Pfizer (PFE) Management Presents at Citi Global Healthcare Conference (Transcript)

| About: Pfizer Inc. (PFE)
This article is now exclusive for PRO subscribers.

Call Start: 14:10 January 1, 0000 2:48 PM ET

Pfizer Inc. (NYSE:PFE)

Citi Global Healthcare Conference Call

December 8, 2016 14:10 ET

Executives

Mikael Dolsten - President, R&D

Analysts

Andrew Baum - Citi

Andrew Baum

All right, I have a couple of slides. Okay. I'll -- so I think we're going to start the session if everyone would like to take a seat, it's the last session of the last day, so from here on in, it’s home run. So -- look, thank you for joining us today. We're delighted to introduce I guess speaker for this keynote, Mikael Dolsten. Mikael is President of Pfizer R&D as many of you know. We've also got Chuck Triano and colleagues who run the Investor Relations team with us in the audience today. I know Mikael wants to stay to give us a brief overview and then we'll just take segue to the Q&A. So thank you for joining us.*

Mikael Dolsten

Thank you very much for inviting us here. Like always, we start with forward-looking statements that include cautionary language about our presentation. You can find a copy of the slide at our filings and our webpage.

So we wanted to just have a kind of a quick glimpse as we have -- look at our track record since 2010-11, year to today. As we have kind of focused only on what we think are the most productive areas. We have built a portfolio with a mix of small molecule, biologicals and vaccines, and a highlight to some of the -- about 20 key approvals since that starting date of which about half are new medical entities, on average three approvals per year, one to two of them being NMEs. And you note, IBRANCE, our leading novel cell cycle inhibitor for hormone receptor positive breast cancer. Prevnar 13, the number one vaccines in the world including more recently, adult indication next to the previous infant; INLYTA second line renal cells carcinoma; XALKORI, [indiscernible] poster child for treatment with precision medicine lung cancer; XELJANZ, the first launched JAK inhibitor for inflammation diseases, RA; Eliquis that are preferred by cardiologists, noval oral anti-coagulants for stroke prevention, venous thrombosis. And to the right, two of the recently acquired drugs with either marketed for some indication like Xtandi in prostate cancer, metastatic prostate cancer, and Crisaborole which is in late registration phase, PDUFA date, early January next year for atopic dermatitis.***

When you look at the pipeline that deliver this flow of Phase 3 and approvals, we have about 90 projects. Slightly more than 40% in Phase 3 registration, slightly less than 40% in Phase 1, and about 20% in Phase 2; about two-thirds are NMEs and about 50-50 are small molecules versus biologicals; and that really is quite aligned with the goals that we set a few years ago.

2016 has been a productive robust year for us. We added a second indication IBRANCE in U.S., the re current breast cancer in fibroid [ph] and we got approval for both, advanced and recurrent breast cancer in Europe. I'm making it clearly - the class leader in both continents.

XALKORI was approved for a second indication, ROS positive non-small cell lung cancer, and we're actually exploring a third indication, a MET positive lung cancer in our clinical development. We added a once a day formulation of XELJANZ and Prevnar 13 got approved for infant in China expanding it to a very important market for future use in prevention of pneumococcal disease.*

We are in submission Phase 4 of a few different drugs. Inotuzumab and Mylotarg are two classical antibody drug conjugates for liquid tumors, both in filing phase for U.S. and Europe. Inotuzumab has also breakthrough designation. In immune-oncology we're able to move our PD-L1 inhibitor to the first filed indication, Merkel cell carcinoma where we have both breakthrough status and [priority] [ph] review.

And finally, we expect project end of this year ertugliflozin to be filed in three different forms together with U.S. Merck, monotherapy, fixed dose with JANUVIA and fixed dose combination with metformin.**

So looking at the earlier to mid-stature of the portfolio in 2016, I think we had a quite good momentum in building up a portfolio with a number of very meaningful and some really transformational drug opportunities.

