Welcome to the Crinetics Pharmaceuticals' third quarter 2024 financial results conference call. At this time, all participants are in a listen-only mode. Following management's prepared remarks, we will hold a question-and-answer session. I would now like to turn the call over to Gayathri Diwakar of Crinetics. Please go ahead. Thank you, Operator. Hello, everyone, and welcome to Crinetics' earnings call. Joining me today are Dr. Scott Struthers, Founder and Chief Executive Officer, and Marc Wilson, Chief Financial Officer. Also joining us for the Q&A portion of the call are Dr. Dana Pizzuti, Chief Medical and Development Officer, and Dr. Alan Krasner, Chief Endocrinologist. A press release announcing the third quarter 2024 financial results was issued today and is also available on our corporate website. As a reminder, we'll be making forward-looking statements, and I invite you to learn more about the risks and uncertainties associated with these statements as disclosed in our SEC filings. Such forward-looking statements are not a guarantee of performance, and the company's actual results could differ materially from those stated or implied in such statements due to risks and uncertainties associated with the company's business. These forward-looking statements are qualified in their entirety by the cautionary statements contained in today's news release, the company's other news releases, and Crinetics' SEC filings, including its annual report on Form 10-K and quarterly reports on 10-Q. I would also like to specify that the content of this conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, November 12th, 2024. Crinetics takes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call. With that, I'll turn the call over to Scott. Thank you, Gayathri. Good afternoon, everyone, and thank you for joining us on our third quarter 2024 results call. We've had yet another incredibly productive quarter with advancements up and down the pipeline, and we continue to strengthen our financial position. For today's call, I will summarize our recent accomplishments shown on slide three, preview some of our upcoming events, and then hand the call over to Marc Wilson for a review of our financials. We'll end, as always, by taking your questions. As some of you may know, November 1st was Acromegaly Awareness Day. We commemorated this day by hosting acromegaly patients at our headquarters to bring life to the impact of our mission of improving patients' lives. That was the picture you saw on the first slide of our presentation today. It was especially timely for Crinetics as we recently submitted our first NDA for our investigational drug, paltusotine, for the treatment and long-term maintenance of acromegaly. We very much look forward to Acromegaly Awareness Day next November. We believe paltusotine will represent a next-generation therapy for people living with acromegaly. We expect to receive the FDA filing notification later in December and expect a standard review period. In the meantime, we continue to focus on building our commercial capabilities and preparing for the anticipated launch of our first drug next fall. As part of these preparations, our national accounts team is meeting with payers to discuss formulary placement and product coverage. We believe that having these conversations early and often allows us to positively influence formulary placement and coverage decisions with the goal of broad access for patients living with acromegaly. In addition, our medical science liaisons are in the field speaking with academic KOLs and community endocrinologists to get their feedback from these clinicians on how treatment protocols are established within their practices and to better understand the patient experience. In addition to preparing for the U.S. paltusotine launch, we're also in the early stages of building capabilities for commercialization of paltusotine and to support global clinical development of our other potential future drugs in the pipeline. As you are aware, we partnered paltusotine in Japan with SKK, and they are doing an excellent job of advancing our Japanese phase three trial in patients with acromegaly. Based on the strength of the clinical data for paltusotine and atumelnant, the depth of our evolving pipeline, and the capabilities of Crinetics today, we believe that we can retain more of the global value of our pipeline by maintaining closer control of the European market and development activities. Towards this, we anticipate submitting the MAA in the first half of next year for the use of paltusotine in patients with acromegaly. We have also recently established operations in Switzerland, hired a general manager for Europe, and are recruiting supporting staff in the areas of regulatory, market access, medical affairs, and operations. We are committed to eventually bringing paltusotine and our other future products to patients in Europe and the rest of the world. But as with all our investments, we will do so in a fiscally prudent way and consider the