Greetings, ladies and gentlemen, and welcome to the Incyte Corporation’s Q3 2010 financial results. [Operator Instructions.] As a reminder this conference is being recorded. It is now my pleasure to introduce your host, Ms. Pamela Murphy, vice president of investor relations and communications. Thank you, Ms. Murphy. You may begin.

Thank you and good morning. On the call today are Paul Friedman, Incyte’s President and Chief Executive Officer; Dave Hastings, Executive Vice President, Chief Financial Officer; Rich Levy, Executive Vice President, Chief Drug Development Officer and Medical Officer; and Pat Andrews, Executive Vice President, Chief Commercial Officer. To begin, Paul will review recent developments at Incyte and Dave will follow with a discussion of our Q3 financial results. We’ll then open up the call for Q&A. Before beginning, we’d like to remind you that some of the statements made during the call today, including statements regarding our plans and expectations for our drug development programs, including the timing of our clinical trials, regulatory submissions, and the potential safety and efficacy of our compounds, as well as our expected financial results and guidance are forward looking statements. These forward looking statements are subject to a number of risks and uncertainties that may cause our actual results to differ materially, including those described from time to time in our 10Q for the quarter ended June 30, 2010, and from time to time in our SEC documents. Paul?

Good morning everyone. We continue to make excellent progress on all fronts, as reflected in the increase in publications and presentations of our clinical results, most notably for our JAK1 and JAK2 inhibitors. In particular, data from our lead JAK inhibitor, Incyte 18424, was the subject of an article in the New England Journal of Medicine, in which the potential of 424 in the treatment of myelofibrosis was described. As there are currently no approved therapies for this disease, we are encouraged by the conclusions of the authors, as well as the comments in the accompanying editorial by [inaudible], which reaffirms JAK1 and JAK2 inhibition as a new targeted therapy for myelofibrosis. Now also tomorrow the full 24-week Phase 2A results of Incyte 28050 in rheumatoid arthritis will be presented at the American College of Rheumatology annual meeting. We are hosting a presentation of the data Wednesday evening, tomorrow evening, that will be one chance for those of you who are not attending the ACR meeting in person. Beyond these accomplishments, we're especially looking to the completion of the two Phase 3 trials with 18424 in myelofibrosis. The controlled portion of the U.S. trial COMFORT-1 has completed, and we expect to release the top line results in the second half of December. Provided the results are positive, we intend to submit a new drug application in the first half of 2011. The European registration trial COMFORT-II, being conducted by Novartis, is also expected to be completed this year, and the MAA submission is planned in the first half of 2011 as well. Full results from both studies are expected to be submitted for presentation this coming June at both the ASCO and the European Society of Hematology meetings. As part of our objective to expand the use of 18424 into…

Thanks Paul, and good morning everyone. I'll start my overview this morning by discussing our cash position, revenue, and operating expenses, and then I'll move to our changes in 2010 financial guidance. We ended the third quarter with $396 million in cash and investments, excluding $47 million remaining in an escrow account reserved for interest payments through October 2012 in the 4.3% convertible senior notes. So far, our cash use this year has been $111 million. This amount excludes $183 million received from collaborators for milestones and up-front payments, $8 million received from the exercise of stock options, and $159 million used to redeem the remaining 3.5% convertible senior and subordinated notes. In terms of revenue, we were pleased to announce additional significant milestone from our partners, which will be recorded in the fourth quarter. Under our agreement with Lilly, we earn $19 million for the initiation of a Phase 2B study in RA, and we have earned $49 million in total milestones from Lilly this year. As part of our agreement with Novartis, we earned $50 million in milestones for the initiation of the joint global Phase 3 study in PV. Now, moving to our operating expenses, our R&D SG&A so far this year are $91 million and $22 million respectively. As we have stated in the past, we do expect variability in our spending in these areas due to the nature and timing of clinical programs and the ramping up of the commercial infrastructure needed to support the potential launch of 424 in myelofibrosis. Now in terms of the 2010 financial guidance, we are making changes in the following four areas. First, we are reducing our gross cash use guidance from the previous range of $160 million to $165 million to a range of $150 million to $155 million. This cash use guidance excludes actual and potential future milestones received from partners and proceeds from stock options. Second, we are increasing our revenue guidance from our previous range of $99 million to $101 million, to a range of $168 million to $170 million. Third, we are reducing our R&D expense guidance from a previous range of $135 million to $142 million to a range of $128 million to $135 million. And finally, we are reducing our SG&A expense guidance from a previous range of $35 million to $40 million to a range of $30 million to $35 million. We are gratified that we have been able to prudently manage our costs and remain in a strong financial position to continue making significant investments in our development pipeline and in the preliminary commercial effort for 424 in its first potential indication of myelofibrosis. And so with that, Paul, I'll turn the call back over to you.

