Seeking Alpha
We cover over 5K calls/quarter
Profile| Send Message| ()  

Executives

Robert I. Blum – President and Chief Executive Officer

John R. Teerlink – Professor of Medicine-University of California San Francisco

John J. V. McMurray – Professor of Medical Cardiology-University of Glasgow

Fady I. Malik – Senior Vice President-Research and Early Development

Andrew A. Wolff – Senior Vice President-Clinical Research and Development and Chief Medical Officer

Analysts

Ritu Baral – Canaccord Genuity, Inc.

Cytokinetics, Inc. (CYTK) Investor Event on ATOMIC-AHF Data at the ESC Conference Call September 3, 2013 8:00 AM ET

Robert I. Blum

Good afternoon, thank you for joining us for the Cytokinetics Investor Event here at the European Society of Cardiology 2013. We are here in Amsterdam and broadcasting from the European Society of Cardiology meetings, today September 03, 2013. My name is Robert Blum, I am President and CEO of Cytokinetics. I’ll be making forward-looking statements. I point you to our SEC filings with respect to the proper caveats to those statements. We don’t undertake any obligation with regard to updating those statements.

I am very pleased to be joined today by members of Cytokinetics senior management team, as well as special guests. Here on slide number 4, you see that I am joined by Fady Malik, Physician, Scientist, Senior Vice President Research and Early Development and a Cardiologist.

Fady is a member of the management team who joined Cytokinetics back in 1998. Fady was Cytokinetics first employee and it’s his vision with regard to the original mechanistic and therapeutic hypothesis that we’ve been executing on in connection with our muscle biology related research and development. He has been responsible for the research and translational medicine and this is very proud day for all of us and then especially for Fady in light of today’s announcements regarding omecamtiv mecarbil.

I am also joined by Andy Wolff, also a Cardiologist, a member of our senior management team since 2004. Andy is our Head of Clinical Research and Development and Chief Medical Officer. Andy took a quite significant role in the design of our clinical studies including this trial ATOMIC-AHF that we’ll be speaking about today. By now I speak also for Andy in connection with this being a proud moment for him and the company.

Today we are also joined by two special guest, Dr. John McMurray and Dr. John Teerlink. John and John are both cardiologist who have been involved in the development and clinical research of omecamtiv mecarbil for some time. I think they bring quite excellent credentials and credibility to the study and evaluation of omecamtiv mecarbil and they have been involved with the studies since the early clinical trials and through to also this study, ATOMIC-AHF, that we’ll be speaking about and I am very pleased that they’ve been able to join us today to provide both the results from the study and also commentary and perspective.

Here on slide number five is our agenda for today, I’ll be making some opening remarks. Then John Teerlink will provide results of ATOMIC-AHF. John just presented these data here in Amsterdam at the European Society, amongst his professional colleagues and now we are very grateful for him also joining us for this investor event.

John McMurray will then follow John Teerlink and provide commentary in perspective about the unmet need in heart failure and also where these results may fit into that place for drug development and opportunities to address the clinical unmet need.

Fady Malik will then take the podium and talk about the program and its overview, some of the original therapeutic hypothesis we had for a small molecule cardiac myosin activator, where the ATOMIC results fit into that and how we now are proceeding development with ATOMIC results towards other results that we expect from other ongoing studies.

Andy Wolff will then lead a question-and-answer session both for those of you here in Amsterdam, as well as those participating in the webcast. I encourage you to e-mail your questions, so that we can ensure they get a proper response. I will then make some concluding remarks.

I’d now like to make a few comments about omecamtiv mecarbil, our heart failure program and also the heart failure syndrome around which omecamtiv mecarbil has been designed and is been developed.

Heart failure is a complex clinical syndrome. It’s a physiologic state in which cardiac output is insufficient to meet the needs of the body and lungs. It’s a chronic condition with an urgent unmet need. It’s a fast growing population tied to ageing demographics and about one-half to two-thirds of patients with heart failure have compromised left ventricular function or systolic dysfunction. Those are the patients to whom we are addressing the development of omecamtiv mecarbil with the hope that this drug candidate may result in improved cardiac performance, improved cardiac muscle contractility and potentially increased cardiac output.

Heart failure is typically classified as is described on this slide. By the New York Heart Association categorization, the U.S. population of heart failure is estimated to be approximately 5 million patients with the majority of them being Class II or Class III heart failure patients. There is a high unmet need given current standards of care in this disease area. There are opportunities both in the acute and chronic setting for novel mechanism evidenced based therapies to reduce mortality and hospital readmission, there are the absence of treatments to increase cardiac performance without associated liabilities currently as it is seem with Inotropic Therapy which will increase cardiac output, but also associated a potential increased mortality risk linked to increases in heart rate and arrhythmias.

Heart failure therapies in terms of the acute care and chronic care are depicted on this slide. You can see that there is an armamentarium of existing drugs that fall into different categories to treat this complex syndrome and inotropes those drugs useful for the expected objective of increasing cardiac performance represent depending on how you look at it about 10% to 20% of the acute heart failure therapies despite their limitation and the goal with the omecamtiv mecarbil program is to develop a medicine that may improve cardiac contractility without associated liabilities and increased mortality risk.

I mentioned the heart failure population is a large one and a growing one. Heart failure is the number one reason why patients in the United States are hospitalized. It is the number one reason why Medicare patients are hospitalized. It’s a population that’s growing with increased aging demographics and given the high unmet need, an important population to address with new drug development.

Currently, there is an unacceptably high risk of mortality and readmission given conventional therapies for the treatment of heart failure. These patients tend to do okay in hospital, albeit there are opportunities for improvement, but where they are at their highest risk is in the post-discharge setting, were there is a high risk of death and readmission in the post-acute and chronic phase unacceptably high and where this represents both a significant need clinically and also economically.

The costs associated with heart failure are already high and increasing. They are expected to increase both as the population ages and as patients live longer, post acute coronary syndromes with compromised myocardial heart function. This is a key issue of ongoing healthcare reform and interest to see about demonstrating where drugs and other interventions can have a role in both presenting readmission and increasing days alive outside of hospital. This is an area of high urgent interest amongst policymakers.

Our goal and that of Amgen in partnership with Cytokinetics in the development of omecamtiv mecarbil is as we prepare for the potential progression to Phase 3 to conduct studies both with the intravenous and the oral forms of omecamtiv mecarbil. The results of ATOMIC-AHF were presented here in Amsterdam this morning. We are pleased with those results as you will hear more in detail in the session and we look forward to results from COSMIC-HF over these next several months, as we plan for the potential progression to Phase 3.

