As a reminder, this conference is being recorded. It is now my pleasure to introduce Jonathan Lim, CEO and Chairman. Please go ahead. Welcome to Erasca's ERAS-0015 preliminary Phase I data update. We are excited to share these data with you and appreciate your joining us today. Here with me are David Chacko, our CFO and Chief Business Officer, Shannon Morris, our Chief Medical Officer, Robert Shoemaker, our Chief Scientific Officer, and Dawei Xuan, our SVP of Clinical Pharmacology. Please note that we will be making forward-looking statements covered under the safe harbor provisions of the Private Securities Litigation Reform Act. We will also be making comparisons and pooling of clinical data across separate non-head-to-head studies, and caution should be exercised when drawing conclusions from such data, as such data may not be directly comparable. Please see the cautionary language included on the disclaimer slide of this presentation and in our latest SEC filings and the risk factors associated with our business. In addition, any statements made today represent our views only as of the date of this webcast and should not be relied upon as representing our views as of any subsequent date. We specifically disclaim any obligations to update these statements. During today's update call, we'll be providing an overview of ERAS-0015, its clinical studies, and the clinical pharmacokinetics and pharmacodynamics data, which will set the stage for showing ERAS-0015's potential for differentiation in the big three tumor types of non-small cell lung cancer, pancreatic cancer, and colorectal cancer, and against a comparator. Shannon will share a deep dive of preliminary clinical efficacy, safety, and tolerability data, and then we'll wrap up with conclusions, key milestones, and Q&A. First, we'll begin with an overview of ERAS-0015 and the two clinical trials underway in the U.S. and China, as well as the PK/PD profile of ERAS-0015. RAS mutations are the most common oncogenic driver mutations identified in approximately 30% of all solid tumors. Over the past decade, we've made substantial progress in addressing this previously undruggable target with recent advances in targeting KRAS G12C and RAS mutations. We believe there are still opportunities to improve efficacy, safety, and tolerability, and combinability for patients. We believe ERAS-0015 has the potential to show differentiation in efficacy, safety, and tolerability across multiple indications through improved PK and potency. We are thrilled to present our data and the advances we have made. ERAS-0015 has many attributes demonstrating preclinical differentiation due to its improved binding affinity to CypA that is 8- to 21-fold higher than the comparator. This led to improved cell-based potency and greater in vivo activity with tumor regression achieved at one-tenth to one-fifth of the comparator dose in multiple mouse models. The PK properties also are differentiated with demonstrated higher oral bioavailability, lower clearance, and longer half-life, which could potentially result in a lower predicted peak-to-trough ratio in the clinic, and preferential tumor distribution and longer residence time resulting from ERAS-0015's higher binding affinity to the CypA that is overexpressed across multiple solid tumors. Earlier this year, we showed promising early clinical data demonstrating translation of these preclinical properties in the clinic. Today, we are presenting substantially more clinical data to help support our assertion that the preclinical differentiation translates to the clinic. Today, we are presenting preliminary first-in-human data for ERAS-0015. However, this early data set is notable in that we will share results from two independent clinical trials conducted in parallel, which allows us to present a larger overall data set as well as speak to the potential generalizability of these data between the two studies. On the left is a schematic diagram illustrating the dose escalation and dose expansion portions of the trial conducted in China by Joyo, from whom we licensed ERAS-0015, which was administered orally once daily in escalating doses from two to 40 milligrams, with opportunity to backfill select dose escalation cohorts as well as expand select doses in a Phase Ib dose expansion portion. On the right is a schematic diagram illustrating the dose escalation portion of the trial conducted by Erasca in the U.S. In this trial, ERAS-0015 was also administered once daily in escalating doses from two up to the maximum administered dose or MAD of 40 milligrams with opportunity to backfill dose escalation cohorts. The primary and secondary endpoints were similar between the two trials and consistent with a first-in-human trial design. Eligibility criteria were similar, with one key distinction in that the China trial allowed patients with any RAS-mutated solid tumor, while the U.S. trial focused on pancreatic cancer, KRAS G12X/G13X lung cancer, and select KRAS G12X/G13X GI tumors. As shown in these baseline characteristics summary tables, patients enrolled in the China and U.S. trials were generally similar and consistent with a population enrolled in first-in-human trials. The table on the left shows the China trial data, while the table on the right summarizes the U.S. trial data. While there are small differences in the percentage of patients with pancreatic or lung cancer that had a better ECOG status in the U.S. trial compared to the China trial, the potential effect on prognosis is counterbalanced by the difference in the number of prior lines of therapy, which suggests that the U.S. population is slightly more heavily pretreated than the China population. This is a slide that we have shown for nearly two years now, ever since our investor update in May 2024 when we first laid out our thesis for in-licensing both ERAS-0015 and ERAS-4001. At that time, we laid out the three key attributes for an ideal RAS-targeting molecule and our thesis that better preclinical activity and PK performance could lead to a lower clinically active dose that could translate to lower risk of solubility-limited absorption, leading to exposure plateau, better GI tolerability due to lower drug load, and improved therapeutic window for any potential off-target toxicities, all of which we think can translate into improved clinical activity. Now let's review the clinical data that we think support our potential for differentiation in the clinic. I'm going to begin by showing why we think ERAS-0015 has demonstrated improved PK properties in the clinic. The rest of our presentation will follow this framework of differentiated PK, differentiated efficacy, and differentiated safety and tolerability with a potential benefit of improved combinability. Consistent with our predictions, ERAS-0015 has demonstrated well-behaved PK characteristics in the clinic in terms of rapid drug absorption following oral administration, dose-dependent increase in PK exposure across the entire dose range evaluated, and low to moderate PK variability, as shown