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Amgen, Inc. (AMGN)

European Society of Cardiology Conference Call

June 19, 2006 12:00 pm ET

Executives

Tony Gringeri - Sr. Director, Scientific Affairs

Scott Wasserman, MD - FACC, Global Development Leader, Clinical Development (Cardiology)

Analysts

Gene Mack – HSBC

Craig Parker - Lehman Brothers

Steve Harr - Morgan Stanley

Elise Wang - Smith Barney Citigroup

Richard Nelson - MorganJoseph

John Davenport -

Brett Holley - CIBC World Markets

Jack Mueller -

Presentation

Operator

At this time, I would like to welcome everyone to the Amgen at European Society of Cardiology conference call. (Operator Instructions) Mr. Gringeri, you may begin the conference.

Tony Gringeri

Good morning everyone, this is Tony Gringeri from the Scientific Affairs Group at Amgen. We’re very pleased to be able to have this teleconference today form the European Society of Cardiology. We’re going to discuss the results of our Phase 2 program of treatment of anemia in heart failure patients with Darbepoetin alfa and our presenter today will be Scott Wasserman. Scott is the Global Development Leader in the Clinical Development Group here at Amgen, responsible for this program and Scott will take us through a series of slides.

Before we begin I wanted to make a couple of announcements. The first is that the slides we will be discussing today are available on the web. The address is www.amgen.com. When you get onto that page there is an Investors tab and under Investors you will see an Events Calendar. This is the first event, Amgen an the European Society of Cardiology.

In addition, this broadcast will be available for replay for three days. The call-in number is 1-800-642-1687 and if you need any of this information or haven’t had the opportunity to copy it down while I’m talking, you certainly can give us a call and we will provide it to you.

Finally, I would like to make our Safe Harbor statement. Some of the information presented here today will be forward-looking and, of course, actual results may vary materially. At the end of the session, we will have a Q&A during which you will be able to ask questions of Dr. Wasserman, but right now I’d like to turn the microphone over to Scott and we will begin the presentation.

Scott Wasserman

Thanks Tony, and I’d like to thank everyone for participating on this call and for your interest as well as your participation. I also wanted to state that Dr. William Abraham as well as Dr. van Veldhuisen regret that they could not present this data to you today. Professor van Veldhuisen presented this data yesterday at the late-breaking trial session of the European Society of Cardiology, Heart Failure Congress in Helsinki, Finland. Unfortunately, at this time he is currently chairing a session and could not be with us.

Dr. Abraham, who is the first author on this abstract had a personal emergency that prohibited his participation at this conference and on this call.

Now I’ll begin. As most people on this call are aware, heart failure is a major cause of morbidity and mortality. This figure is a Kaplan-Meyer Curve from a publication by McMurray and colleagues which demonstrates that the diagnosis of heart failure carries with it a mortality that is worse than many cancers.

Heart failure is the leading cause of hospitalization in patients age 65 years and older. There are over 23 million people with heart failure worldwide. 5 million in the U.S. and over 4 million in Europe. The lifetime risk is 1 in 5 for both males and females and the cost is over $29 billion per year in the United States. Next slide please.

From observational studies, we know that about 20% to 30% of patients with heart failure suffer from anemia. We also know that anemia is important in the presence of heart failure because it carries with it an increased risk of clinical outcomes like death or hospitalization.

An example of this is show here in a publication by Annon and colleagues from circulation, and this from the Renaissance Trial. It demonstrates that a lower baseline hemoglobin is associated with a worst outcome; in this case, survival. Next slide please.

Currently, there is no approved treatment for the 20% to 30% of heart failure patients that suffer from anemia and of the nearly 1 million anemic patients with CKD on dialysis, more than 95% currently receive treatment for anemia. For the greater than 1.3 million anemic patients with CKD not on dialysis, about 20% receive treatment for anemia. For the greater than 2.4 million anemic patients with heart failure, there is no approved treatment for anemia. Next slide.

