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Neurocrine Biosciences, Inc. (NASDAQ:NBIX)

Deutsche Bank 37th Annual Health Care Conference Call

May 09, 2012 11:20 am ET

Executives

Kevin C. Gorman – President and Chief Executive Officer

Analysts

Navdeep Singh – Deutsche Bank Securities, Inc.

Navdeep Singh – Deutsche Bank Securities, Inc.

Hey, good morning everyone and thanks for attending the third and final day of the 37th Annual Deutsche Bank Health Care Conference. My name is Navdeep Singh and I’m one of the Deutsche Bank Biotechnology Analyst, and up next we have Neurocrine Biosciences and representing the company is Kevin Gorman, Chief Executive Officer. Kevin?

Kevin C. Gorman

Thank you, Navdeep and thank you to Deutsche Bank for inviting us to the conference. Before I start out, I’ll direct you to our Safe Harbor statement and our resent SEC fillings for an exhaustive detailing of the risk factors because I will be making forward looking statements today.

So I’m going to basically talk about our two main programs at Neurocrine today. The first one being our elagolix program, a small molecule GnRH Antagonists that we partnered with Abbott and Abbott now fully controls and runs this program.

The second program that I’ll be speaking about is our wholly-owned VMAT2 program for movement disorders. And so let’s start right in with the elagolix program. I usually never stop on this slide, but I will today because endometriosis is a condition that is characterized by at times extreme pain.

This is delectating, this affects young women. These are women who are in the prime of their carriers or their family life and it not only affects them, it affects everyone who interacts with that women and we have a fairly startling image here of a women that has barbed wire around her mid-section and we utilize this image because in the hundreds, if not thousands of women that have spoken to with endometriosis that is a recurrent thing that comes up from them. This is how the feel. This what this disease does to them.

I’m very pleased to say here today that the Phase III protocol that Abbott has designed has now been locked at Abbott. They’ve held the investigators meeting last week with all the investigators in this very large Phase III program. And in the coming days they will begin patient screening, which is the beginning of this trail drug has been shipped to all the sides. So this trail will be launching in just the next few days. The Phase III protocol, the end points are the ones that we defined at the end of our Phase II program that is two co-primary end points, non-menstrual pelvic pain, and dysmenorrhea, dysmenorrhea being the intense pain that is felt during menstruation.

As with our Phase II program, the statistical analysis is going to be a responder analysis that’s been agreed to with the FDA and this trial will be six months in duration and then a safety extension out to one year.

Shortly after the trial kicks off Abbott will be putting it up on clintrials.gov with far more detail and that’s when we will be able to talk about that detail, but very pleased that this trial is getting started and Abbott is putting considerable resources behind this entire program of endometriosis.

Also quite a bit of work has been done and continues to be done by Abbott and some of ourselves doing on market research getting this product ready for commercialization, pharmacogenomics and both qualitative and quantitative market research. Now the second half of this program is even a larger market opportunity than endometriosis and that’s uterine fibroids.

We did not treat any uterine fibroid patients in our large Phase II program that Neurocrine ran. That’s because we had the resources only to concentrate on one program at a time. Abbott, one of the main reasons we selected them amongst the competitive partners that we were looking at, at the time that we partnered us with them is that they were dedicated to develop this drug simultaneously in both indications; endometriosis and uterine fibroids.

So Abbott started up last year a proof-of-concept trial, a large proof-of-concept trial in uterine fibroids. They take patients in and get a baseline measurement of the disease for two months. This baseline measurement is bleeding, it’s interesting in endometriosis the primary problem or complaint and what the primary end point has to deal with is pain.

In endometriosis secondarily is bleeding, our drug takes care of both of those problems in endometriosis. In uterine fibroids, the primary problem and which leads to the primary end point is bleeding excessive, unpredictable, throughout the month bleed especially, heavy bleeding during menstruation.

Secondarily they do suffer from pain and discomfort from mechanistic aspect of antagonizing the GnRH receptor our drug should work in uterine fibroids just as it works in endometriosis. In endometriosis, the primary growth factor of these endometrial explants is Estradiol in uterine fibroids, the growth factors for the fibroid collisions and causing the bleeding is both Estradiol and Progesterone by antagonizing centrally the GnRH receptor we lower in a dose dependent fashion both Estradiol and Progesterone.