continuously evolving reimbursement landscape in making final decisions about where and when to launch. Carcinoid syndrome is the second indication in development with paltusotine. We reported positive results from our phase two study earlier this year, and we remain on track to start the phase three trial on our anticipated timeline. We've had productive interactions with the FDA regarding the phase three protocol and received feedback on details of endpoints, inclusion criteria, rescue criteria, etc. We are finalizing the protocol and expect to begin site activation activity shortly. Paltusotine is just the first of many therapeutic candidates that we have been purposely designed in-house to transform the treatment of endocrine conditions. Beyond paltusotine, our investigational drug atumelnant is in phase two development for both congenital adrenal hyperplasia, or CAH, and Cushing's disease. We previously shared exciting initial data from both of atumelnant's phase 2 studies earlier this year at the Endocrine Society's annual meeting in June. As a reminder, we previously showed partial data from a small subset of patients at Endo. By early next year, we plan to share the complete 12 weeks of data from all the 28 patients recruited across three doses, 40, 80, and 120 milligrams. We expect to initiate a phase 3 study in adults with CAH in the first half of 2025. There's also a very high level of unmet need in children with CAH due to the irreversible effects of early hyperandrogenism and the consequences of supraphysiologic glucocorticoid use. We plan to initiate a pediatric CAH program with atumelnant in 2025. We also shared remarkable initial data at the endocrine meeting about the use of atumelnant in patients with Cushing's disease. Encouraged by the positive emergent data, we are also planning to initiate a full development program in Cushing's in 2025, pending regulatory feedback on program design. We've also continued to make great progress on our early stage pipeline, as shown on slide four, with four new candidates currently the subject of first-in-human enabling activities with INDs anticipated next year if these studies are positive. As we mentioned previously, IND enabling studies of our PTH receptor antagonist in development for hyperparathyroidism are ongoing. Assuming positive results, we expect to file an IND for this candidate in 2025. We've also initiated IND enabling studies of our SST3 agonist for autosomal dominant polycystic kidney disease. Assuming positive results, we expect to file an IND in 2025. Today, we are excited to announce that we recently nominated a development candidate for our TSH antagonist program. As you may recall, a TSH antagonist could be developed for both Graves' hyperthyroidism and Graves' ophthalmopathy, often referred to as thyroid eye disease or TED. We are initiating IND enabling studies for this compound. Assuming positive results, we expect to file an IND in 2025. As you can see from our progress in these programs, our commitment to GPCR drug discovery continues to unlock scientific and medical innovations that have the potential to bring transformative therapies to patients and significant value to our co-owners. We believe we have a unique, deep pipeline of drug candidates. These were all developed by our in-house R&D team and driven by a passion for the pursuit of science and medicine to help patients. Our goal is to relieve the burden of disease so that patients can focus on living their lives. To date, our drug discovery and development efforts have been focused on novel therapies to manage endocrine disorders, including those caused by the secretory activity of endocrine tumors. Today, I'd like to introduce you to non-peptide drug conjugates, or NDCs. NDCs are a new technology that we've developed in-house, enabled by our premier in-house drug discovery capabilities in the area of GPCRs. This novel platform leverages endocrine receptors for highly selective targeting of anti-tumor agents with the goal of treating the underlying tumors themselves. If successful, we anticipate our NDC platform may be applicable to a wide range of different cancers. We're extremely excited about the long-term potential of this approach. By way of background, we've all heard a lot about the success of antibody drug conjugates, or ADCs, in cancers. These combine a targeting antibody that recognizes tumor cell surface markers and delivers a cytotoxic payload to the constituent tumor cells. ADCs are now a well-validated platform and contribute to the therapeutic armamentarium for a wide range of different cancers. NDCs leverage Crinetics' deep expertise in small molecule ligand design for GPCR targets to replace the antibody of ADCs with a fit-for-purpose, novel small molecule. This is non-peptide. Our first NDC candidate from this platform is CRN09682, and its overall design is shown on slide five. The NDC approach is intended to enhance tumor penetration, selectively target specific GPCR-expressing tumor cells, induce internalization, and selectively