in the PK concentration time profile figures. The pharmacologically active doses, which I will refer to as PAD from now on, in humans were identified as 16-32 mg daily based upon the observed mean steady-state average concentration at ≥16 mg doses exceeding the target efficacy exposure threshold derived from an insensitive CDX model, as shown in the steady-state PK profiles on the right. Based on the observed safety tolerability, preliminary efficacy, and PK/PD data collected during dose escalation, we have selected 24- and 32-mg daily as the recommended doses for expansion, which I will refer to as RDEs from now on, for further evaluation in accordance with FDA Project Optimus. We also compared the PK data between China and U.S. trials. As you can see from the PK figures, the single-dose PK profiles between the two trials are largely comparable, which provides reassurance that there are no obvious differences in the PK between Chinese patients and U.S. patients in a cross-trial comparison. ERAS-0015's dose-exposure relationship translated into robust PD activity as measured by the reduction in KRAS mutant allele fraction in ctDNA. At PAD, there was a statistically significant greater reduction in KRAS mutant allele fraction compared to lower dose levels. Notably, all 14 patients treated at PAD achieved at least a 75% reduction in KRAS mutant allele fraction, with five patients achieving complete clearance. This biomarker response data further supports the PAD determined from human PK and translational pharmacology data. Now I'm going to discuss ERAS-0015's potential differentiation in the big three tumor types and against the comparator. The reason why we refer to metastatic colorectal cancer, lung cancer, and pancreatic cancer as the big three is because of the large number of patients affected by KRAS mutations in the U.S. and globally in these three tumor types relative to the long tail of other solid tumor types where the unmet need is significant but not quite as prevalent. Unfortunately, there are approximately 74,000 patients with KRAS-mutated colorectal cancer and over 50,000 patients with either KRAS-mutated lung cancer or pancreatic cancer in the U.S. every year, representing a significant unmet medical need for new therapies. Learning from the storied history of targeted therapy development in oncology over the past few decades, including the experience of predecessor pan-RAS and mutant selective KRAS targeting molecules, we know that the big three tumor types have varying levels of sensitivity to targeted inhibition. We predict that KRAS-mutated lung cancer would have the highest sensitivity to pan-RAS inhibition, manifesting as faster, deeper responses to ERAS-0015 monotherapy administered at the PAD of 16-32 mg. We predict that EGFR-mediated primary and adaptive resistance would be a key issue in KRAS-mutated colorectal cancer, therefore requiring a combination approach with anti-EGFR antibodies to achieve meaningful clinical benefit. Finally, we predict that KRAS mutated pancreatic cancer sensitivity would lie somewhere between the other two tumor types. We know from the comparator that up to 50% of patients with KRAS mutated pancreatic cancer exhibited delayed robust responses that weren't observed until after 14 weeks or more of treatment. We hypothesized that the higher doses of 24 mg and 32 mg may be able to overcome the relative insensitivity of pancreatic cancer to monotherapy pan-RAS inhibition and induce robust responses more quickly. I'm now going to share with you our preliminary Phase I clinical data for ERAS-0015 that further underscores the relative sensitivity in the clinic of the big three tumor types to pan-RAS inhibition. In order to provide you with the most applicable comparison, our data disclosure today will include data cuts based on non-head-to-head studies that we believe are similar to those used for the comparator, though our future data disclosures might not follow this methodology, and the comparator data have been generated since that time, which may differ from what we are presenting today. Beginning with second-line plus KRAS G12X lung cancer, we are pleased to report our data showing robust efficacy. At 8 mg or above, a total of 39 patients were treated in the U.S. and China, and we observed a response rate of 62%. Shown in the middle column, 37 of the 39 patients were treated at the 16-32 mg PAD, and the response rate was also 62%, with remarkable consistency of responses between the two regions. Next, I'll call your attention to the teal box, which shows the results of a subgroup analysis. These data represent patients with KRAS G12X lung cancer who were post-checkpoint and platinum therapy being treated with ERAS-0015 in the second or third line setting and who were docetaxel naive. The purpose here was to understand the clinical activity of ERAS-0015 in a patient population who would traditionally receive docetaxel. In this 16-patient subgroup, ERAS-0015 at the PAD demonstrated an impressive 75% response rate with consistency of responses observed between the two regions. Finally, while the maturing dataset for U.S. patients treated at 24-32 mg is still early with 1 response and 2 patients still on therapy with stable disease, the response rates observed in the patients in the China trial suggest that increased ERAS-0015 dose correlates with higher response rates. On a global basis, the response rates were 64% at the RDEs, which is in line with or better than many of the top targeted therapy drugs in lung cancer. To provide additional perspective of how we believe ERAS-0015 fits within the RAS targeting landscape, on the left you can see examples of first-in-class drugs within the KRAS targeting space, including the KRAS G12C inhibitors and the comparator, all of which achieve response rates in the high 30% and low 40% range. On the right, you can see examples of what we believe are potentially best-in-class RAS targeting molecules with differentiated preclinical properties such as potency in the case of divarasib and potency and PK in the case of ERAS-0015. With the potentially best-in-class molecules, response rates increase to the high 50s% for divarasib, as you can see in the blue box in the upper right, and to low 60s%-mid-70s% for ERAS-0015 in the dark blue and teal boxes in the lower right. The comparator data in this example in the gray box in the lower left are from ELCC 2025. The 40 patients in the denominator are a subgroup of the 73 patients treated in the 120-220 mg range, where the subgroup is defined as those patients who received the first dose of the comparator at least 14 weeks prior to DCO to allow two potential scans. Patients harboring KRAS G12X mutations are second- or third-line post-immunotherapy and platinum chemotherapy and have not received docetaxel previously. In contrast, looking now at the dark blue box on the right, you see that in all comers, ERAS-0015's response rate was 62% at the 16-32 mg/day PAD, who had received their first dose of ERAS-0015 at least eight weeks prior to DCO in the