Good day, thank you for standing by. Welcome to the Coherus and Surface Oncology conference call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star 11 on your telephone. You will hear an automated message advising that your hand is raised. To withdraw your question, please press star 11 again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today. Marek, please go ahead. Thank you, Latonya. Good morning, everybody. Today's call includes forward-looking statements regarding the proposed transaction for the terms of the agreement and plan of merger among Coherus BioSciences and Surface Oncology and their affiliates. These forward-looking statements include, but are not limited to, statements regarding the business combination and related matters, including, but not limited to, satisfaction of closing conditions, prospective performance and opportunities with respect to Coherus or Surface, post-closing operations, and the output for the company's businesses, Coherus's, Surface's, or the combined company's targets, plans, objectives, or goals for future operations, including those related to Coherus's and Surface's product candidates. Factors that may affect future results and may cause these forward-looking statements to be inaccurate include, without limitation, uncertainties as to the timing for completion of the proposed transaction, uncertainties as to Surface's ability to obtain the approval of its stockholders, the possibility that competing offers will be made by third parties, the occurrence of events that may give rise to rights of one or both of parents and the company to terminate the merger agreement or other factors. By their very nature, forward-looking statements involve inherent risks and uncertainties, both general and specific, that are discussed in our presentation slides and the press release that we issued today, as well as the documents that Coherus and Surface filed with the SEC. With that, I will hand the call over to Denny. Thank you, Marek. Good morning, everyone. As you know, this morning, we announced the proposed acquisition of Surface Oncology. The objective of our call this morning is to explain to you the scientific, clinical, and strategic rationale behind this transaction. I'm honored and pleased to be joined today by Dr. Rob Ross, Surface Oncology's Chief Executive Officer. I am also joined by my Coherus team members, Dr. Theresa LaVallee, our Chief Scientific & Development Officer, and Mr. McDavid Stilwell, our Chief Financial Officer. For more than a year, Coherus has systematically searched for IO assets complementary with our next-generation differentiated PD-1 inhibitor, toripalimab, that would potentially extend tori's reach into more prevalent cancers, as well as areas of unmet need and inadequate patient survival. With this effort, we screened over 200 companies for more than 500 meetings. We believe our efforts were comprehensive and thorough. At the end of that process, the world-class science of Surface and the high-quality, clinical-stage, data-rich assets, SRF388 and SRF114, stood out head and shoulders above the others. Coherus brings to Surface the ability to develop these assets in combination with our PD-1 inhibitor, toripalimab. As you will see, the Coherus Surface merger creates one of the few immuno-oncology companies with demonstrated commercial expertise, significant product revenues, and unique leading-edge R&D programs. Let me make 2 additional key points. Firstly, this merger comes at a very opportune time for Coherus, as we are now midway through an 18-month period of 5 product launches and our revenue inflection point with toripalimab progressing towards an FDA approval decision. Secondly, by adding SRF388 and SRF114 to our immuno-oncology portfolio, creates a pipeline prioritization opportunity as we upgrade and refocus on more competitively positioned programs. We project R&D expense reductions of up to $50 million through the 2025 planning period. These efforts, while adding up to $25 million in cash to our balance sheet upon closing. The scientific, clinical, and business model synergies of this corporate combination are considerable. Through rigorous scientific research, Surface Oncology has discovered and developed a number of very interesting IO drug candidates, potentially synergistic with toripalimab. Toripalimab itself is an ideal foundation stone for the IO franchise, Coherus, with a differentiated mechanism of action and well-positioned for success in prevalent cancers. The existing Coherus pipeline is also focused on targeting the immune suppressive mechanisms in the tumor microenvironment. Of course, our commercial revenues now from our approved products will support our development expenses. We're well-positioned to extend the survival of cancer patients and deliver significant shareholder value. Let me talk firstly about the scientific synergies. Agents which activated an immune response in the tumor microenvironment hold promise when combined with checkpoint inhibitors. Both SRF388 and IL-27 mAb and SRF114, a CCR8 mAb, target the tumor microenvironment, relieving immune suppression, allowing T-cell response. Checkpoint inhibitors reinvigorate tumor-specific T-cells. This mechanism of action synergy thus presents promising approaches to treat cancers with high prevalence of unmet need. As a next-generation PD-1 inhibitor antibody, toripalimab is thus ideally suited for combination therapy with these assets. Let me talk now