Good morning. Welcome to Corcept's Ovarian Cancer Program update. I'm Atabak Mokari, Corcept's Chief Financial Officer. I wanna begin by thanking those of you joining us virtually, as well as a big thank you to those of you joining us here in New York. We're delighted to host this event to highlight one of our important clinical development programs. Statements during this meeting, other than statements of historical fact, are forward-looking statements based on our plans and expectations that are subject to risks and uncertainties, which might cause actual results to differ materially from those expressed or implied in such statements. These forward-looking statements are described in our press release that was issued yesterday, and the risks and uncertainties that may affect them are described in our annual report on Form 10-K and our quarterly reports on Form 10-Q. Please refer to those documents for additional information regarding these forward-looking statements and the factors that may affect them. We disclaim any intention or duty to update forward-looking statements. We have a full agenda today. Our CEO, Joe Belanoff, will begin with a company overview. Next, our Chief Development Officer, Bill Guyer, will provide an overview of our oncology program. We're honored to be joined today by Dr. Thomas Herzog, a renowned gynecologic oncologist, who will review the ovarian cancer treatment landscape, our phase II trial results, and our upcoming phase III trial. Following some concluding remarks by Bill, we will proceed to a Q&A session, which I will moderate. For those of you joining virtually, please submit your questions via the app. For those of you joining in person, please submit your questions via the note cards provided, and we will collect them from you. You may also submit your questions by emailing ir@corcept.com. I will now turn the meeting over to our Chief Executive Officer, Dr. Joseph Belanoff. Thank you. Well, it's really nice to see everybody in a room together. It has not happened. I was saying before, I actually I'm not sure the last time I wore this suit. Just glad it still fit. Thank you really for coming. I've been tasked with really talking about the company as a whole, and I'm gonna do it briefly 'cause we have lots of interesting information to go. I think it really does help sort of set the context for everything else that you're gonna hear today. Corcept, as I've said to those of you who've known me for a long time, that even the name tells you what we do, cortisol and receptor. Cortisol is everything that we think about. Sometimes people will ask us, "Are you an oncology company, an endocrine company, a psychiatric company, neurologic company?" The answer to that is, "Well, we're none of those specific things." You can't put us in any of that cubbyhole. What ties it all together is diseases which are affected by cortisol and our drugs which modulate the effects of cortisol. Cortisol, of course, is a critical hormone, essential for life. Absence of cortisol leads to death. It's produced by adrenal glands. Anyone who wants to know where that is, renal is another word for your kidney. They're just above your kidney. It's got an interesting thing, which is a diurnal variation, meaning it's high in the morning, it drops through the day, rises through the night. All of you here are pretty much wide awake and alert because your cortisol is ready to go. It's at its top level for the day. A critical thing is that it binds to virtually every organ of the body. There are receptors for cortisol almost everywhere. When you have a problem with cortisol, it can manifest itself in many different ways. I'm gonna talk about a few diseases, very few, but we're gonna get to ovarian cancer in a second. Just keep in mind, sort of as you think about this, that our platform is really very, very broad. Those of you, and I know in the room there are some, who've been investors for a very long time, you understand how we're really getting to all of those diseases. This is a particularly exciting year because many of the things will read out this year, of which ovarian cancer is just the first. All of our compounds do a specific thing. They modulate activity at the receptor for cortisol, which is the glucocorticoid receptor. That's an important distinction from they don't lower the level of cortisol. Essentially, like they're the dimmer on your light switch. They can turn down, to varying degrees, cortisol activity. They're all competitive antagonists. Our second generation compounds really are very specific to cortisol. Now, I'll mention her a couple times today, but there really is a person who is responsible for all of our second generation compounds. That's Hazel Hunt, our Chief Scientific Officer. Hazel usually resides in England, and for our afternoon conference calls, it's kinda late, so she doesn't participate in many of them. She actually came over here today, and I'm sure all of you will have a chance to meet her as the day goes along. Now, here's something that's very important. When we tasked Hazel actually someone was teasing me about it before. I'm gonna show you a little scientific diagram in a second. You know, we have a great first generation compound. We call it Korlym. It works very well to modulate cortisol, but it also antagonizes the progesterone receptor. It is in another form used to terminate early pregnancy. We really tasked Hazel with seeing if we could separate those activities. That was a very difficult thing many companies had tried before Hazel tried, but ultimately she succeeded. An important thing to really understand, a very important thing, is that even though all of our compounds modulate cortisol, they are not identical to each other. They have different qualities, and I say it at every single quarterly call. Some are better at creating insulin sensitivity. Some are better at creating weight loss. Some are active in oncologic models, some are not. You cannot think of them as a compound. They really are very different from one another in important ways, which has actually created a great opportunity for us, because instead of bringing one compound forward, over time, we will bring many compounds forward because of the specific activities that they have. I'll do this just very quickly. Korlym, progesterone, cortisol, you can see they look an awful lot alike because they all share the steroid portion of their molecule, which is the four rings there. Korlym is a competitive antagonist, but it's just as much an antagonist as the progesterone receptor as the cortisol receptor. What Hazel did, which is really pretty amazing, is she created a library of compounds, more than 1,000 of them now, that are in three different structural series, and all of them are very potent in modulating cortisol activity, and none of them touch the progesterone receptor at all. The primary thing of getting rid of the quality of pre-producing termination of pregnancy by blocking the progesterone receptor and the other medical effects which happen through the progesterone receptor are really absent. Again, I'll make the point, you know, that they are not identical. Here's, just you can see relacorilant, which is the drug we're gonna talk about today, and Korlym, they look different. There are structural reasons why relacorilant antagonizes the glucocorticoid receptor and not the progesterone or any other receptors. Even if you sit, you know, sort of sitting here can see they're not the same molecules. It's a bigger molecule. It's not a steroid and those qualities actually are shared amongst all of our second-generation compounds. Now, here's the most complicated slide I'm gonna show you. I'm not gonna spend much time on it, but what this really tells you is I think it's a fallacy for people to think of this as a simple sort of lock and key system. What happens actually in this system is that whatever you have, either the drug or cortisol, binds to the receptor. The receptor and ligand together translocate to the nucleus. They sit on the DNA, and then a whole host of cofactors, repressors, stimulators actually join the party, and they join the party in very different ways with different compounds. This is really an actual readout of the coregulators. But the important thing to really get from this slide is that they're not the same. Mifepristone is not the same as CORT125134, which is relacorilant, and it's certainly not the same as the compounds below it or cortisol. If you wanna know what happened to the other compounds, names you have not heard, you know, in various ways, they were inferior. It's not just that relacorilant is better than mifepristone in ways that we think is important. It's better than other compounds that actually we created. The point, again, is not the same. These compounds have important differences in actuality in the