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Greetings and welcome to the Prosensa Holding's First Quarter 2014 Earnings Conference Call. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. (Operator Instructions) As a reminder, this conference is being recorded. I would now like to turn the conference over to your host, Celia Economides, Senior Director of Investor Relations and Corporate Communications. Thank you. You may begin.

Thank you, operator, and thank you all for joining us. On behalf of Prosensa, I would like to welcome everyone to our first quarter 2014 earnings call for the quarter ending on March 31, 2014. With me today are Hans Schikan, Chief Executive Officer; Giles Campion, Chief Medical Officer; Berndt Modig, Chief Financial Officer. And joining us for the Q&A is Luc Dochez, Chief Business Officer. Earlier today, we issued a press release containing results for the first quarter of 2014, which is available on our website at prosensa.com. Today we also filed our quarterly financial statements and management discussion and analysis with the SEC. During today's call, we may make forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These include statements about our future expectations, clinical developments and regulatory timelines, the potential success of our product candidates and including drisapersen and financial projections. Actual results may differ materially from those indicated by these statements. Forward-looking statements during this call include statements around our exon-skipping drug pipeline including drisapersen and our financial position. Such forward-looking information involves risks and uncertainties that could significantly affect expected results. These risks and uncertainties are discussed in the company's SEC filings, including, but not limited to, the company's annual report on Form 20-F. In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so even if our views change. With that, let me pass the call over to Hans.

