Good afternoon, everyone. Welcome to this session of the Morgan Stanley Global Healthcare Conference. We are very excited to have Luis Peña from Evommune here with us. Let me just get through a quick disclosure, Luis, before we get started. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. With that, I am Judah Frommer, one of the senior biotech analysts. Like I said, very happy to have Evommune here. It has been an eventful year. You came public shortly after this conference last year. Maybe give the audience a quick intro to the company and how the team came together. Well, thanks very much for the Morgan Stanley and Judah for having me here. My name is Luis Peña, President, CEO, founder of Evommune. The company has been around six years now. I founded it just after I was a co-founder of Dermira. We had sold that to Lilly, that had bought lebrikizumab, which is now Ebglyss and doing very well on the market in atopic dermatitis. The goal for us has been to be a serious player in chronic inflammation, and we have been very disciplined since the inception of the company of putting a brand new program into the clinic with a novel target every 18 to 24 months or so. Fast-forward six years later, we have four programs currently in the pipeline. There really are two co-leads. There is an oral MRGPRX2 inhibitor, which is currently in a Phase IIb study in migraine. There is an IL-18 biologic that just showed very positive Phase IIa data earlier this year. We are scaling up the manufacturing and will be in a Phase IIb study in atopic dermatitis the middle of next year. We have just started talking about a very potent TLR7/8 inhibitor that we plan to put into the clinic in the first half of next year, and there has been some very interesting positive data recently with the TLR7/8, as well as previously. We also have a very deep STAT6 inhibitor degrader program that is preclinical, and we would file an IND towards the end of next year. So very busy and pretty excited about the current pipeline. Great. So plenty to talk about. Maybe we will start with IL-18, EVO301. Maybe just tell us a bit about the design of this molecule, its potential differentiation amongst IL-18 targeted therapies, and a bit of a history on the asset. Sure. We have a very talented medicinal chemistry team, and we do on our small molecule all the discovery work internal. We had a gap between two of our programs, and following that 18-24 month discipline, we had been scouring the world to in-license and fill the gap. We found a company in South Korea called AprilBio, and what they do is they take existing or new biologics or novel biologics, and they bind them to a fob that allows it to bind the albumin. That gives us two really cool properties. One is that it extends the half-life, so the naturally occurring binding protein, which we like a lot, it has been optimized for a long time by nature, but it is cleared very rapidly. From a therapeutic perspective, it is pretty tough. The binding to the fob allowed it to increase the half-life to two weeks, which in the maintenance phase, for example, for atopic dermatitis, you could probably dose every two months or so. That is a distinct advantage. In addition, it also helps it penetrate inflamed tissue, so that was really a bonus that was thrown in, and that might actually add deposition effect over time in the right area as we dose these patients for longer. From that perspective, we really liked the background, the phenotype of, not the phenotype, but the makeup of the molecule. It had already been through Phase I. It was very well tolerated, and it continues to be so. Right after we got the molecule, we took it into a- Phase II-A study that had very exciting data. Okay, great. You are investigating it in atopic dermatitis. Just taking a step back maybe, IL-18 is usually not the first target that comes to mind when thinking about atopic derm, but you have generated some very interesting data in the indication. Before we get to the data, maybe tell us about the rationale for evaluating IL-18 in this indication and why it was a specific target of interest. Yeah. You are right. It has really been over the last five to 10 years that there has been a lot of different publications that have shown elevations of IL-18 levels in many different indications, but no one has really dug into one. GSK generated some data that really caught our eye, and the reason it did so is the following. They had done a single dose study with an IL-18 monoclonal, very similar in potency to our binding protein. After one dose, they showed really somewhat of a similar profile to what we showed in our Phase II-A. They had IGA 0/1 scores in the mid-20s. Reasonable EASI 50, 75, 90 scores, although those are not dose optimized. It looked exactly like the data that we had looked at when we in-licensed lebrikizumab from Genentech. Lebrikizumab had done also a single dose study with topical corticosteroids on top, which somewhat increases the efficacy, but it was okay. After a single dose, they showed IGA 0/1 scores in the mid-20s, percent EASI change similar to what we had. Once we saw that- that to us was pretty clear validation that they had a biologic here with relevance. We very aggressively went after the molecule and then licenses it and put it in a phase IIa with an IV formulation. Okay, so maybe a bit more on the phase IIa data that you reported earlier this year. You mentioned the