Today, the Boundless Bio management team will provide an update on our business, including portfolio prioritization decisions, the streamlining of our operations, and revised financial runway guidance. I am joined on today's call by Chief Medical Officer Bob Doebele and Chief Scientific Officer Chris Hassig. Before we begin, please note that we will be making forward-looking statements concerning our future strategy, plans, expectations, and performance. Actual results may differ materially from those implied by these forward-looking statements as a result of risks and uncertainties associated with our business. These forward-looking statements are qualified by the cautionary statements contained in today's presentation and in our filings with the SEC. This call contains time-sensitive information that is accurate only as of the date of this live broadcast. We undertake no obligations to revise or update any forward-looking statements to reflect events or circumstances after the date of this call. On Friday, we issued a press release announcing important updates to our business. Today, my team will provide more color on each of those decisions. In a continuous effort to maximize value for patients and shareholders, we have prioritized our portfolio as follows. We intend to discontinue all current arms of the BBI-355 POTENTIATE clinical trial, which includes the monotherapy arm evaluating BBI-355 as a single agent in the gynecological tumor setting and the arms evaluating BBI-355 in combination with an EGFR inhibitor, FGFR inhibitor, or CDK4/6 inhibitor. This decision is based on both clinical observations and market considerations. Bob will provide more detail in a moment. Instead, we plan to implement a new arm of the POTENTIATE clinical trial to evaluate BBI-355 in combination with BBI-825 in patients with oncogene amplifications. Chris will explain the scientific base for this pursuit, including the potential synergies of these novel therapies, as well as the potential for complementary safety and other clinical characteristics. We have declared a development candidate, BBI-940, for our novel kinesin oral degrader program, and we remain on track to file an IND in the first half of 2026. Chris will share key highlights from this exciting program, which we believe to be only in class. In alignment with our focused development efforts, we have streamlined our operations, reducing our workforce by approximately 20 positions, which represents about one-third of our staff. We expect these changes to extend our cash runway into the first half of 2028. Now, please allow us to provide some detail around each of these decisions. I will start with a brief background on how we have assembled our portfolio of therapeutic candidates to date. As a reminder, Boundless Bio was formed to try to improve outcomes for patients with oncogene-amplified cancers. These types of tumors, in contrast to those with gene fusions or point mutations, have proven refractory to traditional drug mechanisms and standards of care, leading to poor outcomes, including worse survival. Since we established operations six years ago, we have focused our research on the rapidly emerging area of cancer biology known as extrachromosomal DNA, or ecDNA, which are a key enabler of oncogene amplification. To this end, we built and deployed our proprietary Spyglass platform to interrogate ecDNA biology and identify new or underappreciated targets that may be synthetically lethal in oncogene-amplified tumors. Spyglass has thus far revealed several distinct nodes of ecDNA biology, resulting in three druggable targets, each of which may be synthetically lethal in certain oncogene-amplified cancer settings. These nodes are replication stress, which is a key feature and vulnerability of oncogene-amplified tumors, including those with ecDNA. Consequently, we identified CHK1, cell's master regulator of the DNA damage response pathway to replication stress, as a potential target with particular sensitivity in oncogene-amplified cancer. This led to our discovery and development of a potent selective oral CHK1 inhibitor, BBI-355. The second node is DNA assembly and repair, which is a key feature and vulnerability of oncogene-amplified tumors, including those with ecDNA. We identified RNR as a potential target with particular sensitivity in certain oncogene-amplified tumors. RNR is the rate-limiting enzyme responsible for production of dNTPs required for DNA assembly via the de novo pathway, which is a distinctive dependency of cancer cells. Our RNR discovery effort led to the development of a selective oral RNR dimerization inhibitor, BBI-825. The third node is DNA segregation, including ecDNA segregation, which can also be a key feature and vulnerability of certain oncogene-amplified tumors. We identified a novel kinesin, which is considered nonessential in healthy cells but essential in a subset of cancer settings, as a potential novel cancer target. This led to our discovery and development of a potent oral kinesin degrader, BBI-940, which