Good afternoon and welcome ladies and gentlemen to the Cytokinetics, second quarter 2010 conference call. At this time I would like to inform you that this call is being recorded and that all participants are in a listen-only mode. At the request of the company we will open up the call for questions-and-answers after the presentation, I will now turn the call over to Sharon Barbari, Cytokinetics' Executive Vice President of Finance and CFO. Please go ahead

Good afternoon and thank you for joining the Cytokinetics' senior management team on this conference call today. Also present during this call are Robert Blum, our President and Chief Executive Officer and Dr. Andrew Wolff, Senior Vice President of Clinical Research and Development and Chief Medical Officer. Following the forward-looking statement disclaimer, Robert will provide an overview of the past quarter along with an update on the advancement of our development pipeline focused on the biology of muscle function. Andy will then provide highlights and details on the progress of the company's clinical development program. I will then provide some brief comments with respect to our financials and our investment in research and development activity and Robert will then conclude the call with additional comments regarding our recent activities and discuss the projected company milestones for the remainder of 2010. We'll then open the call for a brief question-and-answer session. The following discussion, including our responses to questions contain statements that constitute forward-looking statements for purposes of the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995 including but not limited to statements relating to our financial guidance, to the initiation, enrolment, design, conduct and result of clinical trial and to other research and development activity. Our actual results might differ materially those projected in these forward-looking statements. Additional information concerning factors that could cause our actual results to differ materially from those in these forward-looking statements is contained in our SEC filings, including our most current quarterly report on Form 10-Q and our current reports on Form 8-K. Copies of these documents may be obtained from the SEC or by visiting the Investor Relations section of our website. These forward-looking statements speak only as of today. You should not rely on them as representing our views in the future and we undertake no obligation to update these statements after this call. Now, I'll turn the call over to Robert.

Thank you, Sharon. During the second quarter Cytokinetics took additional steps to execute on the company's business plan directed to the biology of muscle function. In the second quarter, we initiated dosing in two Phase IIa evidence of effect trials of the lead drug candidate from our skeletal muscle activator program, CK-2017357 or CK-357. One in patients with amyotrophic lateral sclerosis or ALS and the other in patients with symptoms of claudication. With these trial initiations, we are demonstrating clear progress towards our goal of advancing a broad and sustainable pipeline of novel mechanism drug candidates. We are especially pleased with the continuation of the Phase IIa trial of CK-357 in patients with ALS. In recent days, we conducted an interim review of the data with results supporting the continuation of this trial under the current protocol. As Andy will elaborate, we are pleased with what we have seen to-date in terms of the apparent safety and tolerability of CK-357 in these patients as well as the dose proportional and predictable pharmacokinetic profile of this drug candidate in the patient studied. We look forward to additional data from this trial by the end of the year. As Andy and I will both discuss later in the call, Amgen and Cytokinetics continue to work closely together in the development of only omecamtiv mecarbil as a potential treatment for heart failure. We expect to be initiating in the coming months under Amgen's sponsorship a pharmacokinetic trial of two distinct oral formulations of omecamtiv mecarbil in a stable heart failure patients as well as an additional study of an oral form of our drug candidate in renally comprised patients. Moreover, we are together putting the finishing touches on the protocol for our phase IIB trial intended to evaluate the intravenous form of only omecamtiv mecarbil in more acutely ill heart failure patients. Overall, in the second quarter Cytokinetics continued to execute well against clinical development timelines with the goal of progressing our therapeutic pipeline and importantly doing so in a physically responsible way. I now would like to turn the call over to Andy to elaborate on the specific clinical progress achieved during the last quarter in our respective drug development programs and to provide some insights into our plans for the future.

Thank you, Robert. The second quarter was a busy one as our activities starting on advancing our redrug candidate from our skeletal muscle activator program CK-357 into phase IIa evidenced of effect trial designed and conducted by Cytokinetics. In the last quarter, we initiated dosing in our phase IIa evidence of the effect clinical trial of CK-357 and patients with ALS. You may recall that this trial is a double blind randomized placebo controlled treat carrying crossover, pharmacokinetic and pharmacodynamic trail of CK-357 in at least 36 and of the 72 male and female patients with ALS. To remind you, the primary objective of this hypothesis generating trial is to evaluate the pharmacodynamic effects of CK-357 on measures of skeletal muscle function or the applicability in impatients with ALS at single doses of 250 and 500 milligrams. The secondary objectives of the trial are to evaluate the relationship if any, between the plasma concentration of CK-357 and its pharmacodynamic effects to evaluate the safety and tolerability of the two single doses of CK-357 administered orally to patient with ALS and too evaluate the effects of this drug candidate on patient and investigated in terms of global functional assessments. Study assessments include various measures of muscle strength or fatigue, employing both maximum and sub-maximum voluntary contractions as well as measures of pulmonary function. These measurements are taken at base line and there are three checks and 24 hours post dosing after each of two single doses of CK-357 and placebo. A washout period of six to 10 days between doses exists. In this early Phase II, hypothesis generating trail, these multiple pharmacodynamic assessments are made without specifying a single primary endpoint. As Robert mentioned, in July we conducted an interim review of the data from this ongoing trial. I am please…