Thank you, Celia, and good morning, good afternoon, everyone. Thank you for joining us today for our first quarter 2014 earnings call. On today’s call we will be providing you with an update on the status of our lead exon-skipping program drisapersen and update on the rest of our DMD portfolio and an update on our financials. While we covered much of the first quarter during our last earnings call which took place on the 18th of March, this time period to represent its transitional ones for the company as it’s the first quarter as a public company where we operated without our former partner GlaxoSmithKline. On the 13 of January we had announced that we regained the rights to drisapersen from GSK and retained rights to all order programs for the treatment of the Duchenne muscular dystrophy. Prosensa now has the full and incumbent rights to continue the development of drisapersen in addition to each of our other DMD programs of which three compounds are currently in clinical developments. We believe that we are in a favorable, strategic position to advance our R&D pipeline and have been pursuing this effort since then. We continued to expand our knowledge of the disease prior to our pipeline but also throughout comprehensive natural history study which commenced enrollment last summer. This study is close to reaching our target enrollments with 247 patients enrolled out of 250 plans as of today. On the 24th of January, we had our first meeting with the FDA. Following the drisapersen Phase 3 data read out on the 20 September, 2013. At this time GSK was still the IND holder. The IND was transferred to Prosensa on the 18th of February, which was communicated by a letter to investigators and to patient groups. Since that time we have had ongoing interactions with regulators both in the U.S. and Europe and remain on track to providing you with further clarity on a potential regulatory path forward for drisapersen before the end of June. We estimate substantial progress in the transfer of the drisapersen program from GSK. The transition period elapsed on the 12th of May and we have now entered into a 30-day expansion period to ensure that there are no outstanding transition tasks to complete. This is an integrate process involving a number of disciplines across the company. During this period, we have been receiving individual patient data from GSK and are now in a position to further assess these data. Given that this is the largest clinical data set in Duchenne comprising of three placebo controlled and two long-term open label studies treating over 300 patients, we have shared our view of the data with the community in addition to the outcomes of any additional analysis performed where possible. In the longer study to date for drisapersen, boys have been treated over four years with efficacy data reported up to 177 weeks. The main change from baseline in the six minute walk distance test from this group of boys, 10 boys was 24.5 meters minus which includes two boys that have become non-ambulance earlier in the study. Natural History data suggest that entry to DMD boys can lose anywhere from 40 to 60 meters on the six minute walk distance per year or more than 120 meters over a two-year period. Recent investor briefing Dr. Nathalie Goemans, who is the lead investigator on this study reported that these results are very encouraging especially also given the nature of these boys at week 177 of 12.9 years. Along with leading investigators in the field, in the past few years, we have learned much more about the natural course of DMD and key factors for a clinical trial to compare between subjects where so many individual and external factors can also impact outcomes. Based on our assessments of the data, we believe that the Phase III trial may have failed the drug rather than the drug failing the trial. Boys in the Phase III were generally more progressed to the disease than in previous placebo-controlled Phase II studies. This is apparent when comparing the baseline characteristics of the boys in the Phase III trial for those boys in to Phase II trials. Boys in the Phase III trial had a lower baseline six minute walk distance, performed worst in all tests of muscle function and were generally older which is correlated with increased disease progression. Age and baseline six minute walk distance appeared to be key predictors of disease progression. Based on published and our own data in to drisapersen program, we performed an analysis of the Phase III results in boys older than seven with the baseline six minute walk distance between 300 and 450 meters. You may recall that the treatment difference for all boys older than 7 was 7 meters. While this is a post-talk analysis and the results are not statistically significant, when applying these age and baseline criteria, the treatment difference more than tripled to 25 meters. This analysis serves as further evidence of the apparent influence of the extent of disease progression on efficacy as measured by the six minute walk test. Moreover, it became clear that one in every four boys participating in the Phase III study was older than 7 with the baseline of less than 300 meters. Finally, this study was performed in 45 sites in 19 countries which has contributed to the variability in the patient population studied. On the 16th of January, we also provided an initial overview of the top line data for the overall drisapersen program including a number of integrated analysis. We reported a long-term expansion data of DEMAND IV or DMD114349, showing a treatment effect of 46 meters after 96 weeks of treatment which results in 113 patients. An analysis by feeder study and by age supports the hypothesis that earlier intervention and longer treatment duration may be required to show a clinically meaningful effect. The post-walk pool analysis of both placebo-controlled Phase II studies involving 70 patients, showed a statistically significant and clinically meaningful difference from placebo of plus 31 meters with the P value of 0.003. Key safety findings are consistent with previous observations including injection-site reactions, proteinuria and moderate to severe thrombocytopenia. On the 17th of March, at the Muscular Dystrophy Association Clinical Meeting, Dr. Craig McDonald from UC, Sacramento presented the 48-week data from the DEMAND V or DMD114876 study. As you may recall, the treatment phase for this randomized placebo-controlled exploratory study was 24 weeks with a 24 week no treatment follow-up period. The trial was not powered for a statistical significance, was conducted in 13 centers in the United States. These results indicated a clinically meaningful treatment difference of 27 meters with a P value of 0.069 in the primary endpoint which was a six minute walk distance at 24 weeks for the 6 milligram per kilogram per week treatment on further placebo. In the poster presented at the Muscular Dystrophy Association Clinical Meeting it was shown that the treatment benefits in the 6 mgs/kg per week treatment group was maintained at 48 weeks with the main difference of 28 meters versus placebo although not statistically significant. The drisapersen 6 milligram per kilogram treatment showed an overall increase from base line of 15 meters whereas the placebo arm showed a mean decline of 13 meters. The results of this exploratory study support the use of drisapersen at a dose of 6 milligrams per kilogram by subcutaneous injection once weekly in the treatment of boys with DMD eligible for exon 51 skipping. The maintenance of the treatment difference in the 24-week post-treatment phase is encouraging, and is consistent with the possible slowing of disease progression. On the 8th of April we announced our former Chief Financial Officer with Genzyme, Mike Wyzga has been nominated for appointment to our Supervisory Board at the next shareholders meeting scheduled for 17 of June 2014. We welcome Mike as an instrumental addition to our supervisory board and are confident that his extensive financial and transactional expertise will support the company significantly in our efforts to bring much needed life saving treatments for rare genetic diseases to patients. His long-term tenure at Genzyme, one of the most successful companies in the rare disease space will be invaluable as we continue developing therapies for boys with Duchenne muscular dystrophy and building our company. At this time I would like to turn the call over to Giles Campion our Chief Medical Officer to provide you with an update on drisapersen re-dosing plans and our follow on DMD programs.