In Alzheimer we have now focused on secretion inhibitors and we have a clinical Phase 1 data that are favorable, shown potency in reducing amyloid for BACE and the first Gamma Secretase Modulators that has a design and activity in clinical studies. The other component in Phase 1 that I wanted to highlight is to with the best of my knowledge the most advanced dual Tyk2/JAK1, really interesting profile based on what we learned with XELJANZ and particular Tyk2 extend activity to inhibit IL-12, IL-23 like cytokines which we think will be critical for improved profiling diseases like psoriasis, Crohn's, [indiscernible] etcetera.***

I'm very pleased to share with you that's our C. difficile vaccine which is a unique high-technology genetically engineered two-component vaccine has reached positive proof-of-concept criteria showing very high percent of individual reaching the bar for meaningful immunogenicity levels against the two toxins and their levels reached were regarded as very high in a large number of individuals.

Recently at ASH we communicated at Glasdegib a SMO [indiscernible] inhibitor had favorable data in a subset of AML. And we have shared I think six different Phase 3 studies ertugliflozin, a top line level as we prepare for submission. XELJANZ is now reaching its second step, going into new regions, and new indications. Tofacitinib, the active ingredient reported strong data in ulcerative colitis, psoriatic arthritis, and we are in advanced registration phase for the RA indication in Europe. You can also see some of the early phase assets P-cadherin Bi functional antibody, a really novel agent which is now the number 10 immunoncology NME in our pipeline in the clinic.***

A JAK1 inhibitor dosed in atopic dermatitis, we think it has a profile that would hit very nicely to IL-4, IL-13 cytokines that monoclonals have shown to be very important in that disease. And then Avelumab that I mentioned briefly for Merkel cell carcinoma, started six different phase 3 [cross][ph] solid tumors including one additional combo study with Inlyta for renal cell cancer. We think Inlyta has a really interesting profile as a targeted agent together with [IL] [ph] compounds as shared earlier when we combined it with KEYTRUDA from U.S. Merck.****

Very briefly when it comes to internal versus external, we really have our strategic ambition to be a networked R&D organization, some strong capabilities internally welcoming biotech and pharma partners and you can see three example of that approach. Product acquisitions through M&A, Medivation, access to Xtandi, Talazoparib among other things, Anacor which was the company providing crisaborole, the topical PD-4 inhibitor. Next to that we have strategic acquisition of technology and early product. Bamboo is a company engaged in gene therapy and provided to us what we think is the most comprehensive manufacturing of clinical gene therapy material in the United States and also have two project for entry into neurological disease gene therapy scheduled 17 and 18 for first in humans. And then a partnership with Western Oncolytics that provides us with an oncolytic virus particularly interesting for cancer therapy of what we call cold tumors with moderate to low immune activity.****

Finally, Bind as a small technology acquisition provides us with non-particle technology and very timely we had a partnership with them exploring targeted agents in nanoparticle for prostate cancer. One of those agents seems to do very well, preclinical [indiscernible] studies would Xtandi, so we were delighted as these two acquisition very timely coincided.

I would conclude on looking at what's next when it comes to novel science and medical entities in 2017 and 2018. We are taking the next step in immune-oncology, moving the field from monotherapy to doublet and triplets and you can see there is old cohort what we think are really unique doublets and triplets with opportunity to be industry-leading in this next step of immune-oncology. We expect upto three Gene30 [ph] clinical trials going in this time period. About 10 different Phase 2 studies with next-generation JAK inhibitors across derm, rheum, and GI segments. And with vaccines, I'll end and say not yet C. difficile that we will now plan in regulatory discussions to move to Phase 3 during first part of 2017. We hope at the end of 2017 or possibly, earlier 2018, to have a breakthrough like this time of an aureus-V vaccine that we think is unique and can be really important. And finally, we are now in clinical phase with a next-generation of [indiscernible] vaccine covering up to 20 different serotypes.

I conclude on that and thank you for attention.

Andrew Baum

Thank you, Mikael. So maybe before we get into a conversation about the individual assets in your portfolio. Help us understand how you're thinking about building out Pfizer oncology from an organic basis from an R&D function because within your business you have the vaccines part, the small molecule part, biologics part, you have remap [ph] on the antibody engineering; and yet you're dealing from an immunotherapy perspective, if we believe all roads lead to Rome. Highly complex system to understand why some humans are not immune responsive, how to make achievements; and it's going to enroll carefully-timed together across the organization, lots of different parts. So are there any structural organizational changes that you think are required or do you feel the current separation that exists within Pfizer is something that is going to stay in this multiple?

