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Isis Pharmaceuticals, Inc. (NASDAQ:ISIS)

Review Data Presented at the EAS 2012 Meeting Conference Transcript

June 01, 2012 12:00 PM ET

Executives

Stanley Crooke – Chairman and CEO

Sam Tsimikas – Professor, Medicine and Director, Vascular Medicine at UCSD

Lynne Parshall – Chief Operating Officer and CFO

Richard Geary – Senior Vice President, Development

Kristina Lemonidis – Director, Corporate Communications

Analysts

Jim Birchenough – BMO

Operator

Good day, ladies and gentlemen. And welcome to the Isis Pharmaceuticals Conference Call to Review KYNAMRO Data that was recently presented at the EAS 2012 Meeting. As a reminder, this call is being recorded for replay purposes.

I would now turn the call over to Dr. Stanley Crooke, Chairman and CEO. Please proceed.

Stanley Crooke

Good morning, everyone. The purpose of the call today is to have Dr. Tsimikas review in the additional results on KYNAMRO that were represented at the European Atherosclerosis Society 2012 Meeting on March 29th in Milan.

Joining us on today’s are Dr. Sam Tsimikas, Professor of Medicine and Director of Vascular Medicine at UCSD; Lynne Parshall, COO and CFO; Richard Geary; Senior Vice President, Development; and Kristina Lemonidis, Director of Corporate Communications.

Kris will you please read our forward-looking language statement.

Kristina Lemonidis

Sure Stan. I remind you to everyone this webcast includes forward-looking statements regarding the development activity and therapeutic and commercial potential on safety of KYNAMRO. Any statement describing Isis' goals, expectations, financial or other projections, intentions or beliefs including the planned commercialization of KYNAMRO is a forward-looking statement and should be considered an at-risk statement.

Such statements are subject to certain risks and uncertainties, particularly those inherent in the process of discovering, developing, and commercializing drugs that are safe and effective for use of human therapeutics, and in the endeavor of building a business around such drugs.

Isis' forward-looking statements also involve assumptions that it never materialize or prove correct could cause its results to differ materially from those expressed or implied by such forward-looking statements.

Although Isis' forward-looking statements reflect the good faith judgment of its management, these statements are based only on facts and factors currently known by Isis.

As a result, you are cautioned not to rely on these forward-looking statements. These and other risks concerning Isis programs are described in additional detail on Isis' annual report on Form 10-K for the year ending December 31, 2011, and also most recent quarterly report on Form 10-Q which are on file with the SEC. Copies of these and other documents are available from the company.

And with that, I’ll turn the call back over to Stan.

Stanley Crooke

Thanks Kris. Again thanks for joining us today. Let me begin by saying how pleased we are that the U.S. NDA has been filed by the FDA, and that we’ve earned the $25 million milestone payment from Genzyme.

The NDA filing represents another significant achievement in the development of KYNAMRO and the significant step to bringing benefits to the patients who need KYNAMRO.

We are also pleased with the progress of the European filing. Because our initial indication in Europe will likely be broader than in United States, if successful Europe will be our largest initial market.

As I mentioned last month, we’ve already hosted inspectors who performed pre-approval inspection for Europe for our KYNAMRO manufacturing facility and that inspection went well.

I also hope that you will be able to join us in March when Dr. Santos reviewed the long-term safety study of KYNAMRO. In this long-term extension study we have patients treated out more than three years.

These patients demonstrated that consistent reduction of all atherogenic lipids with the safety profile that continues to be appropriate for the indications we are seeking, the unique lipid-lowering profile of KYNAMRO makes this drug a potential game changers for patients with FH.

Today we have the opportunity to provide you with the data that were presented earlier this week at the EAS Meeting in Milan. These data drive from an analysis of the four Phase 3 trials that you’ve already seen and above we’ve been reported in considerable depth.

But this new analysis focus on -- focuses on another lipid factor independent cardiovascular risk factor called Lp(a). This data highlight the potential of KYNAMRO to lower not just apo-B, triglycerides LDL cholesterol in related particles, but this other important atherogenic lipid Lp(a).

Lp(a) is a growing concern in the medical community. In 2010, the EAS consensus panel recommended screening and treatment for elevated Lp(a) and in 2011, the National Lipid Association Expert Panel on FH published guidance noting that elevated Lp(a) places FH patients at even higher risk of cardiovascular events. KYNAMRO is the only drug that reduces all these risk factors and either has no effect or slightly increases HDL.

