ImmunoGen's CEO Presents at 2013 Morgan Stanley Global Healthcare Conference (Transcript)

Sep.11.13 | About: ImmunoGen, Inc. (IMGN)

ImmunoGen, Inc. (NASDAQ:IMGN)

Morgan Stanley Global Healthcare Conference

September 11, 2013 9:10 AM ET

Executives

Dan Junius – President, Chief Executive Officer

Analysts

Yigal Nochomovitz – Morgan Stanley

Yigal Nochomovitz – Morgan Stanley

I think we’re ready to start. Thanks for coming, everyone. My name is Yigal Nochomovitz, biotech analyst at Morgan Stanley. I’m very pleased to have with me his morning the CEO of ImmunoGen, Dan Junius. This is meant to be an interactive session, so there are microphones circulating around the room and I encourage you to raise your hand and ask questions at any point during the conversation. So Dan, welcome.

Dan Junius

Thank you.

Yigal Nochomovitz – Morgan Stanley

Happy to have you here. Maybe at a high level, give us an overview of ImmunoGen programs, both proprietary as well as some of the partner programs for those investors that are less familiar with the story.

Dan Junius

Sure, be happy to. Well, thank you to Morgan Stanley for inviting ImmunoGen to participate this year. I’m very happy to be here.

Maybe to start, just to characterize the company, the company is what we believe is the leader in the ADC – the antibody drug conjugate space. We’ve been developing this technology for quite some time. We have a depth of understanding of all of the important components – the cell-killing agent, the linker, the antibody, the target, the characterization of the target – so we think we bring a lot of expertise into what is becoming a very prominent technology in oncology.

We would characterize ourselves as in one sense development stage, given that our proprietary programs are all in development, the most advanced being in Phase II; but I guess we can lay some claim to being a commercial company as well since the most advanced partner program was approved by the FDA for use in the U.S. earlier this year in February, and I’ll come back to that.

But across the pipeline today, we have, I’ll say, 12 compounds in the clinic. A little bit of an asterisk in that one has been—is an IND that’s been approved but we’ve not yet dosed our first patient, but I’ll take some license and count that as one of the 12. Four of the 12 are proprietary, eight are through partners, and briefly I’ll walk through both. So if we start with the proprietary pipeline, we have four compounds across a range of indications. The most advanced is what we call IMGN901, which is in a Phase II study today for first line small cell lung cancer. The target for this, CD56, is also found on a variety of other cancer types, but at the moment we’re concentrating on small cell as the pathway to registration. We should complete enrollment in this Phase II – and I’m sure we’ll come back and talk about it a little bit more – but we should complete enrollment sometime really within the next several weeks, which should allow us to have data to make some later stage decisions by the middle of 2014.

There’s a second program that we have, is IMGN853. This targets the folate receptor alpha. This is a target that’s over-expressed on a variety of cancers, the most prominent being ovarian but also on adenocarcinoma non-small cell lung cancer as well as endometrial cancer. This is in a Phase I dose escalation study. We’re working there to determine the dose. Once we have the dose, we’ve identified some cohorts that we’ll pursue further that will be disease-specific. We should have the dose identified in the next several months and again should be deep into those expansion cohorts with data sometime around the middle of next year as well.

The third compound for solid tumors is one that we are about to dose our first patient, and that will be before the end of this year. It’s a compound, IMGN289. This we and others find quite interesting because it follows an established pathway in that the target is EGFR. EGFR is attractive and certainly well validated as a target. It happens to be in ErbB-2 family, which similar to Herceptin targeting HER2 or ErbB-2—so it’s ErbB family, not ErbB-2 family, but ErbB family. So we have that as a similarity, and it’s a construct that’s very similar certainly in terms of linker and cytotoxin. It’s identical to what’s used in the approved product use in our technology, Kadcyla. The preclinical data looks very attractive. It’s an active antibody, so we have the opportunity for two mechanisms of action in cell-killing, both from the antibody itself as well as from the cytotoxin that we attach through our technology.

And then the last clinical program is one that’s hematologic – IMGN529. This targets CD37 – again, a construct similar to Kadcyla, same linker, same cytotoxin. Again, an active antibody – it’s an antibody that preclinically showed itself to be more active than Rituxan and then by adding the ADC technology we enhance the overall potency of the compound.