about the clinical synergies. Together, Coherus and Surface Oncology share a patient-focused vision for developing novel immuno-oncology agents that will potentially extend survival beyond what has been achieved with checkpoint inhibitors and chemotherapy. This merger upgrades Coherus' clinical pipeline and leapfrogs us to combinations with the potential to accelerate the development pathway. SRF388 and SRF114, in combination with toripalimab, and potentially also with CHS-006, our TIGIT-targeted antibody, has the potential to expand our immuno-oncology commercial opportunity to non-small cell lung cancer, hepatocellular carcinoma, head and neck cancer, and other tumor types where IL-27 and CCR8 mechanisms play a role in immune suppression. These tumor types are complementary to the toripalimab clinical development program, setting up promising combination approaches to cancer treatment. Now, let me discuss a bit about the business model synergies and benefits. The Surface acquisition brings important business model synergies and financial benefits to Coherus. First, the elimination of program overlap on shared targets generates cost and time savings. Secondly, the transaction enables Coherus to conduct a portfolio review and to prioritize development of the most advanced and the most competitively positioned programs. It expands our partnering opportunities for toripalimab. In addition, combination therapies. We expect to reduce Coherus' currently budgeted R&D expenses through 2025 by at least $50 million through this portfolio prioritization. Additionally, we plan to monetize ex-US rights, SRF388 and SRF114, in 2024 and 2025 after the assets have passed through important clinical milestones, potentially yielding upfront payments and defraying future development expenses. Coherus shareholders will receive 30% share of the value for the Surface programs partnered with Novartis and GSK. Importantly, the transaction is projected to strengthen Coherus' balance sheet, with up to $25 million of Surface' net cash projected at closing. The Surface merger is very opportunistically timed, as we are beginning to realize the potential of our biosimilar strategy, which plays an important role for Coherus as they generate net sales to fund our innovative immuno-oncology product development. We are seeing accelerating revenue growth for CIMERLI per plan, and the recently launched UDENYCA auto-injector is gaining traction, providing a new spark to the UDENYCA franchise. Next month, we plan to launch our ranibizumab biosimilar YUSIMRY with our innovative strategy, made possible by significant prior investment manufacturing scale. toripalimab will become our first branded drug, if approved by the FDA for nasopharyngeal carcinoma, and we are continuing to work with the FDA to get this potentially life-saving drug to patients who currently have no approved therapies in the United States. This merger adds two competitively positioned clinical-stage programs to our pipeline. The combined pipeline of the two companies is represented here. In a few moments, Rob will describe the exciting data that's been generated recently with SRF388 and SRF114. Commercially, use of an approved combination of these candidates with toripalimab would yield sales of two Coherus-owned drugs. With that, I'll now turn the call over to my colleague, Dr. Rob Ross, Surface Oncology's CEO. Rob? Thank you, Denny. It's a pleasure to be joining the Coherus team on today's call to provide an overview of Surface Oncology's programs, discuss the data we announced today, and most importantly, to share our excitement for the proposed merger of Surface Oncology and Coherus. Surface Oncology has a compelling pipeline of innovative immuno-oncology antibodies, which hold the potential to change the treatment paradigm for patients suffering from a variety of solid tumors. However, to truly realize their potential, it is essential that these molecules are developed with both the resources and the companion drugs needed to successfully advance them through the clinic and to bring them to market. Coherus is greatly positioned to do just that. Surface Oncology's programs dovetail with the Coherus business strategy and its vision to become an innovative leader in the field of immuno-oncology. That's why we firmly believe that with Coherus, our programs will have the best possible opportunity to benefit patients and realize value for our shareholders. I'll start by revisiting the combined pipeline, which Denny just shared. This slide illustrates the logic and benefits of a merger of Surface Oncology and Coherus. It presents an exciting opportunity to advance Surface Oncology's novel antibodies and investigate them in combination with Coherus' molecules. I'll discuss more detail about the Surface Oncology novel antibodies now. Moving to the next slide. SRF388 is Surface Oncology's fully human IgG1 antibody that binds and neutralizes the immunosuppressive cytokine IL-27. It is the only anti-IL-27 antibody in clinical development. At Surface Oncology, we have been at the forefront of IL-27 research and biology. This cytokine is not always found in the tumor microenvironment, but when present, it is highly immunosuppressive and serves as an important regulator of checkpoint protein expression. SRF388 binds IL-27 and prevents it from interacting with its downstream receptor, thereby neutralizing its immunosuppressive effects. With this agent, we have demonstrated clinical activity