Good afternoon. My name is Josh and I will be your conference operator today. I would like to welcome everyone to the Aptose Biosciences' Conference Call for the First Quarter ended March 31st, 2024. At this time, all participants are in a listen only mode. After the speakers' remarks, there will be a question-and-answer session. [Operator Instructions] Thank you. As a reminder, this conference call may be recorded. I would like to introduce Ms. Susan Pietropaolo. Please go ahead.

Thank you, Josh. Good afternoon and welcome to the Aptose Biosciences conference call to discuss financial and operational results for the first quarter ended March 31st, 2024. Earlier today, Aptose issued a press release relating to these financial results. The news release as well as related SEC filings are accessible at Aptose's website. Joining me on today's call are Dr. William Rice, Chairman, President and CEO; Dr. Rafael Bejar, Senior Vice President and Chief Medical Officer; and Mr. Fletcher Payne, Senior Vice President, Chief Financial Officer and Chief Business Officer. Before we proceed, I would like to remind everyone that certain statements made during this call will include forward-looking statements within the meaning of U.S. and Canadian Securities laws. Forward-looking statements reflect Aptose's current expectations regarding future events. They are not guarantees of performance and it is possible that actual results and performance could differ materially these stated expectations. They involve known and unknown risks, uncertainties, and assumptions that may cause actual results, performance, and achievement to differ materially from those expressed. To learn more about these risks and uncertainties, please read the risk factors set forth in Aptose's most recent quarterly report on Form 10-Q and SEC and SEDAR filings. All forward-looking statements made during this call speak only as of the date they are made. Aptose undertakes no obligation to revise or update the statements to reflect events or circumstances after the date of this call, except as required by law. We encourage you to refer to today's press release and the 10-Q for additional information and disclosures regarding today's announcement. I will now turn the call over to Dr. Rice.

