Madrigal Pharmaceuticals Inc (MDGL) 2010 Q4 法說會逐字稿

Good day, and welcome to the Synta Pharmaceuticals fourth-quarter and year-end 2010 financial results conference call. Today's conference is being recorded and webcast. At this time for opening remarks, I would like to turn the call over to Rob Kloppenburg, Vice President of Investor Relations and Corporate Communications at Synta Pharmaceuticals. Please go ahead, sir.

Good morning, and thank you all for taking the time to join us today. With me are Dr. Safi Bahcall, our Chief Executive Officer, Keith Ehrlich, our Chief Financial Officer and Dr. Vojo Vukovic, Synta's Chief Medical Officer. This morning, we issued a press that reported results for the fourth-quarter and year-end 2010. This release can be found on our website at www.syntapharma.com.

Before we begin, I would like to point out that we will be making forward-looking statements based on our current intent, belief, and expectations. They are subject to certain risks and uncertainties, and I encourage everyone to look at the SEC filings for additional detail. I will now turn the call over to Dr. Bahcall, after which we will open the floor to questions. Safi?

Thanks, Rob, and thank you all for joining us this morning. I'll begin with a brief overview, and then turn the call over to Vojo to summarize recent clinical developments. I'll then hand the call over to Keith who will provide the financial update.

This past year, we made significant progress with Ganetespib, our second generation Hsp90 inhibitor, which is now recognized in the oncology community as the leading Hsp90 inhibitor in development. Ganetespib is in 11 Phase 2 trials with over 350 patients treated, and has shown clear evidence of anti-tumor activity and favorable safety. As many recent publications and meeting presentations have highlighted, Hsp90 remains one of the most promising anti-cancer targets, both specific gene profiles that may be highly sensitive to single agent Hsp90 inhibition and several different tumor types, as well as in combination as a means of suppressing resistance mechanisms to kinase inhibitors and certain other drug classes.

The development of Hsp90 inhibitors, however, has been limited by the safety profile of prior compounds. In the case of first generation valinomycin derivatives, these were safety issues related to serious blood work toxicities. In the case of other second generation Hsp90 inhibitors, there has been a high incidence of eye toxicities.

Ganetespib, which is structurally distinct from these other compounds in important ways does not show these toxicities. Based on the promising activity we've seen in our trials to date as well as the differentiated favorable safety profile, we plan to take advantage of our leading position, and be the first to fully capture the very broad Hsp90 opportunity. There are two approaches for advancing this program to registration, which we are pursuing in parallel. One is a single agent approach; The other is in combination.

The rationale for the first is based on the increasing number of responses we are seeing as a single agent in our ongoing trials. We are also seeing promising early signs that these responses are associated with specific gene profiles, which is very exciting. As we have reported, anti-tumor activity has been seen in lung cancer, breast cancer, gastric cancer, and others.

The rationale for the second approach, the combination approach, is based on the ability of Hsp90 inhibition to enhance the activity of, or suppress mechanisms of resistance to, certain other drugs such as taxane, kinase inhibitors, and angiogenesis inhibitors. We've seen not only pre-clinical evidence, but also encouraging clinical evidence from our ongoing trial that the combination is synergistic and well tolerated.

I will now turn the call over to Vojo who will summarize some recent results and discuss these points in more detail.

Thank you, Safi.

As Safi noted, we have some very exciting data and a very active clinical development program. In addition to the favorable safety results, which are very important, we have seen objective responses and durable tumor shrinkage in patients with a range of cancers. These patients have been heavily pre-treated, have exhausted all approved therapies as well as in many cases, a number of experimental therapies.

To see that Ganetespib, a single agent, can induce durable tumor shrinkage is very exciting to us and to our investigators. It's clear proof of clinical activity. The onset of clinical activity can in some cases be quite rapid. For example, one lung cancer patient had progressed on four prior chemotherapy and targeted patients, including carboplatin, taxol and avastin, had been in pain for a long time. Within two weeks of starting treatment with Ganetespib he reported being out of pain for the first time in a long time. This patient showed a response on his first eight week scan.

