Kura Oncology at Goldman Sachs Conference: Strategic Insights on ZIFTOMENIB

On Tuesday, 10 June 2025, Kura Oncology (NASDAQ:KURA) presented at the Goldman Sachs 46th Annual Global Healthcare Conference, highlighting its strategic focus on ZIFTOMENIB, a promising treatment for acute leukemia. The company showcased positive data and outlined plans for future trials, while also acknowledging the challenges in the competitive landscape.

Key Takeaways

• Kura Oncology is advancing ZIFTOMENIB, a menin inhibitor, for acute leukemia with an NDA under FDA review.
• The company estimates a $7 billion market opportunity for menin inhibitors, aiming to capture half.
• A robust cash position of $73 million supports commercialization plans without financial strain.
• ZIFTOMENIB’s safety profile stands out against competitors, with no significant side effects.
• Plans for broad commercialization include partnerships and a strong sales force.

Financial Results

• Cash Position: Kura Oncology reported a cash reserve of $73 million as of the last quarter.
• Market Opportunity: The potential market for menin inhibitors in acute leukemia is estimated at $7 billion, with ZIFTOMENIB targeting a significant share.
• Revenue Potential: If priced similarly to competitors, ZIFTOMENIB could generate $5 billion annually from the frontline AML market in the US.

Operational Updates

• ZIFTOMENIB: The NDA is under review, with a potential launch in relapsed/refractory AML later this year. Upcoming data presentations at EHA will explore frontline opportunities.
• Clinical Trials: Two Phase III trials are planned for intensive and non-intensive settings.
• GIST Program: Patient dosing is underway, with data expected in 2026.
• Farnesyltransferase Program: Anticipated data updates at ESMO in October.
• Commercialization: A sales team is in place, supported by a partnership with Kyowa Kirin, enhancing market presence.

Future Outlook

• ZIFTOMENIB Approval: Kura Oncology is optimistic about FDA approval and plans to position ZIFTOMENIB as a backbone therapy in AML.
• Diabetes Program: The company is seeking partnerships for late-stage development.
• Clinical Developments: Phase III trials are set to commence, with data from non-intensive combinations expected at ASH.

Q&A Highlights

• Differentiation: ZIFTOMENIB’s safety and tolerability, with no QT prolongation or myelosuppression, distinguish it from competitors like Revumenib.
• Regulatory Collaboration: The FDA has been supportive and proactive in the review process.
• Commercial Strategy: Lessons from Syndax’s Rebuminib launch are being applied, with a focus on physician education and clinical data expansion.
• Frontline AML: Efforts are directed at improving treatment response and reducing the need for transplants.

Readers are encouraged to refer to the full transcript for a detailed account of the conference call.

Full transcript - Goldman Sachs 46th Annual Global Healthcare Conference:

Troy Wilson, President and CEO, Cura Oncology: Thanks

Andrea Newkirk, Biotech Analyst, Goldman Sachs: 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 Cura Oncology. Thanks so much Troy for joining us.

Troy Wilson, President and CEO, Cura Oncology: My pleasure. Thank you for the chance to participate.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Yeah, 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 we’d love to hear how you’re thinking about the path forward for Cura from

Troy Wilson, President and CEO, Cura Oncology: 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. It’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 relapsedrefractory population.

We are we’ll be showing data Thursday, in two days, at EHA on the of the two frontline opportunities. That’s in the intensive chemotherapy setting. We hope to present data for the non intensive later this year, perhaps at ASH. That’s interesting because ultimately, you’re trying to do two things with 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 time we’re really showing frontline data at the recommended Phase II dose. So I would say look for that. We are we have two Phase III trials that we’re spooling up to start here in the half of the year to support registration in both the intensive and non intensive setting. And ultimately, if we’re able to realize the full potential of ZIFTOMENNEB in acute leukemia, we think the market opportunity for menin inhibitors is about 7,000,000,000.

That’s all lines of therapy. We think ZIFTO can probably take half S. Numbers, 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 twenty 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 farnesyltransferase 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 Kewa Kirin, we’re in an incredibly strong cash position. We had $7.00 $3,000,000 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 zifdomenib. We believe that we should be fully financed with zifdomenib 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 But for now, I think we’re in a really good position to deliver value for patients and for shareholders.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Maybe one big picture question there, just coming off the comments you just made about Keoacurin. How are you thinking about additional partnerships as you think about expansion to GIST, to diabetes with your other programs?

Troy Wilson, President and CEO, Cura Oncology: Yeah, it’s interesting. So it’s a good question. With GIST, GIST is let’s say that it works, right? 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 lethality. And at least in the preclinical models, you drive complete responses in the animals.