After two months of getting baseline bleeding, the patients get randomized into different cohorts and they are characterized by having in each cohort a placebo arm and then a dose of elagolix. Abbott does not disclose and request that we not disclose in this proof-of-concept study, what the doses they’re looking at here, suffice to say, it’s a broad dose range, that Abbott is doing in this proof-of-concept trial and then happy end of that three months of treatment, where the primary end point which is bleeding is taken and compared to the baseline, they then will follow these patients upon a safety basis for three months after that.

On clinicaltrials.gov. Abbott has the completion of the study as being the end of this year. I hope to get more color from Abbott on timelines and seeing where they are in everything with the entire program as soon as they are done with their long range planning which is taking place right now.

Now this reduction in uterine blood flow is not done subjectively as it has been done in the past where women look at pictorial examples of what their sanitary product would be and say yes, that looks like that. It’s actually done in an objective fashion, where they say all of their sanitary napkin, they are sealed up and the hematin content of them is measured and we had a standardized against their own hematin content in that individual patients, so this is a objective measure of blood flow.

Women, normal women’s blood flow per month is about 35 milliliters, to gain entry in this study you had to have a minimum of 80 ml of blood flow, so it’s quite a bit of blood flow, and the goal is to reduce that blood flow in those women.

So I think I’ve gone through the pioneer efficacy end point here these are approximately 300 women in this study about 50 per cohort. There is a number of secondary efficacy end points you can look this upon clinicaltrials.gov, you’ll see a lot of them, number of bleeding days, their severity in days of bleeding, uterine volume, and they are hematocrit fibroid volume that’s also being measured, but the primary end point is the amount of bleeding. So I’m very please now with the start in the coming days of that Phase III endometriosis and the phase that which the uterine fibroid program that’s moving along. All of which as I said is under the control of our partner Abbott.

So now I’d like to move over to our VMAT2 program, and this is a wholly-owned program by Neurocrine, and I’ll say at the offset that we plan on keeping this program to ourselves and commercializing ourselves at least in North America. Now VMAT2 is the Vesicular Monoamine Transporter 2. This is a target that is pre-synaptic and intracellular in the brain and it is responsible for packaging all of the monoamines.

So that as they are produced in the cytoplasm, they are packaged and then now they can be transported and released into the synaptic cleft; by all the monoamines, dopamine, and then serotonin, histamine, norepinephrine. VMAT2 preferentially packages dopamine, and that’s what we are interested in because as a target four movement disorders.

Tardive dyskinesia is the first movement disorder that we’re going to go after with this mechanism, there are several. All of them share the same feature. They have a hyper dopaminergic system going on essentially. So the goal of our program is to down modulate their dopamine system by inhibiting VMAT2, therefore reducing the amount of dopamine that is packaged or released into the synaptic cleft. We don't want to eliminate it obviously, you would get terrible side effects, if you did that, we just want to normalize it.

In these hyperkinetic movement assorted tardive dyskinesia, what you find with these patients and I hope to share with you in the future conference to be able to show you visually on some video is the type of movement disorder that takes place here in these patients. It is debilitating in their ability to eat, to breathe, to hold conversations, it isolates these patients.

It's mainly from the neck up that you see the most severe forms in tongue, mouth, jaw and facial discoordinated movements, but they also have it where the trunk is undergoing involuntary movements, which affects breathing substantially their arms and their legs. so, our goal here and this is caused by the antipsychotics that the patient is taking. So, where you first saw this arise was in schizophrenia patients where the antipsychotics were developed for, and that was the typical antipsychotics, caused a bit of raise that in the literature, it’s reported anywhere from 5% to 35%. I think the 35% is high. we use numbers somewhere between 5%, 8% or 9% is what we see there.

One of the great hopes for the atypical antipsychotics when they came along was that they would not cause tardive dyskinesia, they wouldn't cause this ramping up of the dopaminergic system, because of maybe being more selective presynaptically as inhibitors of the dopamine receptors.

Unfortunately they do cause it. Now they do cause it of the lower incidence. So they are causing at about a 4% to 6% rate. Again, the literature is still a bit all over the place. Some studies even very recently show that there is no difference in the incidence between the atypicals and the typical. So we’re doing a lot of work right now to refine this, a lot of good epidemiological work hasn’t been done to-date because there is no treatment for these patients. So, there is no motivation that’s been there to understand the exact rates that are going on here.

