Good morning, everyone. My name is Frank Tang, and I am with the Investment Banking division at Morgan Stanley. Thank you all for joining us today for the Fireside Chat with ORIC Pharmaceuticals. I am joined here today by the CEO, Jacob Chacko, and CFO, Dom Piscitelli. Great. Thank you both for joining us today. To start off, for those in the audience that are not familiar with ORIC, could you guys give us an overview of where the company sits today, your lead programs, and your priorities now that you have crossed into late-stage development? Sure. Happy to, Frank, and thanks for having us. ORIC Pharmaceuticals. ORIC stands for Overcoming Resistance in Cancer. In a nutshell, that is the mission of the company. We are today focused on executing across two late-stage development programs. rinzimetostat, which is a PRC2 inhibitor that is being developed in prostate cancer in combination with two of the big three androgen receptor inhibitors in prostate cancer. That has just started its first phase III study, a study called Himalayas-1, which is in the castration-resistant prostate cancer setting in patients who are post abiraterone. I am sure we will talk a lot about that today. Then our second program, enozertinib, which is a brain-penetrant TKI for lung cancer, which is being developed in two different populations within the EGFR family of mutations. EGFR exon 20, and then separately, EGFR atypical mutations. That is a program that will have a pretty substantial data update coming up not too far from now in ESMO in Madrid in about a month's time. If all goes according to plan there, and we continue to show a best-in-class profile for that program, we would anticipate starting the first phase III study next year in 2027. A lot going on at the company and extremely well-funded. Let us get into your specific questions. Yeah. I would like to start by going a little bit deeper into rinzimetostat. What are your expectations for Pfizer's upcoming MEVPRO-1 readout, particularly in light of their announcement that top-line data is now expected in Q4 of this year? Yeah. So probably the most common question we get in meetings these days is about Pfizer's data, and what is the expectations for MEVPRO-1. I always hesitate to comment on expectations for another company's program. Maybe what I will just leave it at is, I think we and others on the street have been doing a statistical events analysis around Pfizer's MEVPRO-1 study. That is the first of three phase III studies that Pfizer is undertaking with the same mechanism. Pfizer has got a drug, mevrometostat, which is a PRC2 inhibitor, which they are combining with the third of the AR inhibitors. I mentioned that we are combining our drug with two of the three big AR inhibitors. Pfizer is combining their drug with enzalutamide, which is their AR inhibitor that they acquired from Medivation. They have got MEV-Pro01, MEV-Pro02, and MEV-Pro03, and MEV-Pro01 and MEV-Pro02 are in the CRPC setting, MEV-Pro03 is in the CSPC setting. MEV-Pro01 is the one that Pfizer recently, on their Q2 earnings call, narrowed the guidance for the top-line readout to Q4 of this year. I think that the analysis that we and others on the street are doing essentially suggests that probably bodes well for the trial results. The fact that the top line would be coming in Q4 probably means that the treatment arm is doing well and that the events have been accruing on the control arm. I think folks are now reading statistically a decent chance that that trial will be positive. Obviously, the later, the better in terms of that positivity. But I think most importantly, Frank, is that almost any statistical analysis you can do on the event accrual into that trial would suggest that a readout in Q4 pretty much takes off the table a huge miss in the trial. Meaning that as you start to think about scenarios for how that trial might play out, whether that is a huge win ranging all the way down to a small win, a small miss, or a huge miss, you basically have taken a huge miss off the table at this point and narrowed the range of outcomes for them. Okay. But beyond that, I will leave it to Pfizer to comment on expectations. Okay. That is super helpful. I guess, how do you see any of that impacting you in terms of the types of readouts? The extreme outcomes are gone, but it could be a clear positive or an edge case scenario. How do you view those outcomes? Yeah. If I just take those four scenarios again that any trial could have, which is a huge win, a small win, a small miss, or a huge miss. The fact that you have taken huge miss off the table, at least statistically speaking, should be a good thing because a huge miss obviously would call into question the mechanism of action itself. I think Yeah. For all the statistical and event reasons that we have talked about, it seems highly unlikely that a huge miss is on the table at this point. I think even beyond that, just taking a huge step back and looking at the half a dozen or so data points that at this point Pfizer has shown in various single-arm settings, as well as a randomized controlled trial of their own in a phase II setting, and then two different phase I data sets that ORIC has now presented. Another drug also had some positive data at ASCO GU. I think across half a dozen different data points, the mechanism does truly seem to be additive. When you add a PRC2 inhibitor with an androgen receptor inhibitor, you get pretty