A fundamental feature of this technology is as a targeted chemotherapeutic, the intent is to be able to deliver a potent agent to a cancer cell, impact and kill the cancer cell while minimizing impact on healthy tissue. So as a contrast to traditional chemotherapeutics, it doesn’t have the systemic toxicity that you see with traditional chemotherapeutics. I think that was demonstrated in a very profound fashion and continues to be as we see data from the compound Kadcyla, formerly known as T-DM1, where in all of the studies that have been reported thus far, those that are comparing T-DM1 versus—whether it was against Tykerb, whether it was against Herceptin plus a taxane, has shown with the data generally about a 50% improvement in PFS with a marked reduction in toxicity to patients, so that’s made it a compound of significant interest. Data that was generated and presented at ASCO a year ago from a study looking at patients in second line metastatic breast cancer who had failed in earlier Herceptin therapy showed a significant improvement in PFS, an improvement in overall survival that resulted in the submission and ultimate approval of Kadcyla.

That approval, we would expect would be the first of many. Kadcyla’s being developed beyond second line metastatic breast cancer. There is data that will be coming out late in 2014 for first line metastatic breast cancer. There are several studies that are being sponsored by Roche in early HER2-positive breast cancer, so adjuvant, neo-adjuvant, et cetera. There is also a registration study in second line gastric cancer underway, so Kadcyla promises to be a very effective therapy with significant potential across a range of indications.

Maybe I’ll take a breath and we can —

Yigal Nochomovitz – Morgan Stanley

Sure, okay. Thank you. So maybe starting out with Kadcyla, I think it would be helpful for our audience if you could sort of clarify the technology picture with Kadcyla in terms of which components are ImmunoGen technology – linker, payload – and whether you have rights to use the linker and payload in other assets.

Dan Junius

Yes, I’d actually—in answering it I’d sort of turn it the other way. We own the linker and payload. We have the composition of matter patent on Kadcyla, so we contributed that technology. The piece of technology that came from Genentech was trastuzumab, the antibody that is marketed as a naked agent as Herceptin. But we own the composition of matter patent on the SMCC linker as well as on the cytotoxin itself, as well as methods of manufacture, et cetera. So the reason I turn it the other way in saying Genentech had to come to us for rights to use that, as opposed to them having any ownership of that technology.

Yigal Nochomovitz – Morgan Stanley

Okay, terrific. And then on a high level, can you talk about how does the company think about licensing an ADC technology, and what are the issues that come into play in terms of choosing your technology versus a competing technology? Is it something based on economics, like a bake-off, or is it looking at the underlying technology evaluation or some other issues?

Dan Junius

Yes, that’s a world that’s evolved quite a bit. Our first license, I think, goes back to 2000, was actually the HER-2 license with Genentech, and Genentech licensed access to ADC technology from both us and from Seattle Genetics, the other company with an improved ADC, and worked them both through the development path. So that one was clearly a technical bake-off, and I don’t know what the terms of their licenses were but I can’t imagine it was economically driven, and based on that assessment chose to go forward with our technology. We’re very pleased with that and pleased with the outcome.

I don’t think that since that, we’ve seen any evidence of a pure live technical bake-off where someone has licensed the same target from both parties and then did the development work that we saw with Genentech. I think the way the process generally goes is that, one, a partner would want to make sure targets of interest are available, because all of our licenses are done on an exclusive basis. So to the extent a party had an interest in a specific target and comes to us, and either we’re working on it or it’s been licensed to a third party, that’s not available and that would force them to pursue other alternatives.

Beyond that, I think that most of the work done by parties is to assess available data, clinical data, preclinical data across our technology, other parties’ technologies, and from that they would then make a decision of what path they want to pursue. I don’t think economics are a driver here as I’ve watched terms evolve in this space. As best I can tell, economic terms between us and, say, Seattle, who also has a mature technology, appear to be comparable. Companies going in another direction and going with earlier stage firms with unproven technology, I think there are probably other considerations that come into play. My guess is the economics aren’t as rich. It gives them an early entry point to play with such technology and see if that’s going to apply.

Yigal Nochomovitz – Morgan Stanley

Terrific. So you mentioned Seattle Genetics – maybe take a few minutes just to give an overview of your technology and the key aspects of differentiation for some of the competing ADC platforms. What do you see as unique to your approach?

Dan Junius

Well, there certainly are similarities. There are some differences. I guess even before getting into that, I would make the point that this was a topic of probably greater import four or five years ago when both Seattle and ImmunoGen were looking to build their organizations based heavily on a licensing strategy. I think we both have evolved with proprietary compounds as that’s the predominant method of building value, and I think that while we will still do additional licenses, it’s not as significant a priority as it might have been four or five years ago.