Thank you, Susan. I want to welcome everyone to our call for the first quarter ended March 31st, 2024. Our last call was only about a month and a half ago. So, we've decided to switch up our conference call format today to include a selection of slides that can provide you with a better understanding of our clinical strategy to focus the development of tuspetinib as a triple drug combination or triplet frontline therapy to treat newly diagnosed AML patients. Tuspetinib or TUS, as we refer to it, is Aptose's lead clinical asset. TUS is being combined with venetoclax or VEN and a hypomethylating agent for HMA. This forms the TUS-VEN-HMA triplet drug combination that is being developed for frontline therapy to treat newly diagnosed AML patients. VEN-HMA is currently the standard-of-care therapy for newly diagnosed AML patients and TUS is being bolted on to VEN-HMA standard-of-care to boost the activity and to do so safely. And importantly, we expect to report clinical data with the TUS-VEN-HMA triplet and the newly diagnosed AML patients during the second half of this year. We all know AML is a highly aggressive cancer of the blood and bone marrow and that unmet need still exists for the relapsed or refractory patient population and for the newly diagnosed population. I'll remind you, when we began clinical trials with TUS as a single agent and with the TUS-VEN doublet in the relapsed or refractory AML population, as is the case with many other new cancer drugs. Yet we've always planned to move tuspetinib into frontline therapy for newly diagnosed AML patients. Our trials with TUS single agent and with TUS-VEN doublet and relapsed or refractory patients are now completed. The single agent and the doublet demonstrated excellent safety profiles and distinguished tuspetinib from other agents. Just as important, we observed responses in patients with wild-type FLT3, patients with mutated FLT3; patients with mutated TP53 and RAS genes, patients who failed prior therapies with venetoclax/hypomethylating agents, FLT3 inhibitors, and chemotherapy; and those who had failed prior stem cell transplants, illustrating tuspetinib achieved responses across a remarkable diversity of AML populations. During Q1 of this year, we presented our clinical findings to the FDA as part of a protocol amendment to allow for evaluation of the TUS-VEN-HMA triple drug combination for the frontline therapy of newly diagnosed AML patients. That protocol for the triplet and frontline therapy is now open and our clinical team is engaging clinical sites and preparing to initiate dosing of patients on the study. I want to explain why we've accelerated our strategy to focus on the frontline triplet in newly diagnosed AML patients. As we began to share safety and efficacy data from the TUS and TUS-VEN trials in relapsed or refractory AML patients with our KOLs in pharma, it became clear that the greatest unmet medical need and greatest opportunity in AML is the development of a superior frontline therapy for the treatment of newly diagnosed AML patients. It also became clear that the unique safety and broad efficacy properties of tuspetinib fit the desired profile of a third agent to add to the VEN plus HMA standard-of-care backbone and assemble a superior triplet for the frontline therapy. Before we go further, let's first recognize that progress has been made with the introduction of venetoclax to the VEN-HMA doublet and this was the major advancement in the treatment of AML. However, the complete remission response rates are still too low and survival is still too short and frontline therapy. And we all want to see a more effective frontline therapy. But there was another important factor, leading our KOLs, pharma, and our internal team to focus on frontline therapy. While venetoclax treatment has resulted in more responses in frontline therapy, there is a double-edged sword with venetoclax. It turns out that relapsed or refractory patients who have failed prior venetoclax treatment, respond poorly to salvage therapies and even if they achieve a response, the survival timeline is grim on the order of a few months. This tells us we need a new frontline strategy that may be able to help avoid rapid failure of venetoclax-based therapies. So, what we need is an exceptional third agent that can boost response rates of VEN plus HMA, prolong the duration of responses and survival, improve quality of life, treat a broad spectrum of AML genetic subpopulations, and minimize the likelihood of patients becoming resistant to venetoclax. This is a tall order and other potential third agents in development may only address specific genetic subpopulations, while other agents bring their own complicating toxicities to the triplet. This has opened the door for tuspetinib to address the greatest single opportunity in AML, which is the development of a superior frontline therapy to treat newly diagnosed AML. Tuspetinib is a natural third agent for addition to venetoclax and HMAs. Tuspetinib has an excellent safety profile as a single agent and in combination with venetoclax and HMA and with other drugs. Tuspetinib enhances antileukemic activity when combined with venetoclax and HMAs. Tuspetinib has a very broad scope of activity across genetic subgroups of AML, even those who have high-risk mutations in the TP53 and RAS genes. And tuspetinib targets known venetoclax resistance mechanisms and may help minimize the rapid onset of drug resistance. Because of this unique safety, activity and mechanistic profile of tuspetinib, we're developing the TUS-VEN-HMA triplet to become a new standard-of-care therapy to address the safety, scope, and survival needs of newly diagnosed AML patients. I now want to present just one more slide because it's important to understand how tuspetinib works and how TUS plus VEN show mechanistic complementarity and may minimize drug resistance. And I'll illustrate these mechanistic interactions, the cartoon on the right side of the slide. As you can see, AML cells upregulate key oxygenic signal transduction pathways to drive excessive proliferation and cell division. At the same time, AML sales avoid cell death by modifying the exploration of anti-apoptotic proteins such as MCL1 and BCL2. Often in an AML, the BCL2 protein is up regulated. Venetoclax is administered to patients to target the BCL2 and enable the AML cells to die more readily. However, venetoclax alone has minimal efficacy in AML. That's why venetoclax is combined with the hypomethylating agents to achieve clinical remissions. Unfortunately, over time, the cells can modify a number of key pathways to generate resistance to venetoclax. Multiple mutations can occur simultaneously in the FLT3 and KIT receptor kinases and the JAK kinases of the JAK-STAT pathway and in the RAS MAP kinase pathway, all leading to upregulation of the MCL1 anti-apoptotic protein. Collectively, these alterations allow AML sales to drive cell division and avoid to cell death even in the presence of venetoclax. Now, let's look at the effects of tuspetinib. Tuspetinib directly inhibits the FLT3 kinase, the mutant form of KIT, the SYK and JAK Kinases and the JAK-STAT pathway, and the RSK2 kinases downstream in the RAS MAP kinase pathway and indirectly reduces MCL-1 expression. It's this mechanistic complementary that can make tuspetinib and venetoclax such a powerful combination tool against AML. And Dr. Bejar will describe how we plan to use these agents together more effectively to treat payment. With that, I'll now turn it over to Dr. Bejar, Aptose's Chief Medical Officer and Resident, KOL, for his insights into the AML patient journey and to take you through our clinical plan that is already well in place. Raf?

