Good morning, everyone, and welcome. Today, we will review the initial clinical and translational data from the phase I trial of LYL797, our first-generation ROR1-targeted CAR T-cell product candidate, enhanced with novel anti-exhaustion technology. Please review the press release and Form 8-K issued earlier today, which are available on our website at lyell.com. In addition, the supplemental slides discussed today are available on our website in the Events and Presentations section. Speakers on today's call include Dr. Lynn Seely, our President and Chief Executive Officer; Dr. Gary Lee, our Chief Scientific Officer; and Dr. David Spigel, the Chief Scientific Officer at the Sarah Cannon Research Institute. Dr. Spigel is a medical oncologist, lung cancer expert, and a lead investigator in our LYL797 clinical trial. Before we begin, I'd like to remind you that during today's presentation, we will be making forward-looking statements that are subject to certain risks, uncertainties and other factors that could cause actual events to differ materially from those referred to in any forward-looking statements. For a discussion of the risks and uncertainties associated with our forward-looking statements, please see our press release issued today, as well as our most recent filings with the SEC. We disclaim any obligation to update our forward-looking statements. With that, I'd like to turn the call over to Lynn. Thank you, Ellen, and thank you to everyone joining the call. Today, we are pleased to announce the initial data from our first-in-human phase I clinical trial of LYL797. We have invited Dr. David R. Spigel to present the clinical data and to provide his perspective and context. But first, let me begin with an overview of the data to be discussed today and some background information. In this first data set of 20 patients treated with LYL797, we saw clear evidence of dose-dependent clinical activity. The data includes 16 patients with relapsed refractory triple-negative breast cancer and four patients with non-small cell lung cancer. At a dose of 150 million cells, which is the highest dose level we have cleared to date, we observed a 40% objective response rate, including two confirmed partial responses and a clinical benefit rate, defined as stable disease, partial response, or complete response of 60%. Overall, we observed a dose-dependent clinical benefit rate of 38% across the four dose levels evaluated to date. Our translational data showed that our ROR1 CAR T-cells overexpressing c-Jun and manufactured with Epi-R protocol successfully expanded and infiltrated solid tumors, with evidence of tumor lysis or cancer cell killing on histologic examination. We believe this is the first reported clinical trial demonstration of CAR T-cells infiltrating solid tumors. Patients without metastatic lung disease experienced only mild CRS and the expected cytopenia from lymphodepletion, with no dose-limiting toxicities. Our dose escalation has been progressing more gradually, however, in patients with lung metastases, as we have observed pneumonitis or lung inflammation in some patients. We are continuing to dose escalate patients in separate cohorts, those without and with lung involvement, defined generally as primary lung or metastatic lung cancer or with pleural effusion. We are currently evaluating the dose of 300 million cells in patients without and a dose of 75 million cells in those with lung involvement. All patients are being treated prophylactically with dexamethasone to mitigate pneumonitis. With these data in hand that demonstrated dose-dependent clinical activity and validate the benefit of our reprogramming technologies with our first-generation ROR1 targeted product candidate, we are expanding enrollment to include patients with ROR1+, platinum-resistant ovarian or endometrial cancers. In addition, we expect to initiate a new phase I trial of LYL797 in patients with either ROR1+ multiple myeloma or chronic lymphocytic leukemia in the second half of this year. There is a high incidence of ROR1 expression in these patient populations associated with a poor prognosis, with no approved ROR1-directed therapies and too many deaths from cancer, despite currently available treatments. Our LYL797 clinical program was designed based upon data from an elegant clinical experiment conducted at the Fred Hutchinson Cancer Center, examining why CAR T-cells have been effective in hematologic malignancies, but not in solid tumors. Investigators treated patients with chronic lymphocytic leukemia with a ROR1-targeted CAR T-cell and observed good cell expansion without evidence of T-cell exhaustion, and the treated patients responded. Using the same ROR1 construct, the investigators also treated 14 patients with either ROR1+ triple-negative breast cancer or non-small cell lung cancer, and something very different happened. The cells did not expand well in most patients and rapidly developed markers of exhaustion, such as TIGIT and LAG-3. There was also a lack of evidence of CAR T-cell tumor infiltration in the study. Importantly, none of the 14 patients responded after a single dose of up to 200 million cells. For the first time, it became clear that lack of T-cell expansion and resistance to T-cell exhaustion, resulting from repeated antigen stimulation, are two key barriers that must be overcome to develop a successful CAR T-cell therapy for solid tumors. Lyell's proprietary technologies are designed to endow the body's T-cells with the ability to resist exhaustion and expand in the immunosuppressive tumor microenvironment, and most importantly, to kill cancer cells. The initial translational data we'll