Good morning, everyone, and welcome to the Leap Therapeutics conference call. Following the initial comments, there will be an opportunity for questions. Please be advised that this call is being recorded at the company's request. The company would like to remind you that any statements made during this call that are not historical are considered to be forward-looking statements within the meanings of the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these statements as a result of various important factors, including those discussed in the forward-looking statements section of the press release issued today and the Risk Factors section of the company's most recent annual report on Form 10-K, as well as other reports filed with the SEC. Any forward-looking statements represent Leap's views as of today, January 17th, 2023 only. A replay of this call will be available on the company's website, www.leaptx.com, following this call. At this time, I will now turn the call over to Douglas Onsi, President and Chief Executive Officer of Leap. Please begin. Thank you, operator. Welcome. I'm joined here today by other members of the Leap management team. Thank you to those of you joining us today as we announce a transformative moment for Leap Therapeutics through the acquisition of Flame Biosciences, a privately held venture capital-backed cancer company. When we took Leap public in 2017, our stated mission was to acquire and develop a pipeline of drugs with the potential to change the practice of medicine. Our strategy for our lead product, DKN-01, and any other products we would acquire, is to identify specific biomarkers that will predict which patients are more likely to respond and have better survival outcomes. We intend to be a biomarker-focused oncology drug development company. With DKN-01, we have a lead product that has demonstrated single agent activity in three tumor types: esophageal gastric cancer, non-small cell lung cancer, and endometrial cancer. We have shown that esophageal gastric cancer and gynecologic cancer patients with high DKK1 expression can have strong outcomes with DKN-01, whether as a single agent or in combination with an anti-PD-1 antibody and chemotherapy. In 2022, we initiated our first randomized clinical trial for DKN-01 in combination with our partner BeiGene's anti-PD-1 antibody tislelizumab and chemotherapy in first-line gastric cancer patients. We initiated a new trial in second-line colorectal cancer patients and an investigator-sponsored study in endometrial cancer patients in combination with Merck's KEYTRUDA. As a company, we've always aspired to develop more products than only DKN-01 and have been actively seeking new product opportunities to broaden our pipeline. We believe that we have found the perfect fit in Flame, identifying a second clinical stage antibody program, expanding our GI cancer focus, building on our biomarker expertise and development strategy of bringing personalized medicines to targeted patient populations with a validated target in Claudin 18.2, and the potential for clinical data from a first-in-human trial in China funded by our partner, along with two exciting preclinical programs. Through the merger being announced today, Leap has acquired FL-301, Flame's clinical stage anti-Claudin 18.2 monoclonal antibody, FL-302, Flame's preclinical anti-Claudin 18.2 CD137 or 4-1BB bispecific monoclonal antibody, FL-501, Flame's preclinical anti-GDF15 monoclonal antibody, along with Flame's net cash, which was approximately $50 million as of year-end. Importantly, following the transaction, the pro forma cash balance at year-end, the combined company was approximately $115 million, sufficient to fund the development of our expanded pipeline to mid-2025, well beyond our DKN-01 clinical milestones, even without any additional payments from BeiGene or other potential business development partners. Let me spend a few minutes introducing the new programs and how they fit with DKN-01 and our strategy of developing novel biomarker-targeted therapies for cancer patients. Adding the Claudin 18.2 program leverages the existing Leap team's expertise, operational infrastructure, and experience in gastric cancer clinical and biomarker development that has been built through the DKN-01 program, leveraging our strong key opinion leader, clinical trial site, and diagnostic testing relationships. We believe that DKK1 and Claudin 18.2 will become important patient selection biomarkers in gastric cancer, alongside HER2 and PD-L1 expression, with doctors having the opportunity to order a panel of biomarker tests and choose the appropriate combination of therapies for their patients. As a bit of background, Claudin 18.2 is a key component of the tight junction for cell polarity and sealing the spaces between adjacent cells. It is expressed in a wide range of human malignancies, including gastric, esophageal, pancreatic, lung, and ovarian cancers. Claudin 18.2 is largely inaccessible on normal tissue, but becomes accessible to antibodies like FL-301 and FL-302 during tumorigenesis, making it a highly selective biomarker for targeted cancer therapies. Claudin 18.2 is also a validated target, as randomized clinical trials from Astellas of their chimeric anti-Claudin 18.2 antibody, zolbetuximab, have shown a survival benefit in combination with chemotherapy in a phase II study. Recently announced phase III studies in first-line gastric cancer patients whose tumors express high and intense levels of Claudin 18.2. However, since Claudin 18.2 expression in