U.S. or had at least one post-dose tumor assessment in China, which compared favorably to the 38% response rate for the comparator. Furthermore, the teal box shows a similar population of 16 patients who were second- or third-line post-immunotherapy and platinum chemotherapy and docetaxel-naive with a response rate of 75% that is nearly double what was observed with the comparator. Perhaps most strikingly, the lower bound of the 95% confidence interval for both response rates excludes the 38% value observed with the comparator, which indicates that the clinical activity observed with ERAS-0015 is significantly better than that reported for the comparator. If this observation holds in later Phase studies, ERAS-0015 could be among the very best molecularly targeted therapies in oncogenic mutation-driven lung cancer. Moving on to pancreatic cancer, it has been previously reported by the comparator that among patients with a response, half of the patients experienced their first response after 14 weeks of treatment, which we believe explains why their data cuts and reported response rates from ESMO 2023 to ENA triple meeting 2024 to their corporate update in June 2025 have evolved over time. This table shows the impact of dose, longer minimum follow-up and line of treatment on response rates and explains why the initial response rate in patients with second-line plus KRAS G12X pancreatic cancer at ESMO 2023 was 19.6% at doses greater than or equal to 80 mg using an efficacy evaluable population, including only those patients whose first dose of the comparator was taken at 8 weeks prior to DCO and then evolved to 29% in a more homogeneous efficacy evaluable patient population defined as second-line only and starting the comparator at doses of 160-300 mg at least 14 weeks prior to the DCO. It is this second-line population that was ultimately assessed in RASolute 302, where one of the key eligibility criteria was restriction of the number of prior lines of therapy to one in the metastatic setting. Further restriction of the target patient population to only those patients dosed at 300 milligrams resulted in an ORR of 35% at a later disclosure. Applying this methodology to our data set, you can see that ERAS-0015's response rates increase significantly with longer minimum follow-up and earlier line of treatment, yielding impressive 40%-50% response rates in the PAD, RDE, and 32 milligram only dose ranges in an efficacy evaluable population defined as having received ERAS-0015 in the second-line setting at least 14 weeks prior to the DCO. Notably, the response rates observed for ERAS-0015 in the second-line setting, which is the same population evaluated in RASolute 302, compare favorably to the response rates achieved with the comparator. The preliminary data in pancreatic cancer, consistent with what we saw with the preliminary lung cancer data, suggests that differentiated preclinical characteristics such as potency and PK could potentially drive improved clinical activity. In this subgroup of second-line-only patients, ERAS-0015's 40% response rate in a sample size of 20 patients treated at a similar dose range is more than 10 percentage points higher than what was observed with the comparator administered in a comparable dose range, which is encouraging to see. Now, switching to colorectal cancer, achieving meaningful clinical activity with a RAS/MAPK pathway inhibitor monotherapy has been challenging due to adaptive pathway reactivation, primarily driven by EGFR-mediated upstream signaling. This is why EGFR inhibition is a key strategy to enhance the activity of RAS/MAPK pathway inhibitors in colorectal cancer. However, anti-EGFR antibody monotherapy has demonstrated limited clinical activity in RAS mutant colorectal cancer, as you can see with the low monotherapy response rates. This is because RAS mutations activate the RAS MAPK pathway downstream of EGFR, reducing tumor dependence on upstream EGFR signaling. Consistent with this biology, RAS mutations are excluded in the FDA labels for the approved anti-EGFR antibodies cetuximab and panitumumab in colorectal cancer. However, the combination of an anti-EGFR antibody with a KRAS G12C inhibitor showed a markedly improved response rate to 26%. Likewise, we hypothesized that combining an anti-EGFR antibody with ERAS-0015 would be a rational combination. I'm pleased to disclose that we started enrolling our first combination dose escalation cohort of ERAS-0015 with panitumumab ahead of schedule earlier this year in the first quarter. Three patients have enrolled in a cohort evaluating 16 mg of ERAS-0015 in combination with the approved dose of panitumumab. Two have completed the DLT evaluation period, and no DLTs have been observed as of March 31 data cutoff. Based on the absence of DLTs, paired with anecdotal feedback from the investigators indicating that the AEs are consistent with the known profile of panitumumab, we feel these data provide the best evidence of rash tolerability with our compound. We are excited to report that in the first efficacy evaluable patient's initial scan, a partial response was observed, which is really incredible to see. Given that panitumumab is not expected to have any activity in KRAS-mutated colorectal cancer, we feel these data provide the first indication that the KRAS G12C inhibitor plus anti-EGFR antibody experience, where they did see activity with the combination, may generalize the ERAS-0015 plus anti-EGFR antibody in terms of potentially demonstrating synergistic efficacy. This is the case study of the ongoing response in a 77-year-old male patient with stage 4 KRAS G12D colorectal cancer treated with 16 mg of ERAS-0015 daily in combo with standard of care doses of panitumumab. The patient was heavily treated with three prior lines of therapy before receiving the ERAS-0015 plus panitumumab combo. At the first restaging CT scan, the tumor shrank by 34% and the patient continues on treatment. His TRAEs include low-grade rash, paronychia, pruritus, and mucositis. On the right, you can see the lesion in the liver shrinking from baseline to cycle 3, which is great to see, representing, to our knowledge, the first documented patient to show response to a pan-RAS molecular glue with anti-EGFR combination. We look forward to assessing the safety, tolerability, and efficacy of this combination in other patients in the future. ERAS-0015 safety and tolerability results are promising as well. We are showing data from the U.S. trial only because of the differences in reporting TRAEs versus China, where the approach to reporting TRAEs is significantly different and difficult to generalize to the U.S. population. We also are taking a more conservative approach by showing safety in patients with pancreatic and lung cancer on the left-hand side, treated at the 16-32 mg PAD, which does not include patients treated at lower doses, as well as safety in the eight milligrams and above dose range on the right-hand side. The frequency and severity of rash, GI, and stomatitis are quite promising for ERAS-0015, as