Good day, ladies and gentlemen, and welcome to the Amicus Therapeutics Fourth Quarter and Full Year 2011 Results Conference Call.[Operator Instructions] Now I’ll turn the conference over to Sara Pellegrino of Investor Relations for Amicus. Please begin.

Good afternoon, and thank you for joining our conference call to discuss our fourth quarter and full year 2011 financial results. Here on today’s call we have John Crowley, our Chairman and Chief Executive Office; Bradley Campbell, our Chief Business Officer and Daphne Quimi, our Corporate Controller. They are joined by Pol Boudes, our Chief Medical Officer and David Lockhart, our Chief Scientific Officer, who are available to participate in the Q&A session. As a reminder, this conference call will contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 relating to the business operations and financial condition of Amicus, including but not limited to preclinical and clinical development of Amicus candidate drug products, the timing and reporting of results from preclinical studies and clinical trials evaluating Amicus candidate drug products and the projected cash position of the company. Words such as, but not limited to: believe, expect, anticipate, estimate, intend, likely, should and could and similar expressions are words identifying forward-looking statements. Although Amicus believes the expectations reflected in such forward-looking statements are based upon reasonable assumptions, there can be no assurance that its expectations will be realized. Actual results could differ materially from those projected in Amicus’s forward-looking statement due to numerous known and unknown risks and uncertainties, including the risk factors described in our Annual Report on Form-10K for the year ended December 31, 2010 and other public filings with the Securities and Exchange Commission. Amicus does not undertake any obligation to publicly update any forward-looking statements to reflect events or circumstances after the date on which any such statement is made or to reflect the occurrence of unanticipated events. At this time, it is my pleasure to turn the call over to John Crowley, Chairman and Chief Executive Officer of Amicus.

Great. Thank you Sara. Good evening, everybody. We are indeed off to a great start in 2012. I think a lot of that is going back just over the last several weeks, at and around the JP Morgan conference, with the release of some of the data with the combinations, even proof of concept study in 013. I think as we think about the strong start to 2012 with some of the new data, the new strategy that we’ve articulated, you can look back to 2011 and if I can, I’d like to begin just for a moment and reflect back on what we did in 2011 that we think laid such a strong foundation for 2012. Of course, one of the primary drivers of value for shareholders at Amicus, as our Fabry program with the Migalastat and with that the 011 study for monotherapy approval of the drug. Enrollment of that study into and through the end of 2011 was a critical part of our successes, both in building relationships and bridges with the physician community, in addition to providing the success hopefully as we look to data in Q3 of 2012 for that program, so enrollment in 011, very important. Likewise we laid the foundation for 012 and 013, 2 separate studies we’ll be talking about on this call as well, together with continuing preclinical work to further strengthen the program for Migalastat for Fabry, as well as the broad technology here at Amicus. In 2011 we also continued to build upon the deal that we had signed at the end of 2010 with GSK rare diseases. 2011 was a terrific year in building on that working partnership that we strengthened and advanced with our partners at GSK and in addition we spent a lot of time and…

Great. Thanks, John. Hello, everybody. Before I get into the details of the chaperone ERT combination programs, I’d just like to echo John’s excitement of our Phase 3 Fabry program and the significant opportunity that we believe exists for migalastat as a monotherapy. We are all eagerly anticipating the results of a study that we hope could lead to an important new treatment option for a number of Fabry patients. With that let me shift gears to our chaperon ERT combination platform. Right now we are evaluating several chaperone-ERT combinations and Phase 2 studies in Fabry and Pompe and preclinical studies in Gaucher and other undisclosed LSDs, where we believe there is a significant opportunity to improve current ERT products. As a reminder, as part of our Fabry collaboration with GSK, we are developing migalastat as a monotherapy and in combination with ERT, however outside the Fabry program, we own exclusive rights to all of our other assets. As we have described before, when co-administered with ERT, pharmacological chaperones are designed to bind to and stabilize the infused recombinant enzyme in the circulation of patients on ERT regardless of their mutation type. Preclinical chaperone-ERT and co-administration studies in animal models of Fabry, Pompe and Gaucher have all shown that a pharmacological chaperone can selectively bind to and stabilize the enzyme, prevent deactivation in the circulation and increase uptake of active enzyme into key tissues of disease. In addition in Fabry and Pompe animal models, we’ve shown that this increased activity in tissue uptake has led to greater substrate reduction than ERT alone. Based on these preclinical data that we’ve generated so far, we are conducting 2 Phase 2 open label studies, 1 for Fabry and 1 for Pompe, to evaluate our first 2 chaperone ERT combinations in the clinic. Patients…

