Executives
Amy Sullivan – IR
Ron Renaud – CFO and Treasurer
Jean-Pierre Sommadossi – Chairman, President and CEO
David Standring – EVP of Biology
Analysts
Steve Harr
Brian Abrahams
David Moskowitz
Jason Kolbert
Howard Liang
Idenix Pharmaceuticals, Inc. (IDIX) Q3 2008 Earnings Call Transcript October 30, 2008 4:30 PM ET
Operator
Good morning. My name is Erica and I will be your conference operator today. At this time, I would like to welcome everyone to third quarter 2008 financial results conference call. All lines have been placed on mute to prevent any background noise. After the speakers’ remarks, there will be a question and answer session. (Operator instructions) Thank you. Ms. Sullivan you may begin your conference.
Amy Sullivan
Thank you, Erica. Good morning and welcome to Idenix’s conference call to discuss our third quarter financial results. With me today are Jean-Pierre Sommadossi, CEO; Ronald Renaud, CFO; and David Standring, our Executive Vice-President of Biology.
Before we begin, let me review our safe harbor statement. Today's discussion contains estimates and other statements that are forward-looking under the Private Securities Litigation Reform Act of 1995. Such estimates and statements are based on current expectations and assumptions that are subject to risks and uncertainties and involve a number of factors that could cause actual results to differ materially. Additional information concerning these factors is contained in our filings with the SEC, which are available on the investor section of our website at www.idenix.com. While we may elect to update forward-looking statements in the future, we specifically disclaim any obligation to do so, even if our estimates change. You should not rely on these forward-looking statements as representing our estimates as of any date subsequent to today.
The brief agenda for today is as follows. Ron will quickly review our results for the quarter and provide an update on the partnering status for 899. Then JP will provide a brief update on our HCV program. We will then open the call for Q&A for which David will also be available.
I will now turn the call over to Ron.
Ron Renaud
Thanks a lot, Amy. Now let’s quickly review our financial results for the third quarter. For the third quarter ended September 30, 2008, we reported total revenues of $2.1 million compared with total revenues of $10.9 million in the third quarter of 2007. The decrease is primarily due to a decline of $7.4 million in reimbursements of research and development costs from Novartis. We reported a net loss of $16.9 million or a loss of $0.30 per basic and diluted share for the third quarter of 2008 compared to a net loss of $30.5 million or a loss of $0.54 per basic and diluted share for the same period in 2007.
In these results you can clearly see the significant impact that the restructuring implemented at the end of the third quarter of 2007 has had. Our total operating expenses in 2008 as compared to 2007 are down approximately 50% year-over-year.
Now I would like to also take a moment to discuss our year-end financial guidance. We ended the third quarter with approximately $60.1 million of cash, cash equivalents and marketable securities. With the IDX375 program, to which JP will discuss in a moment, advancing much faster than we had planned our cash burn remained elevated from second quarter to third quarter and we now expect to end 2008 with between $45 million and $50 million of cash, cash equivalents and marketable securities. This is down slightly from our prior guidance of approximately $50 million and assumes no milestone payments, license fees, reimbursement for development programs, and assumes no financing activities during the remainder of 2008. Any licensing fees from IDX899 would be incremental to our year-end cash guidance.
Now I would like to quickly review where we are in the partnering process for IDX899. As you know, we reported favorable data from the final 100 mg dosing cohort and the proof of concept study of IDX899 in treatment naive HIV infected patients in early September. These results were in line with a potent activity observed with each of the other dosing cohorts with the mean 1.8 log reduction after seven days of dosing. Potential partners are impressed with the combination of potent activity, low dose, and the clean safety profile of IDX899 observed to date. With several parties initiating discussions after the 100 mg data were reported. We remain confident in our ability to partner the IDX899 program this year as we are currently in advanced current term sheet discussions. With that I will now turn the call over to JP.
Jean-Pierre Sommadossi
Thanks, Ron. IDX184 as you know is a once daily oral nucleotide prodrug candidate, which is based on our proprietary liver targeting technology and we have shown with a presentation at EASL that this compound is active in vitro against all major HCV genotype 1 to 4.
We have recently completed a first-in-man study of IDX184. Let the remind you that this Phase I study was a double-blind, placebo-controlled single dose escalation study designed to evaluate the safety and pharmacokinetics of IDX184 in healthy volunteers. This study evaluated six single rising doses of IDX184 ranging from 5 mg to 100 mg once per day. Each cohort of the study evaluated 8 volunteers randomized 8 to IDX184 and 2 to placebo.