evidenced by the low frequency of grade 3 and above TRAEs and the low frequency of dose interruptions and reductions, as well as discontinuations. By minimizing dose modifications and discontinuations, adequate drug exposure can be maintained and clinical benefit maximized. We are also showing early signs of combinability of ERAS-0015 with panitumumab and a response demonstrated in the first patient on first assessment, as mentioned earlier. The fact that ERAS-0015 has been able to combine with an anti-EGFR antibody, a drug class known for skin toxicity, without DLTs observed in the two patients who have completed the DLT window, provides the best clinical evidence of the more favorable rash profile of ERAS-0015. We feel that this speaks to the potential for differentiation of ERAS-0015. For context, this slide shows the safety and tolerability data of the comparator from their public disclosures. Dose interruptions of the comparator were not disclosed in the ESMO 2023 dataset, but they were subsequently disclosed in later investor decks for lung and pancreatic cancer in 2024 and 2025. These data further highlight the substantially reduced dose modification and discontinuation rate of ERAS-0015 versus the comparator, with just 12%-17% interruptions versus 34%-43%, 7% dose reductions versus 14%-30% and 0% dose discontinuation, matching the comparator's rate in second-line plus pancreatic cancer. We included a scorecard in our corporate deck a few weeks ago that lays out the potential scenarios for our view of differentiation of ERAS-0015 compared to the comparator. As you'll recall, showing differentiated efficacy in one or more efficacy attributes or differentiated safety in two or more safety and tolerability attributes would be a differentiated scenario. Showing compelling performance data in both efficacy and safety would be a paradigm-shifting scenario in our view. We have populated the scorecard with ERAS-0015's preliminary Phase I data and are pleased to report that the early clinical data suggests the potential for the paradigm-shifting scenario. I realize this is probably the most detailed data chart you've ever seen from a public biotech company, but we wanted to lay out all the key efficacy, safety, and tolerability data to allow you to contextualize our belief in ERAS-0015's differentiation. From an efficacy standpoint, I'll point you to the top row in the efficacy section. Recall that the most relevant data for pancreatic cancer is the clinical activity in second line, as that population is most representative of the RASolute 302 patient population. Although the data are still immature, we achieved 40%-50% response rates achieved in the PAD, RDE, and 32 mg doses, where the comparator achieved 29%-35% response rates in its prior study. In the second row of the efficacy section, you'll find the lung cancer data showing the 62%-64% response rates at PAD and RDE and the 75% response rate in the post-immunotherapy platinum docetaxel naive second/third-line setting. These are significantly higher than what the comparator achieved in its study, as evidenced by the lower bound of the 95% confidence interval, excluding 38%, and are competitive with what's been observed with the most successful targeted lung cancer drugs in their studies. We've talked about the safety and tolerability advantages, and they're summarized here for your convenience as well. To summarize, we're thrilled to report that ERAS-0015's early clinical data suggests potential for achieving the paradigm-shifting scenario based on performance in both efficacy attributes. 11-15 percentage point response rate increases in second-line KRAS G12X pancreatic cancer and 24-37 percentage point response rate increases in second-line plus KRAS G12X lung cancer and second/third-line subgroup. This is in the context of also showing differentiation in all five safety and tolerability attributes, including demonstrating promising early combinability with anti-EGFR therapy. We think these early data and the improvements in efficacy and safety data suggest ERAS-0015's potential to be an exciting new option for delivering benefit to patients and addressing the huge unmet need in RAS-mutated solid tumors. With that, I'll hand the call over to Shannon to go through the clinical efficacy, safety, and tolerability for ERAS-0015 in further detail. Shannon? Thank you, Jonathan. As Jonathan indicated at the start of the call, my goal is to provide a deeper dive into the ERAS-0015 clinical efficacy and safety data with a specific focus on those patients with lung cancer and pancreatic cancer. As a reminder, our overarching hypothesis has been that the preclinical differentiation would translate into improved efficacy and safety in the clinic. We feel that the data being shared today indicate that our hypothesis may be coming to fruition. Let's start with the efficacy data in patients with KRAS G12X lung cancer from the China trial. In the upper left, you see a table summarizing the objective response rates and disease control rates by dose. In the lower left, you can see the waterfall plot, which shows the maximum change from baseline in target lesions. Because no patients with KRAS G12X lung cancer treated with 32 mg ERAS-0015 are included in the efficacy evaluable population, which is the dataset being shown in this slide today, the data summarized here focuses on the doses of 16 mg and 24 mg. As shown in the table, the response rate was 63% in the efficacy evaluable population. Given the heavily pretreated nature of these patients, we performed an additional subgroup analysis focusing on those patients who received both immune checkpoint inhibitor and platinum-based therapies, were being treated on our trial in the second or third-line setting, and had not received docetaxel. While the data are still maturing, the response rate of 73% is impressive and supports evaluation of ERAS-0015 in earlier clinical settings. This next figure provides a visual representation of the time on treatment for each individual patient in the population defined as any patient who received one dose of ERAS-0015. All patients with unconfirmed and confirmed partial responses were continuing on treatment as of the data cutoff date. This is an important point since the response rates we are reporting include both confirmed and unconfirmed responses. Given that our data are still maturing, the unconfirmed responses have the potential to be confirmed. This observation, paired with the fact that many additional patients with stable disease remain on treatment, speak to the strong safety and tolerability data of ERAS-0015, as well as its potential to provide durable clinical benefit to patients. Transitioning from the data generated in China, I now want to share the U.S. data generated for patients with KRAS G12X lung cancer in the efficacy evaluable population. Although the U.S. data set is less mature, the response rate of 60% observed in the 16-32 mg dose range speaks to the generalizability of the China data to a U.S. population. Additional