we are excited to introduce to you today. I will now hand over to first Bob, then Chris, to discuss our learnings and path forward for each of these internally discovered and wholly owned programs. Thank you, Zach. I will first provide an update on BBI-355, our potent selective oral CHK1 inhibitor. As background, I will remind you that BBI-355 is being evaluated in the first in human phase one two POTENTIATE study with the objective to understand safety, tolerability, PK, and preliminary anti-tumor activity as a single agent and in combination with selected targeted therapies against specific oncogene amplifications. The design of the POTENTIATE study is depicted here, including the single agent part one component and the combination arms in parts two and three. Until now, we have been conducting part one single-agent t dose escalation in cancer patients with any oncogene amplifications, part one single-agent dose expansion in patients with ovarian or endometrial cancer with oncogene amplifications, part two module one dose escalation in combination with the EGFR inhibitor, Erlotinib, in cancer patients with EGFR amplifications, and part two module two dose escalation in combination with the FGFR inhibitor, Futibatinib, in cancer patients with FGFR amplifications. We have not yet initiated part three for any cohort, nor part two module three in patients with CDK4/6 amplifications. What we've learned from the clinical experience with BBI-355 is the following. BBI-355 is a potent orally bioavailable CHK1 inhibitor with dose -proportional increase in PK exposure and with evidence of CHK1 target engagement in both skin and serial tumor biopsies. The only notable toxicity of BBI-355 observed to date has been hematologic toxicity, which is an on-target class effect and is ultimately dose limiting. BBI-355 has demonstrated evidence of antitumor activity both in part one and in the part two combination setting. The dose -escalation schema depicted on this slide summarizes the doses and regimens of 355 we have tested to date, both as a single agent and in the combination setting, as well as which dose levels were tolerated and which were not. BBI-355 as a single -agent was well tolerated up to 60 mg every other day or Q2D. In a two days on, five days off regimen, it is well tolerated at 80 mg. Evaluation of a three days on, 11 days off dosing regimen is currently ongoing at 80 mg. In combination, 40 mg of BBI-355 Q2D is well tolerated with either 150 mg Erlotinib or 20 mg Futibatinib. However, 60 mg of BBI-355 Q2D exceeds the MTD when dosed with 150 mg Erlotinib or 20 mg Futibatinib. All dose limiting toxicities of BBI-355 have been neutropenia and/or thrombocytopenia, and nearly all grade three or above drug-related toxicity was hematologic in nature. What we've concluded from our clinical experience with BBI-355 to date is that it, like prior CHK1 and 2 inhibitors, has a narrow therapeutic index due to predicted on-target hematologic toxicity near or at the doses and exposures associated with activity. We had hypothesized based on preclinical data that combination with certain targeted therapies, for example, EGFR or FGFR inhibitors, could elicit heightened tumor sensitivity at doses and exposures that might be well tolerated. However, despite a lack of overlapping toxicities between BBI-355 and the safety profiles described in the labels of the EGFR inhibitor Erlotinib or the FGFR inhibitor Futibatinib, the combinations were not well tolerated at the dose and exposure level, specifically 60 mg Q2D of BBI-355, that we believe is the minimum dose required for robust, sustained anti-tumor activity with these specific combination regimens. After thorough dose and regimen exploration, our overarching conclusion is that BBI-355, at least when administered Q2D, has a narrow therapeutic index due to on-target pharmacology. We do not believe the narrow therapeutic index is easily solvable with the approaches we have clinically tested to date, which, when combined with current market considerations, serves as a deterrent to further clinical development in these settings at this time. Therefore, we have decided not to advance the part one single agent expansion or the part three expansion in combination with the aforementioned targeted therapies. Based on what we've learned from the clinical experience of BBI-355, we do think that there are alternative approaches that could harness its potent selective CHK1 inhibition and expand its therapeutic index. Chris will touch on that in a moment. Before we get to that discussion, and because it is highly pertinent, let me first provide you with a bit more detail on the status of BBI-825, our selective oral RNR inhibitor. BBI-825 entered the clinic in our first in human phase one two Star Map study in 2024 with the objective to understand safety, tolerability, PK, and preliminary anti-tumor activity as a single agent in all comer cancer patients and in combination with select MAPK targeted therapies that can lead to amplification-mediated