Oncternal Therapeutics Inc (ONCT) 2010 Q3 法說會逐字稿

Good morning, everyone, and welcome to the GTx, Incorporated third quarter results conference call. Today's conference is being recorded. I will turn the call over to Dr. Mitchell Steiner, CEO of GTx. Please go ahead.

Thank you, and welcome to our third quarter 2010 corporate results conference call. Before we begin, I want to mention that I'll be making forward-looking comments during today's call. And I direct to Form 8-K we filed October 26 with the SEC, where we discuss in detail the risks and uncertainties that affect our business. This morning, I will update you on our clinical programs Toremifene 80 mg, GTx-758, and Ostarine, also known as GTx-024, as well as our recent financing.

After receiving a complete response letter from the FDA, following the review of the Toremifene 80 mg NDA, we have met twice and have had multiple calls with FDA. We now have agreement with FDA on the design of a single clinical trial that will address the two deficiencies cited in the complete response letter.

In March of this year, we amended our collaboration agreement with Ipsen, our European partner, and obtained a funding commitment for most of the anticipated cost of the second Phase III clinical trial. Ipsen agreed to pay up to EUR42 million for the then-projected cost of the study. In the agreement with Ipsen, if the actual cost of the study, following FDA input exceeded a certain threshold beyond the EUR42 million, Ipsen and GTx agreed to revisit the program and renegotiate terms to address the higher cost. GTx and Ipsen are currently renegotiating the terms of the collaboration, including the level of each companies' funding commitments for the planned clinical trial or whether to initiate the study.

GTx-758, a selective estrogen receptor alpha agonist for first line treatment of advanced prostate cancer, is being developed as an alternative to LHRH analog drugs, like Lupron and Zoladex. We are excited about GTx-758 for several reasons. The simplicity of the mechanism of action, the clarity of the regulatory pathway, and the potential to garner a large share of the established 3 billion worldwide commercial opportunities. GTx-758 acts by specifically binding to the estrogen receptor alpha to achieve castration by feedback innovation of the hypothalamus, pituitary gonadal axis to suppress the secretion of LH of the pituitary gland.

Just as Aperaterum was developed to be a safer version of well-established drug, Keydicondizal, to treat castrate-resistant prostate cancer, GTx-758 is being developed to be a safer version of a well-established drug called DES, which has been used effectively for decades for first line treatment for men with hormone sensitive advanced prostate cancer. Urologists have used DES did not question its efficacy to achieve castration in advanced prostate cancer patients and did not observe the estrogen deficiency side effects, such as hot flashes and bone loss which are commonly seen with LHRH analog drugs.

LHRH analog drugs became standard care for first line treatment of advanced prostate cancer because early data suggested LHRH agonists were safer than DES. At higher doses, DES caused platelet aggregation, which was associated with an increased risk of arterial thrombosis, MIs, and strokes. While DES castrates via the estrogen receptor, the molecule is non-selective. It binds not only with both ER alpha and ER beta, but also interacts with at least 12 other neutral hormone receptors, including the progesterone and glucocorticoid receptors. This cross-reactivity results in the off target and sometimes undesirable side effects such as platelet aggregation leading to thrombosis.

Studies of LHRH agonists versus DES were conducted 30 years ago at a time when men with advanced prostate cancer had a median survival of only 24 to 36 months. With the advent of PSA testing in the earlier use of LHRH agonist therapy, the impact of serious side effects related to long-term estrogen deficiency in men with advanced prostate cancer on LHRH agonist ADT is now becoming better understood. In large, well-controlled prospective studies by GTx and Amgen, it is now well-established that men on ADT are at high-risk for bone loss and fractures.

Moreover, other studies show that men with prostate cancer with on LHRH agonists develop lipid abnormalities and gain more body fat, which leads to metabolic syndrome and insulin resistance. In October of this year, FDA updated the labels of all LHRH agonist drugs to include new warnings about the increased risk of diabetes and certain cardiovascular diseases, such as heart attacks, sudden cardiac death, and stroke. LHRH treatment also is known to commonly cause systematic side effects such as hot flashes.

Another reason LHRH drugs such as Lupron became standard of care has been the direct financial benefit to position from the administration of the drug. An article published on November 4, 2010, in the New England Journal of Medicine, points out that in the 1990s the administration of Lupron and other ADT drugs was profitable for urologists. Today reimbursements for LHRH analog treatments have dramatically in reduced and urologists are no longer making the same kind of profit treatment. In fact, in order to minimize upfront cost of purchasing and carrying ADT in inventory many urological practices are now reducing the use of ADT or encouraging patients to pick up and pay for the LHRH agonist at a pharmacy and to have the drug administered when they come for their visit.

