Curis Inc (CRIS) 2015 Q4 法說會逐字稿

Welcome to the fourth quarter Curis, Inc. earnings conference call.

(Operator Instructions)

I would now like to introduce your host for today's conference, Mani Mohindru, Senior Vice President of Corporate Strategy. Please go ahead.

Thank you, Christi. Good morning, everyone, and thank you for joining us.

During today's call, we will provide you with an update on corporate developments and plans and also discuss fourth quarter and full-year 2015 financial results.

Before we begin, I'd like to advise you that this conference call contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 including, without limitation, statements relating to our strategy, future operations, future financial position, future revenues, projected costs, prospects, plans and objectives of the management, the potential therapeutic benefits of our drug development program, and our plans to advance the development of drug candidates within these programs, as well as our expectations about Genentech and Roche's continuous development and commercialization of Erivedge.

Actual results may differ materially from those indicated by forward-looking statements in this conference call, as a result of various important factors, including those risk factors described in our quarterly report on Form 10-Q for the quarter ended September 30, 2015, and in other filings that we periodically make with the SEC.

And we encourage you to review these risk factors carefully. We caution you that forward-looking statements we make in this conference call only represent our views as of today, and that we may not update any of these statements, even if events and developments subsequent to the date of this call cause our estimates and expectations to change.

I would now like to introduce Ali Fattaey, our President and CEO, who will provide an update on the Company and our development programs. Following Ali's remarks, Mike Gray, our Chief Financial and Chief Business Officer will review our financial results for the fourth quarter and full-year 2015, after which, we will open the call for questions.

Ali?

Thank you Mani. And thank you to the conference call and webcast participants for joining us this morning.

We remain focused on building Curis by advancing our pipeline with the aim of eventual commercialization of innovative and effective drugs for the treatment of patients with cancer. We are pleased to have put our clinical-stage drug candidates CUDC-907 on a path to registration with the recent initiation of our Phase 2 clinical study in patients with MYC-altered relapsed/refractory diffuse large B-cell lymphoma or DLBCL. Also during the fourth quarter of 2015, in our collaboration with Aurigene, we in-licensed two drug candidates.

The first in the immuno-oncology field is an orally available small molecule antagonist of PD-L1 and VISTA checkpoint proteins, that we have named CA-170, and the second is a potent and selective inhibitor of the IRAK4 kinase which we have designated CA-4948. We expect to file IND applications and to advance both of these drug candidates into clinical development in 2016.

I will now provide additional details regarding these three programs today. I would like to begin with CUDC-907. As I mentioned, we recently initiated a Phase 2 trial to determine CUDC-907's efficacy in patients with relapsed/refractory DLBCL whose cancers harbor alterations in the MYC Oncogene.

The design in patient population of the Phase 2 trial was driven by the promising efficacy and safety data presented by our lead investigator, Dr. Anas Younes, from the Memorial Sloan Kettering Cancer Center at the American Society of Hematology's Annual Meeting held in early December last year. In this presentation, CUDC-907 was shown to be well-tolerated, with diarrhea, fatigue and non-symptomatic thrombocytopenia being the common adverse events of note. Dose limiting toxicities of Grade 3 diarrhea and Grade 3/4 hyperglycemia were only observed at the higher or more frequent doses and no dose limiting toxicities were observed with the 60-milligram dose that was given on the five days on, two days off schedule, which we determined to be the recommended Phase 2 dose and the regiment that is being used in the Phase 2 study.

On the efficacy front, 25 of the total 72 were patients with relapsed/refractory DLBCL and of these, 18 were evaluable for response assessment. Now, eight of these 18 patients achieved an objective response, including three patients with complete responses.

At the time of the presentation, all but one of these responses were still ongoing. A retrospective analysis of the molecular pathology of these patients showed that a majority of them -- responses were observed in patients whose DLBCL tumors harbored alterations in the MYC Oncogene, including tumors from all three complete responders that had an increase in MYC gene copy number.

We define MYC alteration as either a translocation of the MYC gene locus, an increase in MYC gene copy number or increase in MYC protein levels, all of which are well-accepted a criteria used in the field to assess MYC status and tumor samples. This potential correlation between clinical responses in patients and MYC alterations observed in the patient's tumor sample is consistent with our recent preclinical findings, where CUDC-907 treatment of DLBCL cell lines in culture can effectively and rapidly eliminate MYC protein levels in a dose-dependent manner at a very low nanomolar concentration.

