Curis, Inc. (CRIS) Q1 2014 Earnings Report, Transcript and Summary

Good morning, ladies and gentlemen, and welcome to the Curis Conference Call to discuss the company's first quarter 2014 financial results and corporate update. [Operator Instructions] As a reminder, today's call will be recorded for replay purposes. I will now turn the call over to Mani Mohindru, Vice President of Investor Relations and Corporate Strategy.

Thank you. Good morning, and thank you for joining us. During today's call, we will provide you with an update on corporate plans and development and also discuss our first quarter financial results. Before we begin, I would 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 related to our strategy, future operations, future financial position, future revenues, projected costs, prospects, plans and objectives of management, the therapeutic benefit of and our plans to develop CUDC-907 and CUDC-427, our collaborated Genentech and Roche's expectations concerning the commercialization of and market opportunity for Erivedge in various territories and expected growth of Erivedge's sales in 2014 and beyond. And our collaborated Debio funds expectations regarding the clinical development of Debio 0932. 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 annual report on Form 10-K for the year ended December 31, 2013, and in other financial -- 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 we are making these forward-looking statements only as of today and that we may not update any of these statements even if the events and developments subsequent to the date of this call can cause these estimates and expectations to change. I would also like to mention that we have an updated presentation on our website that addresses some of the things we will discuss at our call today. I'd now look to introduce Dan Passeri, our Chief Executive Officer, who will provide an overall update and position of the company. Ali Fattaey, our President and Chief Operating Officer, will then follow with an update on our proprietary drug candidates, CUDC-907 and CUDC-427. Following Ali's remarks, Dan will provide an update on our partner's program, and then Mike Gray, our Chief Financial and Business Officer, will review our financial results for the first quarter 2014, following which we'll open the call for any questions. [Operator Instructions] Dan?

Thank you, Mani. Good morning, everyone. I'd like to begin the call by providing a brief overview of our perspective of Curis, and why we're confident that the company continues to be well positioned with very strong fundamentals. First, Curis is in a select group of biotech companies with an approved drug, Erivedge, which is being commercialized by the #1 global oncology company, Genentech Roche. Erivedge is expected to continue providing a healthy royalty-based revenue stream for the foreseeable future and should provide downside protection for shareholder investment. Second, we have a pipeline of proprietary growth candidates in early clinical development, each of which has the potential to provide significant value to our shareholders. Third, we have successfully built and developed a superb clinical team for furthering our capabilities and capacity to investigate the potential benefit of our drugs for our cancer patients. And finally, we're in a very solid cash position, enabling us to execute our plan well in the mid-2016, further allowing us to develop our proprietary pipeline to meaningful data points. Our focus will remain on developing our drug candidates further through clinical development for treatment of specific cancer patient populations. I'd like to ask Ali to provide an update and highlight our plans with CUDC-907 and CUDC-427. Ali?

