Afternoon. Welcome to Verastem Oncology's VS-7375 R&D update conference call. My name is Tawanda, and I will be your call operator today. Please note this event is being recorded. All participants will be in a listen-only mode. After today's presentation, there will be an opportunity to ask questions. I will now turn the call over to Julissa Viana, Senior Vice President of Corporate Communications, Investor Relations, and Patient Advocacy at Verastem Oncology. Ma'am, you may begin. Thank you, operator. Welcome everyone. Thank you for joining us today to discuss our potential best-in-class, highly selective oral KRAS G12D on-off inhibitor, VS-7375. We will share progress from our TARGET-D clinical development program, including preliminary data from the TARGET-D 101 dose escalation and dose expansion trial. This afternoon, we issued a press release detailing these results, along with a slide presentation that we will reference during our call today. Both are available on the investor relations section of our website. Before we begin, let me point out that we'll be making forward-looking statements that are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and actual results may differ materially. We encourage you to consult the risk factors discussed in our SEC filings for additional details. Joining me in today's call to deliver prepared remarks and take your questions are Dan Paterson, President and Chief Executive Officer, Dr. Michael Kauffman, President of Development, and Dr. Jonathan Pachter, Chief Scientific Officer. I will now turn the call over to Dan. Thank you, Julissa. Good afternoon. Thank you for joining us today. We're excited to share the progress we've made across the VS-7375 development program and to discuss why we believe 7375 is a potential best-in-class, highly selective oral KRAS G12D on-off inhibitor that could become the preferred treatment option for patients with KRAS G12D-mutated cancers. Today, more than 60,000 patients are diagnosed each year in the U.S. alone with a cancer harboring a KRAS G12D mutation, which has the worst prognosis of the RAS mutations, yet there's no approved treatment specifically targeting this mutation. Our conviction in VS-7375 is grounded in the design of the molecule, its differentiated preclinical profile, and the emerging clinical profile generated to date. While broader RAS inhibition strategies have helped to demonstrate that RAS remains one of the most important targets in cancer, greater selectivity may ultimately prove advantageous. By specifically targeting KRAS G12D, we avoid unnecessary toxicities that are on target for a pan-RAS inhibitor, but not with a selective KRAS G12D inhibitor. Precision targeting has transformed cancer treatment across multiple tumor types, and we believe that in 2026, we must apply these same principles to KRAS G12D-mutated cancers. Selectively and potently inhibiting the cancer-driving mutation in both the on and the off states could provide meaningful advantages over approaches that target the on-only or off-only KRAS protein or broader RAS inhibition strategies. As you'll see from the data we present today, we believe many patients with KRAS G12D-mutated cancers will require deep and durable pathway suppression to achieve meaningful improvements in outcomes. That belief has guided the design of VS-7375 from the very beginning and continues to inform our development strategy. Our goal was straightforward: develop a highly selective and orally bioavailable KRAS G12D inhibitor capable of delivering meaningful efficacy with favorable tolerability that'd be expected by targeting a specific oncogenic driver mutation. To achieve that, we focused on selectively targeting the KRAS G12D variant to enable deeper and more potent sustained inhibition of the intended target without affecting normal RAS-mediated pathways. We selected a candidate molecule that could hit the target hard and could support broad combination strategies that are often preferred in order to maximize patient outcomes. These principles continue to guide the program today. As we advance the development of VS-7375, we've seen evidence that it's delivering on the attributes we set out to achieve. 7375 has demonstrated deep target inhibition, prolonged target engagement, and a differentiated on/off inhibition profile designed to drive deeper pathway suppression. Importantly, VS-7375 has shown good oral bioavailability and sustained exposure that increases as the dose is raised. Along these lines, we are particularly pleased with the PK and the associated preliminary anti-tumor activity and tolerability results we've seen with the 900 mg once-daily oral dose. We've also been encouraged by the anti-tumor activity seen at the 600 mg dose. However, the exposure at 900 mg delivers the target coverage based on preclinical models without a trade-off in increased adverse events. Collectively, these characteristics support the potential for a best-in-class efficacy with a differentiated side effect profile, while also enabling combination development strategies and opportunities to address areas of high unmet need, including in the frontline treatment settings. Overall, these attributes have given us increasing confidence in the potential of VS-7375 as a preferred oral KRAS G12D inhibitor. Today, we believe that VS-7375 is positioned competitively to treat the major KRAS G12D mutated cancers. First, we have a differentiated profile versus other RAS inhibitors. We believe our truly dual on/off inhibition and long target residence time are exactly the mechanisms you need to drive deep and durable responses. As Michael will share shortly, the emerging antitumor activity we are seeing in our TARGET-D 101 phase I/II trial has the potential for VS-7375 to be the best-in-class KRAS G12D inhibitor. Let me be clear, we see efficacy at the 600 mg dose that we're excited about, but we're also seeing a dose response at 900 mg, which reinforces our decision to bring this dose forward into our phase II trials. We've also demonstrated that our safety and tolerability profile is consistent with the selective nature of targeting KRAS G12D, distinguishing it further from pan-RAS approaches that have major toxicities. This emerging tolerability profile allows us to go higher in dose, also makes it possible for us to combine with multiple standard of care agents. Furthermore, our emerging safety profile shows little to no rash and mucositis, which are quite prevalent with pan-RAS inhibitors. Further on our combination strategy, the preclinical data that John will share will help you understand some of the paths we are pursuing. As announced today, we intend to enter into an agreement to evaluate VS-7375 in combination with ERAS-0015, Erasca's investigational and potential best-in-class oral pan-RAS molecular glue in advanced KRAS G12D mutant solid tumors. In addition, we plan to evaluate VS-7375 in combination with a PRMT5 inhibitor as soon as possible. Lastly, we have multiple paths to registration. We are working quickly to enroll patients into our phase II TARGET-D trials, ultimately to deliver a compelling data package to the agency for potential accelerated approval. To summarize, the data generated to date reinforce our belief that VS-7375 has the potential to become the best-in-class KRAS G12D inhibitor. As we look next at the market opportunity, there is clearly a need for new treatment options because of the sizable patient