Welcome to the Crescent Biopharma Conference Call. All participants will be in a listen-only mode. Later, we will conduct a question-and-answer session. I would now like to turn the conference over to Amy Reilly. Amy, you may begin. Thank you for joining us for our call today to discuss the partnership Crescent announced with Kelun-Biotech, as well as a comprehensive review of our pipeline. Before we get started, I'd like to remind everyone that we will be making forward-looking statements today that are subject to the safe harbor protections provided under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from these forward-looking statements as a result of various important factors, including those discussed in the risk factors section of our most recent Form 10-Q. These statements represent Crescent's view as of today's date, and we disclaim any obligation to update these statements except as required by law. Joining me on today's call is Josh Brumm, our CEO, Jonathan McNeill, our President and Chief Operating Officer, Ellie Im, our Chief Medical Officer, and Jan Pinkas, our Chief Scientific Officer. Following prepared remarks, we'll open up for questions, and with that, I'll turn things over to Josh. Thanks, Amy, and thanks everyone for tuning in today. A number of us on the leadership team joined Crescent earlier this year because of the tremendous opportunity in the dynamic IO and ADC space to make a difference in the lives of people living with cancer. For months, we've been saying that we look forward to the right time to provide more details on our programs and plans, and with the transformational transaction we announced with Kelun, today is that time. I'd like to start by saying hello and good evening to our new partners in China and thank them for their kindness, generosity, and partnership as we work to bring our two companies together in this unique and strategic collaboration. Dr. Ge, Richard, Xiaoping, and Su, we look forward to celebrating with you at JPMorgan in a few short weeks. I also want to thank our Crescent family for the incredible persistence, determination, commitment, and long-hour sacrifice to land multiple planes this week right on schedule, with the partnership, financing, board meeting, and other key initiatives all hitting this week. Finally, I want to thank the Crescent board for your unwavering support to the CBIO team and the vision we all share for this special company. Before we get into the specifics of today's announcements, I want to start with the founding and mission of Crescent. We were founded with assets that originated from Paragon Therapeutics, an antibody discovery engine established by pharma. We became a public company via a reverse merger in June of this year, and we are focused on delivering the next wave of transformative therapies to bring a brighter future for people living with cancer. We have a bold vision to build the next leading biotechnology company. We are executing across two distinct strategies to build our portfolio to achieve this vision. First, it starts with CR001, our PD-1 VEGF bispecific that has the potential to replace Keytruda as the best-in-class foundational IO backbone. Second, building a robust portfolio of best-in-class ADCs. Importantly, as we execute on these two strategies, we can combine CR001 and our ADC therapies to create best-in-class synergistic combinations to transform care for multiple types of cancer. Over the past six, seven months, we've been working quietly to put the meat on the bone for this strategy, and we are excited to share four meaningful updates with you today. First, we will go deep into CR001 and share details on our phase 1/2 study design and our plan to generate data in both second-line plus and first-line patients starting in Q1 2027. Second, we will review our ADC portfolio, including CR002, which is a PD-L1 topo ADC and on track to enter the clinic in mid-2026. Third, we will cover the partnership we announced today with Kelun-Biotech, which is transformational for Crescent, includes both CR001 and CR003, also known as SKB105, and integrin beta-6 topo ADC. This partnership accelerates and expands our strategy of establishing a leadership position in the IO and ADC combination therapies. And to use a sports analogy, we are scaling to where the puck is going in our space. And now, through this collaboration, we have more opportunities to realize our vision. Of course, the final piece of today's update is the $185 million capital raise with participation from leading healthcare investors. This puts us into a strong position as we head into our first set of clinical milestones in Q1 2027. Now, I want to turn things over to Jonathan to review the key elements of our partnership with Kelun-Biotech. Thanks, Josh. Both Crescent and Kelun-Biotech share a commitment to advancing a global pipeline of synergistic combination therapies. We are so fortunate to be partnering with Kelun-Biotech, a leading Chinese biotech company with commercially approved ADCs, including sac-TMT, which is the focus of a multi-billion dollar collaboration with Merck, who's running 15 phase three trials with its assets in multiple tumor types. Kelun-Biotech is advancing 10-plus clinical stage assets and has end-to-end ADC capabilities in the Chinese market. Kelun-Biotech sees the promise of CR001 to be a foundational best-in-class IO backbone to combine with a broad ADC pipeline. They want an asset that replicates the cooperative pharmacology of Ivonescimab and value the intentional design of CR001. With this partnership, we can mutually advance Crescent's CR001 and Kelun-Biotech's SKB105 globally. Crescent will advance CR001 in the U.S. and Europe, with Kelun-Biotech leading both monotherapy and combination studies in China. Kelun-Biotech will advance SKB105 in Greater China, with Crescent leading development in the rest of the world. Both companies are committed to pursuing CR001 and ADC combination studies and sharing clinical data to maximize the value of our respective pipelines. Kelun-Biotech has the opportunity to evaluate CR001 in combination with their full suite of ADCs. Importantly for Crescent, this partnership accelerates and expands our efforts across our pipeline. It enables parallel generation of clinical data for CR001 in both Western and Chinese patients. We