Thank you, Maggie. Thanks, Karen, for inviting us. We are very happy to be here, and in the next 30 minutes or so, I would like to show you why we at Tango are super excited about what's coming up in the year 2026. We have a very compelling story to tell, and a lot of this excitement comes from data that we have generated last year and the years before. vopimetostat, our front-runner molecule, a PRMT5 inhibitor, is a highly potent and selective PRMT5 inhibitor with first and best-in-class potential. The molecule is clinically validated. We have received a lot of tailwind from FDA with respect to potential second-line registration opportunities in pancreatic cancer.
We have also launched proof-of-concept studies or a proof-of-concept study of combining vopimetostat with Revolution Medicines' RAS inhibitors to generate data to position vopimetostat potentially as a foundational backbone in combination for frontline pancreatic cancer. We have multiple additional pipeline opportunities, and I'm going to show some of them to you in the next couple of minutes. We have a very strong financial position, and this financial position is important because it enables us to accelerate the comprehensive vopimetostat registration program in pancreatic cancer. What are we going to do this year? We are going to launch a pivotal trial of vopimetostat monotherapy in second-line pancreatic cancer. We are going to complete and report our data with respect to vopimetostat in combination with Revolution Medicines RAS inhibitor to support our frontline pivotal trials in pancreatic cancer.
We are going to expand vopimetostat data in lung cancer and potentially other cancers to support additional pivotal studies. We are going to evaluate TNG456 efficacy in patients with glioblastoma. We feel very positively and strongly about these opportunities because our molecule has shown MTAP selectivity and potency, which provides potentially best-in-class opportunity. We also have a very exciting safety and tolerability profile of vopimetostat, which is extremely important with respect to potential combinability of vopimetostat with other molecules. Tango is the first company who has ever combined a PRMT5 inhibitor with a RAS inhibitor, and that may be the foundation of a fast and innovative path to first-line approvals. We have a wholly owned pipeline targeting multiple high-value indications.
Our principle is to develop our products in patients with high unmet medical needs and with potential fast-to-market opportunities. I already spoke about vopimetostat monotherapy and combination studies, and I will provide a little bit more background on these trials. TNG456 is our blood-brain barrier penetrant PRMT5 inhibitor, which we develop in glioblastoma and non-small cell lung cancer. TNG961 is an HVS1L inhibitor, which we develop in MTAP and PRCAT1 co-deleted cancers. Let's dive a little bit deeper into our vopimetostat program. If you think about MTAP deletion, MTAP deletions are one of the most common genetic changes in cancer. If a tumor has an MTAP deletion, this deletion confers sensitivity to PRMT5 inhibition. The frequency of MTAP deletion is shown on the left side of this slide.
For example, 15% of patients with non-small cell lung cancer have this genetic alteration, 40% of patients with pancreatic cancer, 45% of patients with GBM, 16% of patients with head and neck cancer. This is a large opportunity for development in pancreatic cancer and other cancers. We have estimated that approximately 60,000 patients with MTAP deletion could benefit from PRMT5 inhibition annually in the United States alone. vopimetostat is a potential best-in-class PRMT5 inhibitor. It has a very differentiated profile. It's highly selective and potent for potentially superior PRMT5 suppression. It is clinically validated. 27% of patients across all tumor types have an objective response rate.
The safety profile is very benign and makes us confident that our molecule is suited for potential combinations with other targeted therapies or even chemotherapies. We have a first-mover advantage here. We are ahead of the game in terms of combining our PRMT5 inhibitor with RAS inhibitors, and we are excited about potential opportunities that evolve from the data that we are going to disclose later this year. I want to show you a couple of data points with respect to our ongoing Phase I/II study. We have completed our dose escalation phase and are in dose optimization in patients with pancreatic cancer, lung cancer, and histology-selective cancers. In terms of pancreatic cancer, the data are supporting clearly the advancing into second-line pancreatic cancer registration trials. For lung cancer, we have fully enrolled our cohort, and we will provide an update of this dataset later this year.
We have seen encouraging data emerging out of the histology-selective cancers, and I will give a little bit more color to what we mean here. vopimetostat at 250 milligram daily shows a best-in-class safety potential. We've shown here a couple of data points in terms of nausea, anemia, fatigue, dysgeusia, and other toxicities, and we are very pleased with the benign safety and tolerability profile. The median follow-up for this dataset is 6.1 months. We have observed only 8% of dose reductions, and not a single patient has been discontinued for related events. We have not observed any grade 4 or 5 related events. This data is very important when you think about moving PRMT5 inhibitors into combinations with other targeted agents or chemotherapies.
Looking at median progression-free survival, in the study that I just mentioned, we have a PFS, median PFS of 7.2 months, and that is roughly doubling or more than doubling what you commonly expect in patients being treated with standard of care chemotherapies. The curves on the left here show examples of chemotherapy treatments and the respective median progression-free survival numbers. These numbers may even be overestimates because it's known that MTAP deletions confer a bad prognosis due to concurrent CDKN2A deletion. This is the trial design of the upcoming monotherapy pivotal trial in second-line pancreatic cancer. It's a hierarchical co-primary endpoint of PFS and overall survival. It's a global study. It's a randomized trial with sites in the United States, Europe, and in Asia Pacific.
