Idera Pharmaceuticals, Inc.
Q1 2016 Earnings Call Transcript

Published: 10 May 2016

[Operator:]

Good afternoon and welcome everyone the Idera Pharmaceuticals' Investor Conference Call. Today's call is being recorded and is expected to last up to one hour. At this time, I will now turn the call over to Idera's Chief Executive Officer, Vin Milano. Please go ahead.

[Vincent Milano:]

Thank you. Good afternoon and welcome everyone joining us on today's call. I'd like to thank you for taking the time to join us today as we provide you with an update on our business activities to the first several months of 2016. Our plan is when we have meaningful updates plus we do today, we will take advantage of these opportunities to conduct conference calls. I am joined on today's call by a number of my leadership team colleagues here at Idera. Before we proceed, Bob Doody will apprise you of our potential to make forward-looking statements. Bob?

[Robert Doody:]

Thanks, Vince. During this call we will make forward-looking statements within the meaning of Federal Securities Laws which may be identified by words like anticipate, expect, belief, estimate, potential and other similar words. Certain statements such as those regarding our expectations for future clinical trials, the timing and potential outcomes of clinical study and our interactions with our regulatory authorities are examples of such forward-looking statements. As you know, forward-looking statements are subject to factors that may cause our results and plans to materially differ from those expected. Factors that may cause these differences include those described in the risk factor section of our annual report filed on Form 10-K and our most recent 10-Q filed with the SEC. Please refer to the press release issued this afternoon and to our filings with the SEC for more information regarding the risks and uncertainties that could cause future results to differ materially from the expectations expressed in this conference call. These statements speak only as of today's date and we disclaim any intention of obligation to update them. Vin?

[Vincent Milano:]

Thanks, Bob. Once again good afternoon to all of you. In December we discussed the exciting data we had presented at the American Society of Hematology annual meeting which demonstrated early signals of clinical activity with IMO-8400, our antagonist of toll-like receptors 7, 8 and 9 in a B-cell malignancy population, as well as the clean safety profile with Sujag [ph] has exhibited to this date. Since December the momentum in our B-cell malignancy development program has continued to increase. Additionally, our development teams have also made important strides across the Board including advancing the dose escalation portion of the clinical trial of intra-tumoral IMO-2125 or agonist of TLR9 in PD1 refractory melanoma patients and refining the design of our Phase 2 clinical trial in Dermatomyositis. Importantly the research team has continued to make great progress with our third generation anti-sense platform. Our conviction grows each day that this technology platform will represent the core pillar of Idera's long-term growth and value creation for years to come. In a moment, I will turn the call over to Joanna to provide you with an update on all of our clinical advancements, who will be followed by Clayton to provide you more color around the strategic advancement of the 3GA platform. And I'll return for some closing remarks. Importantly, I expect you will take from today's update that for next 18 months we're setting up to be a pivotal time for Idera as we expect to see data from our clinical studies, meaningfully advance the 3GA platform into human validation and crystalize how Idera will march towards and arrive at our stated destination which to be a commercial company delivering solutions to patients suffering from rare diseases including cancer populations with great unmet medical needs. With that I will now turn the call over to Joanna and Clayton, and then I will return at the end for some closing remarks before we take your questions. Joanna?

[Joanna Horobin:]

