Great. Welcome, everyone. My name's Jess Fye. I'm a Biotech Analyst at JP Morgan, and we are continuing the 43rd Annual Healthcare Conference today with Crinetics. You're going to hear a presentation from the company's CEO, and then we'll go into some Q&A. If you're sitting in the room and you want to ask a question, raise your hand, and someone will bring you a mic. Or you can send them to me through the portal, and I'll get them on this iPad up here. But with that, let me pass it over to Crinetics CEO, Scott Struthers.
Thank you, Jess, and thanks for having us today. I appreciate the opportunity to be here, and all of you for coming in person. I look forward to providing everyone an update as to where we're going as an organization and our vision, and you might be asking why there's a picture of a fruit tree on our opening slide, and those of you here last year might remember we opened a new facility last year, and as part of that, planted 35 fruit trees around the facility, and they were scrawny at the time, and one had one orange, and that's the picture I showed. This year, we've got a lot of growth, a lot of fruit coming to ripen, and it's very much like Crinetics, where we're planning on growing and building new things in our pipeline.
I want to tell you today about that vision for the future, because if you imagine these fruit trees and you imagine the companies and the company and where we'll be later this year, next year, the year after that, our plan is to continue to grow and build value for both us who own the stock and, more importantly, for the patients around the world who can benefit from the science that we're working on. With that, my safe harbor statement. I want to start out that our central goal and my personal passion is to build the world's premier endocrine company, and nothing short of that is going to be good enough. We're discovering and developing, and now soon to be commercializing, a next generation of therapeutics for endocrine diseases and beyond that.
These new medicines will improve the lives of millions of people around the world, and today I'm going to update you on progress towards that strategy and how we're trying to achieve that goal, so if you look back at the second half of 2023 and then 2024, despite the rocky trading we've seen for ourselves and others this week and in the last few days, our vision has been moving forward up and down the pipeline in building both clinical data and assets, as well as the company's capability itself, and some of that is summarized here, so on the paltusotine front, which is our lead asset, we've completed a phase III program for acromegaly with remarkable data. The NDA for that has been submitted to the FDA. We're working on our MAA submission. We have a PDUFA date for the U.S. in September of this year.
We also showed positive results in paltusotine for carcinoid syndrome, which is a severe complication of neuroendocrine tumors, and we're initiating a phase III trial now. We've built a commercial organization, and we're continuing to build that organization so that we're ready for launch for this year for paltusotine, but also for things coming in the future in the pipeline. Atumelnant is a novel ACTH antagonist where we've shown positive phase II results in studies of congenital adrenal hyperplasia and Cushing's disease. The pipeline continues to expand. Everything I'm telling you about today, we built in-house with our internal laboratories, and we have four new molecules entering IND-enabling studies right now, including one which is a whole new platform of non-peptide drug conjugates for the treatment of tumors expressing peptide hormone receptors, in this case, somatostatin, but we plan to expand that platform into other areas.
In addition to all this, last year we strengthened our balance sheet, and as of the end of the last third quarter, we had $1.4 billion in cash. This takes us into 2029. So financially, we're very strong, and this enables us to build out this vision of the pipeline that I'll be telling you about today. So building on that momentum, I want to take a moment to share with you how we've been able to do all that. I think we've proven that we've built a world-class discovery organization. We've got great drug hunters in the difficult GPCR space. We've got an experienced team that has built a robust pipeline now with nine programs, all internally discovered, all wholly owned assets, and the IP goes into the 2040s.
We continue to invest in new discovery, and there's always a bunch of projects going on in the discovery kitchen, sometimes ones they don't tell me about, so I'm often surprised what may pop out. We've also proven with five global positive phase III trial readouts in the last two years that we can do high-quality global clinical trials, and we're getting better at it with each one. This is our first NDA, and that'll come out, as I said, in September, but I look forward to many new NDAs to come and other global marketing applications. So from all that, expect a steady stream of catalysts in the coming year and years to come.
Now I need to transform the organization into a successful commercial organization, and we're well along our way of doing that, building out these capabilities to support the launch of acromegaly, but also the rest of the things coming from the discovery and then development in our pipeline. And part of that is really to ensure that the next generation of patients have, sorry, that patients have access to the next generation drugs. And I think each of these advances the practice of medicine in that area substantially. And we spend a lot of time talking to patients about what they need, in addition to our colleagues in the clinical side of things, but so that you'll see in our trials we're measuring things that matter to patients in addition to the regulatory outcomes that we need from a filing point of view.