resistance in colorectal cancer. Last December, we made the decision not to further advance BBI-825 in the Star Map study, but I would like to walk through what we learned from the clinical experience with BBI-825 and why it's important to our path forward. BBI-825 is an orally bioavailable compound with rapid absorption and dose proportional increases in PK exposure on day one of dosing, which is depicted in the first PK graph. However, as you can see in the PK graph on the right, there is reduced exposure at steady state on day 15 of dosing, particularly at the higher dose levels tested. We believe the decline in exposure from day one to day 15 is due to CYP induction resulting in increased metabolism of BBI-825 with continuous daily BID dosing. BBI-825 has been well tolerated to date through four dose levels and has not established a maximum tolerated dose. We did not advance BBI-825 into the cohorts evaluated in combination with MAP kinase-directed therapies in this study because we did not feel we were attaining sufficient steady state exposure for that treatment setting. At the time of ceasing enrollment in Star Map, BBI-825 had cleared the 200 mg, 400 mg, and 800 mg BID dose cohorts and was enrolling at 1200 mg BID without DLTs at that level. The overarching conclusion from this study is that BBI-825 administered BID daily leads to CYP induction that limits steady state exposure at a level below what is predicted to be required for anti-tumor activity in the MAP kinase resistance setting. The implications of the two clinical program summaries I provided today are, first, that BBI-355's development along our original plan is limited by a narrow therapeutic index when administered Q2D as a single agent or in combination with certain targeted therapies, and second, that BBI-825's development along its original plan is limited by CYP induction when administered BID on a daily basis. I will now hand over to Chris to walk through an intersection of these two findings and why we think the limitations of each individual agent may be offset when administered together, which provides a data-driven and highly differentiated development path forward. Thank you, Bob. While Bob just summarized the challenges of independently developing either BBI-355 or BBI-825, we believe there is compelling scientific rationale that supports developing them as a combination. The fundamental principle is illustrated here, wherein tumor cells addicted to the de novo metabolic pathway for DNA synthesis experience significant imbalance of their dNTP pools when RNR is inhibited. This results in replication stress and activation of CHK1 to resolve the problem. By simultaneously inactivating CHK1, like with the CHK1 inhibitor BBI-355, the tumor cells are forced through the cell cycle into replication and mitotic catastrophe. The oncology field has previously established that combining CHK1 inhibitors with non-selective RNR inhibitors, such as the nucleoside analog gemcitabine, can lead to synergistic anti-tumor activity in vitro and in vivo. An example of preclinical synergy is shown in the xenograft on the bottom right of this slide. Importantly, this synergy has also been observed in clinical trials, as evidenced on the slide by the combination of two distinct CHK1 inhibitors, SRA737 and GDC0575, with subtherapeutic doses of the non-selective RNR inhibitor gemcitabine, leading to multiple confirmed responses across several tumor types, whereas neither CHK1 inhibitor had activity alone. The historical challenge with combining CHK1 inhibitors with non-selective RNR inhibitors was that the synergistic activity was not limited to cancer cells and has also had synergistic impact on healthy cells such as those in the bone marrow. Despite greater anti-tumor activity, investigators reported substantially higher grade three and above hematologic and other toxicities in both studies. Thus, there was no improvement of the therapeutic index. The increased toxicities associated with this combination are, in part, a consequence of the fact that gemcitabine, as a nucleoside analog, is structurally related to DNA precursors and is actively transported into hematological cells by nucleoside transporters as part of the DNTP salvage pathway. In contrast to gemcitabine, BBI-825 is distinct in that it is a protein-protein interaction inhibitor that is structurally unrelated to nucleosides and is instead a highly selective RNR inhibitor, thereby avoiding collateral damage to normal tissues that are more dependent on the salvage pathway for their DNA synthesis needs. Consistent with this differentiated mechanism, we've observed that gemcitabine, unlike BBI-825, is actually more toxic to normal proliferating myeloid cells than to tumor cells in vitro. Empirically, BBI-825 has not demonstrated evidence of hematological toxicity to date, either in animal toxicology studies or in the clinic. Thus, based on the cancer-directed pharmacology of 825 and its lack of hematologic toxicity, we hypothesized that we may be able to combine