population that remains underserved today. Approximately 40% of pancreatic cancers, 15% of colorectal cancers, and about 5% of lung cancers harbor a KRAS G12D mutation with a total addressable market in the U.S. alone in excess of $2.5 billion. In each of these cancers, the KRAS G12D mutation is associated with a particularly poor prognosis. Therefore, beyond the numbers of patients that could potentially benefit, we have an opportunity to fundamentally alter the prognosis for patients whose tumors harbor this bad acting oncogene. In addition to our initial phase II programs focusing on previously treated pancreatic, colorectal, and non-small cell lung cancers, we see VS-7375 moving rapidly into the frontline setting, typically as part of combination regimens to optimize outcomes at this critical treatment stage. As you will hear today, our goal is to expeditiously generate data that will address the majority of the unmet need and maximize patient benefits across major KRAS G12D tumor types. I would now like to turn it over to Michael to give an update on our clinical development of VS-7375. Michael? Thanks, Dan. As Dan outlined, VS-7375 is being developed with a clear objective: to maximize the opportunity to deliver meaningful outcomes for patients living with each of the major KRAS G12D mutated cancers. We have strongly executed against this vision. In the first half of 2026, we rapidly advanced a broad clinical development program for VS-7375 by enrolling more than 150 patients in our TARGET-D 101 phase I/II dose escalation and dose expansion trial, initiated pre-registration directed phase II trials in pancreatic, colorectal, and non-small cell lung cancers, and we are on track to initiate 3 pivotal phase III trials in these indications by the first half of 2027. That is an ambitious development strategy. As I have said time and again, this is why I decided to step inside the company in December of last year. Programs are not advanced at this pace without firm conviction and laser-focused delivery each and every day. We will now share some of the clinical data across the tumor types that are driving our development strategy, and why we've chosen to continue to prioritize all three indications as we work to bring VS-7375 to patients as quickly as possible. Before diving into the data by tumor type, let me highlight four key takeaways from the clinical experience to date. First, we are observing encouraging antitumor activity across pancreatic, colorectal, and non-small cell lung cancers, as well as in other KRAS G12D mutated cancers like biliary tract cancer. Second, the safety and tolerability profile is very different from the experience our partner in China has shared. Most importantly, we have observed primarily low-grade nausea, vomiting, and diarrhea, and the majority of these adverse events attenuate after the first cycle of dosing. Third, the emerging profile of VS-7375 supports combination strategies with full dose standard of care therapies that we believe can further enhance patient outcomes. Finally, we have dosed the first patient in our registration-directed TARGET-D 201 phase II PDAC trial last week. We anticipate dosing the first patients in our other registration-directed phase II trials very soon. All of these trials will support discussions with the agency around an accelerated approval pathway. With these takeaways in mind, let's get into more detail about the TARGET-D 101 phase I/II trial and the progress we have made. As a reminder, here is our phase I TARGET-D 101 trial design. Overall, we are making a lot of progress across our program. We have enrolled more than 150 patients across the dose escalation and dose expansion cohorts seen on the slide. We are exploring a 1,200 mg once daily dose, as dose-limiting toxicity has not occurred in the 900 mg cohort. While I won't touch on it further today, let me say that we are continuing to enroll patients in our tumor-agnostic cohort, and we're excited to see anti-tumor activity in cancers like biliary tract cancers. We will share more on this cohort in the future. Now let me discuss our updated PK findings. As described previously, based on achieving at least 30% reductions in animal tumors in our four key preclinical models, similar to the threshold required by RECIST solid tumor response criteria in humans, we were aiming for human exposures of at least 2,000 nanogram hours per mil. These levels are highly correlated with the most optimal outcomes in mice and occurred at well-tolerated doses there. We are extremely pleased to confirm that the majority of patients treated at 900 mg who have had PK testing have shown steady-state exposures at or above this important level. We believe that VS-7375 is among the only RAS-targeting agents to demonstrate dose-dependent exposures, thus enabling optimal human PK that is associated with well-tolerated doses driven by its high oral bioavailability. Now let me turn to our PDAC update. In our metastatic pancreatic cancer cohorts, preliminary data demonstrate dose-dependent anti-tumor activity across the 600 mg and 900 mg dose levels. In addition, the anti-EGFR combination cohort has demonstrated preliminary evidence of deeper and more rapid responses relative to monotherapy. Importantly, the vast majority of patients have not yet reached six months of follow-up. As we prepare to enter the first-line metastatic pancreatic cancer setting, we are evaluating VS-7375 in combination with standard of care gemcitabine plus nab-paclitaxel, which I will refer to as Gem-Nab. The combination of VS-7375, 600 mg, and full dose Gem-Nab has cleared dose-limiting toxicity evaluations in patients with previously treated PDAC, and the enrollment of the VS-7375 900 mg cohort plus full dose Gem-Nab is ongoing. We expect to report preliminary first-line combination data in the second half of 2026. In addition to the usual CT scans, which are essential for evaluating patients with PDAC, about 85% of patients have elevated levels of the tumor marker CA 19-9 in their blood. This tumor marker is often used to follow disease because it's easily obtained and generally correlates with tumor mass. While CA 19-9 changes are not an accepted regulatory endpoint, reductions in CA 19-9, particularly when they occur early in the disease treatment course, have been shown to correlate with improved progression-free survival, overall survival, as well as overall response rate. Despite the limited follow-up in our 900 mg PDAC cohort, 13 of the 14 patients with elevated baseline CA 19-9 levels have achieved at least a 50% reduction in their CA 19-9, with several showing greater than 90% reduction. As shown in the graph, these reductions are quite rapid, typically manifesting at the first testing point at three weeks. These rates of over 50% reduction in CA 19-9 levels are substantially higher than those reported for combination cytotoxic chemotherapy regimens typically used in the treatment of both relapsed and even in frontline PDAC. As the median number of prior therapeutic regimens in this 900 mg cohort is two, these early results give us confidence that VS-7375 can confer substantial anti-tumor activity even in patients with heavily pretreated chemotherapy-refractory pancreatic ductal adenocarcinoma. Now let's take a look at two patient case studies from our ongoing 900 mg PDAC cohort. The first patient is a 55-year-old male diagnosed with KRAS G12D mutated metastatic pancreatic