Thanks Bill. So, to follow-on what you just said, I'd like to describe a little bit about the context in which we're developing tuspetinib, namely to the AML landscape today and how it is the patients are treated. So, a newly diagnosed AML patient would likely receive some form of therapy. On rare occasions, patients who have too many comorbidities may elect for palliative care, but the majority of patients received some sort of therapy in first line. The younger individuals and generally, patients younger than age 70 will receive a form of intensive chemotherapy if they are fit enough to tolerate this kind of therapy. This has the potential for curing a subset of patients and has a very high complete remission rate. However, the average age of patients with AML is about 68, meaning that the majority of patients may not be great candidates for high-intensity chemotherapy, instead, would receive lower intensity therapy in the frontline consisting of venetoclax plus hypomethylating agent, which has become the standard-of-care in the past few years. This had a complete remission rate of about 37% and a composite complete remission rate that includes a complete count recovery of about 66%, mainly two-thirds of patients achieving some form of complete remission and median overall survival to the therapy in the frontline setting is about 15 months. Now, what can happen to individuals after they achieve complete remission? Ideally, a candidate who might be able to receive an allogeneic stem cell transplant would do so is that it's potentially curative therapy, and they may receive maintenance therapy after that kind of treatment. Alternatively, a patient who achieved complete remission is not a candidate for stem cell transplant may receive maintenance therapy alone or no therapy as they are hopefully in a deep remission. However, patients may be primarily refractory to initial treatment, meaning they never achieved a complete remission and are immediately considered therapeutically refractory or they may achieve a remission and even undergo transplant in some cases and yet still relapse and have what we can consider therapeutic failure. And outcomes in patients who have refractory or relapsed disease is quite dismal. And therefore, it is really important to try to prevent this outcome. In other words, try to improve the likelihood that patients remain in remission for a longer with frontline therapy because the best way to treat relapsed/refractory disease is to make sure that it doesn't happen in the first place. So, why do I say that we still can improve upon HMA-VEN as it has become the new standard for the treatment of older individuals unfit for intensive induction chemotherapy. From the VIALE-A trial that led to the approval of HMA plus venetoclax as the frontline standard for older unfit individuals, we can break down the benefit in different subpopulations. Those individuals that have a more favorable genetic profile, namely they did not have mutations in TP53, FLT3, or NRAS or KRAS, they had the greatest benefit from this kind of therapy. In fact, their median overall survival was over two years. However, there were some patients that do have some high-risk mutations, they might be in the intermediate benefit category, namely those individuals with FLT3-ITD mutations or mutations downstream of FLT3-ITD in KRAS or NRAS and their benefit wasn't even half as good. Their median overall survival was only about 12 months. And then there was about a quarter of patients who have a TP53 mutation. Those patients have the worst outcomes. The median overall survival was less than six months and apparently, had a little benefit with the addition of venetoclax over an HMA alone. So, there is substantial room for improvement, particularly in these patients that have these proliferative signaling mutations in FLT3 and NRAS and KRAS to improve upon the outcomes that they see with an HMA or venetoclax. And that is where I think we have a prime opportunity for tuspetinib. So, let's talk about that. What are the opportunities for the drug? We know that AML is a disease that has about 21,000 cases annually in the U.S. and with more than half of the patients succumbing to the disorder each year. As I mentioned, the median age is 68, meaning that the majority of patients are close to that age where induction chemotherapy is not a common option and survival is still relatively poor, especially for those older individuals where five-year overall survival rates are estimated to be less than 10%. Now, frontline therapies have made improvements in the last few years, as Dr. Rice mentioned, I mentioned that the combination of VEN-HMA have about a two-thirds overall response rate for CR/CRI and a 15-month median overall survival, but there are a subset of patients that have inferior outcomes. We have seen several studies that are combining three agents, venetoclax, HMA, and a novel agent to try to improve outcomes in those frontline patients and we have seen successes there. In particular, trials with kinase inhibitors have shown composite complete remission rates of 80% to 90% in the frontline setting, which is very promising. Unfortunately, they do have their own liabilities. In part, they tend to be more toxic when combined in that triplet agent, requiring dose reductions not just of the third novel agent, but of the standard-of-care backbone of a hypomethylating agent and venetoclax, meaning that the combined therapy is fall short of the standard-of-care for you to give a placebo instead of the third agent. And of course, many of these trials have used targeted agents, meaning that they are not applicable to the broader range of AML patients only a subset defined by either genetic or other biomarkers. So, there is an urgent need for a safe and more