Mikael Dolsten

You know, you can never be sure about the future but I would say, I think we have a very well aligned strategic structure, and let me say why. So [indiscernible] we have our center for small molecule design in cancer and it's the group that have made all this great targeted agents from XALKORI to fall on Tofacitinib [ph] to IBRANCE and are actually working right now with our next-generation cell cycle inhibitor that will address some of resistance to molecules like IBRANCE off the patients being exposed for years that we hope to having the clinic in within 12 to 15 months.

In the San Francisco area, we have our specialized immune-oncology group that have worked on the recent 4-1BB, OX40 check point modulator that brings us into what we think is leading doublet and triplet. Going back to South San Francisco, we have our cancer vaccine door-to-door with our small molecule vaccine. And the cancer vaccine has sold many years built significant capability with two perform, one is the multi-antigen vaccine that is co-administrated with CTLA-4 antibody locally and likely a PD-1 Pfizer antibody systemically. If now we're not filed for prostate cancer, and we see early interesting as signals. And we also have the oncolytic viral platform that they alluded to through a partnership.

The third group that is [indiscernible], New York, has deep expertise in functional genomics and help us identify future target that can augment activity of molecules like IBRANCE and can act in synergy with checkpoint blockade. They also are our skill center for antibody drug conjugates and nanoparticles. So I hope you got the sense that each of them have unique skills, each of them are embedded in an academic network, you need to start in the northern California or in the metropolitan [ph], New York, that has been actually instrumental for us. For example, our genomics activity [indiscernible] been in close partnership with [indiscernible] laboratories and we're pulling up some new targets that we do in chemistry honors [ph] that we think can give us in the future if [indiscernible] and cancer metabolic target that when combined with IBRANCE improved the long-lasting cell-killing substantially. So this is the type of network we have put together to tap into the best of science in United States but doing it in a complementary riding and overlapping range.

Andrew Baum

So moving down to the products and if we take the premise that here next 10 to 20 years ago, you have a long-term immunotherapy, if not much longer. And the question is how you get more patients to respond? One area which I know Pfizer has a legacy of investment in is antibody drug conjugates, and which is a map which is now what we're surfacing that I know we went to repair that investment disappointment is. Obviously the most drafted those but I know you have a raft of interesting early stage molecules, so we're talking about the PTK-7 target before we came on. So perhaps you could talk to what you have the advanced tolerability efficacy and then we can sort of segway [ph] into how we can leverage that through combinations with checkpoint blockade?

Mikael Dolsten

Yes, it's a great question. So, you know we have noted in recent team on checkpoint combination studies, that checkpoint modulated by themselves to treat the world in tumors that or what we call hot -- that high-level of PDL1 that maybe -- more than 50% of patients are positive while in corresponding similar lung cancer patients that are low and their efficacies is much more modest. Chemotherapy seems particularly in the – in this cold tumors, be able to cause cell death and damage that leads to a subsequent immune response and by combining chemo with the immune-blockade you can get probably the best of the two. We thought that going forward, and systemic chemo will overtime be a bit of the past and that's why we are quite excited about antibody drug conjugate because they carry -- in a targeted manner with better tolerability chemo into the tumor.

And I think the data that you mentioned that you observed with PTK7 showed substantial response rate in well advanced ovarian cancer, in the 30% range. Please remember checkpoint inhibitors in this space would show about half at most. We know that the key with checkpoint inhibitors is the long-lasting durability with antibody growth conjugates who get good response rate, better tolerability than systemic-chemo but you are not likely to get that long lasting response. What we have seen with PTK7 and similar construct in a preclinical studies is that tumors that are really cold, you find or [indiscernible] quickly become enriched immune cells going into these immunogenic cell death. And that's why we are very excited at the moment, we are just in the final defined phase, how our PTK7 -- PDL-1 type of trial would look like. And whether we go with PDL-1 only or in additional studies doublet to immune checkpoint inhibitors.