be presenting today validated these technologies. LYL797 is a ROR1-targeted CAR with a very similar construct to that used in the Fred Hutch clinical trial. What is different is that Lyell's T-cells are reprogrammed to overexpress c-Jun. c-Jun regulates a critical transcription factor in the AP-1 pathway, which plays a key role in driving T-cell effector function. A functional deficiency of c-Jun leads to T-cell exhaustion, whereas overexpression of c-Jun helps the T cells resist exhaustion, even in the setting of repeated antigen stimulation. These cells are also manufactured using Lyell's proprietary Epi-R technology that generates more stem-like cells and the ability to self-renew and persist. When LYL797 ROR1 CAR T cells with these reprogramming technologies, depicted in the middle panel in purple, are compared to a control ROR1 CAR in black or to mock T cells in gray, you can clearly see the significant tumor reduction and enhanced tumor control with LYL797, resulting in prolonged survival in this in vivo tumor model. The first in-human study for LYL797 was designed as a dose escalation study with four dose levels, followed by dose expansion at the recommended phase II dose in patients with ROR1+, relapsed refractory, triple-negative breast cancer or non-small cell lung cancer. The study objectives are safety and tolerability, the objective response rate and durability of response, establishment of the recommended phase II dose, and assessment of T cell phenotype and infiltration. This slide depicts the study's updated dose escalation schema with associated dose levels. The first dose level we evaluated was 50 million cells, which was cleared without a dose-limiting toxicity or DLT. At a dose of 150 million cells, two DLTs of pneumonitis occurred in two patients with underlying lung metastases. However, no evidence of pneumonitis occurred in patients without lung metastases. A decision was made in collaboration with the study's safety monitoring committee to continue to dose escalate in patients without lung involvement. Patients with lung involvement were de-escalated to 100 million cells and treated with a prophylactic regimen of fluticasone, azithromycin, and montelukast. Two patients with lung involvement at this dose level also developed DLTs and pneumonitis, and patients with lung involvement are currently being enrolled into the 75 million cell cohort. All enrolled patients are now being treated prophylactically with dexamethasone, the standard of care treatment of patients with pneumonitis, to mitigate this occurrence. I will now turn the presentation over to Dr. Spigel, Chief Scientific Officer at the Sarah Cannon Research Institute, who will walk you through the clinical data. Dr. Spigel is a leader in clinical trials with a particular expertise in lung cancer and thoracic oncology. He is also a LYL797 lead investigator and so is uniquely qualified to help put our clinical data into perspective. Dr. Spigel? Thank you, Lynn. I am pleased to be here with the Lyell team today to discuss these promising initial results from the LYL797 clinical trial. Let me begin with the characteristics of the 20 patients included in this data set. The mean age is 52 years, and 80% of the patients treated had triple-negative breast cancer, with the remaining 20% with non-small cell lung cancer. These patients were heavily pretreated, with the average number of 6 prior lines of therapy in the metastatic setting. All patients had performance status of 0 or one, indicating an acceptable level of function for enrollment. This slide summarizes the dose-dependent clinical activity observed to date in the trial. Of the 20 patients in this data set, 16 are valuable for efficacy. Four do not yet have 30-day scans available. Two patients, both with triple-negative breast cancer, achieved confirmed partial responses through day 90 at the 150 million cell dose, and we will describe those patients in more detail. Additionally, 60% of patients at the 150 million cell dose and 38% of patients overall achieved clinical benefit from LYL797 in a dose-dependent fashion, with clinical benefit defined as a best response of stable disease or a partial or complete response. This waterfall plot depicts the best response of the target lesions for the 16 efficacy-evaluable patients. The dark purple bars represent the target lesion tumor size reduction from baseline observed in patients treated at the 150 million cell dose level, the highest dose to be cleared to date. This reduction is clearly increased from patients treated with the 50 or 100 million cell doses. Most target lesions represented here were progressing between the screening and the baseline scans, so the stable disease and tumor reduction observed represent a clear change in the rate of cancer progression. When the data are plotted by dose and the clinical benefit rate, defined as stable disease, partial response, or complete response, a pattern of dose-dependent clinical activity is emerging, suggesting that 150 million cells is an active dose. That being said, higher cell doses are needed to achieve greater durability. In addition to having stable disease by imaging, several patients also had additional observations of clinical benefit, including weight gain, decreased pain, and improved liver function tests. We are looking forward to seeing the results from more patients dosed at the 300 million cell dose level and above. We had originally planned to test doses up to 900 million cells, but we are already seeing clinical activity at the low dose of 150 million cells. Safety data in 18 evaluable patients demonstrated that LYL797 have acceptable tolerability