Good morning, everyone, and thank you for joining the H.C. Wainwright 26th Annual Global Investment Conference. My name is Samira Zumer, and I'm an associate here at H.C. Wainwright. We're confident we're going to be able to provide value to you with over 600 companies presenting at this conference in multiple sector tracks devoted to life sciences, cryptocurrency, blockchain and fintech, technology, media and telecommunications, clean tech, metals and mining, and growth. H.C. Wainwright is a full service investment bank dedicated to providing corporate finance, strategic advisory, and related services to public and private companies across multiple sectors and regions. We have a total of 24 publishing senior analysts and over 636 companies covered across all sectors. Please visit our website for more information. Please also join us for one-on-one meetings, corporate presentations, and panels that will be available live and streaming. With that said, we hope you have a productive and enjoyable day, and I'd like to introduce our speaker for today, Lloyd Segal, who is the CEO at Repare Therapeutics, which is a company that specializes in precision oncology drugs, so thank you and welcome. Thank you very much for the kind introduction, and thanks for the invitation to this great conference. We're very pleased to be here. With me is Steve Forte, our Chief Financial Officer, will be available for questions after the presentation. Before we get started, just refer you to our safe harbor notes and to our numerous SEC filings that describe all the appropriate and relevant risks in what we're sharing today. Repare is developing the next generation of precision oncology medicines. There are four key elements to our story, and I'll do my best to cover them today. We start with a differentiated and proprietary clinical pipeline that we developed entirely on our own. A platform we call SNIPRx that focuses on DNA damage repair and synthetic lethality, a very distinct approach in precision oncology that allows us to target new and important targets in cancer. We've got multiple clinical catalysts in 2024 and through 2025, we'll talk about what those are, in a strong balance sheet with $208 million to fund operations into the second half of 2026, with readouts in many of those catalysts. This slide shows our clinical portfolio, which I think really tells the broad story of Repare. Three current and one about to be clinical program, all, as I noted, developed in-house on our proprietary platform. I'll start at the top, give you a broad description, and then get a little deeper on all of these in the next 15 minutes or so. Lunresertib, at the top, and you see three horizontal bars to the right, is our PKMYT1 inhibitor. Like every one of our developed programs in precision oncology, there is a lesion, a biomarker, a genetic marker, if you will, that we look for, and we only focus on those patients in this precision oncology approach. The target is PKMYT1, which we innovated. We were the first to discover and ultimately take clinical a PKMYT1 inhibitor, and Cyclin E1, FBXW7, and PPP2R1A are the markers we select for, and only those markers. We currently have three active programs that I think the street's pretty focused on. One of them, and that is the near-term readout, I'll talk about a bit more, is our combination with our own ATR inhibitor, camonsertib, which we'll read out in the fourth quarter of this year. We've got some chemotherapy combinations, notably FOLFIRI, which just read out in June. I'll talk about that quickly. And an active and enrolling combination with Debio's WEE1 inhibitor, which is slated for readout in 2025. Camonsertib, our ATR inhibitor, which we believe is the best-in-class ATR inhibitor, is focused on ATM loss and 16 other genetic alterations that we think confer a likely response to an ATR inhibitor. We have that currently active in non-small cell lung monotherapy. That's an enrolling program. There are other combinations that we are actively looking at, notably PARP combinations and ICIs, where multiple competitors are active with what we think are less effective ATR inhibitors. 1664 is our PLK4 inhibitor. The marker there is TRIM37-high. Again, we're innovators there, the first selective PLK4 inhibitor. And our first and most exciting opportunity there, as I'll show you quickly, is in pediatric neuroblastoma, where we have shown absolutely outstanding preclinical work and just are blowing away every model that we can look at. Finally, 3467 is our Pol Theta inhibitor. The core marker there is BRCA1/2. It's an ATPase or helicase inhibitor, and that's going to the clinic in 2024. The IND, as you'll note from public filings, is open, and we expect to start enrolling soon. Behind that is a pipeline that we've recently dialed back a bit, given the depth of our clinical work, but actively, we have our partners at Bristol Myers Squibb, who, as part of a multi-year collaboration, are