Curis Inc (CRIS) 2021 Q1 法說會逐字稿

Good afternoon, and welcome to Curis' First Quarter 2021 Earnings Call. (Operator Instructions) Please note, this event is being recorded. I would now like to turn the conference over to the company's Chief Financial Officer, Bill Steinkrauss. Please go ahead.

Thank you, and welcome to Curis' First Quarter 2021 Earnings Call. Before we begin, I would encourage everyone to go to the Investors section of our website at www.curis.com to find our first quarter 2021 earnings release and related financial tables.

I would also like to remind everyone that during the call, management will be 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.

Joining me on today's call are Jim Dentzer, President and Chief Executive Officer; and Bob Martell, Head of R&D. We will also be available for a question-and-answer period at the end of the call. I'd now like to turn the call over to Jim. Jim?

Thank you, Bill. Good afternoon, everyone, and thank you for joining us today. Every day at Curis we push to develop the next generation of transformative targeted cancer therapies that will meaningfully improve and extend patients' lives. In the first quarter of 2021 we took important steps towards that goal, building upon the exciting progress we made last year and expanding into additional areas where we believe we can make a difference. Our novel small molecule IRAK4 inhibitor, CA-4948 is currently being evaluated in 3 clinical studies. First, the Phase I/II monotherapy study in AML MDS, I just mentioned. Second, the Phase I/II study in combination with ibrutinib for patients with relapsed or refractory NHL or other hematologic malignancies. And third, the Phase II LUCAS study, evaluating CA-4948 in patients with lower risk MDS, being led by Dr. Uwe Platzbecker of the University of Leipzig.

We are especially pleased with the progress of CA-4948 and the exciting data update published in the European Hematology Association abstracts this morning from our Phase I/II monotherapy study in relapsed or refractory acute myeloid leukemia, or AML, and high-risk myelodysplastic syndromes or MDS. As many of you have been following, the long isoform of IRAK4 or IRAK4-L, has been recently identified as the key driver of disease in the majority of patients with AML and MDS. We at Curis have the first and only drug that directly targets IRAK4 to enter clinical testing for these patients.

Today, I am also pleased to announce that we have amended our AML and MDS study to add both a combination dose escalation and a monotherapy dose expansion. Preclinical data supporting the combination study was published by EHA earlier today and will be presented in a poster presentation at the EHA conference next month. We expect to begin enrollment in this portion of the study in Q3.

While there has certainly been a lot of attention on our IRAK4 study. It is important to note that we have also been pleased with patient enrollment in the Phase I dose-escalation study of our first-in-class monoclonal anti-VISTA antibody, CI-8993. We look forward to reporting initial clinical data for this study later this year. All told, we opened 2021 with strong momentum, following our updates in December at ASH and the successful execution of key strategic financings and partnerships with premier institutions like the NCI and the European MDS consortium that will support the continued advancement and expansion of our clinical programs.

With that, let's dig into some detail on our ongoing clinical programs, starting with the IRAK4 study in leukemia. In April, we were pleased to report that CA-4948 had received orphan drug designation from the FDA for the treatment of AML and MDS. This special designation represents a significant milestone for Curis as we work to advance CA-4948 through clinical testing and, in time, seek to make it available to the patients who need it most. In the EHA abstract published this morning, we were pleased to report that the data in our AML and MBS study continue to exceed our original expectations, showing consistent single-agent efficacy across the spectrum of late-line AML and MDS patients. Despite these patients having already experienced several unsuccessful prior lines of therapy.

To provide some context, in conjunction with ASH last year, we reported preliminary data from 6 patients as of a November cutoff, showing marrow blast reductions in all 6 patients, with 2 of the patients demonstrating marrow complete responses. And none of the patients experiencing a dose-limiting toxicity at either the 200 or 300-milligram BID dose levels. The data published today, which are from 15 patients and the February 8 cutoff, showed bone marrow blast reductions in all tested doses, 200, 300 and 400 milligram BID and in 8 of 9 evaluable patients with elevated blast counts at baseline.

Of these, one patient experienced a full hematologic recovery CRm, one patient experienced a CRI with negative minimal residual disease, and 2 patients had bone marrow CRS. 3 of these patients presented with the U2AF1 or SF3B1 spliceosome mutation, and all 3 of those patients achieved a marrow CR or better, validating our belief that these spliceosome mutations are specific oncogenic drivers of the long isoform of IRAK4, which CA-4948 is explicitly designed to target. We were also pleased to see that all patients with objective responses showed signs of hematologic recovery.

