Ali Fattaey - President and Chief Executive Officer James Dentzer - Chief Financial and Chief Administrative Officer.

Peter Lawson - SunTrust Robinson and Humphrey Brian Skorney - Robert Baird Chris Shibutani - Cowen Adnan Butt - RBC Capital Markets Rahul Jasuja - FBR Company.

Good day ladies and gentlemen, and welcome to the Curis, Inc. Q4 2016 Earnings Conference Call. At this time all participants are in a listen-only mode. Later, we will conduct a question-and-answer session and instructions will follow at that time.

[Operator Instructions] I would now like to turn the call over to James Dentzer, Chief Financial and Chief Administrative Officer. Sir you may begin..

Thank you, operator, and welcome to Curis' fourth quarter and full year 2016 earnings call. Before we begin, I would like to encourage everyone to go to the Investors Section of curis.com to find our earnings press release and related financial tables.

I would also like to remind everyone that we will be making forward-looking statements, which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties and our actual results may differ materially. I encourage you to consult our SEC filings for additional detail.

Now I will turn the call over to our President and CEO, Dr. Ali Fattaey.

Ali?.

Thank you, Jim. Good morning everyone, and thank you for joining us today. I'd like to start today with providing a brief overview and also contexts for our progress from last year into 2017 and I'll also describe our expectations for this year.

Our business plan calls for Curis to have multiple oncology drug candidates that we develop and that we expect to commercialize in certain territories should they be approved. Our pipeline currently includes four drug candidates, two of which are in clinical development, and two in pre-IND state.

In 2016, we initiated a Phase 2 trial for our clinical candidates CUDC-907, the results of which if successful should play CUDC-907 on a path for potential accelerated approval with the FDA. We also advanced our second drug candidate CA-170 into Phase 1 clinical testing.

Furthermore we initiated IND enabling studies for our two non-clinical candidates CA-327 and CA-4948. Now in 2017 we expect the initial readouts from the clinical trials of CUDC-907 and CA-170 these data should serve as proof-of-concept to demonstrate that each can be an active drug for treatment of patients with certain cancers.

We also expect to file IND for and began to examine CA-327 and CA-4948 in patients with advanced cancers this year. Before I began with the status update for each of these programs, I’d like to note the press release from this morning regarding our recent financing transaction that is secured with Erivedge royalty.

As indicated, we worked with HealthCare Royalty Partners on a $45 million non-recourse loan to Curis that will be repaid with Erivedge royalty payments that we received from Genentech. As I just described, we do have an ambitious year ahead of us with expectation of four programs in clinical development.

The capital proceeds from this facility allow us to not only expand the development of our current clinical candidates CUDC-907 and CA-170, but to also bring CA-327 and CA-4948 into the clinic as expeditiously as possible this year.

We expect that with the existing capital and this facility our cash runway will be extended significantly beyond the initial data readouts for CUDC-907 and CA-170 clinical trials and well into the first half of 2018. It is now my pleasure to provide an update on the status of each of our drug candidate programs.

I would like to begin with CA-170 the first orally administered small molecule checkpoint antagonist to go into the clinic from our collaboration with Aurigene. CA-170 targets the PD Ligands and VISTA inhibitory immune checkpoints.

Patient dosing in the Phase 1 trial of CA-170 began in June of 2016 with a fixed 50 milligrams starting dose using a once daily continuous administration schedule. By the end of 2016, we completed enrollment in the fourth escalating dose cohort of 400 milligram daily dose.

We are currently enrolling patients in the sixth cohort of 800 milligram daily dose. Dose escalation has progressed on track through these levels dose levels with no limiting safety events thus far. All patients have thus far been enrolled in the U.S.

and have either had prior treatment with immunotherapy or have cancers that are not yet indicated for such treatments. We presented preliminary pharmacokinetic or PK and pharmacodynamic or PD data from patients treated in the initial four dose cohorts at the Society for Immunotherapy of Cancer or SITC Annual Conference in November of 2016.

Analysis of clinical plasma PK indicated that similar to non-clinical observations CA-170 is readily absorbed on oral dosing in men has a linear and dose proportional increase in exposure as determined by Cmax and AUC measurements it has a 10 to 12 hour half-life in men, and does not appear to accumulate after multiple dosing.

