Oncternal Therapeutics Inc (ONCT) 2008 Q3 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the third quarter 2008 GTx financial results conference call. My name is Sandy, and I will be your coordinator for today. [OPERATOR INSTRUCTIONS].

I would now like to turn the presentation over to your host for today's conference, Mr. McDavid Stilwell, Direction of Corporate Communications. Please proceed.

Thank you, and good morning. On behalf of GTx, I'd like to welcome you to our third quarter 2008 conference call. We released our results earlier this morning through the newswires. If you do not have a copy of the release and want one, you'll find it on our website at gtxinc.com. We'll have a replay of this call available on our questions until November 20th, 2008.

With me today are Dr. Mitchell Steiner, Vice Chairman and Chief Executive Officer; Marc Hanover, President and Chief Operating Officer; and Marc Mosteller, Chief Financial Officer. Following this introduction, Dr. Steiner will highlight third quarter 2008 clinical and corporate developments. Next, Mr. Hanover will briefly discuss our financial performance. Dr. Steiner will then make closing remarks and open the call for questions.

Before we begin, I'll remind you that information discussed on this call may include forward-looking statements and such statements are subject to the risks and uncertainties we discuss in detail in our reports filed with the Securities and Exchange Commission, including, in our most recent quarterly report on Form 10-Q, filed August 5th, 2008. We expressly disclaim any obligation to release publicly any updates to forward-looking statements made during this call.

Now I'll turn the call over to Dr. Steiner.

Thank you, McDavid. Good morning, and thank you for joining us today.

We continue to make strong progress. Following a recent planned pre-NDA meeting with the FDA, we're on track to submit this quarter the NDA for toremifene 80 mg for the prevention of fractures and other estrogen deficiency side effects. In the first quarter of next year we expect to hear from the FDA whether the NDA will be processed under priority or standard review. Our European partner Ipsen is planning to submit the MAA for toremifene 80 mg to the EMEA early next year. We're also in discussions with potential partners for toremifene in Asia, Japan, and the rest of the world.

In September at the annual meeting of the American Society for Bone and Mineral Research, we presented additional efficacy and safety analyses from the Phase III ADT clinical trial. One safety measurement was serum PSA. PSA is a sensitive marker of prostate cancer progression in men with advanced prostate cancer and is followed closely by physicians and patients to monitor the underlying prostate cancer.

Among men in the modified intend to treat population with a detectable serum PSA of baseline, which is a PSA greater than or equal to one nanograms per mil, there were 27% fewer men with PSA progression in the toremifene 80 mg group compared to placebo. This reduction was statistically significant. Also there were no differences in PSA progression among men with an undetectable PSA at baseline.

In October at the Chicago Support of Oncology Conference, we presented a similar analysis of PSA safety data from those study subjects who were treatment compliant at least 80% of the time. In this analysis, there were 31% fewer men with PSA progression in the toremifene 80 mg group compared to placebo. We also presented at the same conference bone scan safety data, and in a subset analysis of 201 men with a detectable PSA of baseline and no bone metastases evidenced by bone scan initially, toremifene 80 mg treatment did not affect the underlying prostate cancer. More specifically, this analysis showed by the end of the study 4.1% of men treated with toremifene 80 mg had new bone mets compared to 4.8% of men on placebo.

We believe these are important safety data for toremifene. The data from the ADT trial show that toremifene 80 mg treatment can prevent fractures and treat other estrogen side effects of ADT without negatively affecting the underlying prostate cancer. In fact the PSA progression safety data suggests that toremifene may be suppressing prostate cancer progression and are consistent with the mechanism of action of toremifene.

In other preclinical and clinical studies, including a 514-patient Phase IIb clinical trial for the prevention of prostate cancer in men with high grade PIN, toremifene was shown to have prevented prostate cancer compared to placebo. These observations of the anti-prostatic effect of toremifene in men form the basis of the ongoing Phase III clinical trial evaluating toremifene 20 mg for the prevention of prostate cancer in men with high grade PIN.

To update you on the progress of the PIN trial, in July of this year an independent data safety monitoring board conducted a planned semi-annual review of the unblinded safety data from the approximately 1,590 patients participating in the Phase III high grade PIN clinical trial and recommended the trial continue as planned. The DSMB to date has now reviewed safety data from the almost 3,000 patients involved in both the toremifene 80 mg Phase III ADT clinical trial and the toremifene 20 mg Phase III high grade PIN clinical trial with some of these patients taking drug for as long as three years.

