Good afternoon. My name is Chandralyn, and I will be your conference operator today. I would like to welcome everyone to the Aptose Biosciences conference call for third quarter ending September 30, 2022. At this time, all participants are in listen mode. After the speaker's remarks, there will be a question-and-answer session. If you would like to ask a question during this time, simply press star one one on your telephone keypad. If you would like to withdraw your question, please press the pound key. Thank you. As a reminder, this conference call is being recorded. I would like to take this time to introduce Mrs. Susan Pietropaolo. Susan, please go ahead. Thank you, Chandralyn. Good afternoon, and welcome to the Aptose Biosciences conference call to discuss financial and operational results for the third quarter ended September 30, 2022. Earlier today, Aptose issued a press release relating to these financial results. The news release, as well as related SEC filings, are accessible on Aptose's website. Joining me on today's call are Dr. William G. Rice, Chairman, President, and CEO; Dr. Rafael Bejar, Senior Vice President and Chief Medical Officer; and Mr. Fletcher Payne, Senior Vice President and Chief Financial 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 our actual results and performance could differ materially from 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 annual report on Form 10-K at 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. I will now turn the call over to Dr. Rice, Chairman, President, and CEO of Aptose Biosciences. Dr. Rice? Thank you, Susan. I want to welcome everyone to our call for the third quarter ended September 30, 2022. Let's begin the call by addressing an issue that's on the minds of all of our shareholders. We are acutely aware that the biotech market has experienced a significant year-to-date downward trend, and similarly, the company's stock has fallen with the tide to trading at significant lows. Positive news releases, buying of Aptose stock by management and other insiders, investor presentations, and positive meetings with many quality investors have not yielded improved share prices to date. Ironically, as we presented to fundamental healthcare investors with domain knowledge, a common viewpoint emerged that our lead clinical candidate, HM43239, or just 239, looks like a real drug that gives complete remissions as a single agent in very challenging AML patients, and they were surprised that they had been unaware of 239 and its strong clinical activity. From a drug development perspective, Aptose is by far in the best position in which it has ever been. Aptose employees share a sense of purpose to develop safe and potent drugs for patients whose lives are being threatened by acute myeloid leukemia, or AML. We now are wrapping up a very successful phase I trial with 239 in patients with relapsed or refractory AML. We performed extensive dose exploration that demonstrated a highly favorable safety profile and that has allowed us to assemble a superior safety package. We also explored extensive mutational diversity among AML patient populations, and this approach revealed a breadth of favorable responses across a diverse group of very ill and difficult to treat AML patients, including many who already had been treated with and had been failed by the best available therapies. We continue to see rapid blast reductions and impressive response rates in mutationally defined subgroups across three dose levels of 239, and we look forward to providing the full scope of data from the phase I trial during December at the ASH conference. Meanwhile, we continue our outreach to investors to broaden the awareness around the growing 239 data package. This trial has delivered everything we had hoped. It now is complete, and we are moving on to our dose expansion program to explore single agent and combination therapy in enriched AML populations and to position HM43239 for single-arm phase II registrational studies with an eye toward accelerated approval. With regard to the market, we take a calm and long-term perspective. According to a McKinsey article earlier this year, biotech stocks have taken a major hit, and companies without commercial-stage assets have been affected most severely. The cycle is a familiar one for the sector, and with history as our guide, it is a question of when, not whether, the biotech public market will turn more favorable. In the meantime, emerging companies like Aptose might better weather such headwinds by scrutinizing cash management and financing, by continuing recruitment of exceptional talent, by identifying the best options to achieve planned milestones, by quietly and systematically collecting clinical data and de-risking our assets, and by determining the appropriate timing and magnitude of data to be released. That's exactly what we've been doing to give Aptose and our two assets, HM43239 and Lux, the best paths for success within these market conditions. With that said, now I'll move to discussions of our clinical assets, and let's start with luxeptinib or Lux, as we call it. Afterwards, I'll give an overview of HM43239 before handing it over to Dr. Bejar for additional