cancer who received intensive chemotherapy with FOLFIRINOX for four months, where his best response was stable disease, and the tumor progressed. He was then treated with Gem-Nab for only two months when his disease progressed. The patient then began treatment with single agent oral VS-7375 at 900 mg once per day. As you can see on the baseline CT scan, tumors were present on his liver and pancreatic surgical bed, outlined in orange dot outlines. We pasted the same orange dot outlines into his subsequent scan. Following 12 weeks of treatment with VS-7375, the tumor shows a confirmed partial response or a RECIST with a reduction of 47% in the sum of the longest diameters, or SLD, of the target lesions. The investigator also reported substantial pain resolution within one week of initiating treatment with marked reduction in the use of any opiate pain medications. This response is ongoing at this time, and the patient's treatment duration has already exceeded that of both frontline FOLFIRINOX and second-line Gem-Nab. Most remarkably, this patient has experienced no treatment-related adverse events. Now turning to our second case study, which is more recent but strengthens some of our observations above. This patient, a 79-year-old woman diagnosed with PDAC, who received frontline Gem-Nab for six months, nanoliposomal irinotecan for 11 months, and FOLFOX for three months. She entered our trial with substantial abdominal pain and distension caused by peritoneal carcinomatosis and marked ascites, in which the tumor encased the bowels and induced fluid accumulation in the peritoneum, which tends to be very uncomfortable with marked bloating, indigestion, reduced appetite, and weight gain. Within two weeks of initiation of VS-7375 therapy, the treating physician reported that the patient's abdominal pain and distension had resolved. In addition, this patient had an extremely elevated CA 19-9 at baseline, over 17,000 units per ml, normal being less than 37 units per ml. At week three, the CA 19-9 level had already dropped more than 60%, and it fell over 97% at week six, and more than 99% to 117 units per ml at week nine. Let's remember that declining CA 19-9 following initiation of therapy is predictive of better outcomes. Along these lines, the week six CT scan assessment showed complete resolution of the target lesions, along with marked resolution in ascites. Of note, there were apparently non-target lesions that could not be assessed properly due to the residual ascites. Therefore, this is considered a partial but not a complete response. Her main adverse events, which have been transient, were diarrhea, fatigue, and anorexia. The patient is early on in her treatment course, but initial results appear to be highly promising. Although it's likely fairly obvious, it's worth emphasizing that the side effects that these patients have experienced on VS-7375 are substantially better than those that they tolerated during multi-agent cytotoxic chemotherapy. Let's turn our attention to a case which was inspired by our preclinical work. In this case, you will see that the compelling preclinical data describing the combination of VS-7375 with the anti-EGFR therapy cetuximab that we've shared publicly before is beginning to manifest in patients. Please note that anti-EGFR agents have essentially no activity themselves against KRAS mutant PDAC, as well as other KRAS mutant cancers, including colorectal cancer. This patient is a 64-year-old man diagnosed with KRAS G12D mutated pancreatic cancer. The patient had previously received FOLFIRINOX plus radiotherapy with a partial response. Then progressed and was treated for only three more months with FOLFIRINOX before progression occurred again. Let's recall now that the 400 mg dose of VS-7375 alone has not shown significant activity against PDAC. He was treated with this subtherapeutic dose of VS-7375, that is 400 mg, but this time in combination with cetuximab. As you can see from the baseline scan, tumors were present on his pleura and an mediastinal lymph node. He also had lung lesions which were causing substantial shortness of breath. Within one week of initiating treatment, his shortness of breath resolved. At the week six CT scan, the tumor reached a PR by RECIST with a 46% reduction in the sum of the longest diameters of these lesions. At the week 12 scan, the patient's response continued with a 70% reduction in the maximum diameter of these lesions, thus confirming the partial response. Again, as discussed previously, the patient also saw a significant drop in CA 19-9 levels by week three, starting at nearly 1,000 and dropping to less than 200 units per ml. The patient experienced several treatment-emergent adverse events that the investigator believes were not attributable to VS-7375, but instead were due to metastatic PDAC, and in the case of the maculopapular rash, due to cetuximab. Overall, again, as compared with typical multi-agent chemotherapy, tolerability to the combination regimen appears quite good. Let's turn our attention to colorectal cancer. Preliminary data demonstrate antitumor activity observed at both the 600 mg and 900 mg dose levels in combination with the anti-EGFR therapy in patients with heavily pretreated metastatic colorectal cancer. VS-7375 at the 900 mg dose level in combination with cetuximab was DLT cleared last month. Consistent with observations in the emerging PDAC cohorts, no overlapping toxicity between cetuximab and 7375 has been observed to date. Importantly, all patients receiving the 600 mg dose in combination with cetuximab have less than six months of follow-up. Looking ahead, evaluation of the 900 mg dose level in combination with cetuximab will occur in the phase II registration-directed TARGET-D 203 clinical trial, which will begin enrollment shortly. As we know, more and more patients under 50 are being diagnosed with CRC, underscoring the need for effective treatment options. As you will see in this next case, we treated such a man in his early 40s. Prior to participating in our trial, a 42-year-old man diagnosed with KRAS G12D mutated colorectal cancer had received all standard of care agents, including bevacizumab and TAS-102 Lonsurf, as well as two investigational agents. He had massive and diffuse metastatic disease upon entry into our trial. The patient was treated with 600 mg once daily 7375 in combination with cetuximab. As you can see on the baseline CT scan, massive tumors enclosed by the orange dotted areas were present in his liver on the top left and in both lungs on the bottom left scan. The darker areas in the liver and the white areas in the lung are tumor. The total sum of the longest diameters, or SLD, was 370 millimeters, or over 14.5 inches of tumor at baseline. We also note that liver metastases from CRC are typically refractory to chemotherapy. At the week six scan, the patient achieved a reduction in the SLD of 28%, meaning that four inches of tumor disappeared from his CT scan. At the week 12 scan, the patient's response continued with a reduction of 29.6% from baseline, and he continues to do well. We also note that the tumor marker CEA, which is the most common marker in CRC, elevated in over 70% of patients, was highly elevated at initiation of treatment at 4,000 nanograms per ml, normal being less than three nanograms per ml. The patient's CEA level, the carcinoembryonic antigen level, showed a marked and rapid drop by nearly 90% since therapy was