The results we represented two weeks ago at the IASLC Lung Cancer meeting showed the Ganetespib is active in non-small cell lung cancer. When average patients receive Ganetespib as fourth-line therapy and some patients have received as many as 10 prior regimens. In historical trials, response rates in less refractory lung cancer and best supportive care control arms have been less than 1%.

Of 33 available patients in our trial, approximately 33% showed tumor shrinkage which is impressive considering patients have growing tumors before entering the study. Of these, three exhibited durable confirmed resist responses. All the three patients with response are continuing treatment. One of the most exciting aspects of Ganetespib to us, and our collaborators, is the number of important client protein targets, which suggests multi-tumor application.

We have been very excited by the activities seen in lung, but are equally encouraged by responses seen in a number of other tumors. For example, a 39 year old woman with metastatic triple negative breast cancer was recently involved in a single agent Ganetespib trial. She had previously received six regimens of chemotherapy involving nine different drugs and had progressed on all these treatments. At the end of her fourth cycle single agent Ganetespib, she showed a 31% tumor shrinkage.

We also enrolled a patient with -- gastric cancer who had previously received and progressed on six chemotherapies. This patient also showed a greater than 30% tumor shrinkage following single agent Ganetespib. As many of you know, the unmet medical need in those indications is extremely high. Triple negative breast cancer is the most difficult to treat form of breast cancer, and treatment options for gastric cancer are very limited.

As Safi mentioned, we have a two-pronged approach for advancing Ganetespib towards registration. The first is to further understand the nature of these single agent responses including genetic profile and other biomarkers. In association between clinical response to single agent Ganetespib and genetic profile would create the promising path to registration in the biomarker defined subpopulation. We are seeing promising signs. There are just such (inaudible) due to genetic profiles, patients with what might be called Hsp90 addictive cancers.

In addition there's been a great deal of work done showing that Hsp90 inhibition can enhance the activity of, or suppress mechanisms of resistance to, certain other drugs such as taxanes, kinase inhibitors and angiogenesis inhibitors. While there exists the potential for combination with multiple therapies, have been particularly focused on taking advantage of the promising activity seen in combination with taxanes. Taxanes are used in over 0.5 million cancer patients annually in the US alone. In our Phase I trial of Ganetespib in combination with docetaxel, we have identified a dosing regimen we plan to take forward.

As we announced a few weeks ago, we're initiating a registration enabling Phase 2b-3 trial in non-small cell lung cancer. The first stage, Phase 2b portion of the trial, will enroll approximately 240 patients. We anticipate having early results from this stage by the end of this year, or in the first quarter of next year. The Phase 2b portion will be used to establish a safety and activity of the combination as well as to optimize the design of the Phase 3 portion. For example, we may use information obtained in Phase 2b to refine patient inclusion/exclusion criteria in order to enrich the Phase 3 for those patients most likely to benefit from Ganetespib.

We believe that this trial design provides four distinct advantages. The combination applies both aspects of the Hsp90 mechanism, the single agent therapy and the chemo synthesization. Also, it reduces clinical risks of the Phase 3 by identifying patients most likely to benefit. It also reduces operational risk and most of the Phase 3 Synta's and physicians will have experience with the regimen from Phase 2b. And finally, we believe that this operationally seamless design saves considerable time in transitioning from Phase 2b to Phase 3.

Before I turn the call back over to Safi, I'd like to say that I'm very excited by the clinical activity we're seeing, the receptivity among oncologists and the broad opportunity for Ganetespib. The growing number of top-tier investigators who have adopted Ganetespib and are taking it forward in different indications, and the strong vote of confidence in the clinical results seen to date and the potential of this drug.

Safi?

Thanks, Vojo.

The examples Vojo described of patients with little or no alternative treatment options responding strongly to Ganetespib are particularly inspiring for all of us at Synta, and especially for the Synta scientists in our labs who created this molecule eight years ago. I would like to recognize these scientists and thank them for their hard work.