won't have to manage through the translatability across populations because we will have the data. It also increases Crescent's 2026 clinical pipeline to three programs with the addition of CR003, SKB105, and broadens our ADC pipeline focusing on the established targets of both PD-1 and integrin beta-6. Importantly, it also both accelerates and expands the scope of our CR001 and ADC combination data, with the opportunity to combine CR001 with ADCs from both Crescent's and Kelun's portfolios. Taken together, this enables multiple clinical data readouts by the end of 2027 across IO, ADCs, and combination therapies. This illustrates the breadth of combination data that we plan to generate with multiple ADCs across tumor types. We plan to combine CR001 with CR002, our internally developed PD-L1 ADC. The Kelun partnership enables a rapid generation of combo data with CR003 and other ADCs in Kelun's pipeline. Importantly, this clinical data will inform our strategy for CR001 as an IO backbone for many possible other combination studies, combining CR001 with best-in-class ADCs from both internal and external sources. Now, I'll turn it back over to Josh. Thanks, Jonathan. We are truly in an incredible position with multiple ways to win in delivering for patients in this $100 million plus market opportunity. We are advancing a matrix portfolio where we have the opportunities across IO monotherapy, ADC, and standard of care combinations in our selected therapeutic areas of interest. That includes thoracic, GI, gynecologic, and head and neck cancers. As we enter the clinic in multiple programs, we will follow our data and the competitive landscape to guide us as we choose specific indications to develop. I'd also like to take a moment to consider the assets we have in our pipeline to date, noting again that we will be aggressive about adding additional best-in-class ADC assets to combine with CR001. And if you reflect on all of the indications where we could offer best-in-class synergistic combinations, you start to get a sense of the scale of this opportunity and the real value of our pipeline and strategy. Here are two examples of how we could leverage the power of our matrix portfolio. Everyone understands that lung is the largest market, and we've been asked if we think the lung space is open given the advances in bispecifics, to which we unequivocally have said yes. We believe lung is wide open. There remains a substantial opportunity to improve outcomes with new therapies. With the PD-1 VEGF mechanism generating promising data in lung cancer, we have a path to build on this monotherapy data and reach early-line patients with best-in-class combinations of CR001 with our differentiated topo ADCs. And similarly, with head and neck, given the validation of the PD-1 mechanism in this indication and high PD-1 and integrin beta-6 expression in these tumors, this is another significant market where we believe we can be best-in-class with combination therapy and capture significant market share. So as we sit here today, we have generated a very robust pipeline of next-generation therapies that we believe have the potential to address a range of solid tumors. Importantly, we plan to initiate four clinical trials in 2026. This starts with CR001. We plan to be in the clinic in dosing patients with our PD-1 VEGF bispecific in the US and Europe in Q1 of 2026. CR002, our PD-L1 topo ADC, is slated to be in the clinic in the second half of 2026. CR003, also known as SKB105, our integrin beta-6 topo ADC, is also on track to generate and initiate a phase one trial in early 2026 through our partnership with Kelun-Biotech in China, same timeline as CR001. The initiation of our first combo study with CR001 and an ADC is also expected in the second half of 2026 through our partnership with Kelun-Biotech. We have the opportunity to generate additional ADC candidates through our internal work with Paragon and through external partnerships like Kelun-Biotech. The pipeline leads to multiple meaningful data sets anticipated starting in early 2027 and throughout the year across our programs. This includes phase one initial monotherapy data from CR001, CR002, and CR003. We're being thoughtful about our study designs. For example, for CR001, we know that data from second-line plus patients can be challenging to interpret and compare. We will couple the second-line plus patient data with generating CR001 frontline data in parallel. We know generating frontline data early will be important to validate that we are replicating the clinical profile of Ivonescimab. We are also focused on delivering combination data with CR001 plus CR003 and an additional ADC by the end of 2027. Importantly, we anticipate cash runway into 2028, including all milestones from the Kelun partnership and those important clinical inflection points we just went through. Now, we want to review more specifics on the programs in our portfolio, and I'll first ask Ellie to talk about CR001. Thanks, Josh. I'm a medical oncologist by training, and I have worked across various different modalities, including bispecific antibodies and ADCs, so you can understand my excitement about Crescent's pipeline. Earlier in my career, while I was at Merck, I led a KEYNOTE-010 trial, which paved the way for the approval of Keytruda in second-line non-small cell lung cancer, and later at Tesaro, I led a clinical development for Jemperli, which was the first PD-1 inhibitor approved in first-line endometrial cancer, and today it's on track to be a $1 billion product. Having been part of the first big innovation in immuno-oncology, I've been looking forward to opportunities where we can further improve on the efficacy of PD-1 inhibitors. The Ivonescimab data, combined with the potential for ADCs and other combinations, presents a tremendous opportunity to transform the treatment landscape for people living with cancer. I think everyone is quite familiar with how PD-1, PD-1 therapies transformed oncology and led to the biggest blockbuster in the world in Keytruda. On the left, it's just one of the many dozens of successful phase three trials in this class where the addition of Keytruda to chemo significantly improved overall survival in first-line non-squamous non-small cell lung cancer. On the right, the global sales for the class, which surpassed $50 billion in 2024, with all entrants dominating the space, and blockbuster status was achieved for all of these within five years of launch. Given the success of this class, there were repeated efforts to create next-generation therapies, but preclinical and early clinical data failed to translate in larger trials until last year, as most people know, when HARMONi-2, a phase 3 trial for ivonescimab, nearly doubled the progression-free survival with an HR of 0.5 versus Keytruda. These data were remarkable and indicated that there's something synergistic about how ivonescimab engages these two targets so that it is different from prior trials, which co-administered approved PD-1 and VEGF therapeutics. This result generated tremendous excitement in the opportunity for next-generation immunotherapies, particularly trying to capitalize on the cooperative nature of PD-1 and VEGF. Since that initial study, there have been multiple readouts across ivonescimab studies, including the recent HARMONi-6 PFS and Harmony OS update that have been very encouraging and validating for the entire space. So what is it about ivonescimab that's led to compelling clinical results? We believe that it's the cooperativity that's differentiating. It combines two complementary and validated mechanisms in oncology via a blockade of PD-1 and VEGF. PD-1 checkpoint inhibition is aimed at restoring T cells' ability to recognize and destroy tumor cells, and blocking VEGF is intended for reducing blood supply to tumor cells and inhibiting tumor growth. Ivonescimab is a tetravalent antibody that binds to both targets, and with its unique structure, each molecule can bind to VEGF dimers, and each VEGF dimer can then bind to two ivonescimab molecules. This creates daisy chains of drugs, which lead to increased potency for PD-1 blockade. This cooperative binding mechanism may also drive targeting to the tumor microenvironment. When it came to designing CR001, the Crescent team considered changes to the ivonescimab design to develop an even better molecule. However, given preclinical models and early clinical data often do not translate in immuno-oncology, we believed introducing any new mechanistic approach can increase the risk. So our strategy was to create a new molecular entity and build to replicate ivonescimab pharmacology while still having freedom to operate and to create differentiation with the scFv. CR001 is intentionally designed precisely to match the ivonescimab profile. The backbone is Fc-silenced bevacizumab. Cooperative binding increases anti-VEGF activity in tumor microenvironment, reducing safety risks in healthy tissue. Our PD-1 scFv is designed to be the best possible anti-PD-1 epitope and binding domain, same as ivonescimab. Where we differ from ivonescimab is proprietary engineering to enable functional and stable scFv. We believe this has the potential to provide advantages from a stability and manufacturing perspective. Given the encouraging data and size of the opportunity, there are many entrants in this space, but not all PD-1 VEGF antibodies are created equal. Alternative constructs, such as those targeting PD-1, incorporating a VEGF trap, or utilizing other antibody formats, all these differences create risk and will require additional time and hundreds of patients to understand their clinical profile in randomized phase 3 studies. CR001 is one of the few programs intentionally designed to exhibit ivonescimab-like cooperative pharmacology. Crescent is also differentiated by our pipeline of ADCs, which provides opportunities to develop best-in-class synergistic combinations. We have done preclinical work where CR001 demonstrated cooperative pharmacology in vitro with increased binding to PD-1 in the presence of VEGF, resulting in the augmentation of the PD-1 and PD-1 signaling blockade and enhancing T cell activation, which was consistent with that of ivonescimab. These and other clinical data were shared last month at SITC 2025. While we replicated the cooperative pharmacology of ivonescimab, we incorporated proprietary engineering to the scFvs of CR001, which we believe has the potential for developing subcutaneous dosing down the line. Our composition of matter claims is based in part on this proprietary scFv engineering. We feel great about our IP position, and CR001 is a new molecular entity, and we have freedom to operate. With the intentional design of CR001 matching that profile of ivonescimab and the validating data in the field, there are numerous opportunities to transform the standard of care in various solid tumors. On the slide, you see the list of indications where anti-PD-1 or VEGF have been approved, and there are potentially additional indications we could pursue based on the cooperative pharmacology where existing PD-1 or anti-VEGF therapies have not been able to provide benefit. Now, moving on to our clinical development strategy, we are pursuing two parallel paths. First, there are multiple first-in-class opportunities with rapid path to the market by choosing the indications with a high likelihood of success on both PFS and OS and utilizing efficient development strategy with global trials. Outside of lung cancer, there are 40-plus indications where we could be first-in-class outside of China. Secondly, we can leverage following indications where clinical validation already exists. This is another tremendous opportunity. You don't need to look any further than the evolution of the PD-1 market. As I've seen in my experience with Keytruda and Jemperli, being a later entrant in this large IO market doesn't prevent a therapy from attaining blockbuster status, and it also highlights the importance of clinical development strategy and focused execution. Furthermore, we have opportunities to create best-in-class profile in combination with our ADCs. Today, we are excited to outline the prioritized indications and planned study design for our phase one monotherapy trial for CR001 for the first time. These three therapeutic areas support both our first-in-class and best follower approach, and they are thoracic, GI, and GU-onc. Within these areas, we plan to enrich for these eight tumor types that have clinical validation of PD-1 and/or VEGF inhibition with the opportunity to improve on standard of care with dual targeting. Our clinical development