Delving a bit deeper on this point. The blast reduction data reported in the abstract this morning provide further evidence that CA-4948 is effective at reducing a patient's cancer burden. For this late-line patient population, having a drug that can safely and effectively get the cancer out is the immediate goal. In first line patients, those patients whose bone marrow has not been irrevocably damaged by cancer or by prior cytotoxic treatment, it has been shown that if given a drug that reduces the level of leukemic blasts, these patients can achieve clear and substantial hematologic recovery within a few months.

For the extremely sick late-line population, such as the patients in our study, it is important to remember that their cancer has progressed despite numerous prior lines of therapy. As a result, these patients often have deeply scarred dysfunctional marrow, which may delay or even prevent successful hematologic recovery. It is therefore especially encouraging that we have been able to see signs of hematologic recovery even in these late-line patients after only a few months of treatment. It underscores our optimism that CA-4948 may have both a combo therapy and a monotherapy regulatory path.

Overall, we are very pleased with the progress for CA-4948, and we look forward to the EHA conference, where we will provide an updated and expanded data set with a later cutoff date to include additional patients, including those enrolled in our 500 milligram BID cohort. In addition, we will provide an update on safety, pharmacodynamic data, including IRAK4-L expression levels and further genomics information. We have found that the 500 milligram BID dosing regimen has exceeded the maximum tolerated dose according to protocol guidelines. We observed 2 patients with dose-limiting toxicities, one of whom had grade 3 CPK elevation or rhabdomyolysis, similar to what we saw in the NHL study and the other experienced grade 3 syncope. Both patients' AEs were reversible and quickly resolved after discontinuation of dosing. Now that we have established the maximum tolerated dose, we will explore the lower dose levels to determine the appropriate recommended Phase II dose.

I'd like to briefly touch on the preclinical data in our other EHA abstract published earlier today. These data highlighted CA-4948's synergistic antitumor activity in combination with azacitidine and venetoclax in leukemia cells, and will be presented in a poster session at EHA next month. These data demonstrate that CA-4948 potentiates antitumor activity in certain cell lines resistant to clinically relevant concentrations of azacitidine and venetoclax. Further, CA-4948 demonstrated synergistic antileukemic activity in combination with venetoclax and azacitidine in AML cell lines. Even before we saw these data, we knew that CA-4948 was unique. It is oral. It is disease-modifying. It directly targets the key driver of disease, IRAK4-L, which is a novel mechanism of action. And it has demonstrated the ability to provide clear and significant single-agent activity without significant myelosuppression, including complete elimination of detectable cancer burden.

With the latest preclinical data adding a possible synergistic effect as well, we and our clinical investigators are very excited to explore the combination of CA-4948 with azacitidine and venetoclax in the clinic. As I mentioned earlier, this quarter we amended the protocol of our existing study to include expansion cohorts for both monotherapy and combo therapy. The monotherapy dose expansion will begin after the recommended Phase II dose is determined and will include 4 cohorts: patients with spliceosome mutated MDS that is relapsed/refractory to HMA, patients with MDS without spliceosome mutation that is relapsed/refractory to HMA, patients with FLT3 mutated relapsed/refractory AML and patients with FLT3 wild-type relapsed/refractory AML.

The combo therapy study will start dose escalation at 200 milligrams BID and will include 2 cohorts, CA-4948 plus azacitidine for patients with AML MDS who are naive to HMA, and a second cohort of CA-4948 plus venetoclax for patients with AML or MDS core naive to venetoclax. We hope that the design of these cohorts will help to identify the most appropriate regulatory path or paths for CA-4948. We expect to begin enrolling patients in these combotherapy cohorts in Q3. We may also explore a triple combination of all 3 drugs of CA-4948 plus azacitidine plus venetoclax, but that would of course be dependent upon the initial safety and efficacy results from the 2 agent combination cohorts.

Before moving on from leukemia, I would like to touch briefly on the ongoing IST, treating patients with lower-risk MDS that we announced in February. The Phase II LUCAS study is being led by the co-chairman of EHA's scientific working group on MDS, Dr. Uwe Platzbecker, who will be coordinating this study in 17 sites across Europe to evaluate CA-4948 for the treatment of anemia in patients with lower-risk MDS. If this study is successful, it could lead to a potential breakthrough in the MDS field.

