Good morning, everybody. My name is Kelsey, and I will be your conference operator for today. At this time, I would like to welcome everyone to Karyopharm Therapeutics' Q1 2026 financial results conference call. There will be a question and answer session to follow. Please be advised that this call is being recorded at the company's request. I would now like to turn the call over to Mr. Brendan Strong, Senior Vice President, Investor Relations. Please go ahead. Good morning. Thank you all for joining us on today's conference call to discuss Karyopharm's 1st quarter 2026 financial results and recent company progress. We issued a press release this morning detailing our financial results for the Q1 of 2026. This release, along with a slide presentation that we will reference during our call today, are available on our website. For today's call, as seen on slide two I'm joined by Richard, Reshma, Sohanya, and Lori, who will provide an update on the results for the 1st quarter, highlight the importance of the results from our phase III SENTRY trial in myelofibrosis, and provide an update on our endometrial cancer program and related commercial opportunity. Before we begin our formal comments, I'll remind you that various remarks we will make today constitute forward-looking statements for purposes of the safe harbor provisions under the Private Securities Litigation Reform Act of 1995, as outlined on slide three. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in the Risk Factors section of our most recent Form 10-Q or 10-K on file with the SEC and in other filings we may make in the future with the SEC. Any forward-looking statements represent our views as of today only. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so, even if our views change. Therefore, you should not rely on these forward-looking statements as representing our views as of any later date. I'll now turn the call over to Richard. Please turn to slide five. Good morning, and thank you for joining us today. Karyopharm continues to execute through an important period for the company, with recent and upcoming milestones that we believe can unlock meaningful growth opportunities and shape our next phase. Over the past several quarters, we have focused our organization around three priorities: advancing our late-stage clinical programs, maintaining our commercial foundation in multiple myeloma, and managing the business with discipline as we approach significant value-creating milestones. Since our fourth quarter call, we have made meaningful progress across our key 2026 priorities, including reporting top-line results from our phase III SENTRY trial in myelofibrosis, completing enrollment in XPORT-EC-042 in endometrial cancer, and strengthening our balance sheet through the financing completed in Q1. With these milestones and data in hand, we are now focused on the next phase of execution, advancing our regulatory and scientific engagement for SENTRY, preparing for the EC042 top-line data readout, and continuing to manage the business with financial discipline. SENTRY showed a compelling and differentiated profile for selinexor in combination with ruxolitinib, including rapid, deep, and sustained spleen volume responses, accompanied by a promising overall survival signal and evidence of potential disease modification, including greater reductions in variant allele frequency as early as week 24. These findings reinforce the potential of selinexor plus ruxolitinib to address an important gap in frontline myelofibrosis treatment, where treatment options remain limited and the need for therapies that can improve long-term outcomes remain high. We are very encouraged by the level of interest and enthusiasm we are hearing from the myelofibrosis KOL and patient group communities following the SENTRY readout. Our next major catalyst is XPORT-EC-042 in endometrial cancer, where enrollment is now complete. We continue to expect top-line data in mid-2026. This is a biomarker-driven program focused on patients with TP53 wild-type endometrial cancer, particularly those with pMMR tumors, where there remains a significant unmet need and no approved personalized biomarker-driven maintenance therapy. Commercially, we believe we have a strong foundation to build from. Our deep relationships across community and academic accounts and capabilities in sales, marketing, market access, patient support, and medical affairs can be leveraged across future potential launches. In both endometrial cancer and myelofibrosis, we see concentrated treatment landscapes and clear unmet need. Financially, we remain disciplined. We ended the quarter with increased liquidity following our financing in March. We continue to manage spending with a clear focus on the clinical and regulatory milestones that matter most. Our current operating plan provides us with sufficient flexibility through our major near-term clinical and regulatory catalysts, including SENTRY next steps and the XPORT-EC-042 top-line readout, funding us into late Q3 2026. With that context, today's call will first cover the SENTRY highlights and next steps, followed by a deeper discussion of the upcoming XPORT-EC-042 readout, our commercial readiness, and our financial performance with guidance. I'll now turn the call over to Reshma. Reshma? Thank you, Richard. Before we dive into myelofibrosis and endometrial cancer, I want to take a step back and ground everyone in the biology of XPO1 inhibition and why we believe this novel mechanism has the potential to meaningfully improve outcomes for patients across both diseases, as outlined on slide seven. What's particularly compelling about XPO1 inhibition is that it allows the drug to simultaneously impact multiple highly relevant oncogenic pathways. Selinexor selectively binds to XPO1, a key nuclear export protein, and blocks the transport of critical regulatory proteins out of the nucleus. By doing so, selinexor drives the retention and activation of tumor suppressor proteins such as p53, FOXO, p21, and IκBα within the nucleus where they can exert their anticancer effects. This