Conference. My name is Colleen Kusy. I'm one of the Senior Analysts covering biotech at Baird. Today I'm pleased to have with us the team from ORIC Pharmaceuticals, including CEO Jacob Chacko and CFO Dominic Piscitelli. Thanks so much for being with us. Thanks for having us, Colleen. Maybe if you can start things off with a brief company overview, what are the current state of affairs at ORIC? Sure thing. I'll keep that short so we can dive into the details of the pipeline. ORIC stands for Overcoming Resistance in Cancer. In a nutshell, that's the mission of the company. We focus within oncology, specifically on small molecule drug development in solid tumors. Given the expertise of the company, we tend to go deep on both lung cancer and prostate cancer. That is where the two lead programs are focused on their development. I'm sure we'll touch on both of those today. ORIC-944 is a small molecule inhibitor of PRC2, which is relevant in combination, dosed in combination with androgen receptor inhibitors. We're doing dosing with two different AR inhibitors, which we'll talk about later today, in the middle of dose optimization right now. The theory there is that by dosing a PRC2 inhibitor with an AR inhibitor, you get longer, more durable outcomes for those patients with prostate cancer. ORIC-114, which is a small molecule that's being developed in lung cancer, is in three different targeted therapy populations in lung cancer: EGFR exon 20, EGFR atypical mutations, and HER2 exon 20. Both programs are in dose optimization right now. Both are headed to the start of phase 3 studies next year. The company is extremely well funded. We have raised quite a bit of capital this year. We have cash runway past the phase 3 data readouts for both of those programs. That's the state of play today. That's a valuable position. Yeah. That's fantastic. Thank you. Let's start with ORIC-944, the prostate cancer program. The lead drug targets PRC2, as you mentioned, Jacob. Maybe before we get into the data, at a high level, maybe some investors are more familiar with EZH2. Why do you think that PRC2 via the EED subunit is the right approach? Is it similar to or better than hitting EZH2? I know we've seen kind of a mix of data for EZH2 historically. Just talk about the target to start, please. Sure. I always chuckle a little bit because sometimes investors will say they don't, they're not familiar with PRC2. I always guarantee them they definitely are. PRC2 has two druggable subunits. There's EZH2 and there's EED. The companies, over the course of time, ourselves and others, have tried to drug one of the two. EZH2 is the catalytic subunit. You can achieve allosteric inhibition of PRC2 by targeting EED. The name of the game is really just to get a potent inhibitor that's got good drug properties. As you look at that space, whether it was prior EZH2 inhibitors or prior EED inhibitors, what has limited the first-generation compounds has been poor potency, essentially. On top of poor potency with all those compounds, the first-gen compounds, you've got very short half-lives, on the order of one to two hours. Several of those compounds have something called CYP autoinduction, where essentially they are revving up the CYP enzymes, and those drugs are metabolized by CYP enzymes. What that means is you'll get a really funky phenomenon, which is dose-dependent decreases in exposure with some of those drugs, where the more drug that was given, the less exposure the patient saw. That's obviously not a good thing. It's not what you want to have in your drug development. The lead program in the space now is developed by Pfizer. They're targeting the EZH2 component of PRC2. They seem to have developed some better drug properties than the first-gen compounds that have come before. Our compound, ORIC-944, targets the EED subunit also with better drug properties than the generations that have come before. If you just take a step back and focus on the biology, as to is it better to target EZH2 or EED, I would say that if you have two drugs that have exactly the same potency, exactly the same drug properties, one targets EZH2, one targets EED, they ought to be equally good at inhibiting the PRC2 complex initially. Where there could be a benefit to targeting EED is in terms of long-term resistance. That's because EZH2 inhibitors could be susceptible to bypass resistance from EZH1 or acquired mutations in EZH2. Those are not susceptibilities that an EED inhibitor would be prone to. All things equal, you'd rather target EED. Great. That's helpful. Before we get into your data, I think you mentioned Pfizer's EZH2 inhibitor. I think it's maybe helpful to set the stage with the data that we've seen from them since they're slightly more advanced. That drug in combination with enzalutamide and an androgen inhibitor has shown randomized data with longer radiographic PFS than enza alone. Can you just kind of walk us through the highlights of those data and how you think that bodes for your ongoing program for 944? As I mentioned earlier, Pfizer has come up with a drug called Mevrometostat, which seems to have better drug properties than the first-gen PRC2 inhibitors. That seems to be proven out in the clinic as they've now dosed it with an androgen receptor inhibitor, which is enzalutamide. That's their androgen receptor inhibitor that they acquired from Medivation. In two different phase one