BBI-825 with BBI-355 and induce synergistic cytotoxicity preferentially in cancer cells. To test this hypothesis, we first assessed synergy of the two agents in a panel of cancer cell lines. As seen from the data on this slide, BBI-825 potentiates the cytotoxicity of BBI-355, shifting its potency by approximately tenfold. If we apply BLISS synergy analysis, a standard measure of synergy indicating a combination effect is greater than the sum of each independent agent, the BLISS scores show that BBI-825 and BBI-355 are highly synergistic across cancer cell lines, even more so than combining BBI-355 with gemcitabine as an established positive control. The next piece of the equation was to assess whether the two agents are tolerated as a combination in vivo, specifically in the hematologic compartment, since heme tox, particularly neutropenia, is the known dose limiting toxicity for BBI-355. This was a critical step to determine whether we may be expanding the therapeutic window of BBI-355 versus increasing both anti-tumor and bone marrow toxicity to the same extent. Thus, we conducted a pilot hematologic toxicity study in dogs, an established model predicting human hematologic toxicity. Importantly, in this pilot study, all dogs tolerated the combination even with a twice-weekly dosing regimen. There was minimal evidence of combinatorial hematologic toxicity in the arms evaluating the combination of BBI-355 with BBI-825, even at doses and exposures associated with potent cytotoxicity in cancer cells in vitro. This was in stark contrast to the positive control arm combining gemcitabine with BBI-355, which demonstrated substantial toxicity, as we predicted based on gemcitabine's non-selective nature and clinical precedent. The final preclinical step was to establish that exposure levels of the combination agents that were well tolerated in the dog toxicology study could lead to synergistic anti-tumor activity in vivo in cancer models. Indeed, that is what we observed. When combined, doses of BBI-355 and BBI-825 that have minimal activity as single agents induce synergistic anti-tumor activity, including regression, in mouse xenograft models. Importantly, these are at drug exposures that were below those that were well tolerated in the pilot dog toxicology study. Notably, the dosing intensity of both agents was weekly, or QW, which stands in contrast to the Q2D dosing of BBI-355 that was not tolerated at higher dose levels in the clinic, and the BID dosing of BBI-825 that led to CYP-induced metabolism. I'll now hand it back to Zach. The last point that Chris made is critical because weekly dosing could address the fundamental shortcoming observed with each compound as a single agent in the clinic. We anticipate weekly dosing of BBI-825 will not have the CYP induction liability associated with daily BID dosing in humans. CYP induction occurs slowly, and with weekly dosing, it is expected to return to baseline within seven days. We also anticipate weekly dosing of BBI-355 will be better tolerated in humans than the Q2D regimen due to significantly less overall dose intensity and a six-day period of time for the hematological compartment to recover between doses. Thus, we believe there is encouraging mechanistic preclinical and clinical precedent rationale to clinically evaluate a combination of the selective CHK1 inhibitor BBI-355 with the selective RNR inhibitor BBI-825 using discontinuous dosing, with the belief that this specific combination could overcome the shortcomings of either agent alone, the limitations on prior attempts to combine CHK1 inhibitors with non-selective RNR inhibitors, and provide synergistic anti-tumor activity at tolerated doses. It is our intention to initiate clinical development of the 355825 combo, and only this combo, in patients with oncogene amplified tumors within the POTENTIATE study in 2025. We are confident that the proof-of-concept of this novel-novel comboo will read out within the timeframe of our existing cash runway, which I will speak to at the end of this call. Importantly, this clinical approach leverages our understanding of replication stress biology, the CHK1 and RNR targets, and the initial clinical characteristics of BBI-355 and BBI-825. Should this approach work clinically, we believe we are currently the only entity that possesses both a proprietary selective CHK1 inhibitor and a proprietary selective RNR inhibitor. The 355825 combo is one of the clinical shots on goal that Boundless is eager to pursue from this point forward. The second clinical shot on goal that we look forward to taking will be our Kinesin oral degrader. I will hand back to Chris to further describe this innovative program. Thank you, Zach. I'm pleased to provide an update on our Kinesin program as our progress to a development candidate represents a bold effort by our discovery team, and we believe they've come up with something really unique within our industry. From our surveillance of the medical, scientific, and patent literature, we believe we are the