They'll tell you more about that and the company. We're going to do a hybrid format, so Richard's going to start off with some slides, and then we'll do a Q&A afterwards. So I'll pass it over to you, Richard. Great. Thank you, Maury. Thanks for having us here, and I'm looking forward to share, you know, and get into some more questions with regards to the really exciting data we just had at ASCO. Quickly, a little housekeeping to remind you that various remarks we make constitute forward-looking statements, as you see on the slide, so please refer to our most recent 10-Q. You know, when we think about Karyopharm, you know, I think what's critically important is to look at us as a commercial-stage, innovation-driven oncology company, really with a transformative Phase III pipeline, which three Phase III programs are reading out through 2025. There's an incredible level of excitement and looking forward to talk about the EC data. We presented some great data at ASCO, but also at ASCO, a really positive engagement in myelofibrosis and multiple myeloma. As we look across our Phase III programs in multiple myeloma, EC, and MF, and obviously our commercial business, which is foundational to us, in multiple myeloma. And, you know, globally, when you look at selinexor, selinexor is approved in over 40 countries, continuing to grow reimbursement and approvals. And our guidance this year is at $140 million-$160 million with regards to our global revenue. And again, when you look at our cash position and our financials, I think we've made really strong progress over the last couple of months, as we've really transformed our balance sheet. We've been able to extend the vast majority of our debt into 2028, 2029, really enabling us to see the readouts in our phase 3 programs and also strengthened our cash position as we have a cash runway through to the end of 2025. So as we continue to move forward and accelerate our innovation strategy, you know, selinexor across multiple myeloma, endometrial cancer, and myelofibrosis, we believe has the opportunity to be a $2 billion-plus asset and very excited to continue moving it forward. And when you look at that, you know, you see here our pipeline and again, our core pipeline in EC, MF and MM, you know, supported with our ongoing programs and being very focused and very diligent in terms of how we allocate our resources. Just to close, you know, you see in front of it the key areas we want to focus on and really deliver as we move forward across our three key programs, and key milestones for us, again, with the cash runway taking us through the end of 2025, ensuring we can see, you know, really strong data readouts through 2025. So I wanted to keep it very focused, Maury, because I know you have a lot of excitement to get into the data and the questions. So I'll stop on that and looking forward to getting to Q&A. Great. Yeah, that was a great intro. So let's talk about the ASCO update. You recently presented updated SIENDO data at ASCO, which is showing impressive PFS and OS data, with OS not yet mature. Maybe recap the key data and some of the main takeaways from the data. Yeah, absolutely, and thank you for the question, Maury. We really did. We had a stellar ASCO where the highlight really was about our long-term follow-up from the SIENDO trial. Just to recap, SIENDO specifically evaluated—was a phase 3 trial that evaluated selinexor versus placebo as a maintenance therapy in our advanced recurrent endometrial cancer population. In the ITT, right, we did not show a clinically meaningful benefit. However, we did pre-specify evaluation in an important subgroup of patients defined by their p53 wild-type status. So the data, again, that I'm going to focus on right now is from that p53 wild-type subgroup. As of April 1, 2024, data cutoff, what we now see is a very meaningful PFS benefit of 28.1 months with selinexor versus 5.2 months with placebo, and this translates to a hazard ratio of 0.44. Really identifies the benefit, the very unprecedented benefit that you can see with selinexor in this important subgroup of patients. Now, importantly enough, we see a very rapidly evolving landscape, really great for patients. We have an introduction of the checkpoint inhibitors and potentially in the dMMR population, but they were also evaluated in that pMMR population. As a result, we were also focused on the efficacy in that important subgroup of patients who are defined as both p53 wild type and MMR proficient. This is a population that does not benefit with the checkpoint inhibitors. In fact, efficacy is quite marginal. What we see with selinexor is completely the opposite. You can now see a median PFS in that subgroup that is approximately 40 months, relative to