information on our clinical plans. As a quick reminder, luxeptinib, formerly called CG-806 and now referred to as LUX, is our secondary program. LUX is a clinical-stage oral FLT3 and BTK kinase inhibitor that we've had in development for B-cell malignancies and AML. While we observed clear signs of drug activity and clear target engagement of BTK and FLT3, the original G1 formulation exhibited limited absorption, and only one patient administered the original formulation was able to achieve exposures of LUX to enable a complete response. However, we have been developing a new formulation for LUX, the G3 formulation, over several years for more rapid and more efficient absorption and for economic reasons to reduce the amount of drug substance to manufacture. As we reported in September of this year, the new G3 formulation demonstrated up to an 18-fold improvement in oral bioavailability relative to the original G1 formulation when tested as a single dose in patients. As of today, we've tested G3 as a single dose with 10 milligrams, 20 milligrams, 50 milligrams, 100 milligrams, or 200 milligrams in a total of 20 patients and assembled a PK package around the new formulation. We then amend the protocol of our existing phase I clinical program and submitted it to the FDA to incorporate continuous dosing and dose escalation of G3 in the ongoing trial and to phase out the original G1 formulation. We expect to commence continuous dosing of G3 very soon. If the G3 formulation increases steady-state exposures and delivers responses, we then have the potential to pursue certain types of cancers, inflammation, and autoimmunity indications, as well as work to identify an appropriate development partnership for this very unique molecule. Now let me turn to HM43239, our lead clinical program. First, I want to note that an official generic name has been established for HM43239, and that name is Tuspetinib, spelled T-U-S-P-E-T-I-N-I-B. Now let's discuss how Tuspetinib can be applied to the treatment of AML. As most of you are aware, AML is a highly heterogeneous disease characterized by a multitude of genetic and epigenetic alterations. This makes the treatment of AML both diverse and challenging because AML disease in each patient may present with a different set of manifestations and may be influenced by multiple oncogenic drivers rather than a single genomic alteration. Several companies are developing investigational drugs directed at specific targets that are operative in a particular segment of the AML population. With our lead clinical compound, Tuspetinib, we are pleased that it represents a broader scope drug with the potential to treat multiple mutationally defined populations of patients in their fight against AML. Tuspetinib potently does so by targeting a handful of clinically validated kinases essential for key oncogenic signaling and rescue pathways that contribute to drug resistance or recurring disease. Yet Tuspetinib successfully avoids other kinases often associated with toxicities. Indeed, Tuspetinib already has demonstrated clinical responses with compelling response rates in multiple mutationally defined target populations of relapsed or refractory AML patients, both with and without FLT3 mutations. Tuspetinib has achieved these clinical responses at doses with no drug-related SAEs, no drug-related deaths, no drug-related QTc signals, and no differentiation syndrome. I'm happy to report that we have successfully completed the dose escalation and dose exploration stages of our Tuspetinib phase I trial and have treated approximately 60 relapsed or refractory AML patients previously treated with multiple agents, including chemotherapy, BCL-2 inhibitors, hypomethylating agents, FLT3 inhibitors, and other targeted agents. Rather than trying to run up the score in one specific AML subpopulation, we explored the activity of Tuspetinib in a breadth of relapsed or refractory AML patients with extensive mutational diversity. Once-daily oral Tuspetinib delivered for these patients formal responses in several mutationally defined populations of difficult to treat patients, some of which were entirely unanticipated and would not have been identified if we had performed a more narrowly focused clinical program. Simply, the trial yielded everything you could ask for in a phase I trial, including impressive response data that guide us to pursue several mutationally defined patient populations and a hearty safety package that allows us to select our doses for the next stage of development. The proven breadth of activity and superior safety of Tuspetinib lends itself to combination therapy, potentially as the drug of choice, addressing the most sizable markets in AML. We already have reported significant clinical activity and complete remissions across three dose levels, 80 milligrams, 120, and 160 milligrams without DLTs, and we continue to observe additional clinical activity as responses mature. We believe Tuspetinib is a real drug for a real disease and we plan to disclose the full data set around ASH. I'll remind you that the ASH abstracts that will be coming out later this week will not contain the most updated data. The abstracts are placeholders for a broader