Operator, we can now open the call for questions.

Thank you. [Operator Instructions.] Our first question is coming from Bret Holley with Oppenheimer.

I was just wondering, in PV, how the number of patients refractive versus intolerant of HU breaks down based on the data that you have so far.

The ratio's about 3:1, with the 3 being resistant patients and the 1 being intolerant patients. That's what we've found in that population, that there are about three times more patients who are resistant than who are intolerant.

And would you expect a differential level of response to 424 in those different patient populations?

I don't think so. I'd ask Rich to add to what I just said, but I don't see why we should expect that, and when [inaudible] probably has some kind of bearing on that in the Phase 2 study. Rich, what do you think?

So the patients who are intolerant, basically just can't take any dose of hydroxyurea, whereas the patients who are resistant, or so-called refractory, they can take higher doses but they still don't work. So in terms of their response to hydroxyurea, if that were a choice it wouldn't work, and if they chose another treatment there's no reason why those other treatments should work any differently in patients who are either intolerant or refractory to hydroxyurea.

Our next question is coming from the line of David Friedman with Morgan Stanley Smith Barney. Please state your question.

I was wondering if you could just talk a little bit about the plans for MF, not to get too far ahead of ourselves, but just when you're thinking about number one, building out a sales force, if you could talk about some of the timing and steps you'd take. And then the second is when you think about the MF market and the target doc, is it the generalist hematologist or a hematologist-oncologist, or something even more focused than that?

Let me give an answer to that. As far as building out our sales force, we would look to do that next year. We have a good sense of how many reps and district managers we'd need. We've said that that number is between 30 and 70. We're still refining exactly how many it would be. We are in the process now of identifying a firm to work with to recruit that many people in an efficient way in a narrow space of time, and we would probably start recruiting at the end of the first quarter for some of the more senior people and to have them all on board by the end of the third quarter, beginning of the fourth quarter. And as far as target doctors, MF is generally treated in the United States by hematologist-oncologists, and they are more likely to be in the community than they are in academic medical centers. And we would be planning on reaching about 6,500 of them, which should give us more than 80% of the prescribers reached directly through the sales force.

Our next question is coming from the line of Eric Schmidt with Cowen & Company. Please state your question. Eric Schmidt – Cowen & Company: A couple of financial nits for Dave. First, did I hear you right that you've now retired the entirety of the 3.5% convertible senior notes?

Yes. They're gone.

And you've been recording bigger milestones than I had expected. Can you preview for us a little bit what's to come next from either Novartis or Lilly? I know we're looking forward to 2011, but looking for a little bit of guidance there.

As you know, we can't give you granular detail on that. What I would say is that we've had a very solid year obviously from a milestone perspective, and these things are lumpy in nature, so as you think about timing of initiation of studies and likely milestone events, 2011 wouldn't be as significant as 2010.

And in terms of new study initiations, what's the latest in terms of new indications for 050 with Lilly?

I think you're going to have to ask them about that. You're talking about things beyond RA?

That's right.

Obviously we've had what I would regard as productive talks with them. It's their call what they're going to do next, but I think there are some obvious ones. If I were doing it I would want to study the spondyloarthropathies like ankylosing spondylitis and psoriatic arthritis, because that population in toto reaches about a third in prevalence of what the RA population is and the anti-TNFs have worked there and I think it would be a high probability that you would test positive results. So I would go there. I suspect that we will get there, but at the end of the day it's going to be Lilly's call as to what we do next.