The in vitro data are also consistent with antitumor activity of CUDC-907 that we observe in in vivo animal models of MYC-altered of DLBCL and in Birkett's lymphoma models. We expect that we will be presenting our preclinical findings at upcoming scientific conferences this year.

I also want to mention that, in addition to the data presented at ASH in late 2015, interim data from CUDC-907 Phase 1 trial were also presented earlier at the ASCO Annual Meeting earlier, at the European Hematology Association Annual Meeting, as well as at the International Congress on Malignant Lymphoma at the Lugano Conference earlier in 2015.

So based on the totality of the Phase 1 data, as well as our preclinical findings, we believe CUDC-907 is well-suited for further investigation in patients with MYC-altered DLBCL, a very aggressive disease with very poor prognosis and for which no approved or optimal treatment options exist. This also represents a sizable population with MYC gene alterations reported in up to 19% of DLBCL cases, and the increased MYC protein expression reported in up to one-third of all patients with DLBCL. There is some overlap between the genetic alterations and protein expression labels, of course.

In January of this year, we initiated the Phase 2 trial of CUDC-907 in patients with MYC-altered relapsed/refractory DLBCL disease. The trial is designed to evaluate the efficacy of CUDC-907 with or without rituximab. Patients with relapsed/refractory DLBCL with MYC alterations will be treated with either CUDC-907 or in combination with rituximab.

Both treatment groups are designed to enroll up to 60 patients each, with overall response rate being the primary endpoint and progression-free survival, overall survival, duration of response and safety being key secondary endpoints. The monotherapy arm is designed to assess the single-agent efficacy of CUDC-907, and if the data are consistent with our Phase 1 observations, there is potential to expand the monotherapy arm after discussion with the FDA in consideration for accelerated approval in this indication.

The rituximab combination arm is designed to inform a randomized trial of CUDC-907, which is expected as a combination treatment regiment, which will be supportive for full approval. We will provide further updates on the status of the Phase 2 trial over the course of this year.

In addition to the Phase 2 trial, we also have a Phase 1 trial ongoing in patients with solid tumors, including enrollment of patients with a rare tumor referred to as NUT midline carcinoma, or NMC, which is known to be a MYC-driven cancer. In preclinical models of NMC, as well as in models of other solid tumors with genetic alterations of MYC, CUDC-907 has shown significant antitumor activity.

We are also in discussions with clinical investigators to evaluate CUDC-907 in pediatric patients with MYC-altered cancers, such as neuroblastoma and medulloblastoma, both of which are known to be dependent on MYC alterations. These studies are possibly as investigator-sponsored trials.

I would now like to provide an update on CA-170, our orally bioavailable small molecule immune checkpoint antagonist drug candidate, than we in-licensed in October under our broad collaboration with Aurigene. CA-170 is a first-in-class oral small molecule that targets the two checkpoint regulators PD-L1 and VISTA.

CA-170 was selected as a development candidate based on its compelling in vitro and in vivo profile in preclinical studies, as well as its pharmacokinetic, pharmacodynamic and safety properties in vivo. All IND-enabling studies, including GLP toxicologies, have now been completed and we expect to file an IND and initiate the Phase 1 trial in advanced cancers within the first half of 2016.

Now, CA-170 targets PD ligands, as I mentioned, as well as VISTA, which are both members of the B7 superfamily of immune regulators and have some structural similarity in their extracellular domains. Within the tumor microenvironment, the PD ligands appear to be expressed predominantly on tumor cells whereas the VISTA expression is restricted mainly to cells of the hematopoietic origin, including cells of myeloid origin, such as myeloid origin, such as myeloid-derived suppressor cells within the tumor microenvironment.

Origen scientists have shown that CA-170 can selectively rescue T-cell proliferation and function that have been specifically inhibited by PD ligands or VISTA, but not inhibited by other checkpoint regulators such as TIM-3, CTLA-4, or others, suggesting the specificity of CA-170's mechanism of action. CA-170 is active in multiples syngeneic mouse tumor models, such as those with melanoma, colon and breast cancers, and including some models that are not responsive to anti-PD-1 treatment alone.

This is an agreement with what has been reported preclinically by others that PD and VISTA pathways are non-redundant, and that inhibition of both may synergize in mediating antitumor effects. As I mentioned earlier, all IND-enabling studies, including GLP toxicology with CA-170 have been completed now and we are pleased that thus far, CA-170 appears safe, with high therapeutic index in both rodents and primate safety models.

