Okay. Good afternoon, everyone, and welcome to our next session. I'm Sara Nik from H.C. Wainwright's healthcare research team, and it's my pleasure to introduce Aprea Therapeutics, ticker APRE, a precision medicine oncology company developing an oral WEE1 inhibitor designed to address the therapeutic window limitations that have constrained earlier drugs in the class in biomarker-defined cancers. Presenting today on behalf of the company is CEO Oren Gilad. Please join me in welcoming them, and the floor is yours. Thank you. Thank you, Sara, for the invitation, for presenting Aprea with your audience. As Sara said, we are a clinical stage precision oncology company focusing on synthetic lethality by targeting the DNA damage response pathway. I am going to make forward-looking statements, so please refer to our filings, the Qs and the K for risk associated with it. This is a snapshot, here you see on the right, of our pipeline, and you see that we have multiple targets, but it's very focused pipeline. We did use the slogan at the top left there, "One Critical Pathway - Multiple Targets." The focus of today's talk is going to be the WEE1 inhibitor that is in the clinic in dose escalation. We also have an ATR inhibitor that completed dose escalation, and we're looking for combination partners for it. A p53 reactivator, which I'm going to touch on at the end, and a DYRK1, which is preclinical. What is synthetic lethality? What is our approach to cancer therapy? First, I'm going to say that synthetic lethality is very different than chemotherapy. Chemotherapy kills every dividing cell, and we're all aware of the side effects associated with chemotherapy. Look at synthetic lethality as a cell has two backup systems, right? When the two backup systems are intact, the cell is alive. That's a normal cell. Then what happens, there's mutation. So, one backup system is not functioning, but the second backup system compensates for the loss of the first one. That's the biomarker. That's the mutation that leads to pathway inactivation. When we use our drug, we use a drug to target the second backup system, the second pathway. When cells don't have two pathways intact, the cancer cell dies. But the normal cells still have the first backup system intact. That is the approach. The whole idea here is to have a wide therapeutic window, again, unlike chemotherapy. So, we finished the last quarter with $41 million, and our market cap, if you look online, it's about $10 million, but it's not really $10 million because we're on a fully diluted equivalent. We have $103 million. So, we're in the $40 million- $50 million market cap. The cash runway is into Q1 of 2028 with multiple milestones, which I'm going to touch upon. So, let's talk about the program. What is the WEE1? Where are we, the differentiation? The concept of targeting WEE1 for cancer therapy is not novel. It's been shown in the past. AstraZeneca had the compounds, Zentalis is in the clinic, Debiopharm, and us. What we hope to show and demonstrate is that our drug is different and therefore we hope we'll have a wider therapeutic index, wider therapeutic window, so we see less toxicity and increase in efficacy. AstraZeneca didn't reach that. They struggled with their tox, so the drug has been given back to Merck and is no longer in development. Zentalis and Debiopharm still developing their drugs. This is from May. That's the snapshot of our strategy and where we are in the clinical development. I'm going to be focusing on the center and the left side of the slide to tell you where we are. You see it's a 3+3 dose escalation, but we also added at the center in light blue, we added a backfill, which is enrichment, right? Because we want to enroll as many patients as we can to really identify the patient population that is very likely to respond to the therapy before we move into the optimization. We established 150 mg as the minimum efficacious dose. That's where we saw the first partial response. At the 220 mg, we had a confirmed partial response. The patient population is on the left, in the box on the left. There are three different strategies for that patient population that we're targeting. One is indication independent of the mutation, and that's the USC. The second is a very specific indication and mutation. That's [uncertain] new overexpressing platinum-resistant ovarian cancer and KRAS- and p53 colorectal cancer. The third one is mutation independent of indication. That's cyclin E, FBXW7, and PPP2R1A. We did complete a $30 million financing at the end of March, and that's to help and enrich patients in the dose escalation to up to 100, including 50 patients that are USC and cyclin E overexpressing platinum-resistant ovarian cancer. What I hope you can appreciate from the swimmer plot here is that there's somewhat dosage response in this patient population. The bottom line at the 70 mg, that's the pink, we saw one stable disease, and that was a head and neck patient, p16- positive. That's the longest he's ever been on a drug, by the way, and our drug is taken daily orally. When we went up to 100 mg, we saw three stable diseases. 150 mg, we picked up the first partial response, and then 220 mg, longer duration, and additional stable diseases. We're going to provide an update at the fourth quarter of this year when you see more data from this study. This is as of May 6th. You see the treatment-related adverse effect. This is the most important slide in the deck, and it's the most boring slide in the deck. To that point, the drug has been very well-tolerated, and this is the same patient population that we saw the partial response and the stable diseases. 150 mg is very safe, 220 mg is very safe. When we showed that we're treating the 300 mg, an additional update is going to come at the fourth quarter in one of the conferences. Just to give you a couple of examples, because keep in mind that patients who are being enrolled in our study, they're failing multiple rounds and lines of therapies. In this case, this is a patient with a PPP2R1A mutation. Look at the first line of therapy. She was on therapy 126 days, progressed. Second line, 56 days, progressed. Third line, 70 days, progressed. Fourth line, five months, progressed, came to us. As of this date, she was still on treatment, and we provide update for her status. It looks very promising. She showed -50% tumor reduction in the first scan and another close to 10%, so about -55% tumor reduction at that time of the treatment, and very minimal side effects. It was very well-tolerated with a very impressive response. The second patient I am going to share with you is the 100 mg cohort. You see that mutation is FBXW7. The reason we picked FBXW7, because mutation in FBXW7 leads to prevented degradation of cyclin E. So, it is a cyclin E overexpression by the virtue of not being degraded. This patient, as you can see, five line of the prior treatments, 191 days, 45, 43, 12, 15, and she was on our study for 178 days. Again, taking daily orally, and that is at 100 mg. Remember, the 150 mg is the minimal efficacious dose that we established. Stable disease was -15%. So, the tumor shrank, but it is still considered stable disease, right? Because it is not -30% or stronger. On the left here, you see the table summarizing the responders and the response that I talked about, the PRs and the stable disease based on the indication and the mutation. We are expanding to USC and cyclin E PROC. We are going to add additional patients with FBXW7, the HPV, the PPP2R1A. We are going to be reporting durability and response later this year. So, what to expect? This is based on, it is categorized on each of the programs. The WEE1 we just talked about, monotherapy. Everything, all the data I showed, it is all monotherapy. There was no combination in any of the data I showed. So, all the response is the drug itself. We are going to show additional data. As Sara said, it is a biomarker-defined patient population. We also want to explore combination therapy, so that is to come, and given that the 150 mg, the 220 mg are pretty safe and well-tolerated. There is not much of overlapping toxicity, so we are excited about that. The ATR, I mentioned, we are looking for a combination, so expect combination initiation. We are looking for external-funded collaborations. So, we are not allocating much of resources to that program. We rely on external funding for that. The p53, that is the legacy Aprea that had a very successful phase II, MDS, both in the U.S. and in France, went to phase III and came short. We did announce previously that we are going to go back and look at the patient population, try to identify the patients that did respond to the therapy. So, stay tuned and we will share our findings also when they are available. So that is the company. We are publicly traded. We are focusing on synthetic lethality, targeting the DNA damage response pathway, active clinical programs, and additional update, as I mentioned, to come at the fourth quarter of this year. I thank you for your attention.