Let's start with acromegaly, where our goal is to offer a whole new level of care to patients suffering from this disease. They face significant unmet medical needs at the moment, with 77% reporting injection site reactions from the current standard of care, which are fairly large-gauge needles, large injection volumes of viscous solutions that tend to wear off towards the end of the month, which results in these worsening of symptoms in the vast majority of patients. Many patients in acromegaly and also carcinoid syndrome, where these are also used, end up having to take these injections more frequently than every month, which is the recommended dose. If you don't believe me, go on YouTube, do a little bit of homework on your own, and you can find people who will show you exactly what this means to them.
But part of it is not just about that treatment, but it's about the feeling of dependency for others. And I think we'll show you with paltusotine that this changes the game for them. And that was the data from our most recent phase III program, where we had two studies, PATHFNDR-1 and PATHFNDR-2. And PATHFNDR-1 was in switching patients from the standard of care into our once-a-day oral paltusotine. And on the upper left, you see that we showed a very high responder rate, a very low placebo rate, and a bunch of other data that I'll talk to you more about another time. But this gives patients on current standard of care and their physicians confidence that they can shift to a much more tolerable and, I think, better medicine for maintaining their acromegaly.
But we also developed this according to guidelines that were published a couple of years ago about acromegaly, where if you wanted an indication for the treatment of acromegaly, you also needed to start with patients who are untreated, and that was PATHFNDR-2. And some of the summary data is shown on the lower left in responder point of view, but I think the more compelling is the IGF levels on the right side of this slide. And so for those of you, I should remember that not everybody knows what acromegaly is, but IGF levels are the way in which physicians manage the disease and which regulators determine regulatory outcomes. And so the goal is to lower IGF levels to healthy levels as soon as possible.
And with the depot injections, which are given once a month, you need three months to achieve steady state and see whether the dose you've selected is appropriate. They come in three doses. So after three months, you've evaluated the low dose. Another three months, you've evaluated the middle dose. Another three months, you've evaluated the high dose if the patient needs it. So you may very well spend three, six, nine months trying to get a patient under control. We show here that we get most patients under control in two to four weeks. So this is a real change in how you think about newly diagnosed patients, for example, or patients who've been off drug for a while and you want to get them back on. And almost everybody responded to paltusotine with 93% showing lowering of IGF levels. And this was consistent throughout time.
This is the registrational endpoint, let me be clear. But patients are more than just an IGF level, and they're demanding that they also are managed for their symptoms. So we prospectively developed, according to FDA guidelines, a patient-reported outcome tool called the Acromegaly Symptom Diary and the patients recorded their symptoms with time throughout the study. And what you can see on the upper left, and this was a pre-specified secondary endpoint, what you can see for PATHFNDR-1 and PATHFNDR-2 is that patients had symptoms that maintained control on paltusotine, and when switched to placebo, they got significantly worse with a p-value of 0.02. And then in the PATHFNDR-2 program of the newly diagnosed patients, patients who received paltusotine had improvements in their symptom control, whereas patients with placebo got worse.
Now, I mentioned that one of the problems with this is not just the end result, but the consistency of control throughout the monthly cycle, so this is some new data for some of you, new data that we haven't shown before on the right, which is some other analysis of work we've done both on the PATHFNDR-1 study and based on some online surveys, and on the y-axis is what we call an exacerbation rate, so this is when symptoms got worse that day than they've been the days before it, and you can see a fairly consistent 30% or so exacerbation rate, both on the online survey group that we did and in the run-in period when patients in PATHFNDR-1 were receiving the injections from the standard of care.
But then in PATHFNDR-1, if they switched to paltusotine, you can see that those exacerbations reduced with time. So I think this promises or begins to show the potential for more consistent control of these symptoms throughout the month. And I think this is very important to patients and their caregivers. So our mission is really to not just switch people from standard of care to paltusotine, but to get all the patients out there the medical therapy that they need. And there's a problem in this space. There's 27,000 patients prevalent with the condition, and many of these remain undertreated or untreated. And while there's new patients coming in every year, why wouldn't you switch those? Why wouldn't you start those patients on something like paltusotine?