populations within CRPC, one in a post-abiraterone-treated population and another one that was a post-enzalutamide-treated population, they achieved a PFS that was anywhere from three to four times as long as what you'd expect from enzalutamide alone. It blew away the expectations from enzalutamide alone. They were able to replicate that specifically in a randomized study that they presented earlier this year where they focused on the post-abiraterone population within metastatic CRPC. They had a control arm in that study. The control arm performed exactly as you'd expect, which was enzalutamide achieved six months of PFS, and the treatment arm achieved over 14 months of PFS. Again, really profoundly long PFS compared to what you'd expect from enzalutamide alone. Even as you go and benchmark those results relative to Pluvicto, for example, which obviously has been game-changing in the prostate space, it's far better than Pluvicto in that setting. That's what's kind of really helped to de-risk this mechanism where you've been able to see what a drug with good drug properties is able to achieve in combination with an AR inhibitor. Of course, as you mentioned, we're trying to fast follow that with our own PRC2 inhibitor, ORIC-944, in contrast to Pfizer's drug. Pfizer's drug, Mevrometostat, looks like it's got about a four or five-hour half-life. Clearly, that's a lot better than the first-gen compounds with a one or two-hour half-life, but leaves some room to be improved. Pfizer's drug is being dosed at quite high doses, two times a day, I presume, so that they can get adequate target coverage with that four or five-hour half-life. ORIC-944, which is our drug, was designed by the chemists at Mirati. Very good chemistry came out of Mirati. We acquired the program outright in 2020. They, essentially, back to your earlier question, didn't take a view on EZH2 versus EED. They made a bunch of EZH2 inhibitors and a bunch of EED inhibitors and put them all through the paces to just figure out empirically which one had the best drug properties. The one that ended up winning was what is now ORIC-944, which has a 20-hour clinical half-life. Obviously, that's conducive to QD dosing. The benefit here, though, is not the QD dosing versus the BID dosing. Really, what it is, is a 20-hour half-life allows you to have sufficient target coverage over a 24-hour period without running into issues on Cmax-driven toxicities. That's where we think that our drug ought to have a better profile. In some data that we shared earlier this year in May, we had the first glimpses of that better profile. Great. Let's dive into that next. You presented data in the first half of this year that touched on robust PSA responses and a safety profile. Walk us through the highlights of those data. Sure. In those data, we had 17 patients who were treated with our PRC2 inhibitor in dose exploration in combination with one of two AR inhibitors. Maybe just taking a big step back, the prostate landscape has been transformed by three androgen receptor inhibitors: enzalutamide, which is now marketed by Pfizer as Xtandi, apalutamide from Janssen, and darolutamide from Bayer. Those three drugs collectively are small molecules. They're given as pills. They have transformed the way that prostate cancer therapy is done today and had phenomenal results for patients. They collectively do $11 billion of sales globally. All of them are blockbusters many times over. They all eventually get great outcomes for patients. Eventually, the patients' tumors essentially start to become AR independent. That's where those AR inhibitors start to lose their benefit. Pfizer is doing their combination dosing, of course, with their AR inhibitor. There are two other great AR inhibitors out there: apalutamide from Janssen and darolutamide from Bayer. We're partnered with both of those companies. They're providing us with free drug into the current dose exploration work that we're doing. In the data that we presented in May, we had 17 patients that were dosed with either, all of them were dosed with our PRC2 inhibitor, but then the combo agent was either apalutamide or darolutamide. Regardless of which combo agent it was, we saw very good efficacy and we saw a very good toxicity profile. In contrast to Pfizer's data from their randomized experience that they presented at ASCO GU, they had a confirmed PSA 50 response of 34%. Our confirmed PSA 50 response in our early work was 47%. Their confirmed PSA 90 response rate was 12%. Our confirmed PSA 90 response rate was 24%. Albeit small N, still early, still developing, all the appropriate caveats, we were quite pleased to see that daylight between our PSA response rates already and theirs. Even more important than that, because at the end of the day, whether or not the efficacy of our compound ends up being superior or the same as theirs in terms of long-term durability markers like PFS, what's really going to matter here is the toxicity profile. That was an area that you saw immediately, sort of the theory of the case and the better drug properties, the better PK properties, already manifesting itself in the results that we presented in May, where if you hold them up side by side with Pfizer's, what you will see is that both drugs clearly have the two major classes of on-target toxicity you'd expect from PRC2, which is heme tox and GI tox. In ORIC-944, you see a lot less