EASI and IGA changes, but maybe just a broader high-level recap of the design of that study and the top-line results. Yeah. We had a pretty good-sized study where we were looking at two-to-one randomization of the active versus the placebo. We were really looking at percent change in EASI. As it turned out for the study itself, the placebo rates were very low, and that's important these days. We've seen an uptick in placebo response rates in the atopic dermatitis study, a lot of that driven by really two things. One is the severity of the patient population you put in there. The less severe you have, the more spontaneous resolution and the higher the placebo effect. Secondly, sites that don't have experience. If you take a site that does generalized studies, doesn't understand really how to read these lesions and resolution, then you may have an uptick. We were very careful with that. And then we're able to demonstrate that percent EASI changes in the mid-30s. which is right on par with Yeah some of the best studies that have been shown out there, and that's really what we set up the statistics around. No matter how you looked at it was highly statistically significant. We did a Bayesian analysis on it, and that showed a 99% distribution to the good, meaning there was only really a 1% chance that was a random result. Even if you looked at it with the typical normal statistics, you had a 0.01 p-value. So highly statistically significant and very well tolerated. That was important. No conjunctivitis. Okay. It's not in the IL-4/13 axis. Right whereas that tends to be the main side effect that really bugs these patients. We were pleased to see that. So very well tolerated, and we're excited about the path forward. Okay, great. You evaluated a single 5 milligram IV dose in the study. You're planning to start a phase IIb dose ranging study- with, I believe it's three different sub-Q regimens mid next year. So how much room might there be to improve on the efficacy profile for 301 with an optimized dose, do you think? No question- Yeah we're going to optimize the efficacy profile. We were able, in the phase IIa study, to dose, the same dose, 5 mg per kg twice at day 0 and day 28. That was an IV dose. And the reason for that's all we had tox coverage for. That's the only drug we have. As we're going into this phase IIb, we're going to have a sub-Q formulation. That development's done. We have a very stable formulation that puts it in the 120 to 150 mg per ml range, so that we know we can maintain the 5 mg per kg level. And in this induction study, meaning the first 0 to 16 weeks, you have to be very aggressive. Historically, you don't look for convenience at that stage. You look for reaching steady state very aggressively, optimizing efficacy, and then you can look for convenience out to a year beyond that. And so you're probably going to see regimens that are once every 2 weeks, once every 4 weeks, loading doses in there, allowing us to keep that same drug level, but give more doses over that 16-week span. And we think that should definitely drive up the efficacy, just like we've seen with lebrikizumab and other biologics in historical levels. Okay, great. Ahead of that phase II-B initiation, I think you've said you'll share full phase II-A results at a medical meeting. Yes. Is that still the plan, and what can we expect from that update that we haven't seen? That is the plan. From the phase II-A, really the important data on the lesions already out, the percent change gain over placebo, the IGA 0/1. The EASI 50-90 is bounced around a little bit, which happens when you haven't dose optimized. I think probably the most important data will be on biomarkers, TARC IL-22. That wasn't necessarily a given that we would have a broader response, and that's pretty exciting. We look forward to presenting that, hopefully orally at the EADV, but if we don't get an oral presentation there, we'll probably be at the fall clinical in Las Vegas. Okay, great. If we think about potential approval for 301, where do you see it fitting into the treatment landscape? Do you think it could address both biologic naive patients and patients who inadequately responded to biologics previously? Certainly. Yeah. We don't think that that necessarily has to be a focus for approval. First of all, if you look at, for example, psoriasis, we just had a really interesting meeting where two investors came in, and they were both on biologics. It's important for them giving their severity of their disease, that they stay on the biologics. Because one of the things that we know is if you have moderate to severe skin disease, whether it's psoriasis, eczema, the risk for comorbidities goes up substantially over someone that doesn't. So it's really important to stop the march, make your disease better, and not put yourself at risk for metabolic syndromes, cardiovascular disease, diabetes, that may get you in the long haul. So super important to really stay controlled. We have four biologics currently in AD. Given five times the prevalence that we see in psoriasis, for example, where you have 12 plus biologics, nine blockbusters. You probably need 15 to 20. Yeah. The first thing we need to do is fill up the landscape with more biologics, hopefully with new mechanisms like you have with IL-18s. Highly heterogeneous disease, unlike psoriasis, where you see some of the IL-17, IL-17A/F now with almost 100% clearance. We're