Last question. On the response study can you estimate when you think you'll enroll that study and what percent of patients are going to be ex-U.S.?

I'll answer, and if I don't answer completely right, then Rich should step in. We've allowed ourselves a year to recruit 300 patients. I'm hoping we'll be able to do it more quickly than that. We're up and running in the United States. As I said in the prepared remarks, Novartis will start recruiting ex-U.S. early in 2011 and it is our plan to have about half the patients come from the U.S. and about half the patients come ex-U.S. Is that correct Rich?

Yes, exactly right.

Our next question is coming from the line of Rachel McMinn with Bank of America Merrill Lynch. Please state your question. Rachel McMinn – Bank of America Merrill Lynch: Just Dave, I know you're not here to give 2011 guidance, but when we think about cash use going into 2011 obviously we've got the PV study which is somewhat replacing the MF Phase 3, but can you give us a sense of how we should be thinking about that higher commercial expenses as well, but from an R&D perspective is that number going to be meaningfully higher than 2010?

I think we'll be responsible of course and judicious, but we do want to continue allocating capital to what we view as high value programs and we'll continue to do that, and as you mentioned, Rachel, our investments in sales and marketing will increase. What's important to note, though, is that our guidance in terms of having enough capital to get 424 launched is still in place, and we're well-positioned given the amount of milestones we recorded this year.

And then on the topical psoriasis product, there was really no mention this time. How should we be thinking about that product? Can you describe where you are in negotiations or if that's something that you're willing to take into Phase 3 yourself?

I'll start, and then Pat Andrews, who has responsibility for business development, may want to add more. When we look at how the company is maturing and to where we seem to be evolving, that program sits there all by its lonesome as in a therapeutic area where we would if we took it through ourselves we would only have a single product. We believe that the data we have so far would indicate that with a properly run Phase 3 study the drug is registerable and would be a successful dermatology product, but as a single entity that would require a sales force different than the sales force that we're building up for oncology, myeloproliferative neoplasms to start. It has slipped a little in our priority list, and so we would like to find a partner. Sure, we could do the Phase 3, but we believe at this point our money would be better well-spent on some of the other programs and I'll let Pat comment on the status of this development.

So, we [intend to] continue to discuss with some companies partnering opportunities. Because the Phase 2 results were positive and there's been little truly new for patients with mild to moderate psoriasis in a long time, 424 is an appealing product. It's once a day, it has rapid onset, a good efficacy and safety profile. It might be combinable with other therapies. So we have had interest. That being said, the opportunity is a little on the small side for some large companies and the development costs are a little on the expensive side for some specialty derm companies. So we're continuing to discuss to see if we can find a partner now or maybe later who we could trust with this asset.

And then another completely unrelated question and I'll hop off. Just curious on the Phase 3 and the COMFORT-1 and COMFORT-2. The end point is a little bit different than Phase 3 and I'm just wondering if you have patients that are responding but don't meet the threshold by MRI that you've predefined, are we going to see that data? Is that data being collected? And how will you be able to present that? Is there a significant secondary endpoint?

We are very interested in that data, and we obviously have - and I'll also let Pat add from a marketing standpoint what we've learned. Virtually all the patients get significant - I'd say 85% or more get 25% or more decrease in volume by MRI, and virtually all patients get significant symptomatic improvement. Obviously for regulatory approval you have to pick a number and that's a number you have to achieve, and the reason we ended up at 35% is that we generated the data that showed that that 35% corresponded to a 50% decrease in length by palpation, which was the parameter that was considered significant improvement by the international working group. And so when we look at the data that we had in that Phase 2 study, the median's about 33%. And so we powered the study so that we would easily meet the regulatory end point. But more important, I think to you and to us, is what kind of results do you have to get in a patient population to have physicians who want to prescribe the drug. I'll let Pat expand a little bit on the marketing research that we have that is quite reassuring based on what we've gotten in Phase 2 and what we expect to see in the pivotal trials.