We do think -- whether you use ADCs or nanoparticles that are targeted to tumors, filled with selective agent that will have combined and the tumor effect favorable both, immune modulation on the microenvironment, we think that is a really interesting game for cold tumors. While for the hot tumors, we think you probably will do well when you guys double or triple IUIU blockade. So I hope that gave you a sense for how strategically we have placed our best and just -- and for the type of tumors where you have a very poor ability to provoke immune response, initially tumors that have low degree of mutational burden which is required from immune response. Those are the tumors that we will go with CAR-T platform and also with our bifunctional antibodies because you circumvent the need for this mutational burden. And this story is really how we think as Pfizer, we have built immune-oncology platform that will in the future have an ability to target a very comprehensive group of tumor patients, and possibly the most comprehensive availability's standpoint.

Andrew Baum

So on a similar vein as -- but through a different route, increasing number of patients to eminent [ph] responsive. You've obviously now taken extend DNT or portfolio. And you touched upon -- me taking above from the new antigens. I didn't see on your slide an intent to initiate the trial combining with checkpoint blockade but of course, many of your peers have done that, Astrum and others. How are you thinking about that? Where you were targeted? Any thoughts would be interesting.

Mikael Dolsten

Great question, and I'll be brief as this agents are new in our portfolio. We -- you know, we have noticed there was actually a study with XTANDI and PDL-1 inhibitor that did show added value to such small studies and this is an area we're now looking actively into, how our checkpoint inhibitors could work with a drug like XTANDI for prostate. I also wanted to mention that Talazoparib that was part of the Medivation acquisitions is used particularly for tumors that have high limitation of burden as support-inhibitor. And we think that asset will do extremely well with our immune-oncology portfolio. So that's another area where we are looking at actively what would be the best strategies for those two asset.

Andrew Baum

And then in terms of -- and this is again picking up a conversation before we started but perhaps expanding on the side on that sort of – that GUI [ph] phases of chemotherapy because to end one you may increase an epitope spreading, you may cause immunogenic cell death but on the other hands, you're creating subclonal populations of mutated -- mutations and tumor cells which may in fact move you away from having a favorable effect to chemotherapy. Now obviously, we haven't seen the data but interested in how you're thinking about that -- selecting patient populations using diagnostics noted to try and address that.

Mikael Dolsten

Yes. I think it's a great question and that's why, you know, I think there could be some concern to use chemo IL for tumors that are already immunogenic where you just need to release the brakes for PDL-1. There is enough of the immunogens available and you may not want to cause additional mutations at this stage while for cold tumors you really need to have both immune response. I think overtime there will be more sophisticated approaches than chemo, that's why we're investing in a disease where can deliver a much higher payload into tumor because mutation particular appear when the amount of chemo is insufficient. And that's also what we've added is nanoparticle platform where you can load it with as one or two targeted agents which may be a better way overtime to go than traditional chemo.

Andrew Baum

You have aside from evalamap [ph], you have CD137 for 1PP, you have OX40; so perhaps on OX40, we already saw some early data from Roche in combination with that PDL-1 which was underwhelming, frankly. So -- vast acknowledging differences between molecules and so on. As your scientists have looked for that data and thought about what to take home, what was their conclusions about whether it's dosing, scheduling, indication or molecular -- I'm interested in that. And then just last time, just on the other checkpoints, on CD137, notably it doesn't have the hepatotoxicity which Bristol [ph] has. Is that serve you to -- to the lack of all the diminished effect of function, or is that other differences on the Media type end which make us more likely to contribute to the differential safety efficacy.

Mikael Dolsten

Great question and one of my favorite topics. So thank you for bringing it up. Both Both, our 4-1BB, OX40, are designed as IDT-2 antibodies with reduced risk for 788 and cytotoxicity but with great agonist properties. So we think they optimize for signaling through the cells to augment and so staying PDL-1 in used immune responses. We have combined our 4-1BB with avelumab and earlier we combined it also with Keytruda. And data so far, which is early data, we had a little more advanced with Keytruda but data that accumulates suggests to me that this is a productive combination, good tolerability, and seem to do better than the mono PDL-1 from emerging clinical data. I would like to see more to be able to conclude where and how to use it, but I am encouraged what I've seen. OX40 as you said, showed mainly disease stabilization, some senior responses but also confirmed at some biomarkers that it was having a different profile than 4-1BB. So we are planning early next year, you always want to have a good start of the year. Then we are ready to doze to first patient with a triplet of avelumab, 4-1BB and OX40. We think it's the -- from a rational immune design, and from preclinical studies, it has all the bells and whistles to take off the break, augment cytotoxic and helper cell -- immuno cells to play against the tumor.