begun, again, consistent with his radiologic findings. The investigator also reported that abdominal distension was nearly completely resolved within several weeks of initiation of therapy. The patient developed cetuximab-induced acneiform rash, which is common and occurs in over 80% of patients treated with this agent, but it is managed well and rarely results in treatment delays. No VS-7375 associated events were reported. As noted above, we will be enrolling patients at 900 mg of 7375 plus cetuximab in the TARGET-D 203 study, which should begin shortly. We expect to have more data by year's end with this regimen. Let's talk about observations we've seen in non-small cell lung cancer. We have observed promising preliminary efficacy at the 600 mg dose, and we believe that 900 mg can deliver best-in-class efficacy due to dose response observations. As we've stated for the other cohorts, the majority of patients have had less than six months of follow-up. For the 900 mg dose, we will be evaluating that dose in the phase II TARGET-D 202 study, which will begin shortly. In addition, evaluation of VS-7375 in combination with carboplatin, pemetrexed, pembrolizumab is ongoing and is expected to be DLT cleared over the summer months. Our plan is to then test this combination with VS-7375 in a randomized study in the first line setting. Let's take a look at a patient case study. This patient is a 77-year-old female diagnosed with KRAS G12D mutated advanced NSCLC. Initial treatment for this patient was standard pemetrexed, carboplatin, and pembrolizumab, which has shown variable and typically lower activity against KRAS G12D mutated non-small cell lung cancer in retrospective analyses. Consistent with these observations, the patient had a best response of only stable disease on this triplet therapy and was treated for only four months prior to progression. The patient was then treated with 600 mg of single agent oral VS-7375. As you can see on three sections of the baseline scan in the left column, tumors, the white masses surrounded by orange highlights, were present throughout her lungs. The patient had a partial response at six weeks, which is shown here, and the PR was subsequently confirmed at week 12 with a 49% reduction in SLD. The investigator also reported that shortness of breath and tumor pain had improved within a few weeks of dosing initiation. The patient experienced treatment-related grade 3 diarrhea, which was controlled quickly with standard agents. The dose was temporarily reduced to 400 mg and then re-escalated to 600 mg after several weeks with only grade 1 residual intermittent diarrhea. Before turning to our updated safety, these cases demonstrate the potential of VS-7375 to markedly alter the course of disease in patients with heavily pretreated chemotherapy refractory tumors with adverse events that are easily managed. My last section, let's cover the emerging safety and tolerability profile. As a physician and a drug developer, I think it's very important to distinguish between safety, toxicity issues, as well as tolerability issues. As we all know, current chemotherapies and some targeted agents can cause significant toxicities that can be cumulative and/or life-threatening. Contrast, we have been quite encouraged about the emerging profile of VS-7375, which to date is characterized primarily by tolerability issues, including low-grade nausea, low-grade vomiting, and diarrhea, which attenuate after the first cycle. These are tolerability issues that do not appear to represent major toxicities. In fact, we've not yet identified significant major safety issues associated with VS-7375. The majority of the GI side effects are effectively managed with standard supportive care measures. All patients are advised to take VS-7375 with food, which is generally good advice anyway for patients with any cancer. Our patients receive 5-HT3 antagonists prior to initiating therapy, strongly recommended through the first two cycles, and can receive additional medications as needed after starting treatment. You will also see that the rates of these common GI side effects are similar at the 600 mg and 900 mg cohorts, consistent with a localized irritant effect of the drug product rather than a systemic toxicity, which would generally show a dose dependence. No unexpected adverse events were observed, and rates of Grade 3 adverse events remain low. When they do occur, such as the Grade 3 diarrhea, they are transient and manageable. Importantly, no clinically meaningful cytopenias or liver function abnormalities have been reported, and we have not yet observed any clinically significant cumulative toxicities. No Grade 4 or 5 events have been reported to date. Let's turn to the treatment-related adverse event tables. On this slide, I will highlight a few key points. As of June 12th, 2026, VS-7375 monotherapy has demonstrated a favorable safety profile with manageable AEs in the TARGET-D 101 phase I/II trial, including 57 patients at 600 mg and 25 patients at 900 mg. Note that combination therapies are not included in this table and will be reported in the coming months. As you can see from the tables, about half the patients have diarrhea and half have nausea, mostly Grade 1. Grade 3 events are uncommon, and there are no Grade 4 or 5 events across all of the patients to date, including at 900 mg. There is another aspect of the safety data that I think is particularly noteworthy. Investigators were reporting to us that the GI complaints largely abated during the first cycle of treatment. In order to evaluate this more quantitatively, we looked at AEs for patients continuing in cycle two and beyond, which is the majority of the patients. Across the 73 patients shown on the slide who continued treatment beyond cycle one, the GI adverse events have decreased by more than 50%, and the severity is primarily Grade 1. There was no rash or stomatitis, no significant liver function abnormalities, minimal Grade 3 events, and again, no Grade 4 or 5 events. These data support the observations that patients quickly develop tolerance for the GI events, and this bodes well for very long-term dosing with VS-7375. Let's turn our attention to the status of the phase II and III trials. As we close out enrollment of the TARGET-D 101 program this month, we are also advancing the next stage of development for VS-7375. Last week, on June 16th, we announced the first patient has been dosed in the TARGET-D 201 phase II registration-directed trial evaluating VS-7375 to treat patients with KRAS G12D-mutated second-line PDAC. This trial involves randomization to either 900 mg of 7375 alone or in combination with standard biweekly cetuximab. Panitumumab can be substituted in patients with potential cetuximab allergy. We expect the first patients to be dosed in both the TARGET-D 203 registration-directed metastatic CRC trial and the TARGET-D 202 registration-directed advanced NSCLC trial by mid 2026. We expect to enroll the last patient across all of these three phase II protocols by the end of this year. We're also making progress with our trial designs for three frontline phase III pivotal trials for the metastatic PDAC, metastatic colorectal, and advanced metastatic non-small cell lung cancers, and we're planning to meet with the FDA before the end of this year to reach agreement on these three phase III designs. We expect the first patient to be dosed in each of these trials by no later than