Thank you, Vin and good afternoon everyone. Last time I had the opportunity to speak with you all, I had been at the company just one week. Now after being on-board for five months, I am even more excited about the opportunities that lie before us. Today I will provide update across all of our clinical programs. I'll begin with an update on the IMO-8400 B-cell malignancy development program which currently includes two studies. One in Waldenstrom's Macroglobulinemia and the second quarter in Diffuse Large B-cell Lymphoma. Then I will continue with 8400 in Dermatomyositis. And finally I will update you on the very exciting program with IMO-2125. So starting Waldenstrom's study I will talk what has been accomplished since ASH to enable further dose escalation of 8400 and provide some topline remarks related to the safety and clinical studies in the additional patients treated with 1.2 milligram per kilogram twice dose since the ASH dated. As well as an update on patients who have been exposed to 8400 treatment for longer durations. As a quick reminder, we presented data on ASH on the dose escalation stage at the Waldenstrom's study which demonstrated encouraging clinical activity including end-protein reduction, clinically meaningful increases in hemoglobin and reduction in visceral disease. So we're going to those response without associated dose related top efficacy which makes us believe that efficacy could further improve with continued dose escalation. Importantly, we all know there are part response in the one study subject who has documented on refractory disease. These data continue to hold up as of the last - we are seeing clinical data set in 16 as now 19 subjects is evaluable to serological response including in 9 of the 10 patients treated with highest dose. I remember we had two subjects that had a reduction from baseline of approximately 90%. As far as safety goes, today it has seen no important toxicities even with those patients who have had the longest exposures to 8400. The longest duration of treatment in any subject now exceeds the year and a half. So why is this important? The data we shared at ASH increased the enthusiasm for 8400 within the KOL community. What we are seeing with continued enrollment is that there is a consistency in the outcome that we had seen earlier with favorable safety and the reduction in either M-Protein or total ITM and improvement in hemoglobin. This further experience reinforces our conviction, the proof-of-concept has been achieved in a disease which is driven by the 1988 L26 mutation which is ubiquitous in most patients [ph] and hopefully can be extended to in population which includes patients with critical unmet needs at the ABC form of the DLBCL. Here the present for this mutation confronts and exceptionally poor prognosis. We haven't fully opened in ABC DLBCL and we're interestingly amended this protocol to test the higher doses of 8400 to align with those we are now exploring in the population. So to that point, the amendment we've made to the studies are making their way through the various IRB. We have drug available and we are in a position to start enrolling at the higher doses. The first two cohorts that we'll be testing will be 2.4 milligrams per kilogram and 3.6 milligrams per kilogram both with one dosing. In the Waldenstrom study, we are also encouraging the inclusion of more subjects with our group network disease to double up on this important observational response to 8400 and this difficult to treat population which in itself represents the potential registration pathway. Our goal is to complete this dose escalation in both studies and selected dose of Phase 2 development by the end of 2016 which should position us to present clinical and biomarker data from both studies in the first half of 2017 as one of the larger oncology conferences. Additionally, our clinical program team has drawn out the fast forward beyond the outcome of these studies for registration and commercialization. With multiple options we can try depending on where that they could lead us. Needless to say, our team and the KOLs are enthused by seeing IMO to-date and we look forward to finding out just how good the efficacy IMO-8400 can be in these patient population. Particularly in ADC DLBCL in which the need is greater as these patients are very sick and are running out of options and time. Our January 8400 clinical program and update now on the Phase 2 trial in Dermatomyositis. Back in January I had the opportunity to spend time with PIs from our Phase 2 study and developed a most deeper understanding of this rare inflammatory disease which is characterized by widespread distinctive rash, not a weakness and fatigue so the significant mobility for the affected patients. There the very limited treatment options, primarily steroids and [ph] infusions. But these yield incomplete control symptoms in most patients, it's the top disease controls. In discussion with our PIs we made the decision to amend