Thank you, Andy. As our press release contains details of our financial results for the second quarter ended June 30, 2010, let me refer you to that public statement. We ended the second quarter with $87.6 million in cash, cash equivalent and investments excluding restricted cash which represents over 18 months of going forward growth cash burn based on our 2010 financial guidance. Our guidance for the full year 2010 is anticipated to be a growth cash burn between $52 to $58 million and does not include any revenue from our partner Amgen or other revenue sources such as grant funding our potential strategic partnership. Our second quarter 2010 R&D expenses totaled $10.2 million. From a program perspective from the second quarter approximately 79% of our R&D expenses were attributable to our skeletal muscle contractility research and development activity. 7% to our cardiac muscle contractility activity and 12% to our other research and non-clinical development activity including our smooth muscle contractility program and 2% to the wind down activities related to our mitotic kinesin inhibitor development and research activity. For the six months ended June 30th 2010, our R&D expenses totaled $19.3 million from a program perspective for the six months approximately 76% of our R&D expenses were attributable to our skeletal muscle contractility activity, 6% to our cardiac muscle contractility activity and 14% to our other research in non clinical development activities which include our smooth muscle contractility program and 4% to our mitotic kinesin inhibitor development and research activity. As you can see, we continue to focus on financial resources largely on our skeletal research and development program which we believe may provide the nearest term value generation for the company. In addition, in July as a part of a settlement agreement with UBS AG related to the failed auction rate securities, followed by Cytokinetics, the remaining auction rate securities of $7.5 million were purchased at par by UBS AG. That concludes the financial portion of today's call. With that, I will now turn call back over to Robert.

Thank you Sharon. As you have heard in the second quarter, Cytokinetics continue to execute on key milestones associated with each of our programs in development. Beginning with our skeletal program and our Phase IIa trial of CK-357 in patients with ALS, our most recently activities have focused to the conduct of an interim review of the data from this ongoing trial. This interim look allowed us to determine whether we needed to modify the conduct of this study in anyway. The interim review of the tolerability of CK-357 in this intended patient population is encouraging and as Andy indicated, no serious adverse events were reported. Those events that were reported were largely categorized as mild and were not unexpected. In addition to this review, our clinical, regulatory and legal teams have worked very hard to gain site approvals and initiate the remainder of the clinical sites to be involved in this trial while also supporting those that were already up and running. We continue to be impressed with the pace of enrollment of this ongoing Phase IIa trial as well as the enthusiasm from participating investigators who are also working diligently in the field carry results that may inform the promise of this novel approach to treating this uniformly fatal disease. As mentioned previously, we believe that CK-357 demonstrates promise in ALS patients then it also may have the potential to demonstrate activity in terms of improved functional status in patients with other neuromuscular dysfunction. The initiation of our second Phase IIa evidence of effect trial in patients with symptoms of claudication associated with peripheral artery disease demonstrated Cytokinetics commitment to also exploring CK-357 in non neuromuscular indications. We are pleased with this trial's pace of enrollment as well. While it is too early to point to where we…

(Operator Instructions). Your first question comes from the line of Charles Duncan with JMP Securities.

I had a question on 357 with regard to ALS. It's nice to see that the drug candidate appears to be safe at least in so far in your trial. Can that give you any senses as to I'll call it mechanistic proof that you've got a dose that might be working. Is it good to not have any events there? Can you provide more color on that observation?

I did mentioned that the most clearly dose related adverse event was dizziness which we also saw in a dose related fashion in one of our Phase, once that it's actually we saw dizziness through out our healthy volunteers study it was generally mild, but it was there and the study where we have the most doses in a crossover design and could most clearly evaluate the dose response. The incidents of that particular report did increase with increasing dose and we see that again share with ALS. So I think we are in an active range based on that.