In that study IDX184 was shown to be safe and well tolerated in a healthy subject with no discontinuations or SAEs. Dizziness was the most common observed adverse event and please note that this actually, adverse event occurred most frequently in subject receiving placebo. In this study, we actually, we’re pleased to know more about the pharmacokinetic of IDX184 nucleoside metabolite plasma levels showing low levels as one would have expected with the liver targeting drug.
Also importantly, based on plasma levels observed in this study with both the IDX184 but mostly the nucleoside metabolite, which is the reflection essentially of the triphosphate, produced at the liver site. Actually these plasma levels observed in this study and those observed in HCV infected chimpanzees were essentially compatible and therefore we confirm what we had expected that those doses of 25 mg to 100 mg will be active in HCV infected patients. Furthermore, the PK profile observed in this study continued to support the once daily dosing of IDX184 also as we had expected. This study will be followed by a three day phase I B-2A monotherapy proof of concept study in HCV genotype 1 infected patients, which is anticipated to begin in the coming weeks as we had guided before.
Moving on now to our HCV nonnucleoside program. So a compound that we have reported as IDX375. I’m pleased to report that IDX375 is quickly progress IND enabling studies actually has Ron indicated we are about 6 to 9 months ahead of schedule. So preclinical data from this program would be presented by David and his team at ASLD this week. And also in addition we have recently obtained some seven days non-GLP toxicity studies in monkeys and we were pleased to observe in that dose ranging finding study a 10 mg and 100 mg per kilo per day for 7 days as I said that no toxicity both with clinical chemistry and histopath were observed and therefore this study ready now paving the way for the 14 day GLP tox studies in 2 species that basically are the preamble for the IND submission.
Also in preclinical studies this compound continues to demonstrate potent and selective activity and this drug exposure, as we have measured in this 7-day continued to suggest that this drug will be a once-daily dosing.
We also continued to progress very nicely with our HCV protease inhibitor program both with IDX316 and IDX136. We’re also pleased to report that no toxicities were observed also in the dose range finding study with IDX136 both at the 100 mg and 100 mg per kilo per day for 7 days in monkey. When I say no toxicity this include both clinical chemistry and histopath and the similar studies ongoing right now with IDX316.
So, we remain to track to submit INDs for both programs, the IDX 375 and one of the two PIs by mid 2009. By this time next year our goal is to be the first and only (inaudible) with organically discovered drug candidates from each of the major classes of direct acting HCV anti-viral in ongoing clinical studies.
On that note I would like to end our formal remarks and open the floor to Q&A. Operator are there any questions?
Question-and-Answer Session
Operator
(Operator instructions) Your first question comes from the line of Steve Harr.
Steve Harr
Hi, good afternoon.
Ron Renaud
Hi Steve.
Steve Harr
Hi. A couple of questions. The first one just why did you decide these are macrocyclic protease inhibitor given some of the problems with resistance that those drugs have seen so far in human studies for other companies?
Jean-Pierre Sommadossi
Sure. Well, I’m going to let David Standring to share with you our view on resistance. But in the same time why we decided to go with microcyclic is because we believe that in terms of PK, in terms of potency, this is the class that in the medium term we have to think about five years from now we will not talk about gram levels for ACV drug but we will talk about milligram level with potential coformulation. We believe that and we have demonstrated at least in the replicaon like other companies that this microcyclic are extremely potent. We believe in term of the PK and we have shown already in non human primate that we have an excellent drug exposure with once a day and we anticipate actually again dosing regimens in a range of 50 mg to 100 mg once a day. So I think that and we have a pretty good idea in terms of preliminary evidence in term of potential side effects that you can expect with those drugs. And in type of in vitro cell line that we are using to make sure that we’re not going to encounter some unexpected events there. But in terms of resistance I’m going to let David also share our views.
David Standring
Yes I mean as JP pointed out, I think potency in PK are an important part of the resistance profile and we believe that we have the potency and good PK coverage that is very important for covering resistance. But on top of that we showed at EASL that we have a differentiated resistance profile. We have different type of resistance profile from the linear molecules that we current we have there. Like other macrocycles we do have a issue with one particular 168 mutation. But we are active for instance against the 156 mutations that are been seen with the linear PIs and we further differentiated our compound from the other macrocycles that are out there in terms of, for instance, in our 155-Q mutation and showed that we have good activity against that. So we feel that we have a good favorable resistance profile.