nowhere near that in atopic dermatitis. Many more biologics, different mechanisms. You need to mix and match. Over time, probably some of the bispecifics are going to be important. Then many more oral. Really now, the right things are happening for these patients, and that these companies are working on new mechanisms, more biologics, hopefully more oral, and that will all be needed. Okay, great. Maybe just a bit more on the competitive landscape in IL-18 targeted programs. There is a couple programs in development for atopic derm. There is at least one bispecific, probably more, but maybe briefly speak to how EVO301 might be differentiated from other IL-18 programs and what you are seeing on the multi-specific front, too. Yeah. We certainly like the binding protein. Yeah. Very potent. It has been optimized by nature over time. From that perspective, if you can extend the half-life, it is a great molecule. There may also be an advantage in terms of less of a probability or a lower probability of neutralizing antibodies. Yeah which we know is important for durability over time. We like it. Apollo Therapeutics has a monoclonal. I think we're the only binding protein currently in play, and so we probably are slightly behind them. I would root for our team if we were in a race. We are very experienced. Our team collectively, 28 NDAs or BLAs approved, and so there's a lot of experience there. We really are taking the time to set ourselves up now from a manufacturing tox perspective to go very aggressively to phase IIb and III. I think we really have the shot at being the first IL-18 on the market in atopic dermatitis. Then there are a couple of, as you mentioned, bispecifics, preclinical stage. I think that's important. I think it's important to try to continue, especially in this very heterogeneous disease, to add new molecules. To be determined where they're going to come out. As we know already with the bispecifics, one plus one does not always equal two, although they are important. We'll have to see over time as that data evolves. Okay. Then maybe just back to a comment you made a bit earlier, on that GSK asset that was discontinued, that kind of piqued your interest in the target. I think it was evaluated in a phase IIb dose ranging study that was stopped for futility, though one of the doses did seem to perform reasonably well. Any takeaways from that study? Was there something about that trial or the molecule that contributed to that outcome, do you think? Yeah. I have actually had multiple discussions with internal experts, including their head of strategy, and basically one is they are just out of derm. Yeah. The focus is out of dermatology. With that molecule, they rolled the dice on basically looking for convenience in that induction phase. There was 16 weeks, so they really did not dose optimize. They were looking, hey, can you give the drug once? Yeah. Or maybe twice at most, and then get an incredible result. When they did that interim analysis, they had separation when they had given it twice, but really had not dose optimized. For them, it was either best in class or nothing. Okay. They had no chance. But they definitely saw efficacy. Do you have any idea if it will come back in an IBD or T? From what we know is they are focusing on a bispecific in IBD. Got it. It may have an IL-18 arm. Okay. Their belief, it still works. Got it. It is still a reasonable molecule to go up against, but they are really focusing on IBD, which could be a good play for us down the road. Okay, interesting. All right, maybe moving to EVO756, your MRGPRX2 antagonist or X2. It is a target that has received a good amount of interest from drug developers over the last few years, but maybe just give us a little bit of background on the target and some of the history around it. Yeah. If you look at mast cells and sensory neurons and their interplay, they are really a first line of defense. Especially there is about 100 ligands. A lot of them come from microorganisms, some internal cytokines that activate that pathway. It is really a first line of defense when they are hit with one of these ligands. There is a pretty potent inflammatory degranulation driven effect from the mast cells as well as the neuropeptides. From the sensory neuron perspective, it is not just where they are sensing that there is something there, a ligand there, but they actually are driving the inflammatory effect through neuropeptides. I think what may have now clear since it did not work, it worked in CIndU. We had high levels of drug where we were injecting micromolar concentrations of ligand inducing urticaria, and we were able to block that even with very low amounts of our drug, but it did not work in CSU and AD. I think what that is telling us is that it is not a first line of defense type disease. It is a much more complex inflammatory disease. But it still could be a very important molecule for diseases that are. One that emerged very late for us was migraine. Yes. This is work done by The University of Texas. Greg Dussor there has done some fantastic work on a couple of fronts. One is they've infused these ligands, three of them, which initiate this mast cell degranulation through X2 and the sensory neurons in both preclinical models as well as humans, and they were able to induce a migraine response. Right. That is very different. That definitely keeps it in that first-line type of reaction of