While current EPO-stimulating agents can be effective for patients with lower-risk MDS who have low serum EPO, this effect is often transient and is not disease-modifying, and it does not affect progression to AML and further disease complication. With its direct nonmyelosuppressive targeting of IRAK4 and its robust safety profile, we believe CA-4948 could potentially offer a safe and transformative disease-modifying alternative for patients at earlier stages of disease.

Now moving to lymphoma. In an oral presentation at ASH last December, we reported expanded clinical data from our Phase I dose-escalation study of CA-4948 for the treatment of patients with relapsed or refractory NHL or other hematologic malignancies. These data highlighted durable reductions in tumor burden in 6 of 7 evaluable patients treated with 300 milligrams of CA-4948 twice daily, following a median of 4 prior lines of therapy.

It is important to reiterate that seeing clear efficacy with a novel monotherapy agent and seeing that this efficacy is durable over such an extended period of time for these extremely sick patients is enormously encouraging and provided powerful affirmation of our intention to launch the current combination study evaluating CA-4948 with ibrutinib.

This combination study, which began enrolling in Q1, is expected to enroll approximately 18 patients in a 3-plus-3 design with CA-4948 doses starting at 200 and escalating to 300 milligrams BID. Ibrutinib dosing will be whatever is appropriate for the patient's respective NHL subtype. We expect to provide an enrollment update for this study as well as initial safety and efficacy data in Q4.

Now I'd like to turn to CI-8993, our first-in-class monoclonal antibody for the treatment of patients with relapsed or refractory solid tumors. Checkpoint inhibitors that function to enhance T cell priming, such as anti-CTLA-4 antibodies and checkpoint inhibitors that relieve T cell exhaustion, such as anti-PD-1 antibodies, all have 2 key limitations. First, T cells stuck in a quiescent state cannot be acted upon by these checkpoint inhibitors. Second, myeloid-derived suppressor cells or MDSCs, actively impair the effectiveness of these checkpoint inhibitors. VISTA is a primary enforcer of T cell quiescent and can sequester a large proportion of T cells in a quiescent state, preventing them from being acted upon by anti-CTLA-4 or anti-PD-1 antibodies. VISTA is also a primary driver of MDSCs. These cells function to promote T cell exhaustion and suppress pro-inflammatory tumor-associated macrophages.

Finally, we know that VISTA expression can increase dramatically as a compensatory mechanism during treatment with anti-CTLA-4 or anti-PD-1 therapy. For these reasons, we believe that therapeutic targeting of VISTA will be a crucial addition to the arsenal of immune-oncology therapy. We believe CI-8993 is the most advanced anti-VISTA antibody currently in clinical development and has the potential to be a game-changing cancer therapy. The clinical community has already shown a deep excitement and interest in this program, and we look forward to reporting initial clinical data later this year.

To wrap up, I'd like to extend my utmost appreciation to the entire Curis team who have made all of this progress possible. We are eager to build upon our efforts in the quarters to come and advance our next-generation targeted cancer programs to help patients in need. With that, I'll turn the call over to Bill to review our financial results for the quarter. Bill?

Thank you, Jim. For the first quarter of 2021 we reported a net loss of $9.9 million or $0.11 per share on both a basic and diluted basis as compared to a net loss of $9.7 million or $0.28 per share on both a basic and diluted basis for the same period in 2020. Revenues for the first quarter of 2021 were $2.2 million as compared to $2.7 million for the first quarter of 2020. In both cases, revenues comprised primarily of royalty revenues recorded on Genentech and Roche's net sales of Erivedge.

Operating expenses for the first quarter of 2021 were $11 million as compared to $11.2 million for the same period in 2020. Cost of royalty revenues were $0.1 million for both the first quarter of 2021 and 2020. Research and development expenses were $6.8 million for the first quarter of 2021 as compared to $7.5 million for the same period in 2020. The decrease for the quarter is primarily attributable to the upfront license fee expense from our option and license agreement with ImmuNext related to CI-8993 that occurred during the first quarter of 2020. These costs were partially offset by a $0.3 million increase in employee-related cost.

General and administrative expenses were $4.1 million for the first quarter of 2021 as compared to $3.6 million for the same period 2020. The increase in general and administrative expense was primarily driven by higher cost for stock-based compensation, professional and consulting services, partially offset by lower legal cost during the 3 months ended March 31, 2021. For the first quarter of 2021 and 2020, net other expense was $1.1 million and $1.2 million respectively. Net other expense primarily consisted of imputed interest expense related to future royalty payments.