plan offers the potential for very early de-risking, which, of course, is not the norm in immuno-oncology. Usually, the initial phase 1 data gives an indication of activity and general safety, but when a mechanism or pharmacological profile is new, we really can't conclude much. Since we have reproduced the pharmacology of Ivonescimab with the CR001's intentional design, data from our phase 1 trial, including PK, PD, safety, and preliminary anti-tumor activity, will be de-risking and highly validating. We believe with positive data from phase 1 trial, we have the opportunity to accelerate CR001 development and efficiently move into registration-enabling studies of monotherapy and/or in combinations. This will put us in a very strong position in a competitive field. Now, moving on to our phase 1 trial design, which you can see is quite comprehensive. We anticipate dosing patients early next year. We have been engaging with investigators, including top academic centers, over the last several months, and there's tremendous enthusiasm to participate in our trial. Because most of the PD-1 VEGF bispecific clinicals have been conducted in China thus far, for most US and EU centers, this is their first opportunity to evaluate this new class in their clinical practice. The feedback has been enormously helpful and has enabled us to create very robust clinical trial design. We will do traditional dose escalation in a previously treated population, as all first-in-human trials would do. And in the backfill, we have the opportunity to enroll additional patients across eight tumor types to generate data in previously treated as well as first-line patients. Our dose optimization cohorts will be focused on enrolling first-line patients, and we know this is the data that will help us understand CR001's clinical profile in the landscape of other bispecifics, especially its efficacy and safety in frontline patients. While we are prioritizing these eight tumor types, it is important to note that the data we generate in the study, as well as the competitive landscape, will inform us when we choose the indications for our pivotal studies. In this way, we are maintaining maximum flexibility. We designed our phase 1/2 study with a focus on identifying the recommended phase 2 dose and indications for registration trials. Starting in first quarter 2027, we anticipate sharing meaningful data on CR001's clinical profile, including safety, PK, preliminary anti-tumor activity in multiple tumor types in second-line plus as well as in first-line patients. I want to point out that Crescent has the opportunity to generate some of the first Western patient data in this trial in several tumor types, and we expect to benefit from clinical data generated by our partners at Kelun as they evaluate CR001 in China. As Jonathan mentioned, a major focus of our strategy is developing best-in-class synergistic combinations. As you can see, we have plans to evaluate CR001 in combination studies with ADCs across different targets and in multiple tumor types. We will leverage our partnership with Kelun to evaluate CR003, their other ADCs, as well as our internal ADCs, including CR002. So in summary for CR001, because of its intentional design, cooperative pharmacology, and robust clinical development plan along with our ADC pipeline, we have the opportunity to rapidly generate significant value. And now I'll turn things over to Jan. Great. Thanks, Ellie. I'm thrilled to discuss Crescent's strategy to develop novel ADCs. I spent most of my biotech career in the discovery, development, and commercialization of antibody drug conjugates in oncology, including more than a decade at ImmunoGen, where I led non-clinical development of Elahere and all other programs in their pipeline. I joined Crescent during the summer, and in a short period of time, we've made tremendous progress on our own internal ADC programs. The Kelun Partnership adds an important dimension to our strategy to develop best-in-class ADCs. We have a comprehensive approach to ADC development that incorporates evaluation of targets, linkers, and payloads, and we have multiple ways to source them through our own internal development efforts, through our partner Paragon, and the right external partners such as renowned leaders in the ADC field like Kelun. We believe that CR002 and CR003 have the potential to be best-in-class topoisomerase inhibitor ADCs. Topo inhibitor payloads have consistently demonstrated superior efficacy and safety over microtubule inhibitor-based ADCs, and for the first time today, we're revealing the targets of these molecules: PD-L1 for CR002 and integrin beta-6 for CR003. These are well-validated targets with potential across a broad range of solid tumors. Our plan is to develop these as single agents, but also to pursue synergistic combination opportunities with CR001 as well as other standard of care agents. Here are some representative cross-trial comparisons that informed our decision to pursue topo-based ADCs, showing across numerous targets and indications that they deliver better safety and efficacy compared to microtubule-based antibody-drug conjugates. Before I go through our ADC programs in greater detail, I'll ask Ellie to review some of the recent clinical data from this year's ASCO and ESMO conferences supporting topo-based ADCs. Ellie? The promise of next-generation topo ADCs was really a big storyline coming out of ASCO and ESMO 2025 with some very exciting data in monotherapies and in combination. On the left, you see sac-TMT developed by our partner Kelun-Biotech, the first TROP2-directed ADC to significantly improve PFS and OS over standard of care in patients with EGFR-mutated non-small cell lung cancer. On the right, you see exciting data of TROP2 ADC in combination with immuno-oncology drug Keytruda. Trodelvy plus Keytruda resulted in a median PFS of 11.2 months versus 7.8 months when Keytruda was given in combination with chemotherapy. These data highlight the potential of topo ADCs to synergize with IO therapies and deliver best-in-class outcomes for patients. Here, you see favorable safety profiles from these trials. These data are really encouraging and reinforce the promise of next-generation ADCs and our strategy with the payload choice. Great. Thanks, Ellie. Now I'd like to review our