To start, just kind of having you sort of level set the conversation by talking about Contineum's kind of biggest accomplishments over the course of the year. Yeah, so again, I appreciate the invitation to the conference and the fireside chat. Yeah, Corey, as we look at 2025, it was as good as we could have hoped for. It's our first full year as a public company. We were able to execute on four different clinical studies over the course of the year. Not the first mic adjustment of the day. Yeah, four different clinical studies. So with PIPE-791, which is our what we believe to be best-in-class LPA1 receptor antagonist, we completed a phase 1b PET receptor occupancy study, which we think is really important as we embark on a phase two in IPF. It helped validate the dose selections that we already had a high degree of confidence in, but we were able to establish the target coverage at 50% and 90% with the doses that we plan to bring into our phase two study. Beyond that, we fully enrolled a phase 1b exploratory study in chronic pain, and that will be reading out in the first half of this upcoming year. Also, around PIPE-307, so we reported out VISTA data earlier this month. Unfortunately, we missed the primary endpoint, but we felt that we ran a well-controlled study that allowed us to really evaluate M1 receptor antagonism in relapsing- remitting and trying to identify the first remyelinating agent. And we're still working through some of the data with J&J, so there may be more to come in the future. And then lastly, as I mentioned, we are kicking off a phase two clinical proof of concept study in idiopathic pulmonary fibrosis before the end of this month with PIPE-791. And for us, that is the highlight study for 2026 for us. It is looking more like a phase three study from an operational perspective than a phase two. And we're hoping to be able to demonstrate at the end of this study a best-in-class and possibly a best-in-disease approach to IPF. Okay, so a lot to get through here. Maybe to start, for those who are not as familiar with the space, what's the rationale for targeting LPA1 in IPF and other indications like progressive MS and chronic pain? Yeah, so as we look at the mechanistic rationale for LPA1 receptor antagonism in IPF, a lot of this, the seminal work was done by Andy Tager at Harvard Medical School, and he published this in 2008. What he was able to demonstrate was through lung injury, there's an increase in LPA, and LPA is a bioactive lipid, and its natural ligand is LPA1, and what happens when there's an injury, LPA is upregulated, as is the expression profile of the LPA1 receptor, so LPA activates the LPA1 receptor, and that leads to several cascades of events, so first, it leads to fibroblast recruitment. That fibroblast recruitment leads to collagen secretion, and that initiates the fibrotic process, which then leads to chronic lung disease. Separately, LPA also leads to endothelial barrier breakdown, and that increases inflammation in that setting. So by inhibiting LPA1, you can limit some of these effects and reduce fibrosis. As it relates to our pain program, which, again, exploratory program, early stage, LPA again is the bad actor here. So when there's injury that causes pain, this leads to activation of the ascending pain pathway and increases in activity in the cortical regions. What we're seeking to demonstrate is by inhibition of LPA1, both centrally and peripherally, we can have an impact on demyelination peripherally through Schwann cells, and then equally, if not more important, a reduction in neuroinflammation by inhibiting microglial activation. And then lastly, again, sticking with LPA as the theme for progressive MS, our real interest in this was looking at the LPA1 expression profile in the brain. And specifically, it is highly expressed on glial cells, oligodendrocytes, as well as microglia. So we think that progressive MS is a good first approach on that, being able to interrogate it in that setting because it can lead to an improvement in remyelination as well as a reduction in neuroinflammation. Okay, so you've highlighted in the past the long receptor residence time and the high target coverage of 791. Can you talk to how these kind of PK metrics can translate into tangible benefits in IPF? Yeah, so I think that we have done a really good job with the research team in establishing SAR that is different than other companies and being able to optimize compounds against these targets when we compare to J&J in M1 or BMS in LPA1. We originally were looking at the IP estates from Amira and from BMS. We didn't get the profile that we wanted, so we really moved into a novel estate. And what this allowed us to do was access molecules that are extremely potent. They have pharmacokinetic properties that lend themselves to QD dosing. They have high receptor occupancy. And even as we look at the PK profile, sorry, yeah, I think I've covered it. I apologize. Okay, so then when you look at the broader IPF landscape, you have three approved drugs there. Where does an LPA1 antagonist fit into this? Yeah, so looking at the current landscape, yeah, three drugs are approved. Two of them have been around for the last decade or so. So pirfenidone and nintedanib