Welcome to the Kronos Bio conference call. As a reminder, today's call is being recorded. You may listen to a webcast replay of this call by going to the investors section of Kronos Bio's website. I would now like to turn the call over to Marni Kottle, Senior Vice President of Corporate Communications and Investor Relations of Kronos Bio. Please go ahead. Good afternoon, and thank you for joining us to discuss today's announcement about the prioritization of our clinical programs. I'm Marni Kottle, Senior Vice President of Corporate Communications and Investor Relations. Please note that the press release we issued earlier today is available on our website, kronosbio.com. During today's call, all participants will be in a listen-only mode. The slides and replay of our event will be available on our website shortly following the live broadcast. Joining us today are Dr. Norbert Bischofberger, our President and CEO, and Dr. Jorge DiMartino, our Chief Medical Officer and Executive Vice President of Clinical Development. For the question and answer session, we will also be joined by Dr. Yasir Al-Wakeel, our Chief Financial Officer and Head of Corporate Development. I would like to remind you that this presentation includes certain projections and forward-looking statements as of the date of this presentation, including statements related to our plans, projections, estimates, and expectations regarding our discovery pipeline and clinical development plans, the potential benefits of our product candidates, and our financial condition. These projections and forward-looking statements are based on the beliefs of our management as well as assumptions made and information currently available to us, and reflect our current views and are subject to business, regulatory, economic, and competitive risks and certain contingencies and assumptions. In light of these risks, uncertainties, contingencies, and assumptions, the events or circumstances referred to in the forward-looking statements may not occur. None of the future projections, expectations, estimates, or prospects in this presentation should be taken as forecasts or promises. The actual results may vary from the anticipated results, and the variations may be material. With that, I will now turn the call over to Norbert. Well, thank you, Marni, and again, welcome everyone. Today, we announced that the company made the decision to prioritize its clinical portfolio to focus on our next-generation SYK inhibitor, Lanraplenib, LANRA, as we will call it, and our CDK9 inhibitor, KB-0742. We will discontinue our Entospletinib or ENTO phase III trial and plan to close the trial to further enrollment. Patients who have already enrolled in the trial will be able to complete their course of treatment. We're making this decision after recent review and assessment of enrollment data. This assessment projected significant delays with the ENTO trial due to several factors, including the operational challenges we faced in enrolling genetically defined subset of fit patients with AML in a frontline setting, the residual and ongoing impacts of the COVID-19 pandemic, and the inability to activate planned clinical trial sites in Russia and Ukraine due to the conflict in that region. In light of such enrollment challenges and delays, we made the strategic decision to discontinue the ENTO trial. These changes are expected to extend our cash runway from Q4 2024 into Q2 2025. We believe that the most promising path forward for bringing a transformational therapy to patients with AML is to narrow our focus of our SYK inhibitor program to LANRA, initially in the relapsed refractory setting where the need is most acute. Jorge will talk to you more about LANRA, including our ongoing phase I b2 trial in a few minutes. We did not make this decision to discontinue the ENTO trial because of adverse events or lack of efficacy signals, but rather because of a material change in the timelines, the delays with the trial that I just described. What has not changed is my belief and the belief of our scientific teams in the biological rationale that supports SYK inhibition for the treatment of AML. On behalf of all of us at Kronos Bio, I would like to express my gratitude to the clinicians and patients who participated in our ENTO trial for their contributions to advancing potential new therapies to treat AML. I also would like to thank our employees for their dedication and commitment to the AML community and to our SYK inhibitor program. This strategic change has the added benefit of allowing us to bring additional resources to the development of KB-0742, our CDK9 inhibitor. KB-0742 has the potential to address MYC-amplified solid tumors and transcriptionally addicted cancers. We're nearing the end of the dose escalation stage of our phase I two trial and remain on track to share PK, PD, and safety data from that study later this quarter. Additionally, we're making progress with our earlier stage discovery pipeline and continue to work towards future development candidates. Before I turn over the call to Jorge, I would like to take a moment to walk you through what to expect from us in the near and medium term. On track to provide a clinical update on KB-0742 in the Q4 of this year. We anticipate sharing initial efficacy data from the phase II portion of that trial in the H2 of 2023. With regards to LANRA, we anticipate sharing initial data from the ongoing trial in combination with gilteritinib, along with the recommended phase II dose in the Q4 of 2023, or the Q1 of 2024. It