of it and a lot less severity of it. In addition to that, you see one or two off-target toxicities of note in the Pfizer data, in particular alopecia in 40% of the patients, which we don't see with ORIC-944. We had very positive feedback from investigators at ASCO shortly after we presented the data. It was clear to all of them right away that the toxicity profile of 944 is differentiated from Mevrometostate. Great. Is there a theory on what's driving that differentiation in the safety profile you're seeing? For that, I would say our hunch seems to be the same as Pfizer's hunch. When Pfizer at ASCO GU talked about the toxicity potentially being Cmax related, you can just look at PK curves and think about the PK curve for a drug that's got a four or five-hour half-life that's being dosed in large doses two times a day versus a drug like ours that has a 20-hour half-life dosed at much lower doses. It is easier to avoid those Cmax related toxicities if you've got a QD dose with a 24-hour half-life, 20-hour half-life, sorry. What is the latest in your current development? You mentioned you're in dose optimization. Just tell us the latest update there. We are running hard. We've been kind of watching this play out over the last couple of years. We've obviously been watching Pfizer help really dramatically de-risk this mechanism of action over the last couple of years. We've been running very hard on single-agent dosing to establish the single-agent profile, quickly moved into the combo dosing that we just talked about in terms of dose exploration. As of the May update, we had already settled in on the two Project Optimus doses that we would be optimizing for the darolutamide combination. We were very close to figuring out what those doses were going to be for the apalutamide combination. We've been spending the second half of this year focused on that dose optimization work. The goal is that by the end of this year, early next year, we will have selected the dose that we plan to take forward into our eventual phase three study. That first phase three study is going to be in the CRPC setting. We haven't yet decided what portion of the CRPC, which population within the CRPC setting that we will focus on. We'll intend to start that study first half of next year. A lot going on operationally. Building off of the update that you had in the first half on the early PSA responses and the safety, you've guided towards providing another update in the second half of this year to help us set expectations on what to expect from that readout. Yeah, we have a couple of updates coming in rapid succession. One in the second half of this year and then yet another one in Q1 of next year. I would guide folks to really the Q1 update in early next year is going to be the really substantial update in the sense that that'll be where you get a big bolus of new data. Let's start with the second half update and then go to the Q1 2026 update. The second half update will be a bit incremental in nature only because it'll essentially just round out the knowledge of the dose exploration work that we've already done. In that update, we've told folks to expect no more than a handful of patients. It'll really come down to did we end up enrolling one or two more cohorts in combination of ORIC-944 in combination with apalutamide. No more than a handful of patients new as part of that update. Of course, we can show the PSA 50s, PSA 90s for those patients. We have gotten questions about ctDNA. I think that's because there's been some literature that shows that ctDNA is an even better proxy for long-term durability measures like PFS than PSA 50s and PSA 90s. That's certainly something that we've been measuring in the study. We can share those data, including back on those original 17 patients that we shared from May. Of course, safety profiles, things like that. It'll really be more about laying out the rationale for the doses that we chose to optimize for the two different combinations and really setting up the Q1 2026 update. The Q1 2026 update is going to be focused on the dose optimization data. In that update, we'll provide 20- 25 patients in total, split evenly across, roughly evenly across new patients, across two doses, two provisional RP2Ds within the selected patient population that we're going to take into phase three. It'll be a CRPC population, but it'll be either the post-abiraterone population or a post-AR inhibitor population, which are the two that we're exploring, in combination with the selected AR inhibitor that we're going to take into phase three. Great. For the second half update, would you expect a deepening of response in that amount of follow-up? Do you think probably the responses that you saw initially are those kind of mature enough that you wouldn't expect a further deepening of response? Yeah, with this mechanism of action, there is certainly a phenomenon of a deepening of response as you'd expect with an epigenetic modifier. I would say that at the time that we presented the data in May, we had the chance to confirm nearly every one of those patients. We already showed confirmed PSA 50s, confirmed PSA 90s. Those are the numbers that I quoted off. We really don't speak in terms of unconfirmed rates. You've essentially seen what you're going to see in terms of the confirmations. What I would say is really the biggest difference in the data that you have