the X2 pathway. There's a company called Lundbeck that has a monoclonal against PACAP, just one of the three that we think are the most involved. Yeah. That also showed efficacy. PACAP can hit X2, it can also hit PAC1. Amgen had a monoclonal against the PAC1. They showed no efficacy. You would deduce that it is being driven by PACAP and the X2 receptor. For us, it is a pretty reasonable shot on goal to do a study in migraine patients, and it is with a small percentage of our capital, and we are pretty excited about it, actually. Okay. Awesome. Maybe just taking a step back from the learnings of some of the results you have seen in inflammatory derm, I guess maybe just has it changed how you think about the heterogeneous nature of some of these conditions, and maybe learnings on PK/PD as well that you have gleaned from those? From which studies? From atopic derm and CSU. Well, atopic derm, there's no question. Yeah It's a highly heterogeneous disease. Yeah. You see that with DUPIXENT or mepolizumab, about a third of the patients get a complete response, and the other two-thirds don't. That said, for the patients, and we just talked to one where it works, it's spectacular. Yeah. It is important, and it's important to continue to pursue that, but it also says that for two-thirds of the patients, either it doesn't work at all, or it works in combination. The best combinations right now are topicals. Yeah. But down the road, hopefully we can get into a position where we can mix biologics, hopefully. I like the ability to be able to, from a stoichiometry perspective, mix different monotherapies, but the bispecifics, if they work- could be super important. As I mentioned to these patients that we saw earlier, just stopping that atopic march as early as possible is key because it can limit your lifespan. So anyone that you know that has moderate to severe eczema, they need to get to a doctor. They need to block the systemic inflammation. We're getting much closer- with some of the mechanisms that are out there. Still haven't seen anything like BIMZELX, which with an IL-17A/F, you have 100% of the lesions removed in some patients. We're going to continue to work, and over time, hopefully, we can identify the key mechanisms that we can mix together to get there. Okay, great. Like you said, you've started that Phase II-B in migraine prophylaxis. Before we get to the study, maybe tell us a little bit more about the opportunity in migraine, how big the market is, maybe where it could go, and where you see the particular unmet need that you could be solving for. Yeah, it's a pretty significant market. The CGRPs are really the mainstay there, and if you look at some of the Phase III studies that are in their labels, it's pretty modest improvement. I think Nurtec, which was one of the top ones, a 0.8 difference in migraine days over placebo. Which sounds pretty minimal, but for a migraine patient that is suffering to the degree that they are, any advancement is great. And likely in some is much better. But overall, it is really a very incremental step. I think new mechanisms is great, and that mechanism has opened up a $6 billion-plus- market out there, and it is going to continue, I would think, grow. The prospect to have a new oral in the space with a different mechanism, I think it is pretty exciting. We have had a pretty incredible response from the KOL community. If you look at the investigators that are involved in the study, it is the most prominent in the space, and we expect it to enroll pretty quickly. Fingers crossed that this will have an impact on these patients, a positive impact. Okay. I know you touched on it, maybe just put a finer point on the mechanism here. We think about X2 typically in the context of traditional mast cell indications. Just again, the link between X2 and migraine, and to put a finer point on it, you mentioned the X2 ligands that are associated, but PACAP, PAC1, are those kind of the only connections as far as we know? Or are there multiple receptors that we should be thinking about? Well, there could be multiple receptors. Yeah. We know that by what we believe is induction of X2 through these three different ligands that have been given at The University of Texas. You saw induction of migraines. That was clear both in preclinical as well as the clinical studies. That gives you three out of 100, and there may be more. By blocking one of them, you are able to show a difference, so we think that is a reasonable thesis. You can access in the meningeal space, both the mast cells as well. as these neurons that express X2, and our drug can get there. We can get the sufficient amount there safely. Our expectation is that you are going to see some signal. Okay. Maybe that answers the next question, but I guess distribution of the drug in a manner that's relevant to migraine, is accessing that meningeal space the key here? Absolutely. Yeah. We know we can get about 70% of the drug to the skin by actually measurements in interstitial fluid microneedle. Through our preclinical work, we think we can get to 50%, 60% of our drug that's going around systemically in that space, and that should be enough to keep us- Okay well above the IC90 at 24/7. Okay, great. Maybe just the design of the Phase II-B migraine study. What lessons were taken from historical programs and incorporated into this study design? Yeah. I think there has to be two things that happen in