Thank you, Dan. I'll start with a discussion of CUDC-907. CUDC-907 is a small molecule drug candidate, that by design, collectively inhibits 2 primary targets, HDAC enzyme as well as PI3 kinases with selectivity against the alpha and delta isoforms of PI3 kinase. In preclinical in vivo studies, CUDC-907 had shown activity in genograph lymphoma model, including and specially diffused large B-cell lymphomas. CUDC-907 is being evaluated in an ongoing Phase I dose escalation trial in patients with relapsed or refractory lymphomas or multiple myeloma. This first inhuman trial was initiated in January last year, and patients were initially treated using a continuous dosing schedule. The long plasma half-life and apparent drug accumulation, coupled with common occurrence of the mechanism-based side effects of thrombocytopenia, diarrhea and fatigue, led to early identification of the maximum tolerated dose for their daily schedule. We subsequently initiated testing of twice or 3 times weekly treatment schedules in parallel with those escalating cohorts. The dose escalation is currently continuing with these intermittent schedules with patient enrollments at the fastest possible rate at all 3 study sites. Thus far, no-dose limiting toxicities or consistent side effect pattern has been observed with either of the intermittent dosing schedules, both of which are currently at 120 mg dose level. A total of 29 patients have received CUDC-907 thus far, and we anticipate a continued dose escalation to maximum tolerated dose, likely at some point near the middle of this year. After identifying the recommended dose and schedule, we plan to open the expansion phase of this study in the second half of this year, which will test CUDC-907 in patients with select hematologic malignancy, likely to include diffused large B-cell lymphoma and multiple myeloma patients, as well as patients with other lymphoma subtypes as merited by the data. For clarity, an expansion cohort will enroll up to 12 patients of a particular cancer type, such as diffused large B-cell lymphoma and treat those patients with CUDC-907 at the recommended dose. In addition to our investigation of CUDC-907 in hematologic indications, we also expect to evaluate CUDC-907 in patients with certain solid cancers. We expect to provide additional details regarding this trial as we get closer to the time of initiation. At the AACR annual meeting last month, we presented ancillary data that may also provide insights into the mechanism of CUDC-907 action, and as well as patient stratification strategies for treatments. At that conference, we presented preliminary findings from the ongoing Phase I trial, suggesting that CUDC-907 treatment was associated with changes in levels of certain cytokines, including CCL 17 or TARC, which is a chemokine involved in the stimulation and proliferation of T cells required for the survival of certain malignant blood cells. These findings are consistent with our preclinical studies, demonstrating the effect of CUDC-907 on cytokine production in cultured tumor or supporting stromal cells within the tumor micro environment. From analysis of patient plasma cytokine levels, correlative trends were noted between pre- as well as posttreatment plasma TARC levels as measured on Day 15 of treatment with CUDC-907 and the degree of tumor shrinkage experienced by patients. Plasma cytokine and chemokine levels including TARC and a number of other factors are being explored to determine their biomarker and predicted value, if any, as measures of CUDC-907 patient stratification strategies. I will now provide an update on CUDC-427, our oral small molecule Smac mimetic that is designed to promote cancer cell death by antagonizing IAP proteins. First, I would like to begin by thanking our internal team for the comprehensive response to the FDA that resulted in listing of the partial clinical hold without any further requirements by the agency. The team is now fully focused on reinitiation of patient enrollment in the Phase I monotherapy trial. As a reminder, we initiated a Phase I trial of CUDC-427 monotherapy last year. This trial was designed to expand upon promising findings from the Genentech-sponsored first-in-human trial that was conducted in 42 subjects with refractory solid tumors or lymphomas, the results of which were presented during an oral session at the ASCO annual conference last year. During the course of treatment, on our trial, one patient experienced grade 3 elevations in ALT and ASP liver enzyme, as was later bilirubin levels that continue to rise despite discontinuation of CUDC-427 and progressed to liver failure. After rapidly reporting the event to the FDA in November last year, the trial was placed on a partial clinical hold where no new patients could be enrolled into the study. In March of this year, the FDA removed the partial clinical hold after reviewing our complete response data package that included FDA-requested information regarding the patient's case, a thorough safety analysis for all 51 patients treated with CUDC-427 on the Genentech and Curis' sponsored trial as well as an amended protocol design to mitigate risk of liver injury for patients to be treated with CUDC-427. Importantly, the FDA reviewers requested no additional information or changes to the complete response or the amended protocol that we proposed. We are now poised to reinitiate the CUDC-427 monotherapy trial and will use the 14 days on, 7 days off dosing schedule tested previously rather than continuous dosing regimen. The study will initiate with a brief dose escalation from 100 to 300 miligram CUDC-427 dose. And based on pharmacy dynamic, clinical benefit and safety data, we believe that this dose range represents active and safe levels of single agent CUDC-427 for patient treatment. The protocol has also integrated more stringent patient monitoring and avoidance of certain concomitant medications as further safety parameters. Beyond the brief dose escalation and safety assessment, the aim of the study continues to be evaluation of patient benefits following CUDC-427 monotherapy treatment. As we move forward, the study will predominantly enroll patients with ovarian cancer, and we also plan to expand and enroll patients with certain types of lymphomas including MALT lymphomas. We also intend to genetically type patients' tumors and retrospectively determine whether IAP pathway or other genetic alterations may provide insight into patient stratification strategies for CUDC-427 monotherapy treatment. Beyond monotherapy, we remain on track to initiate a separate trial treating patients with CUDC-427 in combination with standard-of-care chemotherapy treatment, including capecitabine and taxanes later this year. The Phase Ib portion of this study is expected to enroll and treat patients with different chemotherapy agents and parallel cohorts, and we expect to provide additional details regarding this trial closer to the start date. I will now turn to Dan to briefly discuss our 2 partner programs, Erivedge and Debio 0932. Dan?