As you recall, the endpoints of the Phase III high-grade PIN clinical trial was based on prostate cancer events, and we believe the pre-specified number of events to conduct the efficacy analysis will occur in the summer of 2009.

The Merck GTx SARM clinical development programs are also making good progress. In October we announced the top line results from the Phase II clinical trial evaluating Ostarine, which Merck has now designated at MK-2866, in patients with cancer-induced muscle loss, also known as cancer cachexia. The clinical trial met its primary endpoint, a clinically significant, absolute change in total lean body mass, which is muscle, compared to placebo and the secondary endpoint of muscle function which is performance.

The Phase II clinical trial involved 159 cancer patients with an average age of 66 years. The cancer types in the study were non-small cell lung cancer, colorectal cancer, non-Hodgkin's lymphoma, chronic lymphocytic leukemia, and breast cancer. There were 35 sites in the United States and Argentina, and the participants were randomized to receive placebo, 1 mg, or 3 mg oral capsule of Ostarine once daily for 16 weeks. Average reported weight loss prior to entry into the trial among all subjects was 8.8%, and the subjects were allowed to have standard chemotherapy during the trial.

The dropout rate during the trial was 33%, lower than the expected 50% rate which has been observed in other cancer/support of cancer clinical trials. The primary endpoint of the study was absolute lean body mass measured by dexiscan, and the top line showed that Ostarine treatment resulted in statistically significant and clinically meaningful increases in lean body mass compared to placebo and compared to baseline in both the Ostarine 1 mg and 3 mg treatment arms.

The top line results also show for a secondary endpoint of the study that Ostarine treatment improved muscle function, or performance, in a 12-step stair climb test measuring speed and calculating power. No improvement in speed or power was observed for the placebo group.

The incidence of serious adverse events, deaths, and tumor progression was similar in the placebo and treatment arms. The most common side effects reports among all subjects were fatigue, anemia, nausea, and diarrhea. As you recall, these patients were also on chemotherapy. Changes in ALT greater than twice the upper limit of normal were observed in two patients in each of the placebo, Ostarine 1 mg, and Ostarine 3 mg cohorts, and no subject discontinued treatment because of ALT changes.

We're excited that Ostarine met the primary endpoints of the Phase II cancer cachexia clinical trial, even with the presence of confounding factors which included heterogeneous cancer population, cancer induced inflammation in the background, and chemotherapy. The positive changes in lean body mass and stair climb performance compared to placebo were similar in magnitude to the changes that we observed in the Ostarine Phase II proof of concept sarcopenia trial which we reported in December 2006. We plan to present the complete study results on the cancer cachexia trial at the upcoming scientific meetings in 2009.

Together with our collaboration partner Merck, we are evaluating Ostarine and other SARMs for sarcopenia in Phase I and Phase II clinical trials in both men and women. Sarcopenia is an exciting opportunity with a market potential we believe to be as large as osteoporosis. The purpose of these trials is to identify the best product candidates to take forward into Phase IIb and Phase III clinical testing for sarcopenia.

We're looking forward to continuing our work with Merck on the future development of Ostarine and other SARMs and to updating you on the clinical development plans for sarcopenia, cancer cachexia, and other musculoskeletal wasting conditions. We're also excited about our preclinical pipeline. Building on our expertise of serums and SARMs, our robust discovery efforts have generated multiple selective nuclear hormone receptor modulator product candidates.

We're currently focusing our efforts on completing the preclinical studies to begin a Phase I clinical trial of GTx758 in the first quarter of 2009. GTx758 is an oral LH inhibitor to advanced prostate cancer which has the potential to reduce testosterone to castrate levels but without many of the estrogen deficiency side effects of current LHRH agonist therapies. This drug candidate has the potential to be the first real advancement in the androgen deprivation first line therapy since the introduction of LHRH agonists in the late 1980s.

The clinical primary endpoint for ADT agents is testosterone levels, and accordingly the development pathway should be straightforward and expeditious. Given our expertise and our strong relationships with urologists we believe this is an attractive product candidate.

Now I'd like to turn the call over to Marc Hanover.

Good morning. The details of our financial results for the third quarter 2008 are included in this morning's press release and are available on our website. I will focus on the highlights.