terms of both chronic and episodic patients that are enrolled. You have to have a minimum number of migraine days, a minimum number of headache days, and make sure you maintain that. It is a lot like atopic dermatitis, as you start to get to the lower severity. then the chance of a placebo response goes way up. We are really monitoring these sites very closely in terms of putting the more severe patients in. What happens, so it turns into. The study is 330 patients. Yeah which is pretty robust. phase IIb study. It becomes a numbers game, right? Yeah. When a Nurtec gets a 0.8 difference in a phase III study, though, that's a very large study. What you do for these earlier studies, you enrich the population with more chronic patients. That usually will show a two migraine day difference over placebo, then that will narrow as you go to a broader population in phase III. We feel like we have a pretty reasonable sample size to be able to see a difference there. Okay. Maybe just talk a bit about dose selection for the study. Maybe this gets back to the distribution question, but is there PK/PD work you've done that supports doses that you chose to include here? We've done quite extensive work. Yeah. This is where actually our skin challenge study that we did very early on was very helpful because we were dosing micromolar concentrations of ligand. We were blocking it with doses as low as 25, 50 milligrams per day. In this study, although we haven't disclosed the exact doses, we're above that. We have two doses that are both above that. Okay. Both doses should actually work, and if we do need more drug on board, then the higher dose gives us a bit of a safety margin for getting more drug to the meningeal space. Okay. I think you said top line data next year. Yeah. In terms of clinically meaningful outcome, is it those two days improvement? Is there anything else you think you'd share in the top line that would inform go forward progress? I think that's Yeah the key data that you'd need there. Okay. Then safety Sure just to make sure it's well tolerated. Sure. There are, and correct me if I'm wrong, some exploratory endpoints in this study around patient subtyping and biomarkers. We do not have data in the indication yet, but do you have any initial thinking on potential patient subgroups that could be relevant? Those are very difficult. Yeah. I think we are doing some exploratory work, but so far from what we have seen historically, it has been very difficult to define the patient populations, and we are looking at a broader population first, and then over time, then hopefully we can zero in. Got it. Okay. I guess for these two, like you said, co-lead assets, I think you have talked about other indications in the past that might be worth exploring. I guess in terms of timing to updates on broader development plans, what should we be looking at? Yeah. I think for next year, we'll initiate the phase II-B study in the IL-18. We've got the phase II-B study ongoing. For migraine, we'll put TLR7, 8 into the clinic, and then the other maybe more imminent clinical program may be a UC study, ulcerative colitis study with IL-18. Okay. And we would likely be limited to the IV dose, so we just have to decide is that going to have enough drug on board for a sufficient amount of time, or would we want to wait for the sub-Q dosing? Okay. That's the biggest decision right now. But this mechanism looks to be really exciting there, and hence one of the bispecifics already is in IBD. Yeah. Okay, great. You touched on it, but it is a pretty recent pipeline update with the TLR7, 8. What brought that to your attention as a target or targets of interest? It is timely. I think we saw some data out of Beeline in lupus recently. What are plans here, and again, what is your view to the program? Yeah. We started working on this years ago, and it was again with the discipline of putting a new molecule in the clinic every 18 to 24 months. We started a small molecule discovery project, and our chemists are really fantastic at coming up with unique scaffolds that are different from anyone else, but also that very closely follow the Lipinski rules. There is enough experience to know once you start falling outside of that and the molecules get lipophilic, higher molecular weight, then you really increase the risk of off-target effects and impacting your efficacy too. We started on that a long time ago, and we are at a point now where we have molecules that— And we have synthesized what we have seen in the clinic through the patents. They compare very well, look very potent. There does not seem to be any limitations in terms of off-target effects. The half-life is good, so the QD dosing. Comparatively, they look fantastic, and certainly I think the lowest hanging fruit is probably CLE in that there is less complexity doing that study. But certainly this play would be in lifecycle management. Yeah. SLE is exciting. Yeah. That was fantastic. Right We do not know exactly what the data is from Beeline, but that is fantastic to have an oral new mechanism with efficacy in SLE, highly unmet need. There could be a number of other indications behind that. I think for us, as a new company, it is a balance of really showing a positive effect early on, then we can take more risk on the back end. Okay, great. We will look out for that. Maybe one last specific company question, I guess. Just remind us of cash burn, where