in patients who do not have metastases to the lung. However, in those with lung metastases, 4 cases of grade 3 pneumonitis were reported, all prior to the implementation of dexamethasone prophylaxis. Mild grade 1 or 2 cytokine release syndrome was manageable with tocilizumab and steroids. No case of ICANS has been attributed to LYL797. The most frequently reported grade 3 or higher related adverse events were pneumonitis and hypoxia, and the expected cytopenia from lymphodepletion. The first patient with pneumonitis had acute grade 5 respiratory failure on day 41, outside of the DLT reporting period. Subsequently, all patients were treated early for any sign of pneumonitis with good results. While the adverse events of pneumonitis are not desirable, we have learned a great deal about them as we have proceeded gradually with dose escalation. As many of you may be aware, pneumonitis, or lung inflammation, is observed with radiotherapy and several approved cancer therapies, such as checkpoint inhibitors and antibody drug conjugates, so medical oncologists are experienced in diagnosing and treating it. Pneumonitis is, in fact, something we see relatively commonly in oncology clinical practice. We believe pneumonitis observed following LYL797 infusion is most likely related to local cytokine production due to the burden of underlying lung metastatic disease. Specifically, pneumonitis has not been observed in patients without lung involvement. It has a predictable onset of between four and 10 days after treatment. Investigators have been treating it early and aggressively with high-dose steroids with good results. We're now using steroids prophylactically in all patients, although pneumonitis has only been observed in patients with lung metastases. We appreciate some of you may question whether dexamethasone prophylaxis may limit the effectiveness of CAR T cell therapy, but data from the ZUMA-1 cohort 6 safety management study of dexamethasone prophylaxis prior to CD19 CAR T cell therapy demonstrated that there was no loss of efficacy or durability through two years of follow-up, while there was a decrease in CRS and neurologic adverse events. As with CRS and ICANS following CD19 CAR treatment, those of us treating solid tumors with lung metastases or primary lung cancer with LYL797 must learn to safely manage pneumonitis as we dose escalate to more effective and durable doses. I'm encouraged by the progress, as are the other investigators, based upon the number of patients being referred for enrollment. To provide more perspective on the level of clinical activity we are observing, I want to tell you about two patients enrolled in the study at our institution. The first patient is a 51-year-old woman with triple-negative breast cancer, previously treated with doxorubicin, cyclophosphamide, pembrolizumab, paclitaxel, and carboplatin. At progression, she received capecitabine and then doxorubicin before entering the LYL797 trial. She received 150 million CAR T cells and tolerated the treatment well with minimal side effects. On abdominal CT scan, the patient had a rapidly enlarging pelvic mass that increased substantially from her screening to her baseline scan in just 30 days. After receiving LYL797, this mass significantly decreased from 17.6 to 11.4 centimeters. Her hepatic metastases decreased in size as well. These lesions remained stable through 90 days, but she unfortunately developed a new lesion. It is certainly possible that a higher initial CAR T-cell dose may have led to a higher number of persistently active CAR T-cells able to prevent that progression. I would also like to describe the course of a patient with non-small cell lung cancer. This patient is a 49-year-old male who had failed multiple lines of prior treatment, including immune therapy and an experimental interleukin-2, before receiving LYL797 at a dose of only 50 million cells. He had no CRS and no grade 3 adverse events from LYL797. The patient had a rapidly growing right upper lobe lesion that had doubled in size in the three months prior to CAR T-cell treatment. After treatment, the patient experienced weight gain, better sleep, and an improved quality of life, and his cancer remained stable for four months. I would like to leave you with the tumor reduction plots of two patients. Both patients had rapidly growing tumors in the month prior to CAR T treatment, as shown in gray. Both of these patients had confirmed partial responses following CAR T cell infusion, demonstrated in purple. These data demonstrate that LYL797 has activity at a dose of 150 million cells. I'm encouraged by the data obtained to date and look forward to treating more patients with non-small cell lung cancer and other tumor types at higher doses. I'm also quite encouraged by the emerging translational data from this study, which Lyell's Chief Scientific Officer, Dr. Lee, will describe to you now. Data which suggests the reprogramming technologies incorporated into 797 are adding value. Thank you, Dr. Spigel. We have a robust translational program built into the LYL797 clinical trial. Our hypothesis is that by reprogramming T cells to resist exhaustion and possess more similar qualities, we can improve T cell expansion and achieve solid tumor infiltration and anticancer activity. Our initial translational data suggests we are indeed on the right path. First, we observed more robust peripheral CAR T-cell expansion than has been previously reported with ROR1 CAR T-cells in patients with solid tumors. Second, LYL797 CAR T-cells had lower expression of exhaustion markers and demonstrated the desired effective memory or stem-like phenotype. And to our