continuing to push forward on assets we've developed together. I'm going to move a little more quickly, but top line in this slide is that lunresertib, our PKMYT1 inhibitor, is a first-in-class oral small molecule inhibitor of PKMYT1, a large defined potential population over multiple tumor types. We have already shown, and I'll share with you some clear antitumor activity that we think is quite remarkable. We discovered this off our platform, and it very much represented proof of concept of our platform, and it's the data that we've shared to date unambiguously show our preclinical hypothesis on synergy from the genetic alterations we select is absolutely showing through. On this slide, you can just see the multiple tumor types that have those three genetic markers, Cyclin E1, FBXW7, and PPP2R1A. We're talking about a massive opportunity, over 90,000 addressable patients across our markets. But the two areas of most immediate focus are ovarian and endometrial cancers, where we have phase II-like enrichments going on as we speak, to read out in the fourth quarter, and colorectal, where we showed some really cool data recently. I'm going to skip over the overview and just get to the meat of some of the data that I think we and the street were most excited about. This was what we shared last October at ENA. As we developed this combination of lunresertib plus camonsertib, our PKMYT1 inhibitor and our ATR inhibitor, we saw this truly remarkable profile in a very small group of patients at a recommended phase II dose. In ten patients at the dose, what we saw is five out of 10 with gynecological tumors. Those are on the left figure that you're looking at, the hashed, the light hashed bars. What we saw is five of 10 of them had a RECIST response, six with a CA-125 molecular response. We were just blown away by the potential of this and recognizing that this was incredibly small as a starter population in a phase I study, as you would expect. We thought that it deserved a lot more clinical work, and we embarked on a phase II-like exploration in two arms of both endometrial tumors and ovarian, platinum-resistant ovarian cancer tumors, and we're aiming in the fourth quarter to share data on between twenty and thirty patients in each of those histologies, and we're going to aim for a proof of concept that we think could give us a path forward to a registrational trial or trials in 2025. On top of the really cool data that came out of our ENA presentation last fall, we shared some really promising data on lunresertib combined with FOLFIRI, particularly in colorectal cancer, and we were really blown away by the nice tolerability profile of lunresertib plus FOLFIRI. FOLFIRI is a tough one to combine, and in a very small number of patients, we saw that we were beating benchmarks on overall, you know, on a PFS-like markers. And I think this, really said to us that this deserves a likely randomized structure for a phase II investigation. We are exploring now how we would do that, whether we do it alone or in partnership with a bigger player. And I think it's fair to say that the community in colorectal cancer was quite excited about this data, and we're looking at our options as we speak. I mentioned the DBO combination, so that's our PKMYT1 inhibitor, lunresertib, with WEE1 inhibitor, in this case, DBOs. And we saw in our preclinical work and what justified starting this combination is just a tremendous body of preclinical evidence suggesting that this could be a very powerful combination across a range of tumor types. I think it's important to outline the significant opportunity, and what you see on this slide is just the significant patients who, in a second- or third-line setting, have limited options and virtually no options outside of chemotherapy, including some, you know, very powerful new ADC combinations. I think it's true in the sense that while there's more and more emerging in ovarian cancer, it's not clear that it's tolerable, or that it's attractive for either providers or patients. And we love the fact that, lunresertib chemo is an oral, really well-tolerated, very, very low relative tox to the other alternatives for these patients. And I think that the street and the oncology community has seen ELAHERE emerge, as more of an ADC, and despite, you know, a black box warning, it's shown that it can really have an impact in a very clear particular opportunity with patients. And we think we have an ELAHERE-like opportunity in a largely non-overlapping with folate receptor alpha population, as a third-line option, or second line in, ultimately second line in, platinum-resistant ovarian cancer. Even larger opportunity in the parallel trials we're running is the really, really nice opportunity in endometrial cancer, where it's a lot less competitive, much lower bar, where we think we'll need to see a 30% OR and sort of five to six months of PFS for good data. In ovarian, I think