Thanks, Ali. I'd like to first provide an overview of Erivedge, which is being developed and commercialized globally by our partners Genentech and Roche under our collaboration. Roche continues to focus its efforts on global commercialization of Erivedge after successfully securing marketing approvals for Erivedge in over 40 countries, including key territories worldwide such as the United States, Australia and a conditional approval in the European Union among others. In addition, Roche is continuing to pursue marketing approvals in many other countries with several submissions currently under review, and several others planned for 2014. As a reminder, Curis is entitled to royalty payments on worldwide net sales of Erivedge, subject to loan repayment obligations to biopharm. Outside of the basal cell carcinoma indication, we're also entitled to certain development and regulatory milestones. During the first quarter of 2014, Roche reported Erivedge worldwide net sales of approximately $27 million, including approximately $11.1 million in ex-U.S. sales, which exceeded the total of 2013 ex-U.S. sales of $9 million, that was for the entire year, and represented a 66% sequential increase when compared to fourth quarter of 2013 ex-U.S. net sales of $6.7 million. U.S. net sales were $15.3 million for the first quarter. That represented a decline of $6.2 million from the fourth quarter of 2013. According to Roche, however, this difference in U.S. market was likely due to a combination of factors including the sales force restructuring, recently implemented by Genentech during the quarter for a more focused position targeting as well as potentially some inventory drawdown prior to an Erivedge price increase in February. We anticipate that Genentech and Roche's net sales of Erivedge and consequently our royalty revenue should continue to grow in 2014, assuming successful reimbursement and commercialization of Erivedge in territories worldwide and an expected return to continued U.S. growth in 2014. Just as a note, we've seen signs of strength in the U.S.'s prescription data in recent weeks, which we believe support our perspective of continued growth. I think also -- it also supports Genentech's premise that it's possibly due to reconfiguring of the sales force. In March, Genentech also presented results of Phase II trial of Erivedge in patients, approximately 75 with new nonrecurrent operable nodule BCC, which is a less severe form of the disease at the American Association of Dermatology Conference. The primary endpoint of this trial was complete physiological clearance of BCC lesions. While the data did not meet Roche and Genentech's target for a percentage of patients to reach complete histological clearance in the study, we believe the data highlighted the importance of longer duration of treatment for improved outcomes and provided insights into intermittent investing schedules in the operable BCC setting. As we have mentioned previously, this trial was not intended for registration purposes and represented the means to assess the role of Erivedge in less severe forms of BCC. We are encouraged that Roche is continuing to examine Erivedge in less severe forms of BCC, including an ongoing randomized double-blind regimen-controlled Phase II clinical trial, assessing the efficacy and safety of 2 different Erivedge regimens in approximately 200 patients with multiple BCCs. The anticipated time on study treatment in this trial is 72 weeks in the primary endpoint as the relative percent -- percentage reduction from baseline and the number of clinically-evident basal cell carcinomas at week 73 with 2 regimens. Roche is also conducting a randomized double-blind placebo-controlled trial to assess the efficacy and safety of Erivedge with surgery in approximately 75 patients with BCC. Anticipated time on drug treatment in this study is 12 weeks and the primary outcome is the percent change in the target surgical defect area post treatment. Similar to Genentech's prior study in operable BCC, these studies are not intended for registration, but we believe that they are important for building additional information and insight for the potential use of Erivedge in various BCC settings. Lastly, continues to invest in exploring Erivedge in disease indications outside of BCC. During 2013, for instance, Roche initiated a Phase Ib/II trial using Erivedge in patients with relapsed refractory, acute myeloid leukemia and high-risk myelodysplastic syndrome. We look forward to the results from the study and we'll update you accordingly. Now turning to Debio 0932. We're impressed with our partner Debiopharm's commitment in investigating Debio 0932, which, as a reminder, is a second generation non-geldanamycin oral Hsp90 inhibitor and that's been investigated in cancers with strong scientific rationale and supporting preclinical data. Debiopharm expects to complete the Phase I portion of the ongoing Phase I/II HALO trial of Debio 0932 in non-small cell lung cancer patients and anticipates initiating a Phase II portion of the study during the second half of this year. So as a reminder, we are entitled to the next milestone payment under our agreement with Debiopharm, after the fifth patient is enrolled in the Phase II portion of the HALO study. In the fourth quarter of 2013, Debiopharm also initiated a Phase I trial of Debio 0932 in combination with the mTOR inhibitor aromas in patients with advanced or metastatic renal cell carcinoma or RCC. We would be entitled to another milestone payment if Debiopharm initiates Phase II testing in the renal cell carcinoma indication. We continue to believe that our wholly-owned and partnered programs hold significant promise for the treatment of cancer patients and we look forward to providing updates on all of these programs in 2014. I would like now to turn the call over to Mike for his discussion of our financial results.