knowledge, we are reporting for the first time in solid tumors, robust and persistent CAR T-cell infiltration into tumors with associated histologic evidence of tumor lysis in some samples, including in tumor biopsies from both of our confirmed responders. We believe our anti-exhaustion technology has enabled T-cell infiltration into solid tumors. Let me now show you these data. CAR T-cell expansion in the first 11 patients across three dose levels is shown in the graph on the slide. Peak expansion occurred between days eight and 11, consistent with data from other CAR T-cell therapy in patients with solid tumors. The median peak expansion for all 11 patients was more than 11,000 copies per microgram of DNA. This peak is more than 5 times higher than that from the previously reported ROR1 CAR T-cell clinical study conducted at the Fred Hutch. We also observed a median peak expansion to about 16,000 copies per microgram of DNA at a dose level of 150 million CAR positive T-cells, a peak threefold higher than observed at the 50 million cell dose. We then evaluated the phenotype of the expanded CAR T-cells to examine whether or not we are accomplishing our goal of reprogramming T-cells to resist exhaustion and maintain a stem-like phenotype. TIGIT is a well-known marker of T-cell exhaustion. The graph on the left-hand side of this slide depicts the percentage of TIGIT-positive or exhausted CAR T-cells in the initial infusion product and at the peak of the expansion in patients with solid tumors. In a previous study of ROR1 CAR T-cells that did not incorporate c-Jun expression and the Epi-R manufacturing protocol, the CAR T-cells rapidly developed an exhausted phenotype after infusion, with nearly 100% of the CAR T-cells identified as TIGIT-positive. In contrast, LYL797 CAR T-cells, shown in the panel on the right, had only a small increase in the percentage of TIGIT-positive exhausted CAR T-cells when assessed at day 11. These translational data demonstrate for the first time in patients, that c-Jun overexpression allows CAR T-cells to resist exhaustion in patients with solid tumors, just as it did in our in vitro and in vivo preclinical models. To further support these data, we evaluated a broader set of exhaustion markers. RNA sequencing and transcriptomic analyses were conducted on the LYL797 study samples. While publicly available ROR1 CAR T-cell data are not available for comparison, we perform an analysis to benchmark against the bookends of a spectrum of T-cell exhaustion. We identified published transcriptomic data from two CD19 CAR T-cell clinical studies in hematologic malignancies, which we use as a low exhaustion T-cell benchmark, and use transcriptomic data of Tumor-Infiltrating Lymphocyte, or TIL, collected from patients with triple-negative breast cancer to represent the bookend of fully exhausted T-cells. As you can see, looking across a broad set of genes, including TIGIT, PD-1, LAG-3, or a published exhaustion-related gene set of 18 genes, LYL797 CAR T-cells most closely resemble the low CD19 exhaustion CAR T-cells, rather than the more fully exhausted TIL. This analysis provides further evidence that the c-Jun expression technology we have incorporated into LYL797 mitigated CAR T-cell exhaustion. From the same RNA sequencing data set, we assessed the differentiation of the LYL797 CAR T-cells in the peripheral blood from patients with samples obtained at days 11 and 22. We have previously reported in pre-clinical studies that LYL797 cells made using our Epi-R manufacturing protocol, have higher proportions of cells with stem-like and memory-like phenotypes. We now show a similar profile for the first time from patient samples. The majority of the LYL797 CAR T-cells in the peripheral blood at days 11 and 22 have a stem-like or effector memory phenotype demonstrated in blue and green, in contrast to just the low percentage with a short-lived, terminally differentiated phenotype, shown in orange. This is exactly the profile we hope to achieve. Notably, you can see in the right panel, this phenotypic profile is consistent with that observed in CD19 CAR T-cells in samples from patients with hematologic malignancy. So far, I've shown you analyses and characterization of the LYL797 CAR T-cells in peripheral blood. But in the solid tumor setting, the critical battleground is in the tumor. We have obtained nine on-study tumor biopsies between days 21 and 30 post-infusion to assess for the presence of LYL797 CAR T-cells. We are pleased to tell you that we have observed the presence of CAR T-cells in all nine evaluable biopsy samples analyzed today. To our knowledge, this is the first report of robust CAR T-cell infiltration into solid tumors in patients. In this slide, on the left-hand side, you're looking at a standard H&E stain histology slide from a tumor biopsy. We then use a multi-marker in situ hybridization assay designed to co-stain for the ROR1 CAR messenger RNA in red and the T-cell specific mRNA in green, to accurately identify our LYL797 CAR T cells. The nucleus of the cell stains in blue. In the white boxes, you can see the presence of green, red, and blue staining, clearly identifying the LYL797 CAR T cells present in this representative on study tumor biopsy. We believe the T-cell infiltration into solid tumors were enabled by our anti-exhaustion technology. This is a similar slide, now showing a tumor biopsy from patient number eight, a 53-year-old woman with triple-negative breast cancer with lung and peritracheal lymph node metastases. She received a dose of 150 million LYL797 cells and experienced grade 1 CRS and grade 3 pneumonitis. She received tocilizumab and high-dose