effective first-line triplet to improve outcomes for AML patients of all genetic subtypes. So, how does that fit into the model we drive before? Tuspetinib as an ideal third agent with a very favorable safety profile could be combined both with intensive chemotherapy in the frontline setting as other kinase inhibitors have done and have been approved or it could be combined as a third agent with venetoclax in HMA in the low-intensity treatment option. This, I think, provides a broad frontline opportunity for tuspetinib and we have chosen as our first steps in the frontline setting to focus on those low-intensity therapy patients where there are no other drugs currently approved as an applicable triplet for this patient population. Doing so allows us to potentially increase the complete remission rates and survival of patients with FLT3 mutations in such a way that doesn't require a reduction of the standard-of-care. This will permit, for example, a randomized clinical study placebo-controlled that would give standard-of-care to both arms without having to dose reduce them in the treatment arm. As far as we are aware, this is the only agent being developed in combination with VEN-HMA that includes FLT3 wild type patients or generally patients without a mutational biomarker, which represents the majority of AML patients, of course. And it's the only agent that broadly includes patients with TP53, NRAS, and KRAS mutations in this frontline triplet paradigm. We hope that based on the safety profile to-date that the tuspetinib-venetoclax-HMA combination will be a safer therapy for unfit patients with other triplets that might bring additional toxicities to the table. So, having expressed the landscape of AML and the rationale for a third agent, I want to talk about why tuspetinib is an ideal for agent. As we mentioned, drugs like gilteritinib have been combined with venetoclax and HMA and they've boosted the complete remission rate substantially in the flip mutant population. So, the proof-of-principle is there that this class of drug can make important advances. But we have seen the limitations that I mentioned that required the dose reductions. Now tuspetinib, I think, has an ideal profile as a third agent that might make it superior to these other agents in that frontline setting, and we've learned this from the extensive clinical data we've generated to-date with the drug. We've done extensive testing, both with tuspetinib as a monotherapy and with tuspetinib in combination with venetoclax that tells us that tuspetinib does not have several of the side effects that could impair its further clinical development, including no QTC prolongation related to drug, differentiation syndrome, evidence of muscle damage, or even prolonged myelosuppression in patients who achieved remission where patients in remission continue to take the drug without interruption and maintain their blood counts. By combining it with venetoclax in the relapsed refractory setting in a large number of patients, we now understand that there aren't significant drug interactions that would require dramatic dose changes of either agent or see developing them at their established doses. And importantly, we have favorable comparisons in direct, of course, with other agents out there. We believe that we can see -- we have demonstrated we can see responses in patients with a prior-FLT3 inhibitors that we don't need to inhibit the pathway as substantially as other agents do, perhaps because of the multi-kinase activity of the drug and that we have seen responses in the large proportion of FLT3 unmutated patients, which really differentiates tuspetinib from other agents like gilteritinib. Importantly, we have that superior safety profile, where we are targeting the VEN-resistance mechanisms that may potentially help prevent VEN resistance or potentially even re-sensitize them based on preclinical studies and by suppressing more oncogenic pathways, may be able to alleviate other potential mechanisms of resistance from arising. Therefore, we believe there is a strong rationale for combining tuspetinib with venetoclax in the frontline setting, particularly where patients are like VEN-naive to all agents. So, what have we done to get there? We've completed the single agent dose exploration where we treated a large number of patients that I'll show you, we've demonstrated the activity of the drug as a single agent in select populations both with and without FLT3 mutations, and we've demonstrated a superior safety profile of the drug in that context. In the doublet study is learned about the safety of tuspetinib plus venetoclax, how it could safely be given without substantial dose modification, and we've characterized the CPK of both agents. This has now put us in a position to submit a triplet protocol to the FDA and where we've also achieved orphan drug designation and fast-track status for patients with FLT3 mutations in this drug. So, the triplet pilot study has already been implemented and clinical sites are now being prepared to enroll our first patients later this year and we hope to select the optimal dose of tuspetinib that will allow us to maintain the standard-of-care dosing of the other agents, which would then enable a randomized placebo-controlled registrational study. We will learn about how best to give these drug combinations safely and mitigate myelosuppression and we'll characterize the activity in those difficult to treat or less likely to benefit subgroups of patients that have TP53 mutations, NRAS-KRAS mutations, as well as several kinds of FLT3 mutations. We'll further characterize CPK and establish the safety and the efficacy profile and finally, look at what impact we might be having on overall survival before we take our next steps. I want to spend