Thank you Han. As Han’s previously mentioned we are now in a 30-day extension period with GSK to finalize the full transition of the drisapersen program. At this stage we have made substantial progress and continue to analyze the individual patient data we have perceived, engaged with investigators and patient groups, prepare for re-dosing and advance the program as quickly and diligently as we can. On May 1st we announced based on positive feedback from both patients and investigators regarding willingness and desire of patients to go back on drisapersen and encouraging analysis of our clinical trial data we will re-dose an initial cohort of boys in the third quarter of 2014. The first wave of re-dosing in the third quarter will focus on sites in North America and Europe. Patients in North America will be re-dosed under existing amended extension protocols and patients in Europe will either participate in an amended or new treatment particle or via an appropriate expanded access program. Following this announcement we held an investigator briefing on May 14th to review the protocol DMD115501 or re-dosing boys in the United States and Canada, eligible boys are those who completed DEMAND V that is DMD114876, those continue in the current DMD115501 protocol and U.S. or Canadian boys who participated in the DEMAND IV study. Boys will be initially dosed in the clinic for the first four weeks but home dosing is intended subject to site requirements and no biopsies will be taken under this protocol which aims to be less burden for boys and their families. PRO044 our next most advanced product candidate addresses a separate sub-population of up to 6% of DMD patients. PRO044 has completed the Phase I/II study in Europe and results were presented in October 2013. An extension study for PRO044 is planned for the second half of this year. We have four additional early stage compounds that address other distinct sub-population of DMD patients. PRO044 and PRO053 each addressing a population of up to 8% of DMD patients, but currently in Phase I/II clinical trials, we expect data from PRO045 in the fourth quarter of 2014 and PRO053 in the first quarter of 2015. We expect confirmatory studies of these compounds to start in the first quarter of 2015. PRO052 and PRO055 are in advanced preclinical development. We have also commenced a research program prospect which includes a new and innovative application of our RNA modulation technology platform. This approach applies to multiple exon skipping. Our initial efforts on prospect focused on exon 10 to 30 region in the dystrophy gene. As an example 10 to 30 multiple skip could be applicable to up to 13% of all DND patients. Proof of concept has been obtained in multiple patients muscle cell cultures. We continued to work diligently to pioneer research and development in the muscular space and are pleased to announce that Prosensa now collaborated of 12 abstracts that’s been accepted for oral post presentations of the 19th Annual World Muscle Society Congress, taking place in October 7 to 11 of 2014 in Berlin, Germany. As one of the premier scientific meetings for the near muscular disease community, we are pleased that the extensive work being conducted by Prosensa and collaborators will be showcased at this important venue. Thank you, and with that I will pass the call over to Berndt Modig our Chief Financial Officer to provide you with an update of financials.