with confirmed responses as a single agent in kidney cancer and in lung cancer, as well as combination activity in liver cancer. Moving to the next slide, let me share a bit on IL-27 biology. IL-27 is an immunoregulatory cytokine that's produced by macrophages and dendritic cells. It has a multitude of immunosuppressive effects within the tumor microenvironment, including constraining NK cell immunosurveillance, increasing checkpoint receptor expression on immune cells, and decreasing pro-inflammatory cytokine secretion. Through a cascade of different effects, IL-27, when present in the tumor microenvironment, can suppress both innate and adaptive immune responses. By binding the IL-27 cytokine, SRF388 neutralizes these immunosuppressive effects and stimulates antitumor immunity. Moving to the next slide, we share the most recent data from our clinical trial investigating SRF388 as monotherapy treatment in a refractory non-small cell lung cancer population of patients. On the right of this slide, in the waterfall plot, you can see the data from 32 response evaluable patients with non-small cell lung cancer, whose data was available at the time of our most recent snapshot, of whom 24 are RECIST evaluable. All but 1 of these patients were treated at our recommended phase 2 dose of 10 mg per kg or above. All had previous anti-PD-1 or anti-PD-L1 treatment, and many of these patients had low PD-L1 expression in the tumor microenvironment. In this patient population, SRF388 demonstrated encouraging monotherapy activity, including 2 confirmed partial responses. Both PRs were in patients with squamous non-small cell lung cancer, and both patients had either low or no PD-L1 expression within the tumor microenvironment. Additionally, both patients were resistant to previous anti-PD-1 or anti-PD-L1 treatment. It is uncommon to see monotherapy activity in this highly treatment-refractory patient population from a novel IO agent, and we believe this bodes well for its future success in combination. Furthermore, one of the exciting aspects of the proposed merger with Coherus is integrating SRF388's activity in non-small cell lung cancer with the known activity of toripalimab in non-small cell lung cancer, which presents the opportunity for a host of potential combination trials moving forward. Moving to the next slide, this is our phase 2 trial investigating SRF388 in hepatocellular carcinoma, also known as liver cancer. We have fully enrolled the 30-patient lead-in in the first-line, single-arm, phase 2 trial of SRF388 in triplet combination with the standard of care, that is, atezolizumab with bevacizumab. Note that this data cutoff is early in the treatment of these patients, and only half of the patients on the trial have had more than 1 on-treatment scan. To date, we have recorded a 27% overall response rate with a 65% disease control rate. It generally takes 3 or 4 on-treatment scans to identify most of the responders. Importantly, only about half of all eventual responses from atezolizumab and bevacizumab alone are detectable within the first imaging cycle. That only half the patients on our trial have had more than 1 imaging cycle suggests that as these data mature, we should expect to see increased response rates, as well as generating important data on progression-free survival and duration of response. Notably, at the recent ASCO conference, Roche shared exciting new data from their anti-TIGIT antibody in a very similar liver cancer patient population. This news is both encouraging for the class of anti-TIGIT antibodies and also speaks to another highlight of this merger. We believe that the merger of Surface and Coherus presents a unique opportunity to combine the promising novel drugs toripalimab, CHS-006, and SRF388, targeting PD-1, TIGIT, and IL-27, respectively, in liver cancer. No other company has agents against all three of those targets in clinical trials, and the scientific and competitive advantages presented by this proposed combination are vast. I'll move on to SRF114 on the next slide. SRF114 is our anti-CCR8 antibody, which is currently in a phase 1/2 dose escalation, safety and tolerability trial. The scientists at Surface have been working on this program from Surface's inception, because targeting CCR8 offers the opportunity to deplete intratumoral regulatory T cells without depleting other T cells, including circulating regulatory T cells and effector CD8+ T cells. SRF114 is a high-affinity, fully human IgG1 that binds to CCR8 and has been engineered to specifically deplete Tregs within the tumor microenvironment. Importantly, in our preclinical studies, we have seen exquisite selectivity to human CCR8 and have not observed off-target binding of SRF114 to any other human proteins. Moving to the next slide, we have known for quite some time that regulatory T cells, also called Tregs, are an important cellular component of the tumor microenvironment and result in profound local immune suppression, allowing tumor cells to avoid antitumor immunity. A long-held goal in immuno-oncology research has been to find a way to remove these regulatory T cells selectively from the tumor microenvironment. Targeting regulatory T cells results in two key challenges. First, the proteins used to target regulatory T cells are often expressed on normal effector T cells. By targeting a protein that's expressed on the regulatory T cell and a normal non-regulatory T cell, you remove both the immunosuppressive regulatory