profound synergy. Taking that big miss scenario off the table is quite helpful because I think the other three possibilities, which would be anywhere from a big win down to a narrow miss, would be, frankly, good for us. What I mean by that is, mechanistically, we have already seen evidence that this works. There is always edge case scenarios that can take place. If Pfizer has safety issues that pop up on the treatment arm, if that leads to dose reductions and therefore lower dose intensity that the patients receive, that obviously could compromise the therapeutic effect of their regimen. I mentioned that they are combining their PRC2 inhibitor with enzalutamide, which is their AR inhibitor. Enzalutamide is a well-known CYP inducer, meaning it pushes down the exposure of drugs that you try to combine with it. They're having to dose higher with their mevrometostat in order to get back to the right exposures that can always insert some level of uncertainty into a trial. They're also taking a relatively, it's a new regimen, actually, that they're using in the phase III, which is dosing in a fed state as opposed to the randomized data where they were dosing in a fasted state. Now, they've shown data that suggests that they're able to exposure match between those two doses and regimens, but anything can happen in a phase III. There's a whole variety of reasons that could lead to an edge case scenario. But of course, everything that I just rattled off is very specific to their drug, to their regimen. Yeah. Would not read through to rinzimetostat, our drug. The key point that lets Dominic and I and the rest of the company sleep well at night as we think about these various scenarios and even an edge case sort of near miss for them is that rinzimetostat on a like for like basis is just a better drug than mevrometostat. If you look at just drug development 101, look at the pharmacokinetics of the two drugs, mevrometostat has done a lot better for patients in this space than other PRC2 inhibitors have come before. Part of the reason is because it has a better half-life than the other PRC2 inhibitors that have come before. Those PRC2 inhibitors, the first generation compounds, had a half-life of about one to two hours. A lot of them had what's known as CYP autoinduction, where they would rev up the CYP enzymes and then themselves be metabolized by the CYP enzymes, and you would see things like dose-dependent decreases in exposure. Mevrometostat, to Pfizer's credit, has been able to solve some of those issues. They don't seem to have CYP autoinduction. They have a relatively longer half-life than the first generation compounds. Their half-life looks to be about four to five hours. What I love about rinzimetostat is it's taking that and then taking it to the next level. What I mean by that is we acquired this program from Mirati. The chemists at Mirati did a phenomenal job of coming up with a best-in-class drug profile for the compound. With rinzimetostat, we don't have CYP autoinduction, and importantly, we have a 20-hour clinical half-life. That 20-hour clinical half-life means that we can dose relatively low doses of the drug once per day. Our phase III dose is 400 mg once daily. That's obviously a fraction of the dose that Pfizer is using with mevrometostat, which they are dosing 875 mg twice daily. And so at the end of the day, that means that we do not run into the same level or ought not to run into the same level of Cmax-driven toxicity that Pfizer is going to see with their regimen, that they themselves have said that they see with their regimen. And so that list of factors that I just rattled off to you that could lead to an edge case near miss scenario for them do not apply in the same way to rinzimetostat. On top of that, you have to look at the other part of the combination regimen. The three AR inhibitors, which are enzalutamide from Pfizer, apalutamide from J&J, and darolutamide from Bayer, have done phenomenally well for patients with prostate cancer. They have transformed the care of prostate cancer patients. Those three drugs collectively do over $13 billion globally in sales, and that is a clear indicator of just how much unmet need those drugs have met for those patients in prostate cancer. When you go survey the physicians and understand the profile of those drugs, what you will hear in every conversation you have is that the efficacy of those three drugs is the same. What is different is that enzalutamide, which was first to market, is a little worse tolerated, has a little worse tox that people worry about than apalutamide, which was the second drug that came to market. And then darolutamide from Bayer, which is the one that we are combining with, is the best tolerated of the three drugs. Yeah. Darolutamide is also not a CYP inducer, whereas enzalutamide and apalutamide are CYP inducers. And so by bettering each component of the combination regimen, we feel very strongly that we just have a better regimen overall than what Pfizer has. And so essentially anything they can do, we can do at least as good, if not better. Yeah. That is the mantra. And so in any of the scenarios you talked about, it would be fantastic for us. Great. You mentioned a lot about the differentiation, but just maybe to cap it off, how do you expect the primary differentiation to be driven? Is it efficacy, safety, or both? Yeah, I think the thing that I can confidently underwrite just based