evidence for the consistency of the data between the China and U.S. trials is provided by the response rate of 71% in that same subgroup population I mentioned for the data from China. That's patients who had received both immune checkpoint inhibitor and platinum-based therapies were being treated on the trial in the second or third line setting and had not received docetaxel. Note that this subgroup analysis includes 7 patients treated at greater than or equal to the 8 mg dose of ERAS-0015 versus the 5 patients treated at the 16-32 pharmacologically active dose range that you saw on the earlier slide that Jonathan presented. Similar to the data from the China trial, all patients with unconfirmed responses remain on treatment such that the responses still have the potential to be confirmed in the future. These data also show that ERAS-0015 administered at doses as low as 8 milligrams induced responses in patients with lung cancer. This case study provides one example of a response we are seeing in patients with lung cancer and the meaningful impact ERAS-0015 can have on an individual patient's quality of life. This patient was a 70-year-old gentleman with metastatic G12V lung cancer who had received both immune checkpoint inhibitor therapy and platinum-based therapy. He started treatment with ERAS-0015 8 milligrams once daily and had a 37% decrease in his target lesions at the first imaging assessment, consistent with an unconfirmed partial response. This partial response was subsequently confirmed at the next imaging assessment, and the patient remains on treatment as of the data cutoff date. To the left, you see CT images at baseline and from the first tumor assessment. The red circles indicate the areas of improved aeration, that's the darker parts, in both his left and right lungs, and this resulted in the patient being able to come off oxygen within one week of starting therapy. In parallel with his disease response, the patient had minimal toxicity from the treatment, with only a grade one treatment-related rash being reported as of the data cutoff date. Now that I've shared our lung cancer data, I would like to share our KRAS G12X pancreatic cancer data using the same format. This slide summarizes the response rate and shows the waterfall plot for the efficacy evaluable patients enrolled in the China trial. For those patients treated in the second-line plus setting at a dose range of 16-32 milligrams, the response rate was 36%. In a subgroup analysis focusing on a more homogeneous second-line only patient population, the response rate was numerically higher at 41%. This figure summarizing the time on treatment for all patients with KRAS G12X pancreatic cancer illustrates that even those patients without distinct RECIST responses can have meaningful clinical benefits manifesting as prolonged stabilization of disease. Of note, all patients with unconfirmed partial responses remain on treatment as of the data cutoff. As mentioned earlier, this is an important point since the response rates we are reporting include both confirmed and unconfirmed responses, and we want to make sure we accurately describe the clinical activity of ERAS-0015 given that the data are still maturing. Overall, while the US data is still immature, when it is combined with the China data, the totality of data indicates that pancreatic cancer is less sensitive to RAS inhibition by ERAS-0015 compared to lung cancer, as evidenced by the difference in response rates between the two tumor types. Despite the lower response rate, ERAS-0015 does induce stabilization of disease in pancreatic cancer within the dose range of 16-32 mg, as demonstrated by the number of patients still on treatment on the waterfall that have deep decreases in target lesions very close to the -30% line. We also see high disease control rates observed in the efficacy evaluable population. Since almost all the patients who had tumor shrinkage without overt RECIST responses are still on treatment, there is potential for those patients to ultimately have RECIST responses as follow-up matures. Finally, the data summarized in the table on the right shows that ERAS-fifteen was associated with numerically higher response rates with longer minimum follow-up and earlier line of therapy. In keeping with our theme, the figure summarizing time on treatment for the U.S. patients with KRAS G12X pancreatic cancer shows that all patients in the efficacy evaluable population with either confirmed or unconfirmed responses, and even many of those with stable disease remain on treatment. As Jonathan mentioned earlier, we're seeing tumor shrinkage in pancreatic cancer as early as the first tumor assessment. Achieving a RECIST response often takes additional time and multiple assessments. Importantly, as we've shown, ERAS-0015 needs to be in the pharmacologically active dose range of 16-32 milligrams to drive meaningful tumor shrinkage as measured by response rates and disease control rates. The case study in this slide provides another example supporting that point. The patient was a 75-year-old gentleman with metastatic G12D pancreatic cancer who received prior standard therapies as listed on the table. He enrolled in the U.S. trial and started receiving 8 milligrams daily ERAS-0015. Unfortunately, at the first assessment, the patient was found to have progressive disease per RECIST based on a new lesion and an increase in target lesions. He continued treatment beyond progression and escalated his dose to 16 milligrams, which is in the lower end of the pharmacologically active dose range. Encouragingly for our patient, subsequent scans revealed the disappearance of the new lesion and a decrease in the target lesions up to -33% at the last imaging assessment. While the official RECIST outcome remains progressive disease, this case highlights the importance of dosing within the pharmacologically active dose range and suggests the potential benefit for patients being treated beyond progression. While we think the preliminary clinical FSGD data we have presented speaks to the potential for differentiation of ERAS-0015, efficacy is only one side of the equation. To ensure our patients have the best outcomes possible, the efficacy must be delivered in the setting of a safe and tolerable drug, which leads us to the safety and tolerability portion of our presentation. This slide summarizes the most frequent treatment-related adverse events observed in the U.S. trial at 16, 24, and 32 milligrams. Events occurring in greater than or equal to 10% of patients include only four terms: rash, diarrhea, stomatitis, and nausea, all of which are consistent with what's been observed in this class. For your awareness, I want to note a related grade 3 pneumonitis case that progressed to grade 5 after the patient decided to discontinue aggressive supportive care. The patient was a 66-year-old male with heavily pretreated metastatic pancreatic cancer who received 24 milligrams of ERAS-0015. The patient presented to the emergency room with grade 3 pneumonitis, immediately