the eligibility criteria to the protocol to more accurately reflect current standards of care which we believe will better facilitate accruals as well as data ground work for subsequent studies. Also by reducing the number of doses we are testing, we have reduced the overall size of the study and based on the good safety profile with 8400 in Waldenstrom, we plan to explore higher dosing, of course we have maintained the placebo control. So in summary, the team has amended the trial protocol in a manner that we believe is more reflective as the current treatment landscape, improved viability to approve the study in a more timely fashion and also requires fewer patients than originally found. We're currently working with the FDA to gain their agreement on this amended protocol and our PIs are looking forward to re-engage in enrollments shortly. My goal is to help these studies fully approved in the first half of 2017. And I will be better positioned in the second half of this year to provide you with an expected time for the trial to complete and data readout. Now let's move to our immune-oncology development program at IMO-2125, our TLR9 agonist which we're doing in collaboration with NDN. As you all know, the immune-oncology space is looking to build up the exciting efforts seen for us with its new lab in NPD. And certainly we represented significant advancements in patient care, there are still 70% to 80% of patients who remain unaided by this approach. Our belief is that a major reason for the lack of effect to checkpoint inhibitors in these patients is that the innate immune system has not been added quickly primed to allow the checkpoint inhibitors to work, thus immune timing strategies are potentially backbone to any immune-oncology strategy. There are many who are attempting to find ways to alter the tumor migrant and essentially revup the immune response. However, we believe the TLR9 agonist has many advantages and it sees the logic target with dendritic cell activation. Our past clinical study with 2125 is designed to confirm the beneficial effect on immune function those are being repeatedly demonstrated in preclinical models with 2125 which may be predicted with clinical benefits. As you may have heard my colleague state in our various investor presentations, this study has an extensive translational component in addition to the usual clinical outcomes of safety and activity. We expect to sure initial translational data from this study in the second half of 2016. This initial dose lining study with IMO-2125 is being conducted in patients with metastatic melanoma who disease was relapsed but not fully responded to PD1 inhibitor. IMO-2125 is being administered intra-tumoral together with Ipilimumab given according to the standard regiment. The first patient was enrolled in December of last year and the study continues to enroll according to plan as we move through the dose escalation cohort. We are successfully obtaining serial tumor biopsys in the study in all patients and then these are being subjected to comprehensive analysis and by the team of dedicated immunologists. Now importantly, these stage are being reviewed with us in real time, so we should be estimate to make truly informed decision about the selection of dose of 2125 to be used in combination regiments for further development. And of course, we're also getting early read on whether these combinations of clinical activity in PD1 refractory melanoma given another important unmet medical need. So to conclude, we have designed this study to learn gross about what is actually going on inside the tumor micro-environment and immune effect as well as what impact that will have on clinical outcomes. We are also moving forward in designing additional studies with 2125 that can start early next year. These studies will look to signs of clinical activity in tumor sites not currently amendable to new therapy. And they also identify normal combinations for future developments. We are very excited about the prospects of 2125 and look forward to seeing the first clinical data and its founding program as well. Anderson has been a tremendous partner in this effort and having such a high level of enthusiasm from some of the most respected thought leaders in Anderson for this approach is something we really benefit from. Again, we're optimistic that some of the translational data from the early cohorts in the current study will be available for presentation at one of the immune therapy conferences later this year. Once we split it and have enough traction, accepted, we will provide you with more information. As for the initial clinical data outcomes from the current study, we expect to have those next year. I'll now turn the call over to Clayton who will spend little time discussing the strategy around the 3GA program. However, I will call it by saying how much I am looking forward to conduct the clinical studies for our first candidates from this very exciting platform. Clayton?