only entity developing drugs against this target. The Kinesin we are pursuing is involved in congregation of chromosomes during mitosis. However, it is considered nonessential in healthy cells. Notably, overexpression of this Kinesin is correlated with poor patient prognosis and reduced survival in multiple cancers. Inactivation of this Kinesin results in delayed mitosis and higher rates of lagging chromosomes, and our research suggests it may be essential for proper ecDNA segregation during cell division. As we dug into this Kinesin, we observed that when we genetically knocked it down, it resulted in lagging ecDNA during mitosis, aggregated ecDNA, and significantly lower overall ecDNA counts. This effect, in turn, led to significantly reduced proliferation of oncogene amplified cancer cell lines. That phenomenon was observed both as a single agent and synergistically in combination with the targeted therapy, such as the FGFR inhibitor shown here. Notably, the effect was cytotoxic, not just cytostatic, in gene-amplified cancer cell lines, as seen on the right. The more we learned about this Kinesin and its role in oncogene amplified cancer cells, the stronger our conviction grew to try and drug it. Because it was novel, and to our knowledge, there have been no prior drug efforts against it, there was no chemical starting point. We screened over a million compounds across multiple orthogonal screening strategies, including AI-enabled screening, to identify a single-hit scaffold upon which we performed extensive medicinal chemistry and ultimately generated highly potent degraders that demonstrate favorable pharmacokinetics and substantial oral bioavailability across multiple species. Through that effort, our team has discovered BBI-940, an oral protact degrader molecule that exceeds our target product profile. You can see that some key features of BBI-940 are: it is extremely potent, it achieves good maximal target degradation, and it is orally bioavailable. We have tested our Kinesin degrader lead compounds across a host of in vitro and in vivo cancer models and have identified multiple solid tumor indications where a meaningful subset is highly sensitive to degradation via this mechanism. We will not discuss our lead indications at this time, but they represent high unmet need solid tumor indications, including from the Big Four. We show here a representative example of anti-tumor activity in an ecDNA-positive triple-negative breast cancer mouse xenograft model. As you can see, BBI-940, as a single agent, achieved sustained regressions at both dose levels tested: 10 mg per kg and 30 mg per kg. The compound was generally well tolerated with less than 10% body weight loss in this model and even less so in other xenograft models not depicted here. Consistent with the anti-tumor activity seen on the prior slide, you can see here that we achieved good plasma and tumor levels with oral administration of our kinesin degraders, and that led to robust sustained degradation of the target, as revealed by Western blot. All of these data are supportive of what we believe is a favorable profile for our kinesin oral degraders and underlie our declaration of BBI-940 as a development candidate. With this brief overview of the program, I will now hand it back over to Zach. Thank you, Chris. Indeed, that was just a taste of the program. Behind the overview Chris provided today, we have substantially more mechanistic in vitro, in vivo, and preclinical safety data that we look forward to sharing at a later date. For competitive reasons, we are electing not to disclose additional potentially enabling information about our development strategy at this time. We think this is a truly unique first-in-class target, and we are eager to maximize our head start relative to the rest of the field. We have initiated IND-enabling work for BBI-940 and reaffirm our timeline to submit our IND application in the first half of 2026. I will now provide two updates on our business operations. In consideration of the portfolio prioritization decisions we have described today, we have made the difficult but necessary decision to streamline our organization, including a reduction in force of approximately 20 employees representing about one-third of our staff. With these changes, alongside our new focused pipeline development efforts, we now project cash runway into the first half of 2028 through the expected initial clinical readouts for both the 355/825 combo and for BBI-940. I want to conclude with two comments. I first want to extend a sincere and heartfelt thank you to the dedicated Boundless Bio employees who contributed to our development to this point and who are now moving on as a result of these portfolio decisions. We would not be where we are without their invaluable contributions, and we wish them well in their future endeavors. Second, I will share my observation on the state of the biotechnology industry. In this current environment where, one, it is a challenge to secure funding for scientific innovation