discontinued ERAS-0015, and was treated aggressively with high-dose steroids and Infliximab. During the course of his treatment, the patient elected to withdraw supportive care and ultimately passed away. As we look across the broader data set, treatment-related adverse events are infrequently resulting in significant dose modifications or discontinuations of drug. This ability to maintain patients on therapy at their intended dose is encouraging, as it suggests that patients are able to stay on their prescribed dose of ERAS-0015, which we predict will contribute to clinically meaningful efficacy. Sometimes it can be difficult to have a true appreciation for the safety and tolerability of a drug unless you really talk to the patients receiving it or the physicians administering it. To provide a more nuanced view of the safety and tolerability of ERAS-0015, this slide highlights a variety of comments made by the physicians taking care of the patients with cancer receiving ERAS-0015. I'm not going to read each and every quote, but I think it's fair to say that these physicians feel that the ERAS-0015 version of the rash, which is the most common event seen with this class of molecules, has differentiated itself on this front. With that, I'll hand the call back to Jonathan. Thank you, Shannon. We are rapidly advancing ERAS-0015, which we believe is a potential best-in-class pan-RAS molecular glue that has shown early clinical differentiation. We've been able to move the program forward quickly, which underscores the significant unmet need and high investigator patient enthusiasm. We've completed dose escalation in less than one year, including identifying two monotherapy RDEs. We're excited about the clinical profile of ERAS-0015, which showed strong and differentiated efficacy, safety, and PK data, along with early signs of combinability with anti-EGFR therapy. It's also worth mentioning that all patients who had an unconfirmed PR are pending and have the opportunity to confirm with subsequent scans. We believe that this profile therefore positions ERAS-0015 to potentially be the preferred RAS targeting agent with meaningfully improved outcomes for patients. Finally, we are grateful to the patients, their families, and the investigators and study teams. Our anticipated milestones are shown here. In addition to reporting the Phase I monotherapy data today, we're pleased to have initiated the mono expansions and combo dose escalation ahead of schedule. We're narrowing the guidance to H1 2027 for select mono expansion and combo dose escalation data. In summary, these are exciting times for Erasca to be developing ERAS-0015 and ERAS-4001 for the benefit of patients globally. ERAS-0015 is one of the most promising drugs I've ever had the privilege of working on in my career. We have the team to be able to execute on these programs, which we believe significantly advance our mission of erasing cancer and specifically eradicating RAS-driven cancers. Based on these promising preliminary Phase I results for ERAS-0015, we believe we've taken an important step forward in this direction. I'd like to thank you for taking the time to join us today. With that, we'll conclude our formal remarks, and I'll turn the call back to the operator for Q&A. Operator? Thank you. We'll now be conducting a question and answer session. If you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment please while we poll for questions. Thank you. Our first question is from Anupam Rama with J.P. Morgan. Hey, guys. Thanks so much for taking the question and congrats on the data. Just a quick one on the patient death and the treatment-related pneumonitis. Just remind us, did you see any additional events of this AE and how we put this AE into context? A second question on when you think about the totality of data here and sort of unlocking combination potentials, you talked about panitumumab. How do you think about that with this data in hand, unlocking of combination potentials and guiding your development strategy? Yeah. Thanks, Anupam. On the pneumonitis, we haven't seen any other grade 4, grade 5, TRAEs. Pneumonitis is a rare drug-related toxicity that is seen in many oncology drugs. For instance, both approved KRAS G12C inhibitors have warnings and precautions for pneumonitis in their labels. You know, the comparator has also reported pneumonitis at a level of 1 out of 50 patients per monotherapy. In this case, the withdrawal of supportive care is really why this progressed from grade 3 to grade 5. In terms of your other question, yeah, the combinability with panitumumab is very promising, and that's really an objective marker of the tolerability from a rash perspective. We also think that the overall lower frequency and severity of rash, GI, and stomatitis TRAEs bodes well for combining this with, you know, other standard of care agents like chemotherapy and checkpoint inhibitors, for instance. Thanks so much for taking our question. Did that answer your question? Great. Thanks. Yep. Our next question is from Maurice Raycroft with Jefferies. Hi. Congrats on the data update. A lot of data in here. Maybe to start off wondering if regarding having more data first half of next year, between now and then, could you provide some sort of incremental update along the way and comment on how you're seeing responses and durability maturing? Then maybe as a follow-up to Anupam's question earlier, if you could just talk more about next steps for development plan and how you're thinking about prioritizing different paths in non-small cell lung cancer or PDAC and whether you'd pursue second line PDAC. Great. Thanks. Yeah, I'll take on that second one first. In terms of development plans, you know, based on the compelling data that we've seen really across all three of the big three, and it's maturing to be fair, but we're gonna move forward aggressively on all three fronts. You know, in terms of lung, there's a clear signal there. In terms of pancreatic, there also is a signal. I think a lot of our focus will be in the first line setting with combinations, especially based on the promising safety and tolerability data. We think that combinability with chemo could be a promising path forward. Then with colorectal cancer, just the fact that we have early signs of combinability with a EGFR inhibitor, all of that is very exciting to see. We're gonna leave no stone unturned in terms of looking at the big three. In terms of future data updates, you know, our data will mature, and we'll be looking at other opportunities to provide updates. Right now we're committing to the first half of next year. Got it. Okay. Thanks for taking my questions. Thanks, Maurice. Our next question is from Jonathan Miller with Evercore ISI. Hi, guys. Thanks so much for taking my question and for, I'll just echo the last comment, a really detailed presentation. Thanks so much for all of that. I would love to ask again about combos in PDAC in particular. Do you think your safety profile is supportive of a FOLFIRINOX combo in first line? How rapidly