effect is particularly notable for myelofibrosis and endometrial cancer, given that greater than 95% and 50% of these tumors, respectively, are p53 wild type. At the same time, it reduces the activity of oncogenic signaling pathways, including NF-κB, which is of relevance to myelofibrosis. Induction of cell cycle arrest independent of the p53 pathway is also critical pathway important to both endometrial cancer and myelofibrosis. The net effect is a coordinated biological response, including decreased tumor cell proliferation, increased apoptosis, and ultimately the potential for durable disease control. We believe this multi-pathway mechanism is a key differentiator for selinexor and underpins the breadth of activity we've observed across multiple cancers, including both MF and EC. With that backdrop, let's turn to myelofibrosis and why we believe the SENTRY data are so compelling, as outlined on slide nine. There remains a clear opportunity to improve upon the current standard of care. While JAK inhibitors have been an important advancement and remain the only approved class, we continue to see relatively rates of spleen volume reduction, limited impact on long-term survival, and minimal evidence of true disease modification. As such, there is an unmet medical need for therapies that go beyond symptom control and deliver deeper, more durable benefit and improve long-term outcomes like overall survival. Moving to slide 10, as I presented a few weeks ago, we're very encouraged by the top-line results from our phase III SENTRY trial. The combination of selinexor plus ruxolitinib delivered rapid and clinically meaningful spleen volume reduction as early as week 12. Importantly, that benefit was sustained through week 36. The co-primary endpoint of SVR 35 at week 24 was 50% for the combination compared to 28% for ruxolitinib alone, corresponding to a statistically significant P value of less than 0.0001. Our second co-primary endpoint was symptom improvement at week 24. While the difference in absolute TSS was not statistically significant, patients in both arms experienced important and similar improvement from baseline. What we find particularly exciting is the intriguing signal of overall survival, arguably the most important outcome for patients with myelofibrosis. The combination of selinexor and ruxolitinib is the first potential treatment in myelofibrosis to suggest an overall survival improvement relative to standard of care. At the time of the top line data, the overall survival hazard ratio was 0.43 with a nominal P value of 0.0222. In addition, post hoc analyses demonstrate that SVR 35 predicts OS, consistent with published analyses in other myelofibrosis trials that have also shown the same. These findings underscore the importance of achieving rapid, deep and sustained SVR 35. The greater proportion of patients on the combination arm at 32% who experienced a variant allele frequency reduction of at least 20% may be indicative of an underlying effect on the disease biology, raising the potential for true disease modification. The rapidity at which we see these VAF reductions reflect the anti-clonal attributes of selinexor and mirrors both the substantial improvement in SVR 35 as early as week 12 and the early improvements in overall survival. Lastly, the combination demonstrated a generally manageable tolerability profile that was consistent with what we understand about each agent individually. We did not observe any new safety signals. With the use of the lower dose of selinexor in dual antiemetics, we've seen an improved tolerability compared to the phase I study. We believe the combination of the XPO1 inhibitor selinexor and ruxolitinib delivers a very compelling and differentiated product profile with the potential to improve outcomes for patients with myelofibrosis. Turning to slide 11, we're excited that these data have been selected for a late-breaking oral presentation at ASCO. We expect to have a manuscript published in a peer-reviewed journal in the middle of 2026. We remain very encouraged by the SENTRY results and look forward to productive discussions with the FDA. Let's now turn to endometrial cancer and why we're so excited about selinexor's potential to address a clear and meaningful treatment gap, particularly for patients with p53 wild-type MMR-proficient tumors. As highlighted on slide 13, this is a large and well-defined patient population. Approximately half of the patients are p53 wild-type, and about 80% have MMR-proficient tumors. Importantly, this is not a niche segment. It represents a substantial proportion of the overall endometrial cancer patients whose unmet need remains high. Equally important, molecular classification is already embedded in the standard of care today. That means clinicians are routinely identifying these patients in practice, which we believe positions selinexor very well for real-world adoption if our phase III data are positive and pending regulatory approval. On slide 14, we believe we have an opportunity to define a personalized biomarker-driven maintenance treatment option for patients with p53 wild-type endometrial cancer. Today, patients with advanced or recurrent EC have no personalized biomarker-driven maintenance-only therapy. Although checkpoint inhibitors are approved in combination with chemotherapy followed by checkpoint inhibitor alone, patients whose tumors are both TP53 wild-type and MMR-proficient gain the least benefit. The RUBY trial, which evaluated dostarlimab in combination with chemotherapy and in advanced or recurrent EC patients, showed a marginal PFS improvement of only 0.77 in patients whose tumors were NSMP or TP53 wild-type MMR-proficient. This highlights the profound unmet need for the subgroup that comprises approximately 50% of all endometrial cancer patients and underscores the urgency to identify TP53 wild-type-directed therapies. It also highlights the substantial benefit that potentially could be observed with selinexor in patients with TP53 wild-type tumors, and especially those whose tumors are both TP53 wild-type