What you do now is the prevalence has gone up dramatically because the atypical antipsychotics have moved out of schizophrenia and are used now so widespread in a number of patient population bipolar, major depression, less (inaudible) patients, even children are being exposed to the atypical antipsychotics.

So what you’re seeing here is prevalence is actually higher in the atypical and that you see that bipolar and depression actually accounts for approximately 60% to 70% of the patient population now. And the schizophrenia is lower at about 30%. So, it really has changed the landscape of this disease. Again there is nothing available out there to treat this disease.

Our lead compound NBI-98854, we’ve been in VMAT2 now for I’d say about seven years. We’ve developed a number of compounds. We’ve got leads, which is 854 and we have backups behind these leads. 854 has been behaving extremely well for us.

I’m showing you here now the preclinical characterization here. When we first started out, what we wanted to make sure is that we had something that was very important at VMAT2 and we do, we have something that’s in the low (inaudible) as inhibiting VMAT2, and it had to be very selective. we didn’t want it hitting other receptors in the brain, we didn’t want it hitting VMAT1, which brings in all of the monoamines and has no preference for dopamine as VMAT2 does have. And we achieved that all preclinically that’s what we’ve nominated as a clinical compound. we've shown its in vivo pharmacology showing that it’s a dopamine depleter.

We’ve done a lot of drug metabolism. we believe that we have minimal risk for drug-drug interaction. We’ve done a lot of pharmacokinetics in mice, rats, dogs and monkeys. at this point in time, rats and dogs are the top species for this compound as agreed with the FDA. We’ve done a full battery of genotoxicity, which the compound ends up negative on all the genotoxicity batteries, both AIMS, chromosome elaboration, in vitro micronucleus. We’ve done the safety pharmacology in all the animals looking at CNS, over CNS symptoms check that up, particularly looking at cardiovascular signals both in the rats, mice and dogs and it’s negative unheard and it has no effects on in vivo QTc prolongation or a pulmonary function.

We completed at the end of last year, the three-month toxicology in both rats and dogs and we’ve completed Seg 1 and Seg 2 development and reproductive toxicology and the compound is clean in those. We’ve ended a Phase IIa study that we completed approximately a month ago and what we use as the prior end point here as agreed with the FDA is the abnormal involuntary movement scale the AIM scale.

The FDA, while there are several scales that are out there, the FDA and ourselves agree this is probably the most appropriate one that exists for this disease. All of them have their pluses and minuses. What this does is this scales the (physician rates) seven different body regions, gives a score of zero meaning no abnormal movements; 1, is minimal; 2, is mild; 3, is moderate; 4, is severe.

So, you could add up to 28 maximum points, a tardive patient will never have a 28 as a score. The most you are going to see in a moderate to severe tardive patient is going to be high teens, 16, 17, 18 things like that. And we go after the moderate to severe suffering patients. This Phase IIa study was a two period cross-over study.

So you take an AIM score at the day before they enter into the study. They either go on placebo or one of the two doses 12.5 milligrams or 15 milligrams of 98854, and then after two weeks they just switch over to whatever they weren’t on in a random fashion. If they were on drugs, they will now put on placebo, if they were on placebo, they now put on drugs and then a day 29, one day after that they’ve been on the second treatment period, another AIM score and what we looked at was day minus one AIMS versus day 29 AIMS, or I should say what we looked at.

After the first treatment period you had an AIMS score that was done on day 15, so that is the AIMS that looked at what happened in treatment period number one that AIMS 29 score is what happened in period number two, you are comparing those two AIMS scores. I will show you some day though when you compare back to base lines that day minus one.

I think as most everyone has heard in this study, out of the eight sites we had one site that miss-appropriately applied the AIMS for. And also allowed in patients into the study that did not qualify for the study. We removed the data from that it is a co-stock analysis I’m showing you here.

What I’d like to stress to you is that there you do not need a trained professional to see what a zero or one looks like versus a three or four. It is dramatic, it is apparent. At that one site patients were scored on several body regions with three and fours, they were independently scored as zeros or ones on video. That mistake can’t happen by even a casual observer.

We removed that site, we then re-ran the statistics on these patients and what you see when you have a baseline mean of AIMS is approximately 15, so these were moderate to severe suffering patients, and they had to a scored at three or four on at least two body regions, and you see that the 50 mg dose was highly effective, which you were seeing a mean of 15 going down to 6, that’s a dramatic startling improvement in these patients.