Significant patient exposure was also observed at the starting 50 milligram daily dose and it reached similar Cmax and AUC levels as what we observed in non-clinical active dose of 10 milligram per kilogram that was used in mouse tumor model studies.

During that presentation evaluation of patient whole blood samples had pre and post CA-170 oral dosing at doses examined thus far have also demonstrated a several fold increase in the circulating population of activated T-cells after CA-170 dosing.

These CD8+ sides of toxic T-cells express markers of activation including CD-69, the OX40 costimulatory receptor and Granzyme B that we looked at. These initial PD readouts indicate that CA-170 is biologically active and can result in immune activation at examine doses has measured in the peripheral blood from treated patients.

Now our current efforts for CA-170 trial in the first half of 2017 are focused on two fronts. First, enrollment of immunotherapy treatment naïve patients with cancers that are eligible for treatment with approved anti-PD1 or anti-PDL1 antibodies in the U.S.

In this regard, we have recently been granted approval to enroll immunotherapy treatment naïve patients with melanoma, non-small cell lung cancer, renal, bladder, forehead neck cancers in an extension of the Phase 1 trial of CA-170 in Korea and Spain.

Additional approvals for enrollment of patients with these cancers in other European countries is expected through this and next quarter. Second, analysis of tumor biopsies from patients pre and post CA-170 treatment to assess their immune profile.

These analyses are include detecting the expression of inhibitory checkpoints on tumor tissue, the expression of cell surface markers on different immune cells that infiltrate within the tumor, as well as gene expression patterns of immune related genes of interest.

These analyses are intended to assess the immune modulating activity of increasing CA-170 doses within the patient’s tumors as well as inform potential correlates of CA-170 clinical activity and or safety signals.

We expect to analyze the initial Phase 1 clinical profile of CA-170 early in the second half of 2017, based on data from approximately 30 to 40 patients with respect to PK, PD safety and clinical activity. I would now like to update on CUDC-907.

CUDC-907 is being investigated to assess its efficacy as a monotherapy treatment in an ongoing Phase 2 trial in up to 60 patients with relapsed/refractory MYC-altered diffuse large B cell lymphoma, or DLBCL.

Studies have shown that approximately 35% of patients with DLBCL have MYC-alterations, which is associated with a significantly poor prognosis in the first and second lines of treatment as well as even after autologous stem cell transplant.

Although small clinical studies using experimental agents with various mechanisms of action have shown clinical benefit in patients with advanced DLBCL randomized studies have shown the treatment of patients with relapsed refractory DLBCL with commonly used chemotherapy resulting approximately 10% to 15% objective response rates and median progression free survival of two and half to three months.

As we have previously reported on the Phase 1 trial of CUDC-907 of the 25 patients with relapsed refractory DLBCL treated with monotherapy CUDC-907, eight patients achieved an objective response including three with complete responses. Importantly five of the responders including all patients with complete response had MYC-altered disease.

Additionally duration of treatment was over six months for responders on CUDC-907 monotherapy. The Phase 2 trial of CUDC-907 is currently enrolling patients in 22 centers in the U.S. and in Europe, and we expect to complete enrollment within the first half of this year.

The primary endpoint of the Phase 2 study is objective response rate in up to 60 patients with MYC-altered relapse refractory DLBCL. Secondary endpoints of durability of benefits and safety will also be evaluated.

We expect to analyze sufficient clinical data from this study by mid-to-early second half of this year to provide the basis for requesting a meeting with the FDA to discuss a potential path for accelerated approval of monotherapy CUDC-907 in this patient population. I would now like to briefly update on the status of our two pre-IND drug candidates.

In October of 2016, we exercise our option to license the second immuno-oncology program in our partnership with Aurigene. The development candidate from this program CA-327 is an orally bio-available small molecule that targets PDL1 and TIM3 inhibitory immune checkpoints.

Initial characterization and preclinical profile of CA-327 was presented by our Aurigene colleague at scientific conferences in November of 2016. CA-327 is currently completing IND-enabling studies and we expect to file an IND for this drug candidate early in the second half of 2017 and began its clinical development soon thereafter.

We have also continued characterization of CA-4948, which is the development candidate from our IRAK4 program in collaboration with Aurigene. CA-4948 has been shown to be active in vivo xenograft models of human lymphoma and we have continued to assess this activity in additional models of other hematologic malignancies as well.