approximately 4 months that we see with placebo. That translates to a hazard ratio of now 0.36. Now, contextualize those data, right? Again, the checkpoint inhibitors have shown some promising data. When you look at that 40 months, which is, again, just the maintenance part of their first-line treatment, this is approximately 4 times the median PFS benefit compared to what the checkpoint inhibitors achieved. And in fact, numerically, the median PFS that we see with selinexor is actually longer than the overall survival data that the checkpoint inhibitors have also seen. So it really suggests that when you look at a patient population defined as both p53 wild-type and pMMR, the potential future treatment paradigm is likely going to be carboplatin, followed by selinexor in this important population of patients. Now, we also looked at the benefit in that patient population who were p53 wild-type dMMR. Substantially smaller, you know, with that said, a very meaningful benefit with a hazard ratio of 0.49. And when you look at the delta in terms of the median PFS between the two arms, you see a very meaningful difference of about 10 months. So again, really excited about these data suggest that selinexor and that p53 wild-type is potentially a future standard of care. We also had an opportunity to present updated overall survival data. Now, these data are still very immature, but very, very encouraging. Across all of the subgroup of patients that were evaluated, you see these very impressive hazard ratios of anywhere between 0.48 to approximately 0.69. So tracking and trending, you know, similarly to that PFS benefit. Lastly, I just want to highlight a new analysis that we conducted, first time presented at ASCO. It's called a Q-TWiST analysis, very important for patients. What it essentially does is that it incorporates the quality as well as the quantity of PFS, and there we see a very meaningful difference of about 10.5 months. Compare this to dostarlimab, their Q-TWiST difference is really about half at approximately only 4 months. So with that said, I'll pause there. Maury, yeah. Yeah, that was a great summary of the data, which is quite impressive. The follow-up question for me is: for this patient population, the p53 wild type, that's pMMR, why are you seeing the efficacy uniquely good in this patient population? Yeah, so you know, a couple of ways to interpret the data. You know, again, when you look at, you know, phase III comparative trials, it's really going to be about the hazard ratio, right? So when we look at the hazard ratios between these two important subgroups, either p53 wild-type pMMR or p53 wild-type dMMR, again, I'll reiterate, very promising, with hazard ratios anywhere between 0.36-0.49. You know, with that said, I'm very cognizant that the median PFS is substantially longer in that pMMR subgroup. And one of the hypotheses is that, you know, p53 induces apoptosis. To efficiently induce that apoptosis, you potentially may need an intact MMR apparatus. So you know, in that p53 wild-type pMMR, yes, you may drive more apoptosis, decreased cellular proliferation that will translate potentially to a longer PFS. But with that said, still encouraged in that dMMR subgroup as well. Got it. And, one of the KOLs at ASCO talked about historical data and why it makes sense for these pMMR patients to not get a checkpoint inhibitor in the frontline or the frontline maintenance setting, and the doctor talked about why Selinexor makes more sense here. Can you recap some of the key points regarding checkpoint inhibitor use from the KOL? Yeah. So a key thing to remember is that right now, we don't, you know, sort of recycle the checkpoint inhibitors, right? So it really suggests that you've got to pick the optimal space and in which to incorporate that checkpoint inhibitor. Given the fact that the checkpoint inhibitor, specifically in the pMMR, has shown an overall survival benefit in that second-line population, it really suggests that the future landscape, again, for this pMMR p53 is going to be Carboplatin, followed by Selinexor, and then if and when the patients progress, you then treat them with pembrolizumab in combination with lenvatinib. So now we have the sequence of therapies that is emerging, and incorporation of each of these different components that is probably going to drive that overall benefit. But yes, you know, in that pMMR, reserve it after that Selinexor has been used. Got it. And the treatment landscape is still evolving somewhat with the checkpoint inhibitors. What proportion of patients do you expect will have had prior checkpoint inhibitor in XPORT-EC-042, and how do you expect Selinexor performance will be impacted by patients who received chemo versus those who got the