We expect to file the IND application and initiate a Phase 1 trial within the first half of 2016 and we expect to initiate the first in human trial with CA-170 in patients with advanced solid tumors, including those that are naive to immunotherapy, as well as patients that are refractory or have relapsed on anti-PD-1-based therapies.

In addition to CA-170, during the fourth quarter of 2015, we selected a second preclinical program within our immuno-oncology collaboration with Aurigene. This program is focused on evaluating small molecule antagonists that target PD-L1, and TIM-3 immune checkpoints.

TIM-3 is also an independent inhibitory checkpoint molecule that is generally co-expressed with PD-1 on highly exhausted cytotoxic T-cells in the tumor tissues, as well as being expressed on certain regulatory T-cells and plays an important role in immune suppression. The lead compounds within this program show potent and selective rescue of T-cell proliferation and function, that is induced by either PD-L1 or TIM-3, but not by other checkpoints, again, indicating its selective profile. We expect that our colleagues at Aurigene will pursue preclinical data from the CA-170 program, as well as the PD-L1 TIM-3 program at scientific conferences this year.

With regards to our other collaboration program with Aurigene, we in-licensed IRAK4 inhibitor in October of 2015, and have designated the development candidate as CA-4948. IRAK4 is a serine/threonine kinase that is important mediator of Toll-like receptor and IL-1 receptor signaling and plays an important role in innate immune signaling.

Based on its function in this pathway, IRAK4 has been a target of interest for a generation of drug candidates for a treatment of various inflammatory diseases. Additionally, in certain human hematologic malignancies, such a subset of diffuse large B-cell lymphomas, oncogenic mutations in this pathway have been identified that resulted in constitutive activation of IRAK4.

Now, preclinical data with CA-4948 and other program compounds show potent antitumor activity in cell base and in vivo tumor model assays, especially those tumor models that have activating mutations in the IRAK4 pathway. In addition to the cancer models, some of the compounds from this program also demonstrate activity in in vivo inflammatory disease models, indicating the potential of targeting IRAK4 in both oncology and inflammatory diseases with our compounds.

We expect that our colleagues at Aurigene will also make presentations on additional preclinical data from this program at upcoming scientific conferences this year. We continue to work with Aurigene to complete the IND-enabling studies for CA-4948 and expect to file an IND application for its clinical testing in heme malignancies in 2016.

We remain resolved to building the Company through advancement of our pipeline. In 2016, our focus will be on executing the progression of CUDC-907 through Phase 2 clinical testing in patients with MYC-altered relapsed/refractory DLBCL and its further testing in patients with solid tumors, including patients with NMC. We are committed to filing the IND for CA-170 to initiate its clinical testing of patients with advanced cancers, and we continue to work closely with our Aurigene colleagues to complete the IND-enabling studies for CA-4948 for its advancement into the clinic in 2016.

We also anticipate that the optimization work will continue to advance in order for us to select the development candidate from our PD-L1 TIM-3 checkpoint antagonist program, leading to the exercise of our option to license compounds from this program in the collaboration.

I would now like to turn to Erivedge, which is being developed and commercialized globally by Genentech and Roche under our collaboration. Roche continues to concentrate on the global commercialization of Erivedge for the treatment of advanced BCC in key territories worldwide.

We recorded royalty revenues of approximately $2 million for the fourth quarter this year, as compared to $1.9 million for the fourth quarter of 2014. For the full-year 2015, our Erivedge royalty revenues were $8 million, as compared to $6.8 million for the year, full year of 2014.

We are pleased to note that Roche continues to invest in Erivedge and has recently initiated two trials with Erivedge. One, in patients with intermediate or high-risk myelofibrosis, where Erivedge is being studied in combination with ruxolitinib, which is a JAK inhibitor, as well as a second study in idiopathic pulmonary fibrosis, or IPF, where Erivedge is being investigated in combination with pirfenidone, the standard of care with IPF.

I would now like to turn the call over to Mike Gray for his discussion of our financial results, after which, we will open the call to Q&A.

Okay. Thanks Ali.

For the year ended December 31, 2015, we reported a net loss of $59 million, or $0.48 per share -- per basic and fully diluted share, rather, as compared to a net loss of $18.7 million, or $0.22 per basic and fully diluted share in 2014. The 2015 net loss includes a one-time charge for in-process research and development expense of $24.3 million associated with our issuance of 17.1 million shares of Curis common stock to Aurigene under the terms of our January 2015 collaboration agreement.