clinic. Okay, this I'm gonna go through really very briefly. Again, those of you who know Corcept know this well. We are an unusual biotech company. We actually make money, and have for many years, and we actually pay for all of our research from that money. We're a business in some sense like our parents would understand. We make money every day, and we plow it back into our own research where we think we can go forward. The platform is large and rich. This is just the first readout. There are many other diseases you're familiar with, liver disease, psychiatric diseases, neurologic diseases, where we're working. Here's an important thing, and I really, again, want, like with Hazel, wanna give a shout-out. We're really built on the back of doing collaborative academic research and have for many years. It's an unusual thing for a pharmaceutical company, you know, really to do. I know the downsides, but we've had tremendous upsides. It's been a great farm system for us, and I really wanna give credit to the founders of what we're gonna talk about today, which is the University of Chicago. This was their research 15 years ago. We were able to bring it in-house and make it go more quickly, but it was really their founding idea that cortisol modulation might be effective in certain cancers, including ovarian cancer. This is just a brief chart of our revenues and cash and so forth. Again, you've seen this before, and what you've really seen in our commercial business is growth really since inception. During the pandemic year, it sort of moderated, but we're back on to, I think, what is gonna be a very good year of growth. This is just sort of the readout for this year. I put this slide in here just so you will understand that, it's, you know, the end of March, and this is a very important readout you're gonna get today. Things are gonna occur all through the year, both in Cushing's syndrome, oncology, our metabolic diseases, and as we'll mention later, we even have a neurologic disease, ALS, where we're starting this year. All the things I've talked to you about for years are really starting to come to fruition at this point in time. This is last slide from me, and I know, there's plenty on here, and that's intentional. We probably have 35 different academic collaborations at any given point in time, half in the United States, half outside of the United States, half preclinical, half clinical that we support, and it really has operated as a way to develop this entire platform. Obviously, we're gonna spend all our time, the rest, talking about oncology. Keep in mind as the year goes along that you're gonna see results from metabolic issues. You'll see something will come out of psychiatric issues, and that's just gonna continue indefinitely into the future. Thanks for your patience and your interest in all this. I think it's actually a very important part of clinical medicine. All right, I'd like to introduce you next to Bill Guyer. Bill's our Chief Development Officer. He's responsible for all of the things that you just saw in bringing them forward, and he has a few comments to make specifically about ovarian cancer and oncology. Great. Thank you, Joe, and I wanna reiterate as well, it's so great to be here live. It's been two years of pandemic, and it's so good to see New York back. This is one of my best cities to visit in all of the world. It's truly a pleasure to be here today to talk about Corcept's mission to really improve patient lives through cortisol modulation. When I look at why I joined Corcept about eight months ago, it really was everything that Joe had just talked about. I dug deep into the science pre-clinically of all the work Hazel had done, looked at the pipeline, and I was excited with the potential that I could see of meeting unmet medical needs through the SGRMs, which are the selective glucocorticoid receptor modulators across many different diseases. I was excited in seeing what we're doing in endocrinology, metabolics, neurology, but also oncology. Today, we're gonna talk about our efforts in oncology with a specific focus on ovarian cancer. Now, we believe we can have a positive effect for patients based upon research like this. Cortisol modulation has the potential for a broad impact across many different tumor types, and here's research looking at 20 different tumor types. In this evaluation, they looked at the GR expression in these tumor types through a validated assay and measuring the H-score. Now, the H-score has a range of 0 to 100, and it really measures the intensity of the GR activity. H-scores greater than 100 are defined as having high GR expression. As you can see on this slide, all of these 20 tumor types had GR expression, but the vast majority actually had high GR expression. Now you'll also see on the graph that there's a range for that H-score. Now that range can be influenced by a few things, one of them being the stage of the cancer. Because as cancers continue to progress, that H-score typically will increase, which means GR expression will typically increase as well. We believe based upon this research with selective glucocorticoid receptor modulators, we can have a positive impact not only on ovarian cancer, but hopefully on many of these cancers listed here. We also believe that this is validated through research from two different academic centers that collaborated, and this is from the Oregon Health and Science University, as well as the University of Southern California, which is my alma mater. In this study, they evaluated 341 women who had ovarian cancer. At the time of debulking therapy, they took samples of those tumors, and they evaluated GR expression, very similar to the previous study that I showed. They looked to see those who had GR expression and high GR expression. About 40% of these women had high GR expression, and as you can see here, those with high GR expression had a significantly lower progression time, and therefore, we saw that we could have potentially a positive impact, not only on those with high GR expression, but we believe we can have a positive impact on anybody with GR expression. Those two research studies, as well as many others, really informed our phase I study design, where we looked at not only ovarian cancer, but also other solid tumors. We were looking at signal seeking, basically evaluating relacorilant in various different doses and also dosing schedule. This was the first time we had studied intermittent versus that of continuous relacorilant. We also studied various different doses of nab-paclitaxel in combination with relacorilant. As you can see on the slide, we see a longer duration of therapy for many of these patients. Overall, about one-third of the patients had a response. Of note as well, the median time for progression-free survival was about 4.6 months. As you hear from Dr. Herzog coming next, that's very similar to what we're seeing in phase II, and I think very predictive of what we see in phase II. In addition to that, we also looked at other solid tumors. When you look at all these other solid tumors, we saw actually the majority of them responded to relacorilant plus nab-paclitaxel. Of note as well, at the very bottom, the vulvar squamous cell carcinoma patient is still alive today, about 3.5-4 years later. All of this research, as well as many other research, really informed our oncology pipeline and where we are today. We're taking a very focused and methodical approach to our oncology pipeline, but I hope to see this expand rapidly in the coming months to years. We've got three different mechanism of action that we're focusing on. The first being apoptosis and trying to restimulate chemosensitivity, and that is relacorilant in combination with nab-paclitaxel in advanced platinum-resistant ovarian cancer. Currently in phase II, soon to be phase III, as you'll hear today. The second mechanism of action is to block a growth pathway. When you use a drug like Xtandi or enzalutamide, that's an androgen receptor antagonist, cortisol can get upregulated, and that can help stimulate prostate cancer growth. We're hoping to block that by using either two different drugs. One is the phase I study of relacorilant plus enzalutamide, and that's being done at the University of Chicago as an investigator-initiated study. The second one is at the bottom, which is exicorilant, which is another selective glucocorticoid receptor modulator, and that's being also studied as a Corcept sponsor trial of phase I/IIa study. We're gonna get the results for those studies in the second quarter this year, and that will help guide us on our next path forward in prostate cancer. Finally, the third mechanism of action is around immunosuppression. As all of you know, cortisol is an immunosuppressant, and if we can block that, we can hopefully help resensitize a drug like Keytruda, which