And again you don’t need a trained professional to see that, you would see that yourself in these, and a highly significant P value even for a trial now that lost seven of its 31 completers, you still have that kind of significance. The 12.5 mg dose just put in there in the anticipation it would be a minimal or no effect dose and sure enough 12.5 milligram dose did not have on a population that large of an effect. On an individual patient, it could have a good effective, but as a population basis, which we do clinical studies for, it didn’t have that large effect, that’s good. We define the lower end, the 50 milligram worked extremely well.

If you look at change from baseline here, you’re now seeing that you have over a nine point reduction of these patients and their change of baseline. That is enormous in the P-value here shows just how enormous that is. Again, I will reiterate this is a first stock analysis. We did remove one site, but with all those patients that were left in that 50 milligram that was a dramatic result. You don’t need statistics to show that.

And then when you also look at the patient global impression of change in the clinicians, global impression of change and looking only at a much improved and very much improved, just seeing approximately in 80% response rate here in the 50 milligram dose and you’re starting to see what looks like the dose response here between the 12.5 and the 50.

So, from a safety and tolerability, we’re very pleased with the study. And again you use all the subjects when looking at safety and anything that happened at one site as far as efficacy will not affect the safety ratings. Of the 37 patients randomized 31 completed, the AEs as you see here placebo with 17%, 12.5 plus 24, 50 was 32 looks like you’re getting more AEs as you go up and dose. In actuality, I can tell you that virtually that entire difference that 32% versus 17% in placebo was all made up by one patient. that patient had a lot of things going on. he was the patient here who showed, who discontinued, because of the adverse event of akathisia. Akathisia is basically a restlessness of the legs needing to move around, not being able to just stay still. that could be a side effect of our drug that would be a mechanistic side effect that you would look like; you look for in our drug, so that very well could be.

The only thing that might be, is that a little bit, which you need bigger studies in order to sort out more is that the antipsychotics caused that. And that patient has a history of akathisia coming into the study, but nevertheless, that is the kind of thing we look for to be able to identify to then use a lower dose of NBI-98854.

There were no treatment related serious adverse events. there was one patient who after of drug, for I think a week or something, they had an exacerbation of the LPD that has nothing to do with our drug, it is not drug-related. Again short study, they’re only on drugs for two weeks in the study, but we didn’t see any signal of emerging suppression, or suicidal ideation or anything there, again, you need longer-term studies in order to fully flush that out.

We did look at the Brief Psychiatric Rating Scale, BPRS, it was 32 at baseline, it improved to 28 adding the study small in, small change you wouldn’t really draw any conclusions from there. although I do have to say that this mechanism and Dr. Laughren at the Psychiatric Division of the FDA has recognized that this mechanism should be an antipsychotic in and of itself. So, not only would we able to treat the tardive dyskinesia, we can actually treat the underlying disease potentially and we’ll be exploring that as we further develop the compound. The pharmacokinetics where dose proportional again no obvious TDI issues, we took (inaudible) what antiseptic product they were on, typical A, typical we took them off, they didn’t seem to be any difference in exposure based on general gender, we had men and women both in here smoking or not, nor BMI.

So those are all good things bode well for larger studies going forward. So again this was generally safe and well tolerated in a post stock analysis, we did see a very strong and significant response with the 50 mg; we got out of this exactly what we needed to get out of the study. We need a proof-of-concept out of the study, we needed to define a lower end; we did. We have a highly efficacious dose of 50 mg, and so now we’re moving forward.

We met with the FDA just last week to lay out to them all the safety data we have and all of the preclinical TOX data that we developed, all the three months data that we developed in mice, rats and dogs. Since we opened the IND with the FDA and to get their approval that we have the margins and what we need in order to go ahead, from the agency into long term meaning three months study now, in the patient population and they agreed.

So that was a very productive, an important meeting for us. In that two week study, the patients came into the office every single day, whether they are in placebo or not because at that point in time, we only had a liquid formulation of the drug, had been made up each day, now we have capsule formulation, so in the upcoming studies that I will be talking about a large Phase IIb study than I’ll be talking about now. The patients go home with their drug, now so they have their own capsules.

And now, we are starting up the longer term TOX study, six and nine month TOX study in rats and dogs are being moved forward.