[Clayton Fletcher:]

Thank you, Joanna. What I'm going to cover today is more on the strategic direction of the 3GA program for the third generation antisense program and help also put some color around their current thinking on timing. Sudhir, of course is here to answer any questions during the Q&A session. I'll start off by complementing the team for the quality and quantity of work that they have completed over the past year or so. As been noted at the outset, as a team we continue to be more and more convinced at the opportunity presented to us by third generation antisense technology, it has a great potential to fully realized the use of antisense for the treatment of diverse diseases. As a brief primer, many of you are likely aware of the challenges that have been presented by earlier versions of antisense which are limited by potency, safety and limitations to organ specific targeting, namely the liver. Subject confirmation in the clinical setting, we believe that 3GA has the potential to significantly overcome these limitations. In short, using our 3GA technology we have been able to pursue multiple gene targets, assess multiple organ compartments demonstrating local activity and which has a novel mechanism of action. We will be discussing the MOA or the mechanism of action greater detail in the second half of 2016. This potentially opens the door for considerable utilization of 3GA across many disease indications. Our goal last year which was meet was to identify development the first two gene targets for the 3GA platform over the many gene targets we have been evaluating. You may recall we highlighted late last year NLRP3 and thus for at these first Q targets. NLRP3 a key component of the pathway is implicated in multiple diseases including interstitial cities, uveitis, NASH and nephritis. DUCH4 as target which is implicated in FSHD or facio scapular humoral muscular dystrophy. Since we've made this announcement, our team has been conduction extensive preclinical studies and appropriate animal models for these disease indications. In parallel, we've also assessed the 3GA commercial opportunity along with the clinical and regulatory path for these candidates. This is helping us to identify which of these diseases enable us to past opportunity to conduct human proof-of-concept studies in 2017 with the goal of delivering this data as quickly as possible. So for the remainder of this year we'll be conducting a necessary activities to prepare for IND filing in early part of the 2017 with plans to enter the clinical shortly thereafter. We'll plan to update you on our choices of first disease for this study later on this year. Another related activity is our ongoing collaboration with GSK on the application of 3GA for the treatment of renal diseases. Due to the confidentiality of our agreement, I'm unable to go into the details of our collaboration, however, I can make a few topline comments. First of all, we are very pleased to have been approached by GSK to collaborate on the drug candidates renal targets from our 3GA platform. GSK has significant experience in antisense space, so we are happy to be able to benefit from the knowledge they bring forward and it's fair to say that they've been impressed with what we've accomplished with them to date as well. Overall, the relationship has been very constructive for both parties and we look forward to continuing to drive forward and move towards the clinical development. So I think if you look at the activities we've completed today with 3GA platform, you can begin to get a glimpse of how we envision the evolution. Every year we plan to identify additional gene targets and diseases that fit within the mission of Idera for development and ultimately commercializations. The opportunity exists for us to choose, to engage in additional collaborations, develop drugs for diseases that don't fit and to Idera's scope as we often see from companies that have the technology platform with broad applications and scope. These types of potential collaborations may also be sources of funding for our company to run our business and finance our development activities and interest. Overall, we're very excited about the prospects for 3GA and we really only just scratched the surface of what this technology can do and what it could represent for the future value to Idera. I will now turn the call back over to Vin for his closing comments, and as mentioned, both Sudhir and I are here to answer any questions during Q&A. Vin?

[Vincent Milano:]

Thanks, Clayton. Before opening up the call for questions, I'd like to summarize and then make a few closing remarks. So overall, I think you will note that we have a number of opportunities for success and value creation here at Idera. At the same time we've been advancing the pipeline forward in a very focused and targeted manner. 8400 is moving ahead in both B-cell malignancies and Dermatomyositis, and 2017 is setting up to be a data rich year for these programs. The 2125 IO development is well underway and we're excited to see the first elements of the translational data later this year. We've made significant strides in the last year of moving the 3GA platform towards human proof-of-concept and we've also gained great experience with the first of likely many partnerships. Now as we continue to move forward through the remainder of this year, we anticipate that we'll be in position in the second half of fine tune the timing specific for the deliverables for 2017 and we look forward to sharing that information with you. I think this demonstrates things are certainly moving in the right direction for Idera. As it relates to our cash position, we noted in our press release, we have cash to take us well into the third quarter of 2017 and we are poised to reach a number of critical inflexion points between now and that time. I'd also like to note that we have a few opportunities to generate additional capital outside of financing. As you are all aware, we have IMO-9200 which represents an interesting opportunity and a large autoimmune disease. We've made it clear that this is not strategically a good fit for us, so out-licensing 9200 is something we are actively working on that could potentially increase our cash position. Secondly, the 3GA platform which has enormous breadth of potential application is one where we've clearly stated our intention to out-licensed compound the company's interested in pursuing diseases outside of our strategic focus such as the GSK collaboration. I think this puts us in a moreover unique position than a number of our peers who have no choice but to solely rely on the capital markets to advance their causes. Lastly, before closing, many of you have asked me personally, during one-on-one interactions exactly what here to Idera and since that question comes up very frequently, I felt it was worthwhile to address this in front of the broader audience today. Personally the principal driver is the 3GA platform, without a doubt the performance of 8400 and 2125 were very important and both drove potential to the important solutions for patients and substantial value drivers for Idera in the nearer term. However, when you endeavor to build a company, that can produce sustained growth over the long-term, the ability to have a powerful technology platform that can internally produce drug candidate after drug candidate for a large number of diseases is damn right exciting. Having previously led a company that was built through continuous business development execution, I can tell you that is a model that today has become far more tenuous and much for unpredictable. So I'm very excited and feel fortunate to be part of this company that has discovered and developed the technology platform that has a potential to overcome the limitations of earlier generation antisense and RNAi technologies. We have generated a great deal of preclinical data against a number of different targets in many different animal models. We have consistently knocked down the targeted gene in these experiments and now we are diligently working towards advancing our first candidate in the human proof-of-concept trials which we anticipate will further demonstrate the power of this exciting platform. So now let's move on to the Q&A portion of the call. Thank you for your attention. Operator, are there any questions for the team?