checkpoint inhibitor? Yeah, that's right. So ECO42 is our ongoing phase 3 trial evaluating selinexor as a maintenance in this p53 wild-type population. We do allow prior checkpoint inhibitor usage. With that said, it's likely going to be very small, at less than 10%. It's a global trial. In the EU, we do not see a lot of checkpoint inhibitor usage. So again, I think that prevalence is going to be quite small, you know, among the entire ITT population. We also don't have any data to suggest that prior IO usage is going to impact the subsequent selinexor performance, so it, you know, it shouldn't have any impact on the efficacy. Got it. For baseline characteristics in phase 3 SIENDO, there was some discussion at ASCO about how there were actually better ECOG performance status in the control arm and a higher CR rate as well, which could imply that for a larger, more balanced study, like the ongoing XPORT-EC-042 study, that Selinexor PFS and OS could do even better versus what you've seen in SIENDO. So what are your thoughts on this, and can you talk about anything more you could say on baseline characteristics for XPORT-EC-042 and how the new phase 3 patients are different from the old phase...? Yeah, it's a great observation, right? When you take a look at the ECOG performance status as well as the CR rates, these are important prognostic factors, right? And it suggests that the selinexor arm actually had patients that were of worse prognosis. So it makes the data even more compelling when you look at the large p53 wild-type or even the subgroup of patients who are p53 wild-type pMMR. In terms of the demographics that we're seeing in ECO42, by and large, they're tracking very similarly to SIENDO. So the CR rates are approximately 40%. You know, the majority of patients are going to be ECOG 0. I think the one difference that we see is, again, you know, sort of that pMMR population. In the SIENDO trial, it was around 60%. You know, in the XPORT-EC-042, our current phase III, that rate is tracking a little bit higher, given the fact that we now have checkpoint inhibitors available, especially in the dMMR population. ... Got it. Makes sense. Then for the ongoing ECO-42 study, what other key phase 3 design features and differences versus the old SIENDO study do investors need to know about? And can you talk about how the enrollment's going for the study, and when do you expect to complete enrollment? Yeah. So the main differences of our ongoing phase 3 relative to SIENDO, so first, the patient population. We're only enrolling patients who are p53 wild type, and we have a strong collaboration with Foundation Medicine. They're using their NGS platform to identify the p53 status in all of the patients that are screened for this trial. The other difference is the dose. So in SIENDO, we treated all patients with an 80-milligram dose. We've done some very extensive dose optimization in this current phase 3. The dose is 60 milligrams and really should enhance the benefit risk that we see in the ongoing phase 3. The third difference is that we really know the importance of dual antiemetics. Selinexor, across all of our programs, we know causes nausea and vomiting. We also know that incorporation of dual antiemetics, so 2 different antiemetics for the first 2 cycles, substantially reduces both the rates and grades of those AEs. So ultimately, you know, we've identified the patient population that's going to benefit. The dose and the antiemetics should also substantially improve upon the toxicity profile. Got it. And, you said for this study, you're going to report the top-line data first half of next year. Is the trial still on track, and what do you expect to demonstrate in the top-line data, and, that would be clinically meaningful and make doctors excited about the new therapy? Yeah, that's right. So, you know, a ton of enthusiasm around the data. I think, you know, coming out of ASCO, it really solidified the benefit that selinexor potentially can provide in this p53 wild-type population. So enrollment is tracking. We do expect top-line results in the first half of 2025. The primary endpoint is progression-free survival, and I think for KOLs and patients, what they really want to see is a delta of at least six months or greater for PFS. And I think if you just look at the data that we presented, clearly we're going to beat that bar. Got it. And, we heard from one doctor at ASCO who was positive on Selinexor's potential. What other feedback are you getting from doctors at clinical sites? And, when you talk to your XPORT-EC-042 investigators, is there alignment on why Selinexor makes sense in this, p53 wild-type pMMR population, or do you have to do a lot of educating around this still? You know, I think