Good day, and welcome to the MEI fiscal year-end earnings call. My name is Gary, and I'll be the conference facilitator today. All participants will be in a listen-only mode. After today's prepared remarks, there will be an opportunity to ask questions. To ask a question, you may press Star then one on a touch-tone phone. To withdraw your question, please press Star then two. Please note, today's event is being recorded. I would now like to turn the conference over to David Walsey, Senior Vice President of Corporate Affairs at MEI Pharma. Please go ahead, sir. Thank you, Gary. Hello, and thank you for joining the MEI Pharma conference call today. My name is David Walsey, and I'm Senior Vice President of Corporate Affairs for MEI. With me today on the call from MEI are David Urso, President and Chief Executive Officer, Justin File, Chief Financial Officer, and Dr. Richard Ghalie, Chief Medical Officer. Before turning the call over to David for opening remarks, I'd like to remind you that during today's call, we'll be making forward-looking statements. Certain information contained in this communication that are not historical in nature are forward-looking statements within the meaning of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995, including, without limitation, statements regarding the potential safety, efficacy, and regulatory and clinical progress of our product candidates, including the anticipated timing for the initiation of clinical trials and the release of clinical trial data, and our expectations surrounding potential regulatory submissions, approvals, and timing thereof, our business strategy and plans, the sufficiency of our cash, cash equivalents, and short-term investments to fund our operations. You should be aware that our actual results could differ materially from those contained in the forward-looking statements, which are based on management's current expectations and are subject to a number of risks and uncertainties, including, but not limited to, our failure to successfully commercialize our product candidates, the availability or appropriateness of utilizing the FDA's accelerated approval pathway for our product candidates. Final data from our preclinical studies and completed clinical trials may differ materially from reported interim data from ongoing studies and trials, costs and delays in the development and/or FDA approval, or the failure to obtain such approval of our product candidates. Uncertainties or differences in interpretation in the clinical trial results, uncertainty regarding the impact of rising inflation and the increase in interest rates as a result, potential economic downturn, activist investors, our inability to maintain or enter into and the risks resulting from our dependence upon collaboration or contractual arrangements necessary for the development, manufacture, commercialization, marketing, sales, and distribution of any products, competitive factors, our inability to protect our patents or proprietary rights and obtain necessary rights to third-party patents and intellectual property to operate our business, our inability to operate our business without infringing the proprietary rights of others, general economic conditions, the failure of any products to gain market acceptance, our inability to obtain any additional required financing, technological changes, government regulation, changes in industry practice, and one-time events. We do not intend to update any of these factors or to publicly announce the results of any revisions to these forward-looking statements. Under U.S. law, a new drug cannot be marketed until it has been investigated in clinical studies and approved by the FDA as being safe and effective for the intended use. With that, I'll now turn the call over to David Urso. Thank you, David, and thank you all for joining us today. On today's call, I'll make some opening remarks and then turn the call over to Richard Ghalie, our Chief Medical Officer, to review our programs. Justin File, our Chief Financial Officer, will then provide some brief financial comments before moving to Q&A. Before getting started, I want to welcome Jay. He was just appointed our CFO as of August first, so this is his first earnings call at MEI, and we're very happy to have him on the team. With that said, I'll make a brief statement regarding the termination of the merger agreement with Infinity Pharmaceuticals before moving on to review our business. Regarding that proposed transaction, while we believe the potential upside of the Infinity merger was compelling for MEI stockholders, we value the perspective of our stockholders. With the proposed transaction behind us, we're committed to pursuing our two promising clinical-stage programs as a standalone