seen and will see from us this year as opposed to in Q1 2026 is that the Q1 2026 update, of course, will again show PSA 50s, PSA 90s, ctDNA on these new 20 -25 patients, but most importantly, some early durability on those patients. I think that's the last box that needs to be checked here. To level set, it won't be a mature PFS number. It just can't be, just given where dose optimization started. It can certainly be some kind of landmark analysis, three month, four month, whatever makes sense at that time with a good bolus of patients that would have had time to stay on for that long. Great. As you mentioned, you're quickly planning on moving towards a pivotal study. I realize some of these plans are still in flux, but what's your latest thinking on the trial design for what a pivotal study would look like? Right. The trial design will potentially vary depending on which of those populations we end up choosing within the CRPC setting. I think Pfizer's already laid out a couple of different trial designs in two different populations within the CRPC setting. Each one of those trials, the post-abiraterone trial for them at least, is 600 patients in total, split across a treatment arm and a control arm, the control arm being a physician's choice of enzalutamide or chemotherapy. We think all of that makes a ton of sense for that population. They, of course, have MEVPRO-2, which is a second phase three study, which is being developed in treatment-naive metastatic CRPC. It sort of depends on in which line you are studying, because in that case, I believe the control arm is enzalutamide alone, not a physician's choice. Some of the study design will come down to that. In terms of study numbers, my understanding is MEVPRO- 1 is about 600 patients. MEVPRO- 2 is about 800 patients. Whatever study we end up deciding is going to be roughly in that ballpark of number of patients. The key, though, is the primary endpoint here is a sole primary endpoint, and it's radiographic PFS, which is why the Pfizer timelines are so fast and why we expect our timelines to be equally as fast. Pfizer started MEVPRO -1 and MEVPRO -2 in October of last year. Primary completion date for MEVPRO -1 is end of this year. That's a 15-month timeline. The last public disclosure from them was that those phase three data would be out next year. They intend to launch that drug shortly thereafter. It's obviously very fast timelines, regardless of which of these populations you choose. We would intend to be just as fast. Great. Obviously, you'll move forward in some sort of combination with an AR inhibitor. Yeah. Right now, as you mentioned, you have supply agreements for apalutamide and darolutamide. Walk us through the decision tree of which drug you'd choose for the phase three. Could you do both? It would be one or the other. We could certainly do both if we had more money. I would say that there's probably no reason to do both, though, because in the sense that you would just be replicating the design of two different phase three studies and just running two different AR inhibitors. The bottom line is any of you are welcome to do your own physician checks to kind of validate this. What you are going to hear from 10 out of 10 physicians who treat prostate cancer patients is that they view those three AR inhibitors, the three big AR inhibitors: enzalutamide, apalutamide, and darolutamide, to be indistinguishable in efficacy, exactly the same efficacy in the populations in which all three have been studied. Where there is some difference is that if you force rank those in terms of safety, you will find that both darolutamide and apalutamide come out ahead of enzalutamide on the safety front. That's really due to less neurotox, less risk of seizures. All three are well-tolerated drugs. At the end of the day, darolutamide and apalutamide are better tolerated than enzalutamide. We could choose either one of those, and we'd be in a good place. What I love about the situation, what I love about the setup for us, and we mentioned this even back on the May call when we shared the data, is that in our hands and in all these past data sets, you don't see any appreciable differences between the two drugs. That puts us in a good position because we could choose either. Great. The plan would be moving forward to at least get a supply agreement. Is that kind of how to think about that? The plan would be for that first, for the first study from an operational point of view, from a financial point of view, for that first phase three study, we are good to go ourselves. ORIC can do it by ourselves, including sourcing the drug by ourselves if we chose to do that. Obviously, Dominic, our CFO, is cheap. He'd rather get the drug for free. He would. What we will likely look to do is just extend the existing supply agreements with one of those companies to provide free drug, free combo AR inhibitor drug, into that first phase three study. There is no bigger BD deal or bigger BD collaboration that would be holding up the start of that first phase three study. Eventually, we probably will seek a bigger BD deal in terms of a global co-co type deal, really because if you think about the biology of PRC2, this ought to be developed all over the place. Not only in CRPC, which is where we're starting, but in earlier lines like CSPC and potentially even outside of prostate cancer, there's a whole slew of areas that