steroids, and her pneumonitis was markedly improved after 48 hours and rapidly resolved. She had a confirmed partial response, and the LYL797 CAR T cells are demonstrated here, infiltrated into the tumor, highlighted by the white square boxes on the right panel. The patient was subsequently referred for resection of her peritracheal lymph node and her slowly progressing left upper lobe lung metastasis four months after LYL797 treatment. We were fortunate to receive tissue from this operation. A stable peritracheal lymph node was resected at the time of the patient number eight surgery and showed no evidence of disease post-LYL797 treatment. The resected lung mass demonstrated areas of necrosis, with remaining area of tumor, as shown on the H&E stain section on the left. Remarkably, the right-hand panel clearly shows LYL797 CAR T cells present in the tumor tissue four months after CAR T-cell infusion, as demonstrated by the punctate red area coinciding with the green and blue staining. These images tell us we are successfully achieving CAR T-cell persistence. While it's exciting to see robust CAR T-cell infiltration, importantly, we also observe histologic evidence consistent with tumor cell killing in several biopsies. Here, we show you three examples of on-study tumor biopsies demonstrating a T-cell-rich inflammatory infiltrate in the settings of remaining scattered tumor cells. This type of histologic picture was frequently observed in our LYL797 in vivo preclinical models and is consistent with CAR T-cell infiltration and tumor lysis. The three biopsies shown here, including samples from both patients with confirmed partial clinical responses, further suggest our ROR1-targeted CAR T-cell product candidate with anti-exhaustion technology, was associated with tumor cell killing. With that, I'll turn the call over to Lynn. Thank you, Gary. To summarize, LYL797 ROR1-targeted CAR T-cells had dose-dependent clinical activity and expanded, infiltrated, persisted, and killed tumor cells in patients with triple-negative breast cancer. We have observed a 40% objective response rate and a 60% clinical benefit rate at a dose of 150 million cells, the highest dose cleared to date. Importantly, we are continuing to dose escalate. I'll also mention that the manufacturing success rate to date at our Lyell facility in Bothell has been 100%. This not only makes us feel good about the decision we made to invest in our own manufacturing capability, but also gives us confidence that we can execute well as we continue dose escalation and begin dose expansion. There's been no significant safety signal observed related to LYL797 in patients without lung involvement, and we are treating all patients with steroid prophylaxis to mitigate the pneumonitis observed in patients with lung involvement. The robust translational data demonstrated persistent infiltration present in all evaluable on-study tumor biopsies, with histological evidence of tumor lysis in some samples. These initial clinical and translational data validate the preclinical models demonstrating the value of c-Jun overexpression and Epi-R manufacturing in LYL797 ROR1 CAR T-cell, and importantly, validate our thesis that our c-Jun and Epi-R technologies can improve the clinical benefit of ROR1 CAR T-cell activity. We are very encouraged by the results we have reviewed today and are focused on moving forward to select the recommended phase II dose for LYL797 expansion cohorts. We need to generate data at higher doses expected to achieve more durable responses. We will also include patients with platinum-resistant ovarian cancer or endometrial cancers in the current cohorts. In addition, we plan to file an IND to initiate a new study evaluating LYL797 in multiple myeloma and chronic lymphocytic leukemia now that we have observed clinical activity. We are also moving forward with our next generation ROR1-targeted CAR T-cell candidate, LYL119. Today, we announced that the IND has been submitted, and we are awaiting clearance from the FDA. The LYL119 protocol includes enrollment of patients with ovarian, endometrial, non-small cell lung cancer, triple-negative breast cancer, and colorectal cancer. This compelling early clinical data from LYL797 gives us even greater confidence to advance LYL119, which incorporates four proprietary technologies to provide more significant anti-exhaustion capability and persistence in our T-cell. In addition to c-Jun overexpression and Epi-R, LYL119 is also enhanced with NR4A3 knockout and Stim-R. NR4A3 gene knockout, edited using CRISPR/Cas9, builds on our approach to resist exhaustion by removing a protein that negatively regulates the AP-1 pathway, and in preclinical models, acts in concert with c-Jun overexpression to markedly enhance the durability of cancer cell killing. Stim-R is a potentially transformational manufacturing process that uses mesoporous silica microrods to present antibodies and cytokines, and to activate T cells in a much more physiological way. These stackable technologies are all designed to improve our CAR T cells' ability to resist exhaustion, persist, and bring durable benefit to patients with solid tumors. So just how much more potent is our next generation ROR1 CAR T, LYL119? This slide shows a preclinical comparison between LYL797 in purple and LYL119 in gold. Both LYL797 and LYL119 demonstrated excellent, and in fact, indistinguishable tumor control and survival at CAR T cell dose levels as low as 1 million CAR T cells, as shown in the top panels. LYL119, however, eliminated tumors and prolonged survival at the very low dose level of only 100,000 CAR T cells in a tumor model that has now been