The other problem is there's many patients who are undiagnosed, and it takes five to 10 years for them to be diagnosed while the disease is continuing to create permanent damage that can't be fixed with medical therapy. So these are the main segments that we're trying to address with paltusotine. We'll take the people on the current standard of care with its gaps, reduce the burden, and improve control. With the undertreated, we need to educate both physicians and the patients to help them seek the type of treatment targets that they know they should deserve. And the untreated, this is a bit of a mystery to me. I don't know why there's so many people that are untreated. So we need to find them, and we need to educate them and motivate them to get into the physician's offices.
The naive I mentioned, the undiagnosed is going to be challenging because it's easy to diagnose acromegaly once you suspect it because you just do some IGF values and a pituitary MRI. But it's difficult to think about. It's difficult to suspect it. But I think what all this says is, yes, there's an existing market for somatostatin injections for acromegaly, but we want to expand that market and bring good quality care to far more patients that are receiving it today. So the second indication we're working on is congenital, well, actually, I kind of skipped one because we got a lot of things to talk about in our pipeline, and I can't talk about all of them today. So let me skip to the next molecule, which is the third indication that we're working on. And CAH affects about 17,000 adult and pediatric patients in the U.S.
What happens here is they have a genetic mutation which prevents their normal adrenals from making cortisone, which you need to live. But instead, it makes these precursors to cortisol, which are things like A4 and other androgens and others called 17-OHP. These have a whole range of different manifestations, whether it's excess hair or acne, particularly the hirsutism is problematic in women. Polycythemia, which is a relatively new word to me, these androgens act like the testosterone in athletes who are doping, and you end up with too much red blood cells, which can have long-term cardiovascular complications. Women have problems with fertility and normal menstrual cycles because of these excess androgens. Men have fertility issues too, and they grow these adrenal-like tumors in the testes, which can impair fertility and also be painful.
And then to manage all this, up until recently, the only tool available was to give them more glucocorticoids to try and suppress this system. But as you start giving more and more glucocorticoids beyond normal levels, you end up with symptoms of a condition called iatrogenic Cushing's disease, where too much glucocorticoids themselves cause problems. So patients are forced to balance, or patients and their physicians have been forced to balance these excessive glucocorticoids with excessive androgens, and it just impacts every aspect of their lives.
Now, what we've shown with atumelnant, which is a blocker of the one hormone that stimulates the adrenal to make both cortisol in the patients that are in healthy volunteers and in patients with Cushing's, or these adrenal androgens in patients with CAH, we've shown a nice dose response with very strong suppression of the key biomarker for CAH, which is A4, androstenedione, and with a 120-milligram group, we start with patients with an average of 1,000 nanograms per deciliter and get them down to 180 nanograms per deciliter. Most of those are then in the normal range. Similarly, many patients at 80 milligrams get down into the normal range and get significant reductions, and the primary endpoint is shown on the bottom then, which was the absolute amount of change from baseline with obviously high statistical significance in all dose groups.
But again, just like acromegaly, it's not just about hormone levels. It's about what are those hormone, how do those hormone levels manifest into the clinical signs and symptoms that patients can see and feel? And drugs should be addressing that, not just hormones themselves. So I was very, very pleased to see that in women, in six out of ten participants who had irregular menstrual cycles or absent menstrual cycles, they got normal. This was associated with reduced or normalized testosterone levels. So we have a mechanistic explanation for it. In males, there's an elevated androstenedione to testosterone ratio indicating that the normal production of testosterone is inhibited. That improved in many patients. Androgen-mediated polycythemia, which is what I was talking about in doping. We had six individuals in the study who had polycythemia, and five of those resolved in this short 12-week period.
Hirsutism and acne, we didn't have enough time. I think we want to see a little bit more time on that. But one of the more striking things we reported was that the name of this disease is congenital adrenal hyperplasia. That's because with this chronic stimulation of ACTH, the adrenals get larger and larger. And we had some very large adrenals in this study, and we showed consistent reductions across patients. And there's illustrations of some of this in our data release from last week, which I thought presented some remarkable advancements in the field. And overall, atumelnant was well tolerated with no severe or serious adverse events. But part of the rockiness we experienced was we showed one patient with a transient elevation of ALT and AST that we were not particularly concerned about, although we take every event very seriously.