CA-4948 is also currently completing IND-enabling studies and we expect to file an IND by mid 2017 for its testing in the Phase 1 clinical trial in patients with hematologic malignancies.

Lastly we are pleased to note Roche and Genentech’s continued commitment to commercialize Erivedge globally for the treatment of patients with advanced basal cell carcinoma, as well as their efforts to explore Erivedge income combination therapy trial for the treatment of patients with idiopathic pulmonary fibrosis or patients with myelofibrosis.

With that I will turn the call over to Jim for a discussion of our financial results as well as providing further details on the loan facility with HealthCare Royalty Partners.

Jim?.

Thank you, Ali. For the year ended December 31, 2016 we reported a net loss of $60.4 million or $0.45 for basic and fully diluted share as compared to a net loss of $59 million or $0.48 per basic and fully diluted share in 2015.

The net loss for the year ended December 31, 2016 includes a non-cash IPR&D charge of $18 million related to the amendment of Curis’ license agreement with Aurigene. The net loss for 2015 includes a non-cash IPR&D charge of $24.3 million related to Curis’ license agreement with Aurigene.

For the fourth quarter of 2016, we reported a net loss of $11.3 million or $0.8 for basic and fully diluted share as compared to a net loss of $13.4 million or $0.10 for basic and diluted share for the same prior year period. Revenues for the year ended December 31, 2016 were $7.5 million as compared to $7.9 million for the same period in 2015.

Revenues were $2.4 million and $2.0 million for the fourth quarter of 2016 and 2015 respectively. Revenues for both periods comprised primarily royalty revenues recorded on Genentech and Roche’s sales of Erivedge. Operating expenses were $65.6 million for the year ended December 31, 2016 as compared to $64.4 million for the same period in 2015.

Operating expenses were $13.1 one million for the fourth quarter of 2016 as compared to $15.3 million for the same period in 2015. Research and development expenses were $31.6 million for the year ended December 31, 2016 as compared to $26.7 million for the same period in 2015.

The increase was primarily due to increased direct spending related to clinical activities of CUDC-907 and programs under the Aurigene collaboration over the prior year period. Employee related expenses increased over the prior year period primarily due to additional headcount.

Research and development expenses were $9.2 million for the fourth quarter of 2016 as compared to $12.0 million for the same period in 2015. The decrease in R&D expense was primarily due to $7.0 million of onetime milestone and supplemental research support payments made under our collaboration agreement with Aurigene in the fourth of 2015.

Offset by an increase to direct spending over the prior year period related to outside services supporting the ongoing clinical activities of CUDC-907 and direct cost for programs under the Aurigene collaboration. Finally, employee related expenses increased over the prior year, primarily due to additional headcount.

General and administrative expenses were $15.6 million for the year ended of December 31, 2016, as compared to $12.9 million for the same period in 2015.

The increase in G&A expenses was driven primarily by higher personnel costs and stock based compensation expense, due to increased headcount and an increase in legal service costs and professional and consulting services.

General and administrative expenses were $3.8 million for the fourth quarter of 2016, as compared to $3.2 million for the same period in 2015. The increase in G&A expenses was driven primarily by higher personnel costs and stock based compensation expense, due to increased headcount and an increase in legal service and consulting costs.

Other expense was $2.4 million for the year ended December 31, 2016, as compared to $2.5 million for the same period in 2015. Other expense was $0.6 million for the fourth quarter of 2016, as compared to $0.2 million for the same period in 2015.

Other expense for all periods primarily consisted of interest expense related to the loan made by BioPharma-II to Curis Royalty, a wholly owned subsidiary of Curis.

As of December 31, 2016, Curis’ cash, cash equivalents, marketable securities and investments totaled $44.5 million and there were approximately 141.1 million shares of common stock outstanding. Finally, this morning we announced the refinancing of our Erivedge debt facility with Healthcare Royalty Partners.

It represents a $45 billion non-recourse loan to Curis, at 9.95% interest to be repaid with Erivedge royalty payments we received from Genentech. This facility has similar provisions as our existing facility with BioPharma, with the exception that this is a significantly larger facility and a significantly lower interest rate.

After paying off the existing $18.4 million balance with BioPharma, the remaining $26.6 million allows us to extend the cash runway into the first half of 2018 depending upon the size and timing of clinical trial expenses. With that we’ll open the call for questions..

Thank you. [Operator Instructions] And our first question comes from Peter Lawson with SunTrust Robinson and Humphrey. Your line is now open..

