Kura Oncology, Inc. (KURA) Earnings Call Transcript & Summary

Thanks, everyone, for joining us. I'm Andrea Newkirk, one of the biotech analysts here at Goldman Sachs, and I'm really pleased to be joined by Troy Wilson, President and CEO of Kura Oncology. Thanks so much, Troy, for joining us.

My pleasure. Thank you for the chance to participate.

Yes, of course. Well, maybe I will open it up to you for some high-level remarks on the company, the overview of your clinical programs. You are just coming off the back of ASCO. So I would love to hear how you're thinking about the path forward for Kura from here.

Sure. So we're at an exciting time in the company. You referenced it in your question. So our lead program, ziftomenib is a menin inhibitor for acute leukemia. We presented data for the registrational study at ASCO. That supports an NDA submission that's under review with FDA. If all goes well, we should be in a position to launch later this year. That's in the initial relapsed/refractory population. We are -- we'll be showing data Thursday, in 2 days at EHA on the first of the 2 frontline opportunities. That's in the intensive chemotherapy setting. We hope to present data for the nonintensive later this year, perhaps at ASH. That's interesting because ultimately, you're trying to do 2 things at AML. You're trying to treat patients earlier and in combination and you're trying to move AML to more of a chronic disease. And so this will be a look into that data. This is the first time we're really showing frontline data at the recommended Phase II dose. So I would say look for that. We are -- we have 2 Phase III trials that we're spooling up to start here in the second half of the year to support registration in both the intensive and nonintensive setting. And ultimately, if we're able to realize the full potential of ziftomenib in acute leukemia, we think the market opportunity for menin inhibitors is about $7 billion. That's all lines of therapy. We think zifto could probably take half of that. Those are U.S. numbers, I should clarify. Beyond that, we're looking to combine zifto to move it to other indications. So we've started dosing patients now in GIST. That's interesting. There really hasn't been a mechanistic innovation in GIST in 20 years. It's all sort of better and better KIT inhibitors building on imatinib. So look for that maybe next year. And then we're also looking forward to sharing data from our farnesyl transferase programs potentially at ESMO. And that will be interesting. That's multiple shots in big solid tumor indications. The final thing I'll say is, we have the -- because of the support of our shareholders and our partnership with Kyowa Kirin, we're in an incredibly strong cash position. We had $703 million in cash as of the last quarterly update. We're on track to receive some significant milestones later this year around the milestones I just discussed for ziftomenib. We believe that we should be fully financed with ziftomenib to frontline commercialization in AML. If there are opportunities to pursue GIST or other solid tumors, I'm not going to say we would never raise equity again. But for now, I think we're in a really good position to deliver value for patients and for shareholders.

Maybe one big picture question there, just coming off the comments you just made about Kyowa Kirin. How are you thinking about additional partnerships as you think about expansion to GIST, to diabetes with your other programs?

Yes, it's interesting. So it's a good question. With GIST, GIST is -- let's say that it works, right? First of all, what are you trying to do? What happens in GIST is patients move from one KIT inhibitor to the next. KIT inhibitors are good at stalling the disease. They don't really drive complete responses. I'd like to say you put the tumor to sleep. What you do with a menin inhibitor and a KIT inhibitor is you create essentially synthetic lethality and at least in the preclinical models, you drive complete responses in the animals. What we're looking to do with this first dataset is, can we show that actually we can reverse resistance to KIT inhibitors. If we can do that, then you say, do I go after the front line? Do I go faster in the later line, but it is highly disruptive to that field because you have the potential to now keep patients on imatinib, which is generic and very well tolerated and very well liked, you could keep them on therapy 2, 3 years, maybe longer at a premium price point equivalent to AML. That opportunity in GIST is as big as AML, right, potentially. When you look at the incident and then the prevalent population, you don't really need a partnership. Kyowa Kirin has the ability [indiscernible]. We'll show them data from the Phase I. We can -- with our commercial force that we're building, we could commercialize in GIST. Diabetes, completely different animal. Diabetes, I think, ultimately, you need to be a multinational to really maximize the value. But we at Kura could create some meaningful value in early clinical development, if we can show that this is disease-modifying, that we can, for example, increase C-peptide, that, I think, gets the attention of the multinationals. We're pursuing a number of different paths. I will say to you, we're never going to do late-stage development and commercialization in diabetes. But there are some clever, I think, development and financing paths where we can extract value for our shareholders and potentially. [Audio Gap] in a way, use it to do stock repurchases, whatever we might do.