As we have been stating for sometime now, our goal is to develop Omecamtiv Mecarbil both as may address the acute care situation in acute heart failure patients and also those patients as they transit to the outpatient setting. The goal is to demonstrate that improved cardiac function initially has made be achieved in hospital can then be translated in the outpatient setting with maintained functional improvements with the goal of reducing death and readmission in that post-discharge period.

So, I am very pleased today to have an opportunity to introduce John Teerlink who at this investor event will share in detail the results of the ATOMIC-AHF study. Those results as I mentioned earlier, have been the subject of a joint press announcement today with Amgen and also a presentation here at the European Society of Cardiology about two hours ago. John has been a consultant and a principal investigator to Amgen and Cytokinetics in the conduct of multiple studies, in those omecamtiv mecarbil as well or better than anybody else and again it’s my pleasure to introduce him to share with you now the results of ATOMIC-AHF.

John R. Teerlink

Thank you, Robert. It’s a real pleasure to have an opportunity to discuss the results of this program. So my purpose is to really focus on presenting the primary results from the ATOMIC-AHF study. ATOMIC-AHF is a Phase 2 dose finding study of intravenous omecamtiv mecarbil in patients with acute heart failure. Now it probably makes this presentation on behalf of the ATOMIC-AHF investigators and the patients who contributed to this progression of the study.

And you heard a bit, omecamtiv mecarbil is a novel, selective, cardiac myosin activator that works through a very unique mechanism of action increasing the rate of entry of myosin into the tightly bound force producing state with actin, essentially demonstrating an increasing number of hands pulling on the rope. In in-vitro and animal experiments, we have seen this molecular mechanism of action translate into the physiologic finding of increases in duration of systole as measured by the systolic ejection time.

This increase in systolic ejection time in animal models were shown to increase stroke volume without any evidence of increase in myocyte calcium or increase in the rate of contraction or increase in myocardial oxygen demand.

When omecamtiv mecarbil is taken to healthy volunteers and patients with stable chronic heart failure, we saw this incredible relationship between the omecamtiv mecarbil concentration and the changes from baseline and the systolic ejection time, of interest these are very similar curves between the two patient populations. And then we saw in the healthy volunteers and in the patients with stable chronic heart failure, this increase in systolic ejection time translate directly into improvements in cardiac performance, as demonstrated by increases in stroke volume, fractional shortening and improvements in ejection fraction.

Yet, the question was, what would happen when we took this agent into acute heart failure patients? And consequently the ATOMIC-AHF study tried to investigate that question as a dose finding Phase 2 study. The main objective was to evaluate the safety, pharmacokinetics and pharmacodynamics, and efficacy of intravenous omecamtiv mecarbil in patients with acute heart failure. The primary hypothesis was at least one dose level of intravenous omecamtiv will be well tolerated and will result in improvement of dyspnea in subjects with left ventricular systolic dysfunction hospitalized for acute heart failure.

As I ha alluded to, it has a complicated study design. It is based on a sequential dosing design, where approximately 200 patients are randomized in a cohort to either omecamtiv mecarbil or placebo and with ascending doses through the three cohorts with interim data monitoring committee analysis to enable advancing to the next higher dose cohort.

The dosing regimens of these cohorts were established by pharmacokinetic simulations which establish different dosing approaches that were geared towards hitting predicted target plasma concentrations ranging from 115 nanograms to 310 nanograms per milliliter. These changes in serum concentrations were predicted to result in increases in systolic ejection time ranging from minimal increases in the Cohort 1, 2 physiologically significant increases in Cohort 3.

Patients were randomized within 24 hours of presentation for acute heart failure and randomized one-to-one to omecamtiv mecarbil or placebo, they were carefully followed during the in-hospital time period, both during the 48 hour infusions and subsequently during the rest of their hospital course with evaluations of their symptoms in extensive adoption of their pharmacokinetics, as well as intensive monitoring of their cardiac biomarkers. There was also a small echocardiographic subsidy performed.

The patients enrolled in ATOMIC-AHF had a history of heart failure and reduced ejection fraction with an ejection fraction less than or equal to 40%. They were all hospitalized for acute heart failure acquiring intravenous therapy with dyspnea due to heart failure at rest or minimal inclusion despite the administration of an intravenous diuretic. In addition, they had to have elevations in their BNP or NT-proBNP.

While this study was a Phase 2 dose finding study, we also investigated and evaluated some efficacy endpoints. The primary endpoint was selected to be dyspnea symptom response through the first 48 hours. There were multiple secondary efficacy endpoint selected, as well as evaluation of PK/PD from this eco substudies.

And now I get to present the actual results of the trial. 613 patients were enrolled in ATOMIC-AHF and they had characteristics consistent with patients who were admitted for acute heart failure with reduction in the systolic function. They had a high prevalence of ischemic heart disease as well as multiple other comorbidities.

In addition, patients enrolled in this trial had excellent background therapy for the chronic heart failure and despite an exclusion criteria which we excluded patients with clinical ACS or acute coronary syndromes, we had over half of the patients with troponin that were above the upper reference limit. In addition, the NT-proBNP in the 9,000 to 10,000 range is among the highest observed in any accurate heart failure study.

The primary efficacy endpoint consisted of evaluation of the dyspnea using a 7 level Likert scale, ranging from markedly worsened to markedly improved. A patient was considered a responder if they met the following criteria; which was that they were minimally, moderately or markedly better at six hours and moderately or markedly better at 24 hours and 48 hours without worsening of heart failure or death for any cost by 48 hours.

So these are the primary results of the initial analysis of the ATOMIC-AHF trial. And in this figure, you can see an increase in the dyspnea response rate from 42% in Cohort 1, up to 51% in Cohort 3. This 51% represents a 23% increase in treatment effect compared to placebo of the pooled placebo group. However, the overall analysis comparing the pooled placebo group to all of the omecamtiv mecarbil cohorts was not statistically significant with the p value of 0.33. A pre-specified supplementary analysis to the primary endpoint evaluated the pairing of the placebo with the omecamtiv mecarbil from the same cohort.

Within this analysis, we still can see that the placebo response rate among the patients in Cohort 3 was 37% while among the omecamtiv mecarbil treated patients in Cohort 3. the response rate was 51%. This represents a 41% improvement in treatment effect in the omecamtiv mecarbil group in the third cohort with the nominal p value of 0.03.