validated by our clinical experience. We believe this improvement in cell killing results from the even more powerful anti-exhaustion technologies we are deploying in LYL119, designed to increase cell expansion, tumor infiltration, and persistence. We are very excited about the potential of this next generation ROR1 candidate, as it could represent a step change in anti-exhaustion technology, and look forward to getting it into the clinic. ROR1 is expressed in many cancers, and expression is associated with a poor prognosis. Based on the initial evidence of clinical activity, we are already screening and are ready to enroll patients with ROR1+, platinum-resistant ovarian and endometrial cancers into our LYL797 protocol, indications where an estimated 50% of patients have tumors that express ROR1. We are also announcing that we intend to initiate a new clinical trial to evaluate LYL797 in hematologic malignancies, including multiple myeloma and chronic lymphocytic leukemia. While there are a number of approved treatments for these diseases, including BCMA and CD19 CAR T-cell therapies, the malignancies relentlessly progress, and patients need new therapies based on novel targets. Before I close, I want to highlight our planned upcoming milestones and to remind you that we have a strong balance sheet of $526 million that provides a cash runway into 2027 through multiple clinical milestones. For LYL797, in the second half of this year, we expect to begin enrolling patients with ovarian and endometrial cancer, submit the IND for multiple myeloma and CLL, and to initiate dose expansion in the tumor types indicated by the emerging data. We intend to update you on our progress in late 2024 or early 2025. Finally, we anticipate presenting additional clinical data at a major medical conference in the first half of 2025. For LYL119, we look forward to the clearance of our IND and plan to provide a progress update on this program no later than the first half of 2025, and expect to present initial clinical data in the second half of the year. And although not the topic of today's call, we look forward to presenting initial clinical data from our tumor-infiltrating lymphocyte program, LYL845, later this year. In closing, I'd like to express our gratitude to the patients, caregivers, investigators, clinical site teams and Lyell employees for their contributions to advance innovative cell therapies to people with cancer. Charlie Newton, Lyell's Chief Financial Officer, will now join us as we open the call for questions. Operator? Thank you. Ladies and gentlemen, as a reminder, to ask a question, you will need to press star one one on your telephone and wait for your name to be announced. To withdraw your question, simply press star one one again. Please stand by while we compile the Q&A roster. Our first question coming from the line of Salveen Richter with Goldman Sachs. Your line is open. Good morning. Thanks for taking my questions. Could you speak to whether you looked at any additional markers beyond TIGIT, and how representative of the overall repertoire of exhaustion markers TIGIT is? And then speak to your confidence that you're preventing exhaustion of the CAR T cells versus delaying exhaustion. Thank you. Good morning, Salveen. Gary, why don't you take that question? Yeah, excellent question, Salveen. I think we highlight TIGIT in part because this is the one marker that we've also identified in our preclinical study, where c-Jun overexpression have made the greatest impact. We also see reduction in expression of other markers, and we're looking forward to share those data in the future. In addition, I think the transcriptomic data that we showed did look at a set of 18 genes, including TIGIT, PD-1, LAG-3, CD29, TOX, et cetera, which are a really broad set of common exhaustion-related genes. And clearly, in that setting, in that analysis, we saw that our ROR1 CAR T cells in the LYL797 study mostly resemble what we see in the CD19 CAR T setting and very different from exhausted TIL. I think one thing, not everyone appreciates is that we know when we're able to help the T cells resist exhaustion, we see much better T-cell infiltration. That's been shown in our preclinical experiments, and I think in the previous ROR1 studies, without our anti-exhaustion technologies, they weren't able to demonstrate CAR T-cell infiltration. We think we're very confident in the fact that these clinical data, as well as our preclinical data, validate these anti-exhaustion technologies. Great. If I could just add one more question, when do you think we'll see data from the 300 cell dose group, in addition to the prophylactic steroid implementation? Yes, we intend to give an update as we move into expansion and, no later than the end of this year or early next year. Great. Thank you. Thank you. Our next question coming from the line of Vikram Purohit with Morgan Stanley. Your line is open. Hi, good morning. Thank you for taking our questions. So we had two, first on lung involvement. So what portion of the triple-negative breast cancer patient population would you estimate has lung involvement, and especially for patients with the general level of pretreatment that you're seeing here? And then secondly, you mentioned that the 300 million cell dose is going to help strengthen the durability signal long term. What would you consider the threshold for a good durability profile in this patient population? Thank you. Dr. Spigel? Yeah, that's a good question. I mean, as we noticed, lung involvement may be an indicator of a risk for pneumonitis. In general, with triple-negative breast cancer, you know, lung involvement can