company. Looking ahead over the next few quarters, we see important opportunities in the continued progress of our two clinical-stage oncology programs, voruciclib and ME-344. I would like to use this call to provide an update on the status of these programs and why we're optimistic about their potential. Both of our assets represent novel mechanisms of action. Voruciclib is an oral CDK9 inhibitor, and ME-344 is a mitochondrial inhibitor that inhibits the OXPHOS pathway. We're investigating the potential of these compounds to overcome resistance mechanisms to standard of care therapies. The BCL-2 inhibitor, venetoclax, for voruciclib, and the VEGF inhibitor, bevacizumab, in the case of ME-344. The ongoing advancement of each program is based on non-clinical, and in the case of ME-344, clinical data supporting proof of principle for their respective combinations. We chose these combination approaches based on clear hypotheses to address known resistance mechanisms of each standard of care therapy, clear medical need, and significant commercial opportunities. We're working with some of the leading oncologists in the company, in the country in both of our clinical studies, and we're pleased with their level of engagement and interest in our programs. We expect data readouts from each program in the coming months. With respect to voruciclib, as previously reported, we've seen promising data from our ongoing phase I study. Recall that voruciclib, as a selective CDK9 inhibitor, regulates the transcription of MCL-1, and through that mechanism, holds the potential to address a known venetoclax resistance mechanism. The ongoing Phase I study is evaluating voruciclib as a single agent and in combination with venetoclax, which is standard of care in AML and used in other hematologic malignancies as well. Richard will provide more detail shortly, but in brief, voruciclib alone and in combination with venetoclax, has been generally well-tolerated in the Phase I study to date, with no significant myelosuppression in patients with B-cell malignancies or AML. The results further demonstrate encouraging early clinical activity in heavily pre-treated patients that progressed on venetoclax, who were administered voruciclib monotherapy and at the initial dose level in combination with venetoclax. The planned voruciclib data readout in early 2024 is expected to include data from the dose-ascending cohorts in the Phase I study, evaluating voruciclib plus venetoclax in patients with AML. Here are some of the leading KOLs we're working with. We're pleased with how the study is enrolling. As for ME-344, we're pursuing a novel approach to cancer therapy with a combination of ME-344, an OXPHOS inhibitor that inhibits the production of ATP in mitochondria, and bevacizumab, a VEGF inhibitor, which inhibits the production of ATP through glycolysis, to deprive cancer cells of the energy needed to proliferate. Bevacizumab is an established standard of care in multiple solid tumors, including colorectal cancer. Our ongoing phase Ib study is evaluating metastatic colorectal cancer patients with ME-344 plus bevacizumab. This novel approach to treatment has also generated enthusiasm among our investigators in the ongoing study. In earlier clinical studies, ME-344 was generally well-tolerated at the dose we're currently investigating, and there was evidence of clinical activity as a single agent. We had a first look at the potential for this combination in a 42-patient controlled window of opportunity clinical study in HER2-negative breast cancer patients waiting for mastectomy. Richard will discuss the decrease in proliferation biomarker Ki-67 observed in that study. We expect that the ME-344 data readout planned in the first half of 2024 will include initial safety and efficacy data from the first 20-patient cohort in the Phase Ib study, evaluating ME-344 in combination with bevacizumab in patients with metastatic colorectal cancer. We believe the potential value of both programs is notable, given that the addressable market opportunities for voruciclib in combination with venetoclax and ME-344 in combination with bevacizumab are significant. venetoclax is currently used across AML, CLL, and double- hit DLBCL, and generated approximately $2 billion in 2022 worldwide sales. venetoclax sales are continuing to grow and are expected to generate $3.4 billion by 2028. Avastin and bevacizumab biosimilars are used to treat a variety of cancers, including colorectal cancer and ovarian cancer. 