Supporting these findings was an exploratory analysis where we looked at the relationship to the dyspnea response of omecamtiv mecarbil doses and concentrations and these findings greatly supported the suggestion that omecamtiv mecarbil provided centime relief in this study with an increasing dyspnea relief with increasing dose as well as increasing plasma concentrations.

The secondary efficacy endpoint of worsening heart failure was also evaluated. In this case, we looked at death or worsening heart failure within seven days of the investigational product initiation and we saw a 46%-sh decrease in the incidence of death or worsening heart failure with nominal p-values ranging from the 0.06 range. This trend toward beneficial effect in terms of reducing worsening heart failure was predominant – and death was driven predominantly by a reduction in the worsening heart failure events.

Other secondary efficacy endpoints were also evaluated and none of these were statistically significant between the cohorts of omecamtiv mecarbil and the pooled placebo. A very important concern one needs to analyze in these agents in improved cardiac performance is the occurrence of supraventricular and ventricular tachyarrhythmias.

Interestingly supraventricular tachyarrhythmias were actually reduced by 50% in the omecamtiv mecarbil treated patients compared to placebo, driven predominantly by a reduction in atrial fibrillation or the instance of atrial flutter. Importantly, when one of ventricular tachyarrhythmias, there was no significant difference between the placebo or omecamtive mecarbil treated patients.

30 day adjudicated events of death in all re-hospitalizations likewise were similar between the two groups, the groups of placebo and omecamtiv mecarbil treated patients. In addition, myocardial infarctions were relatively rare in the trial. There were three in the placebo group and seven in the pooled omecamtiv mecarbil groups.

As I mentioned earlier, troponin’s were protocol specified to be frequently analyzed at specific time points and this figure represents the Troponin change from baseline compared with the pooled placebo in the light grey and the three cohorts of omecamtiv mecarbil in the various shades of purple.

One can see from this figure that there is a modest increase in troponin’s in the omecamtiv mecarbil group and we decided to investigate the potential relationship between omecamtiv mecarbil and these Troponin increases. When we looked at the maximal Troponin change from baseline and compared it to omecamtiv mecarbil concentrations either by looking at the maximal plasma concentration of omecamtiv mecarbil or the total exposure area under the curve for the first 48 hours of administration of the agent, we saw absolutely no relationship, there is no significant relationship between the Troponin changes and the omecamtiv mecarbil concentrations. You can see from p-values of 0.095 and for the maximal concentration and for p-value of 0.83 for the area under the curve analysis.

Adverse events, both common adverse events and serious adverse events were similar and comparable between the two groups. Importantly, these findings extend what we learned and actually met the main goal of the trial to see that omecamtiv mecarbil in this patient population with acute heart failure behaved very similarly to those in the previous trials. In this study, we see a significant increase in the systolic ejection time that is clearly concentration dependent and is significant at each omecamtiv mecarbil concentration been individually.

And as I mentioned, we have seen this relationship between omecamtiv mecarbil concentration and a change in the systolic ejection time in both the healthy volunteer studies and the chronic heart failure patient studies. ATOMIC-AHF adds to this picture, the role of omecamtiv mecarbil in patients with heart failure showing that the relationship is highly similar to both healthy volunteers and chronic heart failure patients.

Omecamtiv mecarbil also was able to demonstrate significant effects on heart rate and systolic blood pressure and these were beneficial effects and as much as the omecamtiv mecarbil produced a greater reduction in heart rate, while also demonstrating a less significant or lower drop and a lower fall in blood pressure.

So overall in summary, omecamtiv mecarbil met its overall objective which was to provide us information on how the agent would perform in the setting of acute heart failure and give indications of the efficacy and safety.

In terms of its efficacy, omecamtiv mecarbil did not meet the primary endpoint of dyspnea relief. However, it appeared to improve dyspnea in Cohort 3 which is the higher dose cohort and had dose related improvements and concentration related improvements in dyspnea relief.

In addition there were trends towards reductions of worsening heart failure. The safety overall appeared very similar to placebo. So, modest increases in troponin were noted. There is no clear relationship to omecamtiv mecarbil concentration and these modest increases in troponin. There was a numerical imbalance in microinfarctions observed in Cohort 3, but no evidence of proarrhythmia and in fact any evidence of a suggestion of reduction of supraventricular tachyarrhythmias.

The pharmacology was similar to that seen in both healthy volunteers and stable heart failure patients and it demonstrated a consistent improvement in systolic ejection time consistent with its mechanism of action.

In addition to small fall in heart rate and increase in systolic blood pressure at higher doses provides additional assurance in terms of safety of this agent. There are multiple people who contributed to this program including the colleagues from Amgen and Cytokinetics and this is rather another opportunity to acknowledge their hard work in this program. So thank you very much.

I think, I get to turn it over to Professor McMurray for any comments.

Robert I. Blum

So thank you John. I’d now like to ask Professor McMurray, Professor of Medical Cardiology, University of Glasgow to provide his commentary and perspective.

John J. V. McMurray

I maybe doing this with or without slides, so I am not sure – no, no slides, good. Okay, well, as Robert said, my name is John McMurray. I am a Professor of Medical Cardiology in University of Glasgow, in the United Kingdom. I am practicing cardiologist with a particular interest in heart failure and I am a clinical trialist.

So what I’d like to do is, make some comments on the trial results that you have just seen and then I’d like to try and put the omecamtiv development program in the context of what else is going on in acute heart failure. So when you do a Phase 2 trial, what you do is you look to the totality of the information to try and figure out whether the compounds and question looks interesting and of course you are looking at two things as always you are looking at signals for efficacy and you are looking for any signals for harm.

And when I look at the results of ATOMIC heart failure, then the things that stands out to me where that there was a trend towards improvements in dyspnea, which I regard as moderately interesting, but I will come back to dyspnea in a few moments.

There was a stronger trend for a much more and might be important outcome which was death or worsening heart failure. Then actually the things that were also very important, but in some ways buried in the results, because John correctly presented them in the hierarchical order that would be specified the endpoints, where the apparent reduction in atrial arrhythmias and perhaps very significantly indeed, a reduction in heart rates.

Now, why do I say, a reduction in heart risk is of any importance. I say that because it is a uniform truth in all heart failure trials. Today it’s been both acute and chronic heart failure trials as a drug that increases heart rates is almost invariably associated with an increase in mortality, a drug that has no effect on heart rates, probably doesn’t do very much and almost all effect of treatments, in fact all effects of treatments that I can think of today that include clinical outcomes, reduce heart rate.