Steve Harr
As we go to, can I switch to 899 for a second?
Jean-Pierre Sommadossi
Sure.
Steve Harr
The data show on average no differences as you go down the dose, and where there any differences in terms of individual patient response. So that if you got to 100 for example some (inaudible) drug and you didn’t have the same order of benefit or is it pretty much comparable charts if you look at it on a patient-by-patient basis regardless of the dose.
Jean-Pierre Sommadossi
Yes it is very comparable. Actually we were very pleased Steve to see that essentially we had a 100% response. And it is a very good point that you raised. What we want to make sure is that not just that the mean is the same, what we want to make sure is that obviously we have a very good response also at 100 mg. Actually, we had indicated if I recall in the press release that we have all 8 individuals between 1.3 and 2.4 log of viral load decline. So it is really 100% individuals above one log which really compared very favorably with competition especially with (inaudible) and then in RTI. So it is clear that also at the 100 mg we have a very potent drug and actually one thing what I think it is a positive of that drug is really the PK that is very tight. The drug exposure and the variability from patient to patient actually is quite minimal and that is I believe I can explain those (inaudible).
Steve Harr
Great. Thank you.
Operator
Your next question comes from the line of Brian Abrahams.
Brian Abrahams
Hi. Thanks for taking my questions and congratulations on the progress. Why don’t you drill down a little bit more on the 1A results for 184? Did you guys see any lab changes, any cardiovascular changes or any dose dependent pattern to the side effect in all volunteers?
Jean-Pierre Sommadossi
Nothing. Actually to tell you at the 100 mg we were surprised because everything is 0-0-0-0. There was nothing. So essentially we have seen nothing and so we cannot report anything.
Brian Abrahams
Okay. Great and can you give us a sense of what the phase I b might look like in terms of the dosing you are planning to go forward with, the size of that study and when we might see results.
Jean-Pierre Sommadossi
Okay. We have no change our target. First of all I think that what I want to make sure is that there is a good understanding of the field is that we were cautioned many times about the dose that way we were going go into phase I b based on the fact that we had reported data 10 mg per kilo in the chimp. I think what we had thought we’ll see and actually we did confirm with the Phase I we have a much better drug exposure in man than we have and monkeys. And that is a reflection also of the major accumulation of triphosphate, a better accumulation of triphosphate in man as we have seen actually in vitro using human hepatocytes compared to monkey hepatocytes or other species. So basically the 1A study confirmed what we had anticipated. And therefore we believe that definitely we’re going to see antiviral activity between 25 mg and 100 mg. So that what will be the study design? It will be a 3-day with full cohort of 10 individuals, 8 on drug, 2 on placebo, all genotype I treatment naïve, 25 mg, 50 mg, 75 mg, and 100 mg. And you will see we anticipate data presented at EASL.
Brian Abrahams
Great. And then one last follow up if I may, then I will hop back in the queue. How do you get I guess a good read on what the liver to plasma partitioning is in man, to the comfortable that you are at similar liver exposure as you were in chimps. Thanks.
Jean-Pierre Sommadossi
So, basically what – the way we sit. One we are talking about the nucleoside metabolite. This is a definitely a measurement of the amount, with a indirect measure of the amount of nucleotide and obviously from the liver site because we now from our studies in non human primate that 97% of any absorbed drug is basically directly to the liver. So, hepatic extraction. So, as we have measured those levels in nonhuman primates, we did the same the nucleoside metabolite and we are basically what was expected was higher level in man as compared with we had in monkeys. Equivalent dose, and there was basically 1 to 10 type ratio. Whether it is a an increased, whether it is an increased of triphosphate basically to us this means that we are in the right doses to expect the antiviral activity that we have seen in HCV infected chimpanzee.
Brian Abrahams
Great, thank you very much.
Operator
Your next question comes from the line of David Moskowitz.
Jean-Pierre Sommadossi
Hi, David.
David Moskowitz
Hi, good afternoon JP. Question on the 184 compound. The FDA required you guys to do these (inaudible) studies the healthy patient studies. Could you share with us whether or not you had to bring that data to FDA to advance the product into the 1 b trials and could you talk about some of the discussions you had with FDA if that is the case.