Hi, Ali.

Just the quick question about expectations around 907, how should we think about the response rates or see our rates for that and the timing when we would see that later?.

Sure. I think the guidance that we provided obviously during the call and we have done, really the two benchmarks for that is what is currently achievable in patients in this setting for DLBCL the relapse refractory setting, which is minimum of two prior treatments and in our study is up to four prior treatments for the patients.

As I indicated, response rates are in the teams currently for these patients with commonly used treatments outside of the experimental treatments and total duration of benefit for these patients has been measured with regards to PFS is in the range of roughly 2.5, 2.6 months based on randomized the study.

That’s one benchmark if you will the lower end of it obviously what we observed in the Phase 1 trial of CUDC-907 was closer to the 30% response rate, which we think is fairly significant in this population and if we look at the subpopulation of the MYC-altered patients it was slightly higher than that in that case.

And as I indicated, our current read on the duration that patients to stay on treatment CUDC-907 at least the responders is over six months, so we think those levels of response rate closer to the 30% and duration of benefit for the patients of six months in terms of disease free state is a more reasonable mark for us to look at simply because that’s what CUDC-907 achieved in the Phase 1 trial.

We also in discussions with our advisors and our regulatory advisors believe that response rates closer to 30% in six months of durability of benefit is significant for these patients and should be considered by the FDA as possibly positive in the second as well.

So that gives you the benchmarks of where we would expect in terms of timing we are nearing completion of the Phase 2 trial enrollments of patients in U.S. and Europe.

The first thing that we will be looking at is the response rate, because that is the primary endpoint of the study and our expectations for the response rate are fairly close to midyear and then shortly after that would be for the durability of the benefit.

We generally would like to be able to present data in concordance with or at least synchronizing with possibility of medical or scientific conferences. But if we’re unable to do that we would do top line releases with respect to the data for CUDC-907..

Thank you. It’s helpful.

And then just, Jim just around the P&L, how should we think about the impact, the net impact on the P&L for 2017 and beyond?.

So you recall that in Q3 and Q4 of 2016, we were going through about $8 million to $10 million per quarter, so obviously an average of $9 million.

I would expect that to bump up a bit as we go into the clinic, of course the pace and size of increase depends on how quickly we can progress through with 907 or 170 and of course with the entering in the back half of the year of the TIM3 and IRAK4 programs.

But I would recommend obviously a bit of a bumper quarter and course with the financing that we just had as long as you’re carrying yourself into Q2 2018 somewhere in that area, you’re in the right range..

Thank you so much. Thanks for taking the questions..

Thank you. And our next question comes from Brian Skorney with Robert Baird. Your line is now open..

Hey, good morning, guys. Thanks for taking my questions. I guess I didn’t hear on the prepared remarks for the expansion cohort that you’re doing, are you doing those at the 800 MYC dose and maybe you just give some color on what those you’re using going forward.

And then also I know you said that in the prepared remarks that you see in the Cmax threshold you saw clinical activity in the roles of those for mouse models.

I guess what dose that you hit in your peer that you’re actually exceeding that the Cmax and AUC as the same you’re getting pretty good concentrations of drug even at the low dose, and then lastly how many patients total have been treated with CA-170 at this point?.

Thank you, Brian. And so maybe starting with your first question in the context of the cohorts that will be treating certainly outside the U.S. and predominantly or almost exclusively focusing on immunotherapy treatment naïve patients from the five types of cancers that have approvals in the U.S. for PD1, PDL1 treatments.

Dose is a good question, maybe allow me to answer your second question with respect to what we observe in terms of exposure and then come back and elaborate a little bit more about the types and what doses we would look at extending the clinical study in the immunotherapy-naïve patients.

Just maybe I’ll say it little bit more clearly, in the animal models or efficacy or activity in terms of tumor growth inhibition in multiple models has been in the 10 milligram per kilogram dose level in animal models that’s what we currently routinely use in multiple different models.

At that dose in animals the Cmax exposure in animals is roughly one micromolar drug concentration. Trough levels in the mouse drops somewhere in the 200 to 300 nanomolar during a one day period and again in the animals similar to the clinical trial we use once daily dosing.