T cell, but you remove the effector T cell as well, which could undermine the effect you're trying to produce. Secondly, peripheral Tregs serve an important role in preventing autoimmunity in healthy human beings. If one targets intratumoral regulatory T cells, but also deplete peripheral regulatory T cells, it could result in significant toxicity manifested by autoimmunity. CCR8 is an ideal target for removing primarily tumor-infiltrating regulatory T cells, because it is not expressed at high levels on normal T cells, and it is not expressed at high levels on the majority of peripheral regulatory T cells. That's shown in the graph at the bottom of this slide, where you can see that on human cells in vitro studies with SRF114 application, you see marked depletion of intratumoral regulatory T cells, but no effect on peripheral regulatory T cells and no effect on intratumoral CD4 and CD8 effector T cells, which are responsible for antitumor immunity. SRF114 has been observed to be a highly selective and potent anti-CCR8 antibody to deplete tumor-infiltrating regulatory T cells. Moving to the next slide, you can see a snippet from the extensive amount of preclinical data that we have generated, evaluating antibodies which target and deplete CCR8-positive regulatory T cells. In this mouse model that we're displaying on this slide, we used a melanoma tumor that is highly resistant to anti-PD-1 treatment, and then studied treatment with anti-CCR8 antibodies, as well as the combination of anti-CCR8 and anti-PD-1 in the mouse. As you can see on the left, as expected, in this PD-1 resistant tumor type, anti-PD-1 treatment has no effect, while anti-CCR8 treatment had a strong effect of preventing tumor growth, and the combination of the two did even better. On the right, you can see that result is recapitulated in the survival graphs, showing that the best treatment in this PD-1 resistant tumor type is anti-CCR8 in combination with anti-PD-1. There is a huge unmet need for patients with cancer who have progressed during treatment with anti-PD-1, or for those whose tumors just don't respond to anti-PD-1 therapy alone. Potentially, SRF114, in combination with toripalimab, could help to address this need. Moving to slide 20, here is the potential mechanism of action of this combined treatment, and it's clearly illustrated. As you can see, that after treatment with anti-CCR8 or anti-CCR8 plus anti-PD-1, the infiltrating effector T cells, the CD8+ T cells, go up considerably as compared to anti-PD-1 alone. You can see that in the immunohistochemistry on the left, where the CD8+ T cells are shown in brown, and you can see that in the scatter plot on the right, where the combination treatment has markedly increased the number of CD8+ T cells, and those CD8+ T cells are the ones that drive antitumor immunity. Our belief is that the combinatorial efficacy seen in this PD-1 resistant tumor model is driven by this influx of antitumor CD8+ T cells. Moving to slide 22, the first patient was dosed with SRF114 in early 2023. Since that time, we have progressed through 3 dose levels, treating 6 patients without any concerning safety signal. We have some early pharmacodynamic data, which we are quite excited about. In data available from the first two patients treated at dose level three, we saw a profound effect of SRF114 on a subset of circulating CCR8-positive regulatory T cells. You can see in the flow plot on the left and in the bar graph on the right, a marked reduction in the CCR8-positive regulatory T cells from immediately pre-dose to 24 hours post-dose, where the number of CCR8-positive regulatory T cells drops from double digits to less than 1% after treatment. We are gratified to see these data because not only does it suggest that SRF114 is having the intended pharmacologic effect, it is happening at a lower dose level than we had previously thought, speaking to the potency of this antibody. Moving to the next slide, one of the many exciting synergies we see with this potential merger is the opportunity to combine SRF114 with toripalimab in head and neck cancer, where anti-PD-1 treatment has shown durable and consistent responses in human beings. Head and neck tumors are typically heavily infiltrated with regulatory T cells, which are strongly positive for CCR8. As you, as you can see on the left, in the immunofluorescence staining, approximately 75% of the regulatory T cells in head and neck tumors are CCR8 positive. On the right, when you look across a broad range of different solid tumors, the tumor type that combines both high levels of CCR8 positivity on infiltrating regulatory T cells, along with high levels in infiltrating NK cells, which are required for the depletion effects of SRF114, head and neck tumors stand out as the top indication to study. In fact, the current phase 1/2 study already contains an expansion arm for patients suffering from this disease. Coherus and their partners have already presented exciting data from toripalimab in nasopharyngeal tumors, which are a subset of head and neck tumors. We believe there is a real opportunity to have a profound combination that is purely immunotherapy-based, with SRF114, combined with toripalimab, in patients suffering from head and neck cancer. In summary, I believe that the merger of Surface and Coherus creates an exciting armamentarium of potentially transformative immuno-oncology therapies, which holds the promise of improving lives and giving hope to