2022 worldwide Avastin and bevacizumab biosimilar sales reached $2 billion in 2022, and are expected to grow to $3.3 billion by 2028. In short, MEI's pipeline is promising and presents substantial opportunity for delivering novel therapeutics for patients and creation and value creation for MEI stockholders. Both voruciclib and ME-344 have the potential, in combination with current standard of care therapies, to overcome known resistance mechanisms and improve patient outcomes. Each program is supported by non-clinical, and in the case of ME-344, clinical data demonstrating antitumor activity and mechanistic proof of concept for the combinations being evaluated. We anticipate reporting data for voruciclib early in calendar 2024, and in the first half of 2024 for ME-344. We look forward to these data readouts and the next steps these data will inform. I'll now turn the call over to Richard Ghalie, our Chief Medical Officer, to provide additional details on our pipeline. Following Richard's remarks, Justin File, our Chief Financial Officer, will provide a brief financial overview before moving to Q&A. Thank you, David, and I'll begin first by discussing voruciclib, a selective oral CDK9 inhibitor drug candidate. The mechanism of action of voruciclib is depicted in this cartoon. Voruciclib blocks the transcription of MCL-1 and MYC at the Pol II level in DNA transcription. In addition, voruciclib blocks the stabilization of the MYC protein, which has a downstream effect on that pathway. In a moment, I will give more detail to the meaning of these two targets. Voruciclib has a favorable PK and PD profile that allows its use orally because it's bioavailable. It is selective to CDK9 compared to other CDK, as shown in the table on the right, where they have more binding affinity and longer residence time for CDK9 compared to the other CDK. In addition, voruciclib had more selectivity to CDKs compared to other kinases. Voruciclib is potent, with an IC50 ranging from 0.2-1.7 micromolar in a variety of cell lines tested. Interestingly, it concentrates in tumors over plasma, which is relevant in patients with solid tumors or lymphoid malignancies with tumors. Now, let's focus on the two targets of interest. The protein MCL-1, it is known that its increase is associated with poor prognosis in patients with acute myeloid leukemia or AML, and in a variety of B-cell malignancies. In addition, upregulation of MCL-1 is an established mechanism of resistance to venetoclax. As venetoclax inhibits BCL-2, it can lead to stabilization of MCL-1, leading to resistance to venetoclax over time. Independently and separately, we also know that MYC is overexpressed in a variety of cancers and tend to be associated with poorer prognosis. In addition, the MYC pathway include KRAS mutation, which will be relevant for the discussion about the potential role of voruciclib. Let's begin first on the aspect of inhibition of MCL-1. As mentioned, it is relevant for AML and B-cell malignancies and as a way to address venetoclax resistance. MEI focused its initial development in hematologic malignancy, beginning with AML. The reason we selected AML is because venetoclax-based therapies are standard of care in approved and elderly patients who are unfit to receive intensive chemotherapy. It is in the NCCN guidelines, it's been established also as the standard of care in a variety of market research, including the one cited on the right. In addition, ongoing studies are being conducted to establish the role of venetoclax as part of the standard of care in chemotherapy-eligible patients. Our hypothesis is voruciclib, combined to venetoclax, has the potential to restore sensitivity to venetoclax and therefore improve durability of response. This slide summarizes the non-clinical data that support the combination of voruciclib and venetoclax in AML. This is a murine xenograft model. In panel A, it shows suppression of MCL-1 level. In panel B, it shows that either agent alone has activity in AML, but the combination is synergistic, with further increase in apoptosis level. And that corresponds to an improvement in survival in the model depicted here in AML. We have similar data with a combination with venetoclax in CLL and diffuse large B-cell lymphoma models. Now, moving to describe the phase I study. This is a typical phase I dose escalation expansion study in patients with relapsed refractory AML and B-cell malignancy in the first stage, which is the monotherapy dose escalation, and in patients with relapsed and refractory AML for the combination with venetoclax stage. As for a phase I study, its endpoints consist of safety, pharmacokinetic. We are also collecting samples for biologic correlate, primarily to look at BH3 profiling and MCL-1 expression, as well as molecular mutation analysis. And we will also collect, of course, activity data. The monotherapy dose escalation component has been completed, with 40 patients enrolled, and we are now currently enrolling in the combination with venetoclax group in patients with