release a potent anti-tumor agent intracellularly, all while minimizing systemic exposure and toxicities. Additionally, NDCs are manufactured by traditional chemical synthesis methods, avoiding the limitations of complex and heterogeneous manufacturing methods required by most ADCs. 9682 is made up of small molecule SST2 agonists optimized to selectively bind with high affinity and potently induce internalization, then trafficking to specific intracellular targets. This is in contrast to paltusotine, which was designed to minimize internalization in order to maximize G-protein signaling at the plasma membrane to inhibit growth hormone and serotonin secretion. The small molecule agonist in 9682 is linked to a monomethyl auristatin E, or MMAE, which is a well-established cytotoxic payload in approved ADCs. The linker was designed to be selectively cleaved by enzymes only present in specific intracellular compartments and not present in the general circulation. When intact, 9682 has little cytotoxicity, but when the MMAE portion is released inside the cell, it causes cell cycle arrest and subsequent apoptosis or cell death. The net result of all this craftsmanship is a low molecular weight compound that readily penetrates solid tumors and, as shown on slide six, selectively delivers its payload to the inside of tumor cells where it accumulates and kills these cells with little circulating free payload and associated toxicities. In preclinical in vivo tumor models, 9682 is very effective at shrinking and often eliminating well-established tumors in mice. The IND enabling toxicology studies so far suggest a more than adequate preclinical safety margin to begin clinical evaluation. The IND enabling studies are nearly complete, and we anticipate filing an IND to support the clinical development of 9682 in early 2025. Details of the design and preclinical results for 9682 are expected to be presented at the North American Neuroendocrine Tumor Society meeting in Chicago later this month. The 9682 clinical development plan will begin with a dose range finding study in patients with SST2-expressing tumors, including NETs. This leverages the routine use of SST2-targeted PET imaging agents in patients to precisely identify patients whose tumors express SST2 and are therefore good candidates for 9682. Strategically, we believe the development of 9682 in patients with non-functional NETs is complementary to the use of paltusotine in patients with the functional NETs who develop carcinoid syndrome. We'll be working with many of the same centers and investigators for the development of both compounds. When metastatic, NETs are typically incurable with surgery or current therapies, regardless of tumor grade. We believe this is a large population with high unmet need, and we are excited to be developing 9682 for these patients. As you can probably tell, we're very excited about the potential of this first-in-class NDC that may provide an important new treatment option for patients with NETs and potentially multiple other SST2-expressing tumor types. Beyond SST2, we'll use our experience with 9682 to learn how to best optimize and develop future NDCs for other GPCR targets and cancer types. As you can see from this update, we have a robust pipeline shown on slide seven, spanning registration, late-stage development, and discovery. Our recent $575 million equity offering positions us to continue delivering important, innovative medicines well beyond the paltusotine launch in acromegaly next year, anticipated paltusotine launch. Our existing pipeline is filled with possibilities to bring new hope to patients struggling with many different endocrine conditions and endocrine-related tumors. Those who have followed the history of Crinetics know that we have always been judicious with our spending and thoughtful about deploying capital in a way that creates both hope for our patients and value for our co-owners. We will continue to carefully steward the resources with which we have been entrusted as we continue the exciting trajectory of growth and transformation at Crinetics. With that, I'll now hand it over to Marc to review the financials. Marc? Thank you, Scott. Turning to slide eight, Crinetics continues to be in a strong financial position, having ended the third quarter with approximately $863 million in cash and investments. As Scott mentioned, we completed a $575 million public offering that closed after the end of the third quarter. This further strengthened our financial position, and our cash, cash equivalents, and investment securities following the equity offering totaled approximately $1.4 billion on a pro forma basis. We project that with the proceeds from the recent offering, we will be able to fund our current operating plan into 2029. That operating plan includes the commercialization of paltusotine for acromegaly if approved, as well as the initiation of multiple later-stage clinical trials in carcinoid syndrome, in CAH, and in Cushing's disease. In addition, we plan to continue