Cardiologists need to know whether to treat anemia in heart failure. It’s clear from the cardiology literature, as well as clinical practice, that heart failure is associated with poor outcomes. If you compound heart failure with having anemia, your outcomes are worse.

The real question that we are trying to answer with our clinical trials program is if you treat the anemia with Darbepoetin alfa, are you capable of making the outcomes better? There is data out there that suggests that treatment of anemia may improve outcomes. Current United States and European cardiology guidelines do not address the management of anemia in heart failure and the cardiology community needs a large, randomized control trial to answer this question definitively. If we could go to the next slide.

The anemia in heart failure story is very similar to the story with cholesterol and coronary heart disease. Back in the 1960s with the Framingham Heart Study, it was observed that high total cholesterol and LDL correlated with bad outcomes in patients with coronary heart disease.

With the advance to treatments to modify lipids such as HMG, Co-A reductase inhibitors like statins, we could lower total cholesterol and LDL and test the hypothesis that lowering cholesterol and LDL would lead to better outcomes in patients with coronary heart disease. This was done in a number of landmark trials such as the West of Scotland paper, as well as the 4S trial.

This paradigm extends itself nicely to our anemia in heart failure program and our ongoing Red-HF trial which will test the hypothesis that the treatment of anemia with Darbepoetin alfa will reduce the risk of death or heart failure hospitalization in patients with symptomatic heart failure. Next slide please.

To date Amgen, in collaboration with leaders in the cardiology community, has performed three Phase 2 trials evaluating the treatment of anemia with Darbepoetin alfa in patients with symptomatic heart failure. All of these trials were multi-center, double blind, placebo-controlled trials randomizing patients to Darbepoetin alfa or placebo. The median maintenance dose was 0.8 to 0.9 mcg/kg, given every two weeks.

In these three trials, there were over 500 subjects enrolled and nearly 300 were treated with Darbepoetin alfa. End points at six months included exercise capacity, symptoms and quality of life measures. We also have safety data up to one year on these patients. Go to the next slide.

Now I’m going to go over the data that was presented today, as well as yesterday, at the European Society of Cardiology-Heart Failure Congress in Helsinki. This data includes results from Study 170, which is the largest of Amgen’s Phase 2 trials, which randomized 319 patients to Darbepoetin alfa placebo as well as a pre-specified pooled analysis of Study 170 and Study 171. Those are the two largest of Amgen’s Phase 2 trials. Next slide.

The objectives for Studies 170 and 171 were to investigate the treatment of anemia with Darbepoetin alfa versus placebo on hemoglobin response, safety and disease outcomes in subjects with symptomatic heart failure and anemia. Next slide.

The common end points for Studies 170 and 171 included efficacy endpoints such as hemoglobin response, change from baseline to month 6 in NYH class; the Minnesota Living With Heart Failure Questionnaire; the patients’ global assessment at month 6; and then pooled analysis of disease outcomes at one year. These included all cause mortality or heart failure hospitalizations which is a composite endpoint of our Phase 3 Red-HF trial; as well as the individual components of the composite, all cause mortality and heart failure hospitalization.

We also looked at a number of safety endpoints, including the incidents of adverse events and the formation of anti- erthyropoitic antibodies. Next slide.

This is just a somatic diagram of the two studies. For those of you that were at ACC, you’ve seen 171 before, but I’ll go over it briefly. I’ll start off with Study 170: it randomized 319 patients in a 1:1 fashion to receive placebo or Darbepoetin alfa. The starting dose was 0.75 mcg/kg of Darbepoetin alfa and given Q2W, or every two weeks, to a target hemoglobin of 14 plus or minus 1gm/dL.

In Study 171 there ware two Darbepoetin alfa arms and one placebo arm. This study actually looked at a fixed starting dose of 50mcg versus a weight-based starting dose of 0.75mcg/kg.