Thanks, Bradley, and good afternoon, everyone. Before I turn to the fourth quarter 2011 and full year financial results, I will quickly comment on our cash position and reiterate the full year 2012 financial guidance that we announced during the JPMorgan conference in January. Cash, cash equivalents and marketable securities totaled $56 million at December 31, 2011 and $60 million at the beginning of 2012, compared to $70 million at September 30, 2011 and $107 million at December 31, 2010. We anticipate that our current cash position will be sufficient to fund operations into the middle of the third quarter of 2013. This projection includes anticipated Fabry program reimbursement and development milestones, but excludes potential regulatory milestones under our agreement with GSK. As a reminder, we are eligible to receive up to $170 million in development, regulatory and commercial milestones, as well as tiered double-digit royalties on global sales of migalastat. We expect full-year 2012 operating expenses to total $37 million to $43 million, net of anticipated cost sharing and milestones related to the GSK collaboration. Turning to the financial results, I will be referring to Table 1 in our press release, which is available on our corporate website at www.amicustheraputics.com. Additional details can also be found in our Form-10K to be filed in the next few weeks. Total revenue was $5.6 million in the fourth quarter of 2011 compared to $0.9 million in the prior year period. For the full year 2011, total revenue was $21.4 million compared to $0.9 million in full year 2010. Our total revenue consists of research and collaboration revenues, recognized under our collaboration with GSK from Migalastat. Research revenue reflects reimbursement from GSK related to our agreement to share total development cost for migalastat. Amicus and GSK equally shared development costs for migalastat in…

Great. Thank you Daphne. So hopefully everybody can see that there’s a lot of excitement here at Amicus building for all of our programs and the advancement of the technology. We’ve seen a great appreciation in our equity over the last month and that’s certainly a good thing and hopefully representative of a lot of the great work being done here at Amicus, but we’ve got much, much more work to do through the course of this year. Through 2012 we will deliver some very important clinical as well as pre-clinical data on multiple of our programs. But we’ll also be providing continued dialog with the investment community and continued perspective on our strategies for how we’ll leverage our technology and our programs going forward in every case with the same goal and that’s to develop therapies for people living with these rare diseases. So with that, we’ll turn it back and happy to take your questions.

Thank you. [Operator Instructions]. We have a question from Ritu Baral of Canaccord.

Thanks for taking the question. I wanted to ask about the combo therapy programs, both Fabry and Pompe’s and sort of how they relate to each other. I’m assuming based on the timeline of Fabry’s data, additional Fabry’s data first, could you talk to the read-through that we should get from the Fabry’s program to Pompe’s and how the 2 enzyme therapies compare and contrast and how the chaperone benefits to either ERT should compare and contrast?

I think there were multiple there. As a prior litigator, I probably should have objected to the questions if possible, but I will try to answer it as best I can and certainly ask David or Pol to weigh in as well. I think if you step back and think about it, what we are talking about here is several fundamental limitations of these first generation therapies. So, enzyme replacement therapies have been around for several decades. They’ve offered enormous benefits for a lot of patients. We’ve seen in different diseases, different levels of efficacy for sure. If you take it to what we are doing in Fabry and what we are doing in Pompe disease, obviously 2 different disease, 2 different enzymes, but the same fundamental problem, and that you are taking large amounts of protein made in bioreactors in multi hour infusion and taking it from a lyophilized powder, reconstituting it into an infusion bag and putting enormous amounts of protein then into infusion bag and indentation from plasma and hoping then through the whole process of receptor-mediated endocytosis that it ends up getting taking up in to the liposome of target tissues. The challenge is several folds with the ERTs. One is, primary that the enzymes that we are dealing with are enzymes that we all without disease naturally make and that live in the liposome. The liposome pH is more like 5, a highly acidified compartment when you’re putting it into the infusion bag at pH, neutral pH of 6, 6.5 or so and then when it hits the plasma at pH 7.3, it becomes a very, very unstable protein. They lose a tremendous amount of their activity. They not only become less potent, we think as you’re seeing them begin to unfold and come apart…

No. Do you see alpha-glucosidase as being more immunogenetic than galactosidase and the interaction between 2220 and glucosidase, are there lessons to be learnt from migalastat and the Fabry enzyme?