and MMR-proficient. As seen on slide 15, the top-line data in the p53 wild-type subgroup of the SIENDO study showed a very strong PFS signal with a median PFS in the selinexor arm of 13.7 months versus 3.7 months for placebo, translating to a hazard ratio of 0.41. As you can see on slide 16, with long-term follow-up, the median PFS benefit for the selinexor arm extends to 28.4 months, corresponding to a hazard ratio of 0.44. When we focus on the patients whose tumors are p53 wild-type MMR-proficient, the data become even more compelling. As shown on slide 17, the median PFS approaches 40 months at long-term follow-up with a PFS hazard ratio of 0.36. These results compare very favorably to the RUBY data in which the MMR-proficient p53 wild-type subgroup showed a PFS hazard ratio of 0.77. Taken together, what we see is not only a strong initial signal, but a benefit that deepens and becomes more meaningful over time. That's the dynamic we're aiming to replicate in XPORT-EC-042. To demonstrate a clear PFS advantage at top line, we also anticipate that the PFS benefit may continue to strengthen as the data mature. The safety profile on slide 18 is from the long-term follow-up from SIENDO. Given that the dose of selinexor was 80 milligrams in the SIENDO trial and prophylactic dual antiemetics for the first 2 cycles were not mandated, we have an opportunity to observe a better safety and tolerability profile in the ongoing 042 trial. Similar to the SENTRY trial, we've been very deliberate in optimizing both the dose and supportive care. In the XPORT-EC-042 trial, selinexor is dosed at 60 milligrams once weekly, and we've mandated dual antiemetics during the first 2 cycles, which is when patients are most likely to experience nausea and vomiting. There is the potential that with an improved safety profile, patients stay on treatment longer, translating to improved efficacy. Overall, we feel very good about how the program has evolved in delivering a more optimized and patient-friendly treatment approach. Finally, turning to slide 19, as Richard mentioned, I'm very pleased that we have successfully completed enrollment in our phase III XPORT-EC-042 trial. We enrolled 257 patients in the Intent-to-Treat population, which with approximately 220 patients in the Modified Intent-to-Treat population, which is the primary analysis population for the study. As a reminder, our statistical plan is designed to be both rigorous and efficient. We will first assess progression-free survival in the mITT population. If that analysis is statistically significant, the alpha will then pass down sequentially to the full ITT population. As we approach the pre-specified number of PFS events that will trigger the primary analysis, we remain on track to report top-line results in the near term. Stepping back, I'm incredibly excited about the opportunity in front of us, not only in endometrial cancer, but also in myelofibrosis. In both areas, we have the potential to establish new standards of care and deliver meaningful benefits for patients where significant unmet need remains. I will now turn the call to Sohanya. Thank you, Reshma. As shown on slide 21, we delivered strong net product revenue growth this quarter, driven primarily by favorable gross to net dynamics, which Lori will cover in more detail. Underlying demand for XPOVIO was lower compared to the 1st quarter of 2025, reflecting the impact of new competitive entrants. This is not new territory for us. We've successfully navigated competitive dynamics and returned to drive demand growth. Turning to slide 22, there are two ways that XPOVIO is positioned that we believe sets us up for future growth amidst an evolving and competitive landscape. First, our focus remains on the community setting, which represents approximately 60% of total U.S. sales, where many community-based physicians and patients value XPOVIO as a flexible and convenient oral option in the second to fourth line. Second, our distinct positioning for XPOVIO as a differentiated mechanism of action in the peri T-cell engaging therapy setting allows selinexor to be used in patients prior to a CAR T, which is an important position given anticipated future expansion of CAR Ts, and also in patients progressing on a T-cell engaging therapy. Therefore, despite an evolving competitive landscape, we remain confident in our ability to drive growth in XPOVIO net product revenue. Now as we turn to slide 23, if we look at our future potential launches in myelofibrosis and endometrial cancer, these are areas where there is strong overlap with community-based accounts with fewer treatment alternatives and higher unmet need than the multiple myeloma market. As we prepare for these potential launches, I would like to underscore the strength and value of our highly experienced teams. We have established capabilities across sales, marketing, market access, and medical affairs, all of which can be utilized to educate on the relevant disease states. This allows us to prepare for launch with minimal incremental investment pre-approval and only modest additional spend post-launch. Let's now discuss the potential commercial opportunity in both myelofibrosis and endometrial cancer, starting with myelofibrosis on slide 25. In myelofibrosis, the only treatment options that patients currently have are JAK inhibitors, with Ruxolitinib monotherapy being the standard of care for the past 15 years, and only about 1/3 of patients that receive Ruxolitinib achieve a spleen volume reduction of 35% or more, with 2/3 Of patients not adequately responding. Slide 26 provides an outline of the potential market opportunity. selinexor plus Ruxolitinib targets a sizable U.S. myelofibrosis market with roughly 20,000 patients living with the disease and limited approval, approved options beyond JAK inhibitors. With around 7,000 newly diagnosed frontline patients annually, about 4,000 of whom are addressable, we see a clear path to meaningful adoption. We believe the combination of selinexor and ruxolitinib has the potential to deliver up to approximately $1 billion in