So the small decrease in heart rates is actually quite a large and important finding. So those are all good things that I see along with the generally very favorable and worse effect profile.

Of course the safety side of things most relatively looked at and there is the small rise in troponin. There is definitely things to be a trend in the study whereby there is more troponin increase within the higher dose of cohorts and the question is, is that a real finding that should be of concern or is there another explanation for it and I think the most important thing that John showed that perhaps suggest this is play of chance rather than being something anymore significant than that is the relationship between change in troponin and plasma concentrations omecamtiv.

So all in all, as a Phase 2 trial this looks really as promising as I think that you can get at this stage in the development of drug for acute heart failure and I’ve looked at many other sets of Phase 2 data that haven’t looked quite as encouraging.

So I’ll add some comments in the study, what they want to do is, I want to say we’re well anticipating to the overall picture of acute heart failure whilst it has happened in the past while it is happening at present, but I am not going to label the points about the clinical importance of acute heart failures out of anybodies here or listening if they don’t understand how important a condition it is. But the really sad thing about this condition is that, at the moment we do not have a single effective treatment.

I know that for certain because we spent a very long time recently rising these guidelines. I was also in the ACCAJ, American Guideline Committee and we concluded the exactly the same thing and the National Institute of Health and Clinical Excellence in the UK is going through the same process at the moment and drawing the same conclusion.

Sadly since this article was published, actually almost 40 years ago absolutely nothing has changed. We still empirically give the people opioids options, loop diuretics and if we get really, really desperate, we give them inotropes, even though we know that those are probably not doing any good in the long run, and nothing has changed since then. And it’s worse than that because the landscape for previous drug development in this area doesn’t look too good and you can see that as a threat or as an opportunity. So I’d say it’s an opportunity and I think we have seen some recent development, it’s a great deal of hope for this whole area, but to get many of the treatments that have been tried have failed.

I’d say partly because the focus may have been wrong, the focus has been on improvement in breathlessness which probably isn’t the most important thing, but why do I say the landscape has changed and why is the new hope. Well, that’s because another drug being developed for acute heart failure recently reported its results at the American Heart Association in November 2012. That was a trial called RELAX-AHF, looking at an endogenous peptide, RELAX and there are RELAX and in around 1,160 patients or so. This treatment was compared to placebo, 48 hours of intravenous therapy compared to placebo.

Well, the trial gave, what I’d describe as mixed results, one of the co-primary endpoints was positive, the other was not. The two principal secondary endpoints were also not reached, but what caused a great deal of excitement, discussion, controversy was the finding in this study that RELAX and Serelaxin seem to reduce both cardiovascular and all cause mortality though of course small numbers of events and some uncertainty about whether this is a real treatment effect.

Clearly findings that need to be replicated and indeed they will be, because a second larger trial with this agent is about to commence. What else is happening in this field, well there is another natriuretic peptide called Urodilatin that is being tested in the clinical trial. We’ve applied BNP nephritides and fields. Our Japanese colleagues used ANT based on evidence that would not result in regulatory approval in North America or Europe.

And the trial I am about to mention is, setting this other natriuretic peptides that is produced primarily in the kidneys and that treatment is being studied in the trial called TRUE-AHF, which is recruiting, how it has recruited just over 100 patients I believe at this stage. I had two co-primary endpoints one of which is cardiovascular mortality, so I noticed these trials are moving away from dyspnea and towards important clinical outcomes.

So what would I say about the current state of play in acute heart failure where we have no treatment and afraid that’s still a hard truth there is no treatment that is evidence based and therefore there is a huge clinical need.

We’ve had several disappointing trials, I showed you there were something (inaudible) in patients with acute heart failure, well actually it looks promising but a confirmatory trial is immediate and that is about to start. Ularitide or Urodilatin is just entering Phase 3. But one thing I would point out is that the profile of action of the drug we’re talking about today is completely different from these other two agents which if you were to characterize pharmacological action in a very simple way it would be to say that they are vasodilator, which amongst the other things means that they will usually lead to reduction in blood pressure. And for that reason, omecamtiv mecarbil potentially might be used in a much broader segment of the acute heart failure population where to be successful.

Now of course the downside of being behind those other two drugs is that it maybe that omecamtiv mecarbil will have to be tested on top of one or other of the Serelaxin and Ularitide, but I think another incredibly important difference between omecamtiv and the other two drugs is the availability of a novel preparation because that increases the opportunity enormously. It allows us to give the drug chronically to start with intravenous treatment during the acute de-compensation to put the patient in oral therapy before discharge and then to continue that chronically.

So I do see this as a drug because of its unique mechanism of action because it isn’t like any thing else that we’ve got because it does target the fundamental problem in these patients which is that their heart is not pumping properly. I do see this drug having immense potential in an area where there is a huge unmet need. So that’s all I will say.

Fady I. Malik

Okay. Well, thank you John and John for the introductory comments and I’m going to put this and I am just kidding. We are looking at both at how this drug works in ATOMIC-AHF and also for your commentary John in terms of putting this in the overall landscape of heart failure therapies.

My comments are meant to really just put this program, put the results of ATOMIC in the context of the overall program we’d pursued for the last 10 or 12 years now. And first, I just wanted to layout what currently our cornerstones of heart failure therapy. Drugs that have shown in the chronic setting, reductions and mortality and morbidity such as ACE inhibitors and angiotensin receptor blockers, beta-blockers, aldosterone receptor antagonist; these drugs have reduced mortality and morbidity in chronic heart failure.

In acute heart failure, as John just described, we really have very little or no evidence-based drugs that we use and whereas commonly used in the setting of drugs that have increased cardiac contractility. However we don’t have any data, in fact we have in both of these cases, negative data associated with their use both acutely and chronically.

So recognizing that, while these three other mechanisms target the neurohormonal consequences of heart failure, what was missing in this fourth cornerstone was really a drug that might improve cardiac contractility in a way that was effective at reducing clinical outcome and in approving clinical outcomes.

So thus we embarked over ten years ago now, on developing cardiac myosin activators and specifically omecamtiv mecarbil as a drug that might be useful for treating heart failure.

Now in a great majority of heart failure, the ideology of the problem is that there is reduced systolic function that means the contractual function of the heart is not normal, the heart’s inability to pump blood to meet the needs of the body is compromised because the muscle of the heart isn’t working adequately; this results in a release of neural hormones that try to increase cardiac function and a vicious cycle of heart failure that’s been described and is effectively treated by blocking these consequences.