a little bit of time just sharing how we are actually going to be giving these three drugs together, and how this compares to other agent mixes that are out there. For the pilot study, our first triplet in the frontline setting, we're proposing to treat about 20 to 36 patients total. These are patients that are going to be older, ineligible for induction chemotherapy, either because of age over 75 or because of comorbidities that would prevent that kind of more intensive therapy or shoot for 50% of the patients having a FLT3 mutation, so we have an understanding about activity both in the FLT3 mutant and in the FLT3 wild-type group, and we'll look at all those other factors that I just described earlier. The way we're going to give the drugs together is by giving VEN and ASA together as a standard-of-care doublet with the addition of daily tuspetinib, as shown in the top graph here. You can see that at day 18 will perform a bone marrow biopsy and if patients have achieved remission, we will hold venetoclax starting on day 22, and this is consistent with the venetoclax label, that suggests that you begin for 21 to 28 days per cycle. We then will allow patients to recover the counts and monitor how long it takes to do so, making adjustments along the way, if necessary. Of course, if a patient has not achieved a remission, then they would continue to take the venetoclax along with the tuspetinib through day 28, when a second bone marrow biopsy will be performed to see if they achieved a remission. And if they have, then allow additional time for the blood count recovery to occur before they move on to their second cycle. The dosing in the second cycle will be adjusted based on the patient's experience with the first. Patients who have no significant myelosuppression would go on to receive the same type of cycle as a second cycle. Those that do will have adjustments to their drugs made according to the VEN-ASA label. So, now let's talk about milestones and when we are likely to have data. So, coming up very shortly will be the EHA Meeting in Madrid. There, we will present the summary of our single agent and doublet data, really providing an update to what we presented at ASH earlier along these lines in our oral presentation given by Dr. Naval Daver. Shortly after that meeting, we expect to have our first patient enrollment in our frontline triplet study. This will begin the treatment in this frontline patient population if continued approval. And hopefully, the presentation of several patients' worth of data at the Annual Society for Hematology Meeting here in San Diego at the end of -- near the end of Q4. The trial will continue, of course, and we hope to have a more mature summary at next year's EHA Meeting in 2025 as we meet with the FDA and prepare for the regulatory steps with multiple milestones for adding additional data along the way. So, I'll briefly go into some of the frontline -- some of that monotherapy data and doublet data that gave us the understanding about how to proceed in the frontline. So, to summarize, tuspetinib a single agent has now been given to over 91 patients as a monotherapy and it has had a very clean safety profile with, again, no drug-related myelosuppression in patients who achieved remission, QTC prolongation, or CPK elevation that would be evidence of muscle damage, and in fact, in the single agent, no drug-related discontinuations or deaths. Here, you can see the percentage of patients with adverse events related to tuspetinib and the most frequent were relatively mild nausea and fatigue with very few Grade 3 or larger related adverse events. Similar profile occurs when we combined tuspetinib with venetoclax in the doublet with no new or unexpected safety signals arising and very similar rates of adverse events, higher rates of neutropenia, and other myelosuppressive markers as would be expected with the addition of venetoclax is very much in line with what we would expect for a venetoclax-containing regimens, in fact, lower rates of febrile neutropenia than expected. And here is the evidence of that single agent activity. This graph here shows evidence of bone marrow blast reductions in patients treated with tuspetinib as a single agent. You can see that more than half of the patients achieved some degree of bone marrow blast reduction. And you can see that this occurred in a variety of different dose levels are shown by the different colors. The other thing I would point out is that patients that had a prior-FLT3 inhibitor are marked with a red triangle. And you can see that patients with prior-FLT3 inhibitors were just as likely, if not more likely, to show a bone marrow blast reduction. However, patients with prior venetoclax, shown by the black triangles, are less represented in the far right of the graph, consistent with our knowledge that VEN-resistant patients are less likely to respond to practically any other therapy as a monotherapy. For that reason, we performed the doublet study of patients with relapsed/refractory disease, receiving tuspetinib and venetoclax and again saw blast reductions in more than half of the patients. And in contrast to the figure on the left, we now see many more of those black triangles on the far right of the graph, showing that even VEN-pretreated patients can have significant blast reductions when treated with the combination of venetoclax and tuspetinib in the relapsed/refractory setting. And once more, multiple red triangles in the right indicating that patients with prior-FLT3 inhibitor are still more likely to respond than patients who don't likely because of their prior-FLT3 mutation status. So, now I'll pass on -- you talk -- to Fletcher Payne, we'll talk more about the investment thesis and some of the near-term milestones for the drug. Fletcher?