U.S. peak annual revenue. Our sales organization is well-positioned for a potential launch in myelofibrosis. We have deep relationships with the key accounts where the majority of patients are treated. As outlined on slide 27, 70% of myelofibrosis patients are treated in the community setting and 30% are treated in academic centers. Across both settings, the majority of patients are treated in a concentrated group of accounts, which enables us to move quickly and execute a focused high-impact launch if approved. Turning now to slide 28, we're energized by the opportunity to reshape frontline myelofibrosis treatment by pairing selinexor with the current standard of care and pending approval to drive rapid uptake and potentially transform patient outcomes. Turning to slide 30, I'd like to share how we're thinking about the commercial opportunity in endometrial cancer, which is the most common gynecologic malignancy in the U.S., with 17,000 newly diagnosed, advanced, or recurrent patients each year, and incidence and mortality rates on the rise. As Reshma mentioned, we believe we have a clear opportunity to establish selinexor as a standard of care in patients whose tumors are TP53 wild-type and pMMR. These patients comprise approximately 50% of all endometrial cancer patients. As we look at other therapies that have driven meaningful benefit in the treatment landscape, for example, the uptake of checkpoint inhibitors in dMMR endometrial cancer and PARP inhibitors in the maintenance setting in ovarian cancer, they achieve peak share within 18-24 months of launch. Similarly, given the high unmet need for maintenance therapy in p53 wild-type patients, as well as our established commercial capabilities, we would expect adoption to be rapid. On duration, our assumptions are influenced by the fact that this would be a maintenance option. While we don't equate PFS directly with duration, the strength of our PFS data from SIENDO gives us confidence that patients can remain on therapy for an extended period. Putting this together, this represents a significant opportunity within a multi-billion-dollar marketplace. Turning to slide 31, in summary, from a commercial perspective, if approved, selinexor is positioned to rapidly transform treatment in p53 wild-type endometrial cancer. We're very encouraged by the opportunity ahead and confident in our commercial readiness to support successful launches. With that, I'll turn the call over to Lori, starting on slide 33. Thank you, Sohanya, and good morning, everyone. I will focus on the key highlights from our first quarter financial performance and how those results position us relative to our full-year expectations. Starting with revenue, total revenue for the first quarter was $35.1 million compared to $30 million in the prior year period. U.S. XPOVIO net product revenue was $29.2 million compared to $21.1 million last year. This increase was driven by a decrease in gross to net, which was 21.8% this quarter versus 45% in the first quarter of 2025 that was impacted by an atypical product return adjustment. Our gross to net reflected lower realized discounts and returns this quarter. Excluding these adjustments, our underlying gross to net was approximately 26% this quarter. Turning to expenses, we remain focused on disciplined execution. R&D expenses were $33.8 million, and SG&A expenses were $26.7 million, both relatively consistent year-over-year. This reflects our continued focus on prioritizing investment in our highest-value clinical programs while maintaining overall cost controls. Net loss was $22.4 million for the quarter compared to $23.5 million in the prior year. As a reminder, net loss includes non-cash mark-to-market adjustments related to our financing structure. From an underlying operating perspective, performance improved meaningfully with a 20% reduction in loss from operations, driven by the increase in total revenue and continued expense discipline. Turning to the balance sheet, we are managing the business with a clear focus on our clinical catalyst and ended the quarter with $91.2 million in cash equivalents, and restricted cash, which includes the approximately $50 million raised this quarter. Based on our current operating plan, we expect our existing liquidity to fund operations into late in the third quarter of 2026. We remain focused on prudent capital management as we advance our pipeline and prepare for our upcoming phase III readout in endometrial cancer. Turning to guidance, we are reaffirming our full-year 2026 outlook. We continue to expect total revenue in the range of $130 million to $150 million, with license and other revenue consisting entirely of royalties over the next three quarters and U.S. XPOVIO net product revenue of $115 million to $130 million. Finally, we also continue to expect combined R&D and SG&A expenses in the range of $230 million to $245 million in 2026. Overall, we believe our first quarter performance and operating discipline position us well to deliver against our full-year expectations in 2026. With that, I'll turn the call back over to Richard. Thank you, Reshma, Sohanya, and Lori. As we have discussed today, Karyopharm has made meaningful progress against the priorities we laid out entering 2026. Across both myelofibrosis and endometrial cancer, we believe the story is consistent. selinexor has a differentiated mechanism of action, the clinical programs have been refined based on experience, and the commercial opportunities are meaningful. We have also worked hard to optimize how selinexor is used, including dose selection and proactive supportive care, with the goal of delivering the right balance of efficacy, tolerability, and real-world usability. Looking ahead, our focus is clear. We are advancing the next steps for SENTRY, including FDA engagement, presentation of the data at ASCO, publication planning, and potential compendia inclusion. In endometrial cancer, we are preparing for the XPORT-EC-042 top-line readout in mid-2026, which we believe represents a major potential value-creating catalyst for Karyopharm. Across the