It seems from the literature and from talking to physicians and in our experience, the Fabry ERT seems to be less immunogenetic than Pompe, but still we see immune responses in virtually all patients in Fabry disease. So we do think the immunology of the ERT and the immunogeneticy of any of the currently marketed ERTs could be a very important factor in terms of the therapeutic efficacy and again, we will have to explore that in a clinic and see what impact we can have. Obviously, from what we’ve seen and from what others have seen, the Pompe enzyme, the myozyme, lumizyme enzyme, that’s in a few markets seemed to be very, very immunogenic. They do have a black box warning, there was anaphylactic with them in the clinical studies, but even more so we think that some of the immune response that you are seeing actually impedes the therapeutic efficacy due to the immune response created by this unfolded, unstable enzyme in blood and that was part of the grant that we were just given from the NDA that Brad referred to. We are going to explore that and again, I think that will be part of the important preclinical data that we’ll have this year, as well as the clinical data from the 010 studies. So if there is an area where we think we can have an impact in Pompe, I think it’s twofold. I think its protein potency as well as the immunogenicity, so we’ll continue to explore this.

And one more question and I’ll hop back in the queue. 012 enrollment, are there lessons learnt from the FACET study? Do you see it being more efficient and you seem to have given it sort of shorter timelines than what we experienced with FACET.

Yes, it’s a little bit smaller study. It’s a 50 patient study. There are no biopsies, so I think that helps a great deal in terms of patient interest, getting into the study. There is no placebo arm. I think that’s important. People will either stay on ERT or go on to our drug. So I think all those weigh in favor and yes we’ve learnt a lot and we’ve built a lot of relationships. One of our key learning is to enroll these studies with the right patient, you have to screen a lot of patients and to do that you have to open a lot of clinical sites and we are well on that path in the 012 study and it’s also, if you remember when we started the 011 study, we did that prior to the GSK relationship. 012 really got up and going last year and we’ve done a lot of that work together with GSK. So in lot of the geographies where we might not have a strong presence, we are seeing great participation from our partners at GSK, helping us make sure we can have the right reach globally.

Thank you. Our next question is from Joseph Schwartz from Leerink Swann.

There was some striking data on the laterius effects of immunogenicity at WORLD in areas like Pompe and I’m wondering, when will we be able to get some data on your ability to zero [ph] revert I guess or how do you expect to study the ability of the chaperone technology, to translate, improve the maturation profile and serum half-life on antibodies?

I think we are looking at it and I’ll ask David and Pol to add some color as well Joe, but again, we are looking at that with continued preclinical work, so a lot of the work that we are doing with the NDA grant and the data that will be generated through this year, will characterize the immunogenicity of myozyme, lumizyme products and also what we might be able to do to mitigate that, specifically with the addition of our drug. There are a number of ongoing preclinical studies at Amicus and we hope to have more of that data through the year, to talk about what we might be able to do to mitigate that response. The 010 study, just to remind you, of course is a short term PKPD study, although we’ll evaluate some of the potential immunogenicity involved in a short term study, we wouldn’t expect to see that we have any changes there and Pol, Dave, do you have any color to add to it – please.

Joe, one of the key measurements in preclinical studies is you can look at a T-Cell response in human T-Cells. So we’ll be doing that over the course of this year and that is part of the Muscular Dystrophy Grant. As John said in the first clinical study, since its only a single delivery of the small molecule in combination with the ERT, we don’t expect to see anything in particular reducing the antibody titers, but in the next set of studies where we have longer term treatment, we’ll be able to see in patients who start with a measurable antibody titer, can show a reduction with time. So that just requires the repeat dosing studies that will be coming after this first single does study.

Okay great. That’s very helpful, thanks. And then as a follow-up, how do you envision the regulatory pathway for combination therapy? Would it have similar end points do you think as monotherapy, but you just want to show an effect on top of ERT or is there some other potential way to bring it to market.?

No, we are looking at other potential avenues in terms of broadening the label Joe. We do think that the monotherapy program for migalastat will be the foundation for the launch. We can envision multiple different ways to move very quickly from this PKPD Phase 2 study, the 013 study, to a confirmatory Phase 3 study, but in every case what we want to be able to show is that the addition of the chaperone provides a better benefit for patients that is essentially superiority over ERP alone. And there may be different ways that we can measure that. It may include some of the end points that we’ve used before, things like GL-3. We think that could be a study that where urine GL-3 input in a short term study could be particularly appropriate, but we will also look at other potential end points, including ones related to immunogenicity, which may end up being a provable end point potentially.

Thank you. Your next question is from Geoff Meacham of JPMorgan.

This is Anupam Rama in for Geoff Meacham. Just a quick question. In the female patient study at WORLD, there were few patients that showed improvement in left ventricular mass. Can you just kind of help us understanding that improvement and put it into context and what that means for Fabry patients and I’m assuming its mutations that are sort of associated with less ventricular mass. Thanks.