Thanks Raf. Good afternoon, all. There are three key points to the TUS investment thesis. First, there's a very high unmet medical need in frontline AML has been discussed before to increase survival across all genetic subtypes. Two, the KOL support TUS as the ideal third agent for triplet study in the frontline patients. Three, TUS is emerging as an ideal agent to combine with VEN-HMA. This is due to the safety profile, the broad activity across FLT3 mutated and FLT3 wild-type patients as well as activity against difficult-to-treat mutated TP53 and the RAS gene subtypes. The design of the TRIPLE study and the data readout lineup well to generate several near-term value-creating milestones. The first milestone will be at EHA in June 2024, where we will report single agent and double agent activity, which supports our contention to move into the frontline in the triplet study. The second milestone will be in the summer of 2024, we will start dosing newly diagnosed patients in our triplet study. The third milestone at ASH 2024, we will report complete responses, MRD negativity, and safety data from the triplet study. During the first half of 2025, we expect a complete enrollment of the study. The fourth milestone will be at EHA in the summer of 2025, where we will report data readout from the triplet study. So, as you can see, the triplet study provides for a number of value-creating inflection points over the coming year. Before I cover the first quarter financial highlights, I would like to start by saying that being on our comments on this call. Additional information may be found in today's press release and the 10-Q filed with the SEC. During the first quarter of 2024, we continued our disciplined financial management of operations, we reduced spending on several fronts, and prioritize our investments in our clinical programs. As always, we continue to evaluate ways to reduce operating expenses. The total outstanding share count as of today, May 14th, is 16,309,393 shares. Based on current operations, the company expects the cash on hand plus our ATM will provide sufficient resources to fund planned operations, including research and development activities through August of 2024. Last quarter, we informed you that a 2024 deficiency letter from NASDAQ regarding the private placement with Hanmi was announced, which was announced in January. Aptose has submitted a plan to NASDAQ to regain compliance. On April 25 of this year, the company received a letter from NASDAQ Listing Qualifications Department notifying the company had regained compliance with the NASDAQ listing rules, 5635(d) and determines if the matter is now closed. Under the company's plan to regain compliance on April 26, 2024, the company announced that it amended the warrant agreement with Hanmi to prohibit the exercise of Hanmi warrants in excess of the NASDAQ 19.99% limitation and less shareholder approval is first obtained. On April 2, 2024, we received a second notification from NASDAQ stating that the company was not in compliance with the NASDAQ Listing Rules because our stockholders' equity as of December 31, 2023 was below the minimum $2.5 million. We intend to submit a compliance plan on or before May 17, 2024, monitor our stockholders' equity, and if appropriate, consider further available options to evidence compliance with the stockholder equity requirement. I would like to direct you to review the company's risk factors and discussions regarding the NASDAQ latter and the going concern footnote in our 10-Q and our 10-K filings. Now, let's review the first quarter financials. We ended the first quarter of 2024 with approximately $9.3 million in cash, cash equivalents, investments, approximately equal to December 31, 2023. The $11.8 million in net financing proceeds in January 2024 was offset by $11.8 million used to fund our operations for the quarter, including our APTIVATE clinical study for tuspetinib. As seen in the income statement, we had no revenues during 2024 or in the first quarter of 2024. During the first quarter of 2024, the net loss was approximately $9.6 million, translating into $0.73 loss per share compared to $13.7 million loss or $2.22 loss per share from the first quarter of 2023. As of May 14th, 2024, Aptose had 16,309,393 common shares outstanding. All references to losses per share and shares outstanding had been presented to reflect the 15:1 reverse split completed on June 6th, 2023. Research and development expenses were approximately $6.4 million for the quarter ended March 31, 2024 compared to $8.8 million for the first quarter of 2023. Program costs for tuspetinib were $3.9 million for the first quarter of 2024 compared to $4.8 million for the first quarter of 2023. Lower program costs for tuspetinib in the current period represents the completion of patient enrollment, window test, then doublet program, and reduced manufacturing costs. Program costs for luxeptinib were $208,000 for the first quarter and decreased by approximately $1.1 million compared to $1.3 million for the first quarter of 2023, primarily due to lower clinical trial costs and lower manufacturing costs. G&A expenses were $3.3 million for the first quarter of 2024 and decreased by $2 million compared to $5.3 million for the corresponding period of 2023. The decrease was primarily due to lower professional fees, lower stock-based compensation in the current period. Now, let me turn it back to Dr. Rice.