As of March 31, 2021, there were approximately 91.5 million shares of common stock outstanding. As of March 31, 2021, Curis' cash, cash equivalents and investments totaled $168.4 million. We expect that our existing cash and investments should enable us to maintain our planned operations into 2024.

With that, I'd like to open the call for questions. Operator?

(Operator Instructions) Our first question comes from Ed White with H.C. Wainwright.

Congratulations on the data. Very good news. Just a first question, Jim. How should we be thinking of the path forward to approval for monotherapy and combination therapy? Maybe perhaps you can discuss potential time lines to approval in AML and MDS. And what strategy, either monotherapy or combo, can get 4948 to the market sooner?

All right. Thanks, Ed. Appreciate the thoughts and the question. It's a little preliminary for us to talk about timelines to approval. But I think our overall approach is really the same approach we outlined in December. We're just, of course, more confident now that the data continues to reinforce it. And that is from initially expecting this was a combo therapy only drug that we were going to have in a selected population of 50% of the population. The December data and of course, now the ASH abstract data seem to support that this is more appropriate for all comers.

So I think that that's the primary end use. The other opportunity that was hinted at in December, and now we can see more clearly is there may also be a monotherapy path in a selected population. And I think now we can say it looks like the spliceosome mutation population would be a good candidate for that. All 3 of the patients that have a spliceosome mutation in this study so far have seen marrow CR or better.

So obviously that, given the genomics association which it makes it for a very compelling monotherapy opportunity and the idea that in a post HMA setting there is no other drug approved, we like the chance of that one as well. Which one will go faster, I don't really know. I think the answer at this point is both seem to be very compelling opportunities, a combination therapy where this gets added to standard of care. And then of course monotherapy in a separate population driven by the genomic signature.

And maybe you could just give us your thoughts on the size of these dose-escalation studies, the cohorts in both combination and monotherapy.

Yes. Bob, would you mind taking that one?

Yes. So these studies will initially be dose-escalation trials using a 3-plus-3 type of design. Fortunately, we're able to start at a very relevant dose that's already been shown to be therapeutically active of 200 milligrams twice daily. And we also have started to define the upper limits as well, as Jim mentioned. We would likely stick within the range of somewhere in the 200 to 400 range for dosing. So the overall dose escalation for these trials is not likely to take too long.

The next question is from Justin Walsh with B. Riley Securities.

Congrats on the progress. So first, could you guys elaborate on the steps needed to establish the recommended Phase II dose at lower than 500 milligrams bid in AML MDS?

Sure. Again, that's probably the best question for Bob. Bob?

Yes, I can do that. So far we've seen really exciting data in a small number of patients. So part of our efforts now will be to look at a variety of different variables, obviously including pharmacodynamics. We do know, for example, that the pharmacokinetics are very well-behaved between, say, the 200, 300 and 400-milligram dose levels. We'll also want to expand somewhat and further understand the efficacy, perhaps looking at perhaps a dosing interval break, things like that. So all of this will take place in the coming months, and hopefully we'll be able to define a recommended Phase II dose going forward in the near term.

Yes. I think if I were to add something to that, Justin, I'd say that the good news from a timing perspective is we expected to hit MTD, we just didn't know when. The only signal that we had from the NHL studies was that it was likely to be CPK elevation of rhabdo. And sure enough we did see it at 500 in the leukemia study. So I think now that we've got the MTD in hand, we're at this high-class headache where 200, 300 and 400 all look therapeutic. I mean, I know that sounds kind of funny to say that, that's your headache. But really it is. So we need to do a little bit of dose exploration at this point to try and to figure out which of these really is the best one to take into Phase II.

Got it. And one more question for me. I saw on the abstract that most of the patients were transfusion-dependent, which isn't that strange for high-risk MDS. I'm just wondering, are you guys tracking this? And have you noticed any improvements in transfusion dependence in the MDS patients?

Yes. So I'll hold that thought for the more detailed discussion at EHA, but absolutely, in MDS, transfusion dependence is really important. In fact a clinical endpoint for a study could be a reduction of transfusion dependence. So we continue to monitor that. That's something that's going to be important, not just for our studies, but also of course for the low-risk MDS study, the [Lucus IST] that's being run in Europe. So hold that thought.