you might want to study a PRC2 inhibitor. Great. As you mentioned, MEVPRO-1 is really reading out not that long from now. It's been a very fast development track. How are you thinking about that readout and the read-through to your ongoing program? I suppose the read-through is high in the sense that it's the same mechanism and same general population. Obviously, I think Pfizer's put up a lot of data that would suggest that the PTS of that phase three study, that first phase three study, ought to be quite high. I do think that there's reasons that I've articulated in terms of the drug properties of 944 that would suggest that both in terms of 944 as well as the AR inhibitor that we select, whether that's apalutamide or darolutamide, our combination should be advantaged versus Pfizer's combination. There are reasons to believe that anything they can do, we can do better. We'll have to just see what their results look like next year. A commercial question, zooming out, potential approval of 944 in prostate cancer. How much of a delay would you expect to MEVPRO's assumed approval? How would you expect to compete against Pfizer? Yeah, so I think Jacob alluded to this before, but MEVPRO-1, which was Pfizer's first study, was started in October of 2024. We're planning to start our first phase three study in the first half of next year. That puts us somewhere between 18- 24 months behind them. Now, the reality is here, this is prostate cancer. This is a significant patient population. If you look at just the metastatic castration-resistant prostate cancer setting, it's over 50,000 patients. It's really split between three kind of groups of patients, right? It's the ARPI naive, it's the post-ABI, and then it's the post-androgen receptor inhibitor. If you just look at the two patient populations that we're enrolling, post-ABI and post-ARPI, they're each around, call it, you know, mid-teen, 1,000 patients per year. So 17,000- 20,000 patients per year. If you just do the math on that, those each represent about a $3.5 billion treatable adjustable market in the U.S. alone. The point being these are big patient populations. Even if you had, if you look at any analog, any market research, being second to market within two years, the second product typically gets about 35%- 40% of that market share. That puts us in a great position being second to market with assuming the same profile. Now, as Jacob said, there's reasons to believe that we could differentiate either on efficacy or safety, which obviously would be upside to that scenario. Yeah, fantastic. Maybe let's touch on ORIC-114 as well. Your second asset is being developed in non-small cell lung cancer. You mentioned a number of different genetic mutations there. The field is a little crowded. Maybe just talk about how you're viewing differentiation of 114 and your development program. Yeah, we don't disagree with you. It is a crowded field. A lot crowded. We do think there's room for differentiation here. The reason we in-licensed this program is really on two fronts. The two things we really like about it are the safety and tolerability, and then the CNS activity. If you look at our kinome screens, which can be found in our corporate deck, we have an exquisitely clean kinome. The reason that's important is a lot of the drugs that are out there, a lot of the products approved and in development, do have both on-target toxicity you'd expect to see. With a wild type EGFR, you'd expect to see GI and rash-related toxicities. You also see a number of off-target toxicities in the form of elevated liver enzymes. You start to see QTC prolongation. Those are just not good things profiled. We could differentiate on that front. Probably more importantly, it's on the CNS front. The reason it's important when you look at lung cancer, about a third to 40% of these patients do present with baseline brain mets. If you look at the data, mobicertinib, tecadia had a nice data set showing this. In about 40% to 50% of these patients, it's a point of first progression as well. Having the CNS active agent here could really differentiate us. We'll have data later part of this year and first half of next year. We'll keep looking. Yes, help us set expectations for the readouts. Yeah, second half and first half. Yeah, second half of this year, we got a pretty substantial data readout. In the second line or later setting, we've got three cohorts of patients reading out. It's second line, EGFR exon 20, HER2 exon 20, and the EGFR atypicals. For each of those patients, we'll have about 25 patients across two provisional RP2Ds. If you remember, the two provisional RP2Ds we took forward here are 80 and 120 once a day. That's a pretty substantial data set. It's about 75 patients in total. When we think of the benchmarks for those, in the EGFR exon 20 in the second line, we think it's about 35%. HER2, there has been some pretty impressive competitive data there. That's closer to 50% or higher. Lastly, with EGFR exon 20, again, it's probably 35% or so. The important thing to remember here is when you compare apples to oranges, you've got to be careful. We have included patients with active brain mets, where others kind of excluded those patients. That's something, those benchmarks that I sent to you are excluding patients with active brain mets. Gotcha. The other piece that we did bring forward later this year was we'll show you some