Thank you, Fletcher. Now, we'll open the call for questions and please feel free to pose a question to any of us. Operator, if you could, please introduce the questions.

Thank you. [Operator Instructions] Our first question comes from Joe Pantginis with H.C. Wainwright. You may proceed.

Good afternoon gentlemen. Thanks for taking the questions. I'll start with two, if you don't mind. So, first, on Slide number 10, when you presented the trial design for the triplet combination, I'm just curious if there was -- what level of before and after was there. So, you met with the FDA in the first quarter, as you said. How much does Slide 10 align with what you originally wanted with them?

So, Raf -- perhaps Dr. Bejar perhaps you can answer that one and put it in--

Sure. Yes, of course. So, this was developed in conjunction with experts in the field, including our lead PI, Dr. Naval Daver, who's done several of these frontline triplet studies. And it really reflects both his experience and the VEN-ASA label. It isn't really a consequence of the back and forth with the FDA on this. We did submit a protocol amendment to our existing study that includes this protocol more than, I think, 45 to 50 days ago now. But this is really a function of our discussions with our experts, not a consequence of discussions with the FDA.

That makes sense. Thanks. And then I guess, as we look to the triplet study now, everyone is going to be highly looking forward to the year-end data. So, I guess internally, what do you view as the benchmark for success to be able to move beyond the pilot?

So, I can take that, too, Bill. I think there's a couple of opportunities, I think, to show benefit here. The expectations are based on prior data that the frontline triplet with a kinase inhibitor like tuspetinib can substantially increase the response rate. Of course, I think the really -- the metric that really matters is overall survival, and that is not data that we expect to have in the short-term. But the expectation with the VIALE-A study is that you see about a two-thirds of the patients responding. I think if we would see something closer to 75%, I think we'd be comfortable that we are at least meaning that, if not exceeding it. And given the number of patients we expect at ASH, I wouldn't expect to see a robust value there. But by the time the study is complete, we've treated enough patients, I think we have a very good understanding based on the response metrics about how well we're doing.

Joe, I'll add a little bit to that because it also relates back to the trial design. What we hope to see and we expect to see by year end is the complete remissions in these patients. We expect to see the robust safety, which we've continued to see all the way through even in the doublet of tuspetinib with venetoclax. And we hope in that, that allows us to maintain the standard-of-care dosing that Dr. Bejar mentioned, because it's really important to be able to maintain the expected levels of venetoclax as well as the hypomethylating agent according to the label of the drug, FDA wants to see that. We want to see that. And that's been a real problem with many of the other drugs out there. Perhaps Dr. Bejar wants to add to that.

That's exactly right, Bill.

Thank you.

Thanks guys. Appreciate it.

Thank you, Joe.

Thank you. [Operator Instructions] And I'm currently showing no further questions. I would now like to turn the call back over to Dr. Rice for closing remarks.

All right. Well, thank you everyone for joining us this afternoon. We're genuinely excited to take tuspetinib into the frontline trip of therapy for newly diagnosed AML patients. And we hope that we relate how Tuspetinib is distinguished from other AML compounds in development, not only because of its safety profile, but because it has shown activity across a broad set of mutations even in wild-type AML, potentially addressing the largest market in AML, not just a subset. As always, we thank our patients, investigators, and employees for their important role in this effort. Our clinical team has been keen in developing our poly triplet study prepared and -- to getting it prepared. I want to recognize them for their execution. We appreciate our shareholders and analysts who continue to support us and we look forward to keeping you updated on our progress to-date and we really do appreciate the questions that came to us today. I want to thank you and have a good evening.

Thank you. Ladies and gentlemen, that concludes today's conference. You may all disconnect and have a wonderful day.