Thank you Giles. We consolidated financial statements of Prosensa have been prepared in accordance with IFRS, as issued by the International Accounting Standards Board, the consolidated financial statements are presented in Euros which is the company’s functional and presentation currency. All amounts mentioned are in Euros unless otherwise specified. Prosensa's cash and cash equivalent as of March 31, 2014, were €77.4 million compared to €82.2 million as of December 31, 2013. The decrease in cash and cash equivalents was mainly due to operating activities. The company's cash consumption, excluding cash flows from financing for the three months ended March 31, 2014 was €4.9 million. Revenue for the three months ended March 31, 2014, was €14.8 million compared to €2.4 million in 2013 due to an increase in license revenue of €13.3 million and a decrease in collaboration revenue of €0.1 million. License revenue for the three months ended March 31, 2014, in an amount of €14.7 million, was exclusively related to the termination of the research and collaboration agreement with GSK. This was due to one-time release of previously deferred revenue balances as well as a €0.2 million revenue related to other services delivered under the research and collaboration agreement with GSK. In the three months ended March 31, 2014 collaboration revenue was minimal due to the termination of the research and collaboration agreement. Research and development expense was €5.3 million for the three months ended March 31, 2014 compared to €4.1 million for the comparable period in 2013. PRO044 has completed PhaseI/II study in Europe and extension study for this compound is not planned until the second half of this year which resulted in lower expenses in the three month period ended March 31, 2014 compared to the corresponding period in 2013. During the three month period ended March 31, 2014, we incurred expenses for the Phase I/II studies of both PRO044 and PRO053. Our research and development expenses increased substantially in connection with these clinical trials. In the three months period ended March 31, 2014, we also incurred research and development expenses for drisapersen as a result of the termination of the research and collaboration agreement with GSK in addition to expenses for the Natural History study prospects PRO052 and PRO055 programs. General and administrative expense increased from €1.18 million to €2.5 million in the three months ended March 31, 2013 and 2014 respectively. The increase is primarily due to share based compensation expense and cost associated with operating as a public company. Net income for the three months ended March 31, 2014 were €7.3 million or €0.20 per share or €0.19 diluted income per share compared to a loss of €3.5 million or €0.12 per share and €0.12 diluted loss per share for the comparable period on 2013. For the full year 2014, we expect to incur a loss, so there is no income tax provision for the three months ended March 31, 2014. For 2014, the financial results for the company will be influenced by the outcome of the current interactions with regulators about drisapersen. Once we have more clarity on this, we will be in a position to provide updated financial guidance for remainder of 2014. I will now turn the call back over to Hans for some closing remarks. Hans?

Yes, thank you Berndt and thanks to everyone again for joining the call today. We remain committed to enabling a brighter future for the patients and to providing long-term patient access for drisapersen and our extensive follow-on programs. We will re-dose in initial group of boys for drisapersen in the third quarter of this year and we will continue to work very closely with key patient groups and experts in the field to enable drisapersen access to all older boys. We have an ongoing dialogue with regulators both in the United States and the Europe and we will communicate around potential regulatory path forward for drisapersen before the end of June. We look forward to updating you as we know more. I would now like to turn the call back to the operator, who will open the line for questions.

Thank you. At this time, we will be conducting a question-and-answer session. (Operator Instructions). Our first question comes from the line of Paul Matteis with Leerink Partners. Please proceed with your question.

Hey, thanks very much for taking my question and congrats on all the progress. So, I just had a first one on your interactions with the regulators thus far. Can you just characterize what you have been discussing with them? Has it just been about the re-dosing or have there been any talks about a potential NDA or a path forward or are you saving that for your next meeting? Thanks.

Thanks for your question, Paul. We had a number of interactions with regulators both in Europe and the United States. We mentioned in the first part of this call that we had a meeting with the FDA on the 24th of January. We also had a meeting with the European Medicines Agency as part of a so called business review meeting on the 26th of February and a number of interactions thereafter as well with both agencies. And of course our goal would be to see how we can provide drisapersen to as many boys as possible which would then mean a regulatory path forward leading it actually to approval. So our aim of these discussions is to see how does regulatory path forward could look like with the goal to helping as many patients as possible with drisapersen, and that is as broad as it should be.

That’s great. And then in the re-dosing can you give us an estimate of how many boys you think will go back in drisapersen? And then also what kind of data if any you’ll be collecting for safety six-minute walk dystrophy, anything that you think could bolster your argument in NDA filing?

Yeah thanks for that question as well. Of course first and foremost when it comes to safety one should realize that we have a safety data base where more than 300 patients were enrolled in various studies at three placebo controlled studies, two open label studies. If you look at all the treatment years of patients who have been treated in all these studies than you come to over 450 patient treatments here. So from a safety perspective we think that we have a fairly large program already. And the re-dosing is planned under a number of different banners. One would be the possibility to treat patients in expanded access programs, where basically it will be for compassionate use purpose. Another one could be to go for protocols and as Giles was mentioning earlier in the call at 501 protocol is typically such a lighter protocol where eventually patients may be treated after initial dosing in hospital potentially even in a home situation as well. And that will be to generate data but because that protocol 501 protocol is already available in United States that will be a fastest way to help those patients as well. So those are some comments about the purpose of this re-dosing plan and also how that could take shape. Giles any additional light from you in this one? And I’ll come back later as to how many patients have indicated that they would like to participate in re-dosing plans, but that is an overwhelming majority. But Giles first maybe you could give some more color on the various shapes that re-dosing could take.

