted in close to a 20% gross-to-net. We expected to drift down about 400 basis points for the subsequent three quarters.

Your next question comes from the line of Ying Huang with Bank of America Merrill Lynch. Your line is open.

Hi. Good morning. Thanks for taking my questions as well. Maybe for Doug, I have a couple for the Alzheimer program. First of all, can you clarify whether you will wait for the titration results before you start the Phase III trial officially for BIIB037? And secondly, do you guys have any data in-house for the correlation between plaque reduction and also the neurocognitive endpoint such as CDR and MMSE from the Phase IIb? Thank you. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: So with respect to titration, our expectation is that we will begin the study prior to reporting out the titration data. I think we have a pretty good handle on the dosing parameters for the study and how we plan to handle that. So, it's our expectation that we won't wait for that data. And then with respect to the correlation between plaque and CDR, I think it's difficult to, in a study of this size, really draw those sorts of direct correlations. Obviously, we'll be looking at those sorts of things to see whether or not plaque reduction per se can be used as a "biomarker" on sort of an interim basis. But I think the study is relatively small to be able to draw those sorts of strong correlations. What I will say is that irrespective of the cohorts that we looked at, and this is from the most recent AAN poster that was presented, whether you're looking at ApoE4 carriers or non-carriers, whether you're looking at mild or moderate patients, the reduction in amyloid appears to be pretty consistent across the spectrum. So, there doesn't appear to be any difference in ApoE4 status influencing amyloid removal nor the stage of disease, roughly breaking it down between mild and prodromal patients.

Your next question comes from the line of Matthew Harrison with Morgan Stanley. Your line is open. Matthew K. Harrison - Morgan Stanley & Co. LLC: Great. Thanks for taking the question. Maybe one for Paul and George. Just you've got a substantial cash balance. You've seen some other companies go out and buy some close-to-market neurology assets. We've seen you guys do some early-stage deals but not sort of close-to-market deals. Any thinking or what might change your thinking to pick up an asset which could be closer to market than maybe spending a little bit more money than you typically have? Thanks. George A. Scangos, Ph.D. - Chief Executive Officer & Director: Yeah, look, we have no formal strategy that says we're only going to in-license early-stage items. I think when we look at acquisitions from the outside, we look at the data, we look at the market potential, we look at the competitive status and we look at value. And if all those things make sense, then we could go ahead and make an acquisition or in-license a compound. So, I think we try and take a look at these from a scientific and medical perspective to make sure that they're valid from a market perspective, to make sure there's a patient need from a competitive perspective. And then, they have to make sense in term of what we have to pay for what we get. And so, I think those are the filters and, we'll – those are the ones we've used, those are the ones we'll continue to use.

Your next question comes from the line of Cory Kasimov with JPMorgan. Your line is open.

Hey. Good morning, guys. Thank you for taking my question. I wanted to go back to Alzheimer's for a minute. I'm curious if you can provide any updates on the progress with your tau inhibitor, when that might enter the clinic. More specifically, last month at AD/PD there's a lot of talk from KOLs about combo strategies in Alzheimer's. So, wondering if you have any pre-clinical data on tau plus a-beta antibodies and just a combination you may evaluate relatively rapidly, or would you wait to see how aducanumab monotherapy plays out first? Thanks. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: This is Doug. We have a couple of different approaches on tau. Both of them are in pre-clinical at the moment. And I would expect that the sort of front-runner amongst those candidates is one of the antibodies that we have under development. Likely to move into the clinic next year would be my best guess at the moment. We're starting to do some of those experiments with combinations, not just with tau antibodies and anti-amyloid antibodies but also beginning to look at the combination of BACE inhibitors with the anti-amyloid antibodies. So I think long term, our view is that this will become a combination market and we're exploring a number of, what I'd characterize as the sort of obvious combinations to look at right upfront. And I think we're fortunate that we've got a collection of these assets that we can begin to mix and match in the preclinical stages to help guide us towards the choices of what makes the most sense to look at once we actually start generating clinical data.

Your next question comes from the line of Robyn Karnauskas with Deutsche Bank. Your line is open.