investing in the product candidates that are emerging from our discovery pipeline, including the four development candidates that have been nominated this year. With respect to the financial results, there were no revenues for the quarter ended September 30, 2024, compared to $0.3 million for the same period in 2023. The third quarter 2024 revenues were derived from the paltusotine licensing arrangement with our Japanese partner, SKK. Research and development expenses were $61.9 million for the quarter ended September 30, 2024, compared to $43.8 million for the same period in 2023. The increase was primarily driven by higher personnel costs, outside services, and manufacturing activities, the majority of which were attributable to the advancement of the paltusotine and atumelnant development programs and the expansion of our preclinical portfolio. For the quarter ended September 30, 2024, general and administrative expenses were $25.9 million compared to $15.5 million for the same period in 2023. These increases were primarily due to higher personnel costs and commercial planning activities. Net loss for the quarter ended September 30, 2024, was $76.8 million compared to a net loss of $57.5 million for the same period in 2023. Net cash used for operating activities for the quarter ended September 30, 2024, was $62.8 million. We plan to provide updated financial guidance during our year-end earnings call in the first quarter of 2025. It is worth highlighting that in the next year, we plan to initiate multiple phase 3 studies in carcinoid syndrome and in adults with CAH. In addition, we are planning to initiate later-stage development in pediatrics with CAH and in Cushing's disease. As such, we expect our quarterly R&D spend will increase as we initiate and advance paltusotine and atumelnant into these clinical trials over the remainder of this year and throughout 2025. We also anticipate increases in SG&A expenses as we prepare for the potential launch of paltusotine for acromegaly. Crinetics has practiced disciplined expense management, and that continues to be our goal as we continue to grow the organization and invest in our deep pipeline, and we are well financed to do so. I will now hand it back to Scott for closing remarks before we begin Q&A. Thank you, Marc. I'm incredibly excited about the future of Crinetics. As we look to the end of 2024 and the start of 2025, we will continue to build on our strong progress. We've consistently delivered on our plans, and we're committed to maintaining this level of execution. We look forward to sharing upcoming clinical and regulatory milestones from paltusotine and atumelnant and updates on the continued advancement of our deep pipeline of emerging candidates. Crinetics continues to be well positioned to become the premier, fully integrated, endocrine-focused global pharmaceutical company. Thank you all for your attention. Operator, we're ready to take your questions. Thank you, sir. And at this time, if you would like to ask a question, please press the star one on your telephone keypads. You may remove yourself from the queue at any time by pressing star two. And once again, that is star one to ask a question. We'll take our first question from Cory Jubinville with LifeSci Capital. Please go ahead. Hey, congrats on the news, and thanks for taking our questions. NDCs and CRN09682, it's pretty exciting. Anything more you could tell us about this program and kind of where you see it best fitting within the existing paradigm? And I guess what else are some of the key challenges that needed to be overcome to develop an NDC, and what are some of the specific advantages you could point to of an NDC approach over, say, ADCs or radiotherapies? Thanks, Cory. So for more details, I'd encourage folks to come to Chicago for the NANETS meeting where we'll be presenting some of the preclinical data on 9682 and data on paltusotine and carcinoid syndrome and can talk at some more length with data in hand. But broadly, the NDC platform is an extension of the types of ideas that led to the formation of Radionetics a few years ago. We believe that these non-peptides, small molecules, provide a variety of different advantages when targeting GPCRs over antibodies in the typical NDC formats. For one thing, GPCRs are very difficult to make antibodies against, yet they're a whole class of selectively expressed cell surface targets. Unlike many of the targets of ADCs, binding of ligands to GPCRs can be tuned to selectively optimize internalization of these conjugates into the inside of the cell, which is something you want to do for selective intracellular cleavage. So I think it opens up new targets. It opens up simpler chemical synthesis. It opens up the ability to tune things in ways that you can't with antibodies. Something as simple as most antibodies will stick around for weeks, whereas we can clear small molecules in a day or two. So I think it offers a number of different potential advantages, but with 9682, we're going to go learn about what these