Ben Strain - Associate Director, Investor Relations George A. Scangos, Ph.D. - Chief Executive Officer & Director Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development Tony Kingsley - Executive Vice President-Global Commercial Operations Paul J. Clancy - Chief Financial Officer & Executive Vice President

Geoffrey C. Porges - Sanford C. Bernstein & Co. LLC Mark J. Schoenebaum - Evercore ISI Eric T. Schmidt - Cowen & Co. LLC Chris J. Raymond - Robert W. Baird & Co., Inc. (Broker) Matt M. Roden - UBS Securities LLC Geoffrey Meacham - Barclays Capital, Inc. Terence C. Flynn - Goldman Sachs & Co. Ying Huang - Bank of America Merrill Lynch Matthew K. Harrison - Morgan Stanley & Co. LLC Cory W. Kasimov - JPMorgan Securities LLC Robyn Karnauskas - Deutsche Bank Securities, Inc. Michael J. Yee - RBC Capital Markets LLC Joseph P. Schwartz - Leerink Partners LLC

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. Ben Strain - Associate Director, Investor Relations: 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 overall share this quarter but at a moderating pace. Our interferon business continued to perform well, driven by the recent introduction of PLEGRIDY. TYSABRI remained the therapy of choice for patients needing high efficacy. TECFIDERA had a more challenging quarter due to a number of issues, including an overall slowing of the MS market, the recent launch of PLEGRIDY, the single PML case reported last year and some first quarter financial dynamics that Paul will discuss. And as Tony will describe a little later, our two hemophilia products, ELOCTATE and ALPROLIX, continued to gain patients and market share during the quarter. On the research front, we continue to advance our pipeline. We recently presented compelling data for aducanumab, which is the first investigational drug for Alzheimer's disease that has demonstrated a statistically significant reduction of amyloid plaque and a statistically significant slowing of clinical impairment. And this week, we're presenting 73 company-sponsored platform and poster presentations at AAN [American Academy of Neurology], which highlight our marketed MS therapies, including TECFIDERA's strong efficacy across a broad range of MS patients in addition to its favorable long-term safety. We also presented new data for anti-LINGO-1 in acute optic neuritis and aducanumab in Alzheimer's disease. We made excellent progress toward initiating multiple Phase III trials. We plan to initiative Phase III trials for aducanumab later this year. We also recently initiated a Phase III trial for TECFIDERA in patients with secondary progressive MS, both of which Doug will highlight. We believe these important investments have the potential to be significant future growth drivers for Biogen. We continued to make progress in our biosimilar efforts. So far this year, Marketing Authorization Applications filed by Samsung Bioepis, our joint venture with Samsung Biologics, for etanercept and infliximab biosimilar candidates have been accepted by the EMA. Biogen is preparing to commercialize these therapies across the EU if approved. There is a growing societal need for high-quality biosimilars to help improve patient access to treatments that they need, and we believe that Biogen's world-class development, manufacturing and analytical capabilities position us well to bring these therapies to patients. So in conclusion, we have another busy year in which we'll focus on the trajectory of TECFIDERA and of our entire MS franchise in order to achieve our commercial and financial goals and ensure that we execute ongoing and planned clinical trials to move our pipeline forward as quickly as possible. So now, I'll turn the call over to Doug who will update you on our progress in R&D. Douglas E. Williams, Ph.D. - Executive Vice President-Research & Development: Thanks, George. At last month's AD/PD meeting, we presented positive interim data from our Phase Ib study evaluating aducanumab in patients with prodromal and mild Alzheimer's disease. And earlier this week at AAN, we presented additional Phase Ib results demonstrating that aducanumab treatment had a consistent impact on amyloid levels in ApoE4 carriers versus non-carriers as well as in prodromal versus mild AD patient subgroups. We plan to present clinical data for these subgroups at subsequent medical meetings. We plan to initiate Phase III registrational studies for aducanumab in the second half of this year. We've been in active dialogue with regulators and we're close to finalizing our Phase III development plan. Our expectation is that our registrational program will include two identical 18-month-long placebo-controlled trials, each including 1,350 subjects with early Alzheimer's disease. We intend to use the CDR [Clinical Dementia Rating] sum of boxes as the primary end point. In each Phase III study, we plan