For the fourth quarter of 2015, we reported a net loss of $13.5 million, or $0.10 per basic and fully diluted share, as compared to a net loss of $5.7 million, or $0.07 for basic and fully diluted share for the same period in 2014. The fourth quarter 2015 net loss includes $6 million in payments to Aurigene for our exercise of options to license the CA-170 and CA-4948 programs.

Revenues for the year ended December 31, 2015, were $7.9 million as compared to $9.8 million for the same period in 2014. Substantially, all of our revenues in 2015 and 2014 were reported under our collaboration with Genentech.

The decrease in revenue for the year ended December 31, 2015, is primarily due to a decrease in license fee revenues associated with the $3 million milestone payment that we earned during the year ended 2014. Revenues for the fourth quarters of 2015 and 2014 were $2.1 million and $2 million, respectively, and were comprised almost entirely of Erivedge royalty revenues.

Operating expenses were $64.4 million for the year ended December 31, 2015, as compared to $25.7 million for the same period in 2014. Operating expenses for the fourth quarter of 2015 were $15.3 million, as compared to $6.8 million for the fourth quarter of 2014. As noted earlier, we recorded a one-time charge in 2015 for in-process research and development expense of $24.3 million associated with the issuance of common stock to Aurigene.

Research and development expenses were $26.7 million for year ended December 31, 2015, as compared to $13.7 million for 2014. The increase was primarily due to increases in spending on our CUDC-907 clinical development program, as well as our programs under collaboration with Aurigene. These increases were partially offset by decreases in spending on our other programs, including CUDC-427.

R&D expenses were $12 million for the fourth quarter of 2015, as compared to $3.5 million for the same period 2014. We incurred $6 million in milestone payments under the Aurigene collaboration during the fourth quarter of 2015, in connection with our option exercises to license the CA-170 and CA-4948 programs.

G&A expenses were $12.9 million for the year ended December 31, 2015, as compared to $11.7 million in 2014, and were $3.2 million for each of the fourth quarters of 2015 and 2014. The increase in annual expense was primarily due to increased spending on legal costs, consulting and professional services, as well as stock-based compensation.

Other expense was $2.5 million for the year ended December 15 -- 2015, and $2.9 million for the year ended 2014. And is primarily comprised of interest expense associated with the loan made by BioPharma II to Curis Royalty, which is a wholly-owned subsidiary of Curis.

Other expenses of $215,000 for the fourth quarter of 2015, as compared to $878,000 for the fourth quarter of 2014. As of December 31, 2015, our cash, cash equivalents, marketable securities and investments totaled $82.2 million, and there were approximately 129 million shares of our common stock outstanding.

Turning to 2016 financial guidance, we expect to end 2016 with cash, cash equivalents and investments of between $27 million and $34 million, excluding any potential future payments from new or existing collaborators. We expect that 2016 R&D expense will be between $40 million and $45 million and the G&A expense will be between $12 million and $14 million. These expense expectations include approximately $1 million and $2.5 million of estimated 2016 stock-based compensation expense, and R&D and G&A expense, respectively, based on awards that are outstanding as of today.

With that, I will turn it back to Ali.

Thank you, Mike. Before we open up the call to questions, I would like to certainly, not least, but last, would like to thank Mike Gray and Jaye Viner, who, as you know, are all aware of are leaving the Company to pursue their other opportunities. We thank Mike, especially, for the many significant contribution that he has made during his tenure as a Chief Financial Officer and Chief Business Officer at Curis, and we wish him well in his future endeavors.

I would also like to thank Jaye for her contribution in building the clinical development organization and bringing the clinical expertise at Curis, as we prep ourselves for our expanding clinical pipeline. She was instrumental in taking CUDC-907 through the Phase 1 testing and determining the dose and path forward for the drug candidate in patients with diffuse large B-cell lymphoma. We wish Jaye well in her future path as well.

The Company has benefited greatly from both Mike and Jaye's experience and insights, and I join the Board and the employees of Curis in thanking them for the years of valuable service. I also want to take the opportunity to introduce David Tuck, our Senior Vice President of Clinical and Translational Sciences, who will be leading the clinical development activities at Curis. David has been with the Company since the first half of 2015 and brings a wealth of experience in the field of immuno-oncology and drug development, as well as biomarker development.