Yeah the prime motivation to restart dosing is being in response to the demand that we’ve had from patients and investigators. But of course in these protocols one we will continue to monitor patient safety that’s obviously a key concern. But we will also within the restrictions are trying to reduce patient burden as much as possible to continue to follow efficacy parameters in particular of six-minute walks. So we’ll be able to continue to increase the amount of experience we have with drisapersen.

And to go back to your question on the number of patients which we’ll be willing to engage in re-dosing programs and we did send out a survey earlier this year after initial contacts with the number of patient efficacy groups who recommended this approach to us and we did reach out to investigators who then reached our patients at their sites. And based on the feedback we got from those investigators some 90% of all patients would like to go back on dosing, which is very encouraging. On top of that since actually September last year already we have received numerous emails and letters and requests from parents all over the world of patients who were in various studies and many of these requests are very emotional and begging Prosensa to go as quickly as possible back to re-dosing and we try to explain in various occasions in patients efficacy group calls as well that a number of steps have be taken but we’re determined to start dosing now from the third quarter onwards.

That’s great and then one more, and I’ll let others, I appreciate all the color. So just on the data for 45 and 53 expected in the fourth quarter and the first quarter of next year. What kind of data could we see there? Could we get any dystrophin or six-minute walk test data? And given that these compounds operate via the same mechanism of action or from the same chemistry do you think that data from these compounds could go into a regulatory filing for drisapersen. Thanks very much.

Yes the programs of 45 and 53, the initial phase is based on trying to find the dose. So we’re looking at a number of variables to help inform picking the right dose to go forward into the treatment phase including things such as molecular response and that includes exon skip and dystrophin, but also we will be collecting efficacy parameters such as the six-minute walk. The other aspect that we’ve implemented into our new programs since the imaging as well, and that we think is going to play increasingly important role in helping us to look at the impact of this type of intervention on muscle disease. We also included that in some of our natural history sites as well.

Thank you. (Operator Instructions). Our next question comes from the line of Yaron Werber with Citi. Please proceed with your question.

Hi, this is Tennen (ph) in for Yaron this morning, wanted to congratulate you again on the progress and just a couple of quick questions. I was wondering, first, if there were any differences between the Natural History of the disease in the U.S. and EU versus the rest of the world, that might support what you are suggesting might have been happening in the Phase III trial.

That’s the work that we are looking at in terms of subsequent analysis, I mean I think the general comment as Hans indicated was certainly that the boys in the Phase III program were more, in general more progressed in their disease. Another influence maybe through different standards of care in different parts of world and certainly what’s characterize Phase II studies which we conducted in 14 and 13 centers in Europe and the U.S. respectively were the standards of care in those areas were relatively homogenous and patients were left progressing their disease and that’s why we feel we had different results in those two trials. So, we think that variability from having multiple sites throughout world and potentially differences in standard of care may well have played a role in the Phase III result.

And just to add to that in the Phase III results, we have done a retrospective post-walk analysis of the Phase III results in those centers which previously participated in earlier drisapersen trials that concerns in total six centers and then we saw in that smaller sets of patients and totally talking about 26 patients, 9 on placebo versus 17 on drisapersen, so fairly small sets. So, I don’t want to give any guidance on drawing definite conclusions from this. What interesting was that we then saw that there was a treatment difference between drisapersen and placebo of 62 meters after 38 weeks with a P value of 0.058 and at 24 weeks? So, shorter duration in those same six sites that treatment difference was over 50 meters and was statistically significant. But again you talk about a small number of sites which previously participated and we don’t know to what extent we can draw definite conclusions about standard of care or let’s say a country impacts may have played roll there but at least this is interesting to note.