tumors is heterogeneous, expansion to patients with lower expression and improved efficacy in patients with higher expression requires an antibody with higher affinity and improved killing activity. We believe that FL-301 is a best in class and differentiated anti-Claudin 18.2 antibody. FL-301 is a fully human antibody with enhanced affinity and effector functions relative to zolbetuximab. It has 10x-20x higher affinity to CLDN18.2 than zolbetuximab in non-clinical models and specificity to both gastric and pancreatic tumors. Through Fc Engineering, FL-301 also has enhanced ADCC, CDC, and ADCP activities, which lead to improved cancer cell killing and greater potency relative to zolbetuximab in non-clinical models. FL-301 is being developed through an exclusive license from NovaRock Biotherapeutics for territories excluding China and is currently in a first-in-human clinical trial in cancer patients in China. We and NovaRock expect to have initial clinical data to present later this year or early next year, Leap intends to use this data to initiate clinically relevant combination studies in gastric or pancreatic cancer patients at appropriate dose levels. Leap also acquires FL-302, a CLDN18.2 CD137, which is also known as 4-1BB, bispecific antibody that is in preclinical development. By enhancing the antitumor activity of T cells in the tumor microenvironment, we believe that there is an opportunity to further improve the activity of CLDN18.2 targeting and generate additional synergy when used in combination with other immunotherapies, including immune checkpoint inhibitors and potentially our own DKN-01. The other preclinical program, FL-501, targets growth differentiation factor 15 or GDF15, which is a cytokine that is produced at elevated levels in response to various stresses, including chronic inflammation, obesity, cardiovascular diseases, cancer, and chemotherapy treatment. High GDF15 expression is associated with cachexia, including the loss of appetite, nausea, and weight loss, and is also a validated target with a successful randomized clinical trial from Pfizer. We are particularly interested in the role of GDF15 in promoting an immunosuppressive tumor microenvironment, much like DKK1, and the broad range of cancers, including gastric, colorectal, pancreatic, and prostate, where elevated GDF15 also correlates with poor prognosis. With the co-combined company resources and our existing team, we will be able to aggressively advance both DKN-01 and the newly acquired programs. Enrollment is off to a strong start, with high investigator enthusiasm for the randomized controlled trial of DKN-01 in combination with BeiGene's tislelizumab and chemotherapy in first-line gastric cancer patients. We continue to anticipate completion of enrollment of the 160 patient study this year, with initial response rate data being available near year-end 2023 and progression-free survival data in 2024. The new study of DKN-01 in second-line colorectal cancer patients is also starting extremely well, and we're looking forward to seeing data from the initial 20 patients mid-year, which would enable moving forward into a second randomized study. We are also looking forward to initial data late this year from the investigator-initiated study at MD Anderson and University of Alabama at Birmingham in combination with Merck's KEYTRUDA in endometrial cancer patients. We'll be presenting a corporate presentation tomorrow at 1:30 P.M. at the B. Riley 3rd Annual Oncology Conference, where Cindy Jay and I will provide a deeper dive into the DKN-01 data, an introduction to the science behind the Claudin 18.2 clinical programs, and the differentiation of those antibodies from the current products in development, and a look at the important clinical milestones ahead. This presentation will be available by webcast. We encourage all of you to listen in through the link on our website at www.leaptx.com. We appreciate all of the efforts of the Flame team and the Flame investors to complete the merger. We're excited to start the year as a new, stronger Leap Therapeutics with a pipeline of biomarker-targeted antibody therapies for cancer patients, particularly GI cancer patients, an enhanced balance sheet, and an important year of development plan execution and clinical data ahead. Thank you all for your time and attention today. We'd now like to open the call for questions. If you'd like to ask a question, please press star one one. That's star one one to ask a question. Our first question comes from Joseph Catanzaro with Piper Sandler. Your line is open. Great. Thanks so much for taking my questions and congrats on the transaction here. Doug, you mentioned potentially the opportunity to expand utility into lower Claudin 18.2 expressers. When we see the Astellas data, I think later this week, what proportion of the gastric population are they able to target with their program? You know, how much further do you think you'll be able to expand that with FL-301? The ability to maybe target lower expression levels of Claudin 18.2, does that open up any other additional opportunities maybe beyond gastric and pancreatic? Thanks. Thanks. No, that's a great question. As you mentioned, we're expecting to see additional data from Astellas for zolbetuximab this week at ASCO GI. You know, the positive top line data from their phase III studies was expected, you know, based on the previous success of the FAST study. As you mentioned, however, in the FAST study, it was the 70% CLDN18.2 expression population that was successful, even