business, we will maintain operational and financial discipline as we execute while continuing to evaluate opportunities to strengthen our financial position and extend our runway. We have an important few months ahead. We are focused on executing with urgency, discipline, and a clear commitment to bring meaningful new treatment options to patients in two areas of high unmet need. We'll now open the call for questions. Operator? Thank you. Ladies and gentlemen, we will now begin the question-and-answer session. Should you have a question, please press the star followed by the one on your touchtone phone. You will hear a prompt that your hand has been raised. Should you wish to decline from the polling process, please press the star followed by the two. If you are using a speakerphone, please lift the handset before pressing any keys. We do ask that you stick with one question and one follow-up. One moment, please, for your first question. Your first question comes from Brian Abrahams from RBC Capital Markets. Please go ahead. Hey, guys. Thanks for taking the question, and congrats on all the progress. Maybe just on the MF study, have you done any additional work since the top-line presentation to look into some of the deaths that occurred for patients on the placebo Rux arm relative to the seli plus Rux arm? Anything standing out that wasn't apparent at all and initially? Anything, I guess what should we be expecting beyond these initial top-line data you reported at ASCO? Thanks. Yeah. Thanks, Brian. I think overall, again, we'll have, you know, totality of our results as we shared at ASCO, but I'll turn to Reshma to expand on that. Thanks, Brian, for the question. Absolutely, you know, we're looking at the deaths that occurred, specifically the 23 deaths that were reported at the time of the top line. We haven't provided a greater granularity in terms of the types or deaths or the deaths across the 2 arms. You know, with that said, you know, when I look at them, they're very consistent with what you would expect, right? Not only in MF, but other oncology trials, right? We're gonna see a lot of deaths due to progression of disease, adverse events, you know, et cetera. Nothing, you know, inconsistent with what you would expect, and more to come, right? You know, as we continue to evaluate these data, we'll certainly look at opportunities in which we can present it at upcoming medical congresses. Thank you. Thanks, Brian. Thank you. Your next question comes from Edward Tenthoff from Piper Sandler. Please go ahead. Great. Thank you very much. Thanks for all the updates. Really an exciting time for Karyopharm, and you guys just keep on fighting. I appreciate that. I'm looking forward to the endometrial cancer data coming up. My question's on myelofibrosis. I'm looking forward to the presentation at ASCO. Can you give us a little bit more information about the potential timing or sort of preparation that you're doing for the meeting with the FDA? You know, when could we find out sort of where their head is on a potential sNDA? Thanks. Yeah. Again, I think overall, Ted, as we've shared, we're very pleased with the results. SENTRY data is very compelling, you know, and meaningful for MF patients. I'll turn to Reshma again to kind of expand on our planned engagement with the agency. Thank you. Yeah, absolutely. Yeah, thank you, Ted, for the question. You know, I just wanna reiterate what Richard said. You know, I think we're very compelled by the profile that we saw, you know, at the time of the top line results. You know, it's not just about the spleen, right? You know, we know that other phase III trials have shown these spleen reductions. You know, I think what is so compelling is that it's occurring in conjunction with this very promising overall survival signal, again. Yeah. Cutoff. It's reflected by this rapid VAF reduction, which again is a potential signal of disease modification. We believe this is happening because of the unique aspects of XPO1 that are specifically targeting the clone, causing this anti-clonal activity and again reflected in the clinical endpoints of SVR OS and then, of course, this disease modification as well. You know, we look forward to engaging with the FDA. They've been strong partners with us, you know, from the very beginning of the SENTRY trial, and we hope to elaborate on our next steps over the course of the next couple of quarters. Great. Excellent. Thank you so much. Looking forward to the presentation at ASCO. Looking forward to seeing you there, Ted. Thank you. Your next question comes from Colleen Kusy from Baird. Please go ahead. Hey, everyone. It's Nick on for Colleen. Thanks for taking the question. Congrats on the progress. Just for myelofibrosis, could you discuss the gating factors for potential compendia inclusion for selinexor? If seli is included on guidelines in the future, could you discuss how you view this opportunity versus an approval? I just had a quick follow-up after that as well. Sure. I'll take the first part of the question. Thank you, Nick, for this important question around compendia. You know, we know that NCCN, other compendia, they are independent bodies. You know, with that said, you know, from our understanding, they're constantly looking at the literature, whether it's published literature, presented data, whether, you know, new treatments should be incorporated as part of their guidelines. We do expect, you know, that they will be well aware of the data that we present at ASCO in the next couple of weeks, any publication that we do anticipate should be published, you know, in the middle of the year. You know, we anticipate because, again, of the importance of these data, that they will be convening either ad hoc or one of their scheduled meetings. Hopefully, you know, fingers crossed, they agree the data are compelling and will be incorporated into the guidelines. I'll let Richard take the second part of your question. Yeah. Nick, on the second part, I think as you know, in myelofibrosis, there only is, you know, 1 class of therapies, and again, you