AML. As mentioned, this is a two-stage component. First, a dose escalation going from 50 milligram every other day upward, and as of now, we have completed enrollment at the 150 milligram dose level. Once a dose that is confirmed to have, well tolerance as well as evidence of activity, then we will proceed to expansion cohort. Currently, there is one contemplated and additional expansion cohort will be discussed with the FDA. In total, the study will enroll over 100 patients with hematologic malignancies, including approximately 70 patients in the combination with venetoclax. This is a brief summary of the data observed in the monotherapy dose escalation. Preliminary data were presented at the ASH 2021, and additional data and final data were presented at some subsequent scientific meeting. In total, 40 patients were enrolled, all heavily pretreated, with a median of 3 prior therapy, ranging from 1 to up to 8 therapies in one patient. Two dose schedule evaluated, initially daily, continuously in 16 patients, and we have at that time pivoted to evaluate voruciclib on a 14 days on, 14 days off therapy in a 28-day cycle. The reason for this pivot is because we have seen in the daily dosing, two patients pneumonitis that we felt were confounded by patient having developed differentiation syndrome, seen in AML patient receiving targeted therapy, as well as prior allogeneic transplant with graft versus host disease. When we switched to the two weeks on, two weeks off schedule, we're able to dose escalate up to 200 milligram without seeing DLTs. We stopped dose escalation, not because of safety reason, but because we wanted to start pivoting to the combination with venetoclax, our target combination regimen. With the monotherapy, we have seen patient having evidence of anti-tumor activity, including 1 patient with AML, who has a morphologic leukemia-free state achieved, and 5 of 10 patients with AML at the 200 milligram dose who had stable disease. Importantly, we have seen in our correlative laboratory studies done with collaboration at academic centers, a decrease in MCL-1 and MYC, using a single cell RNA sequencing from 3 patients with CLL and 2 patients with AML. So overall, voruciclib as a monotherapy at a dose of up to 200 milligram on a 14 days on, 14 days off schedule, was well tolerated, had no DLT. We did not see drug-related neutropenia. We did not see grade three or higher drug-related toxicity, and no patients was discontinued due to drug-related toxicity. As mentioned, we are now enrolling in the venetoclax combination. Up to now, we have not seen DLTs. The PK analysis of the earlier dose level do not show drug-drug interactions, and we are seeing evidence of clinical activity at the low dose evaluated today, manifested by a reduction in transfusions, improved counts, response observed in some patients, and over 85% of the patients continuing beyond cycle one, the DLT windows. Keep in mind, this is observed in patients who have been heavily pretreated with a median of two prior therapies, including venetoclax. Now, let's turn the focus to voruciclib effect on MYC. As mentioned, MYC is overexpressed in a variety of cancers and tend to be associated with poor prognosis. There is no current treatment approved for MYC-mutated tumors. CDK9 inhibition leads to reduced transcription of MYC and stabilization, thus can have a potential treatment effect. We have clinical data from the initial studies conducted in patients with solid tumors by the prior sponsor. Two studies were conducted, one using a 2 weeks on, 1 week off schedule, and the other one using a daily continuous schedule. Relevant to the discussion today is in the daily continuous schedule study, samples were obtained from 25 patients with a variety of solid tumors and tested on a 10-gene biomarker, with samples obtained at baseline and with each subsequent course of therapy. We have seen a decrease in c-MYC expression in 60% of the patients tested in that study. Here are shown only two illustrative examples of two patients. Circled are the MYC, the gene that we evaluated, showing a decrease in MYC over time with each course of therapy. At MEI, we have further expanded the evaluation of that effect on MYC and KRAS by evaluating a number of cell lines listed here, including colorectal cancer and other tumors, that had variety of KRAS mutation, G12C, but also others. Shown to the panel to the right is a dose-response relationship between voruciclib dose and suppression of tumor growth in three different cell line with different KRAS mutation. Lastly, and of interest, is combination of voruciclib with the KRAS inhibitors, sotorasib. This experiment was conducted in a pancreatic tumor cell model. This is intralesional infusion of one or a combination