is never easy to make the decision to end a clinical trial. I'm confident that because of this decision, we're a better company going forward. I'm also confident in our ability to execute on this strategy. While ENTO and Lanraplenib both target SYK, the development programs have several key differences that I would like to point out. One major difference is the patient population we're targeting for enrollment. We're enrolling patients with relapsed refractory FLT3-mutant AML, who had a low response rate and a poor prognosis, in contrast to the frontline setting. There's only one treatment approved for this group of patients, gilteritinib, and the average overall survival for patients in that study that led to approval of gilteritinib was just 9.3 months. There is significant need here and significant room for improvement. Enrolling mutation-based clinical trials always presents challenges, but it is less challenging to enroll genetically defined patients with relapsed refractory disease than those who are newly diagnosed. Newly diagnosed AML patients who are candidates for intensive induction frequently need to be started on chemotherapy within days, limiting the window of opportunity to assess their mutational status and enroll them on a trial. Relapsed refractory patients, in contrast, are already under the care of a hem-onc specialist. This means at most centers, physicians know the genetic mutational status of these patients and are following them closely for evidence that they're starting to relapse. This provides a much better opportunity to identify, screen, and enroll patients in a study before there is need for urgent intervention. As study site operations move closer to pre-pandemic status, our clinical operations team is better able to closely and continuously engage with the sites to facilitate study startup and communication with investigators. I have been in this industry for more than 30 years and have overseen the successful development and commercialization of more than 25 medicines, and I have learned that drug development is rarely a linear process. Being flexible and resilient and continuing to evaluate both the science and what's best for patients are critical to successfully bringing forward new medicines. This is the right decision for our company at the right time. With that, I will now turn the call over to Jorge. Jorge? Thank you, Norbert, and good afternoon. I wanna begin by echoing Norbert's earlier gratitude to the patients and investigators who participated in this trial and to our internal teams. As Norbert said, we remain deeply committed to patients with AML and to our SYK inhibitor program, and we believe focusing on Lanraplenib is the best path forward. At the time we acquired Entospletinib and Lanraplenib, we believed that Lanraplenib had the potential to address unmet need in a broader AML population in the long term, while Entospletinib was the best option for bringing a SYK inhibitor to younger, fitter patients in the near term. With the recent assessment of enrollment timelines, we no longer believe that the Entospletinib opportunity can be realized in the near term, and we're narrowing the focus of our SYK inhibitor program to Lanraplenib. Lanraplenib has a number of advantages over Entospletinib, including pharmacologic profile that is conducive to better patient compliance during chronic dosing regimens. Lanraplenib has once-daily dosing, the ability to be taken fed or fasted, and can be co-administered with proton pump inhibitors for individuals who require these medications to manage their gastroesophageal reflux or related conditions. From a single-agent safety perspective, Lanraplenib has been well-tolerated without any clinically significant adverse events in more than 250 clinical study participants. These properties make Lanraplenib an ideal compound for use in combinations with other oral targeted agents in AML, which are dosed to progression. Based on our ongoing work with Lanraplenib in preclinical models, we continue to believe in a strong biological rationale for targeting SYK in patients with genetically defined subtypes of AML. Specifically, we've confirmed and expanded observations in the literature showing that SYK is implicated as a vulnerability in patients with AML, with mutations of NPM1, FLT3, and MLL rearrangements. Combining Lanraplenib with targeted inhibitors such as gilteritinib or MLL Menin inhibitors in patients with FLT3 or NPM1 mutations, or MLL rearrangements, or with IDH inhibitors in patients with co-mutation of IDH1 or IDH2, represents an attractive strategy to address unmet need in AML. Novel combinations, such as those we're studying in the phase I b2 study of Lanraplenib and gilteritinib, which I'll describe in more detail in a subsequent slide, have to be tested first in the relapsed/refractory setting. Depending on the level of efficacy and safety that is seen in relapsed refractory patients, this study could set the stage for further development in relapsed refractory or even frontline AML. SYK signaling is critical for leukemogenic potential of FLT3-mutated AML. We and others have shown that combined inhibition of SYK and FLT3 can achieve greater than additive anti-leukemic effects. For example, the data on this slide are from a Kronos Bio presentation at the European Hematology Association meeting in Vienna this past summer, and show the results of treating patient-derived FLT3-ITD mutated AML cells with a range of concentrations of lanraplenib and gilteritinib. The red squares show combinations that have greater than additive killing of AML cells consistent with a synergistic effect. We've now demonstrated this effect in vivo using patient-derived FLT3-mutated xenografts in mice. These data will be presented at the upcoming ASH Meeting in December and form the basis of our conviction that this combination will provide higher response rates and longer duration in patients compared to gilteritinib monotherapy. Turning specifically to the medical need, I wanna talk about this group of patients with relapsed refractory disease. There are approximately 15,000 patients with relapsed refractory AML in the United States. Of those, about 30% have a FLT3 mutation. The prognosis for these patients is poor, and there are few treatment options. The only treatment approved for FLT3-mutated relapsed refractory AML is gilteritinib. In the ADMIRAL study that supported the approval of gilteritinib, only 21.1% of patients achieved a complete response, and overall survival was just 9.3 months. While this represents significant advancement over the existing standard of care, it still leaves a very sizable gap that includes those patients who either did not achieve a complete response or whose survival was nonetheless limited. There are no therapies currently approved for use with gilteritinib to address this gap. Based on the data I shared with you on the previous slide, we believe that Lanraplenib could potentially help fill this gap. We enrolled the first patient in this trial this summer and are continuing to enroll in the dose escalation portion of this trial. Investigator engagement has been positive. Our trial, like most phase I trials in AML, is being primarily conducted at centers where mutational profiling of patients is standard of care, and patients are monitored closely for relapse. In contrast to the frontline setting, this provides a greater lead time for identifying and screening potential study participants. This is one of several reasons we do not anticipate the same enrollment challenges we saw with the Entospletinib program. Finally, I wanna shift gears and say a few words about our KB-0742 program. As you're all aware, CDK9 is a long-sought-after target for drug developers. CDK9 is a global regulator of transcription and key cofactor of many oncogenic transcription factors, including the MYC family of transcription factors. The MYC gene is amplified in approximately 30% of solid tumors, including those affecting the lungs, ovaries, and breast, as well as in transcriptionally addicted cancers such as small cell lung cancer, chordomas, and sarcomas. Despite many efforts, no one has been able to successfully define a dose and schedule of a CDK9 inhibitor that shows adequate target engagement along with good safety and tolerability profile. As a result, other CDK9 inhibitors have been challenged in moving beyond dose escalation studies. We believe that KB-0742's selectivity for CDK9 over other CDKs, combined with its oral bioavailability and long plasma half-life, make it unique in the crowded field of CDK9 inhibitors and position it to be the first CDK9 inhibitor to show clinical benefit in patients with MYC-amplified and transcriptionally addicted solid tumors. We and others have shown in preclinical models that tumors with MYC gene amplification are more sensitive to CDK9 inhibition than tumors with normal MYC gene copy numbers. We're aiming to demonstrate this in the clinic, but the first step is to define a dose and schedule that we believe has the potential for antitumor activity while remaining tolerable for patients over the long term. Last year, we showed data from our first three dose cohorts confirming that the PK properties of KB-0742 were almost exactly as we had predicted from preclinical models. This gave us confidence that with further dose escalation, we would be able to define a dose that achieves the threshold level of CDK9 inhibition needed for antitumor activity while maintaining a tolerable safety profile. As Norbert mentioned, we are now nearing the end of the phase I stage of our phase I two KB-0742 study and remain on track to share PK, PD, and safety data as well as our recommended phase II dose later this quarter. After reaching the recommended phase II dose, we plan to enroll two cohorts of patients in the next stage of the trial from the two groups I just described, patients with MYC-amplified solid tumors and those with transcriptionally addicted cancers. Following the Q4 2022 update from the ongoing KB-0742 trial, the company anticipates sharing initial KB-0742 efficacy data in the H2 of 2023. While this was not the outcome that we had hoped for with the entospletinib trial, I'm confident that by prioritizing our lanraplenib and KB-0742 programs, we're making the right decision for patients with cancer as we seek to bring forward new treatments that have the potential to transform care. I'd like now to turn the call back over to Norbert. Norbert? Well, thank you, Jorge. In closing, I'd like to reiterate that we have the resources we need to execute on our clinical programs and an experienced management team to guide the two ongoing clinical trials. With that, I would like to now open the call to questions. Operator? At this time, if you would like to ask a question, please press the star and one on your touch tone phone. You may withdraw your question at any time by pressing star two. Once again, for your questions, that is star and one. Take our first question from Salveen Richter with Goldman Sachs. Please go ahead. Thanks for taking our question. This