is a checkpoint inhibitor, to help really boost that result in adrenal cancer. But since we're here today to talk about ovarian cancer, I wanted to dig a little deeper on that mechanism of action. Now when we say cortisol modulation may enhance and/or restore chemosensitivity, what does that mean? When we talk about apoptosis, what does that mean for cancer? Apoptosis is the tumor-killing effect that chemotherapy is meant to stimulate. That's the programmed cell death that you're trying to help stimulate and therefore kill that cancer. Unfortunately, though, cortisol increases expression of anti-apoptotic genes such as SGK1 as well as others. That's the main gene we typically evaluate. We're using relacorilant as a selective cortisol modulator to compete with cortisol at the GR and hopefully therefore enhance and/or restore chemotherapy sensitivity to a drug like nab-paclitaxel, but we hope to be more drugs beyond just nab-paclitaxel. All of that got us to the point of phase II and now going into phase III, and it gets us to the point of where I'd like to introduce our special speaker, Dr. Thomas Herzog. Now, Dr. Herzog is the deputy director of the University of Cincinnati Cancer Center. He's a professor of obstetrics and gynecology at the University of Cincinnati College of Medicine, and he's also on the board of directors for the Gynecologic Oncology Group, also known as the GOG. It's been a pleasure to work with him over the past few months, especially around his expertise in clinical trial design and regulatory strategy experience. He, as well as all the GOG Partners, have really helped us better understand the phase II results and have been instrumental in helping us design our phase III trial over the past months. He'll be critical as we interact with regulators moving forward. Dr. Herzog, please welcome. Bill, thank you very much. It's a pleasure to be with you this morning and to talk about this exciting platform. I echo the sentiments of being live and in person. We just had a big meeting in Phoenix for the Society of Gynecologic Oncology. Some people were complaining that their feet hurt after about three or four days from dress shoes that hadn't been worn. They're probably all new dress shoes, and a couple of colleagues were actually wearing flip-flops, believe it or not, with their suit on the last day. We're avoiding that at least this morning. Bill, thank you for the kind introduction. I don't think even my mom would say that many nice things about me, so I'm very grateful. It's the difference between a Zoom meeting. Nobody says those things at a Zoom meeting, so it's great. Thank you. Well, it is my pleasure to be here this morning and talk a little bit about the ovarian cancer landscape. We'll spend a couple seconds talking about that and then to really get into, you've heard the background and the why this should or could work, and we'll talk about some real data, which is always much more exciting. I get the opportunity to really, I guess, be the main meal, if you will. I'm excited about that. Hopefully, the questions are dessert, right? We'll do that after this. This is a success story if we look at the prevalence of disease. In the last couple of decades, we have more women alive with ovarian cancer than we've ever had, and they're receiving more and more lines of therapy. We think looking at the literature, with so few studies showing an OS advantage, we really think that it's been the cobbling together of these progression-free survivals that has increased the lifespan for these women. Note that we're not curing a whole lot more women than what we did two decades ago. That's the unfortunate thing so far. Now, we have some new things that are in the arena, and that may change, based on even some of the front-line data that we have with some of the PARPs and so forth. Right now, we think this increase in the prevalence has really been due to those cobbling together, those PFS gains from individual different types of drugs that we can introduce that have unique mechanisms of action. The other thing that's interesting is that, I think people forget how many cases of ovarian cancer are really out there, and I think this shows it well. Although the mortality has decreased slightly, mortality overall, say if you look at 10 years, hasn't changed very much. Our 5-year mortality has changed significantly. We've been able to push out median survival beyond 5 years for even those women with advanced ovarian cancer. I think that's very important. When we think about the ovarian cancer journey for the patient, it's a devastating disease. I was in clinic yesterday and saw multiple patients with ovarian cancer. Unfortunately, most patients who have high-grade serous cancers, which is the majority of the tumors that we see, present with advanced stage disease. Almost three-quarters of the patients present with stage 3 or stage 4 disease, meaning the disease is out of the pelvis when the cancer is diagnosed. Of those patients, up to 70%-80% of those will recur at some point. The majority of patients with advanced ovarian cancer, unfortunately, will have recurrent disease. It's just the question of when, not if. If we look at frontline treatment, that consists of aggressive surgical cytoreduction, either up front or in a neoadjuvant fashion, where we give several cycles of chemo, and then we treat them with maintenance Bev, maintenance PARP, no maintenance, or combination Bev PARP, largely based on molecular markers and signatures, and the presenting symptoms. They then, unfortunately, as I said, recur, and we use a dichotomous break between 0-6 months and greater than six months to define those patients that are platinum sensitive when they recur more than six months or platinum resistant when they recur within six months of the time of having received platinum. We often have patients then that will recur more than six months, and we label them platinum sensitive. They're generally treated with platinum-based regimens again, and maintenance is an option as well in those patients. Unfortunately, we have a number of patients, however, who will recur first time as platinum resistant. You'll see a term up here, platinum refractory. I should explain that and define that because you'll see it on some of the slides as we go through the presentation. Technically, platinum refractory disease is disease that actually grows during primary treatment. These are the worst of the worst patients in that it's a small percentage. The good news about ovarian cancer is that it's a relatively chemo-sensitive disease. That's why, unlike some other solid tumors that you see, you see patients that are on their fourth, fifth, sixth line of therapy because they often respond or at least have stable disease on treatment. How do you get to be platinum resistant? Again, you recur within six months, and that could be primarily, meaning after frontline therapy, or it could be secondarily after you've received treatment for platinum-sensitive disease. The point is that the majority of patients, almost all, are platinum resistant at some time in their natural history of ovarian cancer, especially those that present with advanced stage disease, which again, is the vast majority of patients. What does this look like from a numeric standpoint? We have over 21,000 new cases projected for this year with over 14,000 deaths. It gives us about 20,000 drug-treatable patients per year in the platinum-resistant ovarian cancer space. Platinum resistance occurs in virtually all patients, as I've said. The therapy options that we have, I think everyone's familiar with those. Most of them are either single-agent chemotherapy, such as paclitaxel, pegylated liposomal doxorubicin, or topotecan, which are the FDA-approved agents. That can be alone or in combination with bevacizumab. Then, of course, we have other drugs that are compendium listed, such as gemcitabine, nab-paclitaxel. You know, in terms of, again, looking at the numbers, the outcomes we see with most of these regimens is a progression-free survival median of about 3-4 months. Response rate is generally under 15% if these drugs are used alone, a little bit higher if we add Bev in at the time. Overall survival is under a year for these regimens. We have data, as I mentioned, with nab-paclitaxel. This is a nanoparticle albumin-bound paclitaxel, so it's a different formulation than what we see with paclitaxel itself. There is data. We've done a study within the GOG. It was done within our GOG 126Q, which is platinum-resistant disease, and it's referenced there, Dr. Coleman. You can reference that as to the baseline type of response data that you see. The one thing I would point out in that study that's important is that those patients were all on their first recurrence. Cross-trial comparisons are always dangerous. Of course, we know