from both government and from investors, and two, there is a hyper-proliferation of competitor compounds against known targets, making it more difficult than ever to establish best-in-class differentiation. I believe that going forward, the single most valuable assets with the highest scarcity premium will be first-in-class drugs against innovative biology targets with competitive moats due to significant head start time advantages and/or unique biology insight. We believe that is what Boundless Bio has with our two prioritized development opportunities presented today. Our team is committed to rapidly and efficiently prosecuting these opportunities in a focused way to important clinical readout milestones. This concludes our prepared remarks, and we will now open to the operator to take questions. Thank you. If you would like to ask a question, please press star one one on your telephone. You will then hear an automated message advising your hand is raised. If you would like to remove yourself, please press star one one again. We also ask that you wait for your name and company to be announced before proceeding with your question. One moment while we compile the Q&A roster. The first question for today will come from the line of Andrew Berens of Leerink Partners. Your line is open. Hi, thanks. Zach, you gave some color on this, but how does 355 get metabolized? Can you just go through the dosing scheme that you're planning to use to minimize the PK issues you saw with the CHK1? Where would that put the drug levels, you think, versus the minimally effective doses? Can you give us some idea of how you could demonstrate contributional parts to the regulatory agencies? The last one, I'm assuming we're not going to get validation of ecDNA diagnostic this year clinically. When will we see prospective data using ecDNA enrichment? Thanks. Thanks, Andy. Yeah, multifactorial question there. Let me do my best along with the team to cover each piece. One thing to clarify, I think you started out by asking about PK. It's 825 that has the CYP induction that leads to induced metabolism and therefore kind of caps the exposure. That was with daily BID dosing. What we're anticipating for the combo is weekly dosing of both agents. That should alleviate the CYP induction issue. Also, what's limiting for 355 is the toxicity ultimately with the Q2D dosing. We think the weekly dosing should be able to help alleviate that as well. The beauty of that is it could address the dose-limiting challenges for both agents. Certainly preclinically, due to the preferential cancer synergy, that weekly dosing is sufficient for profound activity both in vitro and in vivo. Those are at dose levels that were well tolerated and that we predict we can get to in humans. In terms of contribution of components, what's nice is that we've already tested both agents as single agents. Anything we observe when combined that's differentiated from what we saw as single agents, that will be easy to attribute to the combo effect. There's a pretty substantial amount of data clinically on both programs to help inform that. Your final comment was about ECHO. We continue to obtain ECHO status or ecDNA positivity status on all patients enrolled and will going forward. We will be able to see whether an ecDNA positivity or negativity seems to correlate or contribute to any clinical activity observed. That will be a retrospective analysis. It will not be a condition of enrollment. The condition of enrollment will be amplification. If at some point in time we determine that it is the ecDNA status that matters more than simply amplification status, we could always make it a prospective enrollment if that is what the data informs. Okay. Thank you. You're welcome. Thank you. One moment for the next question. Our next question will be coming from the line of Michael Schmidt of Guggenheim. Your line is open. Hey, guys. Good morning. Yeah, maybe just going back to 355, I mean, based on your obviously understanding the sort of on-target tox issues at higher doses, but I mean, it sounds like the 60 mg Q2D dose single agent was perhaps one that was reasonably well tolerated. So any learnings coming out of your continued single agent evaluation that you've done so far in terms of just validating the mechanism or the therapeutic concept behind the molecule? Yeah, I think the key learning is that it is a potent CHK1 inhibitor, and therefore you see what you'd expect with potent CHK1 inhibition, meaning that as you get to the higher doses, we see the evidence of pharmacology through a PD marker. As we stated, we have seen signs of clinical activity, including as measured by RECIST. You also get the on-target pharmacology-induced toxicology, which is the neutropenia and thrombocytopenia. Those are all somewhat inextricable, meaning when you're getting good CHK1 inhibition, you get kind of everything I just described. That is what makes it for a narrow therapeutic index and a challenge at least to develop as an oral agent, as a single agent with