patients who are suffering from life-threatening cancers. I'll now turn the call over to Dr. Theresa LaVallee, Coherus' Chief Development Officer. Thank you, Rob. I'm thrilled to be here today to talk about these exciting and differentiated IO programs with scientific and clinical synergies, all with robust data packages and strong disease positioning. On the next slide, Coherus' toripalimab is a next-generation PD-1 inhibitor designed to bind the FG loop of PD-1. As you can see on the left side of this slide, this epitope binding is specific to toripalimab, while pembrolizumab predominantly binds the C'D loop, and nivolumab predominantly binds the N-terminus of PD-1. As shown on the right side of the slide, toripalimab has greater than 10-fold higher binding affinity for PD-1 compared to pembro and nivo. This unique and potent binding has shown differentiation in 3 phase III studies in non-small cell lung cancer, nasopharyngeal carcinoma, and esophageal squamous cell carcinoma, where treatment with toripalimab and chemotherapy showed similar activity irrespective of PD-L1 status. On the next slide, this importantly shows toripalimab has demonstrated clinical activity in a broad range of immunologically responsive tumor types. Furthermore, our partner, Junshi, reported positive phase III studies in small cell lung cancer and triple-negative breast cancer, tumor types that are generally considered moderately responsive to IO agents. The demonstrated toripalimab clinical activity has scientific and clinical overlap with SRF388 and SRF114. To date, the safety profile for toripalimab is consistent with the PD-1 inhibitor class, with no new safety signals. Toripalimab is currently under BLA review with the US FDA for nasopharyngeal carcinoma and has breakthrough therapy designation, as well as the data being presented at ASCO plenary session and most recently in an oral discussion at ASCO 2023, characterized as practice-changing. Here, this strategy has been to identify novel IO combinations to expand toripalimab treatment beyond NPC and continue to improve survival for underserved cancer patients. SRF388 and SRF114 have met all the criteria we were looking for for development with toripalimab. The next slide depicts Coherus' and the field's focus for immunotherapy development. While PD-1 inhibitors have revolutionized cancer therapy, still, only a minority of patients respond. Over the last decade, the field has learned a lot about what makes a tumor immunologically responsive or hot, and others that are PD-1 resistant or refractory. A key mechanism for PD-1 resistance is immunosuppressive cells and cytokines. Blocking these immune suppressive mechanisms in the tumor microenvironment has the potential to reverse PD-1 resistance and convert a tumor to be immunologically responsive. Surface has demonstrated with their SRF388 program, targeting IL-27, an immune suppressive cytokine, that inhibiting this cytokine can activate the immune system and importantly, activate antitumor immunity, demonstrating single-agent activity in PD-1 experience, non-small cell lung cancer, and renal cell carcinoma. IO monotherapy activity, particularly in PD-1 previously treated patients, is unusual and exciting. Advancing clinical studies with SRF388 and toripalimab is of importance and has the potential to address the critical unmet medical need for cancer patients. Other immune suppressive mechanisms that may address PD-1 resistance are Treg cells and the suppressive macrophages. SRF114, as eloquently described by Rob, is a clinical stage program that is early in its development, and in the Phase I first in human study, has demonstrated the activity to eliminate CCR8-expressing Treg cells in circulation, and thus establishes the proof of the antibody's mechanism of action in cancer patients. Coherus' ILT-4 program aims to relieve suppressive macrophages in the tumor microenvironment. All of these programs are scientifically supported in rational combinations with toripalimab. On the left side of this slide, further shows the aim of future IO treatments. After a decade of successful checkpoint inhibitors generating survival for cancer patients, as signified by the tail on the Kaplan-Meier curve, the next decade is looking to increase survival for more cancer patients. The combined portfolio gives an exciting and science-driven approach to activating antitumor immunity in a broad range of tumor types, with early clinical data showing antitumor activity, an acceptable safety profile, and immune activation for anti-IL-27 SRF388. We look forward to further the phase 2 clinical development in combination with our next generation PD-1 inhibitor, toripalimab. I'll now turn the call to McDavid Stilwell, our Chief Financial Officer. Thank you, Teresa. I'll begin by reviewing key terms of the transaction. This is a stock-for-stock deal in which Coherus will issue shares of common stock in exchange for all outstanding shares of Surface common stock. We estimate the value of the transaction at up to $65 million, inclusive of $40 million of enterprise value and $20 million-$25 million in Surface net cash projected at closing. The transaction pricing is based on Coherus' 5-day volume-weighted average price per share of $5.28. The final transaction value and number of shares issued to Surface shareholders will depend on the value of Surface net cash at closing. The transaction has been unanimously approved by the boards of directors of both