So now I’d like to introduce Dr. Sam Tsimikas. Dr. Sam Tsimikas is Professor of Medicine and Director of Vascular Medicine at University of Calfornia, San Diego. Dr. Tsimikas has published over a 150 articles and book chapters in top tier scientific journals like New England Journal of Medicine, Nature Circulation, Research Circulation and the Journal of Clinical Investigations and others.

Importantly, Dr. Tsimikas has contributed significantly to the understanding of the mechanism of atherosclerosis progression and regression. He was instrumental in the development of the biomaker assay that should be clinical available to soon design to predict cardiovascular depth.

Dr. Tsimikas is also been heavily involved in helping understand what Lp(a) is and what the role of Lp(a) in -- and is in cardiovascular health and diseases. Dr. Tsimikas is currently a Deputy Editor of the Journal of the American College of Cardiology and an Associate Editor of the Journal of the American College of Cardiology cardiovascular inventions.

And so with that, I’ll turn the call over to Dr. Tsimikas to comment on his clinical experience with KYNAMRO and the potential of KYNAMRO to chase the life of very sick patients with FH. And as I say, this is an analysis -- a new analysis of the four Phase 3 trials that we’ve already presented to you in very significant detail.

Sam Tsimikas

Thanks very much and I appreciate the opportunity to review some of this new information. So this aspect was tightly, you see here the effects of mipomersen antisense apo-B synthesis inhibitor on lipoprotein little A level in patients with hypercholesterolemia across four Phase 3 studies.

There are four major lipid disorders, elevated LDL cholesterol, low HDL cholesterol, high triglyceride and the fourth one which is not really emerging and the target of therapy high lipoprotein Little A.

And as you’ll see from this review that that is a very common lipid disorder that probably under appreciated, but in the next five to 10 years we are going to see our interest in this particular lipid disorder as the target of therapy, so it becomes very relevant to have drug that can actually lower this significant.

On this next slide you can see some of our, some of my disclosures and relevant to this talk as you can see that my consultant for Isis and Genzyme another related areas.

So let me start like just sort of going over the background on this particular abstract, and as Stan mentioned, the purpose was to evaluate the effect of the mipomersen on Lp(a) levels in these four randomized double blind placebo-controlled Phase 3 studies and patients that have either familiar hypercholesterolemia or severe hypercholesterolemia with coronary heart disease that are already on maximum tolerated medications, which is an important point, because it only speaks to the issue of what do we do this patients that are not controlled by current therapies, can we develop new therapy that will lower Lp(a) levels.

So for this particular analysis we are going to focus on Lp(a) and the reduction in Lp(a) above and beyond what we get from lowering the LDL cholesterol and the total cholesterol levels.

Now the European Atherosclerosis Society and as well as, the National Lipid Association recently provided some guidance and how to look at Lp(a) levels, contribute screening and in particular the European Atherosclerosis Society has recommended the desirable levels should be less than 15 milligrams per deciliter, we’ll review that in a little more detail.

So in this sub analysis of these studies we are going to look at the effect of Lp(a) and in particular how many patients get below the threshold of 50 milligrams per deciliter.

So, on the next slide, just a little bit of background on Lp(a) and particularly how its related to patient that familial hypercholesterolemia because this is the main group that we want focusing in on right now. So let me give you a little background on Lp(a) and go over how it means relevant to these patients.

So Lp(a) is actually a modified LDL cholesterol particle and it compose of two things, one is the LDL component, which is very similar to the LDL -- LDL cholesterol but also there is coven attachment to another protein called apolipoprotein(a) which is a generic risk factor.

And Lp(a) maybe atherogenic through multiple pathways, one of which is through the LDL cholesterol component as with LDL cholesterol, but the other one that we are not finding out a lot more information about is that apoA components also has several mechanisms through which it can mediate atherogenesis and we are not going to review those in detail here. But you can see here that really is kind of a [SSO] that it provides atherogenic risk through multiple pathways.

Now the important thing about Lp(a) in FH patients is that and Lp(a) is actually higher in FH patients and patients that don’t have FH. In other words, it’s higher in FH patients for the same LDL cholesterol level, say for another patient that had -- did not have FH.

The mechanism is not going to be understood, but the level is about two-fold higher than other patients. So that when you identify patient that has familial hypercholesterolemia, it also likely to have higher LDL levels -- let’s say you’ve earned variety of patients with high LDL cholesterol. So it’s important to start looking at these patients with this risk factor in mind.

Now the issue with Lp(a) is that we don’t have any specific therapies to lower at this point. So there is a strong clinical need to identify drug that can actually lower Lp(a), not just in FH patients but in all patients in general.