CR002 program in greater detail. CR002 is a PD-L1 targeted ADC with a differentiated profile. PD-L1 is highly expressed on tumor cells and plays a role in suppressing T cell activation and function in the tumor microenvironment. PD-L1 expression is elevated in numerous solid tumors compared to normal tissues, making it an attractive ADC target. Our CR002 builds on clinical validation from Henlius and the Pfizer molecules while differentiating via a choice of antibody, linker, and payload, and ability to combine with other agents. Zooming in more detail across these molecules, we can see in this slide distinct points of differentiation for CR002. It incorporates a novel antibody that's selected for enhanced internalization and potency and utilizes the GGFG DXd linker payload format. The PD-L1V molecule from Seagen/Pfizer has a traditional val-cit MMAE linker payload format that has a limited therapeutic index in the clinic, and the Henlius molecule is utilizing a novel linker payload format from MediLink, the TMALIN peptide linker and a topo inhibitor. Now, a bit more color about the choice of linker for these ADCs. The GGFG linker is designed to provide a balance of stability and circulation, efficient bystander activity, and payload release in the tumor. You can see that this compares quite well and favorably compared to other agents. While we look at the comparator molecules, the val-cit linker is known to have some instability in circulation, moderate bystander activity, and low tolerability. In addition, the TIMALIN tripeptide linker utilized in the Henlius molecule has seen some clinical safety issues utilized in the HER3 ADC that MediLink licensed to BioNTech. So now if we move to the next slide. Okay. So we've selected a differentiated antibody for CR002 with the goal of achieving enhanced internalization and cell potency. Different antibodies in this assay were screened on an identical DXd ADC format, allowing direct comparison of antibodies and the correlation between target binding affinity and cell-killing potency. Interestingly, there was an inverse correlation between PD-L1 target binding and cell-killing potency, with a representative high affinity antibody from BMS that showed very limited cell-killing potency. And our CR002 molecule was the most potent ADC in this cell-killing assay. When we put this all together, we can see that CR002 demonstrated robust anti-tumor activity in a PD-L1 positive cell line-derived xenograft model. Looking at other comparator molecules in this setting, we can see the high affinity BMS antibody showed limited anti-tumor activity in this model, and in addition, the ofacolimab antibody, which is the parent antibody for the Henlius ADC, was inactive in this tumor xenograft model in this setting, while the CR002 ADC demonstrated complete responses in eight out of eight animals in this setting. So in summary, we believe that CR002 is a highly differentiated topo-based ADC that compares well to other agents in this class, and we're focused on moving this molecule to IND in mid-2026 that'll allow us to initiate a phase one trial in the second half of next year. Okay. Next, moving on to CR003 or SKB105, the ADC that we're in-licensing from Kelun-Biotech to take forward in regions outside of China. First, let's talk a little bit about the target integrin beta-6. There's a wealth of literature demonstrating integrin beta-6 plays a role in tumor growth and invasion. It's also very highly expressed in tumor compared to normal tissue across a range of solid tumors like non-small-cell head and neck esophageal and others. It also has been demonstrated to have a favorable internalization profile, which makes it a very suitable target for antibody-drug conjugates. CR003 is a highly differentiated integrin beta-6 ADC with a topo payload, and it's designed to be best-in-class. A few key features of the molecule are described here. It utilizes a novel IgG1 antibody targeting integrin beta-6. Antibody was selected for enhanced internalization capability in a novel and stable linker payload format with a topo payload. Here, you can see how CR003 is distinct from other molecules in this space, including two ADCs from Pfizer, the legacy Seagen B6A molecule with an MMAE payload and another earlier candidate with the camptothecin-based topo payload. CR003 was designed with a differentiated antibody selected for enhanced internalization and has generated promising efficacy and tolerability data, which supports its first in-human dosings in the near future. The preclinical studies indicated that CR003 demonstrated superior internalization compared to the parent V6 antibody, especially in low antigen density expressing cell lines. This has the potential to enhance cell-killing potency in low antigen expressing cells. If you want to understand how it behaves in vivo, here we can see that CR003 demonstrated superior anti-tumor responses in a non-small cell lung cancer xenograft model at left, where the SKB105 ADC showed beautiful regressions. In addition, in a pancreatic xenograft model at right, the B6A molecule was inactive, while the SKB105 ADC showed regressions in the study. Additionally, CR003 has a superior PK profile compared to B6A. As we can see in the graph at left, the superimposable PK curves for the antibody and the ADC component for 105 demonstrate high stability in circulation, where you can see for the B6A molecule, the steeper rate of clearance for the ADC compared to the antibody component demonstrating linker instability and lack of stability in circulation. In the end, we are excited about our partnership with Kelun-Biotech, enabling us to advance CR003 and incorporate it into our strategy of developing next-generation best-in-class ADCs for solid tumors. The integrin beta-6 function, expression, and internalization make it a favorable target for an ADC, and the differentiated design and compelling preclinical data give us confidence as it progresses into the clinic. Kelun-Biotech is on track to initiate a phase one-two study in early 2026 with initial data about 12 months later, followed quickly by initiation of a combination study with CR001 and CR003 early in 2027. Now I'll turn things back over to Josh for some closing remarks. Thanks, Jan. I think you can sense our excitement of the comprehensive ADC strategy that