David, do you want to comment and I’ll ask Pol to follow-up with any other thoughts.

Just to point out that cardiac abnormalities are very common in Fabry disease. It’s a whole host of different abnormalities and of course being able to see, even some normalization of any of those would be a very positive sign. We shouldn’t over interpret what we’ve seen so far, but we do find it encouraging whenever there is any normalization of an abnormality in any of the key organs of disease. So I think that it’s interesting, but we do have to be carefully not to overstate that quite yet.

[Operator Instructions] We have a follow up from Ritu Baral of Canaccord.

Of course, I have a follow-up question.

Carry on.

Going back to the world data, we also saw some interesting Fabry’s incidence and prevalence data. Can you tell us what you think about sort of the much, much higher incidence rate seen in some of the instant screening studies presented at the conference versus sort of what’s generally accepted as prevalent.

If you look at the text of literature Ritu, it says that the incidence of Fabry is about 1 in 40,000 or 1 in 50,000 and that there are 5000-plus people in the developed world. That characterizes I think the classical early onset form of the disease. The disease for instance, that Genzyme studied, that segment of the disease in its confirmatory studies almost a decade ago for Fabrazyme. But if you really look at it, it’s like many genetic diseases where there is a broad spectrum of symptoms and a broad spectrum of onset of disease. And I think what these epidemiology studies and screening studies are showing is that Fabry is indeed a much, much more prevalent disorder than people have traditionally thought. The studies that were presented at WORLD showed -- I think the 1 from the Illinois screening showed that 1 in 1700 incidents. Others that have been published from Taiwan and other geographies over the last couple of years have shown 1 in 3,000, 1 in 4,000, which make us much more akin to the prevalence you see in something like a Duchenne muscular dystrophy or cystic fibrosis and if those continue to play out, it could end up being that Fabry, together with CF and a few others is among the most prevalent human genetic disorders out there. You are starting to see Fabry diagnosed in cardiac clinics and there were some presentations about that at WORLD. For people that never suspected Fabry before, people with undiagnosed, left ventricular hypertrophies for instances, other cardiomyopathies. You are seeing it in renal clinicians where people are finding Fabry where they have never looked for it before and again, this is a phenomenon and a series of studies that’s been developed over the last couple of years. It’s one that Amicus and GSK are very much interested in, particularly because many of these studies have shown that the ability to find this Fabry disease in people at such an early stage usually translates with these people having what’s traditionally thought to be a late onset form of the disease, where they would be symptomatic at certain points in their life, but they would have the pathology of disease throughout their life and many, many of those mutations with clear majority seem to be the type of mutations that would amenable to chaperone monotherapy. So it’s something we are very, very interested in.

As far as the screening programs and potential increased diagnose, how do you see that impacting the Fabry market as far as timing and do you see that sort of kicking in the next couple of years? Is it more of a 5-year process or a 10-year process?

I couldn’t tell you exactly how long it would be Ritu, but it’s something we have been thinking about even prior to the WORLD meeting with GFK for sure. Others, I mean Shire, Genzyme has done a very good job at beginning to explore some of those other potential patient populations. So as we look at our forecasts internally, we’ve been very conservative about what the chaperone monotherapy population could be. Again, whatever that number is, we still believe that migalastat is appropriate for 40% to 50% of people with Fabry. So I think as more and more people are diagnosed, if it really is that prevalent of a disease. Finding them earlier is only going to be a good thing and having an option of a therapy like migalastat is only going to be a good thing.

And final question, looking at the responsiveness rates in the WORLD data that you guys presented, with the assumption that there is some selection bias in those 80% and 85% figures, how much of it do you think is patients say in the US or Europe who already know what their mutation is and whether they are mis-sends or whether they are on your sort of list of responses mutations. I mean, do most Fabry patients know their exact mutation and where they fall on your responsiveness charts?

I want to make sure I understand your question. You mean in terms of how they got into the study?

Yes, as far as screening dynamics, I mean from what I understand there were many, many at least U.S. Fabry patients know their exact mutation and can look on one of the many charts that you provided to the Fabry’s community and say, "Oh, I’m responsive, I should enter," but at the same time your finding new mutations. So I’m just sort of wondering how that dynamic shakes out, both as far as known and unknown mutations, as well as the U.S. and x U.S.