we, you know, we continue to do a lot of educating, right? I mean, I think this is a really exciting time for women who suffer from endometrial cancers. You know, we went from relatively recently, just Carboplatin primarily being the only available option to now multiple different therapies. You know, with that said, those therapies are going to be used in certain molecular patient populations. So I think educating around which therapy is going to match with that underlying molecular type is going to be extremely important. I think for those KOLs who are following the landscape, they clearly see it. For the dMMR patient population, it's going to be the checkpoint inhibitor usage. Go ahead and use it in that first line. We know for the pMMR patient population, where the efficacy is quite marginal, this is where they're saying carboplatin, followed by selinexor in that p53 wild-type subgroup, and then let's reserve the pembrolizumab and lenvatinib in that second-line space. Got it. Makes sense. And, for the ongoing phase III, you said safety events could happen early on, and safety-related discontinuation trends tends to happen in the first six to nine months, and with antiemetic prophy, safety should be better. Can you talk more about safety feedback you're getting from investigators and your current expectations for AEs and discontinuation rate for XPORT-EC-042? Yeah. So, you know, in general, right, even though SIENDO was conducted with an 80-milligram dose and dual antiemetics were not required, you know, investigators are still quite, you know, positive about that toxicity profile. It's very manageable, selinexor being an oral maintenance option, and in light of the efficacy, really is a, you know, a very beneficial maintenance option. Now, with a lower dose, as well as the incorporation of dual antiemetics, we can further improve upon that. What we see with these toxicities that are critical to these patients, they happen to occur very early on in the selinexor usage. So nausea, vomiting is still, you know, something that we look at very closely. It happens within the first, almost first 1-2 doses, very short-lived. So by the time they get through those first two months, the nausea is completely resolved, and then they remain on the therapy without really having any issues with that, important AE. So it's very front-loaded. Again, with the incorporation of the dual antiemetics, we expect it to be even better. Got it. Makes sense. Also at ASCO, you reported the PK, efficacy modeling, data that you have around the 60 mg versus 80 mg. Can you talk more about, just some of the details that inform how 60 mgs and 80 mg PK and AUC compares, and how the PK modeling predicts that 60 mgs will be sufficient for the phase III? Absolutely. So when you look at the AUCs, right, it's relatively flat when you look, you know, from an efficacy standpoint. So PFS is very similar, regardless of whether you look at low doses, high doses, so a very flat dose response, you know, evaluation. In terms of safety, it's quite different. So there's a very large differential in terms of safety when you compare the low versus high doses. So it really suggests that we can use 60 milligrams to maintain that efficacy, but also substantially reducing the overall toxicity profile. And when we incorporated some modeling into those analyses, it suggests that with 60 milligrams, even the grade 3, 4 AEs could potentially be decreased by almost 10% with that dose. I think there's really a large opportunity to further improve that benefit risk with this lower dose, to say nothing of, you know, again, the incorporation of the dual antiemetics for the first two cycles. Got it. That's helpful. And, maybe talk about power, powering of the study and how the primary analysis is triggered, and how mature the data will be when you do the top-line readout. Sure. You know, we don't disclose our powering assumptions. You know, with that said, for all of our Phase III's, we're well above 80%. And you can clearly see that, you know, we have a lot of room, especially with the data that we've seen just in terms of PFS. The primary analysis is going to be event-driven, so we have a minimum number of events that need to be observed, and when we observe it, you know, we'll go ahead and trigger that PFS primary analysis. Got it. Let's see, you talked about the dMMR patient population. Is it fair to... So, what's the breakdown again for that? You said s- probably over- Yeah ... over 60% for the pMMR? Yeah, over 60%. Right. So it's going to be... Yeah, the vast majority of the patients are going to be pMMR. Got it. Okay. And for efficacy expectations between those two patient populations in the data that you showed at ASCO, it seems like they're pretty