Got it, terrific, very interesting to think about. And one quick other question about potential biomarkers, from what I have seen dystrophy and how those correlated with immunotory improvement in every patient. Can you talk a little bit more about may be using CK or how imaging have improved the ability to analyze muscle function in these patients?

Yes, let’s talk dystrophin I mean for us as well it was absolutely the objective to be able to show a potential correlation between dystrophin expression and functional outcome that is that would be the holy grail because then future clinical trials could be far shorter by only shown dystrophin restoration in a small number of patients and hopefully correlate that to a functional outcome. Now so far based on our own data but also based on the data which are in the public domain as well as based on expert meetings and it was meeting in December 2012 with Publication in early 2013 by number of experts in the field. Unfortunately, we cannot draw that conclusion at this moment in time that dystrophin can be seen as a surrogate endpoint to predict on a per patient basis what the functional outcome could be. Having said that, we think we strongly believe that we have confirmed the mechanism of action of drisapersen through dystrophin restoration whereby the DEMAND II trial results have been most compelling. At the same time, we are continuously looking at other biomarkers as well and CK, creatine kinase which is a market of muscle integrity is just one example. What we did see in the Phase III trial but also in all the other placebo-controlled trials is that we did see reduction of creatine in the drisapersen treated patients and versus the placebo treated patients. And in the Phase III trial that was statistically significant with the P value of less than 0.001. So, that is a very interesting finding especially when you take into account that for example in the DEMAND V study, so the 114876 study in United States where we have 24 weeks of dosing followed by 24 weeks of follow-up without treatments even though in that period we did not see or we saw I should say, we did see a maintenance of the functional outcome but CK in the drisapersen treated patients went up again. So it came down in the first 24 weeks and then in the no treatment period it went up again which is also an interesting finding. So that is regarding CK and we don’t know yet we are at a functional outcome correlation can be found there, we really have to dig more into individual patient data to see relation in certain subsets may exist. And then on top of that we look at other biomarkers like MMP-9. As Giles was saying we look at MRI imaging to see to what extent that infiltration maybe less in most of groups as well. So we’re really embarking on a number potential biomarkers but to come to the conclusion today that there is one specific biomarker which is able to replace functional measurements and that is too stretched, we’re not there yet. Giles any additions or do you think that I explained it well enough.

I think that a comprehensive response Hans.

Thank you. Our next question comes from the line of Paul Matteis with Leerink Partners. Please proceed with your question.

I just wanted to clarify one aspect of the re-dosing. So can you explain, so it sounds like in the U.S. you are continuing an existing protocol in the EU you’re starting a new protocol with also some of the patients being dosed under compassion. [Indiscernible] might getting all that -- I am sorry this is a little bit complex it sounds like there is a few moving parts. Can you help clear that up? Thanks.

Yes, essentially what you said is correct. If the program as was existing at the time of transition to us comprised a large extension study 349 which was involved the Phase 2 study in Europe as well as the Phase 3 study and that was at fight all over the world. Clearly if you want to re-dose in sights around the world, one that’s a logistic issue and two there may be different ways to approach re-dosing based on individual and national requirements. So we’re taking a more customized approach to those studies. In the U.S. there was a single extension protocol 115501 which was still open at the time that we resume right. So for us that it was much easier to keep that protocol open and then to be able to start re-dosing in the U.S. and we will include Canadian sites within that study as well. In Europe we have a number of options, one of that critical part I think is the individuals that have been on nearly four years of dosing and that we’ve turned our attention quickly to them, because they have been on the drug for so long and so that has one of our priority attention.

To add to that Paul we have had a number of interactions with key investigators in these previous case studies to inform them about our plans of re-dosing, to inform them about the protocols by which that could occur and of course to our feedback as well and based on all that feedback and those interactions we have decided to start re-dosing in the third quarter of this year.