of drug, and the readout is shown to the panel to the right, where we see two type of analysis. One is the standard pathology with an H&E staining that shows the control arm, either agent alone, and to the bottom right panel, the combination, showing an evidence of cell death, apoptotic cells, and also in the fluorescent staining, an increased number of cells dying. So that is my summary for the voruciclib program. Now I'm turning to the description of ME-344, a mitochondrial inhibitor drug candidate. This is a very interesting and novel mechanism of action, where the inhibition on the mitochondria is a dual effect, one, on OXPHOS, and two, on purine synthesis, reminding that purine synthesis is made at the surface of mitochondrial cells. The relevance of that mechanism is illustrated in the panel to the right, which I will simplify by saying that mitochondria generate ATP, which are essential for producing energy for cells, and that is done through the OXPHOS pathway. Blocking the OXPHOS with ME-344 would lead to a decrease in ATP source of energy, and eventually, by a cascade of events, to potentially cell death. Separately, purine biosynthesis is done, as I said, at the surface of mitochondria, which ME-344 can block... Purines are essential to cell proliferation, and blocking purine biosynthesis could lead to a decrease in cell growth and proliferation. This is a simple panel of over 200 cell lines that were tested for ME-344 activity in vitro. As one can see, ME-344 is potent at the nanomolar level in nearly all cell lines tested, except a few. MEI conducted two phase one studies, one as a single agent dose escalation to determine the safety, efficacy, and PK, and that study led to the determination that a recommended phase two dose for further development is 10 mg/kg. The next study evaluating ME-344 with the chemotherapy topotecan in a couple of types of solid tumors. 48 patients enrolled in the study. Myelosuppression due to topotecan was observed. We had disease stabilization at 49% of the patients. However, MEI decided to pursue the development of ME-344 in a different direction on the basis of biology. However, before I go to that, this is a table summarizing the safety profile of ME-344 as a single agent in the phase I study, pointing to the fact that neuropathy, which was seen only at doses higher than 10 mg/kg, was the dose limiting toxicity. It was not reported at lower doses. Now, let me describe the new strategy that we would like to employ ME-344 in combination with the anti-angiogenic agents, primarily Avastin or bevacizumab. This stands for a simple observation that when Avastin is administered to patient, it blocks the glycolytic energy pathway, leading to effect on cell growth. However, cells, of course, the ATP I mentioned earlier. Therefore, it is plausible that combining ME-344... Sorry, there is an echo. So I'll continue then. Combining ME-344 to block the mitochondrial energy and a VEGF inhibitor like Avastin would now have a possibility of synthetic lethality and therefore improving anti-tumor control. This hypothesis was tested initially in animal model, of which I present two, one, a colorectal cancer model and one, a breast cancer model, using ME-344 in combination with oral VEGF inhibitor, lenvatinib and axitinib. And seen on this slide is a decrease in tumor growth with the combination compared to either agent alone and improved survival in colorectal model. This led to a study by collaborator at the NCI Spain in Madrid, a multicenter study, a proof of concept study evaluating ME-344 and bevacizumab in patients with breast cancer. The reason breast cancer was selected is because that is a window of opportunity for this type of mechanistic studies, where patients between diagnosis and definitive surgery has a period of time where the study could be conducted. It was a randomized control study in 41 patients. Group A received bevacizumab with ME-344, just one cycle, and group B received bevacizumab alone. The readout was a PET scan to look at tumor vascularization and tumor biopsy, looking primarily at the biomarker of tumor proliferation called Ki-67. Results are illustrated on this slide. Group A, again, is the combination of ME-344 and bevacizumab in green. As you can see, looking at all patients enrolled in this study, there was a significant decrease of Ki-67 compared to what observed with bevacizumab alone. Focusing now on the subset of patients in this study who had a tumor normalization, vascular, vascularization normalization by PET, this effect is further enhanced. This led us to the decision now to proceed in a clinical trial with clinical readout, and we selected colorectal cancer as the first study to evaluate the combination because it's an unmet need and Avastin is used in that setting. So this is a phase I/II study in patient-relapsed colorectal cancer after failure of all standard therapy. Primary objective is progression-free survival. Secondary objective are survival and safety. The study is conducted in separate cohort, beginning with cohort 1, and using the same dose and schedule that was used in the breast cancer study. 