similar overall. Yeah, exactly. I mean, when you look at it from a PFS hazard ratio, right? You know, again, very compelling data, 0.36-0.49 hazard ratio. So it really suggests that it's all about the p53 status. We, I can identify that p53, it's a strong predictive marker for benefit with Selinexor. Got it. And can you remind me for the ongoing study, if there's any safety or efficacy interim in the phase 3 that could enable an opportunity for resizing? And also remind me if you have stats plans to analyze both the pMMR and dMMR subpopulations, and whether both of those could be approvable separately. Yeah. So, you know, the readout in the first half of 2025 is going to be the primary PFS analysis. So we'll be able to see a very robust signal in terms of PFS, preliminary OS, and then, of course, you know, top line, safety as well. Okay. And as far as the interim goes, so there's not going to be any potential for that- No interims ... along the way. Understood. And, let's see. In the last couple of minutes, wanted to talk about myelofibrosis- Yeah ... as well. Maybe recap your frontline data and remind us the rationale for the phase 3 study in treating patients with selinexor and rux in combo, and what kind of treatment benefit do you expect to show relative to rux alone? Yeah ... in this study? It's a great question. Another really exciting program for us. So, you know, Selinexor XPO1 inhibition is, it's actually a very fundamental mechanism within myelofibrosis. It hits both JAK and non-JAK pathways, really suggesting potential monotherapy activity, which we've already demonstrated in that relapsed refractory patient population, but also potential synergy when we combine with other agents, including ruxolitinib. We conducted a phase I study evaluating this combination in JAK-naive myelofibrosis patients, and what we observed is a really compelling efficacy profile. So at week 24, we observed a 79% SVR35 rate, which is a spleen volume reduction of at least 35%, and also a very compelling TSS50 or a total symptom score reduction of at least 50% or greater at around 58%. You know, put this into context with ruxolitinib alone, SVR rates are sub 40%. Even TSS50 is really going to be in those low forties. So very meaningful benefit with this combination versus ruxolitinib alone. There's multiple other differentiating factors with the combination that I just want to highlight. So Selinexor, again, has potential monotherapy activity, which is key because it gives flexibility to physicians if and when they want to treat with this combination. We also see some very important disease modification in terms of reductions of VAFs as well as cytokines, and then it stabilizes, if not improves, the cytopenia. So I think that aggregate, you know, profile that we see with combination really makes it a very ideal and potentially best-in-class combination for this, patient population. We have an ongoing phase 3 that is evaluating the combination versus Rux alone in a JAK-naive patient population. Primary endpoints are going to include SVR35 and TSS50. They're tested hierarchically, so we're going to evaluate SVR first, and then if positive, we'll then roll down the full alpha to that TSS50. Enrollment's going really well with that trial. Got it. Is there anything more on enrollment that you're saying? You're guiding to having the data second half of next year, so- Yeah. Yeah. Okay. Nothing additional. Okay, understood. I think we're pretty much almost out of time. Maybe if you want to just highlight where you're at commercially, and if there's any updates around what you're seeing second quarter that you can provide, and then key updates that investors should be focused on over the next 12 months. Yeah, I mean, just quickly, we won't go into Q2 yet, but I think we feel very, very confident in our guidance for the year, in the US of $100-$120. As we talked to in our Q1 call, you know, we were able to show positive, 4% quarter-over-quarter growth, with new patient growth in both the community and the academics. And a really good, strong, engagement with regards to Selinexor's role in multiple myeloma. Just had our data from SPD, with the 40 versus 60, which really supports our 40 SPD trial, which is ongoing. So a lot of excitement around our multiple myeloma franchise. And as we look moving forward into Q2, I think just continuing to execute with a commercial team that continues to, you know, drive and support our multiple myeloma franchise. And as we look at, you know, moving into 2025 and kind of where we started, excited about the transformative opportunities in our pipeline with three phase 3 readouts reading out through 2025. Got it. Richard, Reshma, thanks so much for joining us today. Thank you. Thank you.