know, ruxolitinib being approved over 15 years ago, and really a high unmet need for these patients. As Reshma's touched on, it's very typical in these areas with new data, you know, to work to get that guideline listing pretty rapidly. If you look at analogs, you know, over the years, rituximab, brentuximab, gemcitabine, et cetera, you know, they generated, you know, meaningful revenue based on physicians deciding to, you know, prescribe based on NCCN guidelines. Given the strong unmet need, I think you typically see, if we only achieve NCCN listing without a label, you know, products can achieve, you know, approximately about 50% of what peak may be, you know, if they had a label. Obviously, this isn't an area that we would actively promote to, but is an area where physicians can choose to use a medicine to make sure they're fulfilling the best interest of the patients. Great. Thank you. Just on the, on the follow-up for the endometrial with 257 patients enrolled in the ITT, so that was just a bit under the 276 number originally you said. Does that still provide sufficient powering to show statistic in the broader ITT population? Yeah. No, I really appreciate the question, Nick. you know, when we originally incorporated this new mITT population, again, that mITT population by and large consists of these patients who are gonna be p53 wild type and dMMR. Yes, you can anticipate, you know, a small subgroup of patients whose tumors are going to be dMMR, and they're also medically ineligible to receive a checkpoint inhibitor. By and large, just assume this is gonna be your p53 wild type, MMR-proficient subgroup. When we originally incorporated that mITT, we assumed just based upon a proportion that 220 that we were targeting for that important mITT would likely equate to approximately 276 patients in that ITT. What we found, though, is that the proportion was a little bit different. We are still very much targeting the 220 for the mITT. That's the key population for the FDA. You know, based upon the distribution, we landed up with 257 patients for the ITT. Because the benefit of selinexor is driven by the p53 status and not the MMR status, yes, we are very well powered to show both meaningful benefit in the mITT as well as ITT populations. Great. Thank you so much. Thanks, Nick. Thank you. Your next question comes from Yanni from Karyopharm. Please go ahead. From Cantor. I don't think Yanni's at Karyopharm, but Yanni, thanks for the question. Yeah. Yeah. Yeah. Yeah. It's aspirational. No, great to hear the continued operational execution here. Yeah, I guess just two quick ones. You know, now that enrollment has completed here for the trial, just looking back at the SIENDO results for endometrial, obviously the outcomes really improved with additional follow-up. Curious if you can at least kind of directionally guide us in terms of, you know, thoughts on where median follow-up would fall here for this trial. Is it gonna be kind of closer to what we saw for SIENDO top line or maybe closer to the, you know, 30-plus month follow-up for the longer term data cut? Yeah. Appreciate the question, Yanni. We anticipate that it's probably gonna be in between the two. You know, we had a top-line result which showed a median PFS specifically in that P53 wild type subgroup of about 13.7 months, and the placebo arm was 3.1 months. We performed a subsequent cut that demonstrated the median PFS had increased to approximately 22 months. Of course, the most recent data, that long-term follow-up increased again to the median PFS of about 28 months. You know, over those three cuts, we anticipate XPORT-EC-042 to likely land in between the top line and the second cut. We'll see, you know, ultimately when we cut the data, it's gonna be driven by when the events occur, right? That is my anticipation going into the top line results of XPORT-EC-042. Got it. Okay. Very helpful. Then, quick follow-up on myelofibrosis. I guess, with SENTRY-2, I think, slated to also put out data later this year, how does that kind of integrate with the effort here to get a publication out and, you know, potentially be included in a compendia listing? Yeah, really exciting trial. I love this trial, right? It really demonstrates or, you know, hopefully will demonstrate monotherapy activity of selinexor in a frontline population. I do want to reiterate it's not exactly the same population of SENTRY-2, largely because we do allow patients with platelet counts as low as 50,000 to be enrolled. Slightly different, but again, it allows us to better understand monotherapy activity of selinexor because investigators have that opportunity to add a JAK inhibitor as early as week 12. We also get some really important combination data. M y hope is with this trial is that we can, you know, significantly change the landscape in MF, right? JAK inhibitors have always been thought to be the backbone. My hope is that we, you know, change and we now change the paradigm to XPO1 inhibitors as that backbone. Important data, I think it's gonna be, you know, relevant for the patient community as well as the physician community. You know, we look forward to presenting the data in the second half of 2026. Then, you know, absolutely, if the guideline committee, you know, choose to adopt and incorporate that as part of the NCCN, obviously that's up to them. You know, potentially, and again, pending the data, it could be a meaningful opportunity for this patient population. Got it. Thanks so much. Thanks, Yanni. Looking forward to get your[inaudible]. Yeah, indeed. Thank you. Your next question comes from Maury Raycroft from Jefferies. Please go ahead. Hi, good morning. Congrats on the progress, and thanks for taking my questions. Just wondering when you meet with FDA on SENTRY, do you plan to share a more mature OS cut or other specific analyses? Who are you gonna bring with you to the meeting? Is there more on the ex-US interaction strategy that you can share? Do you plan to meet with FDA first, or do you wanna align interactions with FDA and EMA? Yeah. Thanks, Maury, for the question. Give me a