I'm Jim Dentzer, the CEO of Curis. Thank you for taking time today to learn more about us. Over the next 25 minutes, I'll walk through a summary of our progress to date. Before I begin, I'd like to remind everyone that during the presentation, I'm making forward-looking statements, which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and actual results may differ materially. For additional details, please see our SEC filings. While Curis has a broad pipeline of novel cancers, we're focusing our efforts on emavusertib, the first-in-class IRAK4 inhibitor with broad application in lymphoma, leukemia, and solid tumors. We now have proof-of-concept data in 34 patients with PCNSL and a second proof-of-concept data set with 21 patients in AML, with both studies demonstrating a significant improvement over standard of care.
More to the point, we believe that these two studies represent the tip of the iceberg. The proof-of-concept results in PCNSL, one of the toughest NHL subtypes to treat, give us confidence that it will also work in other NHL subtypes, including CLL. Similarly, the proof-of-concept results in relapsed refractory AML give us confidence that it will also work in frontline AML. Curis is one of the most experienced leadership teams in biotech, with each of us having over 20 years of experience developing novel drugs at companies like Dicerna, Biogen, BMS, and Merck. The newest member of our team, Dr. Ahmed Hamdy, brings experience of developing both the number one and the number two BTK inhibitor as the CMO of Pharmacyclics and also at Acerta. Ahmed is spearheading our push into CLL, and we're very glad he chose to join the team earlier this year.
This slide highlights emavusertib's novel mechanism of action and how it addresses multiple unmet medical needs in lymphoma and leukemia. On the right side of the graphic, we see how emavusertib blocks both the TLR and FLT3 pathways, the two pathways driving disease in AML. On the left side of the graphic, we see the BCR and TLR pathways, the two pathways driving CLL and NHL. In this setting, emavusertib is used in combination with a BTK inhibitor to enable a dual blade. BTK inhibitors block the BCR pathway, and emavusertib blocks the TLR pathway. With that, let's walk through the data that demonstrate how important this novel mechanism is. We'll start with the opportunity in CLL and NHL. IRAK4 is a compelling target in CLL and NHL because of its ability to downregulate NF-kappaB in a way that's independent from and synergistic with standard of care.
In the graphic on the left, we see that NF-kappaB overactivity is what's driving disease in NHL, and two pathways are driving that overactivity. One is the BCR pathway, which is addressed by BTK inhibitors. The other is the TLR pathway that's addressed by emavusertib. We all know that BTK inhibitors work, and they can provide high response rates, but we also know that they struggle to get complete responses. We believe this is because they block one of the two pathways driving disease in CLL and NHL. In the graphic on the right, we see the preclinical data supporting this thesis. Both drugs induce tumor reduction in monotherapy, but it is only when we combine them that we see the strongest activity and the deepest responses.
When we look at the unmet need in CLL and NHL, we have to start with the understanding that everyone loves BTK inhibitors for a reason. They changed the game in NHL and have become an $11 billion industry that grew 20% last year. But BTK inhibitors have two key drawbacks. First, their inability to provide complete responses means chronic lifelong therapy for patients with the heightened risk of acquiring treatment-resistant mutations. And second, BTK inhibitors come with side effects like bruising, bleeding, fatigue, and cardiac issues that are particularly difficult for older patients. More recent therapies, like the BCL2 anti-CD20 combination, which was approved in 2019, have suggested the promise of a one-and-done or a fixed-duration treatment, which is very compelling.
Unfortunately, those treatments also come with a very difficult side effect profile, and over the last six years, they've been unable to displace BTK inhibitors as standard of care. With emavusertib, we have a therapy that has the potential to provide the good outcome promise of BCL2 and CAR-T, but with an oral therapy and a much more attractive safety profile. The clinical program for emavusertib in CLL and NHL was designed in anticipation of the potential for accelerated filing. In part A, we explored dose escalation across multiple NHL subtypes. In parts B and C, we're focusing specifically on PCNSL. Part B supports an accelerated approval path, with a single-arm study adding emavusertib to a patient's BTKi regimen directly after they've progressed on BTKi monotherapy. And part C supports the confirmatory path with a randomized study in BTKi naive patients.