The second kind of doublets and triplets platform we have is Avelumab, 4-1BB with IDO1. We are right now in clinical studies with our IDO1 inhibitor that we co-discovered with a Belgium biotech company and we think for some tumors that would be a very interesting triplet. We are right now in mono and moving to doublet, hopefully end of 2017 or 2018 we will have triplets. I think both those triplets will be led by Pfizer, that's our aspiration and to the best of my knowledge we are the only company that have internal access to these four different agents, avelumab, 4-1BB, OX40, IDO1.

Andrew Baum

And presumably, I mean when I look at that first triplet that you mentioned, you've got two active costumers for your molecules and a checkpoint, presumably with those thing, you're going to start very, very, very low because of the tox risk, so that will take a while to find the dose before you can -- is that the right way of thinking about it?

Mikael Dolsten

It is a very thoughtful question. We are planning to define on pieces here. I don't think we need to start death low because we have doublet data on both of them; doublet of various combination of avelumab, 4-1BB and OX40. Each of them have shown good tolerability. So I don't think we need to start that some ultra-low and should be able to doze escalate but in principle you're right, there are a number of doze step you need to take. But we certainly June 2017 to be able to get an early read on the clinical activity, across the spectrum of tumors and then moving to dose expansion cohort in specific tumor types.

Andrew Baum

And you high costs molecule, is that in the clinic or about to go into the clinic?

Mikael Dolsten

The one that's next to go into the clinic for us is likely going to be a getter [ph] molecule. It's going to be like in the clinic second half of 2017, it adds to our [indiscernible] and offers another opportunity next to OX40 to target regulatory components of the immune system.

Andrew Baum

And this is from Rinat?

Mikael Dolsten

It's also from Rinat.

Andrew Baum

Got it, okay.

Mikael Dolsten

Rinat leads our checkpoint modulators and also to get with selective, have a capability for CAR-T cells that we are producing there. As you know we're on clinical studies with our new CAR-19. It's an allogeneic platforms so you don't need all these cumbersome, one patient, one harvests, one infusion; you can create an off-the-shelf product. The second indication that we're hoping -- 12 to 15 months or so to going to will be in myeloma with another CAR-T. Again, allogen 8 [ph] unique, likely first in the industry for both of them.

Andrew Baum

Segueing away from immune-oncology just for a second, could we talk about CDK 4/6.

Mikael Dolsten

Yes.

Andrew Baum

Well, obviously you are the industry leader and with that -- with that we have made huge impact already on the disease. The competition is maturing, now with Lilly and with Novartis. I'd like to get your impression of how much the competitive threat from a scientific safety efficacy point of view you see because frankly, we saw a drug which is going -- hepatotoxicity of QTC and is late, but I'm -- I'd be interested in whether you've seen hepatotoxicity anywhere approaching what was seen in the clinical trial with IBRANCE. There is no QTC, we know that. And then if you could comment on Novartis's comments, that they believe they will be first to market with the faslodex combination. How much do you think that's really going to change the competitive landscape, given the faslodex may become more the gold standard for managing of these patients and remind us where you are with a faslodex combination.

Mikael Dolsten

Yes, I think you summarized rivocycline [ph] but did anyone else, when you said it's late into the market with liver and cardiac rates report that's adverse events. That's me quote you, not me stating you. Our Drug as being you know, now used by 40,000 breast cancer patients. It's you know based on Paloma 2 and 3, answer yes. You know really good efficacy, it is well tolerate. Patience seems to report good life quality. That's been some monitoring for mutual feels, but clinically the patient seems to have few problems and we have not seen, this type of issues that you reported from Novartis as being part of our profiles to any significant extend. We think that the molecule has been out in the market very well perceived by physicians and patients. Established market share for as far second line exceeding 40%. And it gives us a very strong position. We are leaders when it comes to breast cancer which is adjuvant therapy to cure patients. Of course we delayed the risk of a recurrence, where we have two studies going, Penelope and Palas [ph] that we will looking forward around 2020.