continuous dosing. The beauty of the combo is that it enables this intermittent dosing that does not require such frequent inhibition of the target. Understood. On 825, just going back to the idea to circumvent the CYP autoinduction at weekly dosing, I guess when I look at the day one, cycle one chart, I mean, the dose response between 400 and 800 seems very narrow, and then there is a big step up to 1200. Is there something else going on even at day one, and is perhaps 1200 mg sort of a target dose you would consider for the weekly dosing? Yeah, Bob will comment on your correcting your observation that there was less proportionality from 400 to 800, but there's a good reason. Go ahead. Yeah. Michael, thanks for the question. The 800 milligram dose was done in a DDI study with Midazolam, and they impact the exposure that we saw there. That was what was unique about the 800 milligram cohort, and that was done specifically out of concern for the potential for drug-drug interaction. Understood. And then just in terms of possible target indications for this combination, would that be a similar setting in terms of the gene amplified tumors, or are there any particular indications or patients that would benefit from that combination? Yeah, no, great question. We will be selecting on the basis of amplification that basal replication stress associated with high copy amplification, including ecDNA, is a driver of sensitivity. Beyond that, in terms of the indication space that we'll explore, as mentioned from some of the clinical studies previously using low-dose gemcitabine as a combination, there were responses across a range of different solid tumor indications. Initially, we'll be exploring that, and we haven't selected any final indications for expansion at this time. All right. Thank you. You're welcome. Thank you. One moment for our next question. Our next question will come from the line of Boris Peaker of Titan Partners. Your line is open. Great. Thanks for taking my question. First, on the 825/355 combo, so your dog tox that you reported was at five days, and I know that it was reasonably well tolerated. I'm just curious, how many days does it take to reach peak heme tox for 355? I guess the question is whether the combo is really well tolerated or maybe the combo delays the heme tox that might be more apparent later down the line. Yeah, no, great question. The totality of this study was a 14-day study. The peak decline for 355 and/or 825 with a combination of gemcitabine, you saw by the reported days. That effect by CHK1 is actually quite rapid. You can detect that drop by between day five and day eight in both of the arms that we tested. There is complete recovery of the heme compartment by day 14, even with the twice-weekly dosing strategy that was deployed for the BBI-825 and BBI-355 combination. I want to note that with the low-dose gemcitabine combination, that was a single administration during that two-week period, but they also recovered by end of the two-week cycle, at least the animals that survived. Gotcha. Maybe real quick on 940, when will we know the indication that you're pursuing, just kind of ballpark of the timeline? I guess maybe broadly, what can we apply from results of other degraders that we've seen to inform your clinical development? Yeah. In terms of indication, we'll probably disclose more as we get into the clinic, as we put a protocol up or a description on clinicaltrials.gov. We just don't really see any reason to reveal that just yet. I guess stay tuned. I'll have Chris answer the second question about what we're seeing in our profile versus other agents. Yeah, no, it's a good question. Just generally speaking, I think each degrader program is unique, and so there's not necessarily any immediate parallels. The key things that are required for this approach to work is getting effective degradation of the target with sufficient coverage that allows for the efficacy. The profile that we showed you on the slides really demonstrates that across species, we have really good oral bioavailability and exposure and target coverage that maintains suppression of the target over the period of dosing with the frequency that we're deploying. There are no other degraders or drugs against this kinesin, so there's not necessarily a perfect parallel. Certainly wouldn't draw analogies necessarily with, for example, the androgen receptor or SARD molecules that have been described by others. Great. Thanks very much for taking my questions. You're welcome. Thank you. I'm showing no more questions in the queue. I would now like to turn the call back over to Zach for closing remarks. Please go ahead. Great. Thank you, Lisa. We appreciate everyone's time today and your support of our mission. With a clear strategy, strong science, and an extended runway, we believe Boundless Bio is well-positioned to drive value through focused innovation and disciplined execution. This concludes our call. Thank you all for participating in today's conference call. You may now disconnect.