But again treating cardiac contractility itself, which would seem intuitive is a way to present the secondary neurohormonal release has not been successful in drug mediated way.

So why focus on cardiac function, but if you look at how cardiac function is, it’s been improved by advised therapy in a select subset of patients with cardiac dyssynchrony in widened QRS; one sees rather dramatic effects in terms of mortality and morbidity. So, improving cardiac function at least with devices appears to improve clinical outcome. And the question that was evolved for us over the years is could we develop a mechanism that would do so via drug mediated way.

So with the analytical therapeutic hypothesis, and I made this slide more than ten years ago now, asking what might be a consequence of targeting the cardiac sarcomere; directly activating the sarcomere downstream of other mechanisms that have been explored before those mechanisms that generally activates like a messengers, increase cellular calcium, increase heart rates, decrease blood pressure and cause arrhythmias and so forth.

We have both the sides that if you could act downstream of those second messenger systems, work directly on the cardiac sarcomere, but you may end up with a drug mechanism that while increasing contractility would have no adverse effects on heart rate or blood pressure, would not increase oxygen demand and improve cardiac efficiency and not cause arrhythmias and potentially this might lead to an effective drug for heart failure.

And so, omecamtiv mecarbil is a result of the efforts of many scientists at Cytokinetics and now partner with our colleagues at Amgen in terms of development and this is a small molecule activator of cardiac myosin, one of the first direct activators of any enzymes inside the cell, but in this case of its motor protein that is intimately tied in terms to the increases to cardiac contractility.

This protein hydrolyses ATP, and transduces it in a cycle of forced production that leads to increased cardiac contraction. We understand the mechanism of this molecule very well. The work has been published in Science 2011 and as John described in his presentation, the consequences of this drug mechanism appeared to have meet the therapeutic hypothesis and preclinical models meaning that we saw increases in contractility in animal models of heart failure, that didn’t lead to increases in oxygen consumption led to decreases in heart rate without adverse effects on blood pressure.

And so we subsequently moved into the clinic and investigated omecamtiv mecarbil in a broad range of clinical trials conducted some by Cytokinetics, some by our partner, Amgen and the totality of the data which impart is laid out here and impart is also been published in Lancet in back-to-back articles by John Teerlink and John Cleland.

Whether it’s integratively put together or understanding of how this drug works in people in terms of the effects in cardiac function and the concentration related effects on intolerance and ischemia. So in excess of the drug effect, meaning it increases systolic ejection time, just John showed you, it has increased omecamtiv mecarbil leads to a shortening of the time that coronary arteries fill and can lead to entire into the ischemia concentrations that exceed 1,200 nanograms per ml, this is what we learned in healthy volunteers and stable heart failure patients.

We also learned that targeting concentrations is low as the 100 to 300 nanograms per ml led to increases in cardiac function, which could be characterized in echocardiograms.

We also learned a lot about the pharmacokinetics of this drug and since this is tied intimately to the pharmacokinetics of omecamtiv mecarbil, we designed dosing regimens in ATOMIC-AHF to test three doses and a dose ranging dose finding way, escalating from the lowest dose to the highest dose, that in the population, we, that in the population we estimated would lead to concentrations of omecamtiv mecarbil that would be just barely in the range were we’ve seen pharmacodynamic effects to more firmly in the range were we’d seen pharmacodynamic effects.

So I am not going to re-summarize Dr. Teerlink’s presentation, which I thought was very clear and laid out what we have learned in ATOMIC. But I just wanted to put some of the findings it the context of what we pursued in terms of the therapeutic hypothesis in the path forward.

So from our point of view, this trial continues to be supportive of the initial therapeutic hypothesis. There were no adverse effects on heart rate or blood pressure and in fact heart rate declined relatively to placebo and blood pressure would increase relative to placebo in this sick population of patients.

There was no increase in the incidents of arrhythmias again in a population that’s prone to arrhythmias and there were dose and concentration related clinical effects both on dyspnea, on systolic ejection time and on the above heart rate and blood pressure.

ATOMIC was really designed from the get go as a dose range finding study to investigate pharmacokinetic, pharmacodynamic and key safety parameters in this high risk and symptomatic heart failure population. And I’d like to describe in some ways as a book end of one of the populations we may investigate in Phase 3 with chronic heart outpatients and with heart failure being the other book end.

Overall, the drug was well tolerated. One thing in John’s presentation, but not highlighted, was that over 95% of the patients completed the entire scheduled infusion and there was really no difference between omecamtiv mecarbil and placebo.

We now have over 300 patients worth of pharmacokinetics data in the target population and one of the target populations that will inform program going forward and the pharmacodynamics signature of the drug was replicated in these heart failure patients and in fact looked identical to the previous relationships we’d described.

So this large data set provides us some very important data in terms of moving the program forward. We now have explored over a range of doses that will help inform the dose selection, the design of dosing regimens in Phase 3, we have the associated placebo data in this population which well, in many of the studies have been done in acute heart failure population, a study in patients with systolic dysfunction alone has not been performed in a while with RELAX and the other studies been performed in patients with either preserved or reduced systolic function.

That gives us a good estimate of the placebo rates for the dyspnea response and a potential magnitude of omecamtiv mecarbil effect on the dyspnea response that at least in the study with that endpoint provides us information in terms of how to adequately power a Phase 3 study.

ATOMIC-AHF is part of a program of several studies that have been conducted and a study that’s ongoing has met the complement ATOMIC-AHF with an oral formulation of omecamtiv mecarbil which is COSMIC-HF. And the information from both of those studies is meant to inform the design of Phase 3, presuming of course that the data from COSMIC and ATOMIC-AHF support progression of Phase 3.

With COSMIC-AHF, as shown on the next slide is a study of oral formulations of omecamtiv mecarbil of which three are being tested, one will be selected after a two dose escalation cohorts and then studied in a dose expansion Phase for three months of total dosing. Pharmacokinetics and safety are key primary things that we plan to evaluate as well as echocardiographic measures of LV function.

And together this data will inform progress of this program, because as we saw in the previous slide, the intention is to develop either IV or oral formulations that are coupled together, patients may start on the IV, move to the orals, one of the ways the drug maybe developed in Phase 3 or in this patients maybe initiated on the oral and progressed on the oral.

Ultimately the goal is to be able to treat the continuum of patients with heart failures. Those hospitalized with heart failure that have increased risk of events, especially when they leave the hospital in particular as well as patients with heart failure that have high risk features such as recent hospitalization. Eventually the purpose, the goal of program is to develop an improvement and clinical outcomes such as mortality and morbidity.