Once again, the dosing was every two weeks, and the target hemoglobin was 14 +/- 1g/dL. The treatment's duration in Study 170 was one year, and in 171 was six months. In these trials, patients were given supplemental elemental iron at 200 mg a day, unless they had a baseline serum ferritin of greater than 800 mg/mL.

Let's go to the next slide. These are the main eligibility criteria for these trials. Patients had to be consenting adults. They had to have symptomatic heart failure for greater than three months. They had to have a left ventricular ejection fraction of less than or equal to 40%. They had to be anemic, in this case defined by hemoglobin between 9 and 12.5 g/dL.

They had to be normotensive, so their resting blood pressure needed to be less than 160/100. They had to be iron replete, as defined by having a transferrin saturation of greater than or equal to 15%. They should not have significant chronic kidney disease, so the serum creatinine needed to be less than or equal to 3.0 mg/dL. They needed to be receiving standard heart failure treatment, which included beta blockers, ACE inhibitors, or ARBs for at least eight weeks, and the patients were not to have received a blood transfusion or have any exposure to erythropoiesis stimulating proteins within 12 weeks of randomization.

Next slide. The baseline demographics and clinical characteristics from the prespecified pooled analysis were well balanced between patients treated with placebo and those treated with Darbepoetin alfa. In this intention-to-treat data set, 209 patients received placebo, and 266 received Darbepoetin alfa. It is important to note the differences in the numbers because, when you look at the numbers in the columns, you should probably best look at the percentages, which are in the parentheses.

In total, 61% were male, 85% were Caucasian; the mean age was about 70 years. The mean hemoglobin was 11.4 g/dL. New York Heart Class: Class II was about 37%, Class III was 59%. The mean left ventricular ejection fraction was 33%. The mean heart failure duration was six years. The primary cause of the most heart failure trials was ischemic heart disease, with 67% having ischemic heart disease. Beta blocker use was excellent: 80% of patients were on beta blockers. I don't have it on this slide, but 91% of patients received either an ACE inhibitor or an ARB.

Next slide. The mean hemoglobin for the Darbepoetin alfa and placebo patients at baseline was about 11.3 to 11.4 g/dL. You'll notice that the patients that received Darbepoetin alfa --those are the ones in the yellow circles -- had a nice gradual rise in hemoglobin over the first three months after receiving Darbepoetin alfa. This resulted in a maintenance hemoglobin of 13.3 to 13.5 g/dL, while the placebo patients' increased to about 11.8 g/dL.

Next slide. These are the pooled safety results. This is the safety data set, and a safety data set here is defined by any patient that received at least one dose of Darbepoetin alfa when in the Darbepoetin alfa group. You'll notice that, compared to the intention-to-treat set, two patients that were actually randomized for Darbepoetin alfa never received study drugs, so that's why there is a difference in the two sets.

You can see that, in terms of any adverse events, it was balanced between the two groups: 88% in placebo, 80% in Darbepoetin alfa. In terms of serious adverse events, 45% occurred in the placebo group, 38% occurred in Darbepoetin alfa. In terms of deaths, there were 18 deaths in the placebo group, and 17 in the Darbepoetin alfa group, which is 9% of deaths in the placebo, 6% of deaths in the Darbepoetin alfa group.

So, for those of you that have seen Study 171, you saw that there were six deaths in the Darbepoetin alfa groups. When we look at the deaths in Study 170, there were 18 in the placebo group, and only 11 in the Darbepoetin alfa group, which gave us a lot of reassurance that we were not harming patients in any way.

If you look at the number of subjects with adverse events of special interest, and these are adverse events that the FDA, and other regulatory agencies as well as the commissions, are quite concerned about, and many of these include thrombotic events, you can see that there is no signal here.

In terms of all the adverse events of special interest, 32% occurred in placebo, 26% in Darbepoetin alfa. Hypertension was 6% in both treatment groups, placebo and Darbepoetin alfa. In terms of deep vein thrombosis, 1% occurred in placebo, 0% in the Darbepoetin alfa. In terms of pulmonary emboli, there was one PE in the placebo group and none in the Darbepoetin alfa group.