With the safety concerns of Lupron, Zoladex, Eligard, and other ADT drugs now in the spotlight, and because the financial incentives to positions for ADT into both drugs have changed so significantly, we are excited to be developing GTx-758 today. If successful, GTx-758 would be the first new form of androgen-deprivation therapy to be introduced in 30 years. Our discovery team designed GTx-758 to be highly selective for the estrogen receptor alpha. So, that it has potential to achieve medical castration without bone loss, hot flashes, adverse lipid profiles, or adverse fatty body composition changes, which are associated with LHRH agonist and antagonist drugs.

A drug with this profile would benefit healthcare payers -- excuse me healthcare providers, payers, and patients. First , it would benefit position practices by eliminating the inventory carrying costs of LHRH analog treatments. Second, it would benefit the payers by minimizing the need for polypharmacy to treat side effects of LHRH analog treatments. Finally, it would benefit patients by potentially reducing the incidences of these serious and systematic side effects of LHRH analog treatments. GTx-758 also has a potential efficacy advantage over LHRH drugs and surgical castration because GTx-758 induces the liver to produce a protein called SHBG, or sex hormone binding globulin.

SHBG is like a sponge that binds, for all intents and purposes, irreversibly to free testosterone, which is the only form of testosterone in the blood available to prostate cancer cells. The result is that GTx-758 treatment not only achieves castrate levels of serum total testosterone but also has the potential to reduce serum-free testosterone to levels below what is typically achievable with LHRH agonist or antagonist treatments, or even surgical castration.

Selectivity of GTx-758 is a key differentiator from DES. GTx-758 only binds to the estrogen receptor and no other nuclear hormone receptors. For estrogen receptor subtypes, GTx-758 preferentially binds the ER alpha and has weak affinity for ER beta. This is important because ER beta and not ER alpha is the only subtype of the estrogen receptor present on blood platelets. And it is through this mechanism that DES treatment is believed to cause platelet aggregation and, result in, increased cardiovascular risk in high doses.

We have tested GTx-758 in humans and monkeys. And GTx-758 resulted in less platelet aggregation in DES. With that said, our clinical studies will provide the real proof. We are encouraged that GTx-758 is very different than DES and does not appear to increase platelet aggregation.

Finally, the regulatory pathway for first-line advanced prostate cancer drugs is will establish with a 30-year history in FDA. The definition of clinical benefit is the reduction of total testosterone to castrate levels before 50 nanograms per deciliter. Recently, in 2008, the FDA approved a new ADT drug called Degarelix, an LHRH antagonist using this regulatory criteria. In September we announced topline results of the 56 day PKPB study of GTx-758 in young, healthy male volunteers. In this study, we established proof of concept of the ability of GTx-758 to achieve medical castration at rates similar to Lupron and the ability to lower free testosterone to levels lower than what typically can be achieved by LHRH agonist and surgical castration. Full data sets will be presented at the Society of Urologic Oncology in December 2010 and three abstracts on the preclinical data will be presented at the Society for the Basic Urologic Research next week.

In the second quarter of 2011, we plan to initiate a Phase II clinical trial evaluating to doses of GTx-758 compared to the Lupron in 105 men with advanced prostate cancer. The study will assess efficacy and hot flashes of four months in a blinded fashion. And then continue open label for an additional eight months to assess BMD and body composition changes. Our expectation is that in addition to achieving and maintaining castration, men treated with GTx-758 compared to Lupron will not have hot flashes, have no increased in the overall body fat and maintain bone mineral density. We expect to have four-month efficacy data from our Phase II clinical study of GTx-758 the first quarter of 2012. We will use this data to power head-to-head Phase III studies of oral GTx-758 against injectable Lupron, in order to have a label that will clearly differentiate GTx-758.

Now, I will share with you the current status of Ostarine for the prevention and treatment of cancer-induced muscle wasting, also known as cancer cachexia. In November 2006, GTx met with FDA to discuss the clinical development plan for Ostarine in cancer cachexia. In the meeting minutes, FDA defined cancer cachexia as "the accelerated loss of skeletal muscle in the context of a chronic inflammatory response." The meeting minutes also document the endpoints required to demonstrate efficacy of Ostarine for cancer cachexia for approval in a Phase III program.