What we’re looking to do with this data set is can we show that actually we can reverse resistance to 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 two, three 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 populations, you don’t really need a partnership. Kyowa Kirin has the ability be deep in. We’ll show them data from the Phase I. We can, with our commercial force that we’re building, we could commercialize GIST.

Diabetes, completely different animal. Diabetes, I think ultimately, you need to be a multinational to really maximize the value. But we at Cura 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 use it to do stock repurchases, whatever we might do.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Got it. And maybe before we jump into Zifdomenib, which I do want to focus on, just remind us quickly on when we might see some updates from these additional pipeline programs?

Troy Wilson, President and CEO, Cura Oncology: Yes. So let’s jump to the end You’ll see, I hope, updates from the farnesyltransferase program potentially at ESMO in October. And there, what we’ve guided to from a corporate milestone is three different cohorts, a cohort of a farnesyltransferase 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 compound called two thousand eight hundred and six.

And you’ll see that compound two thousand eight hundred and six plus cabozantinib in RCC, renal cell carcinoma. I don’t know exactly what form those are going to take, but that’s the data update. The one that’s missing is two thousand eight hundred and six 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 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 generation menin inhibitor. All the data we’ve shown to date is with Zifdomenib. You don’t want to take Zifdomenib 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Got it. Perfect. Let’s focus now on Zifdomenib, 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.

Troy Wilson, President and CEO, Cura Oncology: Yes. So we were evaluating Zifdomenib in the relapsedrefractory NPM1 mutant population. We reported a CR CRH rate of twenty three percent and a median duration of response of three point seven months, restricted mean of I think four point seven 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 sixteen point four months median in the responders. Now if you think the patients are on, let’s call it approximately six 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 talks.

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 for And that’s what’s been missing, right? Venetoclax is very myelosuppressive. FLT3 inhibitors have cardiac tox and some QT prolongation and GI tox. Patients just don’t tolerate them very well.

Menin inhibitors and Zifdomenib 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

Andrea Newkirk, Biotech Analyst, Goldman Sachs: does the profile or where do you see differentiation from Rebuminin?

Troy Wilson, President and CEO, Cura Oncology: Yeah, 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 Revuminib 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 patient let’s take for example what you’re going to see at EHA. Patients take intensive chemotherapy for the week and then they’re on ZIFTIMENIB thereafter. Revumedib per the label requires weekly EKGs and then monthly EKGs thereafter.

And anytime 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 swim lane 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: 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?

Troy Wilson, President and CEO, Cura Oncology: Yes. So of all, there’s no grade one. So DLTs don’t sort of magically materialize. You usually see them they’re dose dependent. So 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 Zifdomenib and QT because we wanted to put that issue to bed. The three examples that you cited were assessed by investigator. Each of the three, 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, and are we going to fight it? No, it’s a safety study, right?

And so 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 ZYNTO.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Great. And if 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?

Troy Wilson, President and CEO, Cura Oncology: So, Ziftamenib 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 hem onc 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 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’ll come in ahead of schedule on the PDUFA date. But we put it in on we put the PDUFA sorry, we put the NDA in on March 30. On May 30, they gave us the answer, sixty 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Good. Good to hear. As you think about potential commercialization, obviously, you do have Syndax out there commercializing, Rebuminib, 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?

Troy Wilson, President and CEO, Cura Oncology: Yes. So the learning, the most important learning is, I was actually pleasantly surprised to see them report $20,000,000 in their first quarter sales. That tells you there is an 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 relapsedrefractory 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 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 Kewakiran are bringing their expertise.

They’re in the field with Portaleggio. Between our commercial organization and theirs, we’ll probably be 50% larger than Syndax. So we’re going to be trying to get the docs in surround sound on ZYFTOMENIB. We’ll be doing two 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 COMET seven data, which is ZIFTOMENIB plus Venaza in the red ops refractory setting. We have eight 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 I think, in The U. S. With two 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 ceftomenib. And all of that activity in the relapsedrefractory setting all the way to the frontline, that’s just going to drive more and more insight.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: 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?

Troy Wilson, President and CEO, Cura Oncology: Yeah, 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, 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 relapsedrefractory AML.

I don’t know to what extent are we going to see spontaneous usage in the frontline? I don’t 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 the venetoclax, right? And it has the potential, I think, to really inflect the curve in particularly as we go earlier and into frontline.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: 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 be expecting? And how meaningful what should we take away from this disclosure?

Troy Wilson, President and CEO, Cura Oncology: 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 ZiftoMetib plus intensive chemotherapy in two settings, frontline NPM1, newly diagnosed, newly diagnosed KMT2A. In the case of NPM1, the response rates are pretty high.

They’re eighty 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 two years. And of that or within the half of them will relapse, sorry, I got that backwards. Half of them will relapse, eighty percent of that half or forty percent will relapse within two 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 week. They start on ZYPTO on day eight.