In terms of heart failure, 25% in the placebo group and 19% in the Darbepoetin alfa group. In terms of cerebrovascular disorders, 2% in placebo, 3% in Darbepoetin alfa. In terms of myocardial infarction, it was balanced between the two, with 2% in both groups, and in terms of seizure, there were two seizures in placebo and one in Darbepoetin alfa.

So this data was actually quite useful for us internally to feel comfortable with going forward with our Phase 3 trial, and it was very instrumental in us making that decision.

So if we can go to the next slide. This is the pooled efficacy results. These are the morbidity and the mortality hazard ratios, and what I want to highlight here is that these studies, alone or in combination, were not designed to evaluate the effect of treatment of anemia with Darbepoetin alfa on morbidity and mortality. We did collect this data, because we were interested in seeing whether we could see any signal, and that would potentially help us and inform us about whether we should go forward with the Phase 3 trial. So let me just take you through the data here.

The hazard ratio for composite endpoint, and in this case it is a composite of all-cause mortality or a first heart-failure hospitalization, this demonstrates an approximately 33% relative risk reduction, suggesting a benefit from treatment with Darbepoetin alfa.

The p-value for the Kaplan-Meier estimates was 0.064. The hazard ratio for heart-failure hospitalization demonstrates a 34% relative risk reduction, once again suggesting a benefit from treatment with Darbepoetin alfa. The p-value for the Kaplan-Meier estimates was 0.091.

The hazard ratio for all-cause mortality demonstrates a 24% relative risk reduction. The p-value for the Kaplan-Meier estimates was 0.418. So while we didn't see statistically significant results here, there were trends that suggested that treatment of anemia with Darbepoetin alfa would benefit patients with symptomatic heart failure.

And then, let's go to the next slide. This is our conclusions. In subjects with symptomatic heart failure and anemia, treatment with Darbepoetin alfa administered subcutaneously every two weeks was well tolerated. It increased and maintained hemoglobin concentration within the target range in a gradual and reliable fashion, and it resulted in non-statistically significant improvements in morbidity and mortality outcomes. These data support the conduct of a larger randomized double-blind placebo-controlled trial to determine the impact of treatment of anemia with Darbepoetin alfa on clinical outcomes in heart failure patients.

And then, the next slide is our RED-HF(TM) Trial study design. We are going to randomize 3,400 patients to Darbepoetin alfa or placebo in a one-to-one fashion. The study population will be patients with hemoglobin between 9 and 12 g/dL, left ventricular ejection fraction of less than or equal to 35%, New York Heart Class II to IV. We will be titrating the Darbepoetin alfa to achieve and maintain a target hemoglobin of 13.0 g/dL, not to exceed 14.5 g/dL.

The primary endpoint is time to death from any cause, or first hospital admission for worsening heart failure, whichever is first. We started enrolling at the beginning of June. We already have patients in the trial, and this will be an endpoint driven trial, which will require approximately three years.

And with that, the last slide is the end of our talk, and I'm happy to open up for some questions.

Question-and-Answer Session

Operator

(Operator Instructions) Your first question comes from Gene Mack.

Gene Mack – HSBC

Hi. Thanks for taking my question. Can you just go over, I saw the efficacy data that you presented for the combined analysis; but do you have that for on a number needed to treat basis? How many patients you would need to treat in order to avoid one occurrence of even mortality or hospitalization? Is it possible to do that?

The second question is, how are you going to adjudicate the cases of hospitalization due to heart failure that do come in in order to make sure that all clinics are sort of looking at that the same way? Thanks.

Dr. Scott Wasserman

Okay. So just off the top of my head I can't do the number needed to treat for you, but I'm sure I can look into that and get back to you. Unfortunately, I'm not a statistician and I'm not that good at math.