companies, and we expect it to close in September. In addition to Coherus common stock, Surface shareholders will receive contingent value rights for 70% of the value of programs partnered with GSK and Novartis, as well as CVRs, representing 25% of any upfront payments Coherus receives for an ex US collaboration for SRF114, and 50% of the upfront Coherus receives for an ex US collaboration for SRF388. As Denny mentioned, the transaction has a positive financial impact for Coherus. The $20 million-$25 million in projected Surface net cash at closing will strengthen Coherus' balance sheet. Potential out licensing of ex US rights to SRF388 and SRF114 could raise significant non-dilutive capital in 2024 and 2025 after these programs have advanced through key clinical milestones. Coherus also stands to receive 30% of the value of milestones or royalties paid through the GSK and Novartis partnerships. Next slide. The acquisition comes at an opportune time as our biosimilar strategy is beginning to deliver the revenue growth we projected. Similarly, market share and net sales are growing rapidly since the activation of the Q code April 1st, as we expected. Today, we are introducing revenue guidance for the 2Q 2023. We expect combined UDENYCA and CIMERLI net sales of $48 million-$53 million for 2Q. For the full year 2023, we maintain our guidance of at least $275 million of portfolio net sales, including at least $100 million of CIMERLI net sales. This transaction will not change our lean approach to operations. Very importantly, we are also today reaffirming our full-year expense guidance range of $315 million-$335 million of combined R&D and SG&A expenses. This range includes approximately $50 million in non-cash stock compensation expense. It excludes the acquisition cost of Surface Oncology and also upfront or milestone payments payable in connection with other collaborations. Over the past year, we have achieved very significant reductions in operating expenses and cash utilization. We will continue to look for opportunities for savings. As Denny mentioned earlier, this acquisition will enable us to prioritize our R&D activities on the most competitively positioned programs. We expect to cut at least $50 million in budgeted R&D expenses through 2025. We continue to project that Coherus could become cash flow positive again in 2024. I will now turn the call back to Denny for closing remarks. Thank you, McDavid. I'd like to return to the combined pipeline and show you all the exciting near-term catalysts we're expecting from the programs. As you can see, our pipeline is robust, diversified, complementary, synergistic, focused on unmet needs, and extending patient survival in cancer. We are full court pressing the entire cancer immunity cycle, not just focusing on checkpoint inhibitors. These targets represent the most forward-thinking in the IO field and our next-generation approaches. I remind you again, we pair this with our revenue drivers and our expanding commercial portfolio. We anticipate strong news flow on both fronts going forward for you. We'll continue as usual with presenting data when available at scientific medical conferences. I look forward to seeing you all in our research day in Q4 this year. Our operator will now open the call to questions. Certainly. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. One moment for our first question, which comes from Robyn Karnauskas of Truist. Your line is open. Hi, good morning. This is Nishant. I'm one for Robyn. Congrats on the progress here. The first question on MA. You talked about bringing, you know, other molecules to partner with toripalimab or even combine with toripalimab. Considering the, your spend and, you know, profitability insight, how should we think about additional M&A? Like, also, should we anticipate like additional partnerships, agreements with toripalimab in future? I have follow-up. Thank you, thank you for the question. I think with respect to the pipeline and pairing toripalimab with other assets, we would probably do such transactions in partnering mode, taking toripalimab post-approval for nasopharyngeal and pairing it up with selected compounds. I don't foresee further M&A of this type with further products in the pipeline. We continue, however, to look at top line and driving the top line with the revenues, I think that's, that goes hand-in-hand with the IO story. Great. Just one, so in terms of combination studies with toripalimab, you know, what should we think about the next test here? You know, considering like, you know, both those Surface assets would benefit from being used in combinations with toripalimab, like, what can you do quickly to, you know, jump into, like, pivotal combination studies here? Oh, that's a great question. I'll let Dr. LaVallee, our chief development officer, address that. Theresa? Yeah, I think we, Rob and I both talked about the obvious overlaps, both scientifically and clinically, but we'll have to do a full portfolio prioritization. As the deal closes, we'll be announcing more and plan to have a science day in the fourth quarter to really walk through how we're gonna prioritize things and take them forward. Great. Thank you. One moment for our next question. Our next question will come from Ash Verma of UBS. Ash, your line is open. Hi, good morning. Thanks for taking my questions. I had a couple, and I'll get back in the line after that. Just for SRF388, for squamous non-small cell carcinoma, it