But to answer your question, there are similarities. We both use a cell-killing agent that is a tubulin inhibitor. I think that’s important to note that the two leading technologies do use a tubulin inhibitor because aside from the targeting that exists with the fundamental ADC technology of using the antibody as a means of hitting a cancer target with less exposure to healthy tissue, the fact that you’re using a tubulin inhibitor provides a second level of discrimination, if you will, for the agent in that if you do have a target expressed on healthy tissue, you’re delivering the ADC, it’s internalizing, delivering the cytotoxin, but if the cell isn’t dividing, it’s not going to do anything. I think it’s important to think about that in terms of how the technology has advanced, because ADCs with less discriminate cell-killing agents are going to face a toxicity issue of, but what’s going to happen with the healthy tissue that expressed the antigen?

So that’s a similarity. I think the most significant contrast is how we attach—we each attach our cytotoxin to the antibody. We use a methodology that’s not disruptive to the antibody itself. It attaches to lysines that are not structural to the antibody. Seattle’s technology uses—goes and actually breaks a cystine link within the antibody and attaches their cytotoxin there. The only difference that can be seen thus far – and it’s not clear that it’s a critical difference as both of us have advanced compounds through into commercialization with the technologies – is that it appears that based on the clinical data we’ve seen thus far, with their technology they dose up to—I think the highest dose thus far is 2.3 mgs per kg. We’ve had dosing with some compounds that have gone up into the 7 to 8 mgs per kg-type range with tolerable doses. The reason that could be important is if you’re working with an ADC where the antibody is an active agent, you want to be able to get up to a higher dose or get more antibody in to have sufficient exposure to have the antibody be active. You may not need that if you’re simply using the antibody as a targeting vehicle to deliver the cytotoxin, so I think that would be the most significant difference.

Question-and-Answer Session

Yigal Nochomovitz – Morgan Stanley

Okay, terrific. Let me just pause here and see if we have any questions from our audience. Okay, great.

So turning to the lead proprietary program, to 901, maybe you could take a few minutes to just discuss the structure of that randomized trial, the change that you made in the dosing, and the fact that you have seen some peripheral neuropathy with that agent and how does that impact the product’s development.

Dan Junius

Sure. A little bit of history – so 901, as I noted earlier, targets something called CD56. CD56 is expressed on a variety of cancers. It’s expressed on healthy tissue as well – it’s expressed, for example, on NK cells. We examined 901 because of the expression across a range of tumors in a couple of different solid tumor studies, as well as in a multiple myeloma study, both as a single agent and in combination. And across those studies, we saw activity that convinced us that we had an active agent. In particular, looking at a solid tumor study focused on small cell lung cancer in later stage patients, we saw activity. Now, not the profound activity that would get people excited, but enough to say that we’re getting—if you’re getting activity in late stage small cell lung cancer patients, you always have to take into consideration what’s the nature of the underlying disease that said, this is active if we’re able to either develop responses or extended stable disease in late stage small cell lung cancer patients.

So it was that clinical underpinning or platform along with preclinical work that we did looking at 901 in combination with the existing standard of care for small cell lung cancer, that convinced us that we should pursue that as the registration pathway. We set up a Phase I/II study, the Phase I portion being to establish the MTD and the dose that we would take into Phase II. We conducted that and established a dose at 112 mg per kg in two consecutive weeks in the three-week cycle, and initiated our Phase II study.

What we found – and as you referenced – as we got deeper into it, we were seeing a level of peripheral neuropathy that was being disruptive to patients receiving the full dosing over the six week cycle that they would get the triple combination of 901, Etoposide and Carboplatin. And at that point in time, we made the determination that we would reduce the dosing, the initial dosing from 112 down to 90, and put other structures into place so that there was manifestation of peripheral neuropathy that the physician could respond accordingly and either delay or further reduce the dose.

Not unusual at all to see that in a study. Obviously we wish we’d seen it in the Phase I to establish it at 90 mg at the outset, but we think that we saw it early enough to allow us to continue to generate good data from this randomized study. It’s randomized two patients at the triple combination for each one patient that gets the existing standard of care. We also expanded the study from what had been originally designed as an 120 patient study to 135 patients to ensure that we had a sufficiently robust data set for the patients who are going to be initially dosed at 90 mg per meter squared.