[Operator:]

Thank you. [Operator Instructions] And our first question comes from the line of Anil [ph] of JP Morgan. Your line is now open. Please go ahead.

[Unidentified Analyst:]

Hey guys, thanks so much for taking the question. Just on 8400 on the IGM decline. Could you talk about time to IGM declines at the highest dose cohort? Also curious to know if you rolled anymore BTK experienced patients and then what you're seeing in terms of response and time to response in IGM declines and those patients? Thanks.

[Vincent Milano:]

Thanks for the question. I'll let Joanna take the lead on this.

[Joanna Horobin:]

Yes, so at the moment we haven't looked at the time to respond. As you recall though, at ASH, we have noticed that there was an interestingly intriguing accounts by dose response so that we were seeing earlier responses to patient's dose behind. So we will be looking at that, we will include that in the analysis of the complete data what we finished according to patients to this study.

[Unidentified Analyst:]

There was a question on BTK.

[Joanna Horobin:]

And we are actively encouraging additional patients to come into this study, I believe at the most we've got three patients that have previously been to our business. That's currently something that we are actively encouraging our investigators to try and learn forth.

[Unidentified Analyst:]

Great. Thanks so much for taking our question.

[Vincent Milano:]

Thanks.

[Operator:]

Thank you. And our next question comes from the line of Ted Tenthoff of Piper Jaffray. Your line is now open. Please go ahead.

[Ted Tenthoff:]

Great, thank you. Maybe just picking up on last question. Walk us through sort of what the data roll out is for 8400 in both Waldenstrom's and DLBCL? And what would be potentially net debt? And then I have a follow-up if I may.

[Vincent Milano:]

Could you - Ted, could you just repeat the last part of that question so you want the timing of their air roll out I mean the last part.

[Ted Tenthoff:]

And then sort of how you envision going forward. So what would be potential next steps?

[Vincent Milano:]

Okay, Thank you, Joanna.

[Joanna Horobin:]

First of all, as I said, we're anticipating completing accruals to the cohorts this year, that is our intent and so that would place us very nicely if report out activities incurred during 2017. Those are really the intent at the moment. With respect to the second question on what's next…

[Ted Tenthoff:]

And also on DLBCL sort of a similar update if I may?

[Joanna Horobin:]

Right. So let me talk about - so I think it will certainly depend on the patients that we have coming into the study as I just mentioned in a way actively encouraging our investigators to try and find patients who have previously seen an hour lasting following Ipilimumab [ph]. Clearly that patient population, if we continue to see with some test we did with the first patient that we reported on last year at ASH could be a very interest part in terms of our potential regulatory path in Waldenstrom. So that is certainly the way we're thinking about that. Now with DLBCL, we are also now in a position that we can start enrolling patients at these higher doses so that's a big plus because we discussed with you before - quite a challenge here because we've got patients and so time to response becomes more important. So we're actively now actually going to be enrolling those patients and in fact the reason for having data cards at this will - because we have an upcoming meeting with all of that DLBCL investigators, so really getting those data and going for that protocol again. Now that protocol is important because in that protocol, we have actually have potential to move seamlessly from same point of escalation stage into a Phase 2 portion of the protocol. The - have been quite significantly amended. With the DLBCL we now have this sort of seamless transition from Phase 1 to Phase 2 together with I think some very thoughtful additions to the protocol which will allow us to look at whether or not we - if like to cross the threshold of activity that would be interesting for perfect development. So as I said, we're anticipating that we will be able to accrue certainly the more than strong dose escalation with DLBCL this year and then seamlessly move into Phase 2 we hope at the beginning of next year.