do you think you could advance a FOLFIRINOX combo or any combo, chemo combo in first line PDAC into a later stage trial? Then just to clarify your earlier question about the grade five event. You know, I think we are familiar with pneumonitis as a rare but serious side effects in general here. You, your medical team, the patient's medical team's official opinion is that this was a moderate grade pneumonitis event that only progressed to life-threatening status because of the withdrawal of supportive care and that we should expect that pneumonitis in general won't be more severe than with other drugs in this category? Yeah, that's right, Jonathan. It was a very rare event that happened in one patient that was at grade three, and the investigator told us directly that he thought that if the patient had continued supportive care, then it might have been a different outcome. Yeah, it's very unfortunate for the patient, but that was the feedback. In terms of combinations with pancreatic cancer, FOLFIRINOX is a possibility. We also think that gemcitabine and Abraxane is a good combination to look at. We'll be exploring whether a modified gemcitabine and Abraxane or non-modified gemcitabine and Abraxane is the way to go. You know, the way to look at it is there's sort of a path that's already been established and shown to be tolerated, but we can explore various combos based on the safety and tolerability data that we've seen. Our next question. Next question. is from Laura Prendergast with Stifel. Hey, guys. Is there any specific indication line of therapy that you guys have, you know, most conviction in right now, Amvis is pursuing? If you could just comment on the adverse event prophylaxis or management versus the molecular glue competitor, comparator that you've been using here? Yeah. Yeah. I'll let Shannon answer that one. Do you wanna talk about that, Shannon? Sorry. This is Shannon Morris. The prophylaxis. Yeah. Yeah. In terms of prophylaxis, we do not have mandatory primary prophylaxis for any of our adverse events. That means that, you know, the patients are not starting prophylactic antibiotics or topical steroid creams or anything like for the rash, nothing for antiemesis. Obviously we do stress very aggressive management if an adverse event does appear. We think that's really important to getting the best risk/benefit profile for the drug. Back to you, Jonathan. Thank you, Shannon. In terms of your line of therapy question, we think with lung, you know, everything is on the table, second-line plus, as well as first line. In pancreatic, our focus will be on first line, but based on the emerging data, second line's not off the table, so we'll be assessing all our options for that. Colorectal cancer is very interesting, especially the promising combinability with panitumumab, so that's an open lane for us. Got it. Thanks, guys. Congrats on the progress. Thanks, Laura. Our next question is from Michael Schmidt with Guggenheim. Oh, hey guys. Thanks for taking my questions. Hey, Michael. Is it correct to assume that the 40-milligram QD dose was just not yet evaluable, and do you have plans of going higher perhaps? I'm not sure if you will. Then a bigger picture question, I mean, obviously you've broken out the data between this study in China and the U.S. study. But obviously still it's a fairly high contribution in terms of Chinese patients to the dataset. I'm just wondering if you could confirm that the study was done at a single hospital in China or perhaps at more than one center, and what your confidence level is that the data is representative of a potential global study in the future. Yeah. Thank you, Michael. Shannon, do you wanna comment on the 40-milligram dose as well as the multicenter nature of the China trial? While we did not see dose-limiting toxicities as defined by the protocol of 40 milligrams, we did see toxicities that we as well as the treating investigators did not feel would support continued dose escalation or continued evaluation at that dose, particularly since we had already had quite good activity observed in that pharmacologically active dose range of 16-32 milligrams. We felt there was no need to push the dose higher. In terms of the China study, that is a study that was done in multiple sites. In terms of generalizability, I think what I think about there is, you know, tumor response is a fairly objective, quantifiable response or quantifiable endpoint, much less sensitive to subjective. It's much less subjective and I'd say gives us much more confidence that what we're seeing in China will generalize to the United States and to continue development. Time will tell, obviously, but we do have confidence in that data because it is so objective and quantifiable. Yeah. The other thing to add is the eligibility criteria for key prognostic and predictive factors are similar between the two studies. The baseline characteristics between the two trials are similar, as we showed on slide 8. The PK profiles between the two populations are similar. Efficacy between the two regions is generalizable because the standard of care treatment options are similar. As Shannon mentioned, the measures of efficacy are quantitative and objective, so changes in tumor size over time as measured by imaging. This was not done in one site. This was done in multiple Phase I sites in China. Our next question is from Sean Laaman with Morgan Stanley. Hey, Jonathan. Thanks for the very detailed presentation. Most appreciated. I've got a couple of questions on the combo. You know, I think you just might have answered it with the 40-milligram comments, but how much dose flexibility do you believe you have with ERAS-0015 when moving into combo regimens, particularly with EGFR inhibition? Thinking forward with the data and the combo cohorts, you know, what safety or PK markers will you prioritize before expanding combos more broadly? Yeah. Thank you, Sean. The dose for the combos we're exploring within the PAD, the pharmacologically active dose of 16-32 mg is a good area to explore further because it's active, as I mentioned in the PK section of the presentation. The fact that milligrams, the lower end of the PAD, looks to be combinable with panitumumab, that's promising. If that clears, it's possible that we could go up to 24 and see if that is tolerated. If not, the fact that we're seeing a response, albeit, you know, in one patient so far, that's very promising. The fact that, you know, it's good validation that even the 16-milligram dose in the lower end of the PAD is an active dose where we're seeing activity that you wouldn't otherwise expect with panitumumab monotherapy. In terms of just the full range of safety and PK, you know, we will be evaluating safety PK and efficacy for the combos. Anything to add, Shannon? Nothing for me. Thank you. Thanks, Sean. Our next question is from Kelsey Goodwin with Piper Sandler. Oh, hey. Thanks for taking my questions and congrats on the update. Two from me. For the first one, for the U.S. PDAC data, using the 8-week follow-up versus