is Toni on for Salveen. Could you envision LANRA going into Ento's previous indication? Just a question on the timelines here. When are all the patients going to be transitioned off of ENTO, and what's kind of the cadence of savings that you would expect going forward in the next few quarters as part of this discontinuation? Thank you. Yeah. No, great question, Toni. For LANRA, the plan right now is really to focus on the relapsed refractory space and these rational combinations, starting with the gilteritinib combination. This is where, you know, we feel the need is the most acute. You know, with regards to your questions on the timeline, we will be informing the investigators of this decision. Obviously, patients who are already on study treatment will be offered the opportunity to complete their study treatment. Yeah, and that's basically what I'll say about that. In terms of the timeline of the cost savings, Toni to your question, I think, to Jorge's point about the unwinding of this trial, we anticipate that will take effect relatively soon. As you think about our cash runway, it goes from Q4 of 2024 into the Q2 of 2025. Quite a substantial cost saving that'll be realized over the next two and a bit years. That really allows us to deliver on the data for both LANRA and KB-0742 that we're extremely excited about. Thank you. We'll take our next question from Tyler Van Buren with Cowen. Please go ahead. Hi, everyone. This is Brittany on for Tyler. Thanks for taking our questions. Just two from us. On ENTO, can you elaborate more on the challenges in enrolling AGILITY? Was there competition from, for patients from other frontline trials? On the upcoming 0742 update, so looking at factors like exposure, safety and target engagement, what will be the major inputs that you are going to use to select the recommended phase II dose? Yeah. Sure. Okay. With regards to the challenges, I don't think we were really faced with competition per se. We were focused on the NPM1-mutated subset. To our knowledge, there's no other trials enrolling that subset in frontline. I think that the challenges that are faced in these frontline genetically defined patient populations are that, you know, basically there's no sort of pre-existing pool of patients. These patients pop up where they pop up when they're newly diagnosed. In most cases, you have a matter of days to get that patient started on treatment. This is always kind of a, you know, an inherent headwind in these types of trials. With regards to the recommended phase II dose of KB-0742, you know, we're gonna be looking at everything. You know, what we need there is to define a dose that actually achieves the target engagement, the minimum target engagement that we think needs to be achieved, and that maintains a tolerability profile that's consistent with chronic dose. We'll take our next question from Michael Yee with Jefferies. Please go ahead. Hi, Norbert. It's Mike. How are you? I'm good. How are you, Mike? Good. We have a question on CDK9. Obviously, you are in dose escalation. You've been dose escalating for a while. I recall that prior disclosure was you had a good therapeutic window, no major neutropenia, and you had some good biomarker data. Tell me, don't you expect to possibly have some sarcoma patients or other patients that could be addicted? It could be small, but you could have those patients. Don't you think we could see some signals of some efficacy in some way? Thank you. Yeah. Hi, Mike. This is Jorge. As you know, as we've said before, we're still in the dose escalation portion of the trial. We're not specifically enriching for particular types of patients at this point because we're really trying to get to an answer on you know, safety and target engagement first. We'll be opening the expansion cohorts once we announce the recommended phase II dose a little later this year. Okay. Just as a follow-up, yeah, I assume it's a three by three. You know, there should be a good number of patients though at the higher doses. Is that fair? It's not a three by three. It's a continuous reassessment, a Bayesian type dose escalation model. Okay. Thank you. Yep. Once more for your questions, that is star and one. We'll move next to Ted Tenthoff with Piper Sandler. Please go ahead. Great. Thank you for taking my question. I appreciate the focus. I know that's not an easy decision. I'm wondering how partnering fits into the strategy now going forward, particularly with some of the preclinical efforts or even LANRA. Obviously, we'll probably wait for that data readout, but just wanna know how partnering maybe fits into the plan going forward. Thanks. Yeah. Ted, thanks for your question. You know, we are of course working on potential partnerships. We've always been interested in it, and we have a fairly sizable business development effort in that respect. That's all I can say. We haven't, you know, finalized anything yet. Okay. Gotcha. Okay. Thank you. Thank you. This does conclude the Q&A portion of our call. I would now like to turn it back to Dr. Bischofberger for any closing remarks. Well, thank you, operator, and thank you all for joining us this afternoon for our update. We look forward to providing further updates as we advance our clinical programs, but also our research discovery and our business development. We hope you'll continue to follow our progress and have a good remaining of the day. Thank you. This does conclude today's program. Thank you for your participation. You may disconnect at any time, and have a wonderful afternoon.