In patients even at the starting dose of 50 milligram total dose in one day on a daily basis, what we observed was a similar Cmax roughly one micromolar as we escalated the dose into roughly 200 milligram to 400 milligram, which is what we've presented thus far from the pharmacokinetic analyses trough levels for us stay above the 500 nanomolar closer to one micromolar range at those doses.

There are two parameters that we obviously look at, one is the high Cmax exposure levels do and also what our trough levels when the drug is coming back down in terms of its concentrations in plasma looks like.

At these current does of 400 milligram or at the moment up to 800 milligram we're quite comfortable that our Cmax exposure levels in the multiple micromolar range is significant. As also with these doses we're able to keep the trough levels for patients on the daily dosing schedule close to the one micromolar range as well.

So we're comfortable with these doses above 400 milligram because it gives us those boundaries of Cmax and trough levels fairly nicely. Thus far in all of the patients that we've also examined from a biomarker perspective, we have seen the activation or increase in a proportion of activated CD8+ positive T-cells in their circulation at these doses.

So what we try to look at in terms of determining the appropriate dose to take forward where the appropriate doses to take forward includes both the exposure at the moment and the pharmacodynamic readouts that we've presented on.

Our view is that in the immunotherapy-naïve patients in the extension in Korea and Spain to start with, we would initiate with higher doses of 800 milligrams, but we would also test lower doses for a particular purpose and that is to be able to evaluate the tumor pharmacodynamic moderate markers not only at the higher doses, but also at the lower doses.

I would refer to this as really extending the doses or expanding the doses in multiple different cancer types at this point. And we're fairly comfortable and confident that above the 400 milligram dose and higher is appropriate exposure for these patients.

In terms of the number of patients, we've now enrolled over 15 patients into this study, and that as included some of the extension or expansion of the dose at the lower doses of the treatment as well. As I indicated, we have not seen anything limiting in terms of safety signals that would limit our ability to dose escalates on track at this point.

Hope that answers most of your questions Brian and if I need I'm happy to clarify any parts of that..

No, that’s great, thank you..

Thank you. And our next question comes from Chris Shibutani with Cowen. Your line is now open..

Yes, good morning, thanks for taking my question. Returning to CUDC-907 based upon the enrollment rates that you’re seeing if you have to continue to expand your study, what do you anticipate a potential timing of best case scenario for being able to do readout on a pivotal trial.

And when you do discuss with the FDA to try and get the accelerated approval would you anticipate that the primary endpoint would be objective response rate in non-PFS? Thank you..

Sure, thank you Chris, and actually a very good question in terms of a patient enrollment and numbers. Our initial read or primary read for the current Phase 2 trial as we've indicated, we want to enroll up to 60 patients with MYC-altered disease to assess the primary endpoint, which is overall response rate.

The reason for the selection of the 60 patients was in order for us to have confidence and the confidence interval to be above the lower boundary, and in closer also into the upper boundary of confidence interval of 95% confidence interval. For the 60 patients was selected in terms of number from statistical analysis in this case.

With respect to what would be required for discussion with the FDA, we think the primary endpoint of overall response rate for this number of patients up to 60 should be sufficient to be able to assess whether the drug is active and has a significant response rate in this, there were also be a requirement of not just the response rate, but what is the durability of the benefit, so the secondary endpoint of durability of benefit becomes important.

Because this is a monotherapy trial, we will not be able to use through PFS for a secondary endpoint in this study. However, we do want to use the duration of treatment and PFS as well as duration of response collectively as a durability of clinical benefit measure in this case, but primary is overall response rate that has to be hit in this case.

If it is positive and we do get a positive discussion with the FDA our expectation is that we would have to expand this Phase 2 trial to slightly north of 100 patients in order to satisfy both the requirements for safety signal assessment, as well as the right of statistics for this Phase 2 trial to be a valuable or be useful for accelerated approval on its own.

So the Phase 2 trial itself when we would expand it to 100 patients should it be positive would serve as the study for accelerated approval itself.

At the time of approval should it come and Curis would have to have a Phase 3 trial randomized trial running at the same time, but the approval is expected for us or at least our planning is that this Phase 2 trial itself is going to be used and this patient data will be used for accelerated approval, of course should the response rates hit the right mark.

Based on our enrollments in U.S. and Europe and the number of centers that we have open should the study results from the 60 patients be positive we're confident we can enroll the remaining patients within 2017..

Great, thanks for the additional info..

Thank you, Chris..

Thank you. [Operator Instructions] And our next question comes from Adnan Butt with RBC Capital Markets. Your line is now open..

Hey good morning, thanks for the question.

First on 907, have you held any discussions with the FDA regarding the plans to date in terms of having a look at the interim and then maybe turning that into a pivotal?.

Good morning Adnan, and thank you for your question. We held a discussion with the FDA as an end of Phase 1 trial in order to discuss the parameters and our plans for the Phase 2 trial to get some guidance in terms of multiple parameters.

That parameters included the patient population, which for the Phase 2 trial we said as relapsed refractory and two minimum prior treatments for the patients that was one. The second was the appropriate endpoints for the Phase 2 trial, which was selected as response rate as being appropriate.

And then lastly was what other endpoints would be needed in order to have a discussion with the FDA for a solid approval and durability of clinical benefit was the secondary endpoint in terms of discussion.

The numbers we've also gone through with presented obviously to the FDA what our plans were with respect to the numbers and we believe that the statistical analysis tells us that those numbers are correct.

Following the analysis up to 60 patients with respect to their response rate we intend to take that information to the FDA and present the data as well as the plan that we had already presented to them.

So that's the extent of our current discussions that we've had with the FDA and the guidance that we received from them as well as from our regulatory advisors and our internal regulatory team..

Ali, thanks for that clarity.

Then in terms of disclosing to the street what level of disclosure do you anticipate at this point what would be that you have to - the data and you’d share the top line or you would just say that you have the data and you're going to discuss that with the FDA?.

It's a good point, Adnan, I think I would say we're thinking about that ourselves is it a more appropriate disclosure in terms of our discussions with the FDA or whether it's more appropriate to present the top line data and then indicate there will be discussing with the FDA to be honest those are the discussions we hold right now at this point, so allow us to be able to give you further guidance as our thinking matures and obviously as our enrollment completes and matures as well, so no guidance on that at moment Adnan..

Sure.

And then the just on CA-170 when do you expect the next clinical update either that’s corporate in terms of patients for at a medical meeting?.

Yes. So in terms of overall clinical profile of CA-170 is really what we strive to be able to bring and presents and obviously, as I indicated, we would love to be able to do that in conjunction with a medical or scientific community, but if the timing doesn’t work and we would potentially do it as the top line release.

We think the numbers of patients that we indicated roughly 30 to 40 patients is the appropriate number of patients to get a good sense of the clinical profile of CA-170, that includes the parameters that I indicated in terms of the behavior of the drug pharmacokinetic, pharmacodynamic as well as how it affects the patients in terms of both activity as well as safety.

So that number should be relatively healthy, but we also obviously intend to do and present this to ensure that there are populations of patients that are both immunotherapy treatment naïve as well as prior treated patients that profile includes that population of patients.

As I indicated, we would - we are expecting to have those numbers of patients close to midyear or the early part of the second half and once that information in terms of the clinical profile parameters are assessed we would like to be able to present that data again either at a scientific medical conference preferably or at the top line release of the information.

In terms of non-clinical data, we would continue to present potentially throughout the year no guidance in terms of whether there is anything specific that we would present.

But in general as we learn more in terms of the non-clinical profile of the drug and all of our programs we do like to present those at scientific conferences or during our Investor conferences as well..

Okay.

Just the last one on 170, in terms of tolerability or an adverse event profile that’s a different than the current checkpoint inhibitors is at overlap or is it too early to tell?.

I think since the patients that we’ve treated come from all stages and different cancer types and they stay on treatment for differ varying times.

It’s very difficult with as I indicated just north of 15 patients to be able to get a sense of either common adverse events or try to do a fair comparison of the adverse events that we have observed to approve treatments that are optimized now and are standard in use and meeting the antibodies against PD1 and PDL1.

So it’s a little bit early to try and do that. I think what I indicated was that we’ve not seen a limiting toxicity or side effect that this allows us to escalate the dose. We do see adverse events and we evaluate dose and trying to determine whether they can be related to immune related adverse events or other in this case.

In terms of tolerability as well as I indicated patients have stayed on treatment thus far for varying times we have had multiple patients that have gone through multiple cycles of treatment note that a cycle of treatment is 21 days.

So in terms of just from the tolerability perspective it appears that patients can take the drug for multiple cycles at this stage..

Okay. That’s it. Thank you..

Thank you, Adnan..

Thank you. And our next question comes from Rahul Jasuja with FBR Company. Your line is now open..

Good morning, guys. Just a couple questions, let me start with CA-170. So I’ve noted from the presentation at SITC that you have data showing in a change in percent of circulating CD8+ T cells.

I was just wondering at this stage do you have any functional that I mean I know you show an increase and L-Select and OX40 Granzyme B your mouse model show an anti-tumor response and maybe it’s early for an anti-tumor response in patients, but have you seen functional killing like chrome release as CTL activity yet?.

I mean obviously these are fairly - first of all thank you, Rahul and good to have you on the call as well. I think it’s –first of all those are fairly detailed specific experiment and obviously much more difficult to do in patients and in non-clinical essays in animal models.

We do look for the functional activity have the T-cells we’ve done conducted experiments in non-clinical setting, but in the clinical setting obviously that’s a little bit more difficult in terms of isolating T-cells and looking at their functional status at this point.

So non-clinically, we do look this appear to be properly activated professional T-cells. Clinically first-by-first in terms of whether and which ones and to what level they’re activated and also not only in circulation.

As I indicated a lot of our focus now is to look for the immune profile within the patient’s tumor before and after treatment which we look at, non-clinically though more work has been done in that regard so..

Okay. That’s great. And then another question sort of related to more of a strategic in a big picture view and trying to understand the role of an oral that VISTA and as well as TIM3 beside the checkpoint the PD1, PD-L1 pathway. So you began enrolling patients that immunotherapy-naïve and maybe this is going to be new of the story here.

What is the strategy in addressing the PD1, PDL1 non-responders given the fact that you’ve got a different shaded mechanism of action given that you’ve, you’re inhibiting VISTA or TIM3 in the other case would there be a plan to target checkpoint inhibitors non-responders?.

Yes. Now that’s a good point and a good question. Thank you, Rahul. As we indicated in the prepared remarks as well of the patients that we have so far treated they’ve all been in the U.S.

and they’ve either been prior immunotherapy treated with PD1s and PDL1s included or they are immunotherapy treatment naïve, but from cancer types that are not the types that are approved indicated for treatment with anti-PD1s. So that’s the first part of it. Seconds, in addition to the extension of the study to outside the U.S.

to access immunotherapy treatment naïve patients in the five cancer types that I mentioned we do continue to enroll in the U.S. for immunotherapy prior treated patients.

And it’s really, exactly for the reason that you’ve indicated Rahul that the differentiation of our drug candidate is not only that there orally available small molecules where we can optimize the dose in the schedule of administering them and they have particular PK properties as a small molecule.

But also because we are bringing not only novel checkpoint antagonist but they’re dual antagonists and can potentially provide the benefit that you’re describing in patients that are prior treated with anti-PD1s or PDL1s.

Non-clinically, we have presented data for mouse tumor models that are non-responsive to anti-PD1 antibody base treatment in mice that responds fairly nicely to CA-170 in terms of tumor growth inhibition and to the same level that an anti-VISTA antibody in those mouse models provides tumor growth inhibition activity.

That’s really the basis for us to also continue to treat patients that are prior treated with anti-PD1 or PDL1 therapies in the clinic as well. Obviously any clinical benefit in that population can be very attractive and can result for us to consider further lines of development in those patient populations..

That’s very helpful. Thank you and Ali good to meet you over the phone as well..

Yeah. Thanks. Thank you, Rahul..

And I’m showing no further questions. I would now like to turn the call back to Mr. Ali Fattaey for any further remarks..

Thank you everyone for joining the call. We’re pleased to provide you an update and also note the recent transaction - financing transaction that we’ve done with Healthcare Royalty Partners.

Mostly though I would like to thank the entire team at Curis for all of their efforts in 2016 as well as everything that we have plans with our objectives for 2017 to carry those out, I also like to thank our collaborators and partners first and foremost Aurigene for the discovery and all of the work that has gone on into our three drug candidates that we are working on with them as well as our partners Genentech and Roche for the commercialization and further development of Erivedge.

But mostly I would like to thank all the patients and their families that participate in our clinical trials in the past and in an ongoing basis to allow us to assess our drugs to see whether they are effective drugs for treating cancer patients. With that appreciate everyone as joining, and thank you..

Ladies and gentlemen thank you for participating in today's conference. This concludes today's program. You may all disconnect. Everyone have a great day..