In terms of this, obviously a question around, well, is that going to be a sufficiently potent dose to impact the patients – again, across the earlier studies that we saw, my observation would be once we hit a threshold level, there wasn’t a meaningful improvement in activity as we increased doses. It would suggest that we had sufficient saturation at I won’t say low doses, but at doses certainly below what we’re seeing at 90 mg per meter squared, to say that that should be a sufficient dose to stimulate activity within the patient.

I’d also point out that even though we were looking at 112 mg per meter squared, remember this is on top of a fairly potent regimen of Etoposide and Carboplatin, so that’s being dosed at its full prescribed level, and even though we’re at 90 mg per meter squared, again it is on top of that full Etoposide/Carbo regimen. So it slowed us down a little bit in terms of having to adjust the dose, but by the same token it’s been very well received by the investigators. Enrollment has been very strong from the moment we made the change. We will complete enrollment this month, which should put us in a very good position by the early to middle part of next year to begin to have the data and examine the data that will inform us as to our next decision.

Yigal Nochomovitz – Morgan Stanley

And maybe talk in a little bit more detail about the evidence that you have at 90 as well as at lower doses that supports efficacy there. I understand you have some data as well in Merkel cell at lower doses that showed some good responses.

Dan Junius

Yes. Merkel cell is an interesting indication, relatively small level of incidence – about 1,000 patients a year in the U.S., about 1,000 patients a year in Europe. And we have some experience with it because it is another CD56 positive cancer. It biologically has similarities to small cell lung cancer, and in dosing patients in one of our earlier studies, we saw—some would say three, some would say the four. The fourth was a little bit difficult to get your arms around, but we saw complete responses in these patients, and that’s out of about 23 patients that we saw overall. So not a high frequency, but very strong responses with a very limited number of doses, so another affirmation to us that we have an active agent.

People question, well, why don’t you pursue Merkel cell on this registration strategy? Because of the small population, because these patients were going to a complete response after four or five cycles, and in one case it was a 40 mg per meter squared, to get directly to your question, so a relatively low dose, it’s more difficult to develop a viable commercial strategy. It doesn’t have the characteristics of a chronic disease with a small patient population where you’d be dosing patients over a period of time. If you’re generating complete responses in a small percentage of patients after four or five doses or four or five cycles, it’s difficult to see how you can develop a viable commercial strategy there.

But it did provide some encouragement around activity. It did indicate that a threshold level, once achieved, can generate activity, and the threshold being well below what we’re looking at the 90 mg per meter squared level.

Yigal Nochomovitz – Morgan Stanley

Okay, great. Maybe if you could spend a few minutes just talking about the dose escalation work for some of your other compounds; and very briefly, you have seen some toxicity there. It’d be very helpful if you could help our audience understand why you’re seeing that, or if that’s to be expected, and what your approach is to finding the right dose across some of your other agents – 853, 529 for example.

Dan Junius

Yes, a broad comment around toxicity. We have—you have to take into consideration the characteristics of our portfolio. Two, soon to be three of our clinical programs are in Phase I – that’s the dose escalation phase. You’re dosing patients until you encounter toxicity. You want to get to what’s termed the maximum tolerated dose. To know what the maximum tolerated dose is, you have to understand what the intolerable dose is. So I think that there is too much being made out of toxicity when you’re going through dose escalation, because you need to get to that point to understand the safety characteristics of the compound.

What we’re doing in the individual, in 853 and 529, 853 we had data at ASCO. We noted we had dosed patients as high at 7 mg per meter squared. We did encounter what we have seen in a couple of other compounds, so we understand the profile. We saw some ocular toxicity. It’s reversible. It can be addressed through dose reduction, so once we saw that, we then began to modify the dose. So we’re working our way through that to understand what the tolerable dose would be that would eliminate that manifestation. It’s not unique to our technology. It’s been seen with other tubulin agents – it was seen with Abraxane, for example, as that was going through development. It was addressed through a dose modification strategy. So it’s not one that we’re terribly concerned about. We understand it quite well and we think that it’s entirely addressable.

We also made the comment in our call after our—I guess it was after our June quarter around our 529 compound. Recall I mentioned at the outset, 529 is a compound that targets CD37. It’s got a very active antibody that we now have added our cytotoxin technology to, our ADC technology. We commented in the call that we had seen toxicities at a much lower dose than we would have anticipated. I think this potentially is attributable to the level of activity of the antibody to be determined, but again not terribly unusual to encounter some toxicity. It’s part of drug development. We’re doing the work to understand the drivers, what we can do to mitigate the toxicity that we’re seeing here so that we can continue to dose escalate.