Before passing the call on to Keith, I would like to make three brief comments. First, on this call, we're focusing on Ganetespib, in particular, our plans in lung cancer. That's because the Phase 2b-3 trial in lung cancer is our largest Company-sponsored commitment this year. We are also encouraged by what we have seen with elesclomol, but the randomized trial for elesclomol is a much smaller near-term financial commitment, and will not start in full randomized mode until fourth quarter. We expect to discuss that program in more detail later this year.

Second, we are fortunate to have attracted many investigators from top-tier institutions such as the Dana-Farber Cancer Institute, Memorial Sloan-Kettering in New York, Johns Hopkins, Vanderbilt, Emery, and many others to work with us on Ganetespib. Because of that, we have a broad and exciting development program with high attention from leading scientists in the field. The collaborative nature of this program with many investigative and cooperative group sponsored studies also means that our costs are much less than if these programs were Company-sponsored.

Finally, we are entering an intensive period of partnership discussions, with several potential partners reviewing more than one program at the Company simultaneously. We are confident we will conclude one or more partnerships this year for one or more of our three most advanced programs.

I will now turn the call over to Keith, who will briefly review our financial results.

Thank you, Safi, and good morning, everyone.

Total revenues in the fourth-quarter of 2010 were $4 million. Total revenues in the same period of 2009 were $4.7 million. A research agreement with Roche, which concluded at the end of 2010, provided $1.9 million on $3.5 million of cost sharing reimbursement revenues in each of those periods, respectively. In addition, we recognized $1 million in the fourth quarter of 2010 for grant revenues earned and paid under the Federal Government's Therapeutic Discovery Tax Credit program.

In the fourth quarter of 2010, our Research and Development expenses were $9.3 million as compared to $9.2 million for the same period of 2009. Our fourth-quarter general and administrative expenses were $3.1 million as compared to $2.4 million for the comparable period in 2009. In the fourth quarter, our net loss was $8.8 million or $0.21 per basic and diluted share as compared to a net loss of $7 million or $0.21 per basic and diluted share for the same period of 2009.

As of December 31, 2010, we had $51 million of cash resources on hand. Based on our current operating levels, we expect our cash resources will be sufficient to fund operations into 2012. Certain new clinical programs contemplated for 2011 will be conducted, subject to the availability of sufficient financial resources.

I'll now turn the call back to Safi.

Thanks, Keith. We'll now open the call to questions and discussion. Operator?

Thank you. (Operator Instructions) Thank you. Our first question is coming from Jason Kantor of RBC Capital Markets.

Hey, guys. Thanks a lot for doing the call and congratulations on some interesting data presented over the last couple of weeks. Anyway, wanted to hit on the cash question. So, two things. One is that your cash is sufficient to fund operations into 2012. Is that just barely getting into January or is that getting you somewhere into the second half of 2012? And then similarly, you say that certain 2011 programs will be conducted depending on access to funding. Which programs are those programs that you've outlined as milestones this year, or are those programs that we just haven't heard about because of pending funding?

Jason, this is Safi. In terms of the cash on the programs, as we said, we're in so many highly intensive partnership discussions around our programs. We don't actually think it's a particularly great idea to get much more specific on the cash position, because we feel it's quite likely to change. Any one of these partnerships could vary substantially increase our cash runway and they could happen fairly soon. In terms of the programs that we're contemplating at the Company, we have obviously an investment in the CRACM program as we've said several times. We're really focused on partnering that program. We've definitely been encouraged by the level of interest that's been shown in the CRACM implant program; however, our focus from that strategically is really around partnering, and if we don't see a partner materialize for CRACM, that's something we would seriously reevaluate how much we want to invest in.

And then you said that the elesclomol study would not start the randomized portion until the fourth quarter, but I think you had put in your press release that you're going to start the trial in the second quarter, so what is the design there?

There will be a dose escalation portion that would lead into a randomized portion. So, we would expect over the next several months on until, of course, we get to the fourth quarter, there would be a fairly small number of sites involved. And at a fairly low cost commitment, but it's also consistent just with the timing and the focus of the Company, which is we're seeing a very rapid growth in interest in ganetespib, and data from ganetespib. And we're building out a global, multi-national, a global study that's intended to be registration enabling, and so that takes a lot of our energy and time. So, kind of a slower ramp up to elesclomol makes more sense.