And so with that I will turn it over to Andy Wolff who will lead a question-and-answer session. Thank you.

Question-and-Answer Session

Andrew A. Wolff

Thanks Fady. So questions are coming in. John, you’ve had a chance to conjugate on these data for a while now, when you put it all together do you think the study met it’s overall development objectives?

John R. Teerlink

Yes, I certainly did. As I think I mentioned during the presentation, the objectives of trial were to try to see how omecamtiv mecarbil performed in the setting of patients with acute heart failure and I think we certainly were able to get a good sense of signals for efficacy that were very encouraging from moving forward along those lines, overall signals for safety and directions of things that we need to look at more carefully as we go forward.

Andrew A. Wolff

Thanks. So clearly one of our concerns going into ATOMIC-AHF was the possibility of omecamtiv mecarbil, precipitating myocardial ischemia and higher plasma concentrations and that’s why we designed the state to include such intensive troponin sampling and probably have generated the largest database of troponin values in acute heart failure patients in existence now.

And so at the end of the day, we have got this very small imbalance in adjudicated MIs and we have very small, but potentially dose related increases and troponin changes and they had no relationship between the change in troponin and omecamtiv mecarbil placebo concentrate, how you put out altogether?

John R. Teerlink

Well, I think what we see is, for me the most convincing or important piece of data that we have is looking at the relationship between these changes from baseline in this troponins and the omecamtiv mecarbil plasma concentrations. I understand that our people are maybe looking at the myocardial infarctions as something to be more carefully scrutinized and we do have and will be able to eventually produce the information that I think will provide people more comfort over those myocardial infarctions.

Some of them were in patients who had PCIs that had stable troponins and then went for PCI and had I think troponin peak after their PCI, so we had to classify as myocardial infarctions, it was by a criteria myocardial infarction, but I think many people would not necessarily attribute it to omecamtiv mecarbil per say.

In addition, I’d remind people a bit; this program has an overall DMC, an overall Data Monitoring Committee that has been monitoring the global program, both the ATOMIC-AHF data and the COSMIC-HF data and have reviewed all these things and they’ve actually been able to read the narratives and interpret the myocardial infarctions and in no time gave us in any indication that they had any concerns over these data.

Andrew A. Wolff

Thanks. One of the viewers across the web asked if you can put the delta in the dyspnea response in the high dose cohort into clinical context, what will that mean to the patient or mean to the hospital?

John R. Teerlink

So it does to be an interesting split in terms of how people view dyspnea on scores. Some people will say that many patients just improve with no matter what. And if you look at our data, if you look at the placebo group depending on certainly the path match placebo group in the cohort, only 37% of the patients met our criterion for dyspnea relief. So that means that 63% of the patients are not getting that symptom relief.

So if I had a choice between reducing mortality or reducing dyspnea, clearly I’d go for reducing mortality. But that’s not to say that reducing dyspnea is not still a very important goal. So what we see in the high dose cohort and this is based upon small numbers and a trial that wasn’t designed to primarily evaluate the effect on dyspnea, what we see in this case is a 41% treatment effect.

Now 41% treatment effect clinically and generally we think of treatment effects above 15% is being useful and important and so this clearly meets that mark, even if you factor in the exaggerated treatment effect that you can see in Phase 2 studies. So I think it’s very important and it needs to be addressed.

Andrew A. Wolff

I will direct the question to you.

John J. V. McMurray

Well, I’d like to follow-up, because I did say that I found dyspnea wasn’t as importance and I don’t, I mean I think mortality and readmission are much harder endpoints and I think John said the same thing, I don’t think we really disagree. If you can improve dyspnea, of course that’s useful, if you can get the patients ampule history and out of hospital more quickly, that’s clearly important and obviously one of the things that stopped the patient being ready to discharge and still being symptomatic.

So don’t want to trivialize it but there are much I think greater goals for a treatment in acute heart failure, dyspnea relief is great what you could do more.

John R. Teerlink

Well, I think particularly with this class of agents, what we know so far is the currently available agents that improve cardiac function if anything worsen outcomes that will obviously improve.

Andrew A. Wolff

What do you think the data on the dyspnea portend or do you think make any predictions for how these studies that had eventually we are going to be looking at a composite endpoint of probably deaths and re-hospitalization for heart failure, do you think that you can take anything away from ATOMIC that will predict how the drug will perform overtime on those endpoints?

John J. V. McMurray

Okay. Well, I will go first and then John can give his perspective. I wouldn’t make too much into dyspnea from that point of view. I am much more impressed by the way the drug works and the one consistent finding that we’ve had throughout the whole program which is that you improve systolic ejection, you improve the ability of the heart to squeeze blood into the arterial tree, because that’s the fundamental problem and that’s what you’re correctly distressing them, much more impressed by that and impressed by the reduction in heart rates and then impressed by the overall tolerability. And for a Phase 2 study, I am not sure of what more you can guess.

John R. Teerlink

So I would agree with what the other John said. I think the ability of dyspnea to predict long-term outcomes. We’ve looked at a number of acute heart failure trials and that has not necessarily consistently held up. What has held up pretty consistently is actually reduction in worsening heart failure that’s in hospital. And so once again with the caveats that this was a secondary endpoint in a Phase 2 dose finding study, I was actually more encouraged to see the improvement in the worsening heart failure.

Based upon small numbers, but we still had 51 events within the pooled placebo of worsening heart failure events or 17% event rate compared to 9% event rate in the Cohort 3 which is a 45% reduction in that incidence of that event and in many of the contemporary trials, actually the worsening heart failure in hospital is the most important predictor of bad outcome later on including re-hospitalization and mortality. So that as a signal is one of my more encouraging findings from the study.

John J. V. McMurray

I think all (inaudible) industry had the data reveal to this. It really was something that if I not yet to exercise upon because it’s potentially very important.

Andrew A. Wolff

So a couple of people have written in asking about dose, one question says, do you think you have right dose or do you think you can go higher, another phrase is that what you believe is the optimal IV dose based on the data as presented?

Robert I. Blum

So I think we still are actually analyzing these data and I think lot of things that I wanted to make clear now is one of the reasons we don’t have a simultaneous publication is not for interest, or with great interest from journals to publish it simultaneously. We just were not able to get all the data and analysis done in time to make that kind of publication. So we are still looking at all that data and that’s not meant to be a cop out. I personally believe that somewhere within the Cohort 2, Cohort 3 range is going to be a dose that we’ll be able to take forward in the Phase 3 in acute heart failure patients.