though it had only nine months of median progression-free survival. Their data wasn't statistically significant for the 40%-69% expression, which had 4.3 months of median progression-free survival. In the FAST study, there was also only a 38% ORR in the full population. You know, we... You know, our view is that expansion to patients, as you mentioned, with lower Claudin expression is down toward the 40% level requires a differentiated antibody with higher affinity and improved cell killing. You know, as we look at, you know, the clinical study that's being run by our partner, NovaRock, in China, you know, we'll be able to explore how patients with lower levels than 70% of high-intensity Claudin binding will perform, then, you know, be able to see beyond gastric and pancreatic, you know, what are the additional tumor types that can be moved into. I think our basic, from what we've seen is there is a variety of data in the literature regarding high Claudin 18.2 expression. You know, at the moment, you know, the view is it's between 30% and 40% of patients, in a variety of studies that have high Claudin expression. The ability to, you know, expand beyond that requires a next generation, you know, and improved antibody. That's something we're, yeah, excited to see, you know, get developed by our team with this transaction. Okay. Got it. I have a follow-up or two here. I know you sort of touched on this, but wondering how you think about the complementarity of FL-301 to DKN-01. Do you think there's opportunity to look at both within the same regimen, or will these operate within different buckets based on biomarker expression? I guess relatedly, you know, what's the overlap between CLDN18.2 positivity and DKK1 positivity within gastric cancer? Yeah, absolutely. I would say that's a big reason why CLDN18.2 was at the top of the list of programs that we wanted to add behind DKN-01. You know, as anyone who listened to our R&D day call last summer or any of the calls that our KOLs give as they talk about the future of gastric cancer, you know, they say they wanna be able to order a panel of diagnostic tests to select the best combination of therapies for patients. That's HER2 and PD-L1 today. Then as new therapies come forward, DKK1, CLDN18.2, and FGFR2b. Your point is exactly where we sit, which is ultimately, I'd like to get to a point where a patient who had DKK1 high or, you know, important DKK1 expression and Claudin high or intermediate, depending on the activity of the antibody expression, could get both DKN-01 and FL-301 or FL-302, an anti-Claudin antibody, as they should both have independent activity. Just like I would eventually like to move DKN-01 forward into HER2 positive patients in a combination with Herceptin or zanidatamab or in HER2. Having both DKK1 and CLDN18.2 programs in our pipeline allows us to build that leading next generation GI cancer franchise and be in a position where, as this panel of tests are ordered, physicians have choices that address the personalized profile of their patient's tumor. Got it. If I could just squeeze in one quick last one. You mentioned that FL-301 was in licensed from NovaRock Biotherapeutics. Can you maybe just speak to the economic terms of that deal and whether there are any expected milestones due in the near term? It's a pretty standard... No milestone payments expected in the near term, but it's a, you know, fairly standard antibody license with, you know, clinical milestones and royalties. We'll report all of that when we file our next SEC filing, our 10-K. Okay, perfect. Thanks for taking the questions and congrats again on the deal. Thanks, Joe. Our next question comes from Joel Beatty with Baird. Your line is open. Great. Hi, thanks for taking the questions. The first one is in the prepared remarks you mentioned the stronger binding compared with zolbetuximab. Could you discuss the implications of that? Yeah, absolutely. You know, we'll be able to talk more about this. I don't wanna steal too much of Jay's thunder from tomorrow's presentation. We'll add some of this data to our website. NovaRock presented a poster at ACR in 2020, you know, where they showed the difference. You know, as you look at the Astellas data, where they were less successful in patients who didn't have, you know, extremely high Claudin and intense Claudin 18.2 expression, you know, the activity is increased. If you can have higher affinity to Claudin 18.2 and more effective cell killing through the Fc Engineering that they've worked into the antibody, and that, you know, it can wind up being, you know, 1,000x-2,000x more potent than zolbetuximab in non-clinical models. We'll have to demonstrate that in clinical development, but it gives you that opportunity, through the clinical stage program to see enhanced activity and then opens up a very interesting opportunity for the bispecific if you can enhance the immune tumor microenvironment by bringing in T cells with the 4-1BB engagement, particularly in an environment where you're going to combine with immune checkpoint inhibitors, you're going to combine with other immune oncology agents. Aspects of this molecule that can help the immune system target and clear a tumor in tumors like gastric cancer that aren't as, you know, immune sensitive as others, could be incredibly important if our goal is to truly help increase overall survival for patients. Great. You know, thinking ahead to the expanded cash runway, could you help frame how much data we could see from FL-301 in that time frame? I think the key part