In terms of the adjudication, that's a great question. We have a clinical endpoints committee that will determine whether a heart failure hospitalization meets criteria. When we had our discussions with global regulatory agencies, we were very clear about our definition of heart failure hospitalization; we had buy-in from global regulatory agencies about our definition, and so they will use that definition when adjudicating heart failure hospitalization.

Gene Mack – HSBC

Okay. Thank you.

Operator

Your next question comes from Craig Parker.

Craig Parker - Lehman Brothers

Hi. I assume that you did echoes on some of these patients. Do you have any data that you can disclose on cardiac output?

Dr. Scott Wasserman

That's a good question. So in order to get cardiac output, you'd have to do a few back of the envelope calculations, and we haven't done those because it's not necessarily standard.

You'd have to look at the left ventricular outflow track diameter and then make an area calculation to get the forward flow velocity. So we haven't done those calculations, and I'm not sure, to be honest, from our echo data that we have the Doppler needed to get that information. So I can't answer that and I don't think we have the data to get that answered.

Craig Parker - Lehman Brothers

Maybe if I could ask a follow-up. I assume that there was not a significant change in your heart class but were there any clear trends in components?

Dr. Scott Wasserman

Sure. So, that's a great question. I think the one thing that I want to make clear is when Amgen made the decision to go forward, we looked at all three trials and we looked at all of the endpoints in all three trials.

In terms of the New York Heart class, we did not see statistically significant improvements in any of our three trials, but all three trials pointed in the right direction. In other words, patients that received Darbepoetin alfa all got better in terms of their New York Heart class in those three trials.

In three independent trials with three independent sets of TIs and independent investigators, all the arrows were pointing in the right direction suggesting a symptomatic improvement and so once again, we felt confident that there was a real signal there.

Craig Parker - Lehman Brothers

Thank you.

Operator

Your next question comes from Steve Harr.

Steve Harr - Morgan Stanley

It seems like you guys have a numerical trend towards higher adverse events for thrombosis when you combine stroke and MI, but in numerical trend in your favor on mortality. If you look at the causes of mortality, what do you have on cardiovascular mortality versus all cause?

Dr. Scott Wasserman

That's a good question. So let's go back to your question about the numerical trend with basically thrombotic events. You'd have to combine DVT, PE, MI and cerebral vascular disorders; and then, based on what I'm looking at it -- if you look at the numbers then do the percentages it actually probably would be about equivalent.

I wouldn't say that there's a numerical trend suggesting that there's a signal there. I mean that was why I pointed out the numbers because the Darbepoetin alfa group has more patients than that, so you can't just look at the actual number of events.

So in terms of cardiovascular versus non-cardiovascular, most of the deaths in these patients are cardiovascular by and far, so it's, I think it's definitely 70% to 80% are cardiovascular deaths.

Steve Harr - Morgan Stanley

It's basically the same in both treatment and placebo?

Dr. Scott Wasserman

Well, unfortunately the numbers here are so small but I if I remember correctly, it was basically -- I'm trying to remember. There wasn't enough, basically because there are so few deaths in this. I mean you're looking at, you're comparing 18 to 17.So I don't want to speculate on whether…

I mean we thought a lot about if you're trying to get with the composite endpoint in choosing all cause mortality versus cardiovascular mortality, we did see what appeared to be some benefit in terms of non-cardiovascular mortality which is why we went with the all cause mortality.

Steve Harr - Morgan Stanley

Great.

Dr. Scott Wasserman

But that's from me trying to read your mind.

Steve Harr - Morgan Stanley

No, that's helpful. Thank you.

Operator

Your next question comes from Elise Wang.

Elise Wang - Smith Barney Citigroup

Hi. Thanks for taking my question.

Just a point of clarification. I'm just looking at the design of the two different studies, the two Phase 2s. Am I correct in reading this that one study had one-year worth of Aranesp treatment versus placebo and the other only had 26 weeks. Is that correct?

Dr. Scott Wasserman

Yes. Study 170, we actually looked at a number of endpoints like New York heart class and quality of life measures, et cetera at six months, but then we continued to dose patients, followed them up to one year for safety as well as clinical endpoints. Then in Study 171, we just treated them for six months.