20 patient will be enrolled, and the readout will be that, four months after the patients, last patient is enrolled. Considered as a positive outcome is a PFS at four months of 20% or higher. That will lead to evaluation of a second cohort and subsequent cohort to be discussed with the FDA. With that, I conclude the clinical update and will turn it to Justin File to talk about the financial overview. Thank you, Richard. As reported earlier today, as of June 30, 2023, MEI had $100.7 million in cash, cash equivalents, and short-term investments, with no outstanding debt. ... We believe our cash balance is sufficient to fund operations for at least the next 12 months and through the reporting of clinical data readouts from the ongoing and planned voruciclib and ME-344 phase I and phase Ib clinical programs, respectively. I look forward to any questions on the broader set of financial information reported earlier today during the Q&A portion of the call. I'll turn that back to David. Thanks, Jay. As you've heard today, I believe we have two exciting programs with expected data readouts, beginning with voruciclib early in calendar 2024 and in the first half of 2024 for ME-344. With the promising pipeline and capital to support our near-term development plans, we're excited about the potential to create stockholder value and deliver improved therapeutic options for patients. Before we turn to Q&A, I'd like to briefly acknowledge that two of our stockholders, Anson and Cable Car, have initiated a consent solicitation process and separately submitted three director candidates to stand for election at the company's annual stockholder meeting this year. We've had several conversations with Anson and Cable Car as part of ongoing efforts to resolve the situation and remain open to further discussions. We will appropriately address the actions of these stockholders in due course. For the purposes of this earnings call, we're here to discuss our programs and upcoming milestones. We ask that you please keep your questions to these topics. I'll now ask the operator to provide the instructions for asking questions and then open the call for Q&A. We will now begin the question and answer session. To ask a question, you may press star then one on your telephone keypad. If you are using a speakerphone, please pick up your handset before pressing the keys. To withdraw your question, please press star then two. At this time, we will pause momentarily to assemble our roster. Our first question is from Yale Jen with Laidlaw and Company. Please go ahead. Good afternoon, and thanks for taking the questions as well as providing a clear view of what's happening currently. Maybe I start with a housekeeping question, that you got about $100 million cash, and in the press release, you suggested that you have on 12 months or maybe a little bit longer runway. Given that you are still in phase I/II study, should we anticipate it to be a more conservative estimate, or there's additional thoughts behind that in terms of the runway? I have some follow-up as well. Thanks, Yale. This is David. I would say, it's, you know, conservative in the sense that, you know, we've got all the capital we need to do the phase one programs, as they're currently planned and as we, you know, have some ideas about augmenting them. But going into phase two is really data-driven, and so it's really impossible to speculate about the next phase of development for these programs. So I think it's an appropriate guidance in that respect. Okay, great- Yeah, like we said, it's at least, you know, 12 months and covering the current work that we're doing. So you could characterize it as being, I guess, somewhat conservative, but we, you know, we did say at least 12 months. Sure. Maybe just in terms of again the housekeeping one, which is the top line, I understand the deal, the prior deals are completed. So should we anticipate still some top line coming just because of the amortization, or we should anticipate that to be stopped, at least in the near term? I'm sorry, could you repeat? We were having a little bit of trouble following the question. Could you please repeat it? Sure. In terms of the top-line revenue that you have- Uh. until this quarter, my question is, would that will continue for the subsequent fiscal year, or simply these revenue numbers is just the amortization of the prior revenue received? Yeah, I