So we've done a fair amount of quantitative and qualitative market research at this point to understand what matters to practicing physicians, particularly hem-oncs treating MF patients. We've tested various product attributes, including the level of spleen reduction and varied those attributes at the high end and the low end of what we might see coming out of our Phase 3 to understand the importance of that attribute as a prescribing decision. And in general the level of spleen reduction can be much less than 35% by imaging, even down to 10% for some physicians, and still be seen as appropriate therapy for their MF patients. This assumes, of course, that the other benefits that we've seen with 424 such as improvement in constitutional symptoms and an acceptable safety profile remain consistent with the Phase 2 data. In short, you can have a clinically meaningful benefit with less than a 35% reduction in spleen volume that's in the Phase 3.

Our next question is coming from the line of Thomas Wei with Jefferies & Co. Please state your question. Tommy - Jefferies & Co: This is actually Tommy for Thomas. Most of my financial questions have been answered. I just have one follow up 424 question. To follow up on your comments just now on market research, spleen reduction, and also earlier with the hemoglobin [inaudible] by JAK inhibition, can you sort of just put it in context for us how you see the overall competitiveness of 424 in light of the new data on JAK inhibitor competitors. I'm speaking of the Cytopia YM and Targetin's [inaudible] compound being presented at ASH.

First of all, the Targegen compound, the S*BIO compound, don't really very effectively take out JAK1. We've discussed this at some length, that to shut down the proinflammatory cytokine pathways you can do that much more effectively if you have JAK1 as well as JAK2 inhibitory activity. You can demonstrate that in cell culture, in animal models, Basically by taking out less of both JAK1 and JAK2 you can shut down the pathway if you have that kind of a profile. If you just are a JAK2 inhibitor you have to go higher in your JAK2 inhibition to shut down the cytokine pathways as effectively. And when you do that you cross over to greater inhibition of bone marrow function. And I think if you look closely at the Targegen data, in its complete form there was fairly high incidence of anemia. The other thing is when you go higher and you are giving hundreds of milligrams a day, which you do with all three of those compounds, you then get into ranges where the milligram burden to the organs of the individual is such that you begin to see non-mechanism based toxicities. And if you happen to also cross over and hit other kinases like FLIP 3, you also can have toxicities. S*BIO and Targegen have both FLIP 3 inhibitors and they have significant G.I. toxicity. The Cytopia compound is a JAK1/JAK2 inhibitor. It's about three years behind us. As I tried to convey to you in my notes, without calling them out, but you have now done that, we have exactly the same results in terms of having people become transfusion independent analyzing data the way they've analyzed it. I've become more and more certain over time that there is a subset of these patients who have a significant component of their anemia from the chronic disease aspect, and those are the people who if you titrate your JAK1/JAK2 inhibition properly you can get a bump in their hemoglobin. I suspect that the people who get hemoglobin bumps with the [image], even that mechanism's not well understood, probably the same subset of patients. There's probably a lot of crossover in that subset. Obviously, there's a tipping point. If you go too high and you take out too much JAK2 you'll overwhelm the benefits that you get from blocking the cytokine pathways. And in that regard, just looking at the Cytopia compound, it's about ten times less potent on JAK2 than we are. It's about 40 times less potent on JAK1. So it is a JAK1/JAK2 inhibitor, but its ratio has a disadvantage compared to our ratio in terms of avoiding that crossover into having too much JAK inhibition. And they haven't studied very many patients. They haven't studied them for very long. I think if you look at the abstract you see that there are toxicities that we don't have. And so when you put it all together, we're ahead and we have the best compound.

Our next question is coming from the line of Avik Roy with Monness, Crespi, Hardt. Please state your question.

Well first, I don't know if Ruxolitinib is more pronounceable than INCB18424, but congratulations on getting an actual name for the drug. My question is what are your thoughts about non-hematologic toxicity, whether with your drug or some of the others. Just based on your experience, your experience in clinical trials and your discussion with opinion leaders, which of the non-hematologic toxicities do you think are most important in terms of adherence and discontinuation?

You mean that we have?

That have been seen generally.