Elise Wang - Smith Barney Citigroup

Okay. But the safety data also was looked at a six-month follow-up period to that?

Dr. Scott Wasserman

No. The safety is combining all of the data and so is the morbidity and mortality. We talked with our statisticians long and hard about this about whether you could do that statistically and I was assured that we are allowed to do that statistically.

Elise Wang - Smith Barney Citigroup

Okay. In terms of then some of the safety outcomes, do you have any sense of some of the temporal implications of the events in regard to when they may have been on Aranesp treatment versus non-Aranesp treatment? Is that anything of relevance here?

Dr. Scott Wasserman

That's a good question. We've looked at that. In general, there's really no signal. I mean these events, they happen.

We didn't see it temporally related to either -- some patients had events after the first dose of placebo and some had it after the first dose of Darbe and some were at it on a full year and had no events -- both placebo and Darbe -- so it was completely as you'd expect. It looks very balanced in terms of adverse events and we didn't see any terms or any type of safety signal in that.

We did have in this trial as we did in all of our Phase 2s and as we'll have in Phase 3, an independent data monitoring committee that looks at all of that and obviously, if they saw anything temporally, as they meet on a regular basis, they would have stopped the trial. Obviously that didn't happen.

Elise Wang - Smith Barney Citigroup

Okay. And then just a last question for you. On the pivotal study, the large Phase 3, what does that power to show on the endpoint?

Dr. Scott Wasserman

So there's 90% power, to show a 20% relative risk reduction.

Elise Wang - Smith Barney Citigroup

Thank you.

Operator

Your next question comes from Richard Nelson.

Richard Nelson - MorganJoseph

Thank you. I was just wondering how long do you think it will take for you to enroll all the patients in the study?

Dr. Scott Wasserman

Right now, we predict that it's going to take about a year-and-a-half. Obviously we don't know what's going to happen. We're doing our best to leverage our experience with previous trials to ensure that our enrollment is timely. It will just depend on how things go.

We've only been open for enrollment now two weeks and based on the way that you can screen, you really can't get into the trial within the first week. We already have four patients and we only have, I think ten sites up at this stage, so we're doing pretty well. I am confident that we will meet our enrollment.

Richard Nelson - MorganJoseph

Is there anything about the enrollment criteria in Study 171 that possibly might have a biased study against Aranesp from the perspective of mortality? Is there anything you learned from that in terms of excluding certain kinds of patients from the study?

Dr. Scott Wasserman

No. That's a great question. We went back and went through those six deaths very, very carefully and I think Elise was kind of asking that question within terms of, was there a temporal relation with events? We went through it very, very carefully: looked at absolute hemoglobins, we looked at rate of rise, we looked at doses of Aranesp, we looked at all of their meds, we looked at everything.

We could not figure anything in terms of trial design or patient characteristics that would have resulted in the six deaths just being in the Darbepoetin alfa group. Now when you look at the two studies combined, you see that it's completely, that signal goes away and if anything it suggests -- if you look at the percentages -- 9% mortality in placebo and 6% in the Darbepoetin arm.

So, I think when we had our meeting at ACC, I think both Professor van Veldhuisen as well as I tried to stress that in small numbers, take it with a grain of salt, let's look at our entire kind of data package, and then based on that we can make some decisions.

The Company looked at all of that data very, very carefully to ensure that we were going to be safe when we went forward into Phase 3. Obviously, because we're endorsing going forward in Phase 3 and we started enrolling we do feel that the trial design is such that patient safety will not be compromised.

Like I mentioned to Elise we have an independent DMC in Phase 3 that will ensure patient safety throughout the course of the trial.

Richard Nelson - MorganJoseph

Will the enrollment be limited to the United States or is it a global enrollment?

Dr. Scott Wasserman

This is definitely a global trial. We're getting up and running, we're well on our way; obviously it's summer so especially in Europe, it's a little challenging but we'll be up and running -- or we are up and running and I don't anticipate any bumps.