to the expanded timeline or the expanded cash runway is to ensure that we can complete the ongoing DKN-01 randomized clinical trial in colorectal cancer trials regardless of any, you know, any business development or external financings and to have, you know, a year of runway on the back of that data. For FL-301 specifically, we are, you know, we are looking forward to seeing clinical data from the study in China from NovaRock. In terms of our own study, we would not expect to be able to open an FL-301 study in the United States in the short term because our goal would be to not have to repeat the monotherapy dose escalation work that's being done by NovaRock in China and be able to jump straight into use higher doses of FL-301 in more commercially and clinically relevant combinations. With PD-1 antibodies in gastric cancer, you know, with other, you know, approved chemotherapies in pancreatic cancer. You know, that it'll take, you know, time for us to be able to have the data to support going in in ways that can, you know, rapidly generate meaningful clinical data. Got it. Makes sense. Last question. It's a bit off topic, but anything you can tell us about the opt-in decision and the status of that related to BeiGene and DKN-01? Yeah, absolutely. Just as a bit of background, you know, we've been speaking with Flame about this potential transaction for well over a year. You know, this was a strategic opportunity that we believed was a perfect fit for us and our goal to build a company that was more than a single product. You know, we actually believe that the transaction with Flame makes Leap a more attractive partner for BeiGene or any other partner with a stronger balance sheet and additional programs to validate a target that could be combined with PD-1 therapy and enhance any GI oncology franchise. You know, as we mentioned at your conference and at Piper's late last year, our agreement with BeiGene gives BeiGene until late in the first quarter to make their option exercise decision. We met with members of the BeiGene team last week at JP Morgan and shared some early activity in both the ongoing trials, and we'll continue to provide them with updates on the data. We expect that they'll be presenting data from their first line gastric cancer study for tislelizumab at ASCO GI this week. We respect that they have an internal process that goes into making their opt-in decision. From our perspective, though, you know, we believe that the case for BeiGene to exercise is very strong. If we're successful in developing DKN-01, BeiGene could have a significant DKN-01 revenue opportunity in their Asian territory from several large indications. If gastric cancer has 500,000 new cases a year in China, colorectal cancer, endometrial cancer, just based on our current studies, and potentially other indications where we've previously seen DKN-01 mono activity, like non-small cell lung cancer. We believe that they could benefit from increased tislelizumab revenue from being in a combination with DKN-01. You know, increased duration on drug and first-line gastric cancer could be nearly 50% more revenue per patient based on the existing data. Could broaden the market to include PD-L1 low patients in the event that physicians continue to be concerned about using PD-1 plus chemo in PD-L1 low patients without stronger outcomes, because we've seen strong outcomes in PD-L1 low patients with the DKN-01 combinations. Could help them expand indications to include endometrial cancer, where we're currently running a trial with KEYTRUDA that could provide the foundation for that new combination opportunity, or possibly colorectal cancer, where PD-1 antibodies have not historically been successful. This would be a proprietary combination that could allow BeiGene to differentiate from the other PD-1 antibodies that are or could be approved in first-line gastric cancer with a proven advantage over PD-1 plus chemo alone. Our view is, you know, we've achieved everything that we hoped could be achieved when we formed the relationship with BeiGene, and it's now in their hands to make their internal decision based on their, you know, strategic assessment of tislelizumab and their overall, you know, internal prioritization. If BeiGene doesn't opt in, you know, the same rationale for the DKN-01 global commercial opportunity and the potential to drive additional PD-1 revenue applies. You know, DKK1 is a novel target with compelling clinical data and important biological mechanisms in areas of high unmet global need, there are many potential strategic partners. As part of this transaction, you know, that it is important that our combined company cash balance will fund the company for more than a year past that randomized data, which would allow us time to re-partner globally, if necessary, or consider partnering for our retained territories if BeiGene does opt in and from a position of greater strength. That's great. Thank you. Our next question comes from Mara Goldstein with Mizuho. Your line is open. Great. Thanks so much for taking the question. I wanted to ask you just about your assessment around the competitive landscape. Obviously, we've talked about the Astellas compounds, but there are a fair amount of other molecules in development and bispecifics as well, and I'm curious about your thought process there, entering into such a crowded field, particularly since you won't advance into a phase I study in the U.S. for, I'm imagining, at least later into 2023. If you could talk about that'd be great. Absolutely. You know, as