Got it. And maybe before we jump into ziftomenib, which I do want to focus on, just remind us quickly on when we might see some updates from these additional pipeline programs.

Yes. So let's jump to the end first. You'll see, I hope, updates from the farnesyl transferase program potentially at ESMO in October. And there, what we've guided to from a corporate milestone is 3 different cohorts, a cohort of a farnesyl transferase inhibitor plus a PI3 kinase alpha inhibitor in head and neck squamous. That's tipifarnib plus alpelisib. You'll see an escalation cohort from our monotherapy, our new FTI, a compound called 2806, and you'll see that compound 2806 plus cabozantinib in RCC, renal cell carcinoma. I don't know exactly what form those are going to take, but that's the first data update. The one that's missing is 2806 plus adagrasib in KRAS G12C mutant solid tumors. That's probably a 2026 disclosure. But the interesting thing, Andrea, that ties all those together is RCC, PI3 kinase, KRAS, they all have the same resistance. They all have a common resistance mechanism that we're targeting. If we're successful, it could be very impactful for combinations of solid tumors. In terms of GIST, probably 2026. We're currently in dose escalation. I'd like to say no news is good news in dose escalation. Look for data maybe in 2026. I don't know exactly when yet. Diabetes, we've guided that we're going to nominate a second-generation menin inhibitor. All the data we've shown to date is with ziftomenib. You don't want to take ziftomenib into diabetes, let it stay in oncology. Look for us to nominate a development candidate and maybe provide more clarity on how we might move that forward.

Got it. Perfect. Let's focus now on ziftomenib, particularly on the back of the ASCO data presentation there. Maybe just walk us through the findings, in particular, the types of responses you saw across different background therapy usage.

Yes. So we were evaluating ziftomenib in the relapsed/refractory NPM1 mutant population. We reported a CR/CRh rate of 23% and a median duration of response of 3.7 months, restricted mean of, I think, 4.7 months. And to your question, what was interesting was we saw responses independent of prior therapy, independent of whether the patients had undergone stem cell transplant, independently of whether they had been on prior venetoclax. Typically, if a patient takes venetoclax, the physicians will tell you like nothing else is going to work. Venetoclax is the last stop before hospice. So the fact that you're seeing responses post venetoclax is pretty interesting. The other thing that's interesting is, we reported an overall survival of 16.4 months median in the responders. Now if you think the patients are on, let's call it, approximately 6 months, what's driving that overall survival? There are theories that menin inhibitors reprogram the epigenome in these patients, resensitize patients to venetoclax and potentially other therapies. The numbers are too small to really prove that conclusively, but I think it's encouraging. What it says is for NPM1 mutant patients, you now have an option, right, selectively for them. On the safety and tolerability side, really benign, no myelosuppression, no drug-drug interactions, once-a-day dosing, which is incredibly convenient. You don't -- no cardiac tox. We did have a couple of reports of QT prolongation that were investigator-assessed, but just a really attractive safety and tolerability perspective. I always say -- I always focus on safety and tolerability, and I often get people who look at scans and say, why is he talking about safety and tolerability? It means the efficacy is subpar. No, not at all. Efficacy is like table stakes here. What you're trying to do is to make -- in the words of one of our KOLs, make AML look more like CML. And to do that, patients have to be on therapy once a day at the recommended Phase II dose, no dose interruptions, no discontinuations. That's what you're driving toward. This data set gives you confidence. When you bookend that against what you're going to see at EHA on Thursday, I think you'll see why we keep touting safety and tolerability because it allows [indiscernible]. And that's what's been missing, right? Venetoclax is very myelosuppressive. The FLT3 inhibitors have cardiac tox and some QT prolongation and GI tox. Patients just don't tolerate them very well. Menin inhibitors and ziftomenib in particular, have the potential to really provide chronic continuation therapy that allows you to drive long-term clinical benefit. That to me was the greatest takeaway. It says it works. Hopefully, it derisks the approval. It's going to get used. I don't know exactly what the size of the market opportunity will be, and it sets up very nicely now into these combination studies, which is ultimately what all the physicians tell you they want to do. We want to go earlier. We want to use these drugs in combo.

How does the profile or where do you see differentiation from revumenib?