We've presented that to regulators as part of our overall development of the drug, both the FDA as early as or as late as last December and then global regulators. We haven't made any adjustments or changes to the protocol or monitoring, but that has triggered a lot of questions I've been spending answering the last day or two. So to me, the whole program is way stronger than it was a week ago, but I understand that there's risk in drug discovery and people fear risk. But what our vision for this drug is, is to move it forward as fast as we can into late-stage study, phase III program in adults, a pediatric study which bridges in phase II-III way, and then also into Cushing's disease, the other indication that I'm not going to talk about today.
but in the area of people living with CAH, we've clearly demonstrated remarkable lowering of these adrenal androgens. If you start to combine that with the data that we've shown in healthy volunteers and Cushing's disease, it's easy to connect the dots to expect that we should be able to normalize the glucocorticoid levels as well. so these unhealthy levels of hormones on the outside of this graph, all those patients we are trying to bring down into that normal healthier range at the lower left corner. and you can see how tight that little healthy box is compared to the scale of the square, which represents the actual patients in our study. and yet in that study, we were able to do that and see these improvements in clinical signs and features, which I talked to you about. so that's atumelnant. We're super excited about it.
It's something we've known about this hormone and these diseases for a century, and this is the first and only ACTH antagonist in clinical development. But like I mentioned, there's always something cooking in the labs, and we've got four new programs going into IND-enabling studies right now. And the first of those, which should be submitting its IND in the very near future this quarter, is CRN 9682. We number our molecules sequentially, so that's the 9,682nd molecule we've made as a company. And this is a whole new idea around how to treat tumors. It's somewhat similar to antibody-drug conjugates, but here we're using our small molecule peptide hormone receptor ligands to drive payloads similar to ADCs to these neuroendocrine tumors.
In neuroendocrine tumors, there's 140,000 patients roughly in the U.S. expressing somatostatin type 2 receptor, but also somatostatin type 2 receptors expressed in about 30% of ER-positive breast cancer patients, most head and neck patients, metastatic melanoma. There's a long list, but this is a small table, and we're going to have a basket study. I'll tell you a little bit more about this project in a minute. Hyperparathyroidism is the production of too much parathyroid hormone of the four glands embedded in your thyroid. Now, because of the activity in the space, many of you have heard of hypoparathyroidism. So hypoparathyroidism is too little PTH. One of the major causes of too little PTH is surgical removal of the parathyroid glands because of hyperparathyroidism. Hyperparathyroidism is too much PTH. There's roughly 200,000 incident cases of this. There's more patients with primary hyperpara than there are with hypopara.
Hyperparathyroidism can be caused by what's called hypercalcemia of malignancy. These are when advanced tumors in different types of cancers start secreting a PTHrP, which creates some severe forms of hyperparathyroidism. There's various hyperparathyroidisms associated with different types of chronic kidney disease. There's quite a pipeline inside that one particular candidate, and that is progressing through IND-enabling studies. Graves' disease affects 1%-2% of the population with a predominant bias towards women. It's an autoantibody that activates the thyroid gland and cells in the back of the eye that cause this thyroid eye disease, which you've probably all seen because of the commercials on TV. Amgen was advertising this last week, saying up to 50% of people with Graves' disease will end up developing TED. If you had the right drug for Graves' disease, you wouldn't get TED.
We expect that a TSH antagonist would resolve not only the TED, but the hyperthyroidism and prevent the onset of TED in those patients. We're working on moving that forward. That's also just recently started IND-enabling studies. Finally, one that's a little outside our normal type of indication, which is an SST3 agonist for autosomal dominant polycystic kidney disease. This is one of the more common causes of kidney failure after diabetes, and it's severe. It's associated with other ciliopathies. This illustrates one of the principles that we operate on, which is endocrinology is not just for endocrinologists. Tolvaptan is actually an antagonist of a peptide hormone that stimulates the reabsorption of water by the kidney. It doesn't work that well, but it's making a lot of money and providing some relief for patients with polycystic kidney.
But otherwise, there's not a lot in the pipeline. So here's one where we have an interesting hypothesis, a good molecule, and we're going to move that forward to see if we can do something for patients with PKD. But let me spend just a moment on this new platform because for those of you who've been following this, we only rolled this out back in November at the North American Neuroendocrine Tumor Society. Now, it shouldn't be that much of a surprise because a couple of years ago, we also used these small molecule targeting agents to target radiopharmaceuticals for a variety of different oncology indications, spun out a company called Radionetics, and Radionetics is now moving multiple compounds with the radiotherapy idea into the clinic. And you may have seen the deal we did with Lilly last summer on that.
