Curis, Inc. (CRIS) Q1 2021 Earnings Report, Transcript and Summary

Good afternoon and welcome to the Curis' First Quarter 2021 Earnings Call. All participants will be in a listen-only mode. After the Company's prepared remarks, call participants will have an opportunity to ask questions. [Operator Instructions] Please also note this event is being recorded. I would like to turn the conference call 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 is Curis, we push to develop the next generation of transformative, targeted cancer therapies that will meaningfully improve and extend the patient's 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 three clinical studies; first, the Phase 1/2 monotherapy study in AML and MDS I just mentioned; second, the Phase 1/2 study in combination with ibrutinib for patients with relapsed or refractory NHL or other hematologic malignancies; and third, the Phase 2 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 abstract this morning from our Phase 1/2 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 have Curis at 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 our 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's enrollment in the Phase 1 dose escalation study of our first in class monoclonal anti-VISTA antibody CI-8993. We look forward to recording 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 political 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 the most. In the EHA abstract published this morning, we were pleased to report that the data in our AML and MDS 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 six patients as of a November cutoff showing marrow blast reductions in all six patients with two 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 milligram, 300 milligram, and 400 milligram BID. And in eight of nine evaluable patients with elevated blast counts at baseline, one patient experienced a full hematologic recovery CR, one patient experienced a CRI with negative minimal residual disease, and two patients had bone marrow CRs, three of these patients presented with a U2AF1 or SF3B1 spliceosome mutation, and all three of those patients achieved the 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 blast, 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 dataset with a later cutoff date to include additional patientsincluding 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 two patients with dose limiting toxicities, one of whom had Grade 3 CPK element elevation or rhabdomyolysis similar to what we saw in the NHL study and the other experienced Grade 3 syncope. Both patients at ease 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 2 dose. I'd like to briefly touch on the preclinical data in our other EHA abstract published earlier today. These data highlighted CA-4948 synergistic anti-tumor activity in combination with azacitidine and venetoclax in leukaemia cells and will be presented in a poster session at EHA next month. These data demonstrate that CA-4948 potentiate anti-tumor activity in certain cell lines resistant to clinically relevant concentrations of azacitidine and venetoclax. Further, CA-4948 demonstrated synergistic anti-leukemic 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 is 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 combotherapy. The monotherapy dose expansion will begin after the recommended Phase 2 doses determined and will include four 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 flip three mutated relapsed refractory AML and patients with flip three wild type relapsed refractory AML. The combo therapy study will start dose escalation at 200 milligrams BID and will include two cohorts, CA-4948 plus is azacitidine for patients with AML MDS who are naive to HMA and the second cohort of CA-4948 plus venetoclax for patients with AML or MDS, who are 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 be enrolling patients in these combo therapy cohorts in Q3. We may also explore a triple combination of all three drugs of CA-4948 plus azacitidine, plus venetoclax, but that would of course be dependent upon the initial safety and efficacy results from the two 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 2 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 for the disease complication. With its direct, non-myelosuppressive targeting of IRAK4 and its robust safety profile, we believe CA-4948 could potentially offer 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 1 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 six or seven evaluable patients treated with 300 milligrams of CA-4948 twice daily following a median of four 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 three plus three design, we'll see CA-4948 doses starting at 200 and then escalating to 300 milligrams BID. Ibrutinib dosing will be whatever is appropriate for the patient's respective NHL subtypes. We expect to provide an enrollment updates 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 we leave T-cell exhaustion such as anti-PD1 antibodies all have two key limitations. First T-cells stuck in a quiescent state cannot be acted upon by these checkpoint inhibitors; second myeloid derived suppressor cells or MDS sees actively impair the effectiveness of these checkpoint inhibitors. VISTA is a primary enforcer of T quiescence 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-PD1 antibodies. This is also a primary driver of MDS. 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-PD1 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 data later this year. To wrap up, I'd like to extend my utmost appreciation to the entire Curis teams, 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 the basic and diluted basis as compared to a net loss of $9.7 million for $0.28 per share on both the basic and diluted basis for the same period in 2020. Revenues for the first 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 of $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 Immunex related to CI-8993 that occurred during the first quarter of 2020. These costs were partially offset by $0.3 million increase in employee related costs. 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 costs for stock-based compensation, professional and consulting services, partially offset by lower legal costs during three 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. Please go ahead.

Just the first question, Jim, I should be thinking of the path forward to approval for monotherapy and combination therapy. Maybe perhaps you can discuss potential timelines to approval in AML and MDS? And what strategy either monotherapy or combo can get 4948 to the market sooner?

Thanks Ed, appreciate the thoughts on 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, we're confident now that the data continues to reinforce it. And that is, from initially expecting this was a combo therapy only drugs that we were going to have in a selected population of 50% of the population and the December data and of course now the ASH abstract data seems to support that this is more appropriate for all comers. So I think that's the primary end use. The other opportunity that was seen to that in December, and now we can see more clearly is there may also be a monotherapy path in selected population. And I think now we can say it looks like the spliceosome mutations population would be a good candidate for that. All three of the patients that have a spliceosome mutation in the study so far I've seen marrow CR betters. So obviously that given the genomic association, which it makes it for a very compelling monitor of the 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.

Thanks, Jim. 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 three plus three type of design. Fortunately, we were 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 starting to define the upper limits as well as Jim mentioned, we would likely tick within the range of somewhere in the 200 to 400 range for dosing. So the overall dose escalation for these trials, not likely to take too long.

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

First, could you guys elaborate on the steps needed to establish the recommended Phase 2 dose at lower than 500 milligrams BID in AML and 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 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 2 dose going forward in the near term.