on the pharmacokinetics is a safety differentiation. Again, with a four or five-hour half-life and having to dose the drug two times per day, you know exactly what the PK curve looks like for Pfizer, which is they're going to have two very large peaks and then two troughs in the course of a day. In order to cover the target, the required amount of target coverage you need over a 24-hour period, they do have to give relatively high doses of the drug. The issue with that, and this is not me saying it, Pfizer said this at ASCO GU back in 2025, is that they do see Cmax-driven toxicity. When you have those two peaks, you're getting to a Cmax that does lead to an accentuation of the toxicity. On-target toxicity for PRC2 inhibitors should be hematological toxicity and then a variety of different GI toxicities. Pfizer sees those, as do we, of course, because if you're hitting the target, you should see those toxicities. Of course, they see it at a greater frequency and a greater intensity than what we see. Yes. That ought to be at a minimum base case, the difference is that we'll have better safety than what they'll end up having. Assuming that both drugs can cover target for 24 hours, I know that we are covering target for 24 hours. I don't know that Pfizer is because they haven't shown those data yet. I just have to assume that they are. Assuming that both drugs are covering target for 24 hours, efficacy should essentially come out about the same between the two regimens, but safety obviously would come out quite different. Everything I just said applies to the castration-resistant prostate cancer settings where you're hoping to see patients stay on drug for anywhere from nine months to upwards of a year or more. You can manage some level of toxicity in that setting, and clearly Pfizer was able to do that. You see the randomized phase II data that they presented last year, which were quite phenomenal in terms of the PFS that they showed, but had a fair bit of toxicity. You can obviously manage some level of toxicity in the castration-resistant prostate cancer setting. The real question comes when you move to the CSPC setting. Pfizer's third phase III study, MEVPRO-3, is certainly a population that we would want to study as well in a future phase III study of our own. Castration-sensitive prostate cancer, you expect patients to stay on drug for four plus years. Certainly with a treatment like this, you would expect even longer than that. That's a setting in which the room for error, the margin for error of having too much toxicity is going to be quite thin. That's an area where you very well could see a safety advantage bleed through into an efficacy advantage. What I mean by that is if we end up with a better, clearly differentiated safety profile versus the Pfizer combination regimen in the CSPC setting, that actually could yield better long-term durability as well because patients are more willing to stay on drug for the number of years that you would expect in the CSPC setting. It's a thorough overview of differentiators. I appreciate that. You've initiated Himalayas-1, your first phase III in castration-resistant. Could you walk us through the design, including the key similarities and differences versus the MEVPRO-1 trial? The design of Himalayas-1, our first phase III study, is very similar to the design of MEVPRO-1. Both are being studied in the castration-resistant prostate cancer setting. The inclusion/exclusion criteria for both studies is, again, quite similar, which is patients have all progressed on abiraterone, and up to one prior line of chemotherapy is allowed for those patients to have experienced as well. It's very clean in terms of like for like patient populations. One small difference that we've done in terms of just trial design, and this is just to kind of narrow the unexpected surprises possibility is obviously for Pfizer, for us, the control arm is a physician's choice, either an ARPI switch or chemotherapy. That is the same for both. Now, one thing that we have done in our trial is just cap the physician's choice to no more than 60% of either one of those things. Meaning that at the end of the day, you will have between 40%-60% of the patients will have received an AR switch, and between 40%-60% of patients will have received chemotherapy in the control arm. I do not believe that Pfizer has put a cap in their study. That is really the only significant difference between the two in terms of trial design. Yeah. Otherwise, their size is the same, which is 600 patients. Roughly 300 patients in the treatment arm, 300 in the control arm. The other, the trial design stats, timelines, everything else is quite similar, which is you would expect about 6.75 months of PFS in the control arm. That is a blend of the expected PFS of an AR inhibitor switch versus chemotherapy in the control arm. Then you would expect about 10+ months in the treatment arm. All of that is solving for a 0.66 hazard ratio on PFS powered at 95%. So it is a very similar trial stats as well. Great. What are your plans for other trials outside of post-abiraterone and CRPC? Yeah. Internally at ORIC, aside from trial execution in Himalayas-1, the other topic du jour is what comes next. Yeah. Planning for success, what will Himalayas-2 look like? What will Himalayas-3 look like in the prostate cancer space? There is certainly, we do not have time for it today, but there is a lot of places you would