The net loss for the quarter was $11.9 million compared with a net loss of $10.2 million in the quarter a year ago. Revenue for the third quarter of 2008 was $3 million compared to $1.7 million for the same period last year. Revenues for 2008 included $315,000 of net sales of FARESTON and $2.7 million of collaboration income from Ipsen and Merck.

Research and development expenses were $9.2 million and general and administrative expenses were $6.1 million for the three months ended September 30, 2008, compared with $9.9 million and $3.2 million for the third quarter of 2007 respectively.

At September 30, GTx had $105 million in cash. GTx has the potential to add to this cash balance and strengthen our balance sheet through the realization of near term collaboration milestones which the company may receive from our partners Ipsen and Merck. GTx has no debt and no warrants.

I will now turn the call back the Mitch.

Thank you, Marc. GTx is unique. Not only are we one of a handful of companies who have a completed positive Phase III clinical trial with plans to submit a new drug application but also we have the potential for a second new drug application next year for another program, the toremifene 20 mg tablet for the prevention of prostate cancer in high risk men, assuming positive results from the Phase III clinical trial are obtained next summer.

We also have the Merck GTx SARM partnership which is working on Ostarine and other SARMs in multiple clinical programs, and we expect to advance these drug candidates to late stage clinical trials for several indications. And capitalizing on our expertise in small molecule nuclear hormone receptors and urology, we are advancing another one of our compounds, GTx758, into a Phase I clinical trial next quarter which has the potential to replace Lupron, Zoladex, and other ADT therapies.

Additionally, GTx has a strong balance sheet with $105 million and no debt and no warrants. This does not even take into account the near term potential to receive multiple milestone payments from our partners Ipsen and Merck. We are proud of what our 144 employees have accomplished. This year we will deliver -- we would have -- this year we delivered our first Phase III success.

We have been purposefully building GTx as a company with the expertise to develop products from the bench through clinical trials and to commercialize them. We now have multiple near term revenue generating opportunities. At the same time, we're advancing our pipeline to deliver innovative product candidates year after year after year. 2008 has been a good year for GTx, and we're even more excited about our future.

Operator, we're now ready to take questions.

[OPERATOR INSTRUCTIONS].

And your first question comes from the line of Joel Sendek of Lazard Capital Markets. Please proceed.

Thanks. Good morning. My question has to do with your discussions with the FDA. We've heard some -- on some other conference calls this quarter that people are very skeptical about the FDA meeting their timelines, and some are even thinking about not even asking for priority review. Did you get any sense at your pre-NDA filing -- or pre-NDA meeting that priority review might not be a valid strategy?

So the question is -- thank you for the question, Joel. This is Mitch. The question is the FDA has been missing a lot of its timelines and pushing them back and there may be sort of a sense that they may make a decision about priority review versus standard review based on whether, you know, what their workload looks like. And I think that from our standpoint we did not get any sense from the FDA one way or the other that their current "workload" was going to affect how they make a decision on whether we get priority review or not.

What we did hear is that drugs that do not have anything -- excuse me, indications that do not have anything else indicated, in other words there's no other drugs available for that indication, and it's an unmet medical need do qualify for priority review. And they stuck to their guns on that, so I guess they're kind of being blind to the reality of whether they're going to meet that deadline versus whether or not we have the right to go down a certain regulatory pathway.

So the regulatory pathway is intact, and in fact I would argue -- and this is Mitch Steiner arguing now -- that you have to think of our application more as a supplemental application in the sense that all the NDA has been approved for FERASTON 60 mg, and the sections that they would have to review are going to be peculiar to the clinical efficacy and the clinical safety and the CMC for this new line extension if you want to consider it that way.

And so in some ways this may be -- and this is Mitch talking now -- this may be an easier evaluation for the FDA than starting from a new chemical entity.

Okay, and along those lines, I mean, it's been said, since maybe the opposite side of the argument is if you look at the 20 mg on the ongoing study and all the safety data you have there, might they ask for that? Or is that totally irrelevant to this application?

It's going to be irrelevant because that's 20 -- in other words, let's say we would have had the reverse. Let me just say it this way. 80 mg is four times higher than 20, and so they would be less interested in what's going on with the 20, because they already have the 60 mg body of information out there for two decades. And so they're going to be looking at the higher dose not the lower dose, and so it's going to kind of be irrelevant in the sense that if there were no safety signals would it help you? No, and we're not seeing safety signals in the 20 mg.