John J. V. McMurray

Let’s hope everything stay well.

Andrew A. Wolff

John what do you think?

John R. Teerlink

I agree let’s say, I was hoping that you were going to say well.

Andrew A. Wolff

So may be I will put this to Fady and possibly even Robert, there was some questions related to the program, based on these data, how we and the Amgen decided whether or when to move to Phase 3 or the COSMIC results absolutely necessary. And related to that, do we believe COSMIC is powered adequately which shows typically significant outcomes or as in the case here should we be more focused on trends and dose response relationships?

Robert I. Blum

So I’ll speak to the first part of that question, maybe ask Fady to speak about the COSMIC design. To be clear, we have not made nor has the Amgen made a decision regarding proceeding to Phase 3, that’s why we do Phase 2 studies. Speaking on behalf of Cytokinetics, the ATOMIC data we believe supports continued progression and development and I think Amgen should be asked the same question as that opportunity presents. I do believe that these data support the therapeutic hypothesis. The ATOMIC results should be viewed together with the COSMIC results in terms of how best to design a proper Phase 3 program and that’s something to which we look forward to reasonably soon.

Andrew A. Wolff

Thank you.

Ritu Baral – Canaccord Genuity, Inc.

Thanks. Ritu Baral, Canaccord Genuity. To the experts up there, can you talk a little more about the imbalance of MIs, anymore detail on when they occurred, especially proximity of the treatment and how that can be significant?

John J. V. McMurray

I am sure that the MIs were, as I try to allude to earlier that many of them were not actually during the infusion of the drug. So well actually I should say many, because there weren’t that many of them. Some of them were not during infusion of the drug and we are quite a bit delayed, one of which was I think 22 days after the drug, yet we still had accounted as an omecamtiv mecarbil related myocardial infarction. So there was not a consistent pattern whatsoever in terms of the occurrence of these relatively rare events with regard temporarily or in regards to the plasma concentrations. So we were unable to find any relationship that would explain the kind of events.

Ritu Baral – Canaccord Genuity, Inc.

Just as a follow up, given what you guys know about those mechanism, what sort of window post treatment would you still sort of look at as far as troponin’s and potential MIs?

John R. Teerlink

Well, so I mean you want to simply think of it in terms of drug exposure, the drug’s has got a half life of about 20 hours and so after three or four days of drug levels have fallen 90% and more.

John J. V. McMurray

Let me comment, I mean I clearly understand that you must look at these things first, I have a vivid example of my own experience of drug development in heart failure or reading too much into small numbers of events can be tremendously misleading and that example was with candesartan in the CHARM program and there was a Phase 2 proof of concept study carried out called RESULT. And in that study there were a few more deaths in the candesartan plus enalapril group than in the enalapril and (inaudible) groups that big delay was bound into a program by the hearers, sponsors, scratch their heads about what to do and then of course we went on to the three large Phase 2 trials, two in these types of low ejection traction patients, which collectively showed a clear reduction in morbidity and mortality. So, small numbers of events at this stage are very, very hard to interpret either good events or bad events.

Andrew A. Wolff

Fady, I think there was a part of the question about the program that we didn’t get through as how we should view data coming out of COSMIC later on, is it powered or is it again something where we are looking for trends, dose response relationships so forth.

Fady I. Malik

Also both Dr. Teerlink and Dr. McMurray are on the executive committee of COSMIC and they can give their perspective on that as well. They were involved in protocol design and they are involved in its [Technical Difficulty]. But the objective as I stated in the slide is the primary objective of the study is to really characterize pharmacokinetics of the drug and outpatient population. So everything that we have come to understand about this drug is related to exposure, as well as the concentration of the drug upstream. So understanding the pharmacokinetics of the drug across a broad range of patients, pretty ranging patients if you will that are at home are important to selecting a dose for Phase study, it is only three months total rate, that’s not adequate to assess the quality and arguing and executing changes in structures that might occur. And of course we will look at overall (inaudible).

John R. Teerlink

Yeah, I think what we just actually bring that point even more directly home were for the primary endpoints of the trial, their all pharmacokinetics endpoints in terms of protocols just by primary endpoints and we do have secondary endpoints, they are looking, once again systolic ejection time because it’s how the question of can we see the biological hallmark of this mechanism action in oral formulation secondary endpoint. We certainly will look at an event basis, but I would reinforce, reiterate and stress how that’s redundant, John’s comments about the danger of whole numbers both good and bad.

Andrew A. Wolff

We have another question from the audience.

Unidentified Analyst

Sorry to comeback with the issue the MIs, but is there any other details in the baseline characteristic of the patients or the characteristics of the MIs themselves that you give any comfort that they are drug related?

John R. Teerlink

So, once again they are only it’s how do you make you are looking for patterns among a number of events that are even hard to make a real line. So it’s difficult to do that. So in my review of the narratives, in my review of the comorbidities and things I have not seen this at all. To reiterate it, it’s hard to make a casual relationship when with almost 5000 troponin’s measured. You don’t see relationship between the troponin’s and the plasma concentrations. If this were really a direct casual mechanism, you’d expect to see a very consistent higher doses causing higher release of troponin.

In fact and I want to reiterate that the p value from these were 0.95 and 0.83 in terms of their relationship between omecamtiv mecarbil concentrations and the change in troponin’s, if anything those non-significant regression lines go negative. So I am not saying that actually do go negative, but because that the captopril can’t exclude it being flat, but they really is not as significant that kind of relationship and then we reviewed the narratives I can.

John J. V. McMurray

I think the most important point to make here that you have made that I’ll reiterate is that the more statistically significantly robust analysis by (Audio Gap) is the relationship between two continuous variables in plasma drug concentrate, that’s much, much, much more portfolio analysis (Audio Gap) any of these things was everybody here knows a large outcome trial. (Audio Gap) absolutely and I think one of the things that people, yes, one of the things the people need to be careful about is translating the current guidelines for use of agents that improved cardiac performance to what they project to see what would happen with (Audio Gap).

Most of the reserving these agents for the variable blood pressures is because of the huge adverse event profile, we’re reluctant to use it anywhere else (Audio Gap) when I give lectures on this, other people will ask people, who here knows that (Audio Gap) can cause death and everybody raised their hands. And I say, okay, how many of you here use those agents, and everybody kind of sheepishly then raise their hand too. As a last resort, if omecamtiv mecarbil fulfills its promise, it will not only be able to be used in all situations where those agents were used, but also could it be viewed as being able to be used in anybody who has reduced systolic regardless of their blood pressure.

