Good morning, everyone. I appreciate it. Thanks for joining us for the Jefferies Healthcare Conference. I have the pleasure of hosting the Zentalis Management Team, and Ingmar, the Chief Medical Officer, is joining us today. I think the Zentalis team is going to start with a brief overview on their end, and then we'll get started with questions. All right. Thank you, Akash, and thank you to the Jefferies team for having us. Good morning, everyone. Thank you for your interest in Zentalis. I'm Ingmar Bruns, Chief Medical Officer at Zentalis. Before we begin, quick reminder, probably need to click this here, that during today's presentation, we will be making forward-looking statements. These statements are always subject to risks and uncertainties that may cause actual results to materially differ from those forecasted. A description of these risks can be found in our most recent Form 10-Q and 10-K on file with the SEC. We're pleased to share our strategy for our potentially first-in-class WEE1 inhibitor azenosertib, and we're very passionate about developing this potential new treatment option for ovarian cancer. The unmet need it could fill, and the value our unique Cyclin E1 biomarker-driven approach could create for patients, physicians, and shareholders. We have recently shared a very large body of clinical data on azenosertib, which we believe demonstrate clinically meaningful benefit for Cyclin E1-positive platinum-resistant ovarian cancer, or as I will call it in the following, PROC. Most recently, in an oral presentation during the SGO meeting, the Society of Gynecologic Oncology meeting in Seattle. The late-stage development plan in Cyclin E1 PROC includes the phase two study, Denali part two, for potential accelerated approval at the FDA, and a phase three confirmatory study for potential full approval, all of which, as always, is based on data and subject to FDA feedback, of course. We are currently executing towards the plan, and we previously announced that we dosed the first patient in Denali part II in late April, and we are expecting to report top-line data by the end of 2026. We also plan to seek FDA feedback on the phase three confirmatory study later this year and plan to initiate the study in 2026. Last but not least, we have a solid financial position with over $330 million in cash as of end of the first quarter this year and with a runway late into 2027, which is beyond the anticipated Denali top-line data. Slides advanced. Yes. Regarding the opportunity, we think there is substantial market opportunity in Cyclin E1 PROC given the unmet need in the patient population and potential best-in-class clinical profile of azenosertib. In the PROC setting, the successful launch of mirvetuximab in folate receptor alpha high patients underscores the demand for biomarker-directed therapies, and patients with Cyclin E1 PROC comprise a large proportion of the patient population with quite limited overlap with the folate receptor alpha PROC population, as shown on this slide here. Based on feedback from clinicians and opinion leaders, we believe there is significant untapped opportunity here for these patients. As you all know, monotherapy chemotherapy has low response rates and fairly limited durability in PROC patients. However, it is the only standard of care for PROC patients who are not folate receptor alpha positive or high at this point. Patients with Cyclin E1 overexpression tend to have poor outcomes in current chemotherapy standard of care regimens, and that is even more highlighting the significant unmet medical need here. We have accumulated a significant amount of clinical data that demonstrate that Cyclin E1-positive PROC patients overwhelmingly respond better to azenosertib with objective response rates over 30% at our primary dose of interest, which again is 400 mg intermittent schedule five on two off. Also, durable responses are seen consistently across our studies, which again are multiple times the response rates from current standard of care single agent chemotherapy. Beyond PROC, we are studying azenosertib in combination with bevacizumab in platinum-sensitive ovarian cancer. Also studying azenosertib monotherapy in USC, uterine serous carcinoma, and through investigator-initiated studies, azenosertib in combination with standard of care in HER2, which is in HER2-positive solid tumors, as well as in combination with standard of care in triple negative breast cancer. These studies could, of course, also provide franchise expansion opportunities here, but we're focused on the platinum-resistant ovarian cancer population right now. That's an important slide. Through our extensive clinical and translational work, we have established Cyclin E1 as a highly sensitive and specific predictive biomarker that can be used to identify patients who might benefit the most from the drug. I just want to reiterate this, about 50% of PROC patients overexpress Cyclin E1 protein based on analysis with the immunohistochemistry assay and a proprietary cutoff that Zentalis has developed. Importantly, Cyclin E protein levels are regulated at the DNA, RNA, and protein levels. I just want to give you an example for this. The protein can over express with no DNA amplification, but due to an abnormally slow protein degradation, and that's not widely known. Important message to send here for us today. The benefit of the IHC assay is that it really captures these different mechanisms of Cyclin E regulation in one assay that can be used to identify patients. Because so far, I think it's still believed that the genetic amplification is really the only relevant marker here. In fact, we cast a much wider net with equal efficacy as based on our data set. We've used the immunohistochemistry assay here, which again, 50% of the patient population. In this vein, it's also important to note that there is a significant