that, but they're even more dangerous when the entry criteria are different. Keep that in mind. A little bit better group, if you will. As we look at this, what are our options? Well, there's really four options, right? You can always go on to a clinical trial, but many patients don't qualify for a clinical trial, don't wanna go on to a clinical trial. I'm in an academic center. We try very hard to get these patients on to clinical trials because we don't have a lot of great options that are the standard of care currently for platinum-resistant disease. These are the three options that we do have. Single-agent chemotherapy that I just alluded to. You could do those agents and others with bevacizumab, or in some cases, PARP inhibitors, and we'll talk a little bit about each of these. The strengths of the single-agent chemo is that we have multiple agents to choose from. It's kind of like having a lot of quarterbacks on a team that are starters. What do they say? If you have three quarterbacks or two quarterbacks that are your quarterback, you don't have a quarterback. This is kind of where we are with platinum-resistant disease. Key limitations are the efficacy just isn't what it should be, and this is why we have such a great unmet need in terms of drug development in this platinum-resistant space. We need more efficacious drugs with longer durations of response. We also have to look at the patient in this setting. I think that, you know, we're really trying to palliate symptoms at this point. Quality of life is very important, and we sort of have to keep that in mind as we treat these patients. Bev in chemo, it does improve the overall response rate and the PFS. I think the AURELIA trial does a nice job of illustrating that. It's very good at when you add the bevacizumab in. It's very good at managing ascites, large volume ascites, as well as pleural effusions. Downside is that although rare, the side effects are quite severe. We can see GI perforations, severe hypertension, proteinuria, and thromboembolic events. Some of those can even be fatal, especially the GI perforations. Bevacizumab has had an amazing journey in ovarian cancer, has multiple approvals. It has always consistently hit its PFS benchmark for improvement, but it has not been able to improve survival in any of the studies heretofore. PARP therapy, I've sung the praises earlier about maybe even changing the landscape a little bit of ovarian cancer in terms of outcomes. We'll have to wait and see. Very promising in those who have a molecular signature predicting response in those with homologous recombination deficiency, so we're seeing excellent efficacy. Do recall, though, that PARPs were originally developed in platinum-sensitive maintenance and in this space with third line and beyond recurrences. We do have data in this space, so that's encouraging. It's oral, which is great, unless the patient has any GI issues. The only problem, though, is that most of the patients with the molecular signature most likely to benefit from PARP inhibition will have already been treated with a PARP at least once, if not twice. I think you're going to see less and less PARP use in this space because we're now using it in the front line and very aggressively in platinum-sensitive recurrence. I think that it won't be such a great option for us anymore because you know, PARP after PARP after PARP data, it just doesn't exist. Now the exciting part. We get to talk about the randomized phase II study of relacorilant that was performed in this platinum-resistant ovarian cancer space. This space where we have very few great options available. This was, as I said, a randomized phase II study, which I think was very well done in the sense that good numbers of patients with approximately 60 in each cohort. Randomization was one-to-one to one. The patients had to have measurable or evaluable disease, and they were allowed to have up to four prior lines of therapy. You can see here the intermittent relacorilant is in the green there. You can see the schedule and the dose there. The relacorilant was given at 150 mg PO, and the nab-paclitaxel was given at 80 mg/m² intravenously on day 1, 8 and 15 of a 28-day schedule. The relacorilant was given on two days initially, then given the day before the day 8 dose, given on day 8 dose of the nab-paclitaxel, and then the day after, and then that pattern. Then the same thing on day 15, around day 15, and then on day 28. It was given, and then you repeat. The day 28 was actually starting a new cycle. That's the day before, if you will, the 29-day cycle. If you go out 7, 1, 8, 15, 22, 29, you can sort of understand then the pattern. The nab-paclitaxel, again, the dose, is 80 mg/m². Notice that the comparator arm, the nab-paclitaxel dose, was 100 mg/m² intravenous. That's in the purple. The reason it's given on the same schedule, the reason the dose is lower in the combination is because the relacorilant actually decreases hepatic clearance of the nanoparticle albumin-bound paclitaxel. The preclinical data, pharmacokinetics, and pharmacodynamics indicated that a lower dose would be optimal. If you look at the continuous arm, this was where the relacorilant was given every day, and then the nab-paclitaxel was given on the same schedule. The nab-paclitaxel was given on the same schedule in all the arms, just the dose was different in the relacorilant arms, in both the intermittent and continuous. Now, the blue will go away in the sense of I'm going to show you data throughout, but there was not a real difference between the comparator arm and the continuous arm. The arm that was carried forward, which is it's precisely what a phase II, randomized phase II trial is designed to do, is to pick the winner for your phase III trial. This was done very well and by the book, if you will, in terms of selecting the intermittent arm to carry forward. We'll show you that data, and we'll drop some of the curves so it's a little bit clearer as we go through. If you see the blue curves disappearing, it's not that we're trying to hide them. It's because we're trying to make it clear of what you're really going to be using carrying forward between the intermittent and the comparator arms. The primary endpoint of this trial was progression-free survival, as determined by investigator using RECIST 1.1. Key secondary endpoints included response, duration of response, overall survival, and safety data. Baseline characteristics are shown here, well-balanced between the three cohorts. If we concentrate on the intermittent versus comparator, you see that the number that are platinum refractory was higher in the intermittent arm. Remember, these are tougher patients to treat. Most studies that are designed, especially for registration, don't allow these patients into the trial. You had over 10% versus under 2% in the comparator arm. I think as someone assessing this data, that's helpful when if it were the other way around and the intermittent arm did better, I think someone would say, "Well, maybe it's because you had a better group." In this case, I think the argument would be quite the opposite, that you had the tougher group actually in the experimental arm, which was the intermittent versus the comparator. Patients, how many of these have prior taxanes? You know, if you're thinking about where you're using a taxane-based therapy as the comparator, virtually all these patients had that. If you look at the number that do worse, we know number of lines of therapy indicates the lower response rate, lower PFS, and lower overall survival. You see here that fairly well-balanced between the two in a comparison there. Get to the punchline here. This is the progression-free survival as determined by investigator between all three of the cohorts. We'll drop out the continuous there for you to see the intermittent versus the comparator there. Median was 5.6 months versus 3.8 months with a hazard ratio of 0.66. P-value was 0.38, so highly statistically significant. You can see those curves stay apart there. No banana sign there. They're still staying apart. This is looking at the sensitivity analysis, and these are always fun to look at, right? For all the different subgroups and so forth. I think from my perspective, it's always better when all the patients benefit and you don't have a bunch of the lines or the point estimates lying to the right of unity there favoring the experimental arm. It's quite the opposite here. You can see that almost all the points are favoring the intermittent relacorilant arm. There's a couple that are right near unity, but you don't see anything that really favors the experimental regimen in any way. It's consistent throughout the subgroups with all the patients that you see there. Even the confidence interval there does not cross one. Again, remember, this is a phase II, so your numbers