are in a real-world setting and in the type of patients that we're already working with neuroendocrine tumors for those who have carcinoid syndrome. So it's highly synergistic with our ongoing efforts for paltusotine, the internal relationships we've developed with the investigators and the patient community, and it's pioneering this new idea about how we might branch out and use our core platform to expand into anti-tumor agents. Excellent. Thanks for taking our questions. I'll hop back in the queue. Thanks, Cory. Thank you. And thank you. We'll next go to Jessica Fye with JPMorgan. Please go ahead. My question. So with several products entering the clinic next year, what's the soonest that we can expect phase 1 data from any of those, and which will it be from? And then if I could sneak a couple in on 9682, can you talk about how you chose the MMA toxin for that product and how different or similar the ligand is to paltusotine? Okay. There's a good batch. Thanks, Jess, and look forward to seeing you later this week. In terms of the timeline on the different programs, I think we'll probably stick away from providing precise guidelines on each of those. Just have to stay tuned throughout the year and see how they come. In part, it's because you also don't know how far you need to go up in dose-response curves to know when you're starting to get meaningful results. It's a little difficult to predict when they'll each complete, but I think you can expect a nice flow of new information from those and some other compounds that are getting close over the next year and a little into 2026, and then in terms of 9682, it's not paltusotine. It's not a direct homolog of paltusotine. It's another SST2 agonist that was selectively optimized to be the best ligand we could get for the purpose at hand, which is to bind selectively and internalize receptors and get the right biodistribution so it spends very little time in the periphery. And all those various factors were considered as we built that conjugate, both the ligand and the linker group. And MMAE was chosen simply because it's a very well-established payload in the ADC world, but we have ongoing activities to explore alternative payloads as well, and that may be seen in some of our backup or follow-on compounds. Thank you. Thank you. Next, we're going to go to Jeff Hung with Morgan Stanley. Please go ahead. Thanks for taking my question. From your early-stage pipeline, how are you thinking about the obesity indications for candidate selection in 2025? What would you need to see with your GLP-1 or GIP programs in order to have confidence advancing those given the increasingly competitive landscape? Thanks. Thank you. And what I think we're seeing in the competitive landscape is some of the limitations that arise if you're not super careful about how you select candidates. These are things as simple as getting to easily manufactured dose levels. Clearly, there's questions around tolerability in some molecules and the doses needed for good weight loss versus good tolerability. And we have a variety of different hypotheses we're testing as we tune these molecules to be what we think can be the best-in-class profile for an easy-to-synthesize small molecule GLP-1 agonist. Basically, the cost-limiting step is we want a really, really good molecule, and we're not going to settle for anything less than what we think is as close as reasonably expected to perfection. Thank you. Thank you. Next, we're going to go to Brian Skorney with Baird. Please go ahead. Hey, guys. This is Charlie on for Brian. Just kind of piggybacking off the last question, noting that your GLP-1 and GIP assets are non-peptides, how are you guys thinking about the potential advantage of a non-peptide compound here relative to other assets in the space? Thanks. I think the whole field in the obesity space is moving towards alternative modes for delivery of the activity. The main challenge on the peptides is twofold. One is manufacturing that I think everybody and their brother has been hearing about. But also, peptides just limit you in the physical-chemical space that you can explore and the delivery methods that you can utilize. And with small molecules, you don't have those limitations. You can tune every dimension of chemical space to get the types of physiologic or pharmacologic activities, pharmacokinetic activities, and test different types of hypotheses to get the right clinical profile. And so I think what today's talk about 9682 and paltusotine gives you a sense of some of the depth of types of things we try and optimize when we're making small molecule drugs. And you'll see us employ all these different types of techniques as we're applying it to the obesity space and in molecules that can be made at scale because this is one of the biggest public health problems in the world, or at least in most Western societies. Got it. Thank you. And Dennis, your line is open. Hi. Thanks for taking our questions. I had one on the non-peptide drug conjugate. Can you remind us of