We had discussions with FDA, who was very supportive of our trial design, our sample size selection, and our dose selection. Now moving to our non-small cell lung cancer activities. We have 41 patients enrolled in our non-small cell lung cancer cohort. 12 of these patients have completed more than 6 months of treatment since enrollment, and we are currently at a median follow-up time of 4.7 months. The cohort is fully enrolled. We are monitoring the data, and we plan to share data from this non-small cell lung cancer cohort later this year. We have mentioned already the histology selective cohort. This is a cohort in which patients can receive treatment who have MTAP deletions irrespective of the histology.
We have observed an objective response rate of 49% with a median progression-free survival of 9.1 months. There are a couple of interesting data points and signals in this study. For example, 3 out of 3 patients with head and neck cancer had a response in this cohort. We are continuing enrollment in this cohort to expand our database in this histology selective cohort. The median progression-free survival of 9.1 months is again, very competitive with respect to standard of care trials that have been published. We have listed a couple of examples here in biliary cancer of unknown primary, mesothelioma, head and neck cancer, and across the board, I think it's clear that vopimetostat more than doubles the progression-free survival numbers shown in these standard of care trials.
Switching gears, we have started a combination trial of combining vopimetostat with Revolution Medicines' zoldonrasib and daraxonrasib in June of last year. This decision was based on the preclinical data that are shown on this slide. You can see a preclinical experiment combining vopimetostat and zoldonrasib at suboptimal doses. Each suboptimal dose for each component alone has no activity in this preclinical experiments. However, combining these two compounds at suboptimal doses eradicates tumors and has a synergistic activity in these preclinical experiments. Pancreatic cancer, as we all know, is a RAS-addicted tumor. Almost all MTAP-deleted pancreatic cancers have a RAS mutation, and roughly 40% of MTAP-deleted pancreatic cancer are RAS G12D mutated. We are very pleased and happy about our collaboration with Revolution Medicines. The clinical trial is shown here.
We have two arms, one combining vopimetostat with daraxonrasib, the other combining vopimetostat with zoldonrasib in patients with any RAS mutation or G12D-mutated cancers respectively. Our enrollment is very good. We have dosed 30 patients, 14 in the daraxonrasib arm and 16 in the zoldonrasib arm. We are very happy to report that for all components of this combination study, we have reached clinically meaningful exposures. We have seen no adverse events, and we are encouraged by the early signals of clinical activity. We will provide a safety and efficacy update of this clinical trial later this year. Now, we are, of course, often asked what is our plan and what is our strategy with respect to the combination moving forward. I want to make a couple of points. First of all, more than 90% of pancreatic cancers are RAS-driven.
Almost all MTAP-deleted pancreatic cancers have a RAS mutation. This leaves you with 18,000 patients with MTAP deletion and RAS mutation in pancreatic cancer in the United States each year. That's a big number. We think that the potential combinability of vopimetostat with a RAS inhibitor gives an additional opportunity of moving our clinical development into frontline pancreatic cancer. We anticipate our data that we will release later this year to support our thinking in that direction. This is the first PRMT5 inhibitor that has been combined with a RAS inhibitor so far. Now, I want to say a couple of words about TNG456, which is a molecule we are also very excited about. This is a next-generation CNS penetrant PRMT5 inhibitor, and I've shown some key data point on this slide.
The molecule has a potency that is slightly lower than vopimetostat with a higher MTAP selectivity. The molecule has a very good blood-brain barrier penetrability, and that's why we are excited to have started a clinical trial that is shown on this slide in patients with glioblastoma and non-small cell lung cancer. We anticipate to provide an update, a clinical update, for this trial later this year. The dose escalation is ongoing. We have just put the first patients with glioblastoma on this study, and we're excited to see the first results, and we will provide an update later this year. Now, in summary, what is it that we're going to show this year? What are our key milestones that we're going to speak about?
We're going to show our vopimetostat and daraxonrasib and zoldonrasib data later this year. We're going to provide an update with respect to our vopimetostat monotherapy data in lung cancer. We are going to start a second-line pivotal trial in pancreatic cancer, and we are going to provide an update on TNG456, as I just explained. We have a very comfortable cash position of $343 billion in the bank, which provides us a cash runway into 2028. I just want to remind you of this initial slide depicting our storyline of vopimetostat as a highly potent and selective PRMT5 inhibitor with a first and best-in-class potential. Vopimetostat is clinically validated, which has received tailwind from FDA with respect to our second-line pancreatic cancer trial design.
We expect to share our proof of concept data in combination with Revolution Medicines' RAS inhibitors later this year. As I have showed you, we have other exciting components of our clinical pipeline. With this, thank you very much.