Right. Thank you.

Thank you. Our next question is coming from Andrew Vaino of ROTH Capital Partners.

Hey, thanks. Just on the g-spib and docetaxel, are there any specific physical chemical synergies that you've seen there that make you want to do that combination?

Yes, Andy, it's Safi again and I'll turn it over to Vojo to talk about some of the clinical observations. There's, as you may know, quite a bit of literature that's been developed evaluating this at various academic centers. We've done quite a bit of work internally as well, and I don't want to oversimplify, there's certainly a number of observations, but probably one way to just at a very high level indicate what the source of the synergy may be is that when you inhibit Hsp 90, when ganetespib inhibits Hsp 90, you're inhibiting protein folding response that's very critical to the cell cycle. So, in some ways, you free cells right in the middle of cell cycle and by doing that, you're freezing them in the middle of cell cycle in a place and a way that they are extremely vulnerable to microtubule targeting agents like the taxanes. There's a pronounced synergy in the cell cycle effects.

You both sensitize the cells more to the taxanes, and you eliminate one of the escape mechanisms that cells try to escape from the G2-M pile up that's caused by taxanes. So, that is certainly one of the most pronounced effects we've seen in the lab and that people have commented on in the literature. There are certain other synergies that people have commented on, but empirically, in addition to the underlying theory, we've seen in all of the combination studies we've done, we've seen very dramatic enhancements of cytotoxicity when you combine these two compounds. We've also had some encouraging clinical data across our two tiles that are looking at this combination and I'll maybe let Vojo mention some brief comments.

Sure. So, we certainly see that when we combine ganetespib with docetaxel in the clinic using a regimen that's really approved that's really supporting our development program, we see that this combination is well tolerated. We've also seen in our lung cancer trial, some patients were treated with both ganetespib and docetaxel in a combination regimen. And we have seen clear signs that patients who responded to ganetespib initially, they continued to respond, and we've seen enhanced responses when docetaxel was added to ganetespib single agent. So, we have some clinical evidence that's quite compelling about the synergy.

Okay. Great. Thank you.

Thank you. Our next question is coming from Jim Birchanoff of Barclays Capital.

Hi, it's actually Ryan Martins in for Jim. I was wondering maybe if you could talk about the Phase 2b portion of your 2b/3 combination trial. What kind of powering assumptions do you have around the PFS, and are you going to have any interim looks at that Phase 2b portion of the trial? And what are your assumptions for docetaxel PFS in that setting?

Hi, Ryan/Jim. We will get into some more detailed discussion of the powering and the trial design in the next few weeks or few months as the trial initiates. We haven't, I think, announced that level of detail yet. I think, suffice it to say that fairly standard assumptions, there's actually a lot of data about what docetaxel does in that setting, and so those were used in the powering. We have quite high power to detect the signal given the size of the trial compared to more typical smaller Phase 2bs, and the answer is yes, we do have some interim administrative looks that we'll be evaluating over the course of the trial, which should give us some data read outs either by the end of this year or early next.

Okay, and then any color on historically what you see with docetaxel in that setting for PFS?

Historically in the registration trials in second line, docetaxel is producing typically a three-month PFS for medians.

Okay, thank you. And on the same combo trial, it seemed like from your comments that you were going to use a different dose and schedule. Is that different from the 200 mg weekly schedule?

Yes, in the Phase 1 combination study, we established a dose and schedule. It's a standard dose of docetaxel and a just slightly lower dose of ganetespib.

Okay, thanks. And finally, just to follow-up on Jason's question around the cash. So, you've said the cash should last into 2012. Just wondering if that is dependent on more than one partnership, or it can just be one partnership that takes you into 2012 for that?

Yes, sorry. The cash into 2012 is without any further cash coming into the Company whatsoever. So, any incremental partnership that we have today, as I said, we're in many different companies talking about three different programs. Any one of those getting closed in the next few months, or by the end of the year, would significantly increase our cash runway.