early data from first line EGFR exon 20 as a monotherapy. Here, we'll show about 10- 15 patients' worth of data. Great. You've also recently secured a supply agreement with J&J for amivantamab. Maybe talk about that combination and why that's an interesting one. Yeah, so that's definitely a differentiated approach. If you look at the first line EGFR exon 20 space, most competitors have basically taken one of two approaches. They've done it as a monotherapy or they've done it in combination with chemo. Now, given our profile, given our CNS activity, we have reached an agreement with J&J to do a combination where they're supplying us free drug. We are exploring that combination in first line EGFR exon 20. We'll have an early look at that data in mid-2026. The reason this is interesting, we know amivantamab is not CNS active. They've kind of showed this based on previous studies. We bring the CNS activity to the table. What they bring is basically it's a CMET. They're a bispecific. They also potentially address certain resistance mechanisms like C797S and MET as well. Lastly, just with the double EGFR, you get broader coverage and potentially deeper coverage as well. The obstacle here is you got to just be careful you don't have too much EGFR-related toxicities. We're doing dose escalation to see if we could deal with that. What would next steps look like for this program? What are the potential markets that you'd look to address? Yeah, we are very data-driven. We always prospectively set out our benchmarks of what makes a go/no-go decision. That's why we're quite comfortable laying out the benchmarks that Dominic just did. By the end of this year, by early next year, we'll see more data, obviously, from ourselves with competitors, figure out how we stack up in each of those three target populations of interest. The decision would be made independently for each of those three populations of interest because you'll have different benchmarks for each of those and different competitor compounds in each of those. Once we've decided which is a go versus a no-go, we can start to talk about what the regulatory plans might look like. Taking one of them, for example, EGFR exon 20, if that ends up being the first one that we take into a pivotal frontline study, it would be a randomized study. The control arm would be chemotherapy. Treatment arm is up for debate because, as Dominic alluded to earlier, we could do one of the two traditional treatment arms that folks in the field have done, which is either monotherapy, where you go head to head with chemotherapy. Some of the companies have done that. The other flavor of that is a combination with chemotherapy in the treatment arm versus chemotherapy. Of course, the third flavor, which is really only open to us, just given Janssen's interest in exploring imivantamab in combo with 114, is a potential amivantamab 114 combo. Obviously, the key de-risking event there will be the data that we'll have middle of next year, which will show whether those two drugs were combinable, the tox profile was manageable. If so, that would be a preferred alternative for the treatment arm potentially. If not, if they aren't combinable, if there's too much tox, we could just default to one of the traditional study designs of either monotherapy or combo with chemo. Gotcha. How quickly could you move forward into a pivotal study for 114? We intend to start next year. Okay. Yeah, there's a lot going on with the company, two different phase three studies, one for each program starting next year. As I mentioned, the cash position, which Dominic can sort of refresh everybody on. I think about that. The key piece is the runway. Yeah. More than the cash position, more than where it gets us in terms of dates, where it gets us in terms of milestones is past the phase three readouts for each of these programs. In fact, in the case of the prostate program, we will be over a year past the phase three readout for the prostate program in the runway that we've got today. A very comfortable position. I know we're just here at the last couple of minutes. Maybe just as we're summarizing here, obviously, a ton of progress, as you mentioned, a ton on the horizon for you guys as well. Just kind of looking ahead, just sum up for investors why they should be paying attention to ORIC over the next 6- 12 months. I would say you're going to get a boatload of data on both programs over the next nine months. Through middle of next year, just in terms of the already publicly articulated data milestones that we have, you obviously have a company that's extremely well-funded where we can be in control of our own destiny. We're funded through the phase 3 readouts on both programs. You've got programs and targets that are of really relevant strategic interest. The lung space has been disappointing in these various populations thus far. We think we have a program that's got a best-in-class profile that can put up those kind of a profile that's worthy of that space, especially with the CNS activity. Finally, in the prostate space, I would say it is very difficult today to find spots in oncology that have markets this large with a competitive dynamic like the one that we've got laying out in front of us. I would tell people to pay attention to that. Absolutely. Wonderful. With that, we're just about out of time. Thank you so much. Thank you. Thanks for calling in.