data set that will be presented at the meeting in December. We also plan to host a quick and virtual KOL call in conjunction with the conference, and we will provide additional information on the timing of that call in the coming days. I also want to call out Dr. Bejar and our entire clinical development and clinical operations groups that have increased the rate of patient accrual for tuspetinib this year by more than 40% over any previous year of this program. Their execution truly has been remarkable. In a few moments, Dr. Bejar will talk more about our clinical plans for tuspetinib. First, I'd like to highlight one additional piece of recent news. In September, we were pleased to add another renowned member to our board of directors with the appointment of Dr. Bernd R. Seizinger. Dr. Seizinger is an accomplished executive leader with more than 25 years of industry experience in both U.S. and European biotechnology and pharmaceutical companies and multiple financial advisory positions. He has held biotech CEO and CSO positions as well as numerous senior executive and board positions, including with Bristol Myers Squibb, where he served as Senior Vice President of Oncology, Drug Discovery and Vice President for Corporate and Academic Alliances. Aptose benefits from our strong board of directors and our scientific advisory boards led by Dr. Brian Druker, and we are happy to add Dr. Seizinger to that distinguished group. I'll now turn it over to our resident KOL, our Chief Medical Officer, Dr. Rafael Bejar, to talk more about our clinical plans. Raf? Thanks, Bill. We achieved all of our goals in the dose escalation and dose exploration segments of this phase I trial of tuspetinib, with doses ranging from 20 milligrams- 200 milligrams. Just to remind you, by the time these relapsed or refractory AML patients reach our trial, each patient harbors an amalgam of adverse mutations, not just a single mutation, and each suffers with disease that is, by definition, resistant to therapy, having already been failed by other lines of treatment, including chemotherapy, targeted therapies, combination therapies, investigational therapies, and even hematopoietic stem cell transplants in many cases. Plus, these relapsed or refractory AML patients are physically compromised by the complications of their advanced disease and the toxicities of prior failed therapies. For these reasons, the patients that need an anticancer agent potent enough to kill the highly aggressive leukemic cells also need one that's gentle enough to spare normal tissues and preserve the function of the normal bone marrow. It's actually quite remarkable that Tuspetinib in this trial with genetically adverse all comers overall response rates are comparable to gilteritinib in a phase III trial at the selected commercial dose. Yet Tuspetinib is treating an arguably much sicker patient population. It's important to remind you that the number and types of often dramatic responses we've observed do not happen by accident in AML. These are not spontaneous remissions. Tuspetinib is an active agent. Tuspetinib has been impressive in its capacity to deliver complete responses and complete remissions in a diverse AML patient population, and not just FLT3 mutant AML, but wild type AML and other challenging AML types with highly adverse mutations. Additional good news is that since our last update, dosing has continued with no concerning drug-related safety signals or trends to date. Through the 160-milligram dose level, we have not observed any drug-related severe adverse events, no drug-related deaths, and we have not observed any dose-limiting effects that have affected other tyrosine kinase inhibitors. In particular, we've not seen adverse events related to the elevated creatine phosphokinase. We've not seen adverse events related to QT prolongation, and we have not seen any relationship between the change in QTc and dose. We are in the midst of completing data verification and analyses from our phase I trial, and we look forward to reporting those data to you this next month during ASH and present to you the genetically defined populations along with compelling case reports in exceptionally challenging patients in which Tuspetinib has demonstrated strong activity. I'll also point out that as we're preparing for our next clinical studies, we've enrolled additional patients at the lower 40 milligram dose level. This reduces regulatory risk by addressing requirements of the FDA's Project Optimus, an initiative that emphasizes dose exploration during early development of oncology products. This has nothing to do with the safety we've observed thus far at higher doses of Tuspetinib, which has been impressive. We are trying to just dot the I's and cross T's with a meticulous approach to withstand potential FDA scrutiny. In addition, supplementary data at the 40-milligram dose level will provide important information as we move into combination studies with lower doses of tuspetinib, and we now have fully enrolled sufficient numbers of patients at the 40-milligram dose. Having said that, we're eager to move on to the next stage of clinical development. Where are we with our next stage clinical trials? I'm pleased to