Now, how was mipomersen or KYNAMRO relevant here? So, because it’s an apo-B continue like a protein, anything that prevents the synthesis of apo-B will actually have the effect of lowering all apo-B continue like a proteins including Lp(a).

And some of these mechanisms have not been fully determined, but just to remind you mipomersen inhibit mRNA production or mRNA inhibition of apo-B and therefore, you cannot make any apo-B protein.

So, all the downstream products of that can get reduced. So you can see from the slide here that you reduced the production of LDL in the liver and then as it get remodels to LDL in the vasculature, there is less LDL available to be made because the precursors are all diminished.

Okay. So this is actually I think very well know at this point in terms of its mechanistic effects. So in the next slide, just briefly Lp(a), as you can see here on the left part of the slide, you see that it’s composed of an LDL particle, which has the typical lipids of an LDL.

And you see here that there is a real attachment of another protein called apoA, which has multiple kringles that you see that are color coated and these are genetically mediated through the LPA gene.

And it’s a very heterogeneous protein in that different patients have different numbers of those kringles, particularly those kringle 4 type 2 repeat that you see there in black, so that in a patient you will have two alios of apoA. You may have two different sizes of LDL particles. And this has to do with how much LDL is circulating in the blood.

I’m not going to go into the detail of this, but the kind of the bottom line is that it’s a heterogenous particle and it’s a component of LDL and apoA.

Okay. So we can go to the next slide. Let me just mentioned one brief thing that Lp(a), very interestingly involved recently and it’s only presented in human and apes. And it’s particularly relevant to human cardiovascular disease.

Now, how common is Lp(a). This is data from the European Atherosclerosis Society publication and this is derived from the Copenhagen General Population Studies and these were three studies of approximately 42,000 patients.

And if you see there the Lp(a) was distributed in a non (inaudible) form. In other words, most patients have low levels. But you see there in the red the cut off is the 50 milligrams per deciliter about 20% of the general population, both men and women have elevated levels.

It’s actually higher in South Asians and African Americans and Africans have even higher levels. So if you take this at a global perspective, there’s over $1 billion Asians that have higher Lp(a) levels. So it’s actually going to become a very important target of therapy because we know it’s atherogenic.

And you can see this on this next slide. This is data from the Copenhagen Studies again and this is, well, it’s called a Genetic Association Study. And the way these studies are done is because very few things affect Lp(a). You can measure Lp(a) baseline on patients and then follow them in this case 50 years. And what you see there on the X axis, you see the hazard ratio for having a Myocardial Infarction.

And then on the Y axis, you see the different levels of thresholds of Lp(a). So, for example, if you see the 95 percentile on the top left and then you look over to hazard ratio, those patients have a hazard ratio of about 3 that having a Myocardial Infarction compared to have patients that have less than 5 milligrams per deciliter, which is in the bottom left of the figure.

And what you notice there is that it’s linear relationship, so that the level of Lp(a) that these FH patients work along with is directly related to the risk of having a Myocardial Infarction.

Now this study was running in FH patients, it was in the general population. So the FH patients would actually be even at higher risk than what you see on the slide because not only do they have the high Lp(a) but they also have high LDL cholesterol levels. So it’s much more important in these patients to identify them, thus having elevated Lp(a).

Okay. So while the studies are showing the relationships of Lp(a) with risk, we are not going to review. There’s one of the aspect that’s now emerging for Lp(a) in that besides the variability in the levels. There is a technical level of variability that is noted in the genetic abnormalities or genetic variations I should say of these patients. So there are single nucleotide polymorphisms in the apoA gene that also mediated additional increase in the LDL levels and additional risk.

So, if you look at the slide, you look at the [odds] ratio of having coronary artery disease from another study that was published in New Journal of Medicine. If you have two variant alios, so these are single amino acids substitutions in the apoA above and beyond the kringle variability. You see that the [odds] ratio of having CAD approximately doubles from one alio to two alios.

So that there is a component of the actual circulating levels and there’s also an additional genetic component of the sniffs that double the risk. So this is equivalent to having in some ways, Heterozygous versus homozygous FH where you have some risk of 1g but you have 2g, abnormal gs you have doubled the risk. So it becomes important to identify the genetic of these patients and to understand their risk both from the plasma levels and from the genetic variability.

Okay. So now let’s go on to review the recent data, the exciting data from the recent publications. So, on the next slide, you can see that these four studies had a very similar methodology, which makes it very nice for us to be able to compare them and to let them together and have more power for getting better data.