In an ideal world, you’d see them all just swimming along in the swim lane plot staying on ZYPTO. 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 Zipto Menop in a post transplant setting.

That’s the sort of the clinical opportunity. The commercial opportunity again is, we think ultimately half of the frontline population at least is men in call it, their tumors are men independent. That would include FLT3, NPM1, KMT2A. That’s eleven thousand 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 $5,000,000,000 opportunity. It’s just it’s basic math, right? So when you see the swim lane 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: What is the extent of follow-up 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 data set?

Troy Wilson, President and CEO, Cura Oncology: You’re going to get so should added this to my previous answer. So the data that you’re going to see is from the six hundred milligram dose patients in the dose escalation plus the dose expansion patients who were all dosed at six hundred. The dose escalation had 200, 400, six hundred. We’re just showing you the six hundred. We may show you the 200 and four hundred in a subsequent data update.

It’s just you can only cram so much data into these presentations. So you’re seeing all six hundred 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 forty seven weeks.

So in the swim lane, you’re going to see patients from, I think the shortest is 20 all the way up to forty seven. 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, later this year or next year to continue that theme, right? How if we do an eighteen month landmark or a two year landmark, what does it look like?

And that’s why I think it will give people confidence as we’re heading now into COMMOD017 that we actually are driving clinical 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Maybe put that into context for us. MRD negative rates. What is the benchmark here?

Troy Wilson, President and CEO, Cura Oncology: 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 forty percent. That’s the rate of MRD negativity that intensive chemo gives you. Does that make sense? Yes.

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 five percent or lower. If you have five percent blast counts with AML, you still have AML. So MRD negativity and there’s typically a limit of detection of 10 to the minus four, ten to the minus five, 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 goes 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 ZIFTOMENEV around in sort of saturating conditions, any time disease pops up, if it’s in the spleen or it’s in the skeletal muscle or the bone marrow, then you differentiate them.

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 ZYPTUMEND doesn’t have any tox because it works to differentiate. So look for us to do ideally better than that 40% MRD negativity eventually.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: How much better does

Troy Wilson, President and CEO, Cura Oncology: it mean? You want to be clinically meaningful. We have 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 COMID-seventeen 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 two big Phase III, it’s like don’t 100 patients can make a difference, don’t skimp, right? Do the right trial, powered appropriately to ultimately deliver the endpoint.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: And as you think about these combinations with cysto, what is an acceptable safety or tolerability profile or what could we expect?

Troy Wilson, President and CEO, Cura Oncology: So, let me answer it this way. Your biomarker is dose reductions, dose interruptions, dose discontinuations, 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 Venaza 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Awesome. And then you also mentioned that you’ll have data from your non intensive combination.

Troy Wilson, President and CEO, Cura Oncology: Hopefully at ASH, right.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Okay. Maybe help us lay the groundwork for what we can expect there.

Troy Wilson, President and CEO, Cura Oncology: Yeah, 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 two 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 fifty percent. The median overall survival is about fourteen months for VENESA. So again, you’ll get this is the snapshot along the way.

We’ve never shown frontline VENESA 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 VENASA? 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, 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 eighteen months. In the intensive setting, eighteen to twenty four months.

That’s sort of our internal thinking. Hopefully, the data continues to support that view.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Great. So if all of these data sets report out positively and you see opportunity both in the relapse setting, the frontline setting here, You’ve spoken about $7,000,000,000 market opportunity for Menin inhibitors, of which Zipto would take a share of that. How do you I guess maybe in your conversations with physicians, ZIFTO versus Revumetib, how are they thinking about the market split there and how to make that decision over which asset to prescribe for their patients?

Troy Wilson, President and CEO, Cura Oncology: So, the KMT2A rearranged monotherapy setting, it isn’t close. Revu is going to take that, right? I just, there the benefit risk is very clear in favor of RevuMed. 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 frontline, 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 possibly can. In our advisory board meeting, one of the KOLs described Ziftermenib 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, then 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Maybe that’s a good segue into our last question here. Just as you think about potential combinatorial approaches that you could take with ZIFTO, what mechanistically is most interesting to you?

Troy Wilson, President and CEO, Cura Oncology: 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. Menin sits in front of the murderer’s row So NPM1, DNMT3A, KMT2A, BCL2, MCL1, FLT3 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: 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?

Troy Wilson, President and CEO, Cura Oncology: 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, I suspect this landscape five years from now will look completely different.

And have we seen this movie before? Yes, in multiple myeloma, right? Proteasome inhibitors, anti CD38. 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.

Andrea Newkirk, Biotech Analyst, Goldman Sachs: Great. Well, with that, Troy, thank you so much. Thanks everyone. You.

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