report that we will have open recruitment for patients of our Part C expansion trial with 120 milligrams of tuspetinib as a single agent. We have identified a safe therapeutic range with a broad therapeutic window spanning the dose levels of 80, 120, 160 milligrams, and have selected 120 milligrams as our primary single agent expansion dose with 80 milligrams and 160 milligrams as bracketing doses that we can adjust to in order to refine our dose selection if necessary. In particular, patients that start at 120 milligrams will have the opportunity to increase their dose to 160 milligrams should they have no better than stable disease after one cycle of treatment. This trial is designed to confirm activity through patient enrichment, specifically genetically defined AML populations, including FLT3 mutant patients who have been failed by a prior FLT3 inhibitor, as supported by our Fast Track designation and our significant response rate to date. In the FLT3 mutated group, we have seen complete remissions in patients that have important gene co-mutations, including those in NRAS, KRAS, NPM1, and TP53, as well as adverse mutations in RUNX1 and MLL-PTD. Some of these mutations are typically associated with resistance to tyrosine kinase inhibitors, yet appear to be sensitive to tuspetinib. These patients continue to have great unmet medical need, and we believe that the ability to rescue these patients and perhaps allow them to receive a stem cell transplant, as we've now done with several patients in our study, would allow us a quicker path to registration. We expect to have these data beginning mid-year 2023 around the EHA timeframe. Having tested tuspetinib in specific genetically defined populations, our plan then would segue into phase II registrational studies to support accelerated approval. Importantly, we've also seen activity in patients who do not carry a FLT3 mutation, so-called FLT3 wild type patients. We will include relapsed or refractory AML patients with unmutated FLT3 that have other adverse mutations, exploring safety and activity in these patients with tuspetinib treatment, both as a single agent and in combination with venetoclax. Identifying meaningful activity in other adverse subgroups could lead to other options for accelerated approval. We soon will also open recruitment in the exploratory combination study of an 80 mg dose of tuspetinib with venetoclax. The paradigm for the treatment of AML is increasingly moving towards combination therapy, and we hope to position tuspetinib as the preferred agent for combination and use in earlier lines of treatment. Once again, the safety profile to date suggests tuspetinib could become the drug of choice for combination with venetoclax and hypomethylating agents. I'm certain you'll have questions regarding our selection of doses for the single agent and combination expansion trials, so we'll hold those discussion items for the Q&A session. We've accomplished a great deal since taking the reins of the Tuspetinib trial from Hanmi Pharmaceutical, and I'd like to thank our top-notch clinical team for their masterful execution of the dose escalation and exploration trial to date and for their efficient preparation in getting these imminent expansion trial ready to go. Now, I'd like to turn the call over to our CFO, Fletcher Payne, for an update on our financial status. Fletcher? Thanks, Raf. Good afternoon, all. Let's review the third quarter financials. As most of you know from following Aptose, we take a disciplined approach to cash management and the streamlining and prioritization of clinical activities for our pipeline programs. As reported last quarter, these efforts extended our cash runway into 2024. Let's review our cash position. We ended September 30, 2022, with approximately $55.4 million in cash and cash equivalents and investments. That is a decrease in our cash by $7 million for Q3. During the quarter, the net loss was $9.8 million, translating into $0.11 per share loss and down from $11.3 million loss from the comparable period in 2021. As identified in the income statement, we had no revenues during the third quarter of 2022. Research and development expenses were approximately $6.6 million for the quarter, down $7.7 million during the same quarter of 2021. Research and development expenses for the 9-month period ended September 30, 2022, were $21.3 million as compared to $25.8 million for the comparative period, a decrease of $4.5 million. The decrease was due to lower costs of the LUX program, offset by costs for the tuspetinib program. G&A expenses were $3.4 million for the quarter, compared to $2.6 million from the same quarter of 2021. G&A expenses for the 9-month period ended September 30th, 2022, were $10.9 million as compared with $15.3 million for the comparative period, a decrease of approximately $4.4 million. The decrease was primarily due to a decrease in stock-based compensation expenses offset by higher compensation expenses, travel expenses, and professional fees. As of November first, 2022, Aptose had 92,294,734 common shares outstanding. More detailed information can be found in our filings on EDGAR and SEDAR. Let's turn it back over to Dr. Rice. Thank you, Fletcher. As