So you see here that these four studies enrolled these high-risk patients and they were randomized to mipomersen or KYNAMRO, 200 milligrams per week subcutaneously versus placebo and were treated for 26 weeks. And then after that it will follow for an additional 24 weeks, so it basically had about a year of follow-up on drug and off drug to follow them for further clinical response.

Now the main end point on the next slide is really in these studies was the percent change in the LDL cholesterol level from baseline to week 28. And the secondary end point, which we are going to focus on here was the change in the Lp(a) levels in these patients in the same day we set. Now, just briefly these laboratory measurements both Lp(a) with all lipid parameters all validated laboratory measures and there is no concern about their accuracy.

Okay. Let’s go to the next slide and actually review some of the patient characteristics in these studies and then go over the key parts of the talk.

So you see here there are four studies that were in these Phase 3 trials. And just briefly go over them, the first one is patients of homozygous familial hypercholesterolemia. These are the very high-risk patients because LDL cholesterol have really over 500 milligrams per deciliter.

And then the second group is the patients that have severe hypercholesterolemia. These are patients that LDL cholesterol of almost greater than 300.

Third study patients that have heterozygous familial hypercholesterolemia that are treated, but are not getting the LDLs appropriately to level that we would deem therapeutics.

And the last studies patients that have hypercholesterolemia have a high risk of having cardiovascular disease. So these are patients that have multiple other risk factors.

Now, the key part of the slide is that these patients require multiple drugs to get their LDL optimally treated but even that is insufficient. So if you see here on the column with the percent of patient on lipid-lowering therapy, you see that there is a statin only arm and then the statin plus other lipid lowering therapy arm.

You see the vast majority of patients here really on multiple medications. Often we have to use three or four different medications and they’re still not enough to get the LDL cholesterol to where we would deem appropriate for reducing their risk optimally.

Okay. Let’s go now over to the next slide and review the key parts of this presentation. So let me just take a minute here to go over each one of these studies and you see that the number of patients are from 34 to 101.

And if you see the mean baseline levels, just to give you a sense of how hard it is to treat these patients despite optimal medical therapy, if you look at the patients that are homozygous familial hypercholesterolemia, they are starting out with an LDL cholesterol of 439 with optimal medical therapy.

Clearly, this is a huge room for improvement here. And if you see the second group, their mean baseline cholesterol levels, LDL cholesterol level was 276 and at the risk of these groups was down a little bit, they go further, further down.

Now, if you look at the mean percent change of LDL cholesterol levels, you will see that the homozygous FH patients have an additional 25% reduction in the LDL cholesterol and in the other groups approximately up to 37% reduction in the LDL cholesterol above and beyond what we can achieve with currently available therapies.

Now, the Lp(a) component is a key part here for this particular presentation because I think you have seen some of the other data and you would see here, we have very robust decreases in the Lp(a) levels and all the groups at approximately 25% to 40%. So notice here is that the LDL, I’m sorry, the Lp(a) levels are above 30 mg per deciliter and let me just briefly remark on this.

If you look at the epidemiological studies, 30 mg per deciliter is the cut-off that we consider to be atherogenic. The European Atherosclerosis Society recommends a level of less than 50 as an optimal therapy probably because at this point, we’re going to very powerful agent to lower our Lp(a), but nonetheless you see that these patients all at baseline have levels above 30 mg per deciliter. So they are all additional risk of having higher Lp(a).

And if you look at the last column here, you see a very robust reduction in their Lp(a) levels. The mean level essentially comes down below 30 to above 30, below 30 in all these four groups. So the takeaway message from this slide is that not only can you lower LDL significantly, but you can also get a very robust reduction in the Lp(a) across the different patient cohorts.

Now, let me discuss in a little more detail in the next slide. What you see here is, in the green are the placebo arms and in the yellow are the treated arms, and the key points from the slide lowering the Lp(a) has noticed that you get an effect very quickly within five weeks, you already have a reduction in all the groups.

And as you follow the patients up to 26 to 28 weeks at the end of the study, you still have continued decline mainly perhaps a little plateau at the end there. Every group response quite nicely and notice that the placebo groups still change to any great extent. So this is really a very specific effect on Lp(a) levels in all these Phase 3 trials.

And in the next slide, you can see there is little more detail. This is individual patient data. These are called waterfall pods and kind of a visual, we want to see here, the green is the variability you get from measuring Lp(a) in a placebo group and each bar represents one patient and the yellow is the mipomersen group and you see here that the vast majority of patients in the mipomersen group had reductions in Lp(a).