to evaluate two doses of aducanumab in both the ApoE4 carriers and non-carriers, with ApoE4 non-carriers receiving higher treatment doses. Estimating enrollment timing is difficult though we anticipate Phase III enrollment duration will be similar to other large studies in Alzheimer's disease. We hope the substantial interest in the program will catalyze recruitment. However, the studies will include early Alzheimer's patients who are often not yet diagnosed. Also, we must ensure that clinical sites have access to amyloid PET imaging. As we initiate the Phase III program, the Phase Ib study will remain ongoing. We expect to present the one-year clinical results for the 6 mg/kg study cohort at the AAIC meeting in July. We also continue to evaluate dose titration, and we expect to present those results next year. Moving on to our other programs, starting with ZINBRYTA. The EMA has validated the Marketing Authorization Application for ZINBRYTA. If approved, we believe ZINBRYTA could be an important new therapeutic option for relapsing MS patients. For TECFIDERA, we recently initiated a new Phase III study, INSPIRE, to evaluate whether TECFIDERA slows the rate of disability progression in patients with secondary progressive MS. There are no effective treatments available today for SPMS, and developing therapies for this patient population is of great interest to the organization. INSPIRE is a two-year placebo-controlled study in 1,170 subjects. The primary endpoint is time to confirm disability progression based on a composite endpoint including EDSS, a timed 25-foot walk test and a nine-hole peg test. The endpoint utilized is similar to that being used in the ongoing TYSABRI ASCEND SPMS study. The scientific rationale to develop TECFIDERA in SPMS is based on both biological and clinical evidence. We believe preclinical data demonstrate that TECFIDERA has cytoprotective and anti-inflammatory properties that may address the lymphocytic infiltrates and neurodegeneration known to occur in SPMS patients. The clinical data from TECFIDERA Phase III studies also demonstrated reduced disability progression in subjects even when they hadn't experienced recent relapses. Turning to anti-LINGO, at this week's AAN meeting we presented detailed results from the Phase II acute optic neuritis study which we believe demonstrate that anti-LINGO is able to remyelinate damaged neurons. New data demonstrate a statistically-significant improvement in recovery of optic nerve conduction latency in subjects treated with anti-LINGO going out to week 32. Also, results from a sub-study evaluating multifocal VEP, a more sensitive measure of optic nerve conduction, were found to be consistent with a full-field VEP findings. Our anti-LINGO Phase II study in MS remains ongoing, and we expect to obtain final results in mid-2016. I'll now turn the call over to Tony. Tony Kingsley - Executive Vice President-Global Commercial Operations: 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 position in the market. We continue to believe that TECFIDERA remains the preferred oral option in the market given its strong efficacy, convenience and safety profile. We are leveraging the full capabilities of our commercial organization to communicate these benefits, maintaining significant sales force focus, executing both physician and patient programming with updated messaging, and increasing our share of voice across both print and digital media. Next, AVONEX and PLEGRIDY combined continued to gain share among interferons this quarter. PLEGRIDY has continued to source patients broadly, which we believe is a positive indicator of the product's appeal. Based on our market research, we believe PLEGRIDY is emerging as the interferon of choice. And we continue to believe that as the interferon market declines, Biogen's ability to grow share within it is attractive. Finally in the MS franchise, we're pleased that TYSABRI showed a full year of positive patient growth in a market with an increasing number of alternatives. From Q1 2014 to Q1 2015, global TYSABRI patients increased 5%. We think this performance is a testament to physician and patient belief in the high level of efficacy that TYSABRI provides to patients. So in summary, our MS franchise revenue increased 19% year-over-year to approximately $2.1 billion. Turning to our emerging hemophilia business, we continue to be pleased with the launch of our long-acting factors. In the U.S., as the first long-acting factors in the market, both ALPROLIX and ELOCTATE continued to gain new patients this quarter, and we've continued to see expansion of usage among hemophilia treatment centers. We now have over 70% HTC penetration for each product, and our data showed that switching rates in both hemophilia A and hemophilia B are running well above historical averages. We believe we are succeeding in our strategy