mean, all of the revenue we're recognizing is all KKC driven from our collaboration with them, so it's not anticipated to continue into the future. Okay, maybe the last question here is in the clinical side, over voruciclib, phase I data readout. What should we anticipate specifically in terms of sort of type of data? Would that, other than the safety, would that be PK, and would that be any biomarker or other aspect? Could you provide a little color on that? Yeah, this is Richard. Yes, it will be a combination of safety data, primarily, since this is the endpoint, the primary endpoint in phase one study. Perhaps a recommended phase two dose. There will be also PK data and, biomarker analysis. All of them will be available. What specific would you already have some biomarker in mind? If so, what that might be? ... Right. So I've mentioned it when I present the monotherapy dose escalation. The biomarker that we are evaluating are BH3 profiling, particularly MCL-1 expression, where I look at multiple molecular biomarkers such as Myc. And we will be looking at potentially other biomarkers that are relevant directly to the effect of CDK9 on the target. Okay. Okay, great. Yeah, I'll get back to the queue and, thanks for the colors. I mean, I guess we could, we could also say that just from a clinical perspective, for the cohort one from ME-344, we will be looking at PFS, and for the voruciclib expansion cohort that's in our, in our protocol right now, we'll be looking at LR. So those are just standard clinical endpoints for the two respective diseases. Actually, let me, if I can, maybe just follow up a little on that. You said that 20% or higher of the threshold for moving forward for the ME-344 study, Cohort 1. What sort of other factors determine that the 20% was the number, sort of cut off? Well, you know, that was a requirement or a gate that we, you know, reached in collaboration with the clinicians. But we really need to dig into exactly what the patient population is before we can, you know, really know what the meaning of that threshold is. It obviously depends on exactly the experience that each patient- Maybe again, one more question here, which is that if compared to what your prior study in the breast cancer or non-small cell lung, was there any comparable number to that PFS? Yeah. Yeah, this is Richard answering. So it's, it's really two very different approach to therapy here. In the phase one study in combination with chemotherapy, we were really looking at cytotoxic effect and looking at response as the primary endpoint. Here, we're really looking at a different approach, where there is synthetic lethality by combining, you know, VEGF inhibitor with a mitochondrial inhibitor. And therefore, the response rate is less relevant. More relevant would be the time to progression. Again, it's a very different disease, so it will be hard to compare breast cancer or rather, I'm sorry, colorectal cancer on one hand with a prior study, which was done in ovarian cancer and small cell lung cancer. Okay, great. That's very helpful and thanks a lot. I I appreciate it. Mr. Willey, your line is open on our end, perhaps you have it muted on yours? No. Thanks for taking the questions. So maybe just one on, on voruciclib, one on, ME-344, and then just a, a modeling or financial question. So on voruciclib, what's your expectations just around venetoclax retreatment post-progression in the context of AML? And I guess I ask the question because there's not a lot of data that's out there in the public domain. Yeah. There's some retreatment experience in CLL that's shown that you can resensitize patients to venetoclax with venetoclax alone. And I'm just kind of curious, as you think about the data you're going to be generating, what's good, what's interesting, what is your working assumption around venetoclax retreatment response rates? Yeah, I mean, in the initial experience with venetoclax in the relapsed refractory AML population was pretty limited. I think it was like 19 patients, and they saw about a 20% response. But that was in a, as you know, that was in a venetoclax-naive population. Now everybody's getting venetoclax. But I think when we talk to our advisors, it's still around the same threshold as what they would be excited by. Again, you know, I think it's a big deal if you can bring back response to a patient that progressed on venetoclax, and, yeah, a 20%-30% response rate in that, in this relapsed population, I think would get everybody excited. Okay. And then, on 344, I think per ClinicalTrials.gov, it doesn't list any of the approved salvage regimens as allowable prior therapy. So are we to assume that these patients are going to be Lonsurf and regorafenib naive? This is Richard. So the... You're right, this