But this is a separate idea using some of the concepts where you can use a small molecule ligand to a peptide hormone receptor to target not only binding to these receptors, but hijack their natural behaviors so that you can efficiently drive internalization of this payload into the cell. The linker has been optimized so that it can only be cleaved inside the cell with very little release in the systemic circulation. And MMAE is one of the payloads frequently used in some of the well-established ADCs. But with small molecule chemistry, you can tune almost all aspects of this, manufacture it by chemical manufacturing, and not have the long half-lives that you have with antibodies, the nonspecific release of payloads, the poor tumor penetration, and you can have multiple cycles of treatment up until you have either tolerability issues or progression on the therapy.
So it's got a number of advantages potentially over ADCs, and that's something that we're trying to now discover in the clinic or prove in the clinic. But the preclinical data is remarkably positive. To me, the most impressive thing about this molecule is the graph on the left. This is data from a biodistribution study. On the top is the amount of free payload released into the tumor. On the bottom in the squares is the amount of free payload released into the circulation of these mice. It's orders of magnitude difference. The circulating free payload is undetectable after the first day. This is exactly the type of optimum biodistribution profile that we were looking for. And then on the right is a xenograft model of a reasonably aggressive small cell lung tumor, which expresses somatostatin receptors.
In this case, we allowed the tumors to get fairly large, 1,000 cubic millimeters. You can see at the two higher effective doses, you reduce those tumors to almost undetectable and undetectable in the majority of animals at the three milligram dose. If we can do this in people, this may be a real new turnaround for a targeted therapeutic, non-radioactive that doesn't exist for people with NETs or breast or head and neck or paragangliomas or mesothelioma. Sorry. That one I stumble over that tumor type sometimes. Anyway, a range of different SST2- positive tumors. Out there, we already have well-established PET scan imaging agents to screen patients to ensure that their tumor has high expression levels of SST2. This is our pipeline in its entirety.
I obviously am skipping some things and not telling you all about all of it. I encourage you to look at our website to learn more details, but what I really wanted to spend a moment on is just some of the vision for the future, so in 2025, with all that said, as part of our development, the reason I think we're really going to be successful is because as an organization, we've got a lot of people with pride, belief, and belief in that vision of creating something special, and that's shown itself, and in 2025, expect us to advance many different things, including the launch of paltusotine, starting four clinical or four late-stage trials, four new INDs.
And we're working hard to get into the obesity space with some high-quality drug candidates there because after all, we are focused on making small molecule drugs at peptide hormone receptors and what other area needs it more than that. For 2026 and beyond, expect to see the proof of the commercial engine kicking in. We'll be launching multiple indications on multiple drugs in multiple regions. In addition, as that pipeline coming out of discovery matures, you'll see a stream of near-term clinical catalysts. They're meaningful in patient populations and the emergence of these new things coming out of the IND-enabling studies. So expect that pipeline to continue to grow. And as we move that forward, we'll also continue to invest in new discovery efforts.
So to wrap it up, I'd like to ask you to take a moment to gaze at this map of where we've come so far and imagine where we may be in the not-too-distant future. We're clearly advancing the state of medicine in pituitary disease. We're expanding now into more general endocrinology, which includes some of the biggest populations of some of the most severe diseases that affect us. And then, as I said earlier, endocrinology is not just for endocrinologists. So we're moving out into endocrine-adjacent areas. And many different physicians, as I said, routinely prescribe medicines that come out of endocrinology forgetting, in fact, that it was originally an endocrine approach. So with that, as you can see, I think we're not only growing, but evolving. We look forward to continuing to evolve and create immense value both for our patients and for our co-owners in the future.
Thank you, and I look forward to taking your questions. How did I do?
Great. Thanks for the presentation. So you provided us an update on the phase II for atumelnant last week and a bit of a stark reaction in the stock. Can you take us through each of the cases of elevated liver enzymes that you saw and just kind of like level set the information there?
Yeah. So let's be clear, and I'm glad to have the opportunity just to be very specific. So we had two cases. One was not attributed to drug. The reason for that is this patient had depression, was on fluoxetine, started bupropion, which is a known potential interaction with fluoxetine. At that point, somewhere right around then, they also had a car accident. Then they started to show somewhat elevated liver enzymes. They finished the study. No changes were made to treatment or adjusted to anything. They finished the study, came off of atumelnant as planned. The liver enzymes did not resolve. When they went off the bupropion, it resolved. The investigator called it not related to drug. We believe that. We agree with that opinion. So let's set that aside. So we had one case that we couldn't explain.