And with regard to compelling evidence of efficacy in the ALS study, we've talked about that before but are you really looking for muscle strength parameters to improve and what's your view on the predictive value of those kind of measures or is it more biomarker look that you would like to see?

Well we are looking at variety of different assessments in the ALS study in particular and certainly measures strength in various muscle groups including large limb muscle groups and grip strength both at maximum voluntary contraction and at sub maximum targets are part of the evaluation. So also we mentioned, but very briefly in the call is the patient global assessment, just to get better or worse or unchanged the same. This addition throughout the same thing, the patient that are worse or unchanged and before (inaudible) and you maybe familiar that there is a patient reported outcome tool called the ALS functional rating score which has been revised and goes by the unwieldy abbreviation of ALS, FRSR but that's been the primary endpoint in several large trial. However it asks the patient to report their symptoms in comparison with how they felt before they had ALS symptom. So that wouldn't be in-depth form appropriate for a single dose trial like ours, but we work with our thought leader investigators to modify that assessment because certain domains could potentially respond to 357 in the shorter term. For example, assessments of the patient, intelligibility of speech, their difficulty swallowing, the clarity of their handwriting, that kind of thing. And so those domains have been taken from the ALS FRSR, a long-term patient reported outcome tool and put into what we now call the ALS functional assessment which allows the physician to make objective assessment supplemented by the patient reports. So all those things are part of what we're looking at in this trial.

One last question regarding December presentation of data at the symposium on ALS. Have you submitted an abstract and is that going be presentation of the data that you have in hand now or do you think that you will have data from kind of the second phase of this study available in December.

We only provide such more concrete information if we know that we have had an abstract accepted for presentation which is the case in terms of that particular meeting. So yes, we did submit and it has been accepted, and we expect by that point in time we will have much more data to share beyond the interim review that we've already conducted.

And then last question is in terms of next steps, once you see that data, do you think that you will be able to put together a protocol that is more definitive kind of study, call it dose and pharmacological parameters that can give you more clinical outcomes?

Yes, it's a bit premature to speculate and obviously that also has to be done in concert with what we would hope then would be discussions with regulatory authorities, but the idea here for this study as it is hypothesis generating to then feed into a hypothesis testing study that would potentially correlate these pharmacodynamic end points with measures of clinical benefit.

Your next question comes from the line of Joel Sendek with Lazard Capital

Let me see, I guess the follow-up to the last question I am just wondering if you can tell us how many patients you've seen so far and if things go well, how many patients might we see at the conference and in December and will you be able to comment on evidence of efficacy by any of those measures that you mentioned before that conference?

So at this time we are not in a position to comment on the number of patients that contributed to this interim review, but yes what we can say is that by the time December goes around, based on these enrollment rates, we expect we are going to be in a good position to report on evidence of effect arising from the data. So it won't just be a safety review. We do not expect it will limited to that but rather instead also that will be in a position to report on some of these effects across these multiple pharmacodynamic assessments.

Okay and when and if we see the abstract, that wont include the pulmonary efficacy, presumably that would be in the poster at the meeting itself?

Correct that doesn't mean we wouldn't choose to when we have such information as would be deemed material issue of press release to proceed the meeting. I can't say we would or would not until we might end posses the data, but it would not likely therefore be in a published abstract.

And then on omecamtiv, just a couple of questions there. Looks like things are proceeding pretty much on track as far as timeline. I guess two questions for you there. Is there anyway to work with your partner to maybe accelerate this, I am wondering how the partnership is working in your view and you know how much to say, you have, because obviously we all like to see an acceleration along those lines and the second part of that question is the time frame for milestone payments, when's the next one you will receive? Can you give us some guidance on that as far as timing?

So I'll take this question in order. With respect to our contribution Cytokinetics is involved extensively in non-clinical and clinical development activities together with Amgen for this program and we have been, if not on the telephone then in person nearly everyday if not several times a day working through a number of matter and I think things are going well. We have not initiated these studies so you could interpret that to mean things could go more quickly, but I do also believe that if you look at the scope of work that's going to be done, you will be impressed with the quality of the effort and as these studies do get underway, I think you will be similarly impressed by and very encouraged by the extent to which Andy and others in his team are engaging together with Amgen and Amgen is taking not only their comments, but engaging Cytokinetics in substantive ways that relate to strategy as well as tactics for the conduct of these studies. So it's all good and I think you will see evidence of that in this second half of 2010. You asked the second question and now I am forgetting what it is.

Yes, when the next milestone payments might be from Amgen?