Ostarine treated compared to placebo patients should have a higher total lean body mass and an improvement in physical function as measured by a functional endpoint. Using those endpoints in a Phase II study, we conducted a 159-patient, multi-center, double blind, placebo-controlled clinical trial in evaluating two doses of Ostarine in cancer cachexia patients who have either non-small cell lung cancer, colorectal cancer, non-Hodgkin's lymphoma, or breast cancer. The trial was completed in October 2008.

These Phase IIB clinical study demonstrated that by 16 weeks of therapy, Ostarine treated patients had an increase in lean body mass of 1.5 kg compared to placebo, or about 3.3 pounds of new muscle. Ostarine treated patients also climbed stairs faster and with more power. The drug was well tolerated and there were no detrimental effects on tumor progression or overall survival. The results of the study were similar to two other clinical studies evaluating Ostarine for sarcopenia in non-cancer patients with both total lean body mass and physical function endpoints were met.

In the first study, GTx conducted a proof of concept Phase II clinical study in 120 elderly men and post-menopausal women. Ostarine treated subjects, compared to placebo, had an average increase of 1.4 kg of total lean body mass over 12 weeks and also climbed stairs faster and with more power. In the second study conducted by Merck, Ostarine was compared to one of their SARMs in 88 post-menopausal women. Ostarine treatment resulted in an average increase of 1.5 kg of total lean body mass and increased strength as measured by leg press. And Ostarine also demonstrated its superior safety profile compared to the Merck compound. Merck presented their results at the Endocrine Society annual meeting held this past June of 2010.

Ostarine has been studied now in seven clinical trials involving over 580 subjects. And in all three efficacy clinical trials, met the primary endpoint of increasing total lean body mass and, a key secondary endpoint of, physical function. We are now preparing for an end of Phase II meeting with FDA, which will be held in December of 2010. FDA input will be obtained for the Phase III clinical development program for Ostarine for the prevention and treatment of cancer cachexia. We expect to have minutes from that meeting in January of 2011. Following FDA input, we plan to start the study in 2011.

The currently planned to study will evaluate Ostarine compared to placebo, in approximately 300 patients with Stage III or Stage IV non-small cell lung cancer who are starting standard platinum doublet chemotherapy. Advanced non-small cell lung cancer patients are the ideal patients to show clinical benefit. Unfortunately, almost all of these patients will lose significant weight while they fight their cancer and have a median life expectancy of only 12 to 15 months. Moreover, in our earlier Phase IIB study, in a mixed population of cancer patients. The subgroup of non-small cell lung cancer patients on Ostarine have greater lean body mass and physical function, measured by stair climb, compared with placebo.

As for the Phase III clinical study design, the primary endpoints of efficacy are overall lean body mass and physical function. And the secondary endpoints, will include quality of life, tolerance to chemotherapy, measures of independence, progression free survival, and overall survival. To further strengthen GTx's balance sheet and allow us to carry out our plans to increase and maximize shareholder value, we recently completed an underwritten public offering of our common stock, raising net proceeds of approximately $37.6 million. I will now turn the call over to him Marc Hanover for a brief review of our financial

Thank you, Mitch. The details of our financial results for the third quarter 2010 are included in this morning's press release and are available on our website. I will review with you the highlights. The net loss for the quarter ended September 30, 2010 was $8.6 million, compared to the net loss of $12.8 million for the same period in 2009. Revenue for the third quarter of 2010 was $1.3 million, compared to $3.6 million for the same period in 2009.

Revenue for both periods included net sales of Fareston and collaboration revenue from Ipsen. Net sales of Fareston was $960,000 and $719,000 for the three months ended September 30, 2000 and 2009 respectively. Collaboration revenue was $336,000 and $2.9 million for the third quarter of 2010 and 2009 respectively. For the three months ended September 30, 2010 and 2009, research and development expenses was $5.6 million and $8.1 million, respectively. General and administrative expenses decreased during the three months ended September 30, 2010 to $4.1 million, from $8 million for the three months ended September 30, 2009.

At September 30, 2010, GTx had cash, cash equivalents, and short-term investments of $19.7 million . In the fourth quarter of this year, we have added and will be adding additional cash to our balance sheet. As Dr. Steiner has previously noted, on November 1st, GTX raised $37.6 million in an underwritten public offering of our common stock. Early this month, we also were awarded a cash grant of $1.2 million by the United States Government under the Qualifying Therapeutic Discovery Project Program .