In part A, the dose escalation part of the study, we saw a clear pattern of activity across multiple NHL subtypes. Monotherapy and lower doses are active, and there's a steady increase in activity as we go to higher doses and to combination. Among the NHL subtypes, we selected PCNSL as the subtype to pursue for our fastest path to first label because the regulatory opportunity is so clear. PCNSL is an orphan indication. It's the hardest NHL subtype to address, and there are currently no drugs approved for it. So in these early data, we saw an emerging pattern of activity across multiple NHL subtypes. What then happened as we expanded into PCNSL? We see this in parts B and part C. What happened is that the emavusertib continued its encouraging pattern of anti-cancer activity.
In the BTKi naive group, the emavusertib by ibrutinib combination outperforms the data published for ibrutinib monotherapy, 63% versus 39%. In the BTKi experienced group, these are patients who've progressed on BTKi monotherapy, so we wouldn't expect any tumor reduction if they stayed on it. We saw clear reduction in 11 of 17 patients and objective responses in 7 of them. The duration of responses we can see on the right looks encouraging as well. Three of four CRs have lasted longer than six months, and one patient's been in remission for over 400 days and another patient for over 800. In 2025, patients across all programs and all of our studies. The safety table on this slide includes specifically with NHL. Treatment was well tolerated. There's no dose-limiting myelosuppression and no DDI.
As we push forward into PCNSL, the obvious next step is to expand into the other NHL subtypes wherever BTKi is used. We know BTK inhibitors work and that they can provide high response rates, but they struggle to get complete responses. When we add emavusertib to a BTK inhibitor, we can get complete responses. Given the clarity of emavusertib's mechanism and the clear pattern of activity we're seeing, even in the hardest-to-address NHL subtype, we look forward to expanding across NHL wherever BTK inhibitors are used. We expect to enroll our first patient in CLL by year-end. As we said earlier, we look to provide the outcomes promised by BCL2 and anti-CD20, but with a better safety profile. The 53% MRD potential with BCL2 and anti-CD20 is compelling, but its difficult safety profile has prevented it from displacing BTKi since its 2019 approval.
Our goal is to bridge that gap, maintain the safety profile of the established $11 billion standard of care, but deepen its efficacy and enable patients to achieve complete remission or the potential for MRD negativity. From a regulatory perspective, we see the world's changing. The FDA and EMA are increasingly receptive to MRD as a clinical endpoint. To be fair, this is a relatively recent development, but emavusertib's potential to deepen responses, eliminate minimal residual disease, and enable time-limited treatment seems well-timed with where regulatory authorities want to go. In summary, BTK inhibitors are great. They change the game in NHL, but they come with limitations, including the need for chronic lifelong therapy and difficult side effects. With emavusertib, we can make the already clear market leader an even more effective therapy by combining it with emavusertib. And that's the NHL story. Let's move on to AML.
As we dive into AML, we find that emavusertib's unique molecular opportunity. In AML, both IRAK4 and FLT3 are immune targets of interest, with both of them driving disease in AML. Why is this important? Let's walk through them. In the graphic on the right, we see how the TLR pathway and the FLT3 pathway drive disease in AML, and that emavusertib blocks both of them. Let's walk through these two pathways individually to better understand how important this novel mechanism is. First, we'll start with IRAK4. It's important to note that there are two isoforms of IRAK4. IRAK4 short is the wild type, and IRAK4 long is oncogenic. This distinction is demonstrated in the four gray boxes on the left side of the slide. The box in the upper left is the control. The box in the upper right shows that knocking out IRAK4 stops leukemic activity.
In the lower right, we see that adding back the wild type, IRAK4 short, has no effect, and in the box on the lower left, we see that adding back the oncogenic isoform, IRAK4 long, restarts leukemic activity. The red and blue graphic on the right side of the slide shows why the identification of IRAK4 long as an oncogene was so important in AML. These data are from the Cancer Genome Atlas, and they show that IRAK4 long is expressed in nearly all patients with AML. Now, we're not suggesting IRAK4 is the only driver of disease in AML. Of course not. There are a lot of drivers in AML. What we're suggesting is that IRAK4 is an important driver. It's expressed in nearly every patient, and the current standard of care doesn't address it.