Yes. So I would say the efficacy looks more similar than different. You do see that, it's small numbers, but the fact that you're seeing activity independent of venetoclax is interesting. Is that real? We'll see. I think where you really see zifto differentiating is on safety and tolerability. So there's no clinically meaningful QT. It's once daily as opposed to twice daily. There's no myelosuppression. There's no drug-drug interactions. Revumenib is both a sensitive CYP3A4 substrate, and it has a dose-limiting toxicity of QT. Now in the KMT2A rearranged setting where revumenib has an approval, that's not an issue, right? Those docs are going to do whatever they have to do to get those patients to a transplant or to a response. If we're talking about chronic therapy where patients -- let's take, for example, what you're going to see at EHA. Patients take intensive chemotherapy for the first week and then they're on ziftomenib thereafter. Revumenib per the label requires weekly EKGs and then monthly EKGs thereafter. And any time you adjust the dose or you take an antibiotic or St John's wort, for example, you've got to ask yourself, do I have the right dose? All of that goes away with zifto. So it's cleaner. There's no DDIs. There's no myelosuppression. I think what you're going to see is, look at the swimlane plots and in particular, are you seeing discontinuations? Are you seeing dose reductions? Are these patients staying on therapy? If you have to hold therapy, you're giving the disease a chance to come back. That's going to make a huge difference.

And you referenced this earlier, but the observations of a couple of QTc prolongations that you saw in your trial, I guess maybe what gives you the confidence that this signal isn't going to turn into something more significant?

Yes. So first of all, there's no grade 1. So DLTs don't sort of magically materialize. You usually see them -- they're dose dependent. So you don't seek -- you don't see -- we haven't seen and one doesn't see QT kind of regularly in a dose-dependent manner. We'll actually publish data that shows there's no exposure relationship between the exposure of ziftomenib and QT because we wanted to put that issue to bed. The 3 examples that you cited were assessed by the investigator. Each of the 3, the patients were on concomitant medications like posaconazole or certain antibiotics that have QT prolongation as part of their label or they had physiological abnormalities, I guess I'd call them, electrolyte imbalance, atrial fibrillation, how you can say a patient who's in AFib has QT. I mean I'm not a cardiologist, but -- and are we going to fight it? No, it's a safety study, right? And so if the investigator -- these -- if the investigator believes there's potentially a connection, like report it. But at the end of the day, what I will tell you is there's no clinically meaningful QT. You're not going to require cardiac monitoring. And that's really the difference is do you burden the physician? Do you burden the patient? Do you burden the site, the family? If you have to come back once a month or more frequently for -- to get hooked up and do cardiac telemetry, that's a point of differentiation. You're not going to see that with zifto.

Great. And as you look ahead to your PDUFA date in November, that was just recently announced, just given the changing regulatory policy, the administration, all the changes that are happening right now, what underpins your confidence in the approval?

So ziftomenib has breakthrough therapy designation for NPM1 mutant AML. And I give you that as a caveat because of what I'm about to say. If anything, our experience has been, our review team and the HemOnc division have been more cooperative, more collaborative, more proactive than they were before. Is that going to continue? I don't know. We've not seen any changes. We're going to do anything and everything to facilitate their review. They invited us to do an application orientation meeting when we first put the NDA in. That's basically a chance for you to walk them through the application and explain to them sort of all the various parts. I will guide you to the PDUFA date. I have no idea if it will come in ahead of schedule, on the PDUFA date, but we put it in on -- we put the PDUFA -- or sorry, we put the NDA in on March 30. On May 30, they gave us the answer, 60 days, right on time. I look at actions. I look at words. I think oncology just is probably a little insulated relative to some of the other divisions that may be getting impacted.

Good. Good to hear. As you think about potential commercialization, obviously, you do have Syndax out there commercializing revumenib, slightly different patient population. But maybe talk to us about what the learnings you're taking from that launch are and how you would approach your own.