That’s great, thanks for the clarity. And I have one more follow up about dystrophin in quantifying it. So I think a lot of investors wonder why your competitors Sarepta reports anywhere from 44% to 46%, dystrophin expression of normal where as your numbers are lower but obviously there is real discrepancies between the methodologies that you use and then also now you’re talking about looking at biomarkers on via MRI. So can you just help us understand the differences between these quantification methodologies and how we should look at differences in the absolute number of dystrophin via various methods? Thanks.

Thanks for that question. First and foremost what we should be very cautious in comparing the numbers the data but also the methodologies used by various companies. In our case we have spent a lot of time on trying to optimize our methodology which is basically I would say an operator independent methodology where we make use of certain software, with software and a computer will decide whether a certain fiber has the certain intensity. So it’s not about an operator deciding whether a fiber is positive or negative because fibers can be slightly positive or slightly negative or half positive half negative, whatever way you want to look at it. So the software basically will decide the intensity of an individual fiber, so in a screenshot under the microscope we will be looking at a huge number of fibers and each of these fibers will be numbered and will then get (ph) at intensity measure. And that will then lead to a curve -- accumulated curve of all the fibers with an intensity let’s say of 300 and all the fibers with an intensity of 250 and 300 and so on. So then you’ve got curve patients and we can do that both for placebo treated patients and for patients on drisapersen and we can also do that for pre-treatment biopsies and post-treatment biopsies, so that was you get a curve and hopefully a shift of that curve for placebo treated patients where you hope that that curve will not shift because pre and post-treatment should be the same with drisapersen patients you will see that the pre-treatment curve will be then shifting to the higher intensity in the post-treatment phase that’s the methodology which we apply and we have submitted an abstract or a publication for that methodology that is currently under peer review and once that is published it can be seen by everyone and hopefully also be copied by anyone in order to come to more standardized methodology for other companies as well. So, in that way when you then look at the results, you cannot just say the percentage shown by another company can be compared to our percentage because that cannot be done because the methodologies are totally different. So that’s why we feel also given what we said earlier that dystrophin cannot be seen at least yet as a surrogate endpoint as a predictor of functional outcome and we have confirmed that our methodology has shown that the mechanism of action of drisapersen goes through exon-skipping and dystrophin restoration. But at the same time, we have seen patients who have a good functional outcome that did not a dystrophin increase or the other way around we have seen patients with dystrophin increase but a less optimal functional outcome change. So that correlation is not there that’s what we can conclude from our own data but neither can we, if we look at the publicly available data which are known from other companies as well. So, maybe that’s an introduction I mean you can make it even more technical if you want to. But again I think you have given a very comprehensive response, so I mean I will leave to the question, if you have any further questions and we can respond.

No, that was very helpful Hans and Giles. Thank you very much and thanks again for taking my follow-up.

Thank you. Our next question comes from the line of Hua Tan with Coumarone. Please proceed with your question. Your line is live. I am sorry our next question comes from the line of Debjit Chattopadhyay with ROTH Capital Partners. Please proceed with your question.

Hey, good morning and thank you for taking the questions. Just wondering and thinking out loud here, I mean the drisapersen DEMAND III Phase III trial had sicker patients, right. So, is there some kind of a correlation, if you look at the Geiger equation, it seems to be fairly predictive if the baseline walking distance is of 315 meters in the low. Did the Phase III correlate with the decreases that you saw with the Geiger equation? And number two on the dystrophin question, may be from MRI, is there an effort underway to look at our ratio of say the muscles versus the adipose tissue because if you have more adipose tissue then exon-skipping the platform may not really work because you are not going to be producing dystrophin if you loss musculature? Thanks.