develop a PRC2 inhibitor even outside prostate cancer that is also on our radar. Staying within prostate cancer, probably the two next most favorite populations for us, one would be castration-resistant prostate cancer, but in the post-AR inhibitor setting. As you think about the class of drugs called ARPis, it is really the three big AR inhibitors, as well as a drug called abiraterone, which is also widely prescribed to prostate cancer patients today. MEVPRO-1, Pfizer's trial, and Himalayas-1, our trial, are looking to address half of the prescriptions of ARPis today, which is post-abiraterone CRPC, but the other half are the three big AR inhibitors. What do you do for patients who have progressed on an AR inhibitor? That would be a trial that could be of high interest to us. Pfizer and we have both shown pretty strong phase I data that suggests a very strong treatment effect in that setting. At least until today, Pfizer has not announced a phase III study in that setting, so that would obviously be an area that would be of high interest to us is to pursue a trial in the CRPC setting, post-androgen receptor inhibitor. Also, where MEVPRO-3 is. Castration-sensitive prostate cancer is also high on our list. Like Pfizer, we also have every intention of going earlier line. As large as castration-resistant prostate cancer is in the two different indications I talked about Yeah. We can certainly provide some of the sizing around that. Castration-sensitive prostate cancer is multiples larger than even that population. That would also be high interest to us. Got it. Either way, whichever one we choose, we're hoping to get the next Himalayas-2 study started next year. We'll see. Yeah. You've guided to rinzimetostat program having a program update expected later this year or in the second half of this year. Can you preview what that is expected to cover? Yeah. I'll take that one, Frank. What we do every year, we give our guidance back in January of each year, so it's kind of our guide, excuse me, for the milestones for the year. And back then, we did say that we'd have intentionally said we have a program update in the second half of this year. So that program update could be one of many things. That could be an update on the Himalayas-1 study, on how we're doing with that program on that study. The second phase III study for prostate cancer that we're pursuing, or it could be some data updates. So a little bit of TBD on what that will include. Got it. Okay. Thank you. Maybe this might be a little bit of a switch back, but could you walk us through the commercial opportunities and dynamics if both mevrometostat and rinzimetostat ultimately reach the market? What factors do you think will help or help drive physician choice between the two agents? Yeah. I think as we think about the commercial opportunity, obviously, this is prostate cancer. This is a very large commercial opportunity. Maybe I'll walk through the studies or the areas of focus that Jacob highlighted. The first one, obviously, is a post-abiraterone patient population. This is where we're studying the first study, the Himalayas-1. There you got about 17,000 patients in the U.S. We think that's about a $3.5 billion total addressable market in the U.S. Globally, we think it's double, so it's about $7 billion globally. The second one is the post-AR inhibitor. That's around 20,000 patients in the U.S. Again, that's about a $3.5 billion total addressable market in the U.S., and about $7 billion globally. If you move into the earliest stage, obviously, you have higher patient populations and longer durability, so that is probably greater than $10 billion commercial opportunity. Again, this is a huge commercial opportunity in prostate cancer. Where we really think we've differentiated so far based on the data that we've shown earlier this year is really on the safety front. Again, Jacob kind of alluded to this, but if you look at both the frequency and the severity of adverse events were significantly better than Pfizer, and that really does translate into market share. You kind of see it with the analog that Jacob referred to with their enzalutamide, which came seven years after enzalutamide, and it's taking a significant number of share. We've done our own independent market research, and assuming equivalent efficacy, but just differentiation on the safety front, we should own the large majority of the PRC2 class overall. Obviously we think just on safety, that should translate into a market leader in the PRC2 class share. That's a great opportunity. Maybe switching gears to your other lead asset, enozertinib. What's your development strategy there, including the treatment setting and regimens that you guys are pursuing? Yeah. So enozertinib is a drug that is almost as advanced as rinzimetostat. We're developing it in lung cancer in two different patient populations within the EGFR family of mutations, I'll call it. So EGFR exon 20, and then separately, EGFR atypical mutation. We're right now studying enozertinib. We've already studied enozertinib in pre-treated populations in both of those settings. But right now the focus is almost exclusively, in fact, exclusively on the first-line setting, the frontline setting. So treatment-naive patients with one of those two types of mutations. We presented a lot of data on both of those populations last year in December at ESMO Asia. That was a mix across different lines of settings. But