I think it’s important – people focus on the comment about toxicity. It’s not without also seeing activity at a very low dosing level, so the fact that you’re seeing both gives you something to work with, as opposed to if you’re seeing toxicity without any patient benefit. That becomes a somewhat higher hurdle to overcome.

Yigal Nochomovitz – Morgan Stanley

Sure. Speaking of the proprietary programs, what’s the sort of the higher level strategy there in terms of what to keep fully owned by ImmunoGen versus when you might think about some partnering to leverage the economics.

Dan Junius

We’ve stated that with the, what I’ll term the existing clinical programs – that would exclude 289 since that was outside the scope of what our thinking is at the time we’ve made the statement, is that we certainly want to keep 100% of the ownership of those compounds through proof-of-concept. We think that that’s a very significant value inflection point and so we wouldn’t consider partnering before that. There has been interest from parties, but we don’t think that’s in the company’s and our shareholders’ best interest.

At the point in time that we achieve proof-of-concept, we will evaluate different strategies. One that I think has significant appeal is to look at, at least for the first compound that reaches proof-of-concept, some structure that would allow for partnering ex-U.S. rights, retain the U.S. for development by ImmunoGen. We do aspire to being able to commercialize our product over time, one or more products. But I think that bringing a partner in at that early stage will provide some risk mitigation, will allow us to work with a global partner who can address many of the regulatory payor commercialization issues on a global basis that may be difficult to us to effectively address while we’re looking to develop a compound.

The other reason I think it can be very important is when you think about each of the compounds that we’re developing, they have application across a range of indications. So if you’re going to effectively develop these, you’re not developing it for a single indication. Once we get proof-of-concept, so maybe when we get there in small call lung cancer, you immediately want to begin to look at the other indications and put together a broader development strategy, and I think by working with a partner ex-U.S., you have the geographic dimension that gets addressed but also the opportunity to more broadly pursue indications that would be more difficult to address advancing it on our own.

Yigal Nochomovitz – Morgan Stanley

Coming back to 901, clearly there’s a decision to be made there – no-go versus go next year. Discuss what are the ingredients into that decision. There’s the PFS endpoint, but clearly overall survival is also relevant to the decision, I would think. How does the FDA think about PFS versus OS in small cell lung cancer, and your view as to the quality of the data that you need to move that program forward.

Dan Junius

The nature of small cell lung cancer and the unfortunately very short or narrow period of time between PFS and OS makes that probably not a difficult one to deal with. The expected progression free survival, or the mean progression free survival is about 5.5 months with extensive small cell lung cancer. Overall survival is nine to 11 months, so you’re not dealing with a significant period of time.

Response rates, actually, with patients to the current standard of care are pretty good – they are upwards of around 70%. The difficulty is there is no durability, so what we’re looking to bring to these patients is extending the durability of the response that they can get from the current standard of care.

As we look at the data and try to assess what our decision will be for further investment in advancing the compound, we’re going to be looking at all of the data. Obviously PFS—by the time we have mature PFS data, we will have some insight into survival as well because it won’t be for the full data set, but for certainly a meaningful number of patients we’ll have some insight to understand survival trends, so hopefully that will be sufficient to allow us to make the decision.

At the same time, what we’re doing is collecting data around the patients that may further inform us, looking at—well, we’ve indicated that roughly 95% of all small cell lung cancer patients express CD56. There is some modest stratification of expression level, so it will give us—as we’re collecting this data, we can understand PFS, understand OS on an aggregate basis, but also understand whether there is some differentiation based on expression and some other characteristics we’re collecting that may give us some insight to make a more informed decision.

Yigal Nochomovitz – Morgan Stanley

In the few minutes we have left, I think it’d be helpful just to hit some of the upcoming news flow for the company, both for you as well as your partners. Sanofi is going to have data for the anti-CD19 drug, 3419, and DLBCL. Maybe talk a little bit about that and how Sanofi is handling that program, as well as the data coming up very soon at ESMO for THERESA in the third line metastatic breast.

Dan Junius

THERESA data will be interesting. This is for late stage HER-2 positive metastatic breast cancer patients. It will be interesting data. I don’t know that it will be—it’s not going to inform anything around the label. Since these patients are already addressed within the existing label for Kadcyla in the U.S., but it should be informative to the oncology community about the applicability of Kadcyla for these later stage patients.