That's right, the milestone payments, so I apologize, I cannot say that we're bound to confidentiality on what would be events that would trigger milestones payments.

Your next question comes from the line of Mark Monane with Needham & Company Mark Monane - Needham & Company: The summer is flying by and that makes me think about the time that (inaudible) we saw the Phase II omecamtiv data which got everybody excited. And I was wondering if you and Andy could please comment on the progress in seeking about CHF and other companies, any strategies have come by that you think are disruptive or potentially additive to strategy that you and Amgen are pursuing?

I will make a brief mention and turn it over to Andy. I am not aware for other competitive or related programs in the development of heart failure that there is anything that's informing any shifts in our strategy, a strategy that we're executing on and that's been in place for sometime that proceeded Amgen entering into collaboration with us. That's both a good and the bad of it. Good from the standpoint of we have a consistent strategy that I think still serves us very well as we proceed forward now together with Amgen. That in the sense that it underscores what I think is a quite significant unmet need in heart failure that I don't think is being largely addressed by other programs that suggest this is problematic for heart failure patients, but I hope that the work we're going to be doing both with the intravenous and the oral form of omecamtiv mecarbil will address that need.

Well, I would agree, I think there are no other companies that are doing what we're doing in particular by targeting the (inaudible) directly. And most of the other new therapies in development of which I am aware are looking at other parts of the equation that are (inaudible) for protective agents, basically may be modest improvements over pharmacology that already exists. Mark Monane - Needham & Company: And in terms of think about the combination strategies with the current medications that are out there. Are there particular set of agents either Ace inhibitors or ARB or the (inaudible), (inaudible) and you think might be even more beneficial then other in thinking about the appropriate management of the patient.

Well I think ace inhibitors and beta blockers to be sure have been demonstrated to increase survival and decrease hospitalization and other three more of end points that they are part of (inaudible) and so I will need to study the drive over a background of those therapies has been to-date and almost all patients are on diuretics and that will continue and that will be received in combination with our compounders as we go forward in clinical trials. The (inaudible) is not as commonly used as it used to be, it's the driver among the ones that you mentioned that actually at least intended to do something similar increases all its function, although we all know it doesn't, do it particularly well and again as I say its been demonstrated potentially to reduce hospitalization but not in that mortality and we're not seeing a lot of patients particular in the United states. Mark Monane - Needham & Company: That's helpful and then on the ALS trial in the evidence of that graduations into the next step. What kind of difference on the scale might be clinically relevant, I mean none of the (inaudible) patients are in long-term care and therefore they are assisted and some are still in the community setting and you can benefit from strategy in incubations to allow and stay in the community center. What kind of change on a scale or on a functional assessment or even maybe a prevention of institutionalization might be clinically relevant when you talk to investigators.

Well generally they'll say that, the ALS functional rating scale, the patient reported outcome tool that I mentioned earlier and not the modification of it that we're using in our study will decline in patients receiving standard of care at about one point per month. And so any meaningful or statistical or just tactical determinant in that slow will really would be making the slope more shallow or making that rate of decline significantly less is due to its meaningful or sometimes if the study is run for lets say for example three months, you would expect a three point decline from zero to three months in the untreated group and so the active group showing that the decline is only 1.5 or 2 points on average would be viewed as highly meaningful.

Your next question comes from the line of Ritu Baral of Canaccord.

I'll start with 357, so your decision not to add an additional dose at this point of the trial, was that driven more by the safety data that you have seen or have you taken a look at the blinded efficacy data?

So I'll start again turn it to Andy. I think as we've commented publicly in the past, in as much as we are going into ALS patients for the first time with this novel mechanism drug candidate we couldn't know whether the doses we were selecting were necessarily the right ones to conduct this clinical research and I think we've concluded that they can be that this is the right range for us to be operating in terms of answering some of the questions that we're trying to answer and that was predominantly informed by the safety review. So it was another interim review intended to look at other matters but rather one we're focused to these aspects of safety.

So I think in looking at the data that we have in front of us, the most I can really say at this point is there was no compelling evidence that suggests that we should either increase the existing doses or need to decrease them from where they are.

Do you still have the option at this point at add a higher dose later or a lower dose later if needed or is that…

I mean we can amend any protocols taking the proper steps with regulators and ethics committees to do so. So that option continues to be there for us if we felt we need to it.

Okay, and have you seen any falls related to the dizziness that you have seen?

No.

And the euphoria side effect, has there been any progress on that mechanism, any theories as to why there is less of that in ALS patients and a healthy volunteers you used in the Phase I?