If you're talking about 18424, and Rich can embellish this answer if I don't say things completely enough, with 18424 even in the myelofibrosis group when you go beyond the hematologic issues I guess the only thing that I would watch for are still its mechanism based toxicities because frankly we have not seen any significant non-mechanism based toxicities. Our ability to specifically take out these kinases and not other known kinases with our agents is pretty [exquisite]. We have very selective compounds in that regard. But in taking out the JAK1 and JAK2, you do modulate the immune system. That's why we're seeing the good efficacy in our patients, and if you modulate the immune system you have to watch for infections. While I think we've been fortunate by virtue of the fact that you don't take this mechanism out 100% and there's off time during the day, we've been fortunate in seeing only mild and minor types of infections. But that would be the other thing that I think you would look for. If you're talking about other people's compounds, I think the FLIP inhibition is problematic, because folks are having a significant amount of G.I. toxicity and then there are non-mechanism based, or at least they appear to be non-mechanism based, toxicities that have to do with lipasemia, amylasemia, some liver signals, with the other compounds. Now those other compounds are being dosed at hundreds of milligrams a day, so it's not too surprising that you would see some of that with the competitors' compounds.

Actually Avik, before you go, just wanted to comment on the Ruxolitinib, which is the pending INN for 424. We're really far along in the process, but they actually have to publish it before it's officially ours, so we've been sticking with 424 as the name everyone knows and loves before trying to transition to the pending generic name. Hopefully we'll know early next year, and if that's it we'll use it more formally. And if that's not it, they'll probably just give us one. So stay tuned for another couple of months before it's final.

Our next question is coming from the line of Josh Schimmer with Leerink Swann. Please state your question. Joshua Schimmer – Leerink Swann: Paul, I was interested in your comments about 424's ability to eliminate transfusion requirements in patients. I guess a couple of quick questions. First, wondering why this hasn't been something highlighted previously, since it does seem to be a fairly important data point to have. And second, are you able to determine yet, a priori, which patients will have hemoglobin increases versus hemoglobin decreases? And if so, what are the predictive features? And if not, what predictive features are you exploring for this?

The answer to the latter part is not yet, and I think it is an important parameter. I think one of the things that has to be determined is how long the effects last, how much the hemoglobins go up, and Rich, do you want to comment any further on that?

I would say that there are patients who get better in terms of their hemoglobin and transfusion independence, and there are also people, as Paul talked about, whose bone marrow hypofunction is the main reason for their anemia, who don't get better, or might get even slightly worse. And that's going to be true for all of the JAK inhibitors. And so we haven't made a big point of it because we think that the main benefits of the drug are improving the symptoms of the disease, shrinking the spleen to a clinically significant degree, and perhaps some other long-term disease modifying effects that will take longer to demonstrate. I think the reason we talked about it now is that there's been such a point made both by the abstract as well as by some of the notes that have been coming out trying to point out how apparently based on the way that the data was presented that Cytopia's JAK inhibitor might have an advantage over ours in terms of anemia, and we just wanted to correct that by showing that if we analyze our data in similar ways you get similar results. We don't know, by the way, how to predict which patients will do better or worse without actually giving them the drug.

So is the hypothesis that it's based on the anti-inflammatory activity? Is that something you plan on exploring, the correlation between baseline inflammatory activity and some of the inflammatory markers and symptomatology in hemoglobin change?

What you're saying makes theoretical sense, but from a practical matter it's extraordinarily difficult to do. You're not going to find that there is a specific level of certain cytokines that you can measure in the blood that would be predictive. They're all high in everybody, and some are astronomically high, and some are medium high, but it doesn't really tell you that those patients are more likely the ones to respond to therapy. I'd be skeptical about ever really figuring it out without giving the drug and seeing.

Our next question is coming from Liisa Bayko with JMP Securities. Please state your question. Liisa Bayko – JMP Securities: I just wanted to maybe ask a couple questions about the sheddase program. I know results are going to come maybe early in 2011. Can you just give us a little more clarity on exactly what the trial design looks like and what would get you excited about pursuing the program to the next step. So what we should be looking for in the data.