are not as robust as what you would have with a phase III, where those confidence intervals would be much tighter. You can see here, if you take out the platinum refractory, those patients, if you look at those patients, they actually did quite well on this particular study. If you look here, if you look at the progression-free survival when you remove those patients, and the reason we're gonna show this curve is because that is the plan for the phase III. What we're trying to do is tell you what would the population of the phase II look like going into phase III if you took out the patients that were primary platinum refractory, and if you took out those that had greater than or equal to four prior lines of therapy. As you can see here, the hazard ratio gets even better. We can knock out the continuous arm, and you can see while the median doesn't change, the hazard ratio is now 0.58. Your P-value is even more impressive at 0.16. These are the swimmer plots here for the three cohorts. What I think is important on this is looking at the median duration of response. You're looking at 5.6 months versus 3.7 months. We'll drop out the blue there, and you can see there the overall response rate similar between the comparator and the intermittent arm, but the duration of response is significantly different. Again, 5.6 versus 3.7 with a hazard ratio of 0.36 and again a P-value that's 0.006. And you can also see here how many patients are still under treatment at the data cut here when this was performed. The arrows indicate the continuing response there. I think it's, like, 7 to 2 in terms of the two arms. Probably not allowed to say with investors, but you know, from a medical standpoint, there is a chance that this data could even be more positive as you get with those patients that are still on treatment. This is looking at the same thing of looking at duration of response when you remove those patients that will not be included in the phase III study. Again, you see duration of response very positive. Becomes even more positive in terms of the hazard ratio, with a hazard ratio of very impressive 0.26 with a P-value of 0.001. Overall survival data is now available, and this is looking at the overall survival for all three cohorts. Again, if we drop out the continuous here, you see that the overall survival was 13.9 months in the intermittent cohort versus the comparator being 12.2 months. Hazard ratio was an impressive 0.67. P-value was 0.66 versus the nab-paclitaxel alone. Again, pretty impressive curves. They almost come together towards the median there or just below the median, and then they're really apart for most of the time there. Again, sensitivity analysis looking at the overall survival. Very impressive again, in terms of the distribution of these different subgroups. If we look at all patients, again, we're seeing the same pattern as what we saw in the PFS sensitivity analysis. Here, if we take out the platinum refractory, or if we look at the platinum refractory again, you see that those patients did very well in this group, as you can see. Again, if we look at the overall survival curves and we remove those patients that are not going to be in the phase III study that's planned. You'll see that the difference is the medians are the same, but the hazard ratio becomes even more impressive at 0.52, p-value is 0.01. Again, very impressive curves in terms of how they stay apart. This is looking at the overall data for all the patients in summary, and I've already shown you all this, I'm not gonna read it all back to you here. From my standpoint, it's consistent throughout the study of looking at the primary and key secondary endpoints with a benefit for those that receive the intermittent relacorilant plus nab-paclitaxel versus nab-paclitaxel alone. These are the p-values and the hazard ratios. Then if you look, if there's any key hazard ratios you wanna pay attention to, you can sort of see how they change more favorably when again, you look at the criteria that you would use for eligibility for the phase III trial, and that's what's shown here. Even more impressive when you look at these comparisons between intermittent comparator for those that are gonna be eligible for our phase III trial. Safety and tolerability. This is all in line with what we would expect from nab-paclitaxel. It appears to me that, clinically, assessing this, that most of the toxicity, if not all, essentially is coming from the nab-paclitaxel. So no big surprises here. In general, what we saw was that the regimen was extremely well-tolerated. Any variances here I think are just due to some small numbers. If you wanna make it a little clearer, we can compare the intermittent versus the experimental arm there. Intermittent versus the control arm, rather. You can see here, most everything was the same. Even the fatigue in that, I think, is probably just a handful or a couple patients that changed that around. When I look at this data in totality from this program, I do think that cortisol modulation appears to be a promising platform moving forward in terms of oncology therapeutics. This study is the first randomized controlled phase II trial, relacorilant plus nab-paclitaxel in patients with platinum-resistant ovarian cancer. Primary peritoneal and fallopian tube cancers are also included in this group. We grouped those together conventionally, so nothing new about how that was done. That's the convention that we use. Under the umbrella of ovarian cancer, we include those diseases as well. This was a heavily pretreated group, as I said, with up to four lines prior therapy, and still substantial benefit was observed and irrespective of which endpoint we used. In all patients, intermittent relacorilant plus nab-paclitaxel improved progression-free survival duration response compared to the control arm. Either. An even greater differential is seen when you exclude the patients again, who we are not planning on enrolling on the planned phase III trial. No additional side effect burden was observed when we looked at the safety and adverse events from this study. I'm gonna tell you about the phase III trial that is planned, and the hope is to get it started second quarter of this year. This is the design of the phase III. Notice it's working, I don't know how much is gonna change, but hopefully not a whole lot because I think it's pretty well designed. GOG Partners full disclosure, I'm on the board of GOG Partners and associate director for GOG Partners was very involved in the design of this trial. I think we understand the regulatory landscape in ovarian cancer very well, and our colleagues in ENGOT in Europe were also involved in the trial, and I'm actually on the liaison committee between GOG Partners and ENGOT. It's been a very good relationship. Leadership from both those groups was involved in the design of this trial. I have to comment that Corcept has been very receptive to our advice and sometimes the advice wasn't delivered as tactfully as it could have been by some of our members. I wanna applaud. Some of the companies I've worked with through GOG have not been as willing to take our advice, and that hasn't always resulted well in terms of regulatory success, but that's another story. Target enrollment for this study is 360 patients. The histology is gonna include high-grade serous and grade 3 endometrioid epithelial ovarian cancers, which is the majority of patients with epithelial cancer. You're over 80%, so it's gonna be a high number that would be eligible based on histology. Those that obviously are platinum resistant, so they progressed within six months of the last dose of platinum therapy. Again, I've said it over and over, who we're excluding. We're getting rid of the patients that are platinum refractory. One of the things people say, "Well, you know, they look pretty good on the phase II sensitivity analysis," and I agree. You could almost argue, it's that's also an unmet need. The problem with platinum refractory, though, is, at times, we're not even dealing with ovarian cancer. Remember, we get into opening the abdomen and very often there's disease everywhere. They get treated with a regimen for ovarian cancer and molecular studies get sent off and signatures and so forth, and then, you know, start having some rectal bleeding. Eventually they get a colonoscopy and lo and behold, it gets reclassified as a colon cancer or something like that. Remember, any irritation of the peritoneal cavity can cause a CA-125 to go up. That's part of the reason why you don't really want platinum refractory on your studies because some of those patients can sneak in, and then once they're on study, intent-to-treat analysis, they're in your data set and you have to live with that inclusion. That's another reason to take those patients out. We have good data. I would reference