Now, some of them had mild reductions, but you can get up to 60% reduction in Lp(a) in a lot of these patients. So the mean is, they have been about 30% but you see here the variability of how patient respond to the drug and the vast, there is a lot more patients in yellow than in green, and it’s kind of what visually you can see from this slide.

So that most of the patient that we treat with mipomersen are going to have a reduction in Lp(a) and a lot of them are going to have very significant reduction in Lp(a).

That is from one study and this is from second study. This is a little bit larger and you see a very similar response and that the vast majority of patients that can treat with mipomersen have significant reductions in their Lp(a) levels.

Okay. What about targets? Now, targets for Lp(a) not well established clinically yet and the European Athero Society has really kind of taken a lead forward to do this and this slide addresses some of the issue related to can we get patients under level of 50, which might be say first target as we start out lowering our Lp(a). Probably, ultimately, we want to get it even lower than that with more specific therapies but 50 may be a good goal to start with.

So if you look at the table here and you see how many patients have Lp(a) levels greater than 50 versus patients that have Lp(a) levels less than 50. What you see here is that large number of the patients that were treated with mipomersen had achieved Lp(a) less than 50, approximately a third to more than a third. So that if you -- if this became validated goal, this would be a very nice way to kind of use the targeting therapy.

This is one of the equivalent thing, how many patients can you get under an LDL level of 100, how many can you get under 70, how many can you get under 130, which is used classically for efficacy of statin therapy.

Okay. So on the next slide, you can see some of the adverse reactions related to mipomersen. Now, this has been describing a lot of detail in the past and there are no surprises here. This is very similar to what you probably have already seen many times before. So I’m not going to over the slide in any detail because it’s already been described previously since we’re just focusing on the Lp(a) aspects here.

So just a summary on the next slide, approximately 8% of patients that were treated with mipomersen had increase in ALT. This is known from before it’s nothing -- there is no new finding from this analysis that has already been reported.

Okay. So summarize this presentation then, I think we can clearly say that mipomersen consistently reduces Lp(a) levels and they are in the highest risk patients for cardiovascular diseases and these patients are already on maximally tolerated therapy. And this is an important aspect because we don’t have a lot of therapies at this point to take niacin to lower Lp(a).

A lot of these patients also able to achieve Lp(a) level of less than 50, which is made from a standard threshold level for lowering Lp(a). The adverse events were mostly related to injection site reactions and flu-like symptoms.

And ultimately in the future, we like to focus on the role of Lp(a) as the modifiable risk factor and do additional studies to confirm that lowering of Lp(a) will also provide benefit of these patients.

We know the risk factor -- we just don’t know yet, if we lower all of these patients, will improve. The hypothesis is that they will improve significantly because there is a lot of residual risk that you leave behind in patients that you treat with statins and it’s not clear yet what we should modify to reduce that residual risk and Lp(a) is probably one of those key components in our patients that have highest risk cardiovascular disease.

Stanley Crooke

Thanks Sam. This data then highlights potential of KYNAMRO to treat another of the unique needs of patients with FH. There is no free treatment. There is an apheresis that addresses the specific challenges faced by these very sick patients and those challenges include elevated Lp(a), elevated LDL, elevated triglycerides. And we look forward to meeting this unmet need and your partners at Genzyme and Sanofi and to bringing this important new medicine to these patients.

And so with that, we’ll open it up for questions. Kris, if you can set us up that would be helpful.

Question-and-Answer session

Operator

(Operator Instructions) And your first question comes from the line of Jim Birchenough of BMO. Please proceed.

Jim Birchenough – BMO

Hi, guys. Thanks for the presentation. So, few questions and I guess you alluded to it in your final comments. But if you go back to studies like the [4S] study have -- we’ve been able to look at whether Lp(a) reductions correlate with any risk reduction? What proportion of patients if any respond to statins in terms of Lp(a) reduction?

Third, question would be on how does FDA think about Lp(a) reduction? And then the final question is there, anyway to sort of identify the patients treated with mipomersen that might optimally reduce their Lp(a) levels just in terms of more targeted treatment? Thanks.

Sam Tsimikas

Great. This is all great questions. So, I am actually impress, you look at the [4S] study with Lp(a), there was a very nice special Kare Berg. Unfortunately, he has actually invent or discovered Lp(a) and he unfortunately past away couple of years ago, but he published a very nice paper on for us, which as you know as the major trial that validated the cause of LDL hypothesis. But in that trial, the patient that have high Lp(a) levels more at higher risk and benefited significantly.