In addition, in December of this year, we will be receiving a cash payment of $5 million from Merck for cost reimbursements for research and development activities. Furthermore, GTx has no debt and no warrants. Now, I will turn the

Thank you, Marc. Operator, we're ready for our first question.

(Operator Instructions)

And, your first question comes from the line of Joel Sendek with Lazard Capital Markets.

Hi, thanks a lot for that comprehensive update. I guess one thing I wanted to talk about, now that you have cash for runway for a couple years and can get these studies up-and-running and get some data, what's your view on partnering any of the drugs, and do you have a priority of one versus the other, or a timeframe that you can share with us?

Thank you, Joe. So, yes, now that we've got some room to support the clinical activities that we have at GTx, our focus is really to move two of our assets; the Ostarine asset and the GTx-758 asset forward to obtain data. For the 758, that data would be data that's head-to-head against Lupron, and would give us a -- actually, as you can tell from my comments, a very comprehensive view of how, from a safety standpoint, we will differentiate ourselves, and those data are not far away.

I mean, you're looking at your four-month data coming out first, and then it will be open label, and we'll be able to update that. And so, within a year's time, basically, we're going to fill that trial, and by first quarter of '12, have the data for that trial. For Ostarine, we're meeting with the FDA, as you know, and we're going to move forward with that and fill that trial, and the goal, again, is to keep that moving, and now with FDA clarity, it also strengthens our position. So, what do I mean by strengthen our position? By having both of these horses running full-speed, and by having FDA clarity for both of these programs, we feel we'll be in the best position for a potential partnership.

Consequently, rather than letting the partnership dictate how we move forward, we'd rather let the clinical trial, the data, and the FDA clarity determine the value of the opportunity. And so, with that said, both horses will run, and we will be very active in getting both of those opportunities potentially partnered, and we think that this is going to be Management's number one goal as we move forward, is to have the data and to have clarity on how we're going to eventually sell these products.

And, will you entertain diligence requests and things like that during the process, or are you going to wait, for example, on 758, wait for that four-month data you'll get in a little over a year, and then open it up to --

No, we will definitely entertain diligence requests; I mean, Ostarine has been fully evaluated by partners that we're in discussion with; 758 is moving in that direction. We've got a tremendous number of inbound calls on 758, being such a novel opportunity. We have a very extensive data set; I mean, between the acute and chronic animal data, and now over 226 patients -- excuse me, subjects, have been exposed to 758, and now about to go into a study that's going to replicate what we saw on our proof of concept study. We have data coming out, as you know, at a couple of these peer-reviewed scientific meetings in November, this month; and next month will be the clinical data.

So, no, we're open to any due diligence that any pharmaceutical company would like to conduct, and this information is readily available, and we are not going to necessarily wait until we have the data. However, at least we know that once you -- once the studies start, then we're that much closer to getting this thing to market, and what we have learned in the past is that partnerships take time, and if you wait to strike a partnership before you move forward to get data, you'll find yourself waking-up one day that, you know, they can wait and we can't. So, by moving the -- by raising this money and moving these studies forward, it puts us in the best position to get data and to the partnership.

Thanks, Mitch.

(Operator Instructions)

And, at this time, you have no further questions.

No, we have a question, don't we?

You do have a question from Simos Simeonidis with Rodman and Renshaw.

Hi, guys, thanks for taking the question.

Yes, sorry, Simos. I don't know what the mix-up was but, anyway, how are you doing?

Good, how are you?

Doing great, thank you.

So, could you tell us what your thoughts are about the size of the first line trial; the Phase II of [for] 758? And, then are you going to use the 1,000 mg and 1,500 mg as the two doses against Lupron?

Yes. So, it turns out that -- first of all, it's a great question because -- take a step back -- I was just reading some information about some of these castrate-resistant and prostate cancer trials that have become quite huge. This is really for the first line space, so GTx-758 is going after a well-established area in regulatory, where basically they have established for prostate cancer -- this is not true for any other cancers to-date, that a clinical benefit is defined as having a total testosterone level less than 50 nanograms per deciliter. And so, what that means is, you don't even have to do a head-to-head study with Lupron if you don't want to, you just have to show clinical benefit.

In our situation, we made the determination that clinical benefit is not all that's going to be important for this drug. What's going to be important for this drug is to be able to show why we are different than Lupron and Lupron-like drugs which, as you know now, is about a $3 billion worldwide market. And, what makes us different is that we're oral, and we don't have these estrogen deficiency side effects, and the only way we're going to be able to "market this," is to make sure that we do the appropriate head-to-head studies.