Hi. Thanks for taking my question. So I just want to ask a question about TYSABRI in stroke. I kind of understand the mechanism, maybe you can talk a little bit more about it. But specifically, how quickly will TYSABRI work, do you think, in a patient? So what gives you the confidence that when they get this injection after stroke, that you could see a benefit? And maybe, update on possible timing of the data. Thank you. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Sure, Robyn. This is Doug. Well, the timing of the data would be the second half of the year. And I think from the standpoint of mechanism, there's actually quite a bit of preclinical data and stroke models either with antibody treatment or knockouts that demonstrate that the size of the infarct is dramatically reduced when you antagonize this pathway. So, what we're going to be looking at in this particular study is two different measures. The first is a reduction in the infarct size, which we would predict to occur based on the biology. The immediate influx after an infarct tends to be neutrophils, followed quickly thereafter within the first 24 hours with a pretty robust lymphocyte infiltrate. And it starts at that lymphocyte infiltrate, contributes to cytokine production that causes further damage and loss of function. So by antagonizing that sort of second influx of lymphocytes, we hope to reduce the infarct size. And we'll be looking at that by imaging five days out. The perhaps more important endpoint that we're also looking at, and obviously it's a relatively small study so we haven't sized it to see it per se, but there are several measures of stroke. There's a rating scale that is used routinely in these types of studies that we'll be looking at day 29 to really assess whether there's any functional benefit in terms of protecting these patients from loss of function as a result of stroke. So, it's really a two-prong study. The first is the imaging endpoint, and that will come fairly quickly and that's where most of the good biology data is. Secondarily though, we'll be actually looking at the performance of these patients either with placebo or TYSABRI to ask the question of whether we've actually shown some benefit from a clinical perspective. And that's what will drive the decision as to whether we move in to Phase III.

Your next question comes from the line of Michael Yee with RBC Capital Markets. Your line is open.

Hey, good morning. Thanks. Just wanted to clarify on the BIIB037 Phase III that you talked about, is it specifically one study in carriers and one in non-carriers and each of those using different doses? And then, you mentioned it was 18 months. Is that just because you want to give confidence or get confidence that there's enough time to separate between the curves? Is that what you're thinking? Thanks. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Yeah, the two studies will essentially be identical, mirror images of each other, and they will incorporate both carriers and non-carriers into those studies. And you're right, the 18 months is really simply a way of assuring that we have adequate time to capture the treatment effect with the various doses that we'll be testing, both the lower and the higher doses that will be incorporated into the study. So it's been designed really based on the observations from the Phase Ib study in terms of the cadence of the treatment effect, and we think that the 18 months is the appropriate timeframe in which to assess in both carriers and non-carriers of the doses we're planning to go forward with.

Your next question comes from the line of Yaron Werber with Citi. Your line is open.

Hi. This is Kumar Hassain (48:21) for Yaron. Thank you for taking my question. For Alzheimer's, will a single primary of CDR-STB sufficient (48:27) and what are the differences in EU and U.S. regulatory requirements? And also, if you can make any comments on IPR and the Patent interference. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: I missed the second question. But the first question on CDR, I think for a population of patients that are largely prodromal but also including some sort of early mild patients, which is what we'll be focusing our attention on in these studies. The CDR endpoint is an accepted endpoint for regulators. It is, remember, a composite score that looks at both cognition and function. And in prodromal patients in particular, you don't actually have functional changes. So it's thought that this is the most appropriate tool for the early spectrum patients in Alzheimer's disease, and that's why regulators have started to accept this as a single primary endpoint in registrational studies, not just in the U.S. but in the EU as well. George A. Scangos, Ph.D. - Chief Executive Officer & Director: This is George. On the IPR question, we're certainly aware of the IPR that was filed. We have several patents that are protecting TECFIDERA. But we're confident in our IP portfolio, and so we don't think it's going to have an impact on our ability to continue to sell the drug.

Your next question comes from the line Joseph Schwartz with Leerink Partners. Your line is open.

Thanks very much. Maybe one on LINGO. Can you explain to us your thoughts on why you're able to see functional benefits in the absence of seeing anatomic evidence of remyelination? What are your latest thoughts on how useful or not a model of AON is for MS, and how are you thinking about that now versus before you ran the latest experiment? Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Well, the LINGO study that we've reported out on in optic neuritis, I think the anatomical data, just based on where these lesions occur, it's difficult to actually get the sort of imaging confirmation that you can get in MS studies where the lesions are much more visible just because of current MRI technology. So, I think we relied on functional measures of remyelination as opposed to imaging measures just because that was more appropriate in the optic neuritis setting. Our results, I think, give us more confidence going in to the readout from the MS studies. This is, in fact, the first time anyone has reported a treatment effect and the ability to observe remyelination in man. Prior to this study, all we had was some very elegant animal experiments but we'd never really created the linkage of those data to what we can accomplish in man. So, I think the exciting part of the data from the optic neuritis study is that we now have evidence in man looking at a couple of different ways of measuring latency on the optic nerve and also the recovery parameters that I mentioned earlier with double the number of patients getting back to a normal level of latency versus the placebo group. I think the consistency of that data across the various ways we've looked at it gives us added confidence going into the MS study that at least we're influencing the biology we hope to influence. So, we'll just have to wait and see what that data shows us. And as I mentioned in the call, the final data will be available in 2016 in the MS study and tell us a lot more than what we know now about how or if to go forward in MS.

There are no further questions. I turn the call back over to Dr. Scangos. George A. Scangos, Ph.D. - Chief Executive Officer & Director: Okay. Thank you all for your questions. Thanks for your attention this morning. And we'll conclude the call.

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