seems like pembro PFS OS benefit is pretty remarkable irrespective of PD-L1 expression. This field is where SRF388 could fit in here. For CCR8, yeah, I wanted to understand, like, the competitive landscape. I think there are five other companies pursuing this mechanism in early stage. Can you elaborate, like, what's the value proposition and how SRF114 may compete with other programs? Thanks. Okay, I'll let Dr. LaVallee take your first question, first. I think it was pursuant to pembro. In the squamous for PD-L1 expression. I think from the SRF388 data that Rob shared with us today, it's incredibly exciting to see particularly tumor shrinkage in patients who have been PD-1 experienced. The second line on small cell lung cancer is an incredibly important space that is highly underserved. Doing combinations and reversing PD-1 resistance is an incredibly exciting opportunity. Moving into frontline, we'd have to evaluate activity in that setting. In terms of SRF114, it's very competitively positioned. All assets currently are in phase I. Did you have a follow-up, Ash? Yeah, if you have a few minutes, I mean, I just wanted to understand two things really. One is just, like, as you look at these programs, right, like, what is the pre-sales opportunity in your mind of this portfolio? Sometimes the cancer can be a little bit difficult to compete in terms of established PD-1 therapies. Is it possible here that you may pursue a lower-cost oncology drug strategy for this portfolio to gain some competitive advantage? Yeah, I think our focus, as we've said, is really looking to extend patient survival and change the treatment paradigm. These combinations really have the potential to expand, not only improve on current PD-1 regimens, but also address patients who are currently treated with PD-1 inhibitors. Focused on the patient, focused on survival is really where we're looking. Yes. I would further add for you, Ash, that, you know, we are focused overall as an organization, in terms of addressing unmet patient need and what, as Theresa said, with the patient need. On the biosimilar side of the business, you know, that's access to very competitively priced drugs, and, you know, that's the paradigm. Over on this side here, though, I think our, as Theresa said, you know, the patient need is to extend survival, and, you know, those are two sides of the same coin. Great. Thank you. Thank you. One moment for our next question. Sure. Hi, Boris. Hi, how are you? Congratulations on the deal. I just had a question here on, the 388. I'm just curious, obviously, you plan to combine it at some point with toripalimab. What is that timeline for that? Do you, and do you need to start building kind of a safety database of the two drugs combined together? Is there some kind of a plan to start a combo study soon? My second question is on the data expectations, both at in 4 Q, when we're gonna see some additional monotherapy data, as well as 1 Q next year for hepatocellular. What are you looking to see combo forward? I'm sorry. What are we looking to... Yeah. In terms of efficacy, what efficacy bar do you really feel you need to see at that point to move this forward? Got it. Great, Theresa? The first question about what do you need to do to put Tori into the study? Clearly, the current study that Surface has ongoing has a 388 arm with pembro. We would quickly amend that study to include toripalimab. The rest of it, the PD-1 class, the nice data package that Surface has generated, has shown very good safety profile and combination with other agents, including angiogenesis inhibitors and checkpoint inhibitors. The totality of the data should be pretty seamless in terms of doing that rapidly. The rest of it will look for prioritization through our full review and discussions with the Surface team and announce after deal closing at the Science Day in terms of what we would need to see to advance things. We will be looking for a high probability of success to go rapidly. Great. Thank you very much. One moment for our next question. Our next question will come from Balaji Prasad of Barclays. Balaji, your line is open. Hi, good morning. This is Xiao, I'm for Balaji. Thanks for taking our question. Just a quick one on the potential CCR8 Treg and PD-1 combo. Just like in normal biology, you, if you are inhibiting PD-1 at the same time, depleting the Tregs, you will have more CDA positive T-cells without trigger any immune AEs concerns? Thank you. I think that's a good question in terms of the combination with immunotherapies. That has always been a concern, is to look at increased toxicity, and the phase I study will continue to address that. We've also seen combinations with other Tregs targeting agents without terrible toxicity. I think that the data having the high selectivity to the CCR8 positive Tregs, as Rob nicely walked through, gives us that selectivity to the tumoral resident Tregs, and that should preserve other autoimmune mechanisms. The data in the clinical study will read out. Yeah. Rob, any further comment on the MOA here with CCR8? Is this the question? I definitely agree with Theresa that, obviously, with any novel combination, you have to wait to see the clinical data. The whole purpose, though, of targeting CCR8, as opposed to one of the many other ways to target Tregs, is that you're really focused on the intratumoral Tregs. That should have a significant impact on the potential safety, right? When you look across the Treg depletion