we open the call for questions, please feel free to pose a question to any of us. Operator, if you could, please introduce the first question. Thank you. At this time, we will conduct the question- and- answer session. As a reminder, to ask a question, you will need to press star one one on your telephone keypad and wait for your name to be announced. Please stand by while I compile the Q&A roster. Our first question comes from the line of Mr. Gregory Renza with RBC. Gregory, your line is open now. Hi, this is Ying Wang for Greg. Thanks, for taking our questions, and congrats on the progress. Maybe first just on HM43239, could you give some more color and help us set expectations around the data updates you plan to provide at ASH in December in terms of patient population, treatment duration, and maybe the type of data you plan to present? Thanks. Yes. Hi. Thanks. I'll take that one initially, and then perhaps Dr. Bejar will jump in. That's exactly what we tried to outline today was the types of patients that we're treating a breadth of patients in AML with mutations ranging from FLT3, RAS, NPM1, DNMT3A, RUNX1, IDH, TP53, and others. We wanted to be able to look at all of these types of patients, the mix of co-mutations in these patients, identify patients that are responding, and determine if there are patient populations that have heightened sensitivity, as well as those who might not respond as well. We'll be presenting all those data. In particular, we'll be highlighting the patients that have been placed on the trial this year since we took the reins of this clinical trial January first of this year. Dr. Bejar, anything further? No, that's a great summary, Bill. Thank you. Our next question comes from the line of Mr. Li Watsek with Cantor Fitzgerald. Please stand by while I open Mr. Watsek's line. Thank you. Miss. Yeah. Oh, miss. Sorry. Yes. All right. Great. Thank you for taking my questions. I guess just one, you know, on the RP2D dose that you propose and, you know, just wondering if you have h ad any interactions with FDA on this dose and, you know, any possibility to move forward with more than one dose? I'll let Dr. Bejar take that one, please. Sure. It's a great question. As I mentioned for our expansion phase, for which we're just beginning to look for patients now, we are using 120 milligrams as our planned single-agent dose. That is not set in stone, and we will have interactions with the FDA in the early part of next year to discuss, in part, what the appropriate dose going forward should be and whether they agree with our assessment. More importantly, we built into the protocol the ability to adjust that dose based on a variety of signals, including any potential safety signals, efficacy signals, or exposure data that suggests that that dose may not be the appropriate dose. We have that flexibility built in. Yeah. Just to be clear, we have selected doses for the expansion trial that's beginning now. Then as we go through that trial, we hope to be able to select out the appropriate doses to take us into what we would hope to be as the single-arm registrational studies. Okay. Thank you, Li. Our next question comes from the line of Soumit Roy. Please be patient while I allow him or her to speak. I'm sorry. Congratulations on all the progress and on rapidly progressing the tuspetinib. I don't know how much you can comment on this, but curious if you have noticed any of your investigators are more inclined to enroll FLT3 mutant patients, or do you think the patient population that continued to enroll in the phase I is still split between the FLT3 wild type and mutants? Well, I'll begin with that one. Thanks, Soumit. I'll begin, and then I'll turn it over to Dr. Bejar. The intent of the original phase I was to get as great a diversity of patients as possible, both FLT3 mutated and FLT3 wild type, and then to look at all the co-mutations associated with them, and again to look then at those patients who might have greater sensitivity or lesser sensitivity. Then we've been able to learn from these potential populations that we'd want to move forward with into our expansion trials. Dr. Bejar? Yeah. As you know, the FLT3 mutated population is about 1/3 of AML. We built the study in particular to ensure that we had about a 50/50 split. There are some controls in there to allow for that to happen, and that's roughly what we've been able to achieve. Going forward in this expansion study, we're not changing that, although we are enriching for certain subsets of populations. Okay. Soumit, with that. Uh, next- I was gonna make certain that that answered Soumit's questions and if he had anything else. We've lost him. Thank you. Okay. Our next question comes from the line of John Newman with Canaccord Genuity. Please be patient, and I will promote him and open his line. Your line should be open, sir. Hi, guys. Can you hear me? Yes. Yes, John. Great. Bill and Raf, I wondered if you could talk more about the specific populations that you are looking to enroll in the expansion study. Also wondered if those would be similar populations that you would look at in combination with venetoclax or if that study might focus on different populations in terms of the