Thanks, Dan. For the quarter ended March 31, 2014, we recorded a quarter net loss of $5.6 million or $0.06 per share on both a basic and fully diluted basis, as compared to a net loss of $5 million or $0.06 per share on both a basic and fully diluted basis for the same period in 2013. Revenues for the first quarter of 2014 were $1.3 million, up from $900,000 for the same period in 2013, primarily due an increase in royalties received from Genentech and Roche's net sales of Erivedge during the quarter. Operating expenses for the first quarter of 2014 were $6 million, versus $5.2 million for the same period in 2013. Research and development expenses of $3.1 million for the first quarter of 2014 were up from $2.6 million in the first quarter of 2013, mainly due to our increased spending on CUDC-907 and CUDC-427. General and administrative expenses were $2.8 million for the first quarter of 2014, as compared to $2.6 million for Q1 2013. Other expense was $800,000 for the first quarter of 2014, as compared to $600,000 for the same period in 2013, and comprised primarily of $950,000 in interest expense in each quarterly period related to Erivedge -- of the Erivedge secured loan made by BioPharma II to Curis royalty. As of March 31, 2014, our cash, cash equivalents, marketable securities and investments totaled $63.8 million, and we had approximately 85.9 million shares of common stock outstanding. Lastly, just on the financial guidance for 2014, we expect to end 2014 with cash, cash equivalents, marketable securities and investments of between $41 million to $46 million. This was our base case cash, which gets us to approximately mid-2016. Importantly, this cash projection excludes potential future milestone and licensed payments from existing and new collaborators. This also excludes any royalty revenues in 2014 related to net sales of Erivedge. Curis royalty is required to pay BioPharma II up to $2 million per quarter of the royalty revenues that it receives from Genentech in 2014 under the terms of the Erivedge royalty secured debt transaction that will retain royalty revenues that exceed this amount, if any, for use in funding our operations. Lastly, we expect that 2014 R&D expenses will be between $16 million and $19 million, and the G&A expense will be between $11 million and $13 million. These expense -- expectations include approximately $800,000 and $2.4 million of estimated 2014 stock-based compensation expense for R&D and G&A, respectively. So that concludes our prepared remarks, we'd like to now open the call for Q&A.