When we started the study, adding the sheddase inhibitor to Herceptin and then to Herceptin plus chemotherapy - and what we were finding was that people who were both HER2-positive and P95-positive were doing pretty well, better than what is described in the literature. The issue is that there's one paper describing this in the literature, although it's accepted that these P95-positive patients, and it's logical, that they would not do as well in general because you've got a very active growth pathway constitutively turned on that cannot be neutralized by Herceptin. And so all we're doing now is we've been able, by contracting with four academic centers throughout the world that have large sets of histopathological samples and histories on patients who had metastatic breast cancer, and we are taking those samples and staining for P95 and also correlating those results with their clinical course. To simply confirm what the [inaudible] paper and our own data say is true, and also to give us a feeling for how much P95 positivity you have to have to not do as well as if you had lower levels of P95, so that we could figure out the ultimate patient population for Phase 3. Now, there is a chance, we think it's not a big chance, but there is a chance that when we complete this analysis that it will not support the hypothesis that our data and the [inaudible] paper have created. We're cautiously optimistic that that's not going to be the case, but we want to complete these analyses and do a careful statistical analysis on the data that we have before we get ahead of ourselves. And so we are on track to have those data by the end of this year, and if, as we are expecting, the data support the hypothesis, it becomes a very interesting Phase 3 program. We'll tell you where we stand just as soon as we've completed the analyses and we will then go and talk to the FDA about a Phase 3 program.

And then maybe just a quick question for David. Can you just remind us of the accounting treatment for these subpayments you've received?

They'll be recorded as revenue in the fourth quarter. Milestones are treated as revenue as soon as they're announced.

And they're the full amount?

Yes.

Our last question is coming from the line of Tom Russo with Robert W. Baird. Please state your question. Tom Russo – Robert W. Baird: Just a quick question for Pat. Based on your conversations with payers to this point, are you willing to make any comment on level of confidence on price versus the [$]40,000 to [$]60,000 thousand range that the company has kind of talked to in the past and maybe where within that range you might think you would be landing at this point?

We have had some more conversations with payers, but truthfully not at a significant level because the oncology market in the U.S. does not have a lot of price constraints on it. Sometimes there's utilization constraints, like you have to have a prior authorization, but there's not really price constraint. So we remain very comfortable within the [$]40,000 to [$]60,000 level that we have previously spoken about.

And then just last question, what is the current expected timing for publication of the Phase 2 data in PV? And then maybe again for Pat, anything interesting from the market research about the demand for 424 there, even before the label indication?

Rich, what was the publication date -

The publication of the Phase 2 in PV would probably be some time next year, depending upon whether it gets accepted at the first journal it gets submitted to, or where we decide to then have to go somewhere else, could really make a difference of months at a time, so it wouldn't be any more granular in the next year.

And then on the question of whether there might be early usage of 424 in PV, as everyone knows, physicians are allowed to write a product for an indication that has not yet been approved. Of course, the manufacturer does nothing to promote that in any way. So it comes down to thinking about what the physician will know about 424 in PV. Generally they would know that through some publications, or possibly at conferences or other things where they might learn about it. Then they have to think about whether they would believe that the benefit is worth the additional risk associated with a product that hasn't yet been approved, and that indication. And then they'd probably factor in whether or not the product would be reimbursed for that indication, which we depend on what the patient's insurance coverage is, or their willingness to pay out of pocket. So those are some of the factors that would influence whether or not there would be a usage of 424 in PV prior to our receiving the indication in that.

Our last question is coming from the line of Mark Monane with Needham & Company. Please state your question. Mark Monane - Needham & Company: My question is this. Where do you see the place in therapy for 424 in patients with PV and do you have any comments on possibly the market size of that specific population?

We would be studying it in patients who are HU resistant or intolerant. And as discussed, that is a 3:1 ratio, and it's about, say, between 20% and 30% of the total PV population of 95,000. And since they really don't have many other alternatives, I would think usage in those segments could be fairly robust once the drug is approved in those indications.

Seeing as we have no further questions, I'll now turn the floor back over to Dr. Friedman for any closing remarks.

Before I make closing remarks, I just want to clarify two points. One is, most of the analyses that I've looked at on the percentage of people in the PV population who are either HU intolerant or resistant is near the top end of the range that Pat just enumerated. So more like 30%. Secondly, we thank you for joining us this morning. There were a lot of good questions, and we look forward to keeping you informed of our progress. And with that, we'll end the call. Thank you again, and good morning. 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!