number of patients that are Cyclin E non-amplified and Cyclin E1 positive. As I just said, 40% of those are still IHC positive, right, even if they're not amplified. Whereas 85% of the Cyclin E1 amplified patients turn out to be positive also in the IHC assay. Together, that of course leads to a much larger population. Coupled with the strong MOA and the connection between Cyclin E and azenosertib sensitivity, the prognostic significance of Cyclin E1 dysregulation in PROC underscores why patient selection with this diagnostic test is tremendously important for our go forward strategy as we present it here. Before I dive into this, let me make a few comments on the current PROC treatment options. Again, as already mentioned, except for the 35% of folate receptor alpha high patients, single agent non-platinum chemotherapy is still the standard of care for platinum-resistant ovarian cancer. Those agents include paclitaxel, topotecan, pegylated liposomal doxorubicin, PLD, as well as gemcitabine to a lesser degree. The response rates of these combinations in published control arms of studies range from 4-13% with a median PFS of three to three and a half months. Literature also has shown that Cyclin E1-positive patients had poorer prognosis with standard of care, and hence their response rates could actually be lower than the average range here or the range here that I just described with 4%-13%. It has also shown that the PFS is shorter. Based on this, certainly new treatment options are much needed for PROC patients, especially those who are Cyclin E1-positive as per IHC. This is quickly an overview of all the clinical data we've generated to date through several trials. The three studies shown here where azenosertib was tested in PROC were 001, that was the original first-in-human study dose escalation, and then Mammoth, which studied azenosertib in monotherapy as well as in combination with niraparib in PARP inhibitor-resistant PROC patients. Last but not least, Denali part one B, which evaluated our primary dose of interest, 400 mg at the, again, five on two off intermittent schedule in these patients. Across the three schedules, sorry, across the three studies, we have treated over 350 patients. A really large database here and a total daily doses of azeno monotherapy at or above 300 mg across different tumors. Two hundred of them were actually platinum-resistant ovarian cancer patients at 300 mg and 400 mg doses. A uniquely large data set here to base the future plans on. We believe we have gained a very solid understanding of azeno safety profile and have seen clinically meaningful response rates as well as importantly durability based on this very significant sample size. Now a little bit about the data. Here it's shown that the integrated safety profile, as I already alluded to, 300 mg as compared to the 400 mg dose in these patients. That's regardless of the Cyclin E1 status. As you see in this admittedly busy table here, the safety profiles are really broadly comparable between the two doses. Overall, we do see manageable heme and GI tox profiles, which are of course owing to the mechanism, right, interfering with cell cycle. Of course, you target rapidly dividing tissues here as the bone marrow as well as the GI tract tissues. The profile nonetheless appears to be more tolerable than that of other WEE1 inhibitor molecules that have published clinical data, such as also in the Ignite study. It is important to point out that despite the observed cytopenias that we see here, there was actually a very low frequency of patients that experienced febrile neutropenia or sepsis. Yeah. Next slide. The waterfall here. Across studies, as you can appreciate here on this slide, we have treated about 70 and 20 Cyclin E1 PROC patients at 400 and 300 mg respectively. In the 400 mg group, as indicated here, there was a response rate of over 30%. That is really something that not only Zentalis, but also our investigators consider as clinically very meaningful. Even though I just want to mention that 400 mg showed a higher response rate, as you can see, the sample size for 300 mg is relatively small. Also, it is a cross-trial comparison. The patient population was more heavily pretreated. Therefore, and also because of FDA's Project Optimus, we need to confirm the dose. That is why what the part II-A is directed towards here. I'll cover that momentarily. It is also important to note that based on the more recent January 2021 data cutoff, the median duration of response in the Denali study, as again presented at the SGO meeting in Seattle earlier this year, increased to 6.3 months. That is a very encouraging improvement in our view. There are patients that remained on study as of the January data cutoff, so this duration of response was also not yet mature. Now finally turning to Denali part I, we have achieved alignment with the FDA on a seamless design for part two, which we believe has the potential to support an accelerated approval pathway. As always, provided that the data continues to be supportive and of course subject to additional FDA feedback. Part I is designed to enroll patients in early lines of therapy compared to Denali part I- B. Patients here also will have to prospectively meet our proprietary IHC cutoff, which has not been disclosed yet for Cyclin E1 overexpression, while part I- B was a retrospective analysis of the overexpression. With this part II, we are leveraging our existing network of sites, which will support the efficient and swift enrollment, which started in April. Part II- A, as I mentioned, will focus on the dose confirmation according to Project Optimus. Once the dose is confirmed, we will seek additional alignment with the FDA on the dose and then also seek their feedback on the bar for accelerated approval. At the same time, the design of the confirmatory phase III study, which