your competitor using 14 weeks, I guess in the China data set for you guys, was the 8- to 14-week timeframe meaningful in patients converting? Obviously, there are a lot of stable disease patients for you guys in the U.S. data set. And then second, maybe building on the 40-milligram cohort, just given the cleaner safety you saw at less than 40 milligrams, why do you think you couldn't push to 40 milligrams and beyond? Thanks so much. Thank you, Kelsey. Basically, in PDAC, as I mentioned, dose seems to be a driver in pancreatic, as does minimum follow-up, so the 8 versus 14 week, and then also, line of treatment, second line versus third line plus. There was an effect of that in both China as well as the U.S. In China, the enrollment over there had about a 4-month head start, and there was much faster enrollment at the higher doses in China versus the U.S. because there are somewhat looser guardrails in terms of the number of patients that you can enroll at each dose. There is a more mature data set in China. That said, that 14 versus 8-week prior to DCO did have an impact on the China data as it did in the US. In terms of 40 milligrams, I'll answer that and then invite my colleagues to chime in. You know, we are seeing very good activity at the PAD of 16-32 milligrams. It does. We weren't sure if we would identify a dose range that could achieve that sweet spot of seeing promising efficacy coupled with promising safety and tolerability. In that PAD, we're seeing both. At 40, that's where you start to see an increase. For instance, in two of the patients, there was a grade 3 rash, as you could see in the safety table. That's where, as Shannon mentioned, we didn't think that the risk-benefit of pushing the 40-milligram dose further warranted further exploration of that dose. Shannon, do you wanna chime in? I think you've described it accurately. You know, when we're sitting here thinking about this from a physician's point of view, right, we're always thinking efficacy in the setting of safety and tolerability. Based on the criteria for the pharmacologically active dose, the exposures of patients are predicted and are shown to be as high as they need to be to get that tumor shrinkage. It really comes down to, you know, optimizing risk-benefit. It was, again, with conversations with ourselves as well as the treating investigators, the ultimate conclusion was that pushing the dose higher would not lead to better risk-benefit. Our next question is from Joseph Catanzaro with Mizuho. Hey, great. Thanks for taking my questions. Thanks for the update. Maybe two quick ones from me. So, you know, there's some precedent in the RAS molecular glue space that, you know, lung patients maybe need a lower dose than PDAC patients to maintain treatment persistence. How do you see that playing out with double oh one five? So essentially, potential dose in lung versus PDAC. And then I guess related, you showed the G12C case study. Wondering if you think there's potentially a similar path for double oh one five in lung that mirrors the CRESCENDO trial. So essentially, you know, head-to-head with the RAS molecular glue class. Though I appreciate there's no approvals here just yet. Thanks. Yeah. Joseph, thank you for the question. I mean, I think in the case of G12C, that was done. In the case of pan-RAS, that may not be required because it does seem to still be a potentially, you know, open lane. I think in terms of the dose in lung and PDAC, we're not convinced that there needs to be a different dose between those, but we're certainly open to exploring that, whether it does seem that pancreatic might need a higher dose, but I think more data and maturity of data will tell. I'll just see if Shannon has anything to add on either of those. No, I think you're exactly right. I mean, I think we feel very comfortable that 24-32 certainly looks like the doses we're going to take into expansion. I think only time will tell in terms of as that data mature, as we see how the responses, what the durability is. I think committing to anything at this point would be premature. Okay, great. Thanks. Thank you. Our next question is from Alec Stranahan with Bank of America. Hey, Jonathan and team. Thanks for taking my questions. Two from me. First, just on the confirmed versus unconfirmed, I guess, what are your expectations around timing and ability to confirm the remaining patients, particularly in the China study where many of the responses were observed? Just on connecting the dots to survival that we'll see in future updates, I guess, curious, based on the literature or what we've seen for competitors, you know, what a 10-15 percentage point improvement in ORR and PDAC could mean in terms of PFS or OS? Or is there maybe another metric such as, I guess, disease control rate, time on therapy, et cetera, that you think could also help inform this? Thanks. Yeah. Thanks, Alec. Well, first of all, I mean, great question. You know, it's worth noting that there's still multiple ongoing responses. So I think the fact that 23 out of 24 responding patients in lung cancer remain on treatment, including all responders treated at 24-32 milligrams, and in pancreatic, 20 out of 23 responding patients remain on treatment, including all responders treated at the 24-32 milligram RDE. It's also worth noting that any patient that had what we call the UPR or unconfirmed PR was actually a pending partial response. So, the reason they had a UPR is because they hadn't yet had their confirmatory scan. So to your point, I think we'll know a lot more in the second half of this year regarding the maturing of those UPRs or pending PRs. I think in terms of the sort of 10-15 percentage points of differentiation and how that maps to durability metrics like PFS, DOR, and OS, Shannon, you should comment further. In general, you know, in targeted therapy, when you have higher response rates for certain drugs, that does tend to correlate with longer durability as well. Maybe, Shannon, you can comment further. No, I think I completely agree. I think the mechanism of action definitely has an impact, right? Immune checkpoints are gonna have a different situation than a targeted therapy. I would say, in general, higher response rates do tend to give more durable or ultimately to improved PFS and OS. Nothing's ever 100% correlation, but we certainly are excited about where we're at. As the data matures, we hope it continues to mature the way we've seen it today. Thank you. Thanks. Thank you. There are no further questions at this time. I'd like to hand the floor back over to Jonathan Lim for any closing comments. I'd like to thank everyone for joining us on this call. Really appreciate the attendance and the questions, and we're really excited about what we're doing over here at Erasca in terms of seeking to eradicate RAS-driven cancer, and we think that with ERAS-0015, this really helps us take an important step forward. We look forward to talking to all of you soon. Take care, everyone. This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation.