Curis Inc (CRIS) 2014 Q1 法說會逐字稿

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 developments 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 and our collaborator Genentech and Roche's expectations concerning the commercialization of and market opportunity for Erivedge in various territories and expected growth of Erivedge sales in 2014 and beyond, and our and our collaborator Debiopharm's 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 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 like 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 partnered programs, and then Mike Gray, our Chief Financial and Business Officer, will review our financial results for the first quarter 2014, following which we will open the call for any questions. During the Q&A period as a courtesy to those individuals seeking to ask questions, we ask that participants limit themselves to one or two questions. Dan?

Yes, 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 number one 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 drug 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 into 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 now like to ask Ali to provide an update and highlight our plans with CUDC-907 and 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 selectively inhibits two primary targets, HDAC enzymes as well as PI3 kinases, with selectivity against the alpha and delta isoforms of PI3 kinase. In preclinical in vivo studies, CUDC-907 has shown activity in xenograft lymphoma models, including and especially diffuse large B-cell lymphomas.

CUDC-907 is being evaluated in an ongoing Phase 1 dose escalation trial in patients with relapsed or refractory lymphomas or multiple myeloma. This first-in-human 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 the daily schedule.

We subsequently initiated testing of twice or three times weekly treatment schedules in parallel dose-escalating cohorts. The dose escalation is currently continuing with these intermittent schedules, with patient enrollment at the fastest possible rate at all three 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 the 120-mg dose level. A total of 29 patients have received CUDC-907 thus far, and we anticipate continued dose escalation to maximum tolerated dose likely at some point near the middle of this year.

After identifying the recommended dosing 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 diffuse 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 diffuse 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 treatment. At that conference we presented preliminary findings from the ongoing Phase 1 trial suggesting that CUDC-907 treatment was associated with changes in levels of certain cytokines, including CCL17, 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 culture tumor or supporting stromal cells within the tumor microenvironment. 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 predictive value, if any, as measures of CUDC-907's activity and their potential use in 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 their comprehensive response to the FDA that resulted in lifting 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 1 monotherapy trial.

As a reminder, we initiated a Phase 1 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 AST liver enzymes as well as [later] bilirubin levels that continued 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 this 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 trials as well as an amended protocol designed 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 the continuous dosing regimen. The study will initiate with a brief dose escalation from 100- to 300-mg CUDC-427 dose, and, based on pharmacodynamic, 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 this study continues to be evaluation of patient benefit following CUDC-427 monotherapy treatment. As before, 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 insights 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 1b portion of this study is expected to enroll and treat patients with differing chemotherapy agents in 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 two partnered programs, Erivedge and Debio 0932. Dan?

Yes, 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 and 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 BioPharma. 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-US sales, which exceeded the total of 2013 ex-US sales of $9 million, and that was for the entire year, and represented a 66% sequential increase when compared to the fourth quarter of 2013 ex-US net sales of $6.7 million. US 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 the US market was likely due to a combination of factors, including a sales force restructuring recently implemented by Genentech during the quarter for a more focused physician 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 US growth in 2014.

Just as a note, we've seen signs of strengthening US 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 the reconfiguring of the sales force.

In March Genentech also presented results of a Phase 2 trial of Erivedge in patients, approximately 75, with new nonrecurrent operable nodular 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 histological clearance of BCC lesions. While the data did not meet Roche-Genentech's target for percentage of patients to reach complete histological clearance in this study, we believe the data highlighted the importance of longer duration of treatment for improved outcomes and provided insights into intermittent dosing 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 2 clinical trial assessing the efficacy and safety of two different Erivedge regimens in approximately 200 patients with multiple BCCs. The anticipated time on study treatment in this trial is 72 weeks, and the primary endpoint is the relative percentage reduction from baseline in the number of clinically evident basal cell carcinomas at Week 73 with two 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. The 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 posttreatment. 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, (technical difficulty) continues to invest in exploring Erivedge in disease indications outside of BCC. During 2013, for instance, Roche initiated a Phase 1b/2 trial using Erivedge in patients with relapsed, refractory acute myeloid leukemia and high-risk myelodysplastic syndrome. We look forward to the results from this study and will 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 being investigated in cancers with strong scientific rationale and supporting preclinical data. Debiopharm expects to complete the Phase 1 portion of the ongoing Phase 1/2 HALO trial of Debio 0932 in non-small cell lung cancer patients and anticipates initiating a Phase 2 portion of the study during the second half of this year. Also as a reminder, we're entitled to the next milestone payment under our agreement with Debiopharm after the fifth patient is enrolled in the Phase 2 portion of the HALO study.

In the fourth quarter of 2013 Debiopharm also initiated a Phase 1 trial of Debio 0932 in combination with the mTOR inhibitor everolimus in patients with advanced or metastatic renal cell carcinoma, or RCC. We would be entitled to another milestone payment if Debiopharm initiates Phase 2 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'd like now to turn the call over to Mike for his discussion of our financial results.

All right, thanks, Dan.

For the quarter ended March 31, 2014, we reported a 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 to 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 -- 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 is our base case cash, which gets us to approximately mid-2016.

Importantly, this cash projection excludes potential future milestone or license payments from existing or 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 but would 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 that 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, and we'd like to now open the call for Q&A.

(Operator Instructions)

Brian Skorney.

Hey, good morning, guys. Thank you for taking my questions. 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 120-mg intermittent dose, and do you feel comfortable that you're getting above clinically meaningful thresholds here, given what you've seen for the IC50 and 90 levels, or do you think you would 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 to say you should really start seeing a meaningful effect?

Yes, 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 by saying that of course this CUDC-907 is a dual inhibitor of HDAC 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, as before we had not seen any evidence of drug accumulation or potential drug accumulation in animal models. However, of course, we saw that or a potential for that with humans on continuous dosing.

Having said that, one of the other things that I wanted to mention is that with the continued dose escalation we are seeing 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've tested, we certainly see equivalents in preclinical models as being active in our preclinical models, including the models that I described, the lymphoma models as well as the multiple myeloma models. And at those doses in the preclinical setting we've seen fairly robust inhibition of both targets or engagement of both targets, HDAC 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 HDAC activity as well as PI3 kinase.

So the sum of the answer to your question is that as we continue to dose escalate we are seeing continued exposure. We are seeing target engagement from the patient blood samples of HDAC and PI3 kinase. And also, as we mentioned, we are seeing a potential change in patients' 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, is 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 corollary that you pointed out with regards to the occurrence of side effects, we are 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 count, 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 engagement, as well.

The target suppression that I mentioned in the -- and the slide is available on the presentation on the website -- for the target modulation, that particular patient was actually treated at the 90-mg dose level, and, as I pointed out, at this stage we are in the 120-mg dose cohort for both the schedules at this point.

Great. And then just quick on 427, just to clarify, is the reinitiation of the Phase 1 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 to the ovarian and lymphoma cohorts, how is that gated?

Sure. Good question. It will be a sequential increase from 100 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 are 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 those would be separate cohorts of patients going forward.

Great. Thank you so much.

Joe Pantginis, ROTH Capital Partners.

Hey, guys. Good morning. Thanks for taking the question. 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 with the study now regarding this and their consistent interest in the drug, if you will?

Yes, thank you. [Obviously] we spent a good -- did a 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 chart a path 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 have 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 1 monotherapy trial, that those investigators have been very keen. Obviously we've worked with them on the Phase 1 trial previous to this. They've also been involved in the Genentech-sponsored study that was conducted.

And the reception that we are receiving with respect to CUDC-427 with regards to monotherapy, as well as our expectations of combining it with chemotherapy regimens has been very strong, and people understand it and do see the benefit of this drug and its potential 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's very helpful. Thank you. And then maybe just a little bit of follow-up on Erivedge. My question will be a little broad, but hopefully we can get a little more 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 dosing parameters, drug exposure, time on drug, etc. Can you just discuss that a little more?

Yes, I think the take-home message on the study, just to remind everyone again, it was never -- our view was that this was never intended as a registration path 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, Mohs surgeons, etc. 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 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 situations. So we think this still bodes well for expanding the market potential of the drug and market penetration.

Great. Thanks a lot, guys.

Brian Klein, Stifel.

Hi. Thank you for taking my questions. Just two quick ones. First on 427, Ali, you mentioned that you will be doing retrospective analyses 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 patient -- 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.

Great. Thanks. And then second question is regarding the potential Debiopharm milestone payments, Mike, could you just remind us what those two payments might be for starting the Phase 2 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.

Great. Thank you.

Chris Marai, Wedbush Securities.

Good morning, guys. Thanks for taking my questions. 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 genetic alterations such as translocations, I think the MALT lymphoma patient 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. Thanks.

Yes, thank you, Chris. It's a very good point that you make. Obviously, in the Phase 1 clinical study that Genentech sponsored there 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 cIAP gene 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 will include MALT lymphomas, as well.

Preclinically we have been continuing to study the role of IAP gene alterations. With respect to MALT lymphomas themselves, there are very few models available for testing that, so 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 the IAP genes 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 type 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 would look to present some of that data at upcoming scientific conferences, as well.

So we are very much focused on this, of course, Chris, and would like to see the potential use of it. No definitive data at this date.

The one thing that I think is important also to note is that CUDC-427 is fairly unique in this field of IAP antagonism in that we are able to administer CUDC-427 on a more sustained dosing schedule. At this point we would be going forward with a 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.

Great. Thank you. Appreciate that. One quick follow-up, if I may, with respect to new data and maybe a significant data update, when's the next time point you expect to update us on 427, the development path forward and 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 marker for us with regards 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 cohorts, 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 it's 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.

Great. Thanks for taking my questions.

Daniel Brims.

Hi. Thanks for taking my questions. Just a quick question on the two 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?

So, hi, this is Mani. In terms of the enrollment, there are two studies, one of which, 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 Erivedge in combination with Mohs surgery, that study started earlier this year. So it's hard for us to anticipate when exactly they will finish, but that's just to give you a timeline at this time (inaudible).

Okay. Thank you.

I'm not showing any further questions at this time. I'd 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 candidate 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 good day.