If there were safety signals in the 20 mg, will that hurt you? Yes, but we're not seeing that. So really the 80 mg is what they're going to focus on because that's a dose that's not the approved 60 mg, and the 60 mg is already three times higher than the 20.

Great, that's helpful. And then just my final question, a housekeeping on. When you -- you said you were going to unblind or run the analysis on the in study in the summer. Does that mean we'll see the data in the summer? Or will that be simultaneous to when you make the disclosure?

I think we're trying to do the -- I think that really means the data in the summer.

Okay, thanks.

Thank you, Joel.

And your next question comes from the line of Eric Schmidt of Cowen & Co. Please proceed.

Good morning, guys. Mitch, as a follow up to Joel's last question on the PIN data, we were thinking that was a three-year timeline and that upon completion of the three-year period in Q2 you'd just announce the data. I think you alluded to this now being an event-driven analysis. Could you clarify?

Yes, that's been -- we've said that every -- let me back up. Thank you for the question, Eric. The answer is yes, it's always been event driven. The trial is a 36-month trial, just like cancer trials can be so many months, but it is event driven. And the interim analysis, as you know, was based on a certain number of events, and we hit those number of events. And then we pulled the trigger, and we looked at the interim analysis. And the same thing is going to be for the efficacy analysis that we're doing next year.

So it is event driven. Now the next question would be, okay, if it's event driven, then do you have to wait the full 36 months before you go to file if it's positive? And the answer is no. In fact, we're in a better position to have three-year data in a majority of our patients at the time that we would file for PIN. And so we're actually in a better position, because if we would have been successful this past year, then we would still submit the data that we have for the three-year safety, but we would have to add additional data at the 120-day -- you know, you have 120 days after you file the NDA to give them additional safety.

In this situation we're going to be locked and loaded with literally everything that we need if we're successful.

Okay. Could you help us on the number of events that are needed at the final analysis?

Yes, we have not disclosed those number of events, and as you know, we didn't do the same thing for the last time because it just got people saying, "Well, what's your event number now? What's your event number now?" And so what we'd rather say is that we believe, the Company believes that we're going to hit that number of events in the timeframe that I just suggested. And could it change? Could it be sooner? Yes, absolutely. Could it be later? We don't think so. So we're trying to make sure that we give a realistic expectation of when you would expect to see the data, and --

And a question --

Go ahead.

No, that's fine. Thanks. A quick question for Marc on the financials. It looks like you're tracking toward the lower end of the net loss guidance for 2008. Is the range of $52 to $60 million still appropriate?

Yes, Eric, it is, primarily because we have -- this quarter we're going to have some increased expenses as it relates to our submission. And so our run rate will be a little bit higher, but the answer to -- the answer is we will be on the lower end of our range.

Okay, great. And last question from me. It just have to do with the SARM program with Merck, and I know you're somewhat constrained about what you can say and also that you haven't yet made a lot of decisions that are upcoming based on a lack of data at this point. But help us out with the timeline. When do you think we will hear next about this program in terms of what compounds are going forward and what indications and when?

Yes, so let me again make it very clear that there is a lot of activity going on between Merck and GTx, and there are compounds in multiple clinical programs. So it's a lot of noise going on -- positive activity I should say, not noise at all. It's very focused, positive activity going on between what Merck has done in the past and completing what GTx has done in the past and has completed and what we're doing together.

Even as early as eight months ago when we got together and did our partnership, we had started some trials together. So there's a lot of activity. The real question becomes when can we -- when will we be at a point where we can come back to the public and say, "Well, this is how we're going to go forward." We believe -- and this is GTx talking now.

We believe that after the cancer cachexia trial being positive -- and interestingly the cancer cachexia trial being positive for Ostarine and having another Phase II, so that means now you have 120 patients, 159 patients, both of them pretty much showing you that Ostarine is doing what Ostarine is supposed to do, then that's all human clinical data. It gives us a lot of ammunition to think about what the next later stage program is going to look like, and I think Merck and GTx are trying to be very deliberate in how we approach that.

It's a long way of saying that there's a lot of good activity going on. To give you more specifically your answer, we hope that we'll be able to give an outline and hopefully even get started on clinical development going forward, and we're going to be telling people the first half of '09. But believe me, GTx and Merck are working very hard to make sure that we can identify what the next appropriate trial would be.