now, as I said, we're focused entirely on the frontline. And within there, the interesting thing, Frank, is that both of those populations are First of all, taking a step back. Non-small cell lung cancer have these various driver mutations that end up leading to pretty atypical lung cancers for patients where you see patients who are young, never smokers, but they're genetically driven tumors. This is an area that has now been— Thankfully, we've made a lot of progress. Other companies have made progress on mutations like ALK and ROS and RET and classical EGFR mutations. The interesting thing about EGFR exon 20 and then separately EGFR atypical mutations are those are two sets of mutations where, to date, there has not been either approved or late-stage therapies that have shown really profound CNS activity. You might ask why does CNS activity matter for a lung cancer drug? The reason is because of the high prevalence of metastases to the brain in these patient populations. In the frontline setting in either of these populations, about 35% of patients will present with brain metastases at baseline. So before they've ever been treated, 35% have brain metastases at baseline. That is actually undercalling the%. What I mean by that is there's certainly a large portion or% of patients who have what are known as micrometastases, which are brain metastases that have come from their lung into their brain that are just too small to see on traditional imaging. The true number is even north of 35% of the patients who present with brain metastases or who have them. And then the brain is often the first site of progression for patients as well. That's why it's so important, and it has become dogma amongst lung cancer physicians that for patients with any of these driver mutations, you want the drug to be brain penetrant. If you look across the various driver mutations in lung cancer, whether that's ALK or ROS or classical EGFR mutations, the best-in-class drug is always, without exception, a brain penetrant drug. The reason for that is that the non-brain penetrant drugs can't handle those brain metastases. They can't prevent the brain metastases, so you end up getting artificially lower progression-free survival in those patients because you're essentially pulling in the PFS of the patients who present with brain metastases. So the overall PFS gets pulled in as well for those drugs. If you look at alectinib or osimertinib, these drugs that have done incredibly well for patients, what is special about them is that their brain penetrance has led to a profile where there is essentially no difference in the progression-free survival in the patients with versus without brain metastases. What struck us was the lack of a brain penetrant compound in these two spaces. So that's what got us excited about developing enozertinib in both of these populations. We have already shown actually pretty compelling evidence of the CNS activity of the regimen in both populations. Then obviously we've got an update in a month's time on our atypical frontline population, where we will hopefully make the case that this is the best-in-class molecule in that space. Yeah, on that point, could you remind us what you expect to show in this update at ESMO, I'm assuming you were referring to, and then what were the relevant benchmarks? Yeah. So we'll have a poster at ESMO on the EGFR atypical patient population. We'll have 20 to 25 patients worth of data. So what we'll show there is systemic response, CNS response, safety tolerability, and some form of durability, most likely a swimmer plot, given the maturity of the data. When we look across the competitive landscape and the benchmarking, we're really looking through three different lenses. One is systemic response, one is CNS response, and the last is safety and tolerability. If you look at the competitors, systemic response rates are somewhere in the low to mid-60s. What's really interesting is when you look at the CNS response rate. What I mean by that, you see a significant drop-off in the CNS response rates from the systemic. Some of these guys have a systemic response rate of mid-60s, but their CNS response rates is in the low 40s. If you truly have a good CNS active drug, you shouldn't see that daylight between the systemic response rate and the CNS response rate. Hopefully we exceed one of those benchmarks and then we at least meet some of the others. The other thing I'd want to focus on is safety and tolerability. With these agents, you're going to have some on-target toxicities. But the other thing you're seeing with some of these other agents is off-target toxicities, which is not something you'd want with these type of agents. You see things like QTc prolongation, elevated liver enzymes, and anemia. We think there's definitely room for improvement. As Jacob alluded to before, the data that we saw with the CNS activity back at ESMO Asia last year was really encouraging. Hopefully we can exceed at least one of those benchmarks I spoke about and be at least as good on the other. For the EGFR exon 20, what will determine whether you move into a phase III and whether you pursue a mono or a combination approach, and how would you think about the upcoming competitor updates in impacting that potential decision? Yeah. We've taken a very pragmatic approach on what to do with the EGFR exon 20 space in particular, given the reality is it is somewhat of a crowded