Yes. So the first learning, the most important learning is I was actually pleasantly surprised to see them report $20 million in their first quarter sales. That tells you there is a interest and an appetite among physicians for these drugs. I think that's terrific. Unfortunately, there isn't a large pool of patients waiting for menin inhibitors in the relapsed/refractory setting. If you do not get a patient on therapy within a week, that patient typically can progress and pass away. So whether they get out there a month ahead or we do, I'm not sure that's going to matter very much in terms of timing to the market. It is -- what we're hearing from physicians is real excitement about menin inhibitors, a desire to use them earlier and in combination. We are -- we've already recruited all of the leadership in commercial, so marketing, market access, medical affairs, we'll be ready with our sales force, which will look roughly like -- similar in size to Syndax. Our partners at Kyowa Kirin are bringing their expertise. They're in the field with POTELIGEO between our commercial organization and theirs, will probably be 50% larger than Syndax. So we're going to be trying to get the docs in surround sound on ziftomenib. We'll be doing 2 things in parallel. One is promoting on-label in NPM1 mutant AML. The other is publishing, presenting, educating about off-label, additional opportunities. So we have the KOMET-007 data, which is ziftomenib plus ven/aza in the relapsed/refractory setting. We have 008 data, which is ziftomenib plus gilteritinib in FLT3, LDAC and FLAG-IDA. Look for us to publish that data, look for us wherever possible to get it into the guidelines. AML clinicians are very good at using these drugs as they think they should use them. It's our job to educate them how to use them safely. And then that on top of -- we're going to be the first, I think, in the U.S. with 2 big Phase III studies. We will be at every major medical center, I suspect, in the U.S. or very nearly every major medical center with ziftomenib. And all of that activity in the relapsed/refractory setting all the way to the front line, that's just going to drive more and more excitement.

Got it. So your understanding of these physicians is very much an appetite to use this drug as they see fit as long as it's in the guidelines even before an official label.

Yes. Well, so for Syndax, I think if Syndax can get into the guidelines, then yes, we can't get into the guidelines until we have an approval. But once we have an approval, yes, they're looking for safety and tolerability. And in most of these cases or many of these cases, it's generic. There isn't really a high hurdle to reimbursement in relapsed/refractory AML. I don't know to what extent are we going to see spontaneous usage in the front line? I don't know. I'll let the physicians decide that. But their desire to put these agents -- this is the most exciting thing to come along in AML since venetoclax, right? And it has the potential, I think, to really inflect the curve in -- particularly as we go earlier and into frontline.

Maybe that's a good segue to your frontline, and you've referenced the data coming actually just in a couple of days at EHA. Maybe help frame some expectations for what is the extent of the disclosure that we can be expecting? And how meaningful -- what should we take away from this disclosure?

Sure. So let's talk about like what are you trying to do in the front line because a common misconception is you're trying to drive the response rates higher. You have -- so we'll show you data of ziftomenib plus intensive chemotherapy in 2 settings, frontline NPM1, newly diagnosed, newly diagnosed KMT2A. In the case of NPM1, the response rates are pretty high. They're 80-plus percent. You'd like to do better, but in particular, you'd like to do no worse. The challenge with frontline NPM1 is not the response rate. It's actually relapse. So there's a 2018 Blood paper that did a retrospective of AML and then by genotype, including NPM1. Half of those responders will relapse within the first 2 years. And of that -- or within the first -- half of them will relapse, sorry, I got that backwards. Half of them will relapse.80% of that half or 40% will relapse within 2 years. So what you're looking for is can I deepen the response? Can I make the response more durable? What are the -- are patients staying on therapy? Do they have to interrupt dosing? Do they have to dose reduce? Are they going to transplant? Remember that if an NPM1 mutant patient is MRD negative, transplant is not advised because there's no clinical benefit. There is a clinical benefit in the MRD positive. So don't be surprised if you don't see a lot of patients going on to transplant. You're really looking, Andrea, to keep them on therapy for prolonged periods of time. With intensive chemotherapy, they're done with that in the first week. They start on zifto on day 8. In an ideal world, you'd see them all just swimming along in the swimlane plot, staying on zifto. The KMT2A rearranged disease is different. Most of those patients are younger. They actually are advised to go to transplant. So you're looking to get them into response, to keep them in response, to move them to transplant and then to get them back on ziftomenib in a post-transplant setting. The -- that's the sort of the clinical opportunity. The commercial opportunity, again is, we think ultimately, half of the frontline population at least is menin -- call it, their tumors are menin dependent. That would include FLT3, NPM1, KMT2A. That's 11,000 patients per year in the U.S. If you can keep those patients on therapy for a year at Syndax's price point, that's a $5 billion opportunity. It's just -- it's basic math, right? So when you see the swimlane plots, consider that. Can we move frontline AML to something where we give patients the option that they can stay on a drug in a chronic setting, perhaps delay or avoid having to go to transplant and keep their disease in remission. That's the headline.