Okay, thanks for clarifying that, Safi.

Thank you. Our next question is coming from Shiv Kapoor of Morgan.

Thank you for taking my question. First, on your strategy for the Hsp 90 program, the ganetespib. Now, I understand, Safi, why you have been adamant about keeping the economics on this drug. The data looks very good, and now I guess the hard question is how do you keep the economics of the drug? What kind of -- are you trying to partner other drugs first, or are you trying to keep the US rights? What are your -- what are the strategies you're employing right now?

Right. Thanks, Shiv. Yes. As you mentioned and we've discussed in the past, we're fortunate to have quite a bit of oncology and clinical development experience, operational experience, so that running these larger randomized trials is not that hard for us to do on our own. And the economics are of course very compelling, particularly when you have multiple shots on goal, single agent in this tumor, single agent in that tumor, a combination with this drug, combination with that drug. And the fortunate position of being the only Hsp 90 inhibitor, or the leading Hsp 90 inhibitor, that everyone is now approaching us.

So, that makes it particularly attractive from an economics perspective, and it's also particularly good that we can do this at very low internal cost, because nearly all of our trials going forward, except for the lung, are investigator cooperative groups sponsored. So, that gives us high breadth of opportunity at low relative internal costs. So, the economics, as you say, are very favorable.

In this kind of situation, we're having discussions with many companies. There's regional Asian companies in several different countries in Asia. There's global, multi-national, US-based companies. There's global, multi-national, European-based companies. We have active discussions under CDA, getting started with many of those and right now, we're approaching those with some flexible notions. But of course, one way of keeping the economics is certainly to start by doing regional deals, for example Asian deals, and then building the value of the program, and then coming back to evaluating potentially larger deals once we've significantly built the value in the program.

Okay, and if you can for me also go over, perhaps some more detail on what kind of insights you've learned about the genetic profile that is more susceptible to Hsp 90. More specifically, are these genetic profiles -- what proportion of patients might be prone to Hsp 90 in a significant way? And second, are these genetic profiles common to other tumors apart from lung cancer?

Great question. Great question, Shiv. That's -- in fact, we've been in a lot of recent meeting presentations at the IASLC lung cancer meeting in Santa Monica, at the TAP meeting just recently in Europe, at the Cancer Progress meeting in New York, and that's a very common question when people look at our data. You're seeing some lung cancer patients who have been on 10 lines of therapy, and had absolutely no response to anything come on your drug and have dramatic tumor shrinkage. So, what's going on? What's special about these patients? And then we're seeing that we had a triple negative breast cancer patient that Vojo talked about. Obviously, triple negative doesn't respond to most of the known drugs out there. What's going on? Then you have a gastric cancer patient, same thing, doesn't respond to most stuff, responding to your drug. What's going on?

And a lot of people are very interested exactly that question, and we're looking at that and, as Vojo said, we're starting to see some signs that there is certain genetic profiles. You might think of them as two questions. Not only are these patients who have tumors that are addicted to certain oncogenes, or how addicted are they to certain oncogenes, like for example, the EML4-ALK transfusion in lung, or certain other ones in breast, or certain other ones in gastric, but how addicted are those oncogenes to Hsp 90?

They're different levels of addiction between an oncogene as a client and Hsp 90 as a chaperone. And that is one of the questions we're looking at, and that is a question that we think is driving the dramatic single agent responses that are seen, as you point out, not just in one tumor, but in multiple tumors. So, one of the things that makes it so interesting on the flood of scientific discussions that have now been opened up in the community around this drug, is that there's this paradigm that's been developed in the last few years, especially since the discovery of the EGFR sensitizing mutation in lung, in '04 and '05, that the name of your drug tells you the type of patient. EGFR inhibitor, you go after an EGFR mutant; KID inhibitor, you go after KID driven gist; HER2 targeting agent, you go after HER2 positive patients.