Jean-Pierre Sommadossi
Sure. Well. As you know that is a good question. As you know any – after completion of any clinical trials you have to send data to the FDA and that is what we did. And basically we have not had any discussions with the FDA at this stage. So we sent all the reports and that we have shared with you today. And we anticipate as we say to initiate the phase 1 b in the coming weeks. We sent basically all the details obviously of the trial, part of the IRB evaluation. And basically everything is currently moving as we anticipated.
David Moskowitz
So, should we assume that you have got to go ahead or do you have to wait for some signal for the FDA to advance these trials?
Jean-Pierre Sommadossi
I will think the other way around. I mean that if there is no hold basically we will assume that we move.
David Moskowitz
Sort of like an IND.
Jean-Pierre Sommadossi
That is correct.
David Moskowitz
Okay, very good. On sticking with 184, so EASL is in April of next year. I guess the question is when would you expect proof of concept to complete and I guess I am trying to get a better understanding for when the – if you will the clock would start ticking on Novartis’ 90-day decision on whether or not to partner that compound?
Jean-Pierre Sommadossi
Sure. First of all as I said we anticipate that we will share the data at EASL. We believe that work should be done by if there is no surprises and I think mostly when we talk about surprises it is really the availability of treatment naive genotype type 1. Let us not forget that there was two ongoing Phase III studies, that when I say two is actually several Phase III regulatory trials with 2 drugs and I am clear that we had a lot of faculty with our COO to find those individuals but assuming that we have no issues in terms of enrollment we target to have all cohort completed very closely by the end of April or early May at the latest. So, what we foresee is we are going to submit an abstract on the Phase 1A. We are going to submit an abstract on the Phase 1 b, and obviously by the time that EASL will occur, we will – we should have essentially almost 100% of the data.
David Moskowitz
And how does that impact Novartis with its 90-day decision clock?
Jean-Pierre Sommadossi
Again, when first of all when we have done this study we have go on to (inaudible) take us I will say 6 to 8 weeks and thereafter we can anticipate that is when we will send a notice to Novartis. So, if you really look in terms of timing we anticipate probably by the end of June to send a notice to Novartis.
David Moskowitz
Very good thanks. And on the 136 and 316, I think – did I hear you say you are going to select one of those compounds for proof of concept and are you on track for the first half of next year?
Jean-Pierre Sommadossi
Yes, absolutely. As you can appreciate the cost for PI is not minimum and we have not been able except the PK to differentiate those two compounds. But definitely 316 is once a day as compared to 136. We have completed now. We are very pleased 100 mg per kilo even over 7 days for PI fully clear on histopath. I can tell you there is some PIs right now in the clinical study that we will be pleased to have this type of safety at least in monkeys. We have (inaudible) 316 and then we will take a decision and definitely we will very likely move one of the two all the way to IND and keep the second one as a potential backup.
David Moskowitz
Great. Then last question. So, the cash balance is now lower than we expected and you are going to end the year at a level lower than we expected. You know in this type of environment with liquidity at a major premium what can you say to us analysts and investors related to whether or not you are going to need to go to the well and raise new capital?
Jean-Pierre Sommadossi
We’ll make sure that Ron is going to deliver. Why don’t you go over that?
Ron Renaud
So David, I mean we’re you know, obviously our cash guidance at the end of the year is only a little bit lower than where we thought we were going to end the year. And you know at the end of the date is day it is for a good reason and that is the 375 program moving along much more rapidly than we expected. So again our primary focus is always going to be given the pipeline the best chance to succeed. But to that end, we remain very confident that our current cash, cash equivalents, and the marketable securities as well as expected royalty revenues on Tyzeka for next year will satisfy our cash needs through late 2009. So that doesn’t factor in any licensing fee that we may get on the 899 front, that doesn’t include anything we may do in the way of our HCV program with Novartis. It doesn’t include any of that. We feel very good that our balance sheet will take us through the end of next year.
David Moskowitz
Thanks very much guys.
Operator
Your next question comes from the line of Jason Kolbert.
Jason Kolbert
Hi guys. Thank you. Can we talk a little bit about 184 and the calculations from the animal studies to the (inaudible) dose and specifically it sounds like they have a very, very clean profile. But can you go over what that animal data looked like again just I mean in the monkey studies it was just very clean.