chance to present the data at ASCO first. Yeah. I don't wanna get ahead of ourselves. I think there's gonna be a lot of really important data that John Mascarenhas is gonna present on behalf of all the investigators of SENTRY. Keep in mind, right, just as we reported a few weeks ago, even the SVR data, you know, sort of like not only shows week 24 data, but you also got some initial glimpses at week 36 as well. We do have a little bit longer follow-up, you know, as part of SVR, as part of those top-line results. We haven't commented on any future data cuts, right. I will say that the study was designed to follow for long-term outcomes, especially for overall survival. Patients and physicians remain blinded to the arm to which they were randomized. They continue on treatment. They continue, again, on the arm to which they were assigned and will continue to follow up for overall survival. We haven't guided on when those subsequent steps or presentations will occur, but, you know, that's the, that's, you know, an opportunity based upon the trial design. In terms of the FDA too, right? You know, as I mentioned earlier, you know, look, we look forward to providing updates over the course of the next two quarters. You know, at this point, we're not providing any granular details around any of our conversations, either with the FDA or the broader rest-of-world regulatory agencies. Got it. Okay. Our team overall, Maury, is working well with our partners. Globally, and as Reshma touched here in the U.S. in terms of, you know, preparing for an sNDA and preparing and working with regulatory agencies around the world to really advance this rapidly, given the high area of unmet need for these patients. Got it. That's helpful. Maybe a quick follow-up, for EHA, we're seeing the SENTRY-2 placeholder abstract there. The guidance for data is second half, I guess. Will the data be at EHA, or can you clarify on that point? Yeah. That is a trial in progress. Got it. What you're gonna see at EHA. Okay. yes, that's just gonna be a trial in progress. yes, we anticipate data from that trial again in the second half of this year. Okay. Got it. Thank you. Thanks, Maury. Thank you. Your next question comes from Jonathan Chang from Leerink Partners. Please go ahead. Hi, guys. Thanks for taking my questions. First, can you remind me what dose is used in the XPORT-EC-042 and how that compares to the SIENDO, and what gives you confidence in the XPORT-EC-042 dose? As a follow-up to that, can you remind me what the safety profile in SIENDO looked like and what gives you confidence that patients can stay on selinexor in a maintenance setting for an extended period of time? Thank you. Yeah, really appreciate the question, Jonathan. In SIENDO, we had a dose of 80 milligrams of selinexor. These patients took 80 milligrams once weekly. Dual, dual antiemetics was not consistently used in that protocol. The reason I mention both of those is because both of those differentiate with XPORT-EC-042. In XPORT-EC-042, the ongoing phase III trial, we optimized the dose. The dose is gonna be the same as SENTRY in that it's now 60 milligrams of selinexor, again, dosed weekly. In the XPORT-EC-042, we also require the incorporation of dual antiemetics prior to each dose for the first 2 cycles, and we did that because we know nausea and vomiting are known side effects of selinexor because of the kinetics, i.e., the onset usually occurs in the first 2 cycles. We mandate it again just for those first 8 weeks, and then, of course, it's optional thereafter. How did we pick the dose? We really looked at a comprehensive data set. Again, we know in SIENDO that the median dose was 60 milligrams. A majority of the dose reductions occurred very early, largely because of the nausea, vomiting, and hematologic toxicity. We also looked at, you know, comprehensive clin pharm data, and this is really where, you know, the AUCs, when we look at 80 milligrams, AUC is achieved with 80 milligrams. At 60 milligrams, there's a lot of overlap in terms of the progression-free survival that was observed across those 2 data points. Yeah, a lot of confidence that that 60 milligrams should be able to improve the safety profile of selinexor. This improvement in the safety profile is going to enable patients to stay on longer and hopefully drive what could be even potentially better efficacy than what we observed as part of SIENDO. One other thing that I will mention is that we know that the 60 milligrams does improve the safety and tolerability profile. I say that because of our SENTRY data, right? SENTRY, again, incorporated 60 milligrams in combination with ruxolitinib. From that data set, very pleased to see reductions both in the rates as well as grades, especially of these GI toxicities of nausea and vomiting that have been well observed with selinexor. Understood. Thanks for taking the questions. Thanks, Jonathan. Thank you. Just as a reminder, if you do wish to ask a question, please press star one. Your next question comes from Edward Tenthoff from Piper Sandler. Please go ahead. Great. Thank you. I didn't realize that there were openings at Karyopharm. I have to submit my resume as well, especially in, you know, the commercial group since that's gonna be expanding. Then that was kind of my follow-up question for, you know, what additional prep are you guys doing both from a, you know, drug supply side as well as what kind of additions need to be made to the commercial organization, if EC hits and if we get on compendium or ultimately get approval in myelofibrosis? How does that change the organization? Thanks. Yeah, I'll start at a high level, Ted. Great question, and would love to talk, of course, if you're interested. But I'll turn to Sonya for the later parts. Overall, you know, the organization is really well established, and obviously has been working, you know, over the last couple years to make sure we leverage the strong capabilities we've built from a supply perspective, a very solid supply chain, you know, very solid manufacturing here in the U.S. and well ready to drive and support