Now, statins are very interesting in the Lp(a) test. If you look to the literature carefully, a lot of time you actually get a slight increase in Lp(a) about 10%, when you give statins and some time you see no changes. It only depends how you analyze the data but statins do not lower Lp(a) that is very clear.

Sometimes they don’t affected, sometimes they increase a little bit. So optimally, we treat patients in clinic with the statin and we measure the Lp(a) after statin does tend to go up a little.

It’s not really clear why that’s the case and we are doing a lot of work in our laboratory to try understand the mechanisms whether this is a beneficial effect or some kind of side effect or some effect of the statins on hepatocyte synthesis on apo-B or apo-A, some of these clear yet.

So statins are not a therapy for Lp(a), they reduce the risk and patient that have high Lp(a) like you saw in [4S] but by themselves they don’t lower Lp(a) levels.

Now your question about the FDA is a good one. There is now lot of debate about target endpoints. And you can still get indication for lowering LDL I believe, but now you see some of the HDL study that are failed, even HDL which have so much epidemiological data, some other therapeutic trials have not worked out. And it still the data why, so if we have a, say a therapy that lowers Lp(a) 40% or even, if you develop one that lower than 80% to 90%.

And we do a trial, we do just clinical study just to lower that, will the FDA accept an Lp(a) reduction endpoint. I don’t know, but I probably don’t think so. I am not in the FDA, we actually interesting question to bring up to them.

Ultimately, it would be nice to have clinical endpoint data. So for example, the way you can design a trial is you have three patients for high Lp(a) not necessarily high LDL on cholesterol by Lp(a), another risk factors, treat them with a specific agent versus placebo and then see if when you lower the Lp(a) X amount did they have an X benefit.

That might the way the FDA may look at it. I don’t know. I’m just speaking from own opinion here. But it’s an interesting question. And I think it will need to be addressed carefully in the next few years, because there is not a large amount of interest in looking at Lp(a). There is now in the last three or four years because our work does 30 or 40 paper showing that it’s very strong generic independent risk factor for cardiovascular disease.

From an (inaudible) daily randomization study, it also suggest that its causal, because like familial hypercholesterolemia, the Lp(a) levels that we have adverse or the Lp(a) that was have all are lifetime. So the risk accrues theoretically when we were born with Lp(a) as it is with say homozygous and heterozygous FH.

So the question that becomes if you lower Lp(a), we can get benefit. Unfortunately, we haven’t a specific agent only lowers Lp(a). So it’s hard to test that hypothesis clinically at this point.

Your last question of mipomersen, whether we identify systemic patients, it appears that the patients of the highest Lp(a) level respond the best and should have -- and actually have another way to do that. I think the key here is, when you have a patient that had the homozygous or heterozygous FH.

I think they should all have their Lp(a) level checked and if they are elevated, that should be followed, after you treat them with mipomersen, follow and see if they got a significant reduction.

I don’t think we can propose right now adjusting a mipomersen dose, let’s take for example, the just Lp(a) levels is not quite at that level yet, but the key metrics from this talk is that when you get an LDL reduction in these patients, you also will get an Lp(a) reduction, which is a bonus, theoretically a bonus benefit in terms of their overall risk.

Stanley Crooke

Thanks, Sam. Yeah, Jim, our focus obviously is to understand the drug in detail. And to make sure that all of the data are available to the sophisticated lipidologist who will be treating these patients.

And I think Sam is representative of those people who recognized that there is lot more work to be done on Lp(a), about a drug brings -- it reduces Lp(a), well reducing all the other atherogenic lipids is conceptually a very valuable addition. And I think we will leave the FDA question at exactly the place with that same message.

Jim Birchenough – BMO

Great. Thanks, guys.

Operator

(Operator Instructions)

Stanley Crooke

If there are no more questions and we will bring the conversation to an end. Just to summarize, in addition to lowering all of the other apo-B containing atherogenic lipids. And we now, demonstrated clearly that KYNAMRO lowers another independent cardiovascular risk factor Lp(a). The data suggest that the people who need the reduction in Lp(a) the most, get the most benefit from the drug. This is a straight forward clinical test, doesn’t require genetic testing and will be simply something else that we -- that we are confident that the lipidologist will treat these patients will be looking at and evaluating carefully in the years to come, very exciting.

Kristina Lemonidis

Thank you.

Operator

Thank you for your participation in today’s conference. This concludes the presentation. You may now disconnect. Good day.

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