will be performed in parallel here or concurrently. This was a question because I just mentioned the patient population will be different with fewer lines of prior treatment. Earlier patients, specifically one to three prior lines, or in case of folate receptor alpha high patients, they need to have received mirvetuximab where available and approved. In that case, it is one to four prior lines. Many investors have asked in the past if we see difference in response in PFS in these less treated patients. We did this subgroup analysis here in the Cyclin E1-positive PROC patients. With all the caveats, of course, of a smaller sample size and overlapping confidence interval, I'm pleased to report that the ORR increases compared as well as the PFS compared to the patients with four or more prior lines of treatment. Of course, that provides additional confidence for the future trials and part two alike. Next slide. About the, so looking ahead, we will continue to focus on executing Denali and getting ready, as I mentioned, to initiate phase three confirmatory trial in 2026. We're also balancing the advancement of our additional pipeline opportunities for azeno and other tumor types as resources allow. What I really hope you take away from this presentation today is that Zentalis is intensely focused on getting azeno to patients, first and foremost with CIIin E1 PROC as our first approval and commercialization opportunity. We believe we can create tremendous value by executing on Denali part II as our priority that we can drive towards potentially registrational top line data by year end of 2026. We are very confident our potentially first and best in class WEE1 inhibitor based on a large body of clinical data that I hope I was able to show you here and in a very manageable safety profile. Certainly, there is precedent in the market for the demand for biomarker-driven treatments in the PROC population, as shown by mirvetuximab. This remains a tremendous unmet medical need with approximately 50% of PROC patients who are Cyclin E1 positive and have a particularly dismal prognosis here. As data mature and the studies progress, we look forward to providing updates in appropriate forums, including medical meetings and investor events. We appreciate your time here. Now I'd like to hand it back to Akash for Q&A. Thanks so much. I really appreciated it. It's interesting. I don't know if I'm going to the charts you showed in terms of how do you think about the way that ovarian cancer is right now, I'm not sure I agree that that's going to be the paradigm even three years from now. I say that as someone who's personally very skeptical about folate receptor alpha being the established biomarker in ovarian. I just came back from ASCO. I'm sure your team was there as well. You have HER2 antibody, ADCs showing a really good response rate in ovarian cancer, which shocked me. CDH6, you don't have very particularly high expression in CDH6. Merck, at their go forward dose, you're showing a 60-70% response rate. They're going to go potentially for accelerated approval. To me, and then also Lilly's data, it was a folate receptor alpha ADC. You can see this with the Genmab molecule as well, but they are not necessarily going biomarker selected. They are also showing signals in folate receptor alpha low and high. It is not just the high population. I think what is missed in a lot of the investor discussion right now is I think there are probably two ways to think about it, which is CCNE. What I think is particularly interesting is how do you stratify these treatments? You think about, particularly if it is an ADC game in first line, how do you think about both target mediated resistance, but also toxin mediated resistance? How does a WEE1 play in a second, third line setting there? That to me seems particularly interesting. I would love to get your take. Assuming we're going to Genmab going to trial is going to hit, and they're not going to have a biomarker for folate receptor alpha, CDH6 hits, and you have two topo toxins. What work has your team done about WEE1's role and activity and CCNA amplification post a topo payload being used? We do not have particular data for post topo exposure, right? We have and have also shown this at AACR combined preclinically with different payloads on ADCs, including TopoONE, but also spindle poisons. Pre-clinically, this is really truly exciting data, as you may have seen. We do think that the MOA of azeno is obviously uniquely positioned to combine with ADCs given the MOA, DNA damage or interference with mitosis. That certainly is an opportunity here. I also want to comment on what you said earli er here. Because I think first line is a little bit ways out for ADCs, and I think the jury is still out. Obviously, the front line chemotherapy combinations are very well established. We all know that it takes a lot and first and foremost, a lot of time to change that paradigm if the data will hold up on the ADC side. We actually do think that most of the ADCs, you will probably agree, have a really chemotherapy-like profile. I think once patients come off these initial chemotherapy lines, which in our mind will probably continue to exist, they have toxicities, experienced toxicities that probably last like neuropathy, alopecia, to just name them. They're probably afraid of another chemo-like profile. We do think that we can position azeno in between in this setting in PROC in particular. That is the actual opportunity here. Understood. Maybe just I'll ask more from your perspective as a scientist because we're, frankly, our team, we're trying to figure this out. We don't know. I suspect there's actually going to be a meaningful drop in efficacy if you are hitting a patient with a topo payload and then you retry them, even if it's a different target. The data there, I think, is relatively scant