you did the IPO and subsequent raise, but what does that fund from an operational perspective that we have talked about? Yeah, we are very well funded. After our last raise, in the end of the second quarter, we have $288 million in cash. That gets us to a year past the phase IIb result with our IL-18. We really have zero financing overhang right now. We have everything that we need to finish the migraine study, conduct the phase IIb with IL-18, then get to our TLR7/8 phase I results which will include biomarker data, and that's important because in a phase I study, you can read biomarkers that are impacting the pathway. TNF, other interleukins, which if you see a decrease, you know you're hitting the target. We have sufficient capital to finish all of that. Excellent. Okay, now we're asking each of our biotech management teams a little mini survey. Okay. So there's going to be three topics here. The first is on China's rise in biotech innovation. How are you thinking about competitive position here? Will this influence your R&D or business development strategy in any way? Well, we're always scouring the world for what's available. That's been a practice that we've done, and that's how we got to our IL-18 binding protein. We certainly keep an eye on China, and I think China is very prolific. at generating many molecules on known targets. Yeah. A little less prolific in terms of true innovation. Yeah. Anything that is different we are working on, we keep under wraps. But for those early-stage molecules, we certainly have a look at them, so that is their superpower right now. It is not so easy when you get into later-stage development. There are many things that happen, many things that occur along the pathway, whether it is a safety issue or a pharmacodynamic delivery issue, that I do not think they are quite as competitive in. I would not ignore them, but that is something that still is a huge advantage here and a huge advantage for our company. For us, again, it goes back to the discipline we started early on, which go early on targets you are discovering yourself, but also scour the landscape. We certainly have no issue in terms of in-licensing something from China or anywhere else. Sometimes if there is something that we are interested in, we might put it in the ear of one of these Chinese companies, and all of a sudden a year later they are like, "Hey, we have a molecule here you might be interested in. Excellent. Next topic is AI, I guess. How's Evommune leveraging AI or thinking about the potential for AI to disrupt biotech development? I think you have to pay attention to it. Yeah. Our TLR7/8 comes from, I think we generated something like four billion molecules in silico- Yeah which before that was impossible. Yeah. At best, you would have millions of molecules with huge teams. Yeah The ability to do that versus a target is really fantastic. We jumped on that very early on, and we continue to look at it. It would be great if we could get the regulatory agencies to be able to. They do actually have access to bigger data sets than a single company does. Right. I know that they've used them to their advantage in the past. I was just at a talk with Scott Gottlieb yesterday, and he's like, "We always had this conundrum that we have access to broader data sets that we can't make available to a single company. But if you could use AI, for example, to merge those two together in a way that could give you earlier perspectives, for example, on safety and off-target effects of certain chemistry, that would be huge. Right. I am hoping that we make huge inroads there. Or just broadly safety databases for off-target effects on small molecules that could be shared across companies. Or even if it is not shared, that you can plug into patents, that may help. But ignore it at your own risk. Got it. Last one, you touched on it, but I guess as you look down the line, potentially most impactful regulatory impact for your business, FDA, pricing, tariffs, anything on the regulatory side that you think could be most impactful to Evommune? Well, I think at the FDA, a lot of turmoil. Yeah. Hopefully that is going to stabilize sometime soon. I think probably the best side of it is most of the reviewers remain there. Yeah. But a lot of the middle managers are gone, and they do a lot of the work. And so that certainly has hurt, and hopefully that stabilizes now. And so we're going to have to continue to monitor that. There's been a lot of disruption on the pricing front. And first of all, there's a lot of room. There's a lot of room. I've been in the game for a long time. I remember being at Genentech, and there was a lot of hoopla over a $2,000 a year tPA drug, over a $200 streptokinase. Now that's a tiny price. Yeah. And so we could reduce prices from $60,000 to $40,000 with minimal impact. Yeah. I think we need to do a lot of that ourselves. The most favored nation status is tough. I am not sure if that is going to stick around, but I think some voluntary price reductions as well as the industry working together is good. I think disruption on the PBM side is good. I think one of the good things about it is for a young company like us, it actually does create opportunities to commercialize ourselves. Right. That is not a bad thing either. Okay. Excellent. All right. We will leave it there. Thank you again for being here. We appreciate it. Thank you. Thank you for having me. Sure.