[Operator Instructions] Our first question comes from the line of Brian Skorney. Brian P. Skorney - Robert W. Baird & Co. Incorporated, Research Division: I guess first to start off on 907, can you review the PK, PD and just give us your thoughts on what level of target inhibition you're likely getting at the 120mg intermittent dose and do you feel comfortable that you're getting above clinically meaningful thresholds here given what you've seen through the IC50 and 90 levels, or do you think you -- what ideally need to step up, or I guess where -- given no dose-related side effects, where would you really be comfortable at a dosing level, say, you should really start seeing a meaningful effect?

Thank you, Brian, this is Ali. And before I get there, first, I would like to thank our employees, our directors, investors and partners, of course, for their continued support. And we look forward to providing you all with further updates on the progress over the coming months, as well, of course. Related to your specific question, let me start it by saying that, of course, this CUDC-907 is a dual inhibitor of HVAC and PI3 kinases. So we can try and model some of the related PK, PD questions as you're describing in preclinical models -- based on preclinical model studies, however, as we've noted, the resident time or half-life of the drug in patients or in humans is relatively different than what we had seen. In animals, either mice, rats or dogs, before we had not seen any evidence of drug accumulation or potential drug accumulation in animal models, however, of course we saw that, our potential for that with humans on continuous dose. Having said that, one of the other things I wanted to mention is that with this continued dose escalation, we are seeing an increasing exposure for the drug in patients with the dose escalation going forward. The doses that we're currently at within the range that we tested, we certainly see equivalents in preclinical models as being, a, active in our preclinical model, including the model that I described, the lymphoma models as well as the multiple myeloma models. And at those doses in the preclinical settings, we've seen fairly robust inhibition of both targets or engagement of both targets at HVAC as well as PI3 kinase. We also presented some of this data, and that's in our current updated slide presentation, as Mani mentioned, on the website, demonstrating that, in patient samples and from their peripheral blood mononuclear cells, we are seeing target engagement both for the HVAC activity as well as PI3 kinase. So some of these -- the answer to your question is that, as we continued to dose escalate, we are seeing continued exposure. We are seeing target engagements on the patient blood samples of HVAC and PI3 kinase and also as we mentioned, we are seeing a potential change in patient's plasma levels of certain cytokines and chemokines. One that we looked at, of course, was TARC. The question of what dose do we need to get to in order to see activity is a very difficult one. Part of that is again, because it's a dual active agent and it's very difficult to model it against one or the other activity in this regard. The other correlated that you pointed out with regards to the occurrence of side effect, we're just not seeing any common side effects occurring at this point. We are, of course, continuing to track the mechanism-based side effects very closely during the dose escalation as I mentioned, including platelet counts, the occurrence of any diarrhea or any fatigue, and at this point, it seems as if the intermittent dosing schedules are alleviating some of those side effects while we are getting target engagements as well. The target suppression that I mentioned in the slide is available on the presentation on the website. For the target modulation, that particular in patient was actually treated at the 90-milligram dose level, and as I pointed out, at this stage, we're in the 120 milligram dose cohorts for both the schedules at this point. Brian P. Skorney - Robert W. Baird & Co. Incorporated, Research Division: And then, just on 427, just to clarify, is the reinitiation of the Phase I dose escalation, is that a sequential study from 100 mg to 300 mg or is that going to be simultaneous enrollment, and how is the expansion of the ovarian and lymphoma cohorts, how is that gated?

A good question. It would be a sequential increase from 100 mg to 300 mg dose level. That's the expectation for the beginning part of the monotherapy study. And with regards to both the types of patients that we're expecting to enroll in the dose escalation, as well as potential expansion into those patients, very similar. Our expectation is that ovarian and lymphoma patients will be predominantly enrolled even within the dose escalation portion of this. And then with regards to expansion, we would expect to treat patients at dose, and the expectation is that the dose would be separate cohorts of patients going forward.

Our next question comes from the line of Joe Pantginis from Roth Capital Partners.