Ronnie Alvarez's study, I was an author on that paper as well, where we really used to look at just platinum resistance and platinum sensitivity. We now understand that we need to better homogenize our population by looking at other things such as was done with the phase II. We know the molecular signature. Line of therapy is something that's new and this also acknowledges histology. When we put all those together, we have a better understanding of who these patients are and what their expected outcomes are. We can design the study statistically with more precision when we better understand that. It's another reason to remove the heterogeneity of getting these patients out over four lines. Primary endpoint for this study will be progression-free survival, but this time, instead of by investigator, it will be by blinded independent central review. Key secondary endpoints will include overall survival. This is the randomization. The patient would then be randomized to relacorilant plus nab-paclitaxel or investigator's choice chemotherapy, and I'll go over those options in a second. Very similar the same essentially as the phase II in the intermittent is that you have the relacorilant at 150 milligrams PO. The nab-paclitaxel again given at 80 mg because of the reduced hepatic clearance. You can see the schedule there. Schedule's exactly the same, and doses are the same. Another thing that I see some folks do is they make some significant changes between phase II and phase III, which I think is always a dangerous thing to do. Investigator's choice chemotherapy, pegylated liposomal doxorubicin at the community standard dose of 40 mg/m², paclitaxel weekly at 80 mg/m² on a 1, 8, 15 schedule every 28 days. Topotecan given at either a daily ×5 or a weekly schedule. You see two choices there that are available. Then the same control arm with the same schedule that was used in the phase II with the nab-paclitaxel. Physicians can choose amongst these four different drugs and five different options, if you will, because the topotecan has two different schedules that they could choose amongst. I think this lays out the study very well, and I think that the thing that is important is that when we look at the use of growth factors, GCSF was used in all the patients on the intermittent arm in the phase II. Because of the tox profile that was seen in terms of side effects and so forth, neutropenia, the decision's been made to allow that to be at the investigator's discretion, which was what was done in the nab-paclitaxel alone arm or the control arm. It'll be equal for both of those. Any of these, if the investigator wants to use it, they can use it, but it's not mandatory in any of the arms on this study, including the experimental arm. This is my final slide. The reason I put this up here is many people always inquire as to why, how do you choose the primary endpoint on these trials, and is PFS gonna carry the water from a regulatory standpoint or not? In my opinion, it will. PFS is subjective. It's not as objective as overall survival. The problem with overall survival is that what I said is, we're gonna use slightly earlier lines of therapy. Many of those patients will go on to get other active treatment. The problem then is that you have other active treatment that confounds the ability to see the benefit of the regimen. As you saw in our phase II, OS curves looked pretty good. Hopefully with more patients, that endpoint would be met as well, but that just remains to be seen. The primary endpoint, in my opinion, should be BICR, and this is a paper that a lot of my colleagues and I, and you can see some of Rich Pazdur from the FDA and some of the other folks from the FDA wrote from an ovarian cancer workshop back in 2017. We just had another workshop on accelerated approvals in December of this year that we did. We've had a lot of interactions with the FDA, and we feel that this is consistent with their review in this particular space. I wanna thank you so much for allowing me to deliver the fun part of the talk and go over the data. I appreciate you all coming this morning to hear the data. Thank you. Thank you very much, Dr. Herzog. Very well done. Really appreciate that. In conclusion, when we look at cortisol modulation, we believe it has a significant potential across the broad range of oncology products, oncology areas, especially ovarian cancer. When we look specifically at ovarian cancer, we believe based upon the preclinical phase I and phase II results, relacorilant is a differentiated product in platinum-resistant ovarian cancer. A few things I just want you to take home today is, you know, we've seen meaningful efficacy improvements across PFS, duration of response, as well as overall survival. The key thing is while Dr. Herzog showed you various different data cuts, this study was powered on PFS, and even though we looked at data cuts, we hit our overall progression-free survival endpoint, and that's a key piece to take away. While we looked at various different endpoints, that was just exploratory to see how this drug was operating across many different avenues. When we look at the addition of nab-paclitaxel with relacorilant, we saw no additional side effect burden. I think that's key as well because a patient cannot see the efficacy benefit if they cannot tolerate the drug that you're giving them. To me, that gives you overall effectiveness. When we look at the trial or phase II trial, we actually had patients staying on therapy longer in the intermittent arm than any of the other arms, the comparator arm or even the continuous arm. I think that speaks to the side effect profile of adding no additional side effect burden. Finally, when we talk about convenient administration, and when Dr. Herzog took you through the intermittent dosing. The key thing I want you to take away from is really that we're giving a high dose when it matters the most. We're giving a higher dose of relacorilant at 150 milligrams. When it matters the most, meaning we're giving it before, during, and after that of when nab-paclitaxel is administered. With that, we hope that as we go into phase III, if we're able to replicate what we've seen preclinically, which was predictive of what we saw in phase I, which was to me predictive of what we saw in phase II, if we can see those same results in phase III, we're gonna see really unprecedented results for these women with ovarian cancer. Where are we gonna go to next? You know, our future opportunities, we plan to move forward in earlier lines of ovarian cancer after we start the phase III study in the second quarter of this year. We also plan to look at other tumors, as I showed you in the preclinical data. You know, combinations with nab-paclitaxel and many other tumor types. We're gonna look at other combinations with other chemotherapies in these other tumor types. As well, we're gonna look at combinations with other anti-tumor agents. I showed you Keytruda plus relacorilant. We're gonna look at other opportunities for other cancer agents. With that, I'd like to now bring up Atabak, and I'd also like to bring up Hazel and Dorothy as we take questions from all of you. Thank you all very much. All right. Great. For the Q&A session, we're joined by Hazel Hunt, Corcept's Chief Scientific Officer, and Dorothy Nguyen, Corcept's Senior Medical Director leading our ovarian cancer program. Thank you for submitting your questions. We will get to as many as we can, and we will consolidate similar questions in the interest of time. Let's begin. First question is, with an approximately 2-month improvement in overall survival and progression-free survival, is that clinically meaningful? Tom, wanna take that? Sure. Yeah, it's a very good question. Obviously, from a regulatory standpoint, you know, this would be a review issue. I think that one thing that is important to understand is that PFS is a very small part of the curve. When you're comparing Kaplan-Meier curves, to me, the more meaningful parameter is the hazard ratio. The hazard ratios were very impressive irrespective of which endpoint you looked at. Obviously, you know, what the assessment cycles are, number of assessments you know, all those things play a role in terms of the regulatory review. The other big thing that plays a role is what's the toxicity of the experimental compound. In this case, at least the early signals are that it's very minimal with no increased burden for the patient symptomatically. I think with that profile, yes, I think it's very potentially approvable. You, Tom, I think, just accidentally said one thing. What he's saying is that the median is just a single point. Yeah. Yeah. I think that, see, people sort of don't get it. It's not even really a numerical median. It's where it crosses the 50% line, whereas the hazard ratio describes all the data, the entire