the first half of 2027. Amazing progress in a short amount of time and much more to come. I'll hand it over to John to give you a sense of the future potential combinations to improve patient outcomes. Jon? Thanks, Michael. VS-7375 is optimized with several properties that make it the potential best-in-class RAS inhibitor for treatment of patients with KRAS G12D-mutated cancers. As Dan outlined earlier, VS-7375 is extremely potent against both the on and the off states of KRAS G12D, approximately 15 picomolar, and it has a particularly long residence time of 18- 24 hours when it binds KRAS G12D. It is extremely selective for KRAS G12D, in contrast to pan-RAS inhibitors such as divarasib. This selectivity of VS-7375 spares T cell proliferation and avoids side effects such as rash and stomatitis. Importantly, VS-7375 shows once-daily oral dose-dependent exposure in patients. The fact that the pharmacokinetics are not saturating at higher doses enables VS-7375 to maximally inhibit its KRAS G12D target. As we announced today, a key part of our development strategy will be with novel combinations to further extend survival for patients beyond what can be achieved with a RAS inhibitor alone. Here, we studied combinations of VS-7375 or the on only G12D inhibitor, zoldonrasib, with the pan-RAS tricomplex inhibitor divarasib in a KRAS G12D pancreatic cancer model. Although the combination of zoldonrasib with daraxonrasib conferred more durable tumor growth inhibition than zoldonrasib or daraxonrasib alone, we see that single agent VS-7375 gave more durable efficacy than the zoldonrasib/daraxonrasib combination. What is especially impressive is that combining our dual on-off G12D inhibitor 7375 and a pan-RAS on-only inhibitor, in this case daraxonrasib, conferred extremely durable tumor regression. Based on data such as these, we will be collaborating with Erasca to test the combination of VS-7375 with Erasca's potentially best-in-class pan-RAS inhibitor, ERAS-0015, in patients with KRAS G12D pancreatic cancer. In our efforts to identify and pursue the best combinations with VS-7375, we have been extremely impressed with the strong, durable tumor regressions we achieve when we combine VS-7375 with a PRMT5 inhibitor across pancreatic cancer models with KRAS G12D mutation, along with MTAP deletion. KRAS G12D mutations together with MTAP deletion occurs in approximately 10%-12% of patients with pancreatic cancer. As you can see here, combination of VS-7375 with BMS' PRMT5 inhibitor, navlimetostat, gives extremely durable tumor regression. In this patient-derived model, all animals achieved a durable, complete response with this combination. Building on these preclinical data, Verastem is also working to enable a clinical combination with a PRMT5 inhibitor as soon as possible. With that, I will turn it back over to Dan. Thanks, John. Before we open it up to Q&A, I want to leave you with three key takeaways. First, we continue to strengthen our conviction that VS-7375 has the potential to become the preferred treatment for patients with KRAS G12D-mutated cancers. The field has evolved from broad chemotherapy approaches to inhibition of RAS broadly, and we believe VS-7375 represents the next step in the evolution through its selective targeting of KRAS G12D across major tumor types, including pancreatic, colorectal, and lung cancers. Second, what excites us most is not any single data point, but the overall story that's emerging. We're seeing encouraging efficacy signals across tumor types, a safety and tolerability profile that supports the potential for long-term administration, and evidence that VS-7375 can be successfully combined with standard of care therapies. Taken together, these attributes position VS-7375 to deliver the efficacy needed to be practice-changing while offering a differentiated profile over other KRAS G12D or pan-RAS inhibitors. It has the potential to establish VS-7375 as a best-in-class therapy for KRAS G12D-mutated cancers and the foundation of a meaningful franchise in solid tumors. Third, while today we focused on VS-7375, we remain equally focused on execution across our business. AVMAPKI FAKZYNJA CO-PACK continues to perform well, and we're pleased that the changes we've made are having an impact. Since the first quarter, we've seen a rebound in strong physician conviction, putting us back on track with our expected growth trajectory. We look forward to providing an update in August during our second quarter earnings call. I also want to acknowledge our announcement last week regarding the results of RAMP 205. These data show that avutometinib plus defactinib, in combination with GemNab, delivered efficacy equivalent to the best results reported to date, and we believe VS-7375 has the potential to deliver the same efficacy with a more tolerable side effect profile. As we said, we will continue to evaluate the potential role of avutometinib and defactinib in metastatic pancreatic cancer, including combinations with 7375 and potential strategic collaborations informed by the overall final survival results from the study, as well as emerging data from VS-7375. Overall, we've had a disciplined first half of the year focused on execution. We're excited by the tremendous progress we've made with VS-7375, and we look forward to providing a more mature clinical update with appropriate patient follow-up in the second half of 2026. With that, let's open the call for questions. Operator? Thank you. Ladies and gentlemen, to ask the question, please first star one on your telephone, then wait for your company name to be announced. Once your company name is announced, please introduce yourself before asking your questions. To withdraw your question, please press star one again. Please stand by while we compile the Q&A roster. Our first question comes from the line of Cantor Fitzgerald. Please introduce yourself. Your line is open. Well, thanks. It's Eric Schmidt. Appreciate the very comprehensive program update and congrats on the execution progress with VS-7375. Maybe just a quick question on the Erasca collaboration. Can you give us a little bit more detail on which party is going to be designing the studies? Is their primary responsibility for running the trials either with Verastem or Erasca, and who's going to be paying for the work as well? Thank you. Hey, Eric. Thanks for the question. We actually haven't really released any details on it yet. As you can imagine, we're in the process of having discussions with others around our other partnerships and don't want to impact those. As we get closer to it, we'll give a little more detail, but we're very excited to have agreed with them to do a study together. Dan, are we expecting that we'll get a PRMT5 announcement in the not too distant future, too? It sounds like you're alluding to something there. Yeah, that's probably a good bet. Okay. Thank you. Please stand by for our next question. Our next question comes from the line of Guggenheim Securities. Your line is open. Please introduce yourself. Yeah. Hey, it's Michael Schmidt with Guggenheim. Congrats on the update. A couple of questions. Nice to see the progress towards launching the registration-directed phase II studies, actually. Any updated thoughts on how you think about the approval hurdle potentially in terms of efficacy for those three phase II studies across the three indications? Yeah, Michael, thanks for the question. Michael, why don't