the common toxicities associated with MMAE ADCs like Polivy, Padcev, and Tivdak? And just curious around your confidence and your ability to thread the needle on efficacy and tolerability. Thank you. Yeah. Thank you. It's a great question and certainly something we explored carefully in our preclinical program. Now we need to see it in a clinical setting. But we obviously were aware of the types of common toxicities for MMAE and looked carefully for that in the preclinical packages. And we think we've got very, very good margins. And in part, that's because we tuned the molecule so there's very little circulating free MMAE. The conjugates are cleared rapidly from the systemic accumulation, but cleaved MMAE is accumulated both rapidly and persistently in tumor cells. And we'll show this data at NANETS. Perfect. Thank you. Thanks. Thank you. And next, we'll go to Joe Schwartz with Leerink Partners. Please go ahead. Thank you. It's great to see you select a TSH antagonist development candidate. So I was wondering if you could talk about what your criteria has been for the characteristics you need to reach in order to be satisfied that the candidate meets your criteria. And how high is the hurdle here compared to what you needed to clear for other programs such as paltusotine and atumelnant? And then from a biological standpoint, how should we think about the relative degree of efficacy which an IGF-1 or a TSH antagonist can inherently offer almost equal based on crosstalk or any other factors? So just the chemistry and the biology, if you could address those, that would be great. Thank you. Yeah. Great question, Joe. Philosophically, we try and make every molecule as high a quality of a drug candidate as we can. Frankly, I'll tell you that when we advanced paltusotine into the clinic, we took a couple of risks. One is there was a slight risk of drug-drug interactions, which we disproved later in the clinic. And there was a slight risk of lower-than-hoped oral bioavailability, which we disproved later in the clinic. So we did very well with paltusotine, I think you'll agree. But as we get into some of these more prevalent indications like Graves' disease or obesity, we're adding extra layers of carefulness, including broad testing against any other potential liability, making sure the physical-chemical properties are good, making sure it's scalable at high levels of production because you're going to have a lot more patients in Graves' disease than you would in acromegaly, for example. So I don't think we've changed our goals that much, but we're just looking with an even closer eye at the quality of these candidates as you get into the very, very large indications. And then I'm sorry, I missed the—what was the second part about that? Oh, it just seems like your TSH antagonist has a different approach. Oh, yeah. Yeah, yeah, yeah. Yeah. So remember in Graves' Disease, the root cause of the disease is autoantibodies which bind to the TSH receptor and activate cell signaling. And our candidates that are TSH receptor antagonists block the activity of those antibodies at the level of the receptor. Now, in Graves' eye disease, what happens in the cells at the back of the eye is those antibodies bind to the TSH receptor that activates the TSH receptor, which then signals down its main pathway of cyclic AMP. But it also cross-activates the IGF-1 receptor. And that IGF receptor also starts signaling into the back of the eye. And Tepezza and the other drugs are aimed at IGF signaling or acting downstream of TSH. So if you block the activity of the TSH receptor, and we've shown this in preclinical studies that I believe we published at Endo last year, you also block the signaling of IGF in the cells from the back of the eye. So generally, we expect this to be more efficacious or at least equally efficacious as the IGF approaches. And it can be used to treat the underlying Graves' at the level of the thyroid. And if we had the right drug for the treatment of Graves' disease itself, we wouldn't be having thyroid eye disease. So one of the challenges for this program is to figure out the sequence of indications that we address in later-stage trials. Very helpful. Thank you. Thank you. Next, we'll go to Douglas Tsao with H.C. Wainwright. Please go ahead. Hi. Good afternoon. Thanks for taking the questions and congrats on the progress. I guess, Scott, maybe as a follow-up to that, I mean, historically, you as a company have been very innovative in terms of using sort of phase 1 studies to provide very compelling proof-of-mechanism data that has really sort of given confidence in de-risk programs as they enter phase 2 and ultimately phase 3. When you think about the TSH program and Graves' as well as TED, from your sort of initial sense, will you be able to accomplish that in sort of a phase 1, phase 1b study? And will that necessarily inform the initial direction you take with that program in terms of the sort of time at which you sort of intervene with Graves' and if patients are already starting to show manifestations of eye disease? Thank you. Thanks. Why don't I let Alan answer that question? Thanks, Doug. Yeah. I think actually a TSH antagonist is very, very. It would be a nice model in phase 1 to evaluate in the sense that we do have biomarkers that we can evaluate in real time as we've done in our previous phase 1 studies before. In particular, thyroid hormone levels, TSH, and T4 responses to a TSH antagonist could tell us, I think, in theory at least, very quickly whether we're hitting the intended pharmacologic target as we've done in other studies before. So now it's a typical phase 1 study. That time course is a little short to measure efficacy in thyroid eye disease. But certainly, this is still, I think, a good candidate for pharmacologic proof of concept even in phase 1. Okay. Great. Thank you. Perfect. And next, we're going to go to Jon Wolleben with Citizens JMP. Please go ahead. Hi. This is Kathryn on for Jon. I have a question about the carcinoid syndrome program, and if you can give any additional color on kind of the feedback from the FDA and how you kind of foresee the phase three program looking relative to kind of what's been guided before, anything that the FDA has kind of required that's sort of been unexpected? Yeah. Why don't I let Dana answer that question? Yeah. Well, thanks for the question. Yeah. The interaction with the FDA on carcinoid went very well. I think that there were many areas that we had agreement on and then needed their perspective on issues like the endpoints and duration of the trial, but we had anticipated a lot of those potential perspectives, and it wasn't very challenging to be able to accommodate those changes into our proposed plan, so we're just finalizing that right now. We are continuing to be on track to get that started in the same timeframe that we've always been saying. Thank you so much. Next, we're going to go to Leland Gershell with Oppenheimer. Please go ahead. Hi. Thanks for taking my questions and for unveiling this new program in NDC. Scott, just wanted to ask sort of a far-forward-looking question with respect to the opportunities here with this new approach as we think about ways in which you can tune ligands to successfully cause the internalization of GPCRs versus not having them be internalized, i.e., with paltusotine. Are you able to identify others that you could approach following the first compound for perhaps other tumor types with GPCRs? Thanks. Yeah. Thanks, Leland. I think there's lots of other opportunities. But at this point, we really want to learn from 9682 about what it's really going to take to be successful in the clinic. And I think those lessons that we'll learn there, both in pharmacokinetics and tumor responses and lines of therapy and things like that, will be very informative for us. So in the meantime, the discovery group is exploring new ideas, new payloads, new targets, things like that. But before we advance the next one, we really want to see how this does. Got it. And then just a question on the TSH antagonist. Good to see that it's nominated. So will you be planning to study that in Graves' and TED as separate kind of campaigns? Or will you be looking at kind of an overarching Graves' development program with TED as constituting a sort of a subset of those patients? Thanks. Well, I think it's maybe a little early to discuss the overall strategy there. You might imagine there's both some questions we need to ask ourselves around the economics of the two different indications and the feasibility of recruiting in the different indications and the competitive environments. But honestly, I think this is the absolutely best approach for both Graves' hyperthyroidism and Graves' associated ophthalmopathy or TED. We just have to figure out how to stage those investments. Great. Thanks very much. Thank you. And we'll take our next question from Catherine Novack with Jones Trading. Please go ahead. Hi. Afternoon, guys. Thank you so much for taking my questions. Just one on CAH. Given that this is an area that has not really seen any new approvals in recent years, what learnings were you able to take from Neurocrine's pivotal programs when you go to design your own that maybe you can learn from anything or have better designs? And then what do you anticipate the standard of care would be following potential crinecerfont approval next year? Well, I think crinecerfont, if it's approved, will be the first drug specifically for CAH ever. We've used glucocorticoids to treat these patients. But I'm excited to see the potential approval there and the type of labeling that is awarded by the FDA, assuming all goes well. And I think it will be incorporated into the standard of care for some patients. What we've learned is about the role of different hormones in this pathway. And we've speculated for years about how much of the HPA axis is controlled by CRF or vasopressin or ACTH. And I think it's pretty clear now with our early data and Neurocrine's phase three data that CRF contributes to the