so far. I think this is going to be one of the, I mean, ovarian, TNBC, NSCLC. This is going to be a huge question. What do you suspect will occur? Will there be a paradigm where you can retreat patients with the exact same toxin with a different target, or do you think it will become commonplace for doctors to actually go to a different MOA after that ADC? Yeah, I mean, needless to say that I'm a little biased, of course, right? We thought about this hard because it is indeed a very important question. My take or our take on this is you can probably not and that the efficacy of the different ADCs with the same payload will be limited, even if you switch the target because eventually the active part, as you all know, is the toxophore, not the antibody. That's also our take on this. You probably have to choose one of them. If there's resensitization in later lines, maybe we all do not know that, right? That's also an opportunity on the sequencing side where we think, okay, wherever the ADCs move in the future with admittedly exciting response rates in pretty small data sets, but certainly exciting. The question really is, okay, you need to pick one and then what, right? That is the opportunity for azeno after as well, right? We see two ways, right? We see it first and foremost really as an early line opportunity coming off chemotherapy in PROC. Also because it addresses the eligible population where they are, frankly, right? These are elderly women and most of them are actually in the community. Of course, their lifespan is limited with any currently available chemotherapy. Would they necessarily want to go to a chemo infusion center or rather take an oral drug with comparable response rate, right? If you look at the subgroup analysis, we are not that far off, right? Probably more manageable toxicity profile. That is our take. Understood. Now, you have seen this in RCC. You're seeing, I think you're going to see this in Head and Neck, where you have a paradigm change in terms of first line standard of care. What happens is actually the late line settings actually end up being much bigger than expected, right? There is a perception right now that PROC is not necessarily the biggest opportunity. Maybe front line is where it's at. How do you expect the size of the PROC population to change over the next five plus years where that's where Zentalis is really going to be playing with their WEE1? Do you think there is going to be a meaningful increase in the PROC pool? Yeah, I think we, as Mireille basically gave the answer already, right? If you extend overall survival, you probably also extend the need for therapy. With this, the addressable population increases and expands overall, right? There is probably also more patients that can actually receive treatment in later lines. We also, while PROC is our focus, of course, for the first registrational commercialization opportunity, we look beyond PROC, right? We also. Where else would you look? CRC? If there is a, give me the top two indications you would look at. Yeah, I think we are for now sticking with ovarian cancer, right? Because it is relatively close. I think PSOC clearly is an opportunity and we maintain optionality here with the BEF combination that we have going already. That is not a registrational trial, which obviously we do not have the proceeds to pursue this right now, but we want to maintain optionality here and do not want to lose time. These are pretty capital efficient exercises here combining with BEF to move this along. But then there's, of course, also opportunities that we've so far covered, very exciting with IITs, again, to be most capital efficient, right? We have HER2 positive solid tumor combinations within HER2 azeno and triple negative breast cancer combination with standard of care, just to name these examples. Understood. Now, maybe just lastly, and look, I think the issue with Zentalis has been, the story has changed, the regulatory path has changed, the dose FDA interactions have changed. It's been incredibly frustrating on our end as well. Let's put it this way, because this is the convo I'll have with an investor. Do they have it right this time? I want to be clear on two fronts. Number one, do you have a clear set of expectations in terms of what the response rate needs to be to get accelerated approval? Is that 30%? I guess number two, when you think about the types of patients you're going to have in that study, right? Because you do show an interesting signal in patients who progress off PARPs. What is the milieu of patients you're expecting to be in that trial? Because I think that's the other question is, again, standard of care and therapies are changing so quickly. Is the prior data that's been generated over the last three years going to be representative of what's going to be in some of these Denali trials? How confident are you on that? Yeah, we're pretty comfortable with the data set that we have right now. The trial is ongoing. We're not facing a completely different milieu here for patients right now. It's a legit question. W e have some admittedly small data sets that give us certainty there within the population in part one B. We are quite confident. I take your comment on lots of changes along the way. I mean, all I can say is there is a new leadership team in place. We are really committed to this. We looked at that. No one was necessarily looking for a job when taking this on, but we saw the opportunity. I think we are aligned in our belief that this is a largely underappreciated company and drug that gives a lot of opportunity going forward here. Hopefully, we can convince you all and investors that we are going forward with the plan as we laid them out and execute on it. Love it. We are out of time, but I really did enjoy the conversation. Thank you so much for all the investors joining us. Thank you.