you take that one? Sure. The paths are pretty well set out in lung and colorectal cancer. In lung single agent, generally activity that FDA and investigators and patients get excited about is a single-agent response rate north of 30% with a durability of six months or better. These are pretty good metrics. Obviously, we intend to do better than those. Colorectal cancer has also been worked out through the G12C RAS inhibitors in combination with either cetuximab or panitumumab. Again, response rates greater than 30%, durability six months or better generally gets it. I think those areas have precedent for sure. Obviously, pancreatic cancer is undergoing the kind of renaissance we saw back with colorectal G12C cancer and, to some extent, some of the targeted therapies in lung cancer now. We're going to be working with FDA, along with lots of other companies, to map out a path for accelerated approval there. We believe that a combination of both good response rates, again, north of 30%, single agent response rate with a good durability, and importantly, a side effect profile that we think is second to none. Keeping in mind that accelerated approval can include efficacy and/or safety, substantial improvement over available therapies, or both, and we intend to win on both. The last thing I'll say is that there are no agents currently in pancreatic cancer that can deliver a single agent response rate anywhere close to 30% or 35%. Obviously, duraxonrasib is in the 35% range for second line. We think we can do at least that well, if not better, and we think we can deliver a side effect profile that is much easier to tolerate than a pan-RAS inhibitor. Thanks, Michael. I guess just confirming, has the FDA agreed to an accelerated approval strategy in general across these indications, or is that still TBD? As you think about upcoming discussions around the planned phase III studies, in pancreatic cancer specifically, what are possible trials that you're considering given potential changes to the landscape? You have the cetuximab combination in addition to the chemo combo. What could a possible phase III study look like in PDAC specifically? Thanks so much. Yeah, Michael, you want to take that as well? Sure. Thanks. Yeah. Look, as you know, we've known each other a long time. I've been through four successful accelerated approvals in my life, and they're always an uphill battle no matter where they are. I think FDA is more open to them now, especially with agents that have good tolerability profiles. The FDA told us at the beginning that we had to take the TARGET-D 101 phase I/II study and break it into separate disease specific studies, that is the phase II studies, if we wanted to go for a pivotal trial in terms of accelerated approval, and that's what we did. Obviously, they will hold us to a very high bar, which will be determined, but we are engaged with those discussions in all three of the cancers. As you alluded to, a major component of any accelerated approval is that your confirmatory, typically randomized study has to be ongoing at the time of regulatory action, and we are engaging with FDA in the coming months before the end of the year for sure to discuss the phase III trial designs across all three different tumor types. In pancreatic cancer, as you alluded to, we have a few options. We are actively working on the dose that we're going to select for combination of 7375 plus GemNab in front line, and we have cleared the 600 mg cohort already, and we are investigating 900 mg. We've seen really good tolerability of the combination. We've had no need to reduce either drug on either side, we will see. The 900 should clear, hopefully, in the next coming months, and then we'll be able to move ahead with that as one of the components of the phase III. The other component of the phase III will either be, most likely, either be a VS-7375 monotherapy, or if the data with cetuximab continue to look as good as we hope they will, it'll be a combo with cetuximab, and that would be another experimental arm. Of course, this will be against dealer's choice or investigator's choice combination chemotherapy, either FOLFIRINOX or GemNab in the control arm. It'll be most likely a three arm trial with two arms within VS-7375, including a potential chemo-free arm. Great. Thanks. Congrats on the update today. Thank you. Thank you. Please stand by for our next question. Our next question comes from the line of RBC. Your line is open. Please introduce yourself. Hey, guys. It's Leo from RBC. Thanks for taking my question. I wanted to ask on the CA 19-9 biomarker, maybe you can expand a little bit more on how reliable it is and maybe how it correlates to both response rate and then ultimately overall survival. You've mentioned 50% reductions on that biomarker. How meaningful of a marker is that for driving a partial response? I guess ultimately, is this marker going to be more of a leading or a lagging indicator of the tumor? Just noticing there's some variability in the baselines, and some patients appear to have it at baseline, not. Maybe if you just expand on how valuable this marker is. Thanks. Sure. Hey, Leo. Thanks for the question. Michael, why don't you take that one? Sure. We won't have time to go into a lot on this marker, but if you know anyone with pancreatic cancer, and I hope you don't, but unfortunately, a lot of us do, you'll know that they go month to month waiting for their CA 19-9 results, assuming they have a CA 19-9. About 80%+, 85% of the patients do have this marker, and then another 10% or so will have CEA as their biomarker. CT scans are typically done every six weeks. Just to be very clear about this, CA 19-9 is actually an enzyme system that's made by the tumor cells that has to do with glycosylation, and it changes sugar moieties, and it's actually a series of proteins that are glycosylated differently, and the levels are measured accurately and have been for a long time. Be clear, the tumor cells themselves make the marker. It is a leader and a predictor of how the patient's tumor mass is going. You also know that pancreatic cancer has a lot of scar tissue. It, in some sense, can overestimate the treatment effect in the sense that if you hold the CT scan as the gold standard, which of course the FDA and investigators do, then it can look a little bit better than the CT scan. That said, it is actually very well correlated with outcomes, there's an extensive literature on this with multiple meta-analyses and multiple different studies that have looked at especially 50%, 80% and 20% reductions in CA 19-9. To give you an example, one of the best and most recent studies on this was the combination of ONIVYDE, that is a nanoliposomal irinotecan with 5-FU leucovorin in the second, third-line setting, which is very relevant to our population. This is very intensive chemotherapy, as you know, and they had about 30% of their patients had at least a 50% reduction in CA 19-9. That correlated with a 17% response rate. Now, we have three times higher the CA 19-9 response rate. We are clearly more active, I would say, we will see when the scans are available. We're clearly more active, though, on the CA 19-9 than this intensive chemotherapy in the second-line. The CA 19-9 changes also correlated very well statistically with both PFS and OS, as well as ORR. It is very well correlated. It's also correlated in the front-line. Patients with reductions, which is typically 