space, there are many other approaches, most of those approaches target peripheral Tregs and also effector T cells, all of which have additional toxicity. Got it. Thanks. One moment for our next question. Our next question seems to come from Douglas Tsao of H.C. Wainwright. Your line is open, Douglas. Hi, good morning. Can you hear me? Yeah. Good morning, Doug. Hey, good morning. Congrats on this transaction. Just in terms of the moving parts, obviously, you're adding to your balance sheet as well as some rationalization. I mean, just to, you know, how much pipeline expansion can you ultimately envision with these new service assets, you know, especially in combination with Tori? Obviously, you highlighted a couple of different tumor types that you would wanna initially target or seem logical to target initially. How much broader, more broadly, can you pursue? I mean, obviously, how much does that depend on what you see from the biosimilars business and from the other product launches over the next couple of years? Thanks, Doug. I'll let Dr. LaVallee take that one for you. Theresa? Hi, Doug, thanks. As we've kind of walked through in the script, today in the presentation, that we've always been focused, and we've said repeatedly that doing additional studies with toripalimab has been planned to see approval beyond NPC. This really fits in with what we had already planned. As we go through the opportunities, the wealth of opportunities here, and do prioritization and have a development plan that we can really bring forward to folks in the fourth quarter at the Science Day, we'll reveal that. We're incredibly focused on being within the budget that we've outlined and returning to profitability next year. The other point I'd make, Doug, is, one of the things we really like about SRF388, it's in the front in a space that's not very crowded. Whereas, you know, some of the other things, such as our TIGIT assets, as you know, there's, it's a little more crowded. There's quite a few people doing quite a few things. I think this is a more straightforward development path in combination with toripalimab. Okay, great. Thank you so much. One moment for our next question. Our next question will come from Jason Gerberry of Bank of America. Jason, your line is open. Hey, thanks. A couple questions just on IO 2017 and the HCC opportunity. First, just the data that's been generated so far, just wanted to clarify. Of the 7 partial responses, how many are confirmed versus unconfirmed? I think you typically need 2 scans to qualify as a confirmed response. I just wanted to understand that given the amount of follow-up involved with the study so far. As we look forward to the first half 2024 update for this asset, obviously right now, the ORRs are kind of trending in line with atezo/bev as a combination. I think we typically need to see, like, 10%-15% better ORR on a cross-trial comparison basis to kind of get confidence that you've got something better. Will you have sufficient scans and follow-ups of all these patients to kind of make a determination with the first half 2024 data update? Thanks. Thank you. Rob, would you like to address that? I'd be more than happy to. As you rightfully pointed out, with the immature setting of the data, with less than or approximately half the patients having more than 1 on-treatment scan, there just hasn't been enough time for many patients to confirm. Right now, 4 of the responses are confirmed. I think the second half of your question had to do with cross-trial comparisons and what we expect from these data. I really want to stay away from setting an expectation now. I think the important thing is that over the next 6 months, the data mature, we get a better sense of what that response rate looks like, both from a RECIST setting and also an HCC-specific RECIST setting. And then also, we care very much about some of the other efficacy metrics, such as duration of response and progression-free survival. Your question about what's the appropriate or where to go with cross-trial comparisons is a very interesting one, because the the the primary reference point has been the phase 3 trial with atezo/bev, with a response rate on the order of about 30%. Interestingly, at ASCO now, with the MORPHEUS data, we've seen over time a degradation of that response rate. Obviously, small patient numbers, and still need more maturity, but the control arm response rate in that trial was sub 20%, actually, right about 11%. We need to get a really good sense of these patients over time and see how they do. Certainly, I believe these data are trending in a very competitive direction. Then the opportunity to combine with a powerful PD-1, as well as the potential to combine with a drug like, the anti-TIGIT antibody, I think is a really a wealth of opportunities for patients with liver cancer. Got it. Thanks, guys. I'm showing no further questions and would now like to turn the conference back to Coherus CEO, Denny Lanfear, for closing remarks. Thank you, operator, and thank you all for joining us this morning to discuss this very, very exciting combination of two companies and the very significant clinical, strategic, and mechanism of action synergies which are driving us forward. We look forward to talking to you all again on our next call in August, and we look forward to seeing you on our research day in Q4. Bye-bye. This concludes today's conference call. Thank you for participating. You may now disconnect.