What's the extent of follow-ups that we'll see from these patients? I guess, is it possible that we'll be able to answer that question of durability or how long these patients can stay on treatment from this initial dataset?

You're going to get -- so I should have added this to my previous answer. So the data that you're going to see is from the 600-milligram dose patients in the dose escalation plus the dose expansion patients who were all dosed at 600. The dose escalation had 200, 400, 600, we're just showing you the 600. We may show you the 200 and 400 in a subsequent data update. It's just -- you can only cram so much data into these presentations. So you're seeing all 600-milligram patients. That's the recommended Phase II dose. We're going to show you as much follow-up as we had as of the data cut, which I think is in March. The longest patients have been on for 47 weeks. So in the swimlane, you're going to see patients from, I think the shortest is 20, all the way up to 47. Is that going to be enough to convince everybody? I think it will -- I think it's going in the right direction. It gives us the opportunity to give you another update either later this year or next year to continue that theme, right? How -- if we do an 18-month landmark or a 2-year landmark, what does it look like? And that's why I think it will give people confidence as we're heading now into KOMET-017 that we actually are driving potentially clinical benefit. You'll also -- I should have mentioned this, Andrea, sorry, you'll also see MRD negativity. So look for robust rates of MRD negativity because that's both a surrogate for survival and the agency has given us a pathway to accelerated approval using MRD-negative CR. So that will be important.

Maybe put that into context for us, MRD-negative rates, what is the benchmark here?

So the retrospective analysis, you're going to do MRD negativity in bone marrow because the hurdle is lower and it's probably a better predictor of survival. On intensive chemotherapy, think of it as sort of 40%. That's the rate of MRD negativity that intensive chemo gives you. Does that make sense? Half of the patients relapse, right? Those are typically the MRD, the patients who still have measurable residual disease. For the audience, remember that a CR is blast counts of 5% or lower. If you have blast -- if you have 5% blast counts with AML, you still have AML. So MRD negativity, and there's typically a limit of detection of 10% to the minus 4%, 10% to the minus 5%, that's really looking for how do we ensure you don't have disease lurking in your tissues or in your bone marrow. And that would go back to why are menin inhibitors so different. So menin inhibitors work to differentiate leukemic blasts. They don't kill them. They just -- they differentiate them into mature cells. If you can keep ziftomenib around in sort of saturating conditions, anytime disease pops up, if it's in the spleen or it's in the skeletal muscle or in the bone marrow, then you differentiate them and you have the potential to keep those patients in response. That's the beauty of this mechanism. That's why it doesn't have -- or at least ziftomenib doesn't have any tox because it works to differentiate. So look for us to do ideally better than that 40% MRD negativity benchmark.

How much better does it mean?

You want to be clinically meaningful. We have a -- I would say, be clinically meaningful, don't set the bar too high, right, so that you make sure that you can get over it. The KOMET-017 Phase III studies, we'll roll the stats out a little later this year. You'll see that they're well powered. They're actually -- yes, they're well powered to hit those endpoints. One of the advantages that our partnership with Kyowa Kirin gives us is the ability to really invest appropriately. If you're running 2 big Phase IIIs, like don't -- 100 patients can make a difference, don't skim, right? Do the right trial, powered appropriately to ultimately [indiscernible].

And as you think about these combinations with zifto, what is an acceptable safety or tolerability profile? Or what could we expect?

So let me answer it this way. Your biomarker is dose reduction, dose interruption, dose discontinuation, right? That's what you're looking for. That can come in various forms. It can come from myelosuppression. It could come from cardiac tox. That's what you're going to see among the competitors. There isn't an absolute bar. You just want as little as you possibly can. You want no additive toxicity, no additive myelosuppression. You don't want to have to -- one of our competitors, for example, they've had to hold their menin inhibitor in combination with ven/aza to allow counts to recover. I think when you see the zifto combo data, there's no impact on the platelets and the neutrophils. You want those coming back as quickly as possible because that protects the patient from fungal infections, which is their biggest risk.

Awesome. And then you also mentioned that you'll have data from your non-intensive combination.

Hopefully, at ASH, right?

Maybe help us lay the groundwork for what we can expect there.