What's different about ganetespib is that a number -- many of these client proteins are client proteins, and that's why to get to your question about multiple tumors. This does have application in these kind of single agent responses in multiple tumors. We're clearly seeing it in lung. We're seeing it in some of these other patients, and so that is something that we will be exploring and I expect we'll be presenting on later this year.

Well, great. Congratulations and best of luck.

Thank you. Our next question is coming from George Zavoico of MLV.

Hi, Safi, Vojo, everyone. Congratulations on a good quarter, and progress with ganetespib. I just want to follow-up a little bit on the biomarker question. So far, Safi and Vojo, you've mentioned some of the usual suspects in terms of biomarkers. Given what happened at ASCO with the Pfizer drug, new ones are emerging. How thorough a net are you casting, and the larger net you cast, the more effort really needs to take place, you need to do to catch potential biomarkers. Are you doing this by yourself, or are you working with a diagnostics company, or are you partnering the biomarker search? Are you doing multiple biomarker searches or looking mainly at the usual suspects?

Hi, George, this is Vojo. So, I'm going to take on this question, and Safi will jump in if needed. As you know, George, we have a pretty broad net of collaborators, and in many of our clinical trials, we have extensive translational research programs that are mostly externally funded by grant and other academic resources. So, we're able to leverage lots of help and lots of resource to help us really understand better what the patient's best response to ganetespib. And we're certainly building on that ,and as Safi mentioned a minute ago, in many of our trials, which are ongoing, this data has been collected, analyzed and we will expect later this year to have some more information, which then will obviously give us the choices to determine what's the best and most appropriate approach because we certainly want to go with the most feasible approach going forward towards registration.

Yes. And so, you've been, obviously, collecting samples from patients that have already been treated. How many tumor samples have you been able to look at and to do the genetic profiling on?

Well, we'll certainly collect genetic samples in the lung cancer trial and I think as we said before, we'll be presenting some of this data later this year. And we also collecting samples, analyzing, in some of our other trials, particularly on the ganetespib responsive trials. So, I think a steady stream of data coming in later this year and continuing for the rest of the year and next year as well.

So, you have some of the samples left from your Phase 1 trials to look at as well then, it sounds like?

In Phase 1, we didn't collect specific tissue samples. That's what we're doing in Phase 2.

Oh, okay.

So, but we'll present details later this year.

Okay. I'm looking forward to that. That's going to be very, very interesting I think. With regard to your development of ganetespib, the latest trial was very late stage, highly pre-treated. Now, you're marching to second line with docetaxel. Ultimately, is your strategy maybe with a partner to put it in combination as first line in small -- in lung cancer, I mean?

Yes. Absolutely, George. I think the opportunity in second line is really big as the treatment landscape is changing. Some of the previously approved drugs for second line have now moved to front line, which leaves docetaxel as pretty much the only treatment option available for many, many second line patients. So, we expect that the ganetespib combination will be quite successful in second line once we get to the point. But, obviously, there's nothing in the mechanism of the drug that prevents us from really exploring other combinations besides the docetaxel, and then look at other indications, front line or maybe in later line single agent certain situations. So, once we have single agent activity, and a good commandability, I think we have many options on the table.

And I'm sure you're talking about that with a lot of your potential partners. Final, I'd like to ask some questions on elesclomol, but I'll hold off on that. So, that's pretty much it. Again, congratulations and look forward to data coming out during the rest of the year.

Thank you. Our next question is coming from Joel Sendek of Lazard Capital Markets.

All right. Thanks a lot. A couple questions here, on the -- all on ganetespib. With regard to the Phase 2b, Phase 3 transition, I'm wondering what input you have from the FDA, or at what point you would have to meet with them in a post-Phase 2 setting or something like that in order to facilitate a potential registration?

Hi, Joel. Yes. The -- that's something that we'll be doing over the course of this year. That's one of the advantages of the Phase 2b-3 strategy. It allows you to gain experience and go to the FDA with a more robust data set as you get ready to have discussions with them about the Phase 3 portion. So, we do anticipate having further interactions and dialogue with them over the course of this year.

And -- but you've talked to them about this already, right?