I pointed out, I think as we look at the competitive landscape, the first thing that we think about is that even for the Astellas program, the studies that they've run as phase III studies aren't, in our view, clinically relevant studies today because they don't include a PD-1 antibody. To be competitive in gastric cancer today, with the approved therapies, Astellas and all of the other CLDN18.2 programs will need to demonstrate that there's additional efficacy on top of PD-1 plus chemo in first-line patients. I believe that Astellas are starting those PD-1 combination studies, and we'll need to see what the level and intensity of CLDN18.2 expression is that's required for zolbetuximab activity, you know, in combination with a PD-1. You know, I've described, you know, what I think are the engineering design advances in FL-301 that give it the potential for improved activity and improved performance compared to zolbetuximab, which is an old chimeric antibody with, you know, relatively lower affinity in CLDN18.2 and effector function. I think that all of the new, newer antibodies in development stand a very strong chance of surpassing zolbetuximab as being better engineered. I think in many ways the, the ground is for well, for studies that are tied to the current development landscape, the advantage of a company like ours that has relationships with key opinion leaders, with gastric cancer sites, that is actively engaged as a priority in the gastric cancer market, with, you know, open studies and a program that is advanced of where FL-301 is right now, puts us in, you know, an excellent position to be able to execute and to, you know, with monotherapy data out of NovaRock rapidly, you know, make FL-301 competitive. Then, as you mentioned, with bispecifics, you know, we do believe that the next frontier is through bispecific antibodies. Adding 4-1BB engagement can enhance that antitumor activity and create additional synergy when used in combination with other immunotherapies. You know, we'll continue to look very carefully at the opportunities to be able to add PD-L1 and other immune checkpoint inhibitors into that mix, and we'll be able to talk about that more over the course of the next year. Okay. I just also wanted to ask, I mean, on, on the Astellas compound, the safety profile looked fairly benign. The issues were really associated with GI side effects, nausea and the like. I'm curious about your thoughts about the affinity of the molecule that you have in the relationship there. Yeah, absolutely. I think that, you know, as we look at, you know, the potential profile for FL-301, as I mentioned, you know, we see that it has, you know, 10x-20x higher affinity to CLDN18.2 in non-clinical models, you know, enhanced ADC, CDC, ADCP activities, which can lead to greater cell killing and potency. For these antibodies, the issue has been efficacy, particularly as you get to, you know, lower or less intense CLDN18.2 staining. You know, we do note that, you know, CLDN18.2 is not prognostic. You know, this isn't a situation like DKK1, where we believe the claudin high population has more aggressive disease or, you know, more likely to have liver metastases or other factors that make them have shorter survival. It is, you know, an available target that is highly specific to cancer. Where it is expressed and you have an antibody that is efficient at killing those cells, can lead to important benefit for those patients and a benefit that is complementary to the, you know, other ways of looking to kill cancer cells or activate the immune system to kill cancer cells. Okay. Thanks, Doug. I appreciate it. Our next question comes from Timur Ivannikov with Raymond James. Your line is open. Yeah. thank you for the question and congrats on the deal. I just wanted to follow up a little bit on the previous questions, and ask the competitive question in a slightly different way. you know, because there's new development in lower expressors where bispecifics and ADC could be more competitive than the antibodies. On the higher end of expressors, you know, we have new CAR T developments also targeting Claudin 18.2. I'm wondering why do you think it's a good strategy to develop your antibodies first instead of perhaps going with the bispecific? The, you know, we'll be aggressively moving the bispecific, you know, through pre-clinical development into the clinic. It is from a timing perspective, you know, more work to be done before it's ready to be advanced into clinical development. You know, as we think about the ADC molecules, they are certainly, you know, very interesting. We do worry about the safety effects because there is CLDN18.2 expression in the normal gastric mucosa. You know, it's, will be an open question to see whether that safety profile, that toxicity that is potential to come from the ADC molecules impacts their utility or the breadth of Claudin expression patients in which, you know, there is a favorable safety efficacy benefit. It's certainly a very interesting approach. You know, there are a number of other bispecifics which look to engage different targets, whether that's CD3, PD-L1. You know, from our perspective, you know, when we think about what we've learned about DKK1, the tumor microenvironment and the cell types that are most important in leading to stronger outcomes, particularly in gastric cancer patients, there is, in our view, a real advantage to 4-1BB that makes us very excited about the bispecific program. You know, I think from the... You know, there is, you know, I