to capture early adopters and then expand our footprint as both patients and physicians have positive experiences with the products. Outside of the U.S., we also recently launched both ALPROLIX and ELOCTATE in Japan and have seen strong initial interest. We believe that Japan represents an attractive long-term growth opportunity for our hemophilia business. I'll now pass the call to Paul. Paul J. Clancy - Chief Financial Officer & Executive Vice President: Thanks, Tony. Our GAAP diluted earnings per share were $3.49 in the first quarter. Our non-GAAP diluted earnings per share in the first quarter were $3.82. Total revenue for Q1 grew 20% year-over-year to approximately $2.6 billion, though decreased 3% versus the prior quarter. The strengthening dollar weakened revenues by approximately $89 million, which was partially offset by hedging for a net unfavorable impact of $49 million. Global first quarter TECFIDERA revenues were $825 million, an increase of 63% year-over-year, however, a decrease of 10% versus the fourth quarter of last year. This quarter's TECFIDERA revenues consist of $648 million in the U.S. and $177 million outside the U.S. There are a few items that impacted TECFIDERA revenue in Q1. Let me provide the details. U.S. TECFIDERA sales included 13 shipping weeks in Q1 compared to 14 shipping weeks last quarter. We estimate the additional week of TECFIDERA sales in Q4 represented approximately $50 million. U.S. gross-to-net adjustments were higher this quarter than prior quarters. Specifically, increased discounts and allowances in part due to donut hole were approximately 400 basis points higher than our estimated run rate for the remainder of 2015. This impacted Q1 U.S. revenues by approximately $35 million. In the U.S., we estimate we ended the quarter with approximately 2.5 weeks of inventory in the wholesale channel, a similar level to last quarter. However, we believe there was a slight drawdown of inventory in the specialty pharmacy channel. Outside the U.S., foreign exchange impact offset by hedging weakened TECFIDERA revenues by approximately $8 million for Q1 versus the prior quarter. And in Germany, we began recording TECFIDERA sales at a lower price as the free-pricing period ended in mid-February. We expect the official price will be made public in May. So shipping weeks, gross-to-net, foreign exchange and German pricing negatively impacted TECFIDERA this quarter. Nevertheless, as we've noted, we saw moderating patient growth especially in the U.S. and Germany, and we're working diligently to improve TECFIDERA's trajectory. Interferon revenues including both AVONEX and PLEGRIDY were $755 million during the first quarter, including $518 million in the U.S. and $236 million in sales outside the U.S. AVONEX U.S. sales included 13 shipping weeks in Q1 compared to 14 shipping weeks in the prior quarter. Foreign exchange impact offset by hedging weakened Q1 interferon revenue by approximately $12 million versus prior quarter and by approximately $25 million year-over-year. TYSABRI worldwide revenue was $463 million in Q1. These results were comprised of $273 million in the U.S. and $190 million internationally. Foreign exchange impact offset by hedging weakened TYSABRI revenue by approximately $12 million for Q1 versus Q4 and approximately $20 million year-over-year. Moving to hemophilia. ALPROLIX revenues in Q1 was $43 million and ELOCTATE revenue was $54 million. For our anti-CD20 unconsolidated joint business which includes RITUXAN and GAZYVA, our U.S. profit share as well as the profit share and royalties on sales of rituximab outside the U.S. were $331 million, an increase from prior quarter, in part due to an inventory build. Royalties were $20 million for Q1 compared to $38 million in the same quarter last year. Our royalty revenues from ANGIOMAX ended on December 15, 2014. Now, turning to the expense lines on the non-GAAP P&L. Q1 cost of goods sold were $312 million or 12% of revenue. Q1 R&D expense was $461 million or 18% of revenues, which includes no meaningful business development activity during this quarter though we continue to anticipate additional BD activity through the remainder of the year. Q1 SG&A expense was $560 million or 22% of revenue. Our non-GAAP tax rate was approximately 25% for Q1, and our rate benefited by approximately 1.5% related to a discrete item. During the quarter, we made $250 million of CVR payments to the former shareholders of Fumapharm. And our weighted diluted shares at the end of the quarter were 236 million. We ended the quarter with approximately $3.5 billion in cash and marketable securities, split approximately 50/50 between the U.S. and ex-U.S. This brings us to our non-GAAP diluted earnings per share, which were $3.82 for the first quarter. As a reminder, last quarter we announced our plan to provide annual guidance and one