The next question is from Soumit Roy with JonesTrading.

Congratulations again on a very robust data. Just a couple of questions -- absolutely. And not sure how much color you can share with us. The -- any mutational status on these responders, if we should think they are mostly spliceosome mutants or it looks like both, could be both [split 3 white ticon] mutant and the split between AML or MDS, how many are from the AML cohort, the responders, how many from the MDS?

Yes. So we're going to want to hold off on some of the genomics discussion for the actual EHA presentation. We're going to not go beyond what we said in the abstract. That said, of course, that's a matter of great interest for us. So you can look forward to having a lot more detailed discussion around that when we get to it.

Absolutely, understandable. Just one last question. When you were setting up 4948 plus aza in the HMA naive setting, should we think of as frontline patients being included whoever is not amenable to [7-plus-3] treatment? And how are the physicians going to think whether to put the patient on 4948 aza versus venetoclax plus aza in these elderly patients?

Yes. Why don't we ask Bob, our oncologist, to walk through that? Bob?

Yes. So absolutely, azacitidine may be a viable treatment for first-line for patients. So this combination in first-line is something that certainly could be considered. One of the advantages that this drug has over venetoclax, for example, is the lack of significant myelosuppression. So this might be a driving factor, especially for a frail elderly patient for a clinician to choose this combination over venetoclax. As we mentioned earlier, we were also exploring a combination with venetoclax itself and may even consider a triplet combination at some point in the future as well.

Congratulations again.

(Operator Instructions) The next question is from Alethia Young with Cantor Fitzgerald.

Congrats on the progress with the abstract. A lot of help for me. Yes. Good stuff. So first, I'm going to ask them one by one because I think they're all equally as important. So when you look at the 6 people you had at ASH, like when we trace back now to how the CRs have deepened, were those the people that had marrow CR and they deepened? Or how should we think about who had the hematologic recovery is the first question.

Yes. We haven't gone into the patient-by-patient detail. I'd say, hold that discussion on a deeper level of the data for the EHA conference. I would say that the high-level observation is really the most important one, is that we were very pleased that we're getting blast count reductions. Remember that this drug is -- it's an anticancer drug. It's not a marrow stimulant. So we weren't really expecting to see heme recovery in this really late-line population. That we started to see it was fantastic.

We would expect that if you can eliminate the tumor burden and heme recovery is possible, depending upon the health of the marrow, it is the sort of thing that you would expect might come over time. The fact that we've already seen it is, of course, fantastic. So we'll be following those patients. And of course the additional ones we put on, on the study in the months to come. But we're very encouraged by what we're seeing so far.

So to follow that up, so EHA will get the information patient by patient. But just at a high level, is it fair to assume that your hypothesis is that responses deepen over time? Or can you say that?

I think the hypothesis is that this drug directly targets the driver of disease, IRAK4 or IRAK4-Long, and that, that should lead to the reduction of leukemic blasts full stop. That's what this drug does, it's an anti-cancer drug. So by hitting the target of disease, the driver of disease, you should see a reduction in cancer burden.

And if the patient's marrow is healthy enough, obviously front-line patients, marrow is going to be much healthier that in late-line. The marrow gets damaged over time not just by the cancer but frankly by the cytotoxic agents, whether it's chemo or aza or ven, all of these agents will cause damage to the marrow. If the patient's marrow is healthy enough to be recovered, we would hope to see it, knowing that it might take some time. But that's going to be, frankly, a patient-by-patient basis, and it's going to depend, of course, how many prior lines of therapy and how deep the cancer has gone in each patient.

Okay. And so I don't know if you can say this, but can you tell us at what doses those CRs were achieved?

We will be showing that at the conference.

Okay. I guess maybe this is more just on the tox seen at the higher dose. Can you confirm if there were -- whether there are any new responses reported, the 500-milligram cohort?

So…

Or any more toxicity, I guess, in a way like -- is it like -- yes, you know what I'm saying.

Yes, I know what you're saying. I'm -- obviously I'm trying to balance the EHA rules, right. We don't want to be bridging the gap between what's in the abstract and what's in the presentation to come. I think what we would say is that we always expected to see tox, we weren't surprised. We were pleasantly surprised that we started to get responses even at the 200 and 300 dose levels. What I can say broadly is that 200, 300 and 400 all look like therapeutic doses. I would say that we were pleased that we've now established NTD, and we're now going to try and figure out which of the doses is there a dose response. Is 200 -- is 300 better than 200 and 400 better than 300 remains to be seen. And as Bob said, we may also want to take advantage, now that we're in Phase I, before we go to Phase 2, of exploring different regimens as well. Now is the time to learn that. But for now, I would say we're frankly in this very high class headache position of seeing 3 therapeutic doses and trying to evaluate which of the 3 is the best one to take into Phase II.