With that said, we did do a proof of concept study. The proof of concept study was done in healthy males, and healthy males tend to be much more difficult to castrate than in older males and, because of that, we do have two doses that work; we have a 1,000 mg dose, and we have a 1,500 mg dose that both castrate. But, the real question is, what is the appropriate dose in an older male with prostate cancer?

To get to your endpoint which is testosterone, you don't need a lot of patients; that's a pretty tight endpoint. So, consequently, we've got -- we're planning on about 35 patients per arm, and that's going to be at 1,500 mg, 1,000 mg, and Lupron.

The goal here is that in the first four months, we would obtain, in a blinded fashion, the hot flash data. We don't expect hot flashes, so it's not that we treat hot flashes, we just don't expect to see hot flashes with GTx-758. We do expect to see hot flashes with Lupron, and by making it blinded, it at least gives us a feel for what the base rate for hot flashes would be, and also allows us to show a percent of patients that get castrate and maintaining castration.

By running an additional eight months, for safety, it allows us now to pick-up information on bone mineral density. We don't expect with 758 to see any detriment to bone mineral density; we know from the literature that Lupron will, and we also know the body opposition changes in Lupron would be an increase in fat, and that's a reason why they get the metabolic syndrome and insulin resistance, which we're not going to see in our study.

Now, why do we pick healthy males to do our proof of concept study? The answer is that that's a very quick way to get to the answer. Why spend a lot of money on a program where you can't castrate, and you can't castrate the sufficient numbers of patients, and by going after healthy males, you've actually set your bar high in the sense that if you set it high and you achieve it, then it will be much easier to castrate an older male.

This is a similar program -- if you look at the Degarelix medical review, Degarelix also started out in healthy males; that's the appropriate way to do it because the brain; the pituitary, and hypothalamus doesn't care whether you have prostate cancer or not, and the mechanism here is endocrine. So, that's why we believe in first-line therapy; 35 patients per arm will be more than enough to help us power our Phase III program.

Great, that's very helpful. And, I know it might be too early to ask about this, but I'm assuming you probably have thought about it, and I was wondering if you could give us information for the Phase III. Do you think you need to see a similar length of treatment in the people of trial; the four months plus eight, or does it have to be longer? And, secondly, would you have to show superiority, or do you think you could potentially get away with having to show non-inferiority?

Yes. So, let me -- the first question is how long do you have to treat? Well, if you go back and look at Degarelix, the primary endpoint, and I'll explain why the agency picks this as a primary endpoint, is the maintenance of castration from day 28 to day 364; so, it is a year. So, even though in the Phase II that we proposing, we're only going to have four-month data. It is very clear, if you can maintain castration with an oral drug once a day, you're going to be fine, because then you just continue it out for 12 months, and

DES, which is a drug that's similar to this drug, only from a standpoint that it works through the estrogen receptor. I mean, DES was given for a years, and patients never developed tachyphylaxis. In other words, it didn't break through and end-up with a testosterone escape, so we're not expecting that because of the mechanism. We're really focused on safety side. But, the regulatory path, at least to-date, is that you do have to show over a 12-month period from day 28 to 364 that you can maintain castration.

Now, why day 28? Well, day 28 because it turns out that drugs like Lupron actually cause testosterone levels to go up before they come down. And, usually by day 28, over 90% of patients on Lupron and those kinds of drugs will be castrate. They do have what's called the testosterone surge, which is a drug that Degarelix and some other drugs in the past, and even Casodex being given in combination with Lupron, were trying to avoid. GTx-758 in the healthy males did not have a testosterone surge, so we're not going to have that same problem.

Now, the question -- so, we do believe that these are going to be one-year studies, and one-year studies are also good for us from a standpoint that we do want to make a head-to-head claim about BMD and also body composition, which you need about a year to get that good quality data. In terms of what do we need to show? Well, Degarelix did not have to show a -- did not have to do a non-inferiority or superiority study for Lupron, when they went head-to-head.

In fact, if you read the review, it was very clear that the agency was quite happy with just showing clinical benefits by showing that you can reduce testosterone to less than 50 nanograms per deciliter, from day 28 to day 364. They ran a head-to-head study with Lupron because they wanted to show that they could castrate sooner, and also to look at some of the other differences between PSA and that kind of stuff; as you know, PSA is not a regulatory endpoint. But, they did not have to do an inferiority -- show non-inferiority or show superiority.