You know to comment on why the incident is different would be so purely speculative that I'll refrain from doing it. We do see meaningfully less than we saw in the healthy volunteers. I'll say that in general and this is across my experience of over 20 years of during drug development and its (inaudible) the literature and conversations like that with others but similar experience to mine. In general, healthy volunteer report more AEs than patients, they just do. And I think the one reason they are used to feeling healthy. So they come into a clinical trial and any little thing that will strikes and the difference becomes an adverse event to them. Patients with chronic illness are used to be chronically ill and I think they tend to report fewer complaints in general. That's just in general with respect to anything.

Great and then could we get any additional specific time lines for your follow-on skeletal muscle content, your back up?

That's a very good question, I don't know that we can give you anything more specific other than what we're doing here in Phase 2a may form the need or not the need to advance one of the backup or follow on compounds as well as the potential partnering of this program may inform decisions around that. So its both a risk mitigation strategy as well as one that may allow us to broaden the scope and reach of the program into other indications. We can only afford to do ourselves so much right now and with that in mind we haven't made the decision to advance into the clinic as much as we maintain that readiness position.

Okay and can I ask about the ongoing partnership interest and talks?

Certainly you can ask, I am mot sure (inaudible). What I will tell you is, it continues and it continues well and we are advancing discussions and its not with a single party but with multiple parties, its not something that I could comment on in terms of when a partnership or partnerships may occur, but we continue to be pleased with their interest that we're seeing. Obviously more data is better but as we engage in further research and non-clinical and clinical development, we share what we can.

And then moving on to omecamtiv. So the Phase IIb that you described today, that was with the IV formulation. Is there any update on next steps after the IIa so basically any update on an oral Phase IIb trial. Do you need the full readout from the soon to be started IIa before starting that trial?

We do not need the readout from the Phase IIb with the IV product to begin Phase IIb with the oral product, but we are looking to data from the pharmacokinetics studies to inform which form of oral to advance into phase IIb so the studies that I mentioned one in renally compromised patients and one comparing two of the oral forms, those studies do inform and are gating to the entry into Phase IIb for the oral program.

Got it. And so those PK PD studies, what's the estimated sort of size and duration of those or are those things that are study that will readout by mid 2011?

I would first of all say its really just a PK study.

Okay.

And they are in the range of numbers that you would accept for pharmacokinetic studies, usually couple those in patients so case studies. The Phase IIa was oral. You could expect maybe larger depending upon, how many different dozes and formulations eventually are under study.

Yes, so we can't really say much more than that although we do intent once dosing has been initiated and the protocol is firm and will likely also be communicated publicly through www.clinicaltrails.gov, we'll be in a better position to elaborate.

Your next question comes from line of Jeremiah Shepard with Wedbush.

In recourse the LSA Phase IIa study, you mentioned previously that it's scheduled to enroll 36 patients to positively at 72 patients. Was there any gaining factor for stopping at 36 patients?

Was there any gaining factor, I don't know that I…

36 is the minimum. There is much flexibility with respect to enrolment and statistical analysis and the study is meant to really CAP to broaden that so look for any evidence as a pharmacodynamic effect that we can find. Obviously half the tail regulators and members of ethics committees, communications to intend to and they would see it at risk in the study and so based on some preliminary calculations of variability of the assessments that we're performing, we imagined that it would probably take at least 36 patients to generate statistically significant changes versus placebo in these assessments and possibly more. And that's why we wrote the protocol to allow us to enroll from 36 to 72 to be informed by interim looks at the data when there are sufficient data to be able to make assessments of pharmacodynamics.

So you've mentioned that you've done this interim analysis just a few days ago or early part July. Is there anymore plans to do an interim analysis or the next analysis be the final analysis?

Well first of all I think we are careful to refer to it as a review and not an analysis.

Okay.

And as I did just say, we do have a lot of flexibility to undertake additional reviews and analysis of the data which are doing things like adjusting ultra air spend and so forth the one we do for our perspective redesign vigorously controlled Phase III study. So I won't say that we will or we won't provide additional interim data but that the option is there.

Okay and in regards to the patterning discussions, right now there's this two on going Phase IIas and I know the planned (inaudible) Phase IIa in the near term. Is there any certain amount of data that you're hoping to have in hand before progressing with partnering discussions.