So when you think about the dose response curve here, like the 300, 400, now the 500, like there was a [rap though] at 300, not in this population, mind you. But do you think that there -- you have a predictable kind of dose response recur between the 200, 300 and 400 now, and that basically 500 is where this starts to creep up? Or do you think there's more work to be done there?

Yes. I would say we still have a pretty small number of patients, I mean, to be fair. I think we're encouraged that across the board all of the doses look to be effective, all of the doses meaning 200, 300 and 400. But gosh, it's such a small number of patients in each one. It's hard to say today that there's clearly dose response and that one dose is clearly preferable to the other 2. That's exactly why we've got to continue the dose exploration in the months to come and try to sort that out.

Okay. And so with these cases of rhabdo, with the grade 31, was there any clinical symptoms? I know with the other one there was a syncope. But can you -- is the syncope like -- is it drug related? And like if so, like can you kind of explain what you think this mechanism of action is?

Sure. Bob, you're probably the best one to talk to that.

Yes. So generally, patients who experience this will have some muscle soreness. Maybe they'll notice a little bit of darkening of urine. In all of the cases, patients have not had any organ dysfunction like renal failure or anything like that. And they've all recovered fairly rapidly from this. We think in several of the patients there have been other factors that may have also contributed to that, for example, heavy exercise or on a statin, for example, that may have -- that has a warning for rhabdomyolysis. So it's potential that this drug pushed those patients to the point where they experienced it. And from that extent, we do feel that it is drug related, but other potential factors.

I think the primary factor for us, Alethia, in declaring 400 as our maximum tolerated dose and backing away from 500 was not the syncope, it was the rhabdo because we were looking for it, frankly, after the NHL experience. We did expect to see it. We were pleased that, as Bob said, we believe based on the NHL study that if you are on a statin, this may exacerbate that. So if you already have one factor that would push you to CPK elevation, that if you stay on the statin and add our drug, it might push you that much further in the direction. Same thing with heavy exercise. If you're doing a lot of heavy exercise, maybe this exacerbates that. So we were looking for that effect. And that we did see it, didn't surprise us. But even though it's only one of the 2 DLTs, that's really the one that in our mind says, okay, we saw what we expected to see, let's back off to 400 and then, of course, take a look at the other doses as well to see which of those is the best.

Okay. And so with the grade 3 rhabdo that you saw, did anyone have like kind of statin exercise baseline things that would have done though?

Yes, Bob?

Yes. So 2 of the patients on the lymphoma trial, as we've mentioned previously, one of whom had the grade 3 rhabdomyolysis was also on a statin. And the other patient in that case actually felt quite a bit better after being on the study drug for a short time, went out and exercised heavily and then developed this muscle soreness and symptoms after that. So we think -- so what we've advised going forward for the clinical trial is for patients and investigators to discuss with their patients if they are on a statin, whether it's necessary to continue that statin.

And if they can come off that statin, they would suggest to do that. Similarly, to avoid extremely vigorous exercise while on the treatment. And we think that might be part of the reason why we didn't see this side effect until higher doses on the leukemia study.

Got it. And then maybe my last one, do you think there's a differential kind of monotherapy response between MDS and AML patients?

Yes, Bob?

Well, yes. So we -- we'll actually give a much more detailed description of the specific patients. But obviously we've treated both patients so far and we've seen achievement of marrow CRs in both groups of patients. So we'll have to see. The MDS population is the population where these spliceosome mutations are much more common. And you know that we've announced as part of this presentation that the 3 patients who have spliceosome mutations all achieved marrow CR or better.

This concludes our question-and-answer session. I would like to turn the conference back over to James Dentzer for any closing remarks.

Thank you, operator. I'd just like to thank everybody for joining us on the call today. We greatly appreciate the patients and families participating in our clinical trials. And of course, as I said earlier, I'd like to thank the team at Curis for their hard work and commitment. Also our partners at Aurigene, ImmuNext and the NCI for their ongoing help and support. We look forward to updating you all again very soon at the EHA conference. Operator?

The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.