the team has put together. We plan to continue to utilize our in-house capabilities, but also leverage partnerships that can enhance this part of our business as we've done with Kelun-Biotech. This partnership validates our strategy and sends a strong and intentional signal that Crescent is open for business. We are committed to sourcing the best assets and collaborating with top companies to continue building our robust portfolio as we deepen our leadership position in this space. We believe this partnership is a major step forward in accelerating and expanding our efforts to deliver the next wave of therapies for people living with cancer. We are also moving to where the field is going, positioning our portfolio to capitalize on synergistic combinations with CR001, our foundational IO backbone, as well as multiple ADCs in our pipeline. We have a matrix portfolio that provides lots of opportunity for us to play a significant role in one of the largest markets in biotech. We are excited about the competition in this space. To answer the question on how can Crescent compete, not only can we compete, but we are establishing ourselves as a leader in the ever-evolving field of oncology as we have differentiated assets, including the potential best-in-class PD-1 VEGF bispecific and robust ADC pipeline, differentiated clinical strategy with multiple ways to win in a massive market opportunity, a team with deep experience in oncology and a proven track record of execution, and as we've displayed today, an aggressive view on building and leveraging partnerships like Kelun to drive towards our bold vision globally. Focus on execution is what's ahead of us now, with four clinical trials initiated next year, generating multiple data readouts in 2027 from CR001, our ADC, and combination therapies. We have the strategy, the team and capital to deliver on our vision. The financing we announced today enables us to execute these trials and drive towards a meaningful, data-rich 2027. Thank you so much for listening and attending today's call. We'll now open it up to questions. Operator. If you would like to ask a question, please press star one on your telephone keypad now. You'll be placed into the queue in the order received. Please be prepared to ask your question when prompted. Once again, if you would like to ask a question, please press star one on your phone now. Our first question comes from Akash Tiwari of Jefferies. Hey, this is Manoj on for Akash. From a molecular and potential clinical efficacy aspect, how do you view CR001 architecture differentiate itself from LaNova asset? Even Kelun has decided to partner with you despite their close relationship with Merck. Also, where do you see the PD-L1 ADC to be an optimal indication? Because Pfizer now is focusing on the second line head and neck and seems not to be pursuing the first line opportunity. Do you think CR002 could have an opportunity in the first line head and neck? Thanks. Ellie, you want to take this question? Sure. Thank you, Manoj, for great questions. Regarding your first point about how we think we can compare to LaNova's compound, structurally speaking, we are using the VEGF profile that is matching that of ivonescimab, which is the only PD-1 VEGF bispecific to date with multiple positive phase three trials. I understand that LaNova's phase one trial is still running in China. So we are waiting to see how that data looks like, whereas CR001 has a unique benefit of, with its VEGF intentional design of matching that of ivonescimab. If we show in early clinical study matching profile of ivonescimab, then we will gain a lot of conviction that we can also match the key features of ivonescimab demonstrated in the later stage development, such with many successful phase 3 trials. Yeah, and I would just maybe add that Ellie went through the way we designed each part of this molecule very intentionally. And I do think that the robustness of the manufacturability, the stability, the improvements that we've made while keeping the core pharmacology intact from ivonescimab is going to pay big dividends across this molecule. I think we all know the challenges of manufacturing and what those could present in developing a drug. I think we feel very confident in that process and our ability to have really kind of cleaned up and put together a very robust molecule. I think we've said publicly that we can concentrate up to 150 mg per mL. I think ivonescimab has around 10. I mean, these are the things that will provide major benefits for this molecule going forward. And then your second question, it was a little hard to hear. Would you mind repeating that question? So where do you see the opportunity for PD-L1 ADC? So if Pfizer recently kind of stopped their first-line head-and-neck opportunity and then moving to completely focusing on the second-line, so do you think your molecule can differentiate in first-line head-and-neck? Or how do you view that opportunity there? Oh, yeah. Thanks. That's a really great question. So we have a very mature comprehensive portfolio that shows how we want to develop our CR002 PD-L1 topo ADC in conjunction with our CR001 PD-1 bispecific antibody. I understand that Pfizer's compound was focused on second line non-small cell lung cancer, and then recently they decided to stop their first line head and neck study based on competitive landscape. With our optimized profile of antibody, linker, and payload, we believe CR002 can have differentiated and potentially best-in-class profile, which gives us an opportunity to go into not just the head and neck and non-small cell lung, but into other indications. But in head and neck and non-small cell lung cancer, we believe we can provide best-in-class profile as monotherapy as well as in combination with the CR001. Yep. Thank you. Thank you. And our next question comes from Eric Schmidt of Cantor Fitzgerald. Thanks and congrats, Crescent team, on this myriad of updates. Maybe first question on CR001 and the proof of concept data you're hopeful to be able to achieve in early 2027. The phase 1 study is obviously multi-staged, multifaceted. Do you think you'll have data from the backfill cohorts or the expansion cohorts by early 2027? What does that proof-of-concept data might entail? Thank you, Eric. Our initial data release, which is aimed for