In Europe, I think you do have to show that you're at least the same, so it would be a non-inferiority-type trial, but I don't know 100% because we have not met with Europe, so we don't know. But, in the US, if we run the Lupron head-to-head, it's mainly to allow us to have the safety data that will allow us to differentiate ourselves in the marketplace.

Great. And finally, are you still going to do the two Phase I's for formulation food effect? And, it seems like you decided not to going -- to do a Phase II in second line.

Well, no. So, good question. So, the first question is, we do have planned for December a food effect study and a formulation study, and, if we -- the food effect study is required, because it does turn out that drugs like this may be -- the absorption may be impacted by food, so we want to make sure we understand that early. And then -- but, that's an easy study; that's giving a couple doses over a couple days with or without food, so it's not a big study, big Phase I. But, it's important to get it done.

And then, the second study that we're doing is a formulation study. The formation we have now is fine, but if we can optimize it, that would be great. And so, we're starting from a position that, if we have to go forward into our Phase II and prostate cancer patients with the formulation we have, we'll be just fine. But, I have pushed our group to see if they could come-up with a formulation that requires a less drug.

The question about second line. Our thinking is, once we know the dose in first line, and that's why we are doing two doses versus Lupron, then we'll use that dose to go into second line. So, to conserve our cash, that's probably a better clinical pathway. And, in that setting, and if we're anything like DES, or anything like a drug called Estramustine, which Estramustine is drug that was given IV, still used today, and the concept was that you had an estrogen moiety attached to a nitrogen mustard, and the thought was that the estrogen moiety would direct the drug to the prostrate cancer cells, and that the nitrogen mustard would kill the cells. It turns out that the liver chops it up so quickly that, really, the effect you saw in these advance prostate cancer patients were primarily through the estrogen effect.

So, think now, with a second line. Second line means that you've got somebody on Lupron or a drug like that, or even surgical castration, and their PSA starts to come up, or they have symptomatic progression or radiologic progression, in the face of being less than 50 nanograms per deciliter, and they call that group castrate-resistant prostate cancer. If you add DES; if you add Estramustine, which are estrogen-like drugs, you will lower PSA, and these patients will respond. GTx-758 has a similar mechanism and, again, we took advantage of some of the safety features, and we do believe that if a Lupron patient, or a patient on first line fails, that we will see activity in second line. But, I'd rather do with the dose that's the right dose and then go ahead and show those data.

Again, that is a small study, again, because your hard endpoint there would be PSA, and the mechanism by which our drug would work in a second-line setting, is that we lower free testosterone lower than can be achieved with castration drugs like Lupron, or even surgical castration.

Great. Yes, that makes sense. Finally, if I may ask on Toremifene; final question, I promise.

Sure, and you can ask all the questions you want.

Just to get a little more clarity on your comments on what's going to happen -- what could happen with Ipsen. Is it possible where we could see a dissolution of the partnership, or a situation where you don't do the trial --?

Yes, I think that's a real possibility. and the reason it's a real possibility is, as you know, we're very fortunate to have so many things going on at GTx, but that takes resources, and we have to be very measured with these resources. I mean, the TREAT 2 study is in excellent study; we're literally one study away from approval. And, the FDA has approved the at entire NDA; we had only two issues, deficiencies in our complete response letter. We've addressed both of those with the FDA. We feel confident that the trial does pretty much like the first trial does in terms of efficacy; we'll have an improved product, that's the good news.

The other good news is that Ipsen is a wonderful partner; they're fully committed to the program. They do have Decapeptyl in Europe, which is a big product for them. That's an ADT product; that's an LHRH agonist, and a great companion product for them. The problem for GTx is that we are -- you know that -- those data would be five years away, four years away, and we have to focus on where we can bring near-term shareholders value to help us get to the four or five year mark, you know? And so, from our standpoint, we just have to make sure that it works for GTx and works for our shareholders, and keep our eyes on what's going to be important near-term, and making sure that we don't sacrifice too much for long-term.

That makes sense. Thank you so much for taking the questions.

Thank you.

This concludes the Question-and-Answer portion of today's presentation.

Great. Well, thank you, Operator. We would like to thank you all for your interest in GTx, and we look forward to providing you with updates on our future progress. Thank you, again, for joining on today's call.

Thank you for your participation in today's conference. This concludes the presentation. You may now disconnect. Have a great day.