Richard Nelson - MorganJoseph

The three years that you anticipate requiring, is there a specific number of events that will drive that endpoint?

Dr. Scott Wasserman

Sure. It's going to be 1,450 events; so approximately 1,450 events which we think will take about three years.

Richard Nelson - MorganJoseph

Great. Thank you.

Operator

Your next question comes from John Davenport.

John Davenport -

Hi. Thanks for taking my call. I was wondering if there was PGA scores that were taken with this and if there's any data on that?

Dr. Scott Wasserman

Sure. So I'm sure that you're well aware that the PGA -- well you might not be aware of it, but -- in Study 126 which was the smallest trial, we were able to show statistically significant benefit. Then Study 171, we showed a trend towards benefit and then for whatever reason in this larger trial, we didn't see any real significant change and I don't have a good explanation for that.

John Davenport -

Okay. Thank you.

Operator

Your next question comes from Bret Holley.

Brett Holley - CIBC World Markets

I noticed in the RED-HF trial, the enrollment criteria called for left ventricular ejection fraction less than 35%; it appeared in the Phase 2s that it was less than 40%. Is there anything we can read into? Did you see a greater benefit in sicker patients?

Dr. Scott Wasserman

No, that's a great question. In general, heart failure trials either used less than or equal to 35% or less than or equal to 40%. Obviously, there should be a slight difference in terms of event rates with less than or equal to 35%.

It was just, we just wanted to ensure that we were characterizing the correct patients and we just wanted to make sure that the patients had moderate left ventricular systolic dysfunction and that's why we went with 35% versus 40%. 40% is between the mild to mild to moderate and so we were trying to obviously choose a little bit of sicker patients.

Brett Holley - CIBC World Markets

Thanks.

Operator

Your next question comes from Jack Mueller.

Jack Mueller -

I wonder if you could also characterize your thinking behind making the change in the target hemoglobin level from 14g/dL to 13 in the Phase 3 trial?

Dr. Scott Wasserman

In the Phase 3 trial, it's 13 not to exceed 14.5g/dL as opposed to basically 14 plus or minus 1 is 13 to 15g/dL. It was a part of our negotiation with global regulatory agencies, that's where the current target hemoglobin comes from.

Jack Mueller -

Okay. Thank you.

Operator

Your next question comes from Craig Parker.

Craig Parker - Lehman Brothers

Hi. Thanks. I know we're starting to split hairs here about relatively a small data set but did you happen to look at ischemic versus idiopathic cardiomyopathy and see if there was a difference in treatment effect?

Dr. Scott Wasserman

Yes, we did. Once again, you kind of answered your own question with a small data set. We didn't see anything but once again, as you noted, it's a small data set. We did look at that and we did not see any difference.

Craig Parker - Lehman Brothers

Can I just clarify the three years comment about the study? That's three years including the year-and-a-half accrual?

Dr. Scott Wasserman

We anticipate that it will take a year-and-a-half to accrue the patients and then it will take basically the remainder of three years to have enough events. Now, obviously, this is an event-driven trial similar to treat, so it will be based on the event rate.

So obviously, enrollment can affect that because if you don't enroll enough patients you're not going to have enough events or if for whatever reason, we come up with a magic pill to cure everyone's heart failure, it will be really slow. There are things you can not predict and we did our best with current available data in our Phase 2 program to figure out what the appropriate event rate was going to be.

Craig Parker - Lehman Brothers

Thank you.

Operator

Thank you. At this time, there are no further questions.

Tony Gringeri

Thank you very much. With that we'll conclude the call and I just want to remind everyone that for the next 72 hours, there will be an encore dial-in at 800-642-1687 with the same conference ID as this meeting, 1688137 in case you wish to hear the conference replayed or view the slides.

Thank you very much, everyone, and we'll see you again next time.

Operator

Thank you. This concludes today's conference call. You may now disconnect.

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