Yes. I think, I would 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 study 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 treated that your headache, but really it is. So, we need to do a little bit of dose exploration at this point to try and figure out, which of these really is the best one to take in the Phase 2.

Got it. And one more question for me. I saw in the abstract that that most of the patients were transfusion dependent, which isn't that strange for higher 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 hold that thought for the more detailed discussion at EHA, but absolutely in MDS transfusion dependence is really important. In fact, a clinical end point for a study could be 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 that LUCAS IST that's being run in Europe. So hold that thought.

Our next question is from that Soumit Roy with JonesTrading. Please go ahead.

Hi, everyone. Congratulations again a very robust data. Just a couple of things and not sure how much color you can share with us. Any mutational status on this responders, if we should think they're mostly spliceosome mutants or it looks like both could be fit through you [indiscernible] or mutant? And the split between AML or MDS, how many from the AML cohort responders, how many from the MDS?

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. Any one sitting up 4948 plus aza in the [indiscernible] naive sitting. Should we think of as frontline patients being included whoever is not amenable to seven plus three treatment? And how would the physicians kind of think whether to put the patient on 4948 aza versus venetoclax plus aza in the elderly patients?

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

Yes, so absolutely, azacitidine maybe a viable treatment for first-line for patients. So this combination in first line is something that certainly can 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 factorespecially for frail elderly patients 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 triplet combination at some point in the future as well.

[Operator Instructions] The next question is from Alethia Young with Cantor Fitzgerald. Please go ahead.

Thanks for taking my question and congrats on the progress with the abstract. First, I am going to ask them one by one because I think they're all equally important. So, when you look at the six people you had to ASH like when we trace back now to how the CRs have deepened were those the people that had met CR that deepened or how should we think about who had the hematologic recovery? That's the first question.

Yes, we haven't gotten 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 that's an anti-cancer 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 the study in the market to come, but we're very encouraged by what we're seeing so far.

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

I think the hypothesis is that this drug directly targets the driver of disease IRAK4 or IRAK4-L and 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 or the driver of disease, you should see a reduction in cancer burden. And if the patient's marrow is healthy enough, obviously frontline patient's marrow is going to be much healthier than in late line. The marrow gets damaged over time, not just by the cancer, but frankly by the cytotoxic agents whether its 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 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 dose those CRs were achieved?

We will be showing that at the EHA conference.

Okay. I guess maybe this is more just on the toxin at the higher dose. Can you confirm that whether there're any new responses reported at the 500 milligram cohort? Any more toxicity I guess in way like -- you know what I am saying.

Yes, I know what you are saying. Obviously, I'm trying to balance the EHA role. So, 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 talks. And hard surprise, 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 MTD, and we're now going to try and figure out which of the dose is there a dose response, is 200, 300 better than 200, 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 1 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 division of seen three therapeutic doses and trying to evaluate, which of the three is the best one to take into Phase 2.

So when you think about the dose response curve here like the 300, 400, now the 500. There was a ramp the 300 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, you know, basically 500 starts to creep up or do you think there is more work to be done there?

I would say, we still have a pretty small number of patients I need to be fair. I think we're encouraged that across the board, all of the doses look to be effective, all the doses meaning 200, 300 and 400. 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 two. That's exactly why we've got to continue to dose exploration in the months to come and try to assess that out.

Okay. So when these two things with rabdo with the Grade 3, 1, was there any clinical symptom? I know with the other one, there was a syncope? But can you -- is the syncope related -- is it drug related? And like, if so, like, can you kind of explain what you think the mechanism of action is?

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

So generally, patients who experienced this will have some muscle soreness, maybe they'll notice a little bit of darkening of urine. In all 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 other patients, there have been other factors that may have also contributed to that, for example, heavy exercise or a pattern for example that may have been as a warning for rhabdomyolysis. So, those potentials that this drug pushed those patients to the point where they experienced and from that extent, we do feel that it is drug related but other potential factors.

The primary factor for us to Alethia in declaring 400 is our maximum tolerated dose and backing away from 500 was not the syncope, it was the rabdo because we were looking for it frankly after the NHL experience. We did expect to see it. We were pleased with 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 the CPK elevation that if you stay on the statin and add our drug, it might push it that much farther in the direction. Same thing with heavy exercise, if you have 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 two 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 dresses as well to see which dose is the best.

Okay. So, with the Grade 3 rabdo that you saw, did anyone have like kind of pattern exercise baseline things that would have done though?

Yes, bob.

Yes. So, the two of the patients on the lymphoma trials, we've mentioned previously, one of whom had the Grade 3 rhabdomyolysis was also on a statin and the other patients in that case actually felt quite a bit better after being on the study drug for a certain time, and went out and exercise heavily and then developed muscle soreness and symptoms after that. So, we think, so what we've advised going forward for the clinical trials for patients and investigators to discuss with their patients, if they are on a statin or they're necessary to continue that statin. And if they can come off that statin, they would suggest to do that and similarly to avoid extremely vigorous exercise while on the treatment. And we think that part of the reason why we didn't see this side effect until higher doses on the leukemia study.

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

Yes, bob.

Yes. So, we'll actually give the much more detailed description of the specific patients, but obviously we've treated those patients so far and we've seen achievement in marrow CRs in both groups of patients. But we'll have to see that the MDS population is the population where the spliceosome mutations are much more common and that we've announced as part of this presentation that the three patients who have spliceosome mutations all achieved a marrow CR are better.

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

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, Immunex and the NCI for their ongoing help and support. We look forward to updating all you again very soon at the EHA conference. Operator?

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