Maybe I'll just start off on 427 as well. Just wanted to get a sense of -- during the clinical hold, the partial clinical hold, I'm sorry and the subsequent removal of this partial hold, what has been some of the feedback, whether it's KOLs or physicians involved in the study now regarding this and their consistent interest in the drug if you will?

Thank you. In reality, we spent a good -- very good analysis in terms of an assessment of CUDC-427 safety profile and analysis of the individual patient's case that had the liver enzyme elevations and liver failure. And, of course, the PK, PD and clinical benefit associated with it. I think that analysis, both, obviously helped us to try to fast forward for the drug internally. It addressed the questions that the FDA had. But I think, that same analysis has also obviously helped the investigators who've been involved with it with CUDC-427, understand the drug better and appreciate the benefit and the safety profile associated with it. I can say that the investigators that are currently beginning to do the Phase I monotherapy trial, those investigators have been very keen. Obviously, we've worked with them on the Phase I trial previous to this. They've also been involved in the Genentech's conference study that was conducted. And the reception that we are receiving with respect to CUDC-427, which is actually monotherapy, as well as our expectations of combining it with chemotherapy regimen, has been very strong, and people understand it, and do see the benefit of this drug and its potentially use, so we're very much poised for starting the monotherapy and testing the patients as we mentioned in the monotherapy ovarian, as well as an interest in the lymphoma setting as we pointed out. So that expanded interest continues to be there for CUDC-427.

That was very helpful. And then, maybe just a little bit of follow-up on Erivedge. My question will be a little broad, but hopefully, it kicks a little more of color. With the operable study that did not meet, I guess, you would call it, the Genentech-defined endpoints or hurdles for success. Could you add a little more color with regard to was this more of just dosing parameters? I know you touched on a little bit, Dan, as well, but just dosing parameters, drug exposure, time on drug, et cetera. If you'll just discuss that a little more?

Yes, I think that the take-on message on the study, just to remind everyone again, it was never -- our view was that this was never intended as a registration path external trial. It was a survey to gain insight on the best utility of the drug, how to maximize benefit to patients and educate physicians, the end users, dermatologists, most surgeons, et cetera. I think the positive metrics that came out of that study was that, by increased duration of exposure to the drug, you can enhance the therapeutic benefit. The criteria that were used for internal purposes at Genentech-Roche had to do with whether or not operable would be pursued per se as an indication. And those -- as you can imagine, those thresholds would be very high based on the success of surgery. So overall, we've felt the study continues to add support to the promise of this drug for benefiting BCC patients, particularly those where surgery is not amenable, maybe even classified as operable, but very complex situation. So we think this still bodes well for expanding the market potential of the drug and market penetration.

Our next question comes from the line of Brian Klein from Stifel.wit Brian Klein - Stifel, Nicolaus & Company, Incorporated, Research Division: Just 2 quick ones. First on 427. Ali, you mentioned that you will be doing retrospective analysis to determine whether IUP -- IAP, excuse me, would be a reasonable target for patients. Are there any biomarkers that you could utilize on a prospective basis that you've already identified to help guide treatment?

There are no genetic prospective markers that we can use for patient inclusion, enrollment of the patients. We had extensively looked at patients various cytokine levels as had Genentech in the past. And at the moment, those do not reach the threshold of prospective analysis. So everything at this point will be retrospective. Brian Klein - Stifel, Nicolaus & Company, Incorporated, Research Division: Great. And then second question is regarding the potential Debiopharm milestone payments. Mike, could you just remind us what those 2 payments might be for starting the Phase II non-small cell lung cancer trial and then starting the second study?

Yes, they're both mid-single million dollar payments. That's about the best I can give you.

Our next question comes from the line of Chris Marai from Wedbush Securities.

It looks like you've presented some strong evidence of mechanistic efficacy with respect to inhibition of IAPs for 427, and I was just wondering, we saw some early evidence of activity against specific generic alterations, such as translocations, I think the MALT lymphoma patients looked particularly encouraging. I was wondering where you guys are in progress at looking at that and the potential mechanism and opportunity for 427 in genetically defined populations?