70%-80% of patients in front-line with FOLFIRINOX, for example, will have some reduction in their CA 19-9, and that correlates with better outcomes than those patients that have no reduction or a rise in the CA 19-9. Again, it's a leading indicator. It's something that patients follow all the time. What you might notice from the cases we put out is that the patients who had a couple of scans, if you look, you'll see that their CA 19-9 preceded the scans, and if the CA 19-9 stayed down or went down even further, the scans tend to get better over time. It takes a lot longer to remove these pancreatic tumor beds, which consist of a lot of fibrotic tissue, so-called desmoplastic reaction, than it does to kill the tumor cells themselves. We want to give the drug a long time to clear the tumor beds, that is the body, a long time to get rid of the dead tumor tissue, and we are following, of course, CA 19-9 along with the CT scans in parallel. Thanks, Michael. Thank you. Please stand by for our next question. Our next question comes from the line of Mizuho. Your line is open. Please introduce yourself. Hi, this is Sam on for Graig. Thanks for taking our question. Maybe a little bit more color on the current strategy for the 1,200 mg, assuming it gets cleared. Any updates on what the clinical plan is forward for that dose? Thank you. Hey, thanks for the question. Michael, you want to take that one? Yeah, I apologize, I couldn't hear very well. Both questions sort of got muddied. It was really around the question around our plans for the 1,200 mg. Yeah. The 1,200 mg really represents the maximum administrable dose, if you will. The current tablets in the formulation that we have are 100 mg tablets, and giving people nine tablets for 900 mg is doable. They don't love it, obviously, and we all have taken pills before, we know that nine's a lot, 12 pills is really on the edge. It is absolutely good drug development, and it's required for any approvals to explore the maximum tolerated dose, which we have not reached, or the maximum administrable dose, which is probably 1,200 with this current formulation. We're in the DLT period right now. I've got nothing exciting to report about how patients are doing. Hopefully we will clear that, we will declare victory if we clear that dose, we will stop in terms of the current formulation. We're obviously working on pills that are larger, meaning they hold more drug, and we're working on alternative formulations as well, we'll be able to look in the future. The 1,200 is really to finish off the current characterization of the drug and understand what the highest administrable dose will do. We probably will, in the future, look into it a little bit more closely, assuming tolerability is similar to what we've seen so far. Right now it's really just to close off that aspect of the drug description. Just to remind everybody, we're seeing really good coverage at 900, which makes us really confident in that dose. Got it. Thank you for that. Please stand by for our next question. Our next question comes from the line of H.C. Wainwright. Your line is open. Please introduce yourself. Hi, everyone, this is Andres Maldonado from H.C. Wainwright. A couple quick questions from us. First off, from a mechanistic perspective, can you give us a little bit more color as to why cetuximab appears to drive that deeper response we saw with the subtherapeutic dose, specifically at 400 mgs in PDAC? In that context, can you maybe provide a checklist for us on what you really need to see in that data that really supports that chemo-free PDAC path? Maybe a quick follow-up to some of the commentary on CA 19-9. Obviously, the meta-analysis correlations with OS and PFS that you mentioned are intriguing, and I want to take it a step further. Is it safe to say that that meta-analysis also correlates to the CA19 correlate to lower levels of phospho-ERK for these patients? Thank you very much. Thanks for the question. Jon, why don't you take the first one, you can have the second one if you want as well. Okay. I'll start with the first one. There's a lot of building evidence for the importance of EGFR as a combination strategy with RAS inhibitors in pancreatic cancer. Going back to 2019, there were some nice publications by Mariano Barbacid showing that if you block RAS signaling, you really need EGFR inhibition in animal models of pancreatic cancer. There was a beautiful paper by Channing Der's lab in February of this year. They did CRISPR knockout of every gene in the genome together with combination with the RAS inhibitors across pancreatic cell lines. The number one hit was if you knock out EGFR, you greatly increase the efficacy of a RAS inhibitor. They used multiple RAS inhibitors, multiple pancreatic cell lines. They also showed that whenever they treated a pancreatic cell line with a RAS inhibitor, they saw a great increase in phospho-EGFR, showing that it's trying to activate EGFR to get around. We, of course, have preclinical data we've shown before where if we combine Cetuximab with VS-7375 in pancreatic models, as we see in colorectal models, we see very nice regression. That together with our clinical observations, have made us excited about this combination. Michael, do you want to take the question about what it'll take for us to go forward with the Cetuximab combination relative to VS-7375 alone? Sure. I think it's a bunch of different things, as you might imagine. The most important thing, of course, in any of these fatal cancers is efficacy. If we can see a higher response rate with preferably better durability, and mechanistically, if you hit two pathways, you should see both a higher response rate and better durability. That would be the major driver. The trade-off, obviously, is people will have to take an intravenous medication every couple of weeks. The side effects of cetuximab and panitumumab are well-described. The acneiform rash is well managed. Standard doxycycline or minocycline with either steroid cream or what have you, is typically very effective. You saw some of our patients really don't get much else besides the rash. I think it's really going to come down to efficacy. We won't have long-term durability, but we will certainly have the ORR, and the preliminary data are very intriguing for a potentially chemo-free frontline regimen, which will be a lot easier to take than any of the current chemotherapies that are given for pancreatic cancer. Andres, I think you had a third question. Can you repeat what that was? Yeah. There's a question on phospho-ERK and whether that relates to the CA 19-9. Correct. Yeah, John, I don't know if, from a scientific point of view, I'm not aware of any literature on a direct correlation between those two. CA 19-9 is a direct measure of tumor cell mass, not necessarily pancreatic cancer cell size, as I keep emphasizing this rather fibrotic reaction that we do see a lot in pancreatic cancer. Live cells are the cells that make the enzymes that lead to CA 19-9. I don't know that, frankly, phospho-ERK levels have been studied because, in the past, the only thing we've been treating pancreatic cancer with has been multi-agent chemotherapy. I will say two things, though. I think that given that we know that RAS is the strongest driver of pancreatic cancer now, we've been seeing this really clearly. The main endpoint of that is phospho-ERK, I'd be shocked if we don't see the correlation of phospho-ERK with both regression by scans but also with CA 19-9. Secondly, we are adding, actually, a mandatory biopsy cohort in pancreatic cancer patients to our 101 study. One of the main things we'll measure there, we'll measure both phospho-EGFR and phospho-ERK in that case. We actually will learn the answer to your question, although we don't know it today. Perfect. Thanks, and congrats on the data. Thank you. Please stand by for our next question. Our next question comes from the line of B. Riley. Your line is open. Please introduce yourself. Hi, this is Yuan Zhi from B. Riley. Thank you for taking our questions. Dan, you guys showed the encouraging spider plot of CA 19-9 within the 900 mg cohort in PDAC. What about the trend in the 600 mg cohort? Michael, you want to take that? Did we look at this 19-9 in the 600 mg cohort as well? Yeah. I can take it if you like. Yeah. We alluded to it. When we say we see a dose response, we mean it both for CA 19-9 and the preliminary radiographic results that we're getting. We see that 900 delivers much more anti-tumor activity. 