And I will also tell you that GTx and Merck are working very closely together so that GTx and Merck are sharing preclinical activities. In other words they're doing preclinical stuff. We're going preclinical stuff. They're doing clinical stuff, and we expect to continue to do clinical stuff. And so it's really truly a join partnership as opposed to having a relationship with a large pharmaceutical company where we're sort of the innocent bystander and get all the blame but no success. That's not at all happening in this relationship.

Thanks a lot.

[OPERATOR INSTRUCTIONS].

And your next question comes from the line of Howard Liang of Leerink Swann. Please proceed.

Thanks very much. Good morning. I have a question regarding the FDA meeting. Can you tell us whether you were able to get anything out of the meeting, whether either it's encouraging or not encouraging, from your perspective?

That's a great question, Howard. Let me see if I can help give you the level of excitement that GTx has going forward. You know, we've been working on this NDA for the last 18 months. We made the decision that we weren't just going to do a supplemental in the sense that you get grandfathered in with all these studies that may not have been required ten years ago when FARESTON was approved.

So we did a gap analysis. We did additional studies. We basically submitted a full meeting package to the FDA. As you know, we also have an SPA, and as you know, we also make sure that filed everything under the 1994, I think it's 1994-95 draft guidance for osteoporosis drugs. So GTx has done everything possible from a regulatory standpoint to make sure that we cover -- we follow everything that is in the public domain plus having a special meeting, a special protocol meeting with the FDA.

In addition to that, we went ahead and submitted to the FDA full reports on additional studies that were done. Plus they saw the Phase III ADT clinical trial of both the efficacy and the safety. And based on that we then went and had a pre-NDA meeting with the FDA.

We're also working with an electronic vendor, because the FDA requires that you file your NDAs now electronically. So we're literally at the brink of sending this stuff to get it electronically formatted, and you meet with the FDA, because you don't want to have everything electronically formatted before you have your meeting in case the FDA comes back with additional studies and additional changes that require a delay.

Well, the good news is there will be no delay. The FDA answered all our questions. There was nothing -- no surprises. In fact, it was much more on the side of encouragement, and so GTx is very excited about moving ahead to file without delay our NDA and that we were so happy we took the strategy to have everything ready to go and that we do not expect to lose any time because of the recent pre-NDA meeting if that gives you any sense of encouragement.

Okay, great. And a question for Marc regarding the near term milestones from either Ipsen or Merck, can you tell us sort of what we might expect in the near term?

Yes, Howard. I can't disclose the specific timing per our agreements with both Ipsen and Merck. But obviously with Ipsen we're coming up with some -- there are some upcoming milestones based on submission. We're also coming up on milestones with approval hopefully. And with Merck, of course, we have a host of milestone opportunities based on our agreement, which again I can't delineate. But suffice it to say that I wouldn't mention it in my comments today unless I felt like it was something that we could achieve in a near term range, and that's just subject to the agreement.

Okay, great. Then just the last question for Mitch. Regarding the finding of toremifene and the delay for the PSA progression, Mitch I know that you know this very really well. Can you sort of explain to us what will be the mechanism for a serum to delay PSA progression?

Yes, so the mechanism would be that it works on the cancer itself, and if you look into the literature, it's not peculiar to toremifene. All serums have the ability to be anti-prostatic, and tamoxifen has been used in advanced prostate cancer and hormone refractory. As you know we're going after the patients that are hormone sensitive, and in literally every study that's ever been done preclinically and clinically in all the tox work, serums have always been anti-prostatic.

So the mechanism is that it appears that in order for prostate cancer to grow, you need to have a balance between testosterone and estrogen, and even though we focus on testosterone because that's manly, it's very clear that even in animal models you can't get prostate cancer unless you add estrogen. So estrogen's important.

In fact, what we know now, and interestingly this science came about after we had started our trials -- early trials, not the latest trial -- is that even the estrogen story is more complicated with estrogen receptor alpha and estrogen receptor beta being two receptor types that have sort of a yin yang activity in the prostate, where ER alpha accelerates growth and ER beta actually slows it down. So the role of estrogen is very important in prostate, and the mechanism of toremifene is that toremifene does block estrogen at the prostate level. And that whole beauty of it is that it leaves bone alone, as you can see in our ADT trial and hot flashes and so on.

So the anti-prostatic mechanism has been well known for estrogen, and the beauty of the ADT trial is showing that PSA progression is reduced. And even if you look at the bone scan data where there's about almost a 1% difference -- even though it's not statistically significant because it's small numbers between bone scan progression in patients on toremifene versus patients on placebo, it mirrored what you saw in your PSA progression data. So it's not only evidenced by a serum marker, but it's also evidenced by the bone scans.