The last visit, the last blood sample, that patient had an elevated LFT of both AST and ALT. They'd had a little bump earlier in the study, and then they'd been back down to normal, and then they had this. We don't have a great explanation for it. You see these in clinical trials. This has been in our briefing packages both to the FDA, along with all the other safety data, no special interactions. But with the safety data, as we're planning our phase III trials, we're not making any adjustments to those trials. We've not been asked to make any adjustments to those trials. We've not been asked to probe deeper into it, although our pharmacovigilance group is digging through everything we can to understand any potential safety flag that we may see in any of our studies.
But that has generated a lot of questions the last day or two.
Got it. And no changes in bilirubin?
Oh, I'm sorry. Yeah. No changes in bilirubin on either of those subjects. No evidence of any sort of liver injury other than that elevated ALT, AST.
Was there any hint of anything liver-related in the preclinical data?
No. The biggest thing we had in the preclinical data is in the dogs. Because of the mechanism, we made them adrenally insufficient. So we had to go back. And so we had some findings in the beginning, not specific to that. But then we added back glucocorticoids, fixed their hypoadrenalism, and it was the hypoadrenalism that was the dose-limiting toxicity.
Got it. So as we think about what could be shaping up to be a differentiated clinical efficacy profile for this product, what do you see as kind of the optimal development plan to really showcase the product?
So I think there's a couple of aspects to that, right? I mentioned that patients have unhealthy hormone levels both on the axis of things made from the adrenal and because they're often taking too much exogenous glucocorticoids. The goal is to find we'll be measuring both, particularly A4 is a well-established biomarker in this. So we want to bring that down significantly, hopefully to normal. We want to use that to enable the physician and the patient to lower the glucocorticoid levels down to normal is the target. And then how we express that in terms of statistical powering and endpoints is something we're working on internally and with regulators.
But beyond that, we're also going to be measuring all these implications that patients can see and feel of their disease and provide a narrative about what this will mean to them and their physicians on the things that really impact their daily life beyond just the hormonal biomarkers themselves. So I look forward to getting back to you on that as we have our finalizing our protocol, our regulatory interactions. We'll start the phase III program this year, hopefully in the first half. And then we'll announce all the details as we get them worked out.
Great. So you're heading into this milestone approval for Crinetics, expecting your first product approval with paltusotine later this year. What's a reasonable framework to think about the peak sales opportunity there in acromegaly? And how should we think about the path to get there?
Yeah. So I think this is going to be one of those where we're launching into an established market. We're going to need to tell the story about why this is better, educate it, not making a claim, educate people, both physicians and the patients, about the benefits and profile of paltusotine. But then we also need to help improve the practice of medicine. So we were at the Acromegaly Consensus Conference in Seville in September where we reported some of our early work. And we're finding that many physicians in the community are not practicing the type of medicine with the existing agents to getting patients to the targets that the consensus guidelines recommend. So clearly, we have some education to do. And many patients are not being treated at all because people are accepting outcomes as good enough that really aren't according to treatment guidelines.
So all these things say that I'm very confident we can expand the market, which really means improving the population of patients who are well cared for. But at the same time, there's going to be some headwinds into doing that as we have to work our way through switching and getting an appointment with your physician and things like that. But one thing I don't think will be a big barrier is from the payers. We have a very strong patient market access group. We've had a lot of good interactions with payers. And I think we find that they are, shall we say, receptive. I wouldn't want to say supportive. But I think they appreciate the benefits we're bringing, the economic benefits we may be bringing to them, and how this is a next generation of care beyond what's out there on the market today.
Great. Little time left. When could we hear Crinetics reveal more about your efforts in the oral GLP-1 space?
Yeah. So we've got a very active group. So right now, we've just divided our discovery efforts into three main teams: the traditional endocrinology, this new platform in NDCs, non-peptide drug conjugates, and metabolism. And we're circling in on some really good candidates. But I got to say, that is obviously a hyper-competitive space. We're not looking to sell those assets to somebody. We're looking to build assets that we can develop a long way ourselves. And we will probably be a bit quiet about how much we have to share and why we think we have differentiated profiles. So I have to walk a fine line between the disclosure I want to share with our co-owners out here in the community and the competitiveness that this particular aspect faces. But I'll try and find some way to satisfy the curiosity in the not-too-distant future.
Okay. Great. I think we're out of time, so thank you.
Thanks, Jess. Appreciate it. Thank you, everybody.