600 definitely has good activity, but 900 is 50% more drug, and you saw the PK results, and it looks very impressive on the PK side. We're definitely getting more anti-tumor activity, and that does manifest in the CA 19-9 as well. Got it. Since we are short on time here, maybe a quick question. For VS-7375, is that compound metabolized through the CYP3A4 mechanism? Jon, you want to take that? Yes, is the answer. Thank you. Okay. That was a quick answer. Yeah, we are getting up on time here, so we should just get through the last few questions. Thank you. Please stand by. Our next question comes from the line of BTIG. Your line is open. Please introduce yourself. Great. Thanks for taking the question. This is Jeet Mukherjee. Two quick ones, hopefully. One, are you seeing time to response vary in the 101 trial versus the GenFleet trial? Two, how do you see 7375's profile comparing against 1,200 mg zoldonrasib as of now? Thank you. Michael, you want to take that? Yeah. I think time to first response is similar to the GenFleet trial, although I think our patients seem to be more heavily pretreated, just at least in terms of the time that they were on prior therapies and perhaps some of the duration of their second-line treatments. As GenFleet found, non-small cell tends to be more rapid responses than the GI cancers, which I think none of us, certainly none of the oncologists we speak with, are surprised. We seem to be generally in the same ballpark. Again, I think in the GI cancers, we eat away at these tumors over time, and it's actually quite nice to see that people get their next scan, and what's happening is that some more of the tumor is gone. I think it might be a little bit longer for the GI tumors. Non-small cell, again, seems to be quick. There was a second question, I think. I can take that as well. Yeah. Yeah, go ahead, Jon. Yeah. No, I think it's quite interesting. Really what I'm extremely excited about is we don't have an exposure ceiling. We're able to keep dosing higher to maximally inhibit the target. I think across. Probably all other RAS inhibitors, we see this exposure ceiling where they just get to a certain exposure, they can't get higher. Certainly for zoldonrasib, if you compare 600 mg QD to a somewhat lower dose, you see a similar exposure. I think that for that reason, zoldonrasib has a 30% confirmed plus unconfirmed. Not extremely strong. Actually, you see a number of patients where the best response is somewhat substantial PD progression. I think that's maybe a symptom of leaving some patients behind and not getting sufficient exposure as we can get. Thank you. Please stand by for our next questioner. Our next question comes from the line of Alliance Global Partners. Your line is open. Please introduce yourself. Hi, guys. Matt on for Jim Malloy at AGP today. Just two quick ones. Should we anticipate R&D spend increasing a bit in relation to the Erasca collab and the upcoming PRMT5 collab in 2026, or is that more of a 2027 event? Is there any more color you can give us on the patients receiving cetuximab plus VS-7375 in TARGET-D 101, mainly related to safety, as I know that part of the trial is not as far along. Yeah, I would just say in general, R&D expenses related to the G12D program should increase as the year goes by as we start both the phase II trials and then gear up for the phase III trials. The collaborations, we haven't really spoken about what they may add. What was the second part of your question? Sorry. It was if you could just give us a little more color on the patients receiving cetuximab plus- Oh, the cetuximab. - VS-7375. Yeah. Yeah. Michael, you want to take that? Yeah, I mean, the patients receiving cetuximab are similar to the patients that are on the monotherapy as well. Can you give me a little more specificity on what you're looking for? Yeah. Just if the patient population was similar as well as if the safety profile looked similar between the patients receiving VS alone and with cetuximab. Sure. No, great. Now I got it. Yeah. This is identical populations. In fact, in the ongoing, in the trial that just opened, that enrolled, it's actually randomized patient population second line, but in the TARGET-D 101 study, the phase I/II study, the patients were the same. They had to have at least one prior therapy, then they just ended up on whatever slots were open. In terms of the side effect profile, what it really looks like, it looks like 7375 plus cetuximab, and the main contribution of cetuximab, of course, is this nearly ubiquitous rash. I mean, it's touted as 80%, but frankly, it's probably just about everybody gets cetuximab. They get a bit of an acneiform rash. Typically, it's grade one these days because they get prophylaxed. As you know, cetuximab's been around for a very long time, docs know how to take care of this and minimize it. There's no exacerbation of any of the 7375 minimal side effects. As I mentioned on the call, the 7375 side effects are attenuated substantially after the first cycle, patients are just frankly pretty happy on it. Great. Thank you, guys, and congrats on the progress. Thanks. Thank you. Please stand by for our next question. Our next question comes from the line of Jefferies. Your line is open. Please introduce yourself. Hello, this is Anand Shan for Faisal. In the treatment emergent AE table at the end of the slides, you had two grade four events, including one anemia. Could you provide more color on those and how or why those were not deemed treatment-related? Thanks. Michael, you want to take those? Sure. The anemia was associated with a GI bleed that was absolutely due to the pancreatic cancer invading the GI tract. That's not due to our drug; that's due to the pancreatic cancer that's in the GI tract. The hyponatremia similarly was due to, I believe it was also a pancreatic patient, but I'm not absolutely certain. That was, again, due to somebody whose sodium just dropped precipitously when they were third spacing with ascites and so on, which is very common, and that was easily rectified with standard slow infusion hypertonic saline, and then the patient was brought back. Thank you. Ladies and gentlemen, I'm showing no further questions in the queue. That concludes today's conference. Great. Hello? All right. Thanks, everybody. That concludes today's conference call. Thank you for your participation. You may now disconnect.