space, and there's continuous data coming out from competitors. We expect one additional data to come out from one of the competitors in the coming months as well. We do think that's an interesting space as well. We think the market opportunity there, again, is pretty significant as well. We will have an update in the second half of this year. What we're doing there is we're studying it in three different ways. We're studying it both as a monotherapy, in combination with chemo, and in combination with amivantamab. In order for us to move forward into a phase III program, we really need to have a differentiated profile. So obviously we're looking at the benchmarks that are out there today, as well as the ones we expect in the later part of this year. If we're differentiated, we'd move forward into a phase III study next year. If we're not differentiated, we'd probably look to partner the program. Understood. At the end of the day, Frank, we have to be best in class in order to move forward into the phase III setting for either of these populations. Obviously the benchmark competitors are somewhat overlapping, but not totally overlapping between the two. It's an independent decision that we make as to whether we advance neither of these populations, one population, or two into a subsequent phase III study or studies. I guess, given those decisions and given the differentiation we've now talked about, how would you characterize the commercial opportunity that you expect for enozertinib? Yeah. These are smaller than prostate, and I agree with that, but I do not agree when people think this is a small patient population. These are both blockbuster opportunities, both the EGFR exon 20 and the atypical. When you look at the EGFR exon 20, there's about 4,000 patients in the U.S. So if you do the back of the envelope math, that's over a $1 billion TAM in the U.S. alone. If you jump over to the EGFR atypical, that's around 6,000 patients. It is a larger patient population. We estimate that to be a total addressable market of about $2.5 billion in the U.S. alone. Again, if you look at the targeted space, you look at a best-in-class molecule, that best-in-class molecule should capture the large majority of that market share. So we're really interested in the space. We are really excited about the data that we showed at ESMO Asia. Again, we will have an update latter part of this year. That is great. We are looking forward to it. Moving on to the corporate side, could you give us an overview of your cash balance and runway? You ended the quarter with roughly $388 million guided to runway of second half of 2028. Does that cover the potential phase III for enozertinib as well? Yeah. We are in a very good position from well-capitalized from a cash position. We have $388 million at the end of Q2. As you said, we have got runway into the second half of 2028. That does assume both the phase III study for rinzimetostat, Himalayas-1, that is included in that cash runway. It also assumes we are starting a phase III study for enozertinib in the first half of next year. That is a fully burdened cash number. Again, that is cash runway into the second half of 2028. The reason that is really important is based on our timeline of starting the Himalayas-1 study, we would expect our top-line data from that phase III study in the first half of 2028. Our cash runway is past that top-line data readout for that phase III study. Got it. That is great. Now, final question from me is, with two potentially best-in-class assets, how do you think about the strategy of building as these programs continue to mature versus partnering? We think very carefully about it. It's a topic that's top of mind for us is really, we know the value of the two programs. If we truly hit this best-in-class profile for even one of the programs, let alone two of them, we're obviously building something of incredible importance here for cancer patients. Dominic and I, and the rest of the team, we're not dogmatic about what the potential path forward is. We're always evaluating opportunities. Really it's just about maximizing the reach of both programs in terms of the development strategy that we would want to undertake. For the lung cancer program, it's relatively more straightforward in terms of the types of trials you might run in one or both populations. Certainly in prostate cancer, I alluded to it earlier, Frank, there's a broad development program you can undertake in just prostate cancer with rinzimetostat. Even beyond prostate cancer, there's a number of areas that the preclinical evidence would suggest that program, a PRC2 inhibitor, ought to be studied. There's combinations with KRAS inhibitors in either colon cancer or lung cancer. There's combinations with ER-directed agents in breast cancer. There's a whole host of other areas where we may want to develop rinzimetostat. So that could be one that lends itself more easily, more readily to a larger partnership at some point, whenever is that right time. We're right now heads down focused on execution for the two programs and we will always continue to think actively about what's the right way to broaden the development strategy for each of the programs. Beyond that, no other specifics I can offer. Thank you. That's something investors are obviously keeping a keen eye on. Well, thank you both for joining us, and we look forward to the next conversation. Thank you for having us.