We've had a number of interactions with the FDA of course, and we certainly file all of our protocols and register them. And we do expect to continue to have discussions with them over the course of this year.

Okay, and then just a clarification. I think you've mentioned this before, but the original patients in the Phase 2b portion, will any of them continue into Phase 3, or do you stop and then start clean with a new enrollment and recruitment process in Phase 3?

It's two different patient populations. So, it's a phase -- there's one patient population for Phase 2b and there's a separate patient population for Phase 3. They're not merged.

They're not merged, okay. So, could that potentially serve as two different studies in a way, or do you think that enrichment will make it such that they're kind of different? Any early thoughts on that strategy?

No, those would count as two separate studies. One could certainly be supportive for the other.

Okay, understood. All right.And then just a couple quick things. Any data at ASCO, and how many total patients have you had with triple negative metastatic breast cancer with the drug?

Yes, we have a number of our studies presenting at ASCO. The 06 single agent lung study will be presented at some point this -- middle of this year. We actually can't be sure exactly what will be presented at ASCO until we get, obviously, hear from them about what's presented, but we're certainly hopeful that a number of our trials will be presented either there or at other meetings this summer. The breast cancer patient is really our first breast cancer patient. So, that was quite remarkable in our Company-sponsored Phase 1 trial.

Okay, thanks a lot.

Thank you. Our next question is coming from Robin Davison of Edison Investment Research.

Oh, yes. Hello, there. Greetings from London. Just a couple of quick ones. First of all, the sort of cash reach of the Company, I'm assuming that that doesn't include use of the loan facility? You're not taking that into account when you say the $51 million will take you into 2012?

No, it doesn't assume the use of that equity line at the moment.

All right. Okay. Other ones, I'm just wondering when we might see some of the data from earlier particularly the GIST study, which seems to be the one that's at the forefront there.

The GIST and the heme studies, as we said in some of our earlier announcements or releases, we're -- we've seen some interesting data there, but we're really focused on lung cancer right now, because that's where we're seeing most dramatic single agent responses, and where the taxanes are widely used and we can exploit that synergy. We may come back to GIST and heme later as more investigator-sponsored or cooperative groups sponsored. In terms of when we would present that data, that would again be probably middle of this year or second half of this year, depending on which meetings investigators want to present at and get accepted at.

Right. Okay, also I'm interested whether there's likely to be any further investigator-sponsored or cooperative-sponsored studies starting up this year. Obviously, there were quite a few in the fourth quarter, (inaudible) a few anyway. Are we likely to see more this year?

Yes, we have up to half a dozen new studies expected to start this year.

Right. I also -- and really the same question for elesclomol, whether there's any interest from investigators in taking that into other indications in an earlier stage perhaps?

Absolutely. This is Vojo. I think we recently announced that GOG, a major cooperative group in the United States focusing on gynecological cancers, has initiated a combination trial of elesclomol and taxol in ovarian cancer. We are, as Safi mentioned before, in advanced planning stage to initiate the lung cancer program, and we're in active discussions with investigators about other potential opportunities for elesclomol as well.

Right. Okay. Actually, I probably should have clarified this earlier. With ganetespib, have any of these potential new investigator-sponsored studies, they would be with other combinations other than docetaxel. Is that -- would that be a reasonable assumption?

For ganetespib, yes. We have several, actually have many investigators approaching us about combinations with kinase inhibitors, combinations with signal transduction inhibitors, combinations with angiogenesis inhibitors. So, that is of high interest to us, and of course, I think we mentioned the radiation. We have seen some very encouraging data combination with radiotherapy, which is a totally different approach and is something that has been hypothesized for a long time. There's a lot of rationale for why those two approaches can enhance each other. So, we expect that to get started this year as well.

Okay, great. Excellent. Thank you very much.

Thank you. That concludes the question-and-answer session. I will now turn the conference back over to Dr. Bahcall for closing remarks.

Thank you, everybody, for your time and attention today. That ends this call.

Ladies and Gentlemen, this concludes today's call. You may now disconnect.