So not surprised, consistent with the mechanism of action shown from years of research, basic research in independent labs across the world, and now we're seeing it in our human clinical trial. So this is encouraging. Now, remember now the only test that we need to hit is that we have to make sure that toremifene in the ADT patients is not making the underlying cancer worse, because that's important when you're talking about cancer care products. One, you have to be efficacious, and two, you can't compete with the -- I mean, in this case Lupron in its efficacy in keeping prostate cancer in remission. And in fact, if anything, it looks like it may augment and help.

Great, thank you very much.

Thank you.

And your next question comes from the line of Aaron Reames of Wachovia Capital Markets. Please proceed.

Thanks for taking my question. I just had follow up just on the Merck SARM relationship. Do you -- and maybe this has already been addressed, so I apologize if it's redundant. But do you have an idea of when Merck might be more willing to outline what their program, their internal program, looks like and when we might see data on any of those programs? Has there been an update on how that may be conveyed to investors in GTx? Or if you can expand upon that, that would be helpful.

Yes, and the answer is Merck and GTx -- let me say it a different way. Merck understands that GTx has to let the public know what we're doing, okay. It's more for GTx than it is for Merck, because this is a program that's one of our major programs. Merck has already disclosed in their annual report -- and if you look at MK-2866 in their annual report this year, they've already disclosed that SARMs are a priority for them in sarcopenia.

So that's been publicly disclosed and prioritized by Merck. Going forward, we are trying to work with Merck to lay out a program. It's not because Merck doesn't want to be transparent. It's because we really have just gotten the clinical data, and they're just getting clinical data. And we want to make sure that before we tell the public what we're going that we've done our research and that we have designed the trials and that we've met with the FDA when appropriate. And all of that kind of stuff is going on right now.

And so what I can tell you is that as soon as we know what we're doing going forward, and we believe we'll be able to share that with the public over the next half of the year, but that doesn't mean to say we're not going to start to do something over the next half of the year. It's just saying that the clarity in the program and actually starting the program is going to actually happen simultaneously, and we're just trying to work through that and give our partner an opportunity because they just got this data for the first time. And we're using this data plus the Phase II data that we reported in December 2006, plus their clinical data set, plus their preclinical information, our preclinical information, their regulatory discussions, our regulatory discussion, and their market research, our market research, to come up with the next best steps.

Okay, great. And then the last question I had, has there been any further I guess conclusion on whether sarcopenia would be defined as one or two standard deviations below normal in terms of how you would define that actual indication?

Well, I think the question's a great question, and I think it's a little bit more complex than that. And the reason for that is that in addition to talking about lean body mass, there may be some kind of performance measurement that will put a patient in the high-risk group for frailty. And all of that's being sorted out. It is not as clear, for example, as cancer wasting where you can obviously see that if somebody's losing weight we cancer you've got a problem. In sarcopenia the bar is a little higher, and that's in addition to showing that you increase lean body mass, i.e., muscle, you're going to have to show that that muscle translates into some kind of clinical benefit to the patient.

How to define that clinical benefit is where a lot of that discussion is being had, and you just have to stay tuned because the good news is that we're ahead of everybody else. More good news is that it's uncharted territory, so that we're still going to -- you know, being ahead of everybody else, we're going to define what those definitions will be, and that we couldn't have done it, we couldn't be approaching that problem, without being confident that GTx isn't doing it alone.

We're in fact doing it with Merck. And as you know, Merck and other large pharmaceutical companies had to deal with the same issues when osteoporosis first came along, because as you know, bone loss of aging is common, and when does bone loss of aging become a disease? And the answer is when you lose enough bone that you're now more susceptible to fractures. And so we're kind of doing the same thing for sarcopenia, so we're being patient, and we want to make sure that with an opportunity as large as sarcopenia that we do it right.

Okay, great. Thank you for taking my questions.

Sure.

I'm not showing any further audio questions at this time, so I would like to turn the call over to Dr. Steiner for closing remarks.

Thank you, operator. We'd like to thank you all for your interest in GTx. We look forward to updating you on our future progress, and thank you again for joining us on today's call.

Ladies and gentlemen, thank you for your participation in today's conference. This concludes the presentation, and you may now disconnect. Have a good day.