update per year during our second quarter earnings. This change is intended to synchronize with our internal planning processes and ensure a continued focus on the long term. As a result, we won't be updating our formal guidance this quarter though I'd like to briefly characterize how we're thinking about the remainder of the year. There are two key items that we're keeping a watchful eye on for the rest of the year. First, while foreign exchange has been a headwind, any additional strengthening of the dollar could exacerbate this impact on revenue. And second, we continue to expect TECFIDERA will represent the largest contributor to our overall revenue growth. If the U.S. trajectory does not improve, we may come in at the lower end of our previously provided revenue growth. Now I'll turn the call over to George for his closing comments. George A. Scangos, Ph.D. - Chief Executive Officer & Director: Okay. Thank you, Paul. In closing, the year is shaping up to be an eventful one for us. Obviously, a top priority for us is the growth of our entire MS portfolio, including TECFIDERA. We believe that TECFIDERA is a compelling treatment option for MS patients, and our long-term outlook for TECFIDERA and for our entire MS portfolio remains strong. We believe that our portfolio provides leading choices for patients among interferon, oral and high efficacy therapies, and we're working hard to overcome the headwinds that we saw last quarter. And of course, we'll continue to focus on increasing the numbers of hemophilia patients who are taking advantage of the benefits of ELOCTATE and ALPROLIX. This year is also an important one in terms of advancing the pipeline. We'll move aducanumab into Phase III as quickly as possible, and we'll focus on execution of our ongoing trials for the other compounds in our pipeline. We anticipate data on several pipeline compounds this year, including a Phase III trial of TYSABRI for the treatment of SPMS, the Phase II trial for TYSABRI in acute ischemic stroke, and Phase II data for Neublastin in neuropathic pain. And of course, we're looking forward to the data from the Phase II trial of our anti-LINGO antibody in MS next year. We believe that each of these therapies has the potential to be a significant therapeutic advance. And so with that, we'll close our remarks. And, operator, you can now open up the call for questions.

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. Tony Kingsley - Executive Vice President-Global Commercial Operations: 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. Mark J. Schoenebaum - Evercore ISI: 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. Mark J. Schoenebaum - Evercore ISI: 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 other piece is that, frankly, the temporal issues I think also support the fact that it's unlikely that there was any unblinding. Because 92% of the events, the ARIA events that occurred, occurred within the first five doses of administration. We didn't actually see a change in cognition until 12 months, or 54 weeks to be precise. So, there was a significant gap between any of the observed ARIA in these patients and the treatment benefit that we recorded with CDR sum of boxes and the MMSE endpoint. So, that gap in time I think should also give you some comfort. And then with respect to clinical, is ARIA a clinical observation? It's a really good question, Mark. I think it may actually be an indication of biology in the case of our antibody. I think it's difficult to say. What I think is important though is that about two-thirds of the cases of ARIA that we saw had no symptoms associated with them. In those patients, the roughly 35% that did show some symptoms, they were primarily mild to moderate, self-resolving within 4 weeks to 12 weeks. So, I think there's still a lot for us to learn about ARIA and what it means and how we manage patients through that. But it is a question that I think will continue to be explored and the answers will play out over the course of the next several years.

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. Matt M. Roden - UBS Securities LLC: 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. Matt M. Roden - UBS Securities LLC: 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. Geoffrey Meacham - Barclays Capital, Inc.: 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. Ying Huang - Bank of America Merrill Lynch: 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. Cory W. Kasimov - JPMorgan Securities LLC: 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. Robyn Karnauskas - Deutsche Bank Securities, Inc.: 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. Michael J. Yee - RBC Capital Markets LLC: 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. Joseph P. Schwartz - Leerink Partners LLC: 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.