Thank you, Chris. The bigger point you make, obviously in the Phase I clinical study that Genentech sponsored was one patient, one MALT lymphoma patient that had a complete response, an unconfirmed complete response. That individual patient was later shown to have an amplification of the ICI APG, which we think may have contributed obviously to -- or that had the potential of contributing to the benefit that, that patient saw, which is part of the reason that with the monotherapy trial that's about to begin, we will not only enroll ovarian cancer patients, which was the initial focus of this study, but include lymphoma patients, which you will include MALT lymphomas as well. Preclinically, we have been continuing to study the role of IPG in alterations with respect to MALT lymphomas themselves. There are very few models available for testing that makes it slightly difficult, but we are going at generating preclinical studies that can address genetic alterations and whether they represent a potential path for monotherapy treatment of this. We also, of course, look at not only just IPG themselves, but other IAP pathway components. We've looked at that in databases that are available -- publicly available to look at the occurrence or the incidence of various IAPs or IAP pathway components. Certain cancer types seem to have a potential for higher prevalence of that. Some of the ovarian cancers are included in that and that's part of the reason we want to make sure that we genetically hype all of these patients for any apoptosis-related gene and IAP pathway components to see whether that can correlate or provide insights into parameters of sensitivity. I should point out that we've also been doing preclinical studies. The team has been doing an excellent job on that, of looking at gene expression profile analysis, and whether those gene sets, or that we can identify gene sets from expression profile side that can be used as signatures for prediction of sensitivity. Those, at this point, are not mature enough for presentation, but certainly we'd look to present some of that data at upcoming scientific conferences as well. So we're very much focused on this, of course, Chris, and would like to see the potential use of this. No definitive data at this stage. The one thing that I think is important also to note is that CUDC-427 is fairly unique in this field of IAT antagonism in that we were able to administer CUDC-427 on a more sustained dosing schedule. At this point, we would be going forward with the 14 days on, 7 days off treatment, whereas the majority of other IAP antagonists in development are being delivered on a once-weekly basis. We certainly think that sets CUDC-427 up better for being able to be administered as a monotherapy and potentially engage the targets should the genetic alterations be a sensitivity marker for that.

One quick follow-up if I may. With respect to new data, and maybe a significantly data update, when's the next time point you expect to update us on 427, the development path forward, maybe some data? It looks like ASH might make some sense, or is that really going to be more focused on 907?

I think ASH is a good market for us with regard to CUDC-907. I think we would expect to present some data at ASH, including data from the dose escalation part, and if any, may be merited from the expansion cohort if they're available. So ASH is a better marker for that. CUDC-427 wise, obviously we're looking at initiating the trials now, the monotherapy, as well as parallel initiation of the combination treatment regimen study in a separate trial. I think we will do our best to provide any data when if merited with regards to CUDC-427. I don't think we can use ASH as a marker at this point, but we would certainly look for any opportunity to present updates on the data as well.

Our next question comes from the line of Daniel Brims.

Just a quick question on the 2 new BCC studies that Roche is initiating. Have those -- when are those expected to start enrolling, and have -- has there been any estimate of when completion might be for those studies?

This is Mani. In terms of the enrollment, there are 2 studies, one of which is the multiple BCC study, started enrollment last year, I think somewhere around the second quarter of last year. And the other study, which looks at average in combination with most surgery, that study started earlier this year. So it's hard for us to anticipate when exactly they will finish, that's just to give you a timeline at this time [indiscernible].

I'm not showing any further questions at this time. I would now like to turn the call back to Ali Fattaey for further remarks.

Yes. Thank you again for everyone being present on the call, and appreciate your questions. I would like to reiterate that we would like to thank our employees, directors and investors, and partners for their continued support, and of course, we look forward to providing you with further updates on our progress with our proprietary drug candidates, and any from our partner programs that may be upcoming in the following months. Thank you very much.

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