To stay with Kadcyla, we would expect to see data late next year around the first line metastatic study that’s underway, MARIANNE, that they have slated for submission in 2015. In 2015, we should also see data for their second line gastric study, so there will be on a regular basis data coming out on Kadcyla.

You asked about Sanofi and 3419. That’s one that they have in Phase—I think three different Phase II studies, two of them for DLBCL, one for ALL. We know that they are excited about that, they’ve put a lot of work into it in terms of being prepared to advance that into later stage studies. We don’t like to get ahead of our partners in terms of either announcing when data will be available or certainly disclosing the data, but we’re excited to see them moving that to the stage where they’ll be disclosing data at an upcoming conference.

For everyone’s awareness, Sanofi is in a relatively broad partnership with ImmunoGen. They have three compounds in development, two of the ADCs. They actually have a third that’s a naked antibody that we developed on their behalf when we had a broader research collaboration. That particular antibody targets CD38. CD38 has become a relatively attractive target with some rather prominent partnerships put in place with major players for CD38 targeting compounds. And the third clinical compound they have targets DS6 – this is an ADC. The target is found on ovarian cancer, so it’s been in a dose escalation study for some time. I would expect we would be hearing about both of those compounds over a reasonable period of time.

Staying with partners for a moment, we have eight partners. I think I mentioned at the outset there are eight clinical compounds today with those partners. Two of the most recent with Lilly and Novartis are earlier stage and are moving compounds forward, but I think that for the clinical portfolio, we’ll see a significant amount of data coming forward between now and, say, mid-2014, potentially in some cases providing updates a la 3419 with their Phase II data; with others, our first glimpse of what the clinical data looks like for a variety of compounds.

For our proprietary portfolio, as I mentioned again, a lot of our data is going to cluster around the middle of 2014. That’s when we would expect to have the data on the small cell study. We would look to announce the results of our decision and top line data at that point in time. The actual data itself will be targeted to an appropriate medical conference mid-2014 or maybe shortly thereafter, depending on when the data is available.

853, we did have data at ASCO. We would expect to have an update roughly again mid-2014 for the balance of the dose escalation study and potentially some insight around what we’re seeing from some of the disease-specific expansion cohorts. 529, with the lay or the need to look at a pathway forward with 529, we had hoped to have initial data at ASH this year. That’s going to push that out a little bit, so it may be mid-’14, it may be later in the year. We just have to see how all of that evolves.

And then for 289, this again is the EGFR targeting compound. Assuming we get our first patient dosed in the next couple of months, we just have to see how patient enrollment goes, dose escalation goes. I think that one of the elements that investors will be looking at is have we been able to address the skin toxicity that you see with existing antibody-based agents for EGFR expressing tumors, and it’s possible that we would have enough enrollment to have some insight into that to potentially talk about that by mid-’14. But even by mid-’14, we’ll still probably be in the dose refinement stage.

Yigal Nochomovitz – Morgan Stanley

And in the last minute we have, just a few financial questions. Talk a bit about the CFO search and the characteristics of individuals you’re liking to fill that role, as well as any potential plans as far as Kadcyla monetization and how you think about that as far as driving your financial needs.

Dan Junius

Well getting to the second question first, we ended our fiscal 2013 with about $195 million in cash, and the guidance we have given is that we have sufficient cash to take us through our fiscal ’15. So we’ve got a reasonable runway with the inflow of royalties from Kadcyla, with other partner revenues that are generated. We feel quite comfortable with our current position.

Royalties – you know, royalty monetization is an option that we are very pleased to have available to us, but given the fact that we don’t in the short run feel that we need to do any meaningful financing, that’s one that simply is there as another tool once we have that type of decision to make.

On the CFO search, we’ve had quite a bit of interest. What we are looking for with a CFO is one who brings to the company insights from their experience in working with other companies, good street knowledge, someone who has credibility with the analyst community, and frankly someone who can function well within the executive team and help us with many of the important strategic decisions we’ll have to make as we’re seeing our proprietary portfolio evolve over the coming quarters and years.

Yigal Nochomovitz – Morgan Stanley

Okay, terrific. I think we’re going to have to call it there. Thank you very much, Dan, appreciate it, and good luck with the rest of the year in 2014.

Dan Junius

Thanks, Yigal. Thank you.

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