curve. You know, theoretically, you can imagine two curves were identical to the median, and the median change would be not nothing, there'd be no difference. Then one in one group lived and all the other ones died, you'd still have a median that was identical, but the hazard ratio would be dramatically different. I think that that's really, for somebody who's looking at the whole data set, the critical thing to look at. Yeah. Next question is, what is the regulatory path forward? Have you had an end of phase II meeting with the FDA? Bill? Great. Thank you for that question. We've submitted our end of phase II meeting request, and we're eager to meet with the FDA as soon as possible. We feel excited with all the data that Dr. Herzog has shown you, plus more in the full meeting package. We plan that the FDA should be just as excited as we are to discuss the data. Okay. A follow-on question to that. Have you considered submitting this package for approval now? What is the likelihood of receiving accelerated approval? Well, that'll be left up to discussions with the FDA. We feel very excited about the data, and that'll be part of the discussion when we talk with the FDA. Yeah. I'll just amend that because this is something that we've been talking about now almost for a year since the progression-free survival data. I've said, you know, what I'll say exactly again, you know, our anticipation is we're gonna be doing a phase III study. It's up on clinicaltrials.gov, and that's what we think is gonna be required to get to approval. We're very optimistic about that, but that's our expectation, and I want to make sure that investors have the same expectations consistent with what we have. That said, we're gonna have an interesting conversation with the FDA in the near future. Okay. Next question is how do the results of the nab-paclitaxel only arm look relative to what you would have expected? Tom? Yeah. They're very in line. If you look at the Coleman data, I think the response rate on the 126 study was 23%. The PFS in this study with what I would consider a more unfavorable population based on the number of lines of therapy and allowing platinum refractory in would actually be better. I think theirs was 4.3 months? 4.6. 4.6, and ours was. Yours was 5.6. You know, not trying to again cross-trial comparison, but it was at least as good or better. I think the control arms were consistent. I think overall that there were no concerns raised about the, you know, the control arm under or overperforming. Okay. I guess a follow-on question to that, and you talked about the investigators' choices that compared to arm in the phase III. Can you talk a little bit more about the rationale for that versus the nab-paclitaxel alone? One other thing I'd add about having the nab-paclitaxel in the randomized phase II as well as a choice in the randomized phase III is this is a very strong comparator. If you look at the AURELIA data again, you know, you'll see that how badly some of those drugs perform. Topotecan, I think, was under 5%, and then you added Bev, and it went up. We're looking at drugs that are approved that really in our larger phase III trials, you can look at a immune study, JAVELIN Ovarian 200, and look at how PLD performed. I think it was 8%. You know, we're looking at nab-paclitaxel as being at least as good as paclitaxel, which was by far the strongest in the AURELIA trial, which led to approval in that setting with Bev in that space for platinum-resistant disease for the Bev approval. Then if you look at Teneriello's data, which admittedly was given along with Bev in a straight phase II, and then the Robert L. Coleman data from the GOG, you see that there was really very good performance of the nab-paclitaxel, really even outdoing the weekly paclitaxel. It's a very strong comparator, and I think that that's important to point out. As far as why you design a trial with physician's choice, it really helps enrollment tremendously. Remember, many of these patients have had different journeys to get to this point for their recurrence. Some came through platinum sensitive, some primarily recurred, some of them had, you know, they got something else. They received weekly paclitaxel, for example, maybe with Bev. Then now they're on your study. Well, they wouldn't be eligible if you just made it a weekly paclitaxel study because the peripheral neuropathy and all those things are cumulative. It gives you the ability as a clinician to choose what is best for the patient, and the patient doesn't wanna go on something that they just failed three months ago. It really helps enrollment tremendously, and I think it allows you to make the best choice for the patient based on their toxicity from prior treatments, and what's gonna be in her best interest. I really like the Now you have to limit it somewhat as was done here, but I think, you know, you can't have do whatever you want, but you have to put up standard of care treatments. I think the trial design addresses that very well. Let me just make just one summary point because I think that's all very, you know, important information that you heard. Nab-paclitaxel in our study as a single arm performed as, I think, better than any other single arm treatment that you can find in the literature. Mm-hmm. That's your baseline to compare to what happened with relacorilant. It wasn't being compared to a drug that had an 8% response rate. It was the strongest drug which was available. I think that offering it again and for all the reasons Tom's talking about, I think is very important with the whole group. I think you have to consider the results in that context. Mm-hmm. Next question is, you mentioned excluding primary platinum refractory patients from the phase III. Can you define that more? What does that patient population look like? Maybe discuss something about why you're excluding it. Yeah. I alluded to it during the talk, in that, first of all, it's a very difficult patient to be able to treat because they generally don't respond well to most anything. Occasionally, they're admixed with even cancers of another origin, upper GI tract or lower GI tract, for example. Most studies from a regulatory standpoint do exclude them to try to make the population more homogeneous, which the regulatory agency prefers. Next question is about how do you think about the level of GR expression as a prognostic factor or potentially as a guide for treatment? Yeah, I'll take that. So this goes back to one of the slides that Bill showed, which is something we've talked about before. Not all tumors have the glucocorticoid receptor on them. In fact, you could see sort of the end of the chart, some which had very little. Ovarian cancer does have glucocorticoid receptors, and as you get deeper into treatment, it actually has more glucocorticoid receptors that's upregulated as you go through various cycles. Now, before I answer your question directly, I think that a really important thing, and I just don't want it to get lost here. Tom made the point, but I'll make it again, which is the entire group separated. I mean, that's a really unusual thing in a phase II studies. Believe me, I've been part of, you know, phase II studies where, you know, essentially, you know, the egg is rotten, but you're looking for the part that, you know, somehow isn't. This was not the case. All the people separated, you know, regardless of their various characteristics going in. The phase III study is, in some sense, just literally looking to replicate that result in a larger group of patients. Now, it is true that the people who, in this study, who had the highest GR expression, H-scores greater than 100, did better than those who did, but all of them did well. We're not going to use that as an exclusion criteria going into the phase III study because we think that all patients with platinum-resistant ovarian cancer have the chance to benefit from relacorilant addition. We will keep track of it because from a research point of view, it's an interesting thing. All patients with platinum resistant ovarian cancer who've had multiple treatments will be eligible for the phase III study. Okay. Next question is, can you comment on what is the timeline for completing the phase III study, including completing enrollment and data availability? Bill? The timing, we hope to enroll the study within a year and then run the study for approximately a year. It's about a two-year timeframe. We've got equal number of sites in the U.S. and Europe. It's 40 sites in each, U.S. and Europe, so a total of 80 sites. It's gonna be, as I've told both European investigators as well as U.S. investigators, while it's equal in both geographies, it's competitive enrollment. Those who enroll the fastest, we would appreciate the most. Just one thing to add, 'cause Tom's a little modest about this. I