mutations. Yeah. Thanks, John. Thanks for the question, but, I'll have Dr. Bejar address that one. Sure. In the single-agent arm of our expansion trial that's coming up now, we're enriching for two patient populations in particular. One is a FLT3 mutant patient population that has received prior FLT3 inhibitors. I think that's a population of great unmet medical need and probably the group with the highest likelihood of being amenable for a single-arm registrational study as an accelerated approval. We're also enriching for patients that have highly adverse mutations, like mutations in TP53 or complex karyotype. Those are largely FLT3 wild type patients, although not exclusively so. Now in the combination arm, we aren't enriching for any particular population there. We're really, again, just like we did for the original study, accepting all comers. We have the opportunity to see if there are any unexpected populations that respond, including those that are FLT3 wild type. Yeah. Let me just add to that a little bit. We have, as we've collected our most recent data, we've been able to look at the various co-mutations that occur in patients and identifying some subpopulations that are having impressive response rates. We hope to be able to then watch those again as we go forward in the expansion trial. Again, they would fall under the patient populations that Dr. Bejar just described. We'll be watching for several specific co-mutation profiles in patients that may bring us other potential accelerated approval pathways. Anything else, Dr. Bejar? Yeah, I think in, you know, one of the rationales for doing what you just described, Bill, is that this drug is much more than just a FLT3 inhibitor, right? With the activity that we have against targets like SYK and so on, some of the patient populations that might be more targeted by that activity are ones we're gonna look at very closely. Thank you. Thank you, John. Our next question will come from the line of Matthew Biegler of Oppenheimer. Same. I'm gonna ask about the G3 formulation. Have you guys announced the starting dose for the reboot? Would that provide a similar exposure level to the highest dose tested in luxeptinib's phase Ib, which I think was 900 mg? Yeah, but correct me if I'm wrong. Thanks. You are correct. The last dose that we've used for the original formulation is 900 milligrams BID. Then when we went through our various studies with different dose levels of the new G3, it was clear that it looked like the 50 milligrams twice a day should be able to equate with the same exposure that we had seen with the 900 milligrams of the original. Our plan is to start with 50 milligrams twice a day with continuous dosing. Dr. Bejar, did you wanna add anything to that? Yeah. We purposely wanted to start a little bit more conservatively since this is a new formulation. Although we modeled what continuous dosing would look like, we wanted to make sure that we weren't going to exceed our prior exposures that have been cleared for safety. 50 milligrams BID is the starting dose, but we have the ability to then further dose escalate based on the signal and data we receive at that cohort. Have you guys had to do any more tox studies on either Lux or the G3 formulation since? Have you had any kind of safety signals or DLTs in that that would be of note? I can take that one. No additional tox studies since we've gone into the clinic. Before we took G3 into the clinic, we actually did a full preclinical development GLP tox studies to enable us to go in, and clearly it was safe, sufficiently safe for us to go in at these doses and even to look at continued dose escalation. Dr. Bejar, anything you wanted to add to that? We've seen no signals of any type of toxicity. Agreed. In the clinical program where we've dosed patients with a single dose, we haven't seen any concerns or issues from that. Right. Gotcha. All right. Okay, thanks. At this point, no concerns. Thanks. Good question, Matt, but we haven't seen any concerns today. You know, it's a new formulation, so we will watch very carefully at the exposure levels, the safety, and also for the, hopefully for responses. Thanks. Our next question will come from Mr. Joe Pantginis with H.C. Wainwright. Give me just a few moments, and I will promote him so that his mic is open. Mr. Pantginis? Hey, guys. Can you hear me? Hello, Joe. Yes. Great. Thank you. Good afternoon. Quickly first on tuspetinib. Sorry. You might have said this. I'm just making sure. With regard to the combination arm with venetoclax, just a little review of the mechanistic reason why you're starting at 80 versus 120, and does that dose also have bracketing doses like the monotherapy study that you can adjust to? Yeah, good question, Raf? That's a very great question. We purposely lowered the dose a little bit to just make sure that we didn't run any early toxicity issues. Not that we expected any in particular, but we wanted to make sure that we were treating patients at a dose that we thought was going to be both effective and safe. I'll remind you that at 80 milligrams of a single agent, we saw multiple complete remissions in our study. We think that lowering that dose isn't gonna really be sacrificing