So, what we are doing in tardive now in the Phase IIb study, this is going to be a randomized placebo controlled trial, it’s not going to be a cross over, it’s a parallel design that is coming up. There are going to be two doses of 98854 versus placebo here and while this hasn’t been completely finalized, I think it’s 99% there with our clinical and pre-clinical group.

The doses are going to be the 50 milligram dose and a 25 milligram dose. It’s going to be placebo controlled for the first six weeks and then the primary end point, which is the AIMS score versus their base line will be taken against placebo. And then the placebo patients are going to be re-randomized to one of the two drug arms in a blinded fashion and then at the end of six additional weeks. So for a full 12 weeks then we will look for durability of the response there and look for the persistence of effect that we (Inaudible).

All the secondary end points that we had in this previous study are going to be in this study. In addition to that what we are going to now start to be doing in these longer term three months studies is we are going to be looking at the effect of our drug on their underlying psychosis, their schizophrenia. So, we will be about finding the panel score to these patients to see if indeed our drug is acting synergistically with their antipsychotic with the underlying disease.

It will be approximately a 120 patients. We haven’t completed the towering yet of this study and it will take up to 35 sites here. We’ve learned a lot from this last trial that we did. So, we are adding in a number of things into this upcoming study to make sure that we can’t have a single site like we suffered from in that first study. This is taking us a bit longer than to get the study up and off some of the things, we’re going to say goodness we had video of each and every patients in that previous study that we can go back to.

We will have that again, but this time on baseline prior to randomization, there will be an independent video reader who will see every single patient at all 35 sites and that person has final say as to that patient qualifying for the trial. So we won’t have any force going in the 17s into the study. We’ll have two investigators add to each site, one investigator is going to be the one that gives the care as the patient comes in along with the nurse. That’s going to be their primary care giver at that site.

The second investigator only sees that patient for 15 minutes, about three times to apply the AIMS score and we are doing much more rigorous and training of that investigator on the AIMS score. So there is never going to be a relationship between the patient and the investor, the physician who is applying the AIMS score here. Those are just some of the things.

It’s taking us probably a couple of months longer than the start of study, because of all these added features that are into it. So we’d hope to start it by early summer. We’re probably going to be starting it by approximately July. So we’re going to be a couple of months off. I’d hope to have data for you at the very end of this year. It’s probably going to be very early first quarter, when we’ll have data from the study.

I’ll just end up here real fast is that financially we’re in very good shape. Last week, we really start financial results. We have just over $200 million of cash on hand. We plan on burning between $40 million and $45 million this year as our VMAT2 program is ramping up. And so we’ll end this year still in a very nice cash position with $170 million in cash investments and receivables, and we have approximately 66 million shares outstanding no debt, no warrants very simple balance sheet.

Thank you very much and I apologize for going so far over, but we do have about three minutes for questions.

Question-and-Answer Session

Kevin C. Gorman

Are there any questions from the audience?

Unidentified Analyst

I am new with your stories bear with me. On your GnRH, can you explain what your advantage is versus the current GnRH on the market and especially with the Abbott to data product?

Kevin C. Gorman

Yeah, the cap product, which is Lupron.

Unidentified Analyst

Yeah.

Kevin C. Gorman

Yeah, there are a number of Lupron like products that are now available out there. These are Peptide Agonists, and what they do is, they buying to and they agonize the GnRH receptor, they initially cause a flare in estradiol and all the other sex hormones in men that cause a flare and testosterone. But what they do after a couple of weeks, three weeks or so, is they down regulate the receptors, strip it off the surface, so they function as a complete and total antagonists. Look at them as an irreversible antagonist if you will. So what they do is, they sold billions into the prostate cancer market, they’ve been very successful there because they dropped testosterone down to zero and that’s what you want. It’s basically a chemical castration if you will.

In women, it takes a woman who is 22, 23 years-old, by and large they want to get pregnant also, but they are having extreme pain with their endometriosis. It takes them down to menopause. Takes them to about a 58 year old women. They start having dramatic bone loss immediately, which leads to their black box warning on it and they have hot flashes, severe hot flashes and it can take, after it’s given as the (Inaudible) after they go after it can take months after they are off it until they finally are ovulating again and maybe be able to – or trying to conceive.