For example, during his tenure at Bristol-Myers Squibb, he was involved in the development of ipilimumab, as well as other immune checkpoint inhibitors' development. He has been an important addition to our team, and will be leading the clinical efforts at Curis.

I would now like to open the call to questions.

(Operator Instructions)

Our first question comes from the line of Adnan Butt, RBC Capital Markets. Your line is open.

Thanks and nice progress on multiple ends here. First on 907, in terms of taking the Phase 2 that's ongoing into a registration-enabling study, has -- what is the threshold that Curis is looking for, and then when would it hope to discuss those thresholds or the ability to do so with the regulators?

Thank you, Adnan, and thanks for the question. So far, as I indicated, let me just rehash just some of the Phase 2 design and the patient population and gives you a good sense of timing as well.

The patient population is literally the same population that we enrolled for the Phase 1 trial, so relapsed-refractory patients with diffuse large B-cell lymphoma with the exceptions that the Phase 2, we'll select patients based on their MYC alteration before treatment. We do intend to enroll up to 60 patients in the monotherapy arm of this study.

That's an open-label study, which means we will be able to view the data and we have certain look-in points that we have established for ourselves during the enrollment process. We expect the enrollment to take somewhere in the 12- to 15-month time frame for this study.

As I indicated, if the data, as we look forward, are consistent with what we've observed in the Phase 1 trial, meaning that similar levels of response rates, then we expect to discuss that with the FDA and ask for an expansion of this Phase 2 trial, the monotherapy arm to put the drug on registration path, again, using objective response rates as the primary endpoint.

Okay, Ali. Maybe I can ask one on CA-170. The therapeutic window appears pretty wide. So when would you expect to reach therapeutically relevant doses in the Phase 1? How quickly could you assess activity?

That's a good question. So we are -- feel quite comfortable that the drug is obviously safe in the models that we've observed. Again, this is consistent, both with other checkpoint inhibitors, antibodies that have gone into the clinic, and it's also consistent with the mechanism of relieving checkpoint inhibition in that it is these kinds of drugs are able to relieve repression of activated T-cells.

They're not really intended to activate T-cells. That's part of the reason that we think that we have such good therapeutic index, certainly with the oral small molecules as well.

Having said that, as we indicated, majority of our data in the in vivo activity models indicate that the drug is somewhere active in the 10 milligram per kilogram dose level, whereas in the safety models, we have taken the drug all the way up to a 1,000 milligram per kilogram per day administration and has remained safe.

This does allow us to initiate the Phase 1 trial at a comfortable dose, one that we think based on calculation, should result in repression of immune activation, but again, the first study in patients in the Phase 1 trial will be a dose escalation. We'll start at a healthy dose for the patients but we will see as we go; first, safety, first and foremost.

But as we escalate, we will do both evaluation of the biomarkers that we intend to look at, and, of course, any of the activity, clinical activity that may emerge of part of this study. So I couldn't exactly tell you, Adnan, which dose or which cohort we expect to see it. We're just feel as if that starting dose should be a good dose for the patients. We will look at safety first and expect to see both immune activation and, hopefully, benefit for the patients in clinical form as soon as well.

Ali, so in terms of updates, would we just hear that it's moving from cohort 1 to 2 to 3, or you would be able to update on activity at some point?

I think the latter, Adnan. I don't think this is the case where every dose cohort, we would make an announcement that we've gone to the next cohort. I think we -- the better thing for the shareholders and for the drug candidate is allow us to experience how to actually give the drug.

Our expectation is oral daily dosing and a continuous dose escalation but these things, yet, we have to go into the clinic first and get that experience before we come out and describe what types of activities and safety and everything else that we've seen. So I doubt that we will do this cohort by cohort.

Thanks and if you can just let me ask Mike a question since this is his farewell call. Hi, Mike. So does guidance assume exercise of any future programs from Aurigene [investments]?

Yes, the guidance assumes exercise of one future program in immuno-oncology, which is a $3 million option exercise in 2016.

Okay, thanks.

Thank you. Our next question is from the line of Joe Pantginis, ROTH Capital Partners.

Hi, guys. Good morning. Thanks for taking the question. Mike, good luck on your future plans as well. Ali, first, with regard to 1 -- I'm sorry, 907, you said Phase 2 status updates. Can you be a little more granular on that if you can, I mean, with regard to potential data updates at, say, major medical conferences?

We certainly -- I would say the ASH would be an ideal timing for us to present. The abstracts aren't due for a period of time. We certainly would like to update at the ASH Conference, anything that we observe noteworthy-wise for Phase 2. But certainly, we would be wanting to update on the finality of the Phase 1 trial.