have been the standard of care for an extended period of time. They both have some significant liabilities. And if you look at IPF patients from diagnosis, the average lifespan is anywhere from three to five years. So you are setting up a death sentence at that point. Given the issues associated with the current standard of care, you have 30%-40% of patients who refuse to go on drug because of the known tolerability issues. And for those who do go on drug, 50% of them roll off after one year. So they're basically accepting that I will take the quality of life that I have now rather than a longer life with a poorer quality moving forward. So that creates a big hole for the 130,000 patients with IPF in the United States. The new drug that is coming out through BI, nerandomilast, it's a PDE4B inhibitor. Interesting data that came through, and we expect this to be part of the standard of care. I don't know that it will be a frontline therapy immediately because there are some question marks around this as well. So their phase two was very different than their phase three, but they have a DDI issue when taken with pirfenidone, and they also exacerbate the GI issues associated with Ofev. So we think that the market is ready for another entrant with a better safety and tolerability profile and potentially a better efficacy profile. So in the long run, we believe that an LPA1 antagonist will form the backbone of IPF and PPF therapy, and then we will add on polypharmacy to enhance that. Okay, and then the differentiation relative to Bristol's LPA1? Yeah, so there's three key areas of differentiation. One, BMS's drug is BID. So this is the easy one. There's no getting around a BID drug, and it's very clear from our PK traces that we are a QD drug. We believe, and I think that the field agrees, that higher target coverage would lead to higher efficacy. And with the doses that we've tested and we've validated through our PET receptor occupancy studies, with the doses that we're bringing into the phase two, we will have 90% plus receptor occupancy. We believe from BMS's phase two that at best they had 50% receptor occupancy and probably are dipping below that at trough. So that higher level of receptor occupancy should lead to better efficacy. At least that is our goal. And then lastly, on safety and tolerability. So it's been well noted that BMS has had a hypotension signal across all of their studies from their healthy volunteer into their phase two. And to avoid that in the phase three, they are doing a dose titration. We have not seen those signals, and we believe that some of the PK with having a slow association and dissociation rate, we have a built-in titration just given the slow kinetics of the molecule. So I think as we look at this, there's three key areas of differentiation: dosing, potency, and potentially safety and tolerability. Okay, and then so regarding your planned phase two for 791 and IPF, what can you share in terms of trial design and sort of expectations going into that study? Yeah, so the study is kicking off this year. What I can share that we've shared publicly is it's a 26-week study. The primary endpoint will be the same as what everyone looks at, so change in forced vital capacity, so a spirometry measure. What we want to be able to demonstrate at the end is a best-in-class approach to LPA1 receptor antagonism. So without divulging the size of the study or timelines, what we want to be able to share at the end is an apples-to-apples comparison with BMS's phase two. Of course, we'll keep an eye on their phase three. In their phase two, we believe that they missed their doses. They had a 30 mg BID dose that really didn't show anything different than placebo in the IPF portion. And then they showed some activity at 60 mg BID. We believe that they weren't satisfied with the target coverage because now in their phase three, they've included the 60-mg BID and they've added in a previously untested dose of 120-mg BID, which is not a common occurrence for pharma heading into their pivotal programs. Okay, and then thinking ahead beyond phase two, what's the regulatory pathway that you would need in IPF? Historically, you need two well-controlled studies, and a phase two can count as a well-controlled study. As we move into our pivotal studies, though, of course, we will be looking at IPF and PPF, so we'll likely be looking at two phase 3s as well, but there may be a regulatory pathway that allows us to look a little bit sooner. Okay, and then meant to ask this earlier too, but earlier this year, you published some data using donor slices from patients with IPF to kind of test reduction markers of fibrosis. Any learnings from that that kind of help you inform your phase two study? Yes, so we looked at human fibroblasts, we look at donor slices, and we also looked at bleomycin models. And we published a paper on that. We saw reductions in COL1A1, reductions in fibroblast chemotaxis. There are a number of different biomarkers that we were able to establish there. I think most importantly for us is looking at those precision-cut lung slices. We were able to see an upregulation in LPA1 or an increased expression in IPF tissue relative to healthy donor tissue. And we were