occur, but patients obviously can have metastatic disease that does not include the lung. So we're being very cautious here. Patients with any evidence of metastases or pleural effusion, we're instituting prophylaxis with steroids to try to mitigate that risk. Now, the risk has been very predictable and manageable, and we think if we identify it early, we can help patients recover from that. Your question about the durability of the response, yes, we need to see better durability, and we believe that as we increase the dose, we've clearly shown our CAR T cells are expanding, they're persisting, they're infiltrating into tumor. So as we get more of them, we believe that's going to give us an even better result. Similar increases in durability have been seen with other cell therapies as they get to increase dose. Understood. And one follow-up from my standpoint. How does today's data update kind of impact your thinking on prioritizing 797 versus 119, if it does at all? Absolutely. We remain enthusiastic about both product candidates. I think the most important thing about LYL797 is we are seeing this dose-dependent clinical activity, and we have validated our anti-exhaustion technology. So number one, we know that we have an active drug. We need to, of course, determine the appropriate dose and how to manage the pneumonitis, but I think we have an active drug. And, and as, you know, maybe in a moment, Dr. Spigel can comment, it's very common with anticancer therapies to have to learn how to effectively optimize the benefit while minimizing the toxicity. I think with respect to LYL119, it has even more powerful anti-exhaustion technologies, which are really directed towards helping increase tumor infiltration. And so we believe that that has an even greater opportunity to enhance durability. So we feel like this is a real step forward for the field. It's the first demonstration with anti-exhaustion technologies, that we've been able to really demonstrate this nice, and impressive CAR T-cell infiltration into solid tumors associated with cell killing. And now, we need to continue forward and optimize. But Dr. Spigel, maybe you can comment on some of the examples you've seen in oncology where, we've had to do such. Yeah, it's a, it's a good, it's a good question and point. Look, what we're excited about in terms of the investigators is evidence of activity, and so now kind of making sure that everything is safe for patients. And as Lynn points out, you know, this is not new to us. We've as investigators, we've seen things emerge like pneumonitis with agents such as checkpoint inhibitors and more recently with antibody drug conjugates. This is something that's become quite familiar in investigation and now in clinical practice, as those drugs are commonly used in multiple tumor settings, including breast cancer and lung cancer. Pneumonitis is, you know, something you don't want for any of your patients, but we at least understand now how to identify it, how to recognize it in the clinic, and then, of course, how to make it reverse with things like steroids and supportive care, sometimes antibiotics. It is something I think all community oncologists are now accustomed to addressing, recognizing, and treating. And maybe you could comment on the CD19 CRS and ICANS and how that's evolved over time. Yeah, that's a good point. You know, I think back to a lot of new drugs that have kind of emerged, even things such as checkpoint inhibitors in 2015. You know, that seemed scary with all the inflammatory toxicities that doctors were not oncologists were not used to treating and now are pretty routine. You know, CRS, I think, and certainly ICANS, were quite daunting for community oncologists to imagine treating. You know, and those were, those were things we didn't think could make it into the community. And as you know now, that's, that's something that community oncologists are very attuned to, recognize, and has really not stopped the development of those programs from a research perspective or therapeutic modality in the approved setting. So use of agents such as tocilizumab, early hospital intervention, help us feel more comfortable managing those patients. It's something we talk to patients and their families about, and they still want those treatments. Got it. Very helpful. Thank you. Thank you. Our next question coming from the line of Eric Joseph with JP Morgan. Your line is open. Hi, good morning. Thanks for taking the questions. Can you clarify the level of activity, the clinical benefit rate that you're seeing in patients that- D idn't have lung disease or lung mets so far? Just yeah, that, and just curious about the context of, the disease, disease background of the patients where you, did observe partial responses. And, and then in thinking about sort of time to response, can you comment on that? I'm just wondering whether some of the stable disease events so far might have the potential to deepen with longer follow-up. Thanks. Sure. I'll start with that. So I think the, we have seen the 40% overall response rate or objective response rate in, at the 150 million cell dose. And I think, the patients that we observed this in, all of these patients are advanced metastatic patients that have had multiple lines of therapy. And, I'm sorry, I can't remember the other question. One was time to onset. Oh, time to onset. Actually, maybe you can comment on that, Dr. Spigel. Yeah, it's variable. I mean, the numbers are small, but, you know, patients are being followed very closely. Some patients and investigators reporting clinical benefits within the first week, actually. One of my own that I presented in the