Then we have combination studies in breast with a PSD-K inhibitor, we're running a few studies in other tumor types, head and neck, the pancreas, subset of full mandatory, we expect some data to share in 2017 and 2018. And then I already mention that we will put in 12 to 15 months or so, to have another sieve cycle inhibitor that can deal with resistance that inevitably unfortunately cure patients being on talk [ph] to drugs. And we have also developed a insights on how CDK 4/6 inhibitor. And move cancer cells to senescence but they take a long time before they go from 18 to cell death [ph]. And we have identified the vulnerabilities and a planning a you know, to also address additional drugs.

So I just did that journey to give you a sense of a clinical extremely strong position, breast cancer, early breast cancer or beyond breast and future combinations based on our insight. Convective first predicts that, which is the name for Fulvestrant. And we actually had date on Fulvestrant in our PALOMA-3 studies while our PALOMA-2 was based on letrosome [ph]. And (IBRANCE) combined very well with Fulvestrant.

Andrew Baum

But in terms of the registration trial with Fulvestrant.

Mikael Dolsten

I think Fulvestrant is a brand name -- that’s label template provided that they thought recurrent breast cancer is including Fulvestrant to AstraZeneca intramuscular given drug…

Andrew Baum

But that was the drug used in the trial?

Mikael Dolsten

That was the drug used in PLAOMA-3 trial, letrozole used in PALOMA-1 and 2. We have additional trials looking at other hormonal blockade including combined -- compared to chemo for certain patient type of study quote.

Andrew Baum

So -- we are going to be running out of time very shortly but one question I wanted to ask is, given Christmas is around the corner and when you're thinking about your wish list for 2017 in terms of business development; what areas you thinking in terms of either platforms or therapeutic areas; I mean you can be -- as I'm sure you won't be specific but any indication you can give of why you think you would like to bolster your organic competences. I'm sure the audience would find interesting.

Mikael Dolsten

Yes, okay, I'm reading -- I was thinking to just have a less ambitious Christmas gift and maybe that's a New Year, and thinking about what drugs do the portfolio. On one I would say we will continue to have appetite for our strategic investment areas. Right now I think we have a very comprehensive immune-oncology portfolio but we would always built and if there is a new agent appearing, you may have seen that we have invested recently in -- novel -- see, there are four construct that are aimed to be local active in the tumor to circumvent that systemic talks seen with [indiscernible]. We have two collaboration on Bioathlon [ph]. So that would be an example of novelties. Strong checkpoint modulators that to better we're active locally than systemic [indiscernible] is one example.

We have invested quite a lot in Gene's therapy, we have spectacular data to get with our Islamic song vote. Please check out the (NYSE:ASH) presentation, it's just spectacular, nine patients where you can give them synthetic factor 9 of any that down. Intense affected 9 that makes them independent of any further infusion while previously were dependent on infusions. And we're going to Duchene's Muscular Dystrophy, it would love to see us being able to change fatal outcomes for boys with that disease and we'll certainly keep our eyes open if there is another gene therapist as we have one of the -- I think best manufacturing facilities for clinical studies. Maybe you know, I should end to say that there are certain new science area; one is Nash in the metabolic space, we have, you could see last slide we have two clinical phase, KHK inhibitor and an ACC inhibitor, certainly that's -- I think a novel exciting space.

One of the few areas of metabolic disease where you could come to market without big outcome studies and I think it would be a disappointment if I didn't mention that you will always be open on your eyes for breakthroughs in neurological diseases like Parkinson's and Alzheimer's and then it's going to be a combination therapy. Maybe, new agents that deal with newer inflammation which seems to be a major culprit, that would be nice New Year's gifts. So I'm opening in the corridor for anyone that have a good suggestion of how we make the New Year's gift list comes through for -- and in myself -- and we love to have good tips. Thank you for listening in today.

Andrew Baum

I don't think I can say anything better. Listen, many thanks Mikael for joining us, thank you for the audience today and if you have further doubts, please don't hesitate to reach out. Many thanks.

Mikael Dolsten

Very pleasant to talk to you thank.

Andrew Baum

Likewise.

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!