Yes. There -- so there, the intent is not to get to transplant, right? These are the unfit patients, typically 75 years or older or otherwise intolerant to intensive chemotherapy. They -- you typically treat them until progression. You're going to try to do 2 things. You're going to try to wean them off of venetoclax as quickly as possible. You're going to try to keep them in a response as long as possible. The CR rates are lower. They're more like 50%. The median overall survival is about 14 months for ven/aza. So again, you'll get -- this is the first snapshot along the way. We've never shown frontline ven/aza combo data. You're looking to, can I drive higher CR rates, again, by allowing counts to recover, right? You're clearing the leukemia, but can you get the neutrophils and platelets back? What does your MRD negativity look like? Even though that's not an accelerated endpoint, that's important. Can you continue them on ziftomenib while weaning them off of ven/aza. That's what you're trying to do. You'll get some suggestions of, again, is there a median OS? Is there a median duration of CR? Hopefully, there isn't. If there isn't, then that's kind of telling you you're on the right track. But it should qualitatively look similar to what you're seeing in the intensive setting. Just the goal is not to get them to transplant, right? But qualitatively, you want all these patients to go out. We think you can keep patients on ziftomenib in the non-intensive setting for maybe 18 months. In the intensive setting, 18 to 24 months. That's sort of our internal thinking. Hopefully, the data continues to support that view.

Great. So with all of these datasets report out positively. And you see opportunity both in the relapse setting, the frontline setting here. You've spoken about $7 billion market opportunity for menin inhibitors, of which zifto would take a share of that. How do you -- I guess, maybe in your conversations with physicians, as they think about zifto versus revumenib, how are they thinking about the market split there? And how to make that decision over which asset to prescribe for their patients?

The -- so in the KMT2A rearranged monotherapy setting, it isn't close. Revu is going to take that, right? And I just -- there, the benefit risk is very clear in favor of revumenib. Anywhere else, what they tell us is the convenience, the lack of the requirement for cardiac monitoring, the lack of myelosuppression really tips in favor of zifto. We're still going to be out there fighting for every patient. I think the speed with which we've been able to advance to the front line, the rapidity, we're showing you more data and more frequently than any of our competitors. I think that speaks to how easy it is to combine zifto with all these other standards of care, they recognize that. That's what they're looking for. Yes, they want to drive antitumor activity. They want to make it as easy as they possibly can. In our advisory board meeting, one of the KOLs described ziftomenib as a cruise medicine. And I was like, is that a term of art, I don't know. And so somebody fortunately said, what does that mean? And he said, "Look, many of these patients are 60 years or older. They have leukemia. They want to go into a response and take a cruise with their families. Zifto is ideal. It's once a day. It doesn't interact with anything. I don't have to monitor them. I can send them away and say, go enjoy Alaska." He said, that's a real advantage in this setting. He said even once a day versus twice a day makes a huge difference because compliance with AML is so key. So we're going to have to prove it. We're going to have to earn it, but I think it's a good setup.

Maybe that's a good segue into our last question here. Just as you think about the potential combinatorial approaches that you could take with zifto, what mechanistically is most interesting to you?

Ultimately, I think you want to use a menin inhibitor with every other agent. It should be the backbone of every line of therapy. There's preclinical evidence of synergy with both venetoclax and FLT3. It -- menin sits in front of the murderers row of oncogenes in AML, right? So NPM1, DNMT3A, KMT2A, BCL2, MCL1, FLT3 and they're all there. And if it's safe and well tolerated? The answer would be, why would you not use it, right? It is the most important mechanism, I think, to come along in AML probably since the beginning. And our job is to get it out to as many patients on a worldwide basis as we can.

Do you think physicians would need to see it studied rigorously in a trial, these specific combinations? Or are they just going to try it on their own just based off of what their patient may already be on?

I think the more safety, tolerability and activity data you show them, the more confidence you give them. Many of the sites that the analysts and investors talk to are academic, they're always looking to put patients on trials. I don't know again how much spontaneous usage there'll be in the community setting. But yes, I mean, with -- I suspect this landscape 5 years from now will look completely different. And have we seen this movie before? Yes, in multiple myeloma, right, proteasome inhibitors, anti-CD38, you -- it's all about combinations. It's all about going earlier. It's all about sparing transplant. It's the same movie, which is why I'm optimistic on the clinical and commercial opportunity.

Great. Well, with that, Troy, thank you so much. Thanks, everyone.

Thank you.