opening comments, actually, although not objective, radiographically, within the first seven days, the patient and his spouse were commenting on clear clinical benefit and changes that were very favorable. And we've seen, we've seen other clinicians, investigators report similar benefits in the clinic before we've done any imaging. So that's within the first one to two weeks. But we're following the protocol-specified assessments of imaging, you know, to objectively measure that. Okay, great. Thanks. Maybe just a quick follow-up. I know it's small data set overall here, but just anything so far in terms of any correlations you're seeing so far between response activity and sort of levels of ROR1 expression? Just wondering whether as you look to include... expand into different indications, whether you might refine sort of the threshold for what constitutes a ROR1 positivity to select the the- Yeah. In terms of patient- Sure. Thanks, Eric. These patients were all selected to be ROR1 positive. I think the assay is performing quite well. It is too early days for us to... These are too small numbers, as you might expect, for us to start to talk about correlation between ROR1 expression and response. And we are continuing, as we do with ovarian and endometrial cancer, to use the same cutoff and the same assay, 'cause we're pleased with how it's performing. Okay, great. Thanks for taking the questions. Thank you. Our next question coming from the line of Jason Zemansky with Bank of America. Your line is open. Good morning. Congratulations on the progress, and thank you for taking our questions. I was curious, are you exploring any other protocol adjustments, for those with, lung involvement? Anything to maybe get that, that 75, times ten to the sixth cell threshold up, especially if, if you're seeing, a dose-dependent response, you know, closer to the 300, mark? And then kind of part and parcel to that, is what you're seeing from the pneumonitis, can you tell, is it cell dependent, versus more of a general response, especially as you think about, you know, moving to 119? Thank you. Sure. Thanks for the questions, Jason. Dr. Spigel, do you want to comment? Yeah, sure. Those are great questions. So in terms of kind of adjustments to the program, so you know, the safety committee meets on a regular basis, and we've already instituted a program of dexamethasone or steroid prophylaxis in our patients with lung metastases. So we've not given up on trying to help those patients. We're just trying to do that in as safe a manner as possible, and I've already tried to expand from 50 to 75, to try to get to that 150 and 300, but in a safe fashion. So we're watching that very closely. And you know, the steroid prophylaxis, we're anticipating that that could be a remedy, as the early onset in the first four to 10 days correlates with the T-cell expansion. We think that that could mitigate toxicity and not compromise efficacy, but, you know, we want to do this in a very careful, deliberate way. In terms of trying to remember the second question was, He was asking about 119 and- Yeah, well, maybe I'll defer to you on that. Sure. So I think the question was around, do we think that this is a. We personally believe this is a local cytokine reaction in the setting of the cell therapy with lung metastases. And I think with 119, we will be starting with a lower dose and gradually escalating. But the point with 119 is it has these very powerful anti-exhaustion technologies, which really should help the T-cell infiltrate the tumor better and expand within the tumor. So we anticipate that we have an opportunity to see even better durability with 119. Great, but I was just a little curious. Do you have a sense if it's the pneumonitis that you're seeing is more a product of 797, or is it a general response, you know, to you know, having a CAR T in the lung? Yeah, I understand. So, we believe it's a local cytokine reaction to having CAR T cells treating lung disease in the lung. Got it. Thank you so much for the color. Thank you. Thanks for the question. Our next question coming from the line of Mitchell Kapoor with H.C. Wainwright. The line is open. Hi, good morning, everyone. This is Dan on for Mitchell. Congratulations on the data. Did any of the non-small cell lung cancer responders have any, or I guess the only one have, pneumonitis? And did you see any responses beyond the two at the 150 million dose level, or at least in a positive direction, if you could comment on that? And I'd like to ask follow-up, if possible. Sure. So there was no pneumonitis in the four patients with non-small cell lung cancer. The patient had 300 million cells that associated had a best response of stable disease. Awesome. Thank you. And have you seen anything at the 300 million cell dose level that's particularly of note? So very early days. One patient treated at the 300 million cell dose reported here. And so, no, we need to continue to dose escalate and get- Awesome. Thank you. And do you know when we can expect the next data drop and about what to expect from that data drop in terms of timelines, or I guess how long the patients have been treated? Yeah. So we anticipate having the next data update later this year or early next year when we move into dose expansion for- Thank you. Thank you. Now I'm showing no further questions in the queue at this time. I will now turn the call back over to Dr. Lynn Seely for any closing remarks. Thank you all for joining us this morning, and we look forward to updating you on our progress. Ladies and gentlemen, that is our conference for today. Thank you for your participation, and you may now disconnect.