we're looking at sort of 20% or better OR in the same five to six months. In endometrial cancer, much fewer opportunities for patients and a much more wide-open space, same biomarkers, you know, over 3,600 second-line patients here. I don't think I need to highlight how important colorectal cancer is, but I think this page is really meant to underscore why we're so excited about that FOLFIRI combination and why others might be excited to pursue it with us. And finally, our camonsertib program is currently active, as I mentioned earlier, in a 20-patient monotherapy study. Again, small patient set that we saw really exciting opportunity in terms of the PFS we saw in a small number of patients in our studies and the studies that are emerging from AZ. And I could add Merck Serono to that list, in combinations, including immune checkpoint inhibitors and PARPs in the case of Merck Serono. Just spell out how interesting the opportunity is, both as a monotherapy, and as a combination. Non-small cell lung is huge, ATM loss. You know, I think, my chief medical officer put it best, she said last week, this is double the opportunity of ALK, and, that's as a monotherapy, and we think that there's a very, very significant opportunity here. I'm going to switch gears to our PLK4 program. Less visibility on Wall Street and, high visibility on a very focused group of patients who desperately need treatment here. We took our RP-1664 agent into Children's Hospital of Philadelphia, who are leaders in the field of pediatric neuroblastoma. They have about a dozen models of pediatric neuroblastoma. They had hardly seen any responders in multiple different disease-modifying agents that they looked at. What you see here is in six different models. This is work done by Children's Hospital of Philadelphia with our compound. Just unbelievable tumor regressions in all but one case, where you see in the bottom middle figure was a very significant TGI, and we just think that the potential of this compound in pediatric neuroblastoma is massive for a patient population of kids who desperately need a good treatment option. Initially second line, but we think ultimately as a first-line option, depending on how we see this playing out clinically. This is now in a phase one trial. We're getting our dose, we're understanding tolerability. That started in February, and our next key milestone is the transition over to pediatric patients with RP-1664. I'm going to wrap up with Pol Theta. Our Pol Theta inhibitor is about to enter the clinic. As I pointed out earlier, the IND is open, as a matter of public record. You can find it on ClinicalTrials.gov. We are excited about this agent, as I think the rest of the industry is, because in some very high growth sectors of oncology, notably ADCs and RLT, but not limited to that, 'cause we've done a lot of work with PARP 1/2 or PARP 1 selective agents preclinically. The key thing about Pol Theta as a very unique cell cycle inhibitor is that it can... or cell cycle mediator, is that it can actually enhance the therapeutic window and impact of across PARPs, RLT, and chemotherapy. And it does this without adding any tox, which is obviously the challenge in all of these modalities. And I think that's why you're seeing and hearing about as much excitement as you are about pol theta as a class. And we're watching closely our competitors developing a compound IDEAYA in partnership with GSK. We think we have what could be a best-in-class. We're looking forward to seeing data from them and sharing our own data once we get through our initial dose escalation. As you can see on the right of the slide, these are massive markets all of which are becoming increasingly competitive, with pharma balance sheets behind them. We just picked these two out because I think what you see is our PARPs, where, you know, you've got marketed agents with long, long histories and penetration in the clinic. Commercially, you know, we ran out of time in the BRCA2 model on the left, and you see the depth of the regression without any adverse effect on body weight. This was deep and durable as regression gets in our experience. So I'm just going to wrap with the recent and expected milestones, 2024 and through 2025. As I just noted, our Pol Theta agent, our RP-3467, is expected first patient in very shortly. And I think there's a lot of anticipation on the street for our lunresertib and camonsertib expansion cohort data in both ovarian cancer and endometrial cancer, where in each of those, we expect to present in the fourth quarter 2025 20 - 25, sorry, 20 - 30 patients, so about 25 patients each. The goal being proof of concept in at least one, if not both, and a path forward for a registration opportunity in 2025. In 2025, we also expect to share lunresertib and Debio 0123 WEE1 combination data, and our camonsertib monotherapy data in non-small cell lung cancer, amongst other things. So with that, I'll wrap and.