Now, let's look at FLT3, which is mutated in a third of patients with AML. And more specifically, why combining FLT3 inhibition with IRAK4 inhibition is so effective. The graphics on this slide are from the 2019 Mograbi paper, which we think does a great job of articulating why FLT3 inhibitors as a class aren't more effective in treating AML patients who harbor FLT3 mutation. In the graphic on the left, we see that IRAK4 activity increases after treatment with a FLT3 inhibitor. In the middle graphic, we see that blocking either IRAK4 or FLT3 in monotherapy can induce tumor reduction, but the effect is temporary. You need to combine IRAK4 and FLT3 to get the longer, deeper response. In the graphic on the right, we see the logical extension, that blocking both IRAK4 and FLT3 results in extended survival.
So given the strong synergy between IRAK4 and FLT3, the third of the patient population with FLT3 AML represents a clear opportunity for emavusertib. In the frontline setting, composite CR rates are typically around 60%, with fit patients receiving chemo, ± midostaurin or quizartinib, and unfit patients receiving venetoclax. The fit and unfit populations converge in the relapsed refractory setting, where patients will typically receive gilteritinib, and the expected composite CR rate drops to 21%. In our study, we targeted patients who had progressed after they had failed a FLT3 inhibitor. In the salvage line setting, we might expect that the composite CR rate would drop again, perhaps to 10% or lower. As we now know, our data were quite a bit better than that. In the waterfall chart left, we see the single induct.
In the swimmer plot in the middle, we see that these responses came quickly and were durable, and in the chart on the right, we see how these data compare to the current standard of care. Even though the majority of patients treated with gilteritinib were naive to FLT3 inhibition, and the majority of patients on emavusertib had already failed on a FLT3 inhibitor, emavusertib clearly outperformed gilteritinib, the current standard of care for patients with FLT3 AML. Just as we saw in NHL, the safety data in AML are equally encouraging. To date, we've dosed over 225 patients across all of our studies. The table on this slide includes the 102 patients with AML that were treated with emavusertib. Treatment was well tolerated, and no dose-limiting myelosuppression was observed. We're currently working with key opinion leaders to design a registrational head-to-head study randomizing against gilteritinib.
It's a big study, so we'll want to ensure that we have sufficient financing before we kick it off, but it's designed to demonstrate that emavusertib is the next- generation best-in-class treatment for all patients with FLT3 AML, and that's it for leukemia. In short, emavusertib is a novel drug with a compelling monotherapy opportunity in a genetically defined population, with the potential to establish a new standard of care for AML patients with FLT3 mutation. We want to repeat our FLT3 AML study, this time in a head-to-head against gilteritinib. We think we can repeat it. As mentioned in the introduction, the primary focus of our work has been in NHL and AML, but we're also working with several partners in academia and the NCI on the potential for emavusertib in solid tumors.
In preclinical studies, emavusertib has been shown to potentiate both chemotherapy and immunotherapy in solid tumor malignancies. emavusertib's been evaluated in five investigator-sponsored trials in solid tumors. We expect preliminary data from these studies beginning later this year, and as these data mature, we hope to gain a better sense of emavusertib's potential in the competitive landscape and the scope of the potential opportunity in solid tumors. Now that we've walked through emavusertib's potential in NHL, AML, and solid tumors, let's review some of the high-level corporate information. Inclusive of the financing in July, we finished Q2 with roughly $17 million, and we have a strong IP position with comp of matter to 2035 before any extensions. In closing, novel targets in biotech are rare, especially ones with such wide commercial potential.
All of us at Curis are grateful for the opportunity to develop this first-in-class, and we believe best-in-class novel therapy for patients with cancer. Thank you for your time today. We appreciate the opportunity to provide this update on our progress.