No, granted, I am not sure you would want to be giving this kind of agents with blood pressure 180, we wouldn’t do that. But in some one who has a blood pressure of 130 with a bad EF who comes in with bad symptoms, I’d certainly consider that.

John R. Teerlink

I have nothing to add, really now trying to make a point in my presentation as I see this drug being and that can be used in other agents being investigators.

Robert I. Blum

And I would correct the one other thing came up during the discussion in terms of saying that we have limited enrolment to patients with EGFRs about 50 and that was actually, the EGFR of 50 was actually the mean value of each EGFRs in the trial. We led in patients who had much lower EGFRs.

Andrew A. Wolff

We have another question from the audience.

Unidentified Analyst

Is there anything you saw today that will lead to changed design of COSMIC-HF in terms of troponin’s?

John J. V. McMurray

No, mainly because we thought long and hard about the COSMIC – I mean, COSMIC, again to go back to (inaudible) another COSMIC heart failure is to demonstrate that the norm formulation has the signature effect of this trend to improve cardiac contractility.

Unidentified Analyst

Focused more on safety in terms of it?

John J. V. McMurray

Yeah, I understand, I believe that that is built into the design I believe that we will plasma concentrations was within the safe, completely safe range and of course we will find out. We will obviously measure troponin and we will obviously record clinical events, but there is nothing that obviously would change what we are doing and don’t forget, we have the same DSMB who are seeing that trial at ATOMIC heart failure and I think they would also be correct to tell us if they feels otherwise that obviously reduce the protocol and give them their approval.

Unidentified Analyst

Is this the first trial that’s measured troponin aggressively?

John R. Teerlink

Yes.

John J. V. McMurray

Yeah.

Unidentified Analyst

Like RELAX, any data for troponin, RELAX and (inaudible)?

John J. V. McMurray

It’s like what happens we have to do this in a trial with (inaudible) required to measure in case of every visits and this is what happens, not surprisingly overtook some patent issue with measuring liver enzymes if you have to do this, then you find things that nobody ever knew before. So we have by far the largest experienced proponent, zero proponent measurements in acute heart failure.

Andrew Wolff

Okay, thank you. We will take one more question from the Internet. Why do think the improvement in worsening heart failure didn’t translate into an improvement in this day’s lived out of hospital at 30 days?

John R. Teerlink

Well, okay, so I apologize, because it’s going to sound like a broken record, because the days lived out of hospital has very wide range in patients and in order to show differences in that, you really need a large number of patients. So that was why – I don’t think we were at all power to investigate that question.

Andrew A. Wolff

Thanks.

Robert I. Blum

So with that I think we will conclude the Q&A and I thank those participants here in Amsterdam and also those who e-mailed us questions for asking those questions and thanks to our panelists for addressing them.

I will make a few concluding remarks. As CEO of Cytokinetics, it’s especially gratifying to have an opportunity to have the results of a program like this presented, especially Phase 2 results as late break of clinical trial here at such an important cardiology conference. The European Society of Cardiology is proving to be the largest gathering of cardiologists worldwide and this conference is no exception to that. These data we presented today to a very full room, a very large room and I think as you heard here in this investor event they have also been warmly received by the cardiology community.

Clearly, this is a Phase 2 study, the study was designed to ask certain questions, we’ve answered them. In terms of this acutely ill heart failure patient population, a high risk, high vulnerability group to be sure, where we’ve learned a lot about safety and tolerability, pharmacokinetics and pharmacodynamics of omecamtiv mecarbil that informed the continued development of omecamtiv mecarbil.

The next step will be to look at the COSMIC data. We look forward to that data. We expect some time in the first half of 2014 to inform the potential progression to Phase 3, but the results of ATOMIC-AHF, I believe do support continued development. We are working together with our partners at Amgen where we have recently announced the expansion of our license to Amgen to include Japan, so we now have the potential for a global registration program that may allow for both the intravenous and oral forms of omecamtiv mecarbil to progress in further development. We look forward to that possibility. We will continue to engage our partner in those conversations about these data and also data still to be expected.

We are very pleased with the results of ATOMIC-AHF. We invite everyone on this call and others who may listen to its replay to ask us more about these data and we will certainly do our best to ensure you get your questions answered.

With that, I’d like to thank my fellow panelists who participated in this program. Especially I’d like to thank John Teerlink and John McMurray for their steadfast dedication to the clinical investigation of omecamtiv mecarbil and also we look forward to working with you collaboratively as this program continues to progress.

With that, we will close this investor event and thank everybody for their participation.

Copyright policy: All transcripts on this site are the copyright of Seeking Alpha. However, we view them as an important resource for bloggers and journalists, and are excited to contribute to the democratization of financial information on the Internet. (Until now investors have had to pay thousands of dollars in subscription fees for transcripts.) So our reproduction policy is as follows: You may quote up to 400 words of any transcript on the condition that you attribute the transcript to Seeking Alpha and either link to the original transcript or to www.SeekingAlpha.com. All other use is prohibited.

THE INFORMATION CONTAINED HERE IS A TEXTUAL REPRESENTATION OF THE APPLICABLE COMPANY'S CONFERENCE CALL, CONFERENCE PRESENTATION OR OTHER AUDIO PRESENTATION, AND WHILE EFFORTS ARE MADE TO PROVIDE AN ACCURATE TRANSCRIPTION, THERE MAY BE MATERIAL ERRORS, OMISSIONS, OR INACCURACIES IN THE REPORTING OF THE SUBSTANCE OF THE AUDIO PRESENTATIONS. IN NO WAY DOES SEEKING ALPHA ASSUME ANY RESPONSIBILITY FOR ANY INVESTMENT OR OTHER DECISIONS MADE BASED UPON THE INFORMATION PROVIDED ON THIS WEB SITE OR IN ANY TRANSCRIPT. USERS ARE ADVISED TO REVIEW THE APPLICABLE COMPANY'S AUDIO PRESENTATION ITSELF AND THE APPLICABLE COMPANY'S SEC FILINGS BEFORE MAKING ANY INVESTMENT OR OTHER DECISIONS.

If you have any additional questions about our online transcripts, please contact us at: transcripts@seekingalpha.com. Thank you!

Source: Cytokinetics' CEO Hosts Investor Event on ATOMIC-AHF Data at the ESC Conference (Transcript)
This Transcript
All Transcripts