is not listed on clinical trial, but the protocol, it really about it was what the FDA wanted. So patients should have received and progressed on or did not tolerate standard chemotherapy, which is, you know, platinum-based, nitrogen-based, 5-FU. In addition, if they have a mutation that is addressable, like BRAF, they had to receive it. If they are eligible for checkpoint inhibitor, they should have received it or not tolerated, and only then they could enroll in the study. So we may have patients who have received regorafenib and/or Lonsurf or not. So it's not a requirement, but we anticipate that some patients, many in fact, would have received them in this study. Then maybe just to follow up on the 20% four-month PFS rate that's required to gate the enrollment of stage 2. I guess when you look at, I think it was the SUNLIGHT study that was just published, I think they saw a six-month PFS with Avastin Lonsurf of north of 40%, and then I think with Lonsurf alone, close to 20%. So I'm just trying to, I guess, maybe think about the threshold that you're establishing here in the context of some of the historical data that's out there. Right. You're, you're absolutely right about this, report, the phase 3 study, in fact, that was reported at ASCO GI, came in when we were just launching this study. So just let me explain where the 20% threshold came, but then also what it means for us going forward. The 20% threshold was driven by the monotherapy kinase inhibitor, so the regorafenib phase 3 study. And the, our advisors, which is, as you may know, is the Academic GI Cancer Consortium, who's running the trial, said that they would like to see something upward of maybe double of what was seen with regorafenib alone in this patient population. So that's where the 20% came. This is not our ceiling, this is the, the floor. We need to see at least something better than get to, to go to phase 2, to the cohort 2. A separate question that you're asking is, you know, if we just get 20% only, is this enough? Would we get excited knowing that Lonsurf has a 40% PFS at months four to six? And you're right. I think the answer to that is gonna be, it depends who we enroll. If we enroll patient with failed Lonsurf or Lonsurf or another TKI, then the what would get us excited would be very different than if we have patients who really failed prior chemo immunotherapy, I'm sorry, prior chemotherapy with bev, and then they come on that study. So I'm not trying to dodge the answer. I'm trying to say it will be determined by the kind of patient we enroll, not unlike what David mentioned about voruciclib. If we see response in voruciclib, patient progression voruciclib, there will be, you know, the excitement level will be very different if we see response on, you know, patient who respond to other drugs and then progressed, then went back on the, on the combination responded. So it's primarily driven by the patients we enroll, as is often the case in phase one studies. You know, when we enroll, we look at the data, we analyze, and we make conclusion based on what we see. Okay, that's helpful. And then, just lastly, I guess when you look at the 4Q R&D number implied from what you reported year-end, it looks to be demonstrably down sequentially, I think sub-$3 million. How should we think about that number just going forward? And is that somehow impacted by, the Kyowa transaction, some true up there, or is that, is that just a, a true number per the quarterly report and that's just gonna accelerate as you guys, do more clinical development here? Thanks. Yeah, it's Jay. I'll take that. So yeah, you're correct in your assessment. We're not giving specific guidance as to R&D into the next fiscal year, but I will tell you, you know, of that, about $52.5 million of R&D, about $26 million of that was specifically related to zandelisib. We do know that that trial continues to wind down. We do expect that to run out by about October timeframe and probably not incur expenses any more than $1 million, less than that, most likely. The Q4 activity is just seeing the, you know, the continued wind down of the zandelisib trial in Q4. And like I said, we expect that to go ahead and wind down. Then, in addition to some of the other cost reductions that we've made throughout the second half of the year, overall R&D, yeah, you're right, it'll be down significantly from the prior year. Okay. Thanks for taking the questions. Sure. Thank you. This concludes our question and answer session. I would like to turn the conference back over to David Urso for any closing remarks. Thank you for joining the call today, and we appreciate your participation. The conference is now concluded. Thank you for attending today's conference presentation. You may now disconnect.