any activity there, but might give us a little bit more window now that we're adding another agent that is gonna bring some toxicity to the table as well. As with the single agent arm and our combination arm in this expansion, we will have the ability to adjust that dose either upward or downward. This additional data that we're gathering at 40 milligrams with a single agent now will help us understand what that would look like if we needed to drop that dose in the combination arm down to 40. Got it. Thanks, Joe. Anything else? Yeah. Yeah, please. Just a little bit on LUX. You did mention even with earlier studies and, you know, having the new form, potential supply constraints just 'cause you're using so much drug, where do you feel you are right now to be able to supply the G3 for all of your, you know, current plans to start? We don't see any limitations at this time on the G3. Again, this is gonna be a three-by-three study. We would expect that maybe 12-15 patients would be able to give us a really good read on these patients. We don't feel like we have any restrictions on the G3 drug supply at this point. May everything work out so well that we need to manufacture more. Yeah, got it. Then, you know, when you look at, yeah, Bill, you gave a little bit of a, you know, an additional teaser there that, you know, you sort of have discussed in the past about, you know, the potential for inflammatory or autoimmune disorders. When you consider that, do you have, you know, potential, indications or protocols, you know, even in draft form, and is that impacting any potential ongoing business development discussions? Well, I can't speak about any ongoing business development discussions, but, what I can say is, based on the kinases that are targeted by Lux, a number of those are involved with inflammation, autoimmunity, some of these other, diseases of that type. So at the research level, we've gone to great lengths to make sure we understand exactly what's going on inside the cells. A variety of different inflammatory cells, B cells, T cells, looking at the mechanisms and the pathways that are affected, and then even taking that into multiple animal models. We've seen activity, and we've begun to publish some of those data, and we will plan to continue publishing more of those as we go forward. Part of. The big part of that is trying to understand the breadth of activity of LUX, and it looks like it could be taken into those other indications if we can come up with a formulation that consistently delivers the desired levels of exposure with LUX. Again, we might have been able to take the original formulation into these other indications where you likely have to have lower exposures and long-term dosing. We still would prefer to be able to use the G3 formulation and deliver far less of the API and fewer tablets and just a much more efficient dosing. Again, I hope to be able to take it into those other indications into the future. Some of that we may be doing on our own and some will in conjunction with other companies. Time will tell on that, and we'll let the data drive us. Great. Thanks, Joe. Thanks for the added color, guys. Sure. Okay. Prior to taking our next caller's question, may I remind you by dialing star one one on your telephone keypad will allow you to raise your hand and be put into the queue for any potential additional questions. Stand by while I prompt Mr. Edward Tenthoff to ask his questions. Mr. Tenthoff. Hey, guys. How are? Thank you. Hey, Ted. Yeah. Unfortunately, I was pressing star one and all of my questions have been answered, but I just wanted to congratulate you on the progress. Looking forward to more data at ASH and then also the expansion cohort data starting next year. Thanks so much. Okay. Thanks a lot, Ted, for being here. Yeah, I also wanted to reemphasize to everyone, even though we talked about LUX a number of times here, we want to reemphasize HM43239 is our lead program. That is where the vast majority of our effort, our cash is going to be expended. That drug has been de-risked in so many ways with activity, clinical activity and still well tolerated. I just want to reemphasize that the drug is going to be focused there. Okay? Operator, were there any other questions? No, sir. We have no additional questions or persons in the question queue. Therefore, at this time, I would like to turn the call back over to you for any further closing comments. All right. I just wanna thank everyone for joining us this afternoon. 2022 thus far has been a year of truly solid execution on the clinical front. I wanna make sure that we thank all of our employees, our investigators, our contractors, and above all, the patients who continue to help us advance this important work. We are also very thankful. We appreciate our shareholders and analysts, all of you that are on the call. Thank you for your support. We look forward to keeping you apprised of our progress, and we can't wait to see it at ASH a little bit later this year. Everyone, thank you and have a great evening. Bye-bye. Thank you for your participation in today's conference. This concludes the program. You may now disconnect. Okay. All right. Thank you so much, Chandraly n Drillen.