mean, the Gynecologic Oncology Group, where he's on the board in the United States, is the group that does ovarian cancer studies. They are the group that bring things forward to the FDA, and they took on this study, you know, and I'm confident will really shepherd it through, and the equivalent is true in Europe. Our phase II study was a terrific effort led by Dorothy, but I'll joke a little, she did it herself. We had no kind of institutional help with that. Yeah. It still enrolled quite well. If you remember in the pandemic, it enrolled about a quarter quicker than we thought it was because I think as doctors saw the results, they entered patients more rapidly. Yeah. We're hoping that Bill's timelines really are exactly what he says they are. Okay. The next question is, how did you arrive at the number of patients for the phase III trial? What are your powering assumptions, et cetera? Dorothy, would you like to answer that? How did we arrive at the number of patients? Yeah. 3 power assumption. Power assumptions. We're powering the study to evaluate progression-free survival, and that power is 80%-90%, and then we have the OS as a secondary endpoint. It's my recollection, based on the results of the phase II study, this is 90% powered for progression-free survival. Is that correct, Bill? That's correct. With a hazard ratio of 0.7. The average. Yeah. Okay. With a hazard ratio of 0.7. It's gated, hierarchical. Hierarchical gating, meaning that the PFS we evaluated first, and then we will look at the key secondary endpoint first of overall survival, which are important for regulators. Yeah. Okay. Even though PFS, just let me add, is again, if we're able to replicate what we saw in phase II and phase III across all of those parameters, PFS, DOR, and OS, we'll see significant, again, unprecedented results if we're able to replicate that. Okay. The next question is the safety profile of treatment regimens in this patient population an important factor? Tom? Absolutely. So again, if you think about what the goals are of treating someone with platinum-resistant disease, it's to keep them alive for as long as possible. Quality of life becomes a very important parameter that we follow, and it affects our choice of treatment. That's why this platform is particularly appealing in this patient group, where you have a drug that you add on to another agent that doesn't cause additional symptom burden. Safety and toxicity are key parameters. I guess a follow-on question to that is the safety profile of this combination, relacorilant plus nab-paclitaxel, how does that look relative to alternative treatments that you use? Yeah, it looks really favorable. This is, if approved, a regimen that I would use, and I know my colleagues would use. Okay. Next question is, how should we interpret that the overall response rate was similar across the different treatment arms relative to the comparator? Tom, you can answer or I'll answer. I mean. Sure. It's a very high overall response rate. I mean, it's tiny. If you caught what Tom was talking about, in this group of patients with multiple lines of treatment, you often see single-digit response rates. Having about a third of the patients respond really across all lines is really saying something. I mean, the comparator arm did extremely well in the study, as well. I think a really critical thing that was interesting, and it appeared last year but really held up, is that of those who respond, the duration of response for the people who got relacorilant is substantially greater. That actually is why the curves separate, because the people who do respond for much longer. Now, I wish I could say, and I've thought about this a lot over the last year, a priori, who are they gonna be? Unfortunately, you know, we don't really have a signature for that. Consider sort of the value proposition and as Tom's talked about here, you have a medicine which is really not adding side effect burden, and your value proposition is sort of tails you tie, heads you win. Like, why wouldn't I, as a patient, why wouldn't you consider a treatment where you have the possibility to be in that group that has the long duration of response? Otherwise, you're just in a standard group without actually medical cost. Let me add one more point to that too, 'cause that was a great answer. I would again remind you, ORR was a secondary endpoint. Our primary endpoint was PFS, and we powered the study on PFS. Some studies in phase II powered on ORR, overall response, but we did not. We powered it on PFS, and we hit that primary endpoint in our phase II study for all patients. Okay. The next question. How do you think relacorilant fits into the current treatment landscape, and particularly relative to single-agent chemotherapy, Avastin and the PARP inhibitors you mentioned earlier? Tom, would you like to take that? Yeah, I just sort of alluded to that when we were talking about the adverse events and the safety profile. Again, this is a regimen that if it performs as it did in the phase II, is going to be something that will be welcomed into the GYN oncology treatment community. The therapeutic index of this drug looks very favorable. I think that it would be a welcome addition to the landscape, especially with the activity. You know, you mentioned the response rate, but also the duration of response, which is really important. We didn't really get into the concept of stable disease as well, and that can be looked at further in terms of overall clinical benefit, which is a secondary endpoint of the phase III. Based on the mechanism of action and sort of what we're seeing with those durations of responses, I would predict there'll be significant clinical benefit. Obviously, we need to see that in the phase III data. I mean, I wanna add some. I would echo that, and also you have to realize that not all patients, given what Tom described with regards to the side effect profile, would be eligible to get bevacizumab. Because the PARP inhibitor therapy has evolved to come earlier, many patients in this setting would have already had PARP and would not likely have a choice to be receiving PARP. It's a really good- Yeah, yeah. Really good point, Dorothy. It's just that the PARPs just aren't used in this space any longer because the patients with the molecular signature that would respond, again, would have received at least one line and probably two lines by the time they get to this point. Okay. Next question is, how big is the market opportunity in the U.S., for the expected phase III patient population? Yeah. I think that, Tom's slide is accurate. I mean, it's 20-25,000 patients is really this population in the United States. Okay. Looks like two more questions. The key learnings. Can you share your key learnings from the phase II study on patients that can benefit from relacorilant? In particular, is there an opportunity to move to earlier lines of treatment as it seems that as you have progressive lines of treatment, you become more chemo insensitive? I'm gonna pass it over to Tom in a second, but I just wanna make sure everybody understands. I mean, you know, we're going for our first approval in oncology, and we have a circumscribed population where we think we can provide real benefit. That's who we're studying right now. Tom, glad to have you speculate as to where potentially there may be other uses beyond that. Yeah. Purely speculative because I'm not inside your brain, and I don't know what you're gonna do, but I would suspect that if the phase III is positive, that you would wanna look at using it in earlier lines of therapy. It would just make sense, especially as it looks so far, the safety and adverse event profile would favor putting it in combination. You may be able to combine with frontline regimens and platinum sensitive regimens and so forth. It's a very appealing asset from that standpoint, again, because it doesn't add toxicity. Okay. Our last question is: Given that there's a high level of GR expression in many solid tumors, and activity that you've seen in other tumor types, what's next for you? Bill? Well, we're currently also in, again, prostate cancer, and we're in adrenal cancer. You know, as I looked at my first slide of all the different cancers that have GR expression, you know, we're taking a look at all of those in a prioritized fashion to really evaluate internally where we believe we can have the greatest result and meet the highest unmet medical need for patients. It's a deep discussion internally, but yes, we will be picking a few more out of that list of solid tumors to move forward with. Which one today, I cannot speak to, but there will be others. Okay. Great. Well, thank you for joining us today for a very productive update on our ovarian cancer program. Please reach out to us with any follow-up questions. Have a great day. Thank you. Thank you.