Jean-Pierre Sommadossi
Sure. Jason, we are not going to go further in terms of details until EASL. We anticipate we’re going to write an abstract and submit all the details with all the data both on the Phase 1 A and compare with what I was just giving as a top line with the HCV chimp and some potential PK/PD relationship as well.
Jason Kolbert
Okay, can be switch gears to 375. Can you tell us a little bit about that nonnucleoside? Is it a binder [ph] for example?
Jean-Pierre Sommadossi
Well, we have our expert here with David. David why don’t you give more details on 375.
David Standring
Yes 375 is a binder. It basically has very nice potency about 2.3 nanomolar, good potency also against the enzyme and especially favorable PK profile. We believe that this compound has very good exposure in a variety of animal models and on that basis I think it is an exciting candidate from our point of view.
Jason Kolbert
And when you think about how to develop a nonnucleoside in a clinical setting, you know, do you think about doing early combination work and how does that come together?
Jean-Pierre Sommadossi
Well, the reason I think that we hope that we will be in an exciting position in 2010 to be one of the first one to really combine those programs. I think we are and will be in the situation as we were in the HIV field 10, 15 years ago. I think we can read the crystal ball but who knows what we need? Do we need a combo of a PI? You know we can talk about high resistance and with low resistance but at the end of the day everything is just theoretical. I think that we hope you know, because you never know with regulatory authorities we gave a guidance at the beginning of the year we felt we can go into a 7-day as we used to be to go and now we can’t. So, hopefully what we foresee if we have clean drug in the clinic after 4 weeks and I think I have mentioned that in the past and with supportive preclinical tox we believe that the FDA should allow us to start to do some combination of those direct acting antivirals. So, we will have a little bit of luxury to be able to really evaluate what is the best combination, do we need a PI, plus a nuke [ph], plus a need a PI plus a nuke, do we need a nuke and then a non-nuke. We will be in areally unique position to be able to answer the question. So, this is what we look you know, by the end of 2010 to be in a position where essentially we can fully evaluate. We believe as soon as we have 4 weeks of data with each member of this class and assuming that we have no issuing in terms of safety, that if again the regulatory landscape is the same as today we hope that we will be able to evaluate those combinations. Because today you know Jason someone will tell you, it is better to have a nuke and a PI. Someone else will tell you, be better non-nuke and a PI. Who knows? But I think only with clinical evaluation we will be able to answer those questions.
Jason Kolbert
And now I really agree with you. It is going to be really exciting times. Let me end with kind of one last question for Ron and it is when we look at 899 and we try to understand what a deal structure might look like. You are obviously entertaining different things can you point to any other examples in terms of magnitude of what you are looking for and if there was one more piece of clinical data that you could get allowing the 899 program to continue, what piece of data would you like to have in order to really enhance your negotiating capability for a deal?
Ron Renaud
Yes, I think in terms of deal terms you know as maybe you and I have discussed in the past there is no real good proxy out there in the HIV landscape for a good benchmark deal as a lot of the HIV programs have been, internal programs that most of the large pharmaceutical firms and there has been very little in terms of a deal flow at least recently on early stage HIV programs. So we’re out kind of blazing our own path on this one in terms of what we think is the right opportunity for 899 and to that end we are having different discussions and I think for us it is about getting the best economic value for 899 to enable us to reallocate that resource to our HCV program and give those programs the best chance to succeed. In terms of having any incremental data to drive the deal or enhance the deal. I can’t say that is it really necessary at this point. I think when you know, as I mentioned in our remarks about the 100 mg data and having some additional parties come into the fray, I think really it is a series of kind of tick boxes that we have already been able to tick bar, hit the ticks on. And that is it efficacious? You know so far the data shows that it is. Is there a high varied resistance? So far we show that it is. And is there safety there? And the safety seems to be bearing itself out quite well and I think most importantly is the low dosage formulation. That really puts us in a unique position versus anything else that is out there. I mean there is a lot of noise in that space and we have been able to cut through all of that noise and differentiate 899 and I think the folks that we have been talking to fully understand that.
Jason Kolbert
Thanks guys. We will see you on the West Coast.
Ron Renaud
Okay.
Jean-Pierre Sommadossi
Thank you.
Operator
Your next question comes from the line of Howard Liang.
Howard Liang
Hi, good afternoon JP.
Jean-Pierre Sommadossi
Hi Howard.
Howard Liang
Can you remind us whether in the Phase I A (inaudible) whether you saw any GI issues?
Jean-Pierre Sommadossi
We did.