activation of the adrenal. But the stimulation of the adrenal is not completely dependent on CRF, whereas it does appear to be nearly completely dependent upon ACTH, as we expect. So I think we've chosen the ideal target in the pathway and be looking forward to talking more about the rest of the data we have in the not-too-very-distant future. And at that time, we should be able to clarify more about our phase three plans too. Great. Well, looking forward to the rest of the data. Thanks very much for taking my questions. Thanks, Kathryn. We'll take our next question from Yasmeen Rahimi from Piper Sandler. Please go ahead. Good afternoon, team. Thank you so much for the really nice surprise. I definitely caught many of us for this really wonderful update. And I'm sure a ton of work went into this. So I guess the question to ask is, in terms of development for NANETS, what would a path look like? I mean, I think many of us may think of these tumors more slow-growing, take a long time to show a separation. Could you maybe educate us what a path would look like? And next, if you decided to pursue that, that would be really important. And how big that market would be if you've done any work in that regard? Yeah. Thanks, Yaz. I hope we're able to provide a few surprises every now and then. And we've got a very active discovery group that is working really hard. We just want to make sure we got things ready for prime time before we start talking about them. But Alan, maybe you want to comment on some of our ideas on development for this? Yeah. Yeah. So we're planning on starting with an oncology-style phase one study, which is a little bit different than our phase one endocrine trials. The first step, of course, is to escalate doses from a safe starting dose in volunteers with tumors and increasing that dose in subsequent cohorts till we get close to a maximally tolerated dose. The kinds of tumors we're talking about that would be included in such a trial would be patients who have SST2 receptor-expressing tumors. Those are largely patients with neuroendocrine tumors, although I will point out that there are variants of neuroendocrine tumors and even tumors which are not technically neuroendocrine tumors, which can express these receptors. We're going to be pretty agnostic as to which patients we study because these are patients often who have a great deal of medical need. These are patients who would have progressing disease. We'll first define the right dose and then proceed to dose expansion cohorts where, once we have sort of a dose which we expect to be well-tolerated and potentially therapeutic, we would explore a variety of different kinds of tumor types based on the origin of the neuroendocrine tumor. Assuming that's all successful, then we would look at this kind of novel potentially therapeutic compound in patients who have progressive disease and need adjunctive therapy to improve outcomes in phase two and potentially phase three as well. This is a very novel approach. It's a very exciting approach. This is, I would say, a fairly underserved patient population. There's a lot of research going on in the neuroendocrine tumor and related tumors now, but not a lot of great options, particularly beyond PRRT, which is a radioactive therapy. This is a non-radioactive therapy, which we hope would be similarly effective or better. And you could imagine a lot of advantages to using a small molecule as opposed to a very discreet treatment with a radioactive therapy in the long run. So we're very excited. We would follow this kind of oncology path to approval hopefully someday. And just to follow up on your population size, we're still working on some of that. But you'll recall we've said that the carcinoid syndrome patients are roughly 20% of the total population of the neuroendocrine tumor patients. And the vast majority of neuroendocrine tumors do express SST2. So we expect this, just in the NETs space, to be quite a bit larger population than just the carcinoid. And then you'll see, if you look in the radiopharmaceutical space, where there's a lot of entrants in the SST2-targeted radiopharmaceuticals, that they're starting to expand out into some of the other tumor types. In particular, there's certain types of breast cancer that express SST2. Many head and neck cancers express SST2 and some of the pheochromocytoma, other types of more rare cancers. So that's something we're working on, making sure we understand the full potential. But it's not small. Thank you so much. Congrats again. Great. Thank you. Great surprise. Thank you. I'd now like to turn the call back over to Scott Struthers for any closing or additional remarks. No. Thank you, everybody. Thank you for your attention to our story and your support in our financing and participating with the success and growth of the company. We appreciate it and look forward to talking to many of you in the coming days and weeks. Thank you. This does conclude today's program. Thank you for your participation. You may disconnect at any time.