It's a good question I know that you'd want as I in your positions to handicap sort of the timing of when such an announcement could occur for partnering. The way we're approaching partnering is not at all predicated on availability of fi0nal data from these phase 2a studies. This is a program for which there has been years of investment and research as well as non-clinical and mal-clinical development and it's the totality of the information that will drive the partnering discussions. I imagine there are some potential partners who would prefer to wait for that data, there are certainly others for whom I do not expect that to be the case and will see where the dynamic of discussions may ultimately lie in terms of negotiating a deal that would ultimately be acceptable to both party. So I wouldn't assume that per se the data is required to close a deal.

Your next question comes from line of George Zavoico with McNicoll, Lewis & Vlak LLC. George Zavoico - McNicoll, Lewis & Vlak LLC: Couple of quick questions, lot of questions have been answered already. Can you just explain why the AOS trial has doses of 250 and 500 and claudication 375 and 750, what's the rationale for that difference?

The LS was designed first when we were less progressed through the single dose escalation trial and healthy volunteers and those doses were at the time doses we felt were clearly likely to be well tolerated even potentially in patients who are frail and sicker than healthy volunteers. By the time we then turned our attention to the claudication study, we progressed further in the dose escalation for maximum tolerated dose and felt that we could go to somewhat higher doses. That's primarily it. George Zavoico - McNicoll, Lewis & Vlak LLC: Okay, and then with regard to the claudication, firstly of all, it's a larger indication, so that's good. But its also heterogeneous one with patients that have various alternatives for surgery and that sort of thing to help restore the blood flow. And I guess that explains why with the crossover each patient serves as their own control which is very important I guess in this indication. But do you have any restrictive less or more restrictive inclusive criteria to eliminate or include patients with who are down with a surgery for example or stable claudications that sort of thing to help perhaps enroll the trail faster or to keep the patient population as homogenous as you can.

I think our main goal in this study is to get a fairly homogonous patient population and as we've described, the assessment in that study are built around bilateral fuel raises. So basically you're just asking the patient to go up on to toes, step there for a second, back down for a second, up for a second. In our preliminary experience prior to actually beginning the randomization, our investigators hold to our investigators confirm that every patient they have, the half claudication upon doing repeated yield raise tested would come to claudication. So it appeared to be an end point that would be less froth with the very ability and things like treadmill testing or six minute walk. I think we got to get a homogonous group of patients that have cash claudication and at least foreign leg per se and that can demonstrate that they can do yield rates testing through claudication or come into the study, so I think they are somewhat more homogonous than maybe the case of some other claudication trials, but again we're looking here for some evidence of the pharmacodynamic effect in some of these population and not necessarily for results that would indicate definitively clinical benefit on other end points in a more heterogonous population. I think if we showed that we can increase the number of fuel raises or the work performed until the onset of claudication and then until intolerable claudication versus complete fatigue of the calf muscle, I think that would convince most potential partners and experts in the field that the drug is doing what it is intended to do and probably would for one exercise time on more standard assessment to use in claudication trials in the (inaudible) patients that would be enrolled in those studies. But that wasn't really our goal with this particular study. George Zavoico - McNicoll, Lewis & Vlak LLC: Yes, an evidence of efficacy trough. And in that regard is it all single dose or multiple dose with possible extensions?

This study is a three period trial where each patient gets a single dose of placebo more than 375 milligrams and more than 750 milligrams in a random order and a double blind fashion and they are assessed before and at certain time points after each of those three double blind doses. And that's really what it will be. George Zavoico - McNicoll, Lewis & Vlak LLC: And similar question in pending heart failure trials, it sounds like most of them, the PK is really the key end point probably because they guess you are evaluating various formulations in various (inaudible) administration. Again is that single dose, multiple dose and what sort of rationale for that design.

I'm sorry. George Zavoico - McNicoll, Lewis & Vlak LLC: The pending trials with Amgen, the new heart failure trials. It sounds like they are mostly PK for various alternative formulation.

I don't think I can make anymore comments regarding the design of those studies that we've done at this point and when they are initiated and they go upon clinical trials that (inaudible) can get information there and be maybe able to say more about the matter at that point. George Zavoico - McNicoll, Lewis & Vlak LLC: Okay fair enough and finally have you submitted any abstracts you're planning to present anything at the heart failure society meetings in September?

We don't comment on submissions. We just comment on…

There are no further questions at this time. I'd like to turn the call back over to Robert Blum, Cytokinetics President and CEO for closing comments.

So I would like to thank all the participants on our teleconference today for continued interest in Cytokinetics. I look forward to updating you on our activities and progress. Operator with that we can conclude the call and wishing everyone a good day.