Howard Liang
You did.
Jean-Pierre Sommadossi
We did.
Howard Liang
You did. Okay.
Jean-Pierre Sommadossi
We did. There was some emesis already in the – actually we didn’t do the same type of study in the Phase I A but in the early normal volunteer we had already some –
Operator
Hello. Mr. Liang.
Howard Liang
Yes, I can hear you. Hello.
Operator
Ms. Sullivan? Ladies and gentlemen, there will be a slight delay in today’s conference. Your line will again be placed on mute until the conference begins. Ms. Sullivan?
Amy Sullivan
Yes.
Operator
You may begin your conference.
Amy Sullivan
So, we are back. We got disconnected. Technical difficulty, and we are right in the middle of answering Howard’s questions. I don’t know if you want to continue with that.
Ron Renaud
Hello, are you still there?
Amy Sullivan
He won’t be back Ron, but you can answer the question.
Jean-Pierre Sommadossi
(inaudible) we didn’t have – just complete Howard’s question asking if we had the same safety with 283, actually with M283. Within the phase I we had seen already some emesis and no more volunteers.
Amy Sullivan
Operator, are there any additional questions.
Operator
Yes, ma’am. There are no more questions.
Amy Sullivan
Can you ask one more time since we had that technical glitch?
Operator
(Operator instructions) Your next question, follow-up question comes from the line of Howard Liang.
Jean-Pierre Sommadossi
Sorry about that Howard.
Amy Sullivan
We did not know what happened there.
Howard Liang
So, if I could continue about, if you can go back to the chimp study, I think you said your PK from Phase 1A was comparable to the chimp, what you saw in chimp, can you talk about – I think the chimp study there was just more than one animal probably noteworthy?
Jean-Pierre Sommadossi
Five animals.
Howard Liang
Can you talk about how big of a range there was –?
Jean-Pierre Sommadossi
Again, Howard as I had said to Jason, we are going to put an abstract for you with all the details and we are talking about, to give you a top line, about 4 to 5 fold differences. Okay, it is about that.
Howard Liang
Within 5 animals, 4 to 5 –
Jean-Pierre Sommadossi
So, what we did. Okay let us – going more and more into details here. Basically what we have done and what we are going to present is in the HCV infected chimp for each chimp over 4 days we have measured trough level everyday on the nucleoside metabolite, which as I said is basically what you obtain from the triphosphate being (inaudible) and by (inaudible) and release the nucleoside. So, what we did in each animal we measured trough level, 24 hours after administration. This nucleoside metabolite. So, we have about to give you an idea, we have about 20, 25 measurements in the whole HCV study, in the chimp study, and thereafter we basically with the study we can basically have a better idea where we stand in terms of same concentration in the Phase I study and I would expect related to dosing. And basically we knew last time, we had a pretty good idea that at least we thought that we will have a better triphosphate formation and we should have a better drug exposure in man as compared to non human primate but I could not tell you that until we have the data. Now we know that that is the case and we will give all the details in term also some PK/PD data at EASL and we are not going to report anything before any scientific meeting is too late for ASLD as you know. And you will have in the field will evaluate we will all the data in detail for you.
Howard Liang
Okay. One more. Can you ask how, have you had more animal toxicology data and how long was the study would that support?
Jean-Pierre Sommadossi
We have two weeks, we have two weeks chronic tox, two species, and we are not going to start the next move in terms of the chronic tox, Howard, as we will move into a 3-month chronic tox with one month peel off, but you know, let us face it. We are not going to stop that before sometime early next year. Okay. And we don’t need to?
Howard Liang
Okay. And then your Phase I b, is it I don’t know if you said this, is it going to be in treatment naïve patients?
Jean-Pierre Sommadossi
Yes, it is and that is requested by the FDA that they want only treatment naïve genotype I in the proof of concept?
Howard Liang
Okay, and will there be follow up therapy like a center of care for the rest of the year.
Jean-Pierre Sommadossi
Yes.
Howard Liang
Okay. Great thanks very much.
Jean-Pierre Sommadossi
Thank you.
Operator
There are no further questions. Do you have any closing remarks, Ms. Sullivan?
Ms. Sullivan
Yes, thank you. I just want to thank everyone for their time today you’re your interest in Idenix. If you have any additional questions, please feel free to call. Thank you.
Operator
This concludes today’s conference all. You may now disconnect.
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