Thanks Debjit for your question and I will leave the NOI question for Giles who is really expert in our company on MRI, also given his past experience at other companies. And talking about your question about baseline criteria so indeed when we look at the Phase III results and we look at this subset of patients and again post-talk analysis so retrospective but if we look at boys who have a baseline between 300 and 450 than we did see in the age category above seven, we saw a 25 meters delta between placebo and drisapersen, not statistically significant. In total, we talk about a total group of 49 patients in that cohort which then let’s say sharply contrast with the patients who have a baseline below 300 meters at an age above seven where there are also more than 40 patients in that segment and that’s where you see the largest variability and we are seeing that especially those patients who have a lower baseline than 300 and older above seven that those patients really have potentially impacted the outcome of the Phase III trial because that’s where you see huge variability. There are patients who lose ambulation, there are patients who lose a large delta in the six minute walk distance whereas if you compare them to the boys who are seven years or younger that’s we saw then 21 meters different, also not statistically significant. In total 80 boys there, less variability in that group, so we think that age and baseline really are two important characteristics to better understand the Phase III data but also to help in the design of future studies in the DMD space in general because the Phase III really has been, given that a lot of information to the company to be able to better design future studies and of course we will be sharing that information - actually we do now already but also eventually in publications and on scientific meetings with age and baseline are two important characteristics but there maybe more. For example the length of steroid treatments is something we’re still to look into, and we know for example this is done to anecdotal reports that some of the patients in the Phase 3 trial were specifically put on steroids and start -- not on start the study because the inclusion criteria it had to be in steroids for at least six months. So we’re steroid naive patients who then were put on steroids in order to be able to enter the study six months later. So we do not know yet what impact that may have had. So we’re still not with the possibility to look at individual patient data assessing that but of courses one parent described it very clearly I think when we got very compelling letter from a mom who was writing while you are analyzing how this drug works, I know that it works. And at a certain moment we have to find a balance between ongoing analysis and really trying to understand the data in every single detail versus our goal of providing drisapersen access to as many boys and as quickly as possible. Now on MRI I would like to hand over to Giles to say something more about that and the question that you had about imaging.

Yea I mean, I think in terms of both trying to understand the patient population that we’re studying and to understand the natural history imaging could really help us. And precisely for the reason that you mentioned that exon skipping to be effective as to interact with the nucleus of the muscle fiber. And if the muscle particularly in muscles supporting ambulation being substantially replaced by fat or fibrosis then you would anticipate less of an impact. And I think that’s where MRI can come into its own, because it can provide both the qualitative and quantitative assessment of what the muscle tissue is doing particularly for ambulant patients. So if you have an individual even though that he has a baseline six-minute walk that would be considered adequate but on imaging you realize that most of that muscle is replaced with fat than any therapeutic will have a poor chance of showing an effect. And so I think increasingly we’re thinking about different boys, certainly when they are on the cost of lowing ambulation, the six-minute walk is probably now a good measure of therapeutic effect, and that’s one of the things we’re investigating. And I think MRI certainly from the longer studies that have been carried out could show real insight and we think it’s going to be important for the subsequent programs as well. So that infiltration can be measured MR, looks T2 waiting the sequences and also the technical term [indiscernible] which can look at the amount of fact infiltration as well.

Thank you and just one more follow-up question. Some of the boys are fairly older in the DEMAND III study. I was just wondering if there was an imbalance in ACE inhibitor used across the two groups. And are you also looking at pulmonary function going forward? Thanks.

Yeah I mean, I think that’s an important question. I think one of the bigger imbalances was in the older age group there were substantially more individuals on drisapersen placebo. So I think that is an important consideration. As far as looking at pulmonary functions; I think the sense is the pulmonary function is something that is unlikely to change in ambulant boys substantially within a year’s timeframe and there have been a number of studies that we look to that, that may be more relevant longer term extension studies. With that question operator I think that we will close this call and I’d like to just make a few closing remarks again and we repeat what I mentioned earlier. We at Prosensa remain committed to enabling a brighter future for Duchenne boys and to provide really long-term access for drisapersen and our follow on programs. As mentioned we will re-dose initial group of boys who drives a person to third quarter of this year, we’ll continue to work very closely with key patient groups and experts in the field to enable drisapersen access to a lot of boys. And finally, we have an ongoing dialog with regulators both in United States and the Europe and will communicate around a potential regulatory path forward for drisapersen before the end of June. And with that I would like to close this call and thank you for your interest in Prosensa and joining our today’s meeting. Thank you.