think as we look at these fields, I think you want to move multiple programs forward and see if they find potentially different niches, or, you know, different levels of Claudin expression where they have a particularly or different combinations, where they have a particularly attractive, risk-benefit or synergistic activity. You know, that'll come with more development work on our part and more work in the clinic. Thanks for that. Just a quick couple of quick housekeeping questions. First, I'm not sure I saw when the transaction is expected to close. I think you mentioned a special shareholder meeting. Then just to for Flame itself, just to clarify, I think they had a study on ClinicalTrials.gov that was withdrawn. Was that withdrawn just because of the Chinese study or because they knew the transaction was coming? You know, what was the reason for the withdrawal of that study? Sure. Let me start with this. The transaction was a simultaneous sign and close, so the transaction is closed. The shareholder meeting, because we were issuing more than 20% of Leap's current common shares, the deal is structured so that the preferred shares, which are the remainder of the Flame consideration over the 19.99% of common stock that we could issue, can't convert to common until we have a separate shareholder vote. We will look to, you know, file a proxy statement and hold that shareholder meeting, you know, over the course of the next few months. That would allow the preferred stock to convert to common. It's the shareholder vote is not to approve the transaction, but it's to approve the conversion of what will currently be non-voting convertible preferred stock into common stock. I think with respect to the existing, you know, Flame clinical studies, you know, historically Flame as a company was founded around their interest in IL-1 beta. You know, our first introduction to Flame was, you know, nearly two years ago when Dr. Monica Bertagnolli, who was then a member of Flame's board, is currently the Director of the National Cancer Institute, someone who's very interested in, you know, the potential development of IL-1 beta, you know, introduced us to the company and they were, you know, in the process of acquiring, you know, additional assets beyond the IL-1 beta program. You know, the, when Novartis conducted their canakinumab CANOPY studies for IL-1 beta and those, you know, studies were unsuccessful, it caused Flame to rethink its corporate objectives and its opportunity, you know, as a standalone company. The process that led to their deal with us was a, you know, a very significant strategic effort on their part. They had many different parties bidding and expressing interest in the range of programs that they'd brought together. They had formed the conclusion that they weren't going to develop these assets themselves and then really look for a strategic partner with the team, with the expertise, with the complementary pipeline that could be the right home for the shareholder base that they've built and that the assets that they had developed. Certainly for us, that shareholder base, you know, includes, you know, many of the top-tier biotech industry investors, the kinds of fundamental investors that you want to see back your company. We're, you know, very appreciative of their interest in us, their belief in what the Leap team can do with DKN-01 and with the Flame assets that we've acquired. That was their strategic pivot, was to not try to open and develop these new studies internally and build the team and infrastructure they would take, but it would be to find an existing team. For us, as I said, it was. You know, Flame was a unique opportunity, you know, to enhance our pipeline with a program that is a perfect strategic fit, to enhance our balance sheet with an additional year of cash, and you have to take advantage of those opportunities when they appear. Okay. actually, sorry, one more quick question, but this one is on DKN-01. I just want to make sure I understand the changes on the ClinicalTrials.gov. Are you adding a higher dose for Part C? If I'm understanding correctly. If so, why are you doing that? Yeah, we're not adding a higher dose. In Part C, we have two different chemotherapy regimens involved, modified FOLFOX6, which is more commonly used in the United States, and capecitabine and oxaliplatin, as we used in Part A. Those chemotherapy combinations are given on different schedules, and so we are looking to match the DKN-01 dosing schedule to the times when patients would otherwise be coming in, and to the as close as possible to the tislelizumab combination. You know, instead of giving DKN-01 on days one and 15 at 300 milligrams, you know, we've increased that if it's a three-week cycle to 600 milligrams with an extra kinda dose in cycle one. You know, as you remember, we saw that there were patients where, particularly with DKK1 high disease, more aggressive biology didn't even get to day 15, getting that extra drug to them early, we think, could be helpful. Then, you know, it's 400 milligrams every other week. Again, looking to try to mirror the PK/PD profile with the different schedule matching the chemotherapy. It's not intended other than in the initial cycle to drive additional dose. It's meant to be more convenient for patients and something that we think will continue to drive attractive safety and efficacy profile. Okay. Thank you very much for the questions. Thank you. We are showing no further questions. Thank you again for dialing into today's call. Have a good day.