I think it shifted it a bit in a favorable direction Ritu. We don’t mean to imply that because of the screening study you can extrapolate that to say that 80 plus percent of people could be amenable to the chaperones and monotherapy. I think there was some selection bias where patients or their physicians knew that the Amicus Phase II study has been successful and people with missense mutations broadly and that’s certainly like the R301Q, a little more prevalent in Fabry patients. So some of those patients very well may have presented knowing some of that. But I can tell you, and Dr. Bichet went through this in his presentation. Again, we have quite a range of mutations presented in this study. Of the 67 patients, there are 59 unique missense mutations that are confirmed and 13 of those were newly discovered mutations and in a lot of the geographies outside of the United States and again, a majority of these patients are outside the U.S., people presented not knowing at all what their mutations are. So I think as we look at this, as we try to be conservative, discounting some of these numbers for some pre selection bias. We still are very confirmable with our predictions, that roughly half of the people living with Fabry will be amenable to the chaperone of the monotherapy.

This is Brad. I think your logic initially is probably right, that in general in the U.S. and Europe and probably Japan, there is a little bit more awareness of mutation type either by the patient or the physician and as we go to the more developing countries, that’s less true and it’s not a perfect correlation, but as John said, we think the numbers will still hold and then as you get into the newborn screening and other kinds of other high risk screening populations, if we do uncover those more late onset types of mutations, then you’d expect that number to go up over time.

And Ritu it wasn’t, it clearly wasn’t complete pre-selection either. Out of the 140, they were 13 mutations that were completely new. They have never even been reported before. And they were ones that we had never seen, we had never tested and once we knew, once we got the information, then we tested them, but the patient actually brought the mutation in the door for the first time before it was even known it us. And there were also more than 20 patients in that first 140 who did not have missense mutations. So it wasn’t even just a selection for people with known, who have known to have a missense mutations as a fair number who were screened did now even have missense mutations or did not have a single missense mutation.

Thank you. Your next question is from Bill Tanner of Lazard Capital.

Thanks for taking the question. John, for you, just on 011 study, I know that the inclusion criteria, they are ERT naïve or not having been treated for 6-months prior and I’m wondering if you can make any comment as to which -- are most of the patients truly naïve or have they just not been treated and I have a follow up.

I have to follow-up with you, because I don’t have the exact list, but I could tell you we saw in Phase 2, that it was about a split between previously naïve and people who had been on [ph] a period of time. In this study given that a lot of the patients came from outside the United States, I’m pretty sure that the majority of them had not been on ERT. I don’t know Pol.

Yes, that’s right.

Yes, that’s correct. So a majority of the patients had never been of ERT. I don’t have the exact numbers for your Bill, but we can get that.

Go ahead, I’m sorry.

I was going to say with the shortage, I would be careful to draw too many conclusions there, because that’s just confounded the background of what patients were going through.

And then how should we just think about the severity of the disease for the patients that are enrolled. I mean, I guess the most obvious inference of patients wanting to stay on in the open label. The extension part is that its working and they feel good or both I guess. I’m just curious on the severity of their disease in terms of really needing to be on therapies --- such as someone who would have been on Repligal or Fabrazyme and had to get off, well against Fabrazyme because of the shortage and really needed the ERT.

Yes. No absolutely. Two things that are really important about this study. One is, that either it’s the largest Fabry disease study -- pivotal study every conducted with 67 patients and the second thing, more relevant to your comment Bill is that, what we’re studying is a true representation of a spectrum of patients living with Fabry disease and we have a couple of dozen males in this study, we have females, so it’s important, especially given that the population consists of a significant number of females. So we have some many, many patients in this study who would be considered at the severe end of Fabry disease in terms of their symptoms. In every case a patient is certainly symptomatic, they have Fabry diseases and because we put in that GL-3 criteria, that they have to have at least 4 times the upper limit of normal to get in the study, there is not a straight correlation between the urine GL-3 and the various disease, but there is a general correlation. So because of that, this is I think not only a broad representation of patients, but certainly patients who are very symptomatic with their Fabry disease.

And I guess, last question, is there a stopping rule then for patients who go on to the open label by the extension in terms of the GL-3 clearance going down or kidney function getting poorer. What’s the -- any criteria there? Any rule there?

No, I don’t believe so.

It’s Pol and there is no stopping rule. It’s up to the physician and the patient to decide what’s going to happen.

Thank you. There are no more questions at this time. I would like to turn the call over to management for any closing remarks.

Well, that’s all we have. That was a great call. Great, great questions. So again, off to a great start for the year, but a lot more work to do. Great, thank you. Good night.

Ladies and gentlemen, thank you for your participation in today’s conference. This concludes the program. You may now disconnect. Have a wonderful day.