also able to show inhibition of that through PIPE-791. Okay, and then I guess the last thing on the IPF front, just be interested in kind of your current take on the market opportunity that's in front of you? In my opinion, it's really untapped. Ofev does have a lot of liabilities associated with it, and despite that and the fact that patients don't want to go on that drug and that it doesn't make them feel better, it will do over $4 billion a year in sales this year, so it's pretty remarkable that even with all of the issues, patients will put themselves through this. What do you most worry about with this asset and with your pending phase two study? What keeps you up at night with this? The unknown, I guess. We're moving into a study that is typically difficult to recruit. I think that we are probably attacking this at the exact right time where BMS is no longer recruiting patients. Amgen isn't recruiting patients. We believe GSK is no longer recruiting patients. So there aren't huge pharmas who are swamping the market. So I think that that gives us a leg up. So it's really recruiting within a reasonable timeframe. What makes IPF studies so difficult to recruit? A lot of patients, these are frail patients. They don't drive. A lot of them are on oxygen. It makes it really difficult for them to come to and from the clinic. And there aren't that many patients. When you're looking at BMS right now, they're enrolling over 2,000 subjects. That swamps a lot of the market. Yep, yep, yep. Okay, all right, so some of the other indications for chronic pain, just want to touch on them quickly as we're sort of running out of time. Can you just talk a little bit more about the rationale behind LPA1 for chronic pain? Yeah, so there's quite a bit of literature around LPA1 and chronic pain and neuropathic pain. We've decided to move forward in osteoarthritis and chronic lower back pain. And what you find in the literature, for instance, in osteoarthritis is that the level of LPA in the synovial fluid correlates with the level of disease severity. And it's that LPA that activates the LPA1 receptor. We are taking our step into the clinic around pain very carefully. So rather than doing rodent models to justify 791 in a pain setting, which we know a lot of investors in the scientific community question, we went directly into a non-human primate study. And what we were able to show through a pretty objective measure of functional MRI is an increase in cortical signaling relative to pain in these non-human primate studies, which then can be blunted with PIPE-791. So that was the data that really got us excited to consider this, but we're taking this carefully. This is a small study. It's exploratory. It is placebo-controlled, but it is not powered. And we're treating this as 40 subjects, each on four weeks of dosing between OA and chronic lower back pain and then a crossover. Like I said, this isn't powered, so we're going to treat this as 40 N-of-1s and look for trends. And as we've done in our preclinical work, we're running this as a kill experiment. So if we see trends that convince us to move into a phase two, we'll continue to pursue that. But in the absence of that, we would stop progression within pain. Okay, and then shifting gears here in our last couple of minutes, are there any preliminary learnings from the phase two VISTA trial with PIPE-307 in relapsing MS? And are there read-throughs from RMS to the work going on in depression, or should we not kind of over-interpret this result? I'll start with the second one. No, we don't believe that there are any read-throughs. The only read-through that there would be was around safety or tolerability. And the safety and tolerability profile that we saw in the VISTA study correlates with what we saw in the phase one SAD and MAD study. So very consistent there. From a biological perspective or from a mechanism perspective, obviously we're both looking at M1 receptor antagonism, but focused on very different areas where with relapsing-remitting, we were looking at OPC differentiation to drive remyelination. With the depression portion of this, it's more around glutamate burst and increasing dendritic spine architecture, which then leads to a neuroplastic effect in the MDD setting. Okay, okay, so our last minute here as we wrap this up, I want to ask for a little sneak peek into 2026 and kind of set the stage for how you're thinking about your key catalysts and objectives next year. Yeah, so we have our first catalyst, and again, I'm going to caveat it with pain studies are tough, and this is an exploratory study. But the first catalyst is going to be releasing top-line data from our chronic pain study in the first half based on what is on ClinicalTrials.gov, because that's what I'm limited to talk about with the J&J collaboration, but they are guiding towards completion of their study in the middle of next year. So the main endpoint there is change in MADRS. And then arguably the biggest catalyst for us is BMS's phase three data from what we understand top-line data is expected in the fourth quarter of next year. Okay, excellent. Well, that way we're out of time, Carmine. Thank you very much for being here. Awesome. Appreciate it. Thanks, Corey.