first quarter 2027, will include data from dose escalation as well as backfill cohorts with comprehensive safety, tolerability, PK, pharmacodynamics, as well as preliminary anti-tumor activity from second-line plus patients, as well as first-line patients in multiple tumor types. Thanks, Ellie. And when you think about pairing CR-001 with either 002 or 003 and looking at a novel combination of that sort, what do you need to achieve in the phase 1 studies in order to be able to start those combos in 2027? Thank you. Thank you, Eric. That's another great question. As a novel combination strategy is one of our key focus. We believe establishing recommended phase 2 dose and understanding comprehensive exposure response of monotherapy of CR001 and CR003 is critical, and once we have a great understanding of preliminary safety and efficacy profile of each compound, then we will find an efficient and safe way to combine these two novel therapies and create best-in-class profile in multiple indications. Yeah, and I would add that this is another advantage of the partnership we announced today with Kelun-Biotech, which says as we generate that initial clinical profile data, both in the Western patient populations and the Chinese patient populations, Kelun-Biotech has the opportunity to pair 001 with their full suite of ADCs, including any ADC that has an established clinical dose. So that is one element that would allow us to, in partnership with Kelun, generate combo data both with our own portfolio, but also their portfolio of ADCs as well. Great. Thanks. And congrats again on the progress. Thanks, Eric. And our next question comes from Phil Nadeau of TD Cowen. Good morning. Let us add our congratulations on the deal and all the progress. Two questions from us. First, in terms of the 001 dose escalation, do you think you have a good idea of the recommended phase two dose given what we've seen from ivonescimab, or is there any reason to think 001's doses could be different? That's the first question. And then second, in terms of CR003, what are the data that support integrin beta-6 being a good combo with a PD-1 VEGF bispecific? Are there any preclinical results that suggest that is a particularly good target that could have synergy with CR001? Thanks. Ellie, why don't you take the first question first, and then we can answer the second question on IB6. Yes. Thank you, Phil. With our CR001, intentionally designed to match the key features of ivonescimab, and then we have shown in preclinical settings that we have a match in comparable pharmacology, it gives us a lot of benefit going into clinical study and developing this drug in an efficient manner. However, it is very important for us to study CR001's PK, safety, tolerability, and efficacy in a comprehensive fashion and understand our dose. So while we have a great advantage with this our structure, we will follow our data and carefully determine recommended phase two dose based on the data that we are generating from this study. Got it. That makes sense. Yeah. And Eric, a second question. So I think there's emerging data preclinically and clinically that topo-based ADCs can combine well with traditional checkpoint therapy. Obviously, the combinations with bispecifics are still more nascent on that end. But I think we can just point to the recent sac-TMT and PEMBRO data in non-small cell, as well as the Trodelvy and PEMBRO data in TMBC to really emphasize that topo-based ADCs and molecules like that can combine well. Yeah. And I just highlight again the value of the Kelun partnership. I think we've been thinking about just a combination since the founding of the company. It's been great to see recently Pfizer, BMS, BioNTech, and others talking about where this puck is moving. And through the Kelun partnership, I think we're going to have a chance to be some of the first to generate the bispecific combo data, which is really interesting for us. And I think will give us the opportunity to highlight and showcase that we believe we have the best-in-class bispecific here with CR001. That's very helpful. Thanks for taking our question. And congratulations again on the deal. Thank you very much. Our next question comes from Robert Driscoll of Wedbush Securities. Thanks, guys. And congrats on this kind of deal coming together. Maybe just to follow on maybe from a couple of the other questions, is there any preclinical data for the combination of CR002 and CR001 that gives you confidence in the synergistic potential, or maybe you just like to kind of talk about kind of an ADC PD-L1 combining with a PD-1 VEGF? Thank you, Robert. It's a great question, so CR002, our PD-L1 topo ADC in combination with the IO, we think it provides us unique and great opportunity to create synergistic effect because how we are laying out this matrix portfolio and going over eight indications in three therapeutic areas, PD-1 and PD-L1 expression in these tumor types have been well validated, and we are anticipating great synergistic effect by going after PD-L1 topo ADC as well as creating immunogenic cell death with the synergistic effect leading to PD-1 VEGF bispecific. In clinical realm, Pfizer has already produced encouraging data of their PD-L1 ADC successfully combined with Keytruda showing encouraging activity both in head and neck, head and neck squamous cell carcinoma as well as non-small cell lung cancer. Got it, and maybe just one more. In terms of Kelun's clinical strategy for CR001, talk a little bit about that. Any additional details you can provide there? Have they kind of outlined any initial combination strategies of interest from their internal pipeline? Thanks. Yeah, that's a great question. So we certainly would refer you to Kelun for discussions around their plans for their pipeline. But as part of this partnership, they have the right to combine 001 with any asset in their pipeline. And you can refer to their pipeline and see that they have multiple clinical stage assets targeting targets such as TROP2, HER2, Nectin, and Claudin. And they do share our vision on the importance of synergistic combinations. And so we look forward to sharing updates as those trials progress. Brilliant. Thanks very much. And congrats again, guys. Thank you. As a reminder, if you would like to ask a question, please press star one on your phone