They can only take it for two six months courses in their life. This is a chronic disease that lasts all the way from their late teens, early 20s through menopause. So, our drug is oral, those dependently lowers estradiol. So, it gives the amelioration of the painful symptoms of endometriosis, but it doesn’t cause the hot flashes, it doesn’t cause the dramatic bone loss and once they start taking the drug as they’ve controlled let’s say over six months, however long they take it for they control the pain, they get their non-menstrual pelvic pain, plus they (Inaudible) control. They come off the drug and they pick up their next menstrual cycle immediately.

So, what they want to do is become pregnant then they can start doing that immediately. And pregnancy actually can put a woman into remission in this disease for three or four years. So, and many of them again want to become pregnant, so the drugs can either be used in long-term, which the peptides can’t because of their black box warning, they are an on off switch. We dose dependently don’t regulate. So that it is no longer enough estradiol to be the growth factor for the endometrial explants, but it is still enough estradiol to keep good cardiovascular health, good bone health in the women.

Unidentified Analyst

And you have the bone loss data?

Kevin C. Gorman

And we have done. We’ve done six-month bone loss data and show with our 150 mg dose given once a day, we have minimal to no bone loss and yet significant pain reduction. Pain reduction that is as good as the goal standards of Lupron or Depo Provera. So here you get all the benefits of that, but you don’t have to downsize and actually we have a lot of headroom as far as bone goes with that.

Unidentified Analyst

And in terms of the pain reduction, how does that compare to the naproxen have a disciplinary indication. So why would you want to do a pain reduction?

Kevin C. Gorman

You’re saying the naproxen.

Unidentified Analyst

Yeah.

Kevin C. Gorman

Yeah. So what women normally go on, as they go on a birth control pill initially when they first present with symptoms or mild symptoms to their gynecologist, it’s (inaudible) and birth control, those actually work extremely well, up until the disease keeps progressing, which dose don’t stop the progression of the disease, when they become moderate to severe, those don't work, they’ve stepped up into the vicodin or (inaudible) to help them on their worst days. and then, they ultimately end up with getting multiple ablations that go on some multiple surgeries or finally into a hysterectomy. We offer them a pharmacological choice here that they can avoid that.

Unidentified Analyst

How about your IP left?

Kevin C. Gorman

IP is a composition of matter after 2027, and we have one question back there.

Unidentified Analyst

I think in your Phase III design, you have as compared to placebo.

Kevin C. Gorman

Yeah.

Unidentified Analyst

Why aren’t you comparing to Lupron and Depo, which is approved for the indication, because your treatment periods are exactly the same duration, six months?

Kevin C. Gorman

Yeah. And when it comes to, when getting scientific advice in the Europe, then it will be compared to an active comparator. In the U.S., we are not required to go against an active comparator in the United States. In our Phase II program we did a non-inferiority study against DMPA in six months of treatment and we showed the drug on every measure to be non-inferior to DMPA. And DMPA was approved by showing non-inferior to Lupron.

We also did a study in a Phase II study in Europe utilizing our drug against Lupron to gain some experience there and it behaved favorably against Lupron there. In the U.S. if you don’t have to go against an active comparator, you don’t. That’s one explanation, my second explanation, is Lupron is a complete failure in this disease. Women refuse to take Lupron, we could spend 10 years trying to recruit into that study, with the Lupron Arm in the United States.

We had to go into Eastern Europe where women have no insurance and no availability of those drugs to be able to recruit into a Lupron arm. The women would rather suffer the disease – the effects of the disease than the side effects of Lupron.

Unidentified Analyst

And is that going to create a reimbursement problem down the road?

Kevin C. Gorman

I don’t see why it would, but I will put the caveat there only just because I have to, as we haven’t done and it’s up to Abbott to do this, is there expensive payer research. But for having a chronic disease and Lupron can only treat for a one-year out of the patient’s life versus having an oral disease at a lower price that can actually treat the disease for their entire life, then I wouldn’t see why the peers would have a problem with that.

Unidentified Analyst

Longer term study too.

Kevin C. Gorman

The six month will only allowed to be use for six months.

Kevin C. Gorman

Actually they are going to have a extension that goes out to 1 year, which allows for one year of dosing and then Abbott would do the extension of that.

Navdeep Singh – Deutsche Bank Securities, Inc.

Extension of that, right.

Kevin C. Gorman

Exactly right.

Navdeep Singh – Deutsche Bank Securities, Inc.

That makes sense to me.

Kevin C. Gorman

Okay. Well, I want to thank you very much and I’m sorry for going on, my host is probably fidgeting here. Thank you.

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