uptake for endometrial cancer and myelofibrosis as we continue to work to achieve labels and be able to commercialize in both those areas. But I'll turn to Sonya 'cause meaningful work has been already in progress and meaningful opportunities as we move forward. Thanks, Richard. Yeah, very proud of the established team that we've set up, and there is a significant amount of pre-launch activities underway right now. I'll break it down into two components. The global medical and scientific affairs obviously has been engaging strongly with KOLs, strong presence at congresses, really understanding the treatment landscape and gathering those insights. From a commercial landscape, we've been extremely busy developing messaging, both promotional branded messaging, peer messaging, key account mapping, segmentation, and so on. Lots of work going on. Again, as Richard mentioned, we have very strong capabilities. From a customer-facing model standpoint, there is very strong overlap at the key accounts and coverage of the key accounts. Specifically in myelofibrosis, it's a very concentrated group of accounts, we should be able to hit the ground running. In terms of endometrial cancer and the sales force coverage, again, strong coverage at key accounts both in the academic and community medical oncology setting. In terms of the specialty gyn docs, there'll obviously be an incremental increase in sales coverage. This specialty gyn doc group really is also a very concentrated group of treating physicians. We're very excited coming from a position of strength here and ready to have you join our team. Thanks so much. Looking forward to all the data coming out. Thank you, Ted. Thank you. Your last question comes from Michael King from Rodman & Renshaw. Please go ahead. Hi. Good morning, guys. Thanks for taking the question. A couple of quick ones, if I may. Just wondering, the data that we'll see at ASCO, how closely is that gonna map to the I mean, I always know the FDA gets a lot more data than what we see in public. Just as far as the data analysis and the timing is concerned, how much more will you take I guess the question is, will you take another cut at the data before you present it to the FDA after investors and your peers see it at ASCO? Yeah, thanks for the question. We're not commenting on the data that, you know, we're presenting to the FDA, right? You know, in general, you know, as I mentioned earlier, you know, we'll provide greater clarity on our interactions with the FDA and next steps over the course of the next couple of quarters. I'm really excited about ASCO, right? I mean, these are the first time the data are going to be presented by, you know, publicly. I'm, you know, obviously really proud of the team for all of the work that they've put into it. Really excited to see John Mascarenhas, you know, one of the leading KOLs, present these data on behalf of all the SENTRY investigators. I think it's a great opportunity for people, you know, to really appreciate, right, sort of the benefit that selinexor in combination with ruxolitinib can provide to this population and the key differentiating aspects of this combination relative to, you know, other treatments that have been evaluated in myelofibrosis and certainly, you know, the current standards of care. You know, I hope you can be there live. I think it's gonna be a great show. I wouldn't miss it for all the money. I am there. Oh, that's awesome. That's great. Yeah. I think it's gonna be a really great opportunity, especially for the patients with this disease. To pick up on your comment about precedent, you know, FDA is a precedent-driven organization and, you know, all the approved MF drugs have had some kind of a glitch in their dataset. You know, I mean, you guys didn't hit SVR 35, but you did hit VAF, you did hit survival. I just want to if you can just help us put it into context, relative to approvals for things like pacritinib, momelotinib, et cetera? Sure. You know, that pacritinib and momelotinib, those are two great examples because, you know, while their focus also was on SVR and TSS, you know, pacritinib clearly got an accelerated approval on SVR only. Really important precedence because I think it highlights the FDA's appreciation and the importance of SVR as an important endpoint in myelofibrosis. In momelotinib I think that example is also very relevant. Although those trials were also focused on SVR, TSS, those trials didn't necessarily show benefit as per their statistical analysis plan. In this situation, the FDA definitely showed flexibility, I would say creativity, in identifying populations and other endpoints that clearly demonstrate that unmet need. You know, I provide those, you know, examples because it shows that this FDA is willing to look at, you know, the totality of the data, the data beyond just, you know, what's included as part of the primary endpoints. They're willing to look at other measures of clinical benefit and, you know, potentially provide a path forward for those meaningful treatments. Great. Appreciate that answer. Thank you, Michael. Thank you. Thank you. There are no further questions at this time. Mr. Richard Paulson, President and Chief Executive Officer, you may continue. Thank you, operator, and thank you again to everyone for joining us today and for your continued interest in Karyopharm. You know, as you've heard, we are very encouraged by the progress we have made across our late-stage programs and remain very focused and disciplined in our execution to the next stage of important milestones. Most importantly, we remain committed to advancing selinexor's potential to bring meaningful new options to patients with both endometrial cancer or in the areas of endometrial cancer and myelofibrosis. As we've heard, we look forward to seeing many of you at ASCO during our oral presentation of our SENTRY results. Thank you for joining today. Ladies and gentlemen, this does conclude your conference call for today. We thank you very much for your participation, and you may now disconnect. Have a great day, everyone. Goodbye.