now. Our next question comes from Stephen Willey of Stifel. Congrats on the update. Maybe just a couple of questions here. So one logistic. Will you be selecting for a PD-L1 expression status in the backfill and dose optimization cohorts? Do you want to have a cutoff in place to best interpret the preliminary efficacy that you're seeing? And then just have a follow-up. Thank you, Steve, for that question. We will have an opportunity to provide you more detailed information on the inclusion and exclusion criteria as well as our development strategy down the road. But we definitely considered a very comprehensive approach of enrolling patients with various PD-L1 expression, but also we considered existing clinical data to improve our probability of success in the phase one trial. Okay. And then maybe just a bigger picture question. I think some of the KOL concern around frontline ADC-based combos are centered around just being able to keep patients on drug long enough to capture that OS benefit that you get with PEMBRO. So just curious how you think about longer-term differentiation versus something like a Dato-DXd. Do you achieve that with a cleaner target, a better TI, a different maintenance dosing strategy? Just wondering if you have just any thoughts here that you can share. Thanks. Yeah, that's a really great question. As multiple ADCs are being developed in frontline settings, providing robust efficacy but also favorable safety profile are both important to make sure that patients can benefit from long-lasting treatment. And here, with our strategy of optimizing antibody for internalization and tumor cell killing and stability of the linker and the payload, we believe we have an opportunity to balance testing efficacy as well as safety tolerability that will ultimately benefit the patients to have a PFS and OS benefit in the first line setting. And it's something that we will keep an eye on and monitor very carefully as we develop CR002 and 003 in monotherapy as well as in combination with the 001. All right. Thanks for taking the questions. And our next question comes from Charles Zhu of LifeSci Capital. Hi, this is Ffion for Charles. Thanks for taking our question. And congrats on the progress. What are some key learnings from Summit and Akeso developing Ivonescimab that you would highlight as particularly informing how Crescent will approach clinical development with 001? Do you intend to pursue a monotherapy development of ADC assets? If so, to what extent might 02 and 03 monotherapy programs overlap or diverge from eight indications for CR001? Thanks. Thanks, Steve. Great questions. On the lessons learned, there's definitely some things that we're going to implement into our clinical strategy. Ellie, maybe you want to talk about some of that and then our views on the monotherapy for ADCs. Sure. Thank you, Steve. We are in a great position of benefiting from available clinical data and emerging information from various bispecifics. Regarding Summit and Akeso's case, we are learning how to translate the data studied in China and then in the global setting. As we have pointed out, CR001 is starting phase 1 to study in the global setting. This gives us a unique benefit of starting with the Asian as well as Western population. And we will be working with the FDA, EMA, and global regulatory agencies to understand how best to develop CR001. And regarding monotherapy development plan for ADC as well as a combination, we will study CR002 and 003 in multiple different solid tumors. And after careful exploration of efficacy and safety profile, we'll find an indication for its best development test for monotherapy as well as in combination with 001. Yeah. And I would just say that in addition to the power in the stats and the lessons learned from indications to go after, the space is wide open. I think we continue to be differentiated with the assets, our clinical strategy, and our focus on execution. I think, as I pointed out in the call, there's multiple ways to win here. And I think in this particular situation, it's a credit to the work that's been done ahead of us, but it does pay some dividends to be a very fast follower to learn from these lessons. And again, the combination approach to this and part of our key part of our strategy also is going to be very beneficial to getting those best-in-class therapies across all available indications. Thanks so much. Congrats again. And our next question comes from Mitchell Kapoor of H.C. Wainwright. Hi, this is Katie on for Mitchell. I guess my question is, have you guys begun FDA early interactions for these studies? Is there any additional color you can add to synchronizing the regulatory requirements across this many studies? Yeah. I think what we've said about FDA interactions is, one, we typically don't comment on those, and we stick to the milestones that we put out there publicly. We're well on track to initiate dosing in patients in CR-001 in early 2026. From From the CR-003 SKB105 perspective, I won't speak for Kelun, but I think it's safe to say that we're well on track to begin those studies in China in early 2026, as we point out in our milestones. Beyond that, I think instead of generating the data, data leads the way with regulators. We'll continue to generate high-quality, robust data sets, illustrated by the phase 1 trial design. That will also be a key role in thinking about combining these assets and thinking about combo therapies as well. And we will continue to provide milestones on the trial initiations and the timing of those data readouts. Great. Thank you. Of course. And if there are any final questions, please press star one on your phone now. And it appears we have no further questions at this time. I'll turn the call back over to our hosts for any closing remarks. Thank you very much. Thank you for everyone for listening and your great questions. We're very excited about the path forward that we laid out today for Crescent. Very exciting time for patients as well as we start to think about the next generation of IO therapy and the additional bringing forward of the combination therapies for patients and improving patients' lives. So with that, we'll conclude today's call and look forward to seeing you around the conference circuit and want to wish everyone happy holidays. Thank you.