There are still patients ongoing in the Phase 1 trial, in particular patients in the combination with rituximab expansion arm that is still ongoing. Likely, that we will present at ASH, again, not committing right now, just because the abstracts aren't quite due yet but certainly, ASH can be a conference for CUDC-907 for us.

That's helpful, thanks. If I can just focus one quick question and a little more broader question on the Aurigene collaboration. First on 4948, do you have specific plans yet or are you in wait-and-see mode with regard to moving into inflammatory indications?

Our expectations are and where we've been looking at this star candidate and they -- it has been in heme malignancies. Lymphomas are certainly an area, and B-cell malignancies, including DLBCLs are an area that we would like to look at as well as other heme malignancies but it will be predominantly heme malignancies that we will be looking at with CA-4948.

Sure, understood. I guess the broader question with regard to 170 or even just compounds coming from the program, as you look to -- a lot of your pre-activities before getting into the clinic and identifying sites and such activities, could you describe the type of feedback you've been getting from the sites with regard to the general views towards having an oral immuno-therapy compound, since all of the focus is on the biologics right now?

Yes, I can tell you that there is high interest, both in the concept of taking an oral small molecule from multiple centers that David has been in discussion with and investigators that would very much like to take this drug into the clinic for testing in their patients. There is also a level of excitement for taking a drug with this profile, target profile, in particular, for dual targeting of PD-L1, as well as VISTA.

Both of those seem to be very attractive for investigators. The fact that it's an oral inhibitor as well as the opportunity to target these particular checkpoints has been of excitement. David has been in discussion with multiple centers, several of which we will be entering and enrolling patients in the Phase 1 trial.

Thanks a lot, guys.

Thanks Joe.

Our next question is from Boris Peaker, Cowen.

Great. Thanks for taking my questions. So first, maybe on 907, do you have a sense of what -- or how frequently this alteration, MYC alteration has found? Have you done or do you explain -- plan to explore various tumor types to just kind of get a sense of the landscape?

Sure. As I mentioned, at least what is published in the literature with respect to MYC alterations in diffuse large B-cell lymphoma, which is a fairly common occurrence, up to 19% of patients has gene translocations of MYC. And roughly one-third or so of patients with diffuse large B-cell lymphoma have upregulation of the protein.

As I mentioned, there is an amount of overlap associated with that, meaning, many patients that have translocations have MYC protein upregulation. That's obviously the driver, the protein being the driver in this case. With regards to other malignancies, in solid tumors, we predominantly find gene amplifications, increasing copy number with respect to MYC.

is an interesting one, simply because that is where we find higher expression of MYC. In other solid tumor cancers, prevalence, higher prevalence of MYC translocations appear to occur in patients with triple negative breast cancer, for example. Subpopulations of patients with colorectal cancer and hepatocellular cancer.

And then as I mentioned, a few different pediatric cancers, and in particular, medulloblastomas that are driven by cemic amplifications, a high percentage of them, especially the poorest prognosis group, or the highest risk group.

And then a significant portion of patients, pediatric patients with neuroblastoma that are driven by NMYC amplification NMC. I hope that answers your questions. And the DLBCL, obviously, is where we have majority of our data and up to one-third of those patients are thought to be altered for MYC in one form or another.

Great. That answered the question. One of my other question is for Mike. On your last caller, I just want to get a sense of what's the timeline for paying off the Erivedge royalty debt?

2019 is what we're currently forecasting.

And the partnership will end --?

The composition matter IP goes to late 2020s, end of 2028. So there's a lot of royalty life after that debt is repaid.

Got you. All right. Well, thank you very much for taking my questions.

Thank you. That does conclude our Q&A session for today. I would now like to turn the call back over to management for any further remarks.

Thank you. Lastly, I would like to extend a thank you to all the employees of Curis for their hard work and bringing our programs to the state that they are in, and allowing us to progress the Company to one that is focused on developing effective drugs for patients with cancer, and our eventual goal of commercializing some of these drugs.

I would also like to thank all of the patients and their families who participate in our trials and make these studies and analyses possible. And lastly, again, I would like to thank all of the hard work that Mike and Jaye have done for the Company to bringing us to this stage as well. Thank you.

Ladies and gentlemen, thank you for your participation in today's conference. This does conclude today's program. You may all disconnect. Everyone have a great day.