[Ted Tenthoff:]

Okay. And then if I may just on the Street and Erickson platform. I really appreciate your guys enthusiasm for this and starting to come at the - what the first targets are? I guess my question is for Clayton and for Vin and for everyone just add sort of a higher level. Is this scenario where you know and I guess maybe we even throw 8400 in the mix too but is this a scenario where you guys will look opportunistically to partner, 3 gene antisense and 8400 beyond the other assets or is it really more the goal to kind of generate proprietary program to take further and create value?

[Vincent Milano:]

So Ted let me begin. With regards to 8400, our current thinking is that's going to be credit for our own account. We have not contemplated looking through partners for different disease with 8400. With regards to third generation though very, very different answer - we see the opportunity in third generation to build our own business by taking about target that very much fit into this rare disease including rare cancer space and all the things that we're going to very actively work from research to development and hopefully down to the commercialization. As Clayton mentioned in his comments, the opportunity because of the number of different compartments and the broad - of this possibility of this platform, we can imagine - you can imagine with us that there could be fields of interest that other companies have that would not be strategically lined up with that space or those spaces. And they could represent collaboration partners. So we'll be doing both with regards to third generation. Clayton?

[Clayton Fletcher:]

Such as potential collaborations, Ted, I think you mentioned trying to create unique proprietary molecules for this partners that would definitely be the approach that we would be going down. So we wouldn't want to be broadly casting that, we would want it to be very targeted in the molecules we produce for any partnership.

[Ted Tenthoff:]

All right, good stuff. I'm merely excited about where you guys are going.

[Vincent Milano:]

Thanks, Ted.

[Operator:]

Thank you. [Operator Instructions] Our next question comes from the line of Heather Behanna of Wedbush Securities. Your line is now open. Please go ahead.

[Heather Behanna:]

Hi guys, congrats on the progress. Just a couple of follow-ups on Waldenstrom; one is if you could tell us how many of the patients to-date have actually had the MYD88 mutation and how many of them have responded?

[Joanna Horobin:]

Okay. So our focus on the 10 patients treated at the higher dose. As you recall we were talking about 9 of those 10 patients having had a reduction in the IGM or M-Protein. Also 10 patients - but we have intimation about like the 88-G mutation on 7, we know that 6 of those patients have a mutation, we know that one would negative to mutation and those the other three patients at this point we don't have enough information but of course as you know we had most of these patients will have this mutation.

[Heather Behanna:]

Right. And then when you talk about the reduction in IGM, what is considered from all of your discussions with KOLs and what you've seen a meaningful clinical response as far as the decrease in IGM level?

[Joanna Horobin:]

That's really good question because I think one of the things we need to remember here is that these patients who have all of course being previously treated - fatal disease in itself is actually beneficial, clear terms of benefit for these patients. And so when we're talking about response to-date, we're talking about serological response which is essentially looking at the drop here at M-Protein or IGM from that baseline. And so that's really what we're referring to. Not the more if you can repeat response that we reported on at ASH which included a lot of other factors. We're reporting today on IGM and M-Protein reduction and also we're continuing to follow which carries a very meaningful benefit to patients that we see an increase in hemoglobin.

[Heather Behanna:]

Perfect. And then just one more quick follow-up on the DLBCL, do you expect the dose for each program in Waldenstrom and DLBCL to been the same? And are you starting DLBCL with the new protocol at the 1.2 milligram twice a week or the 2.4 milligram once a week?

[Joanna Horobin:]

Our goal are healing would that we wouldn't have a single dose across the B-cell malignancy program. And we are poised to start treating new patients coming in why DLBCL with higher doses.

[Heather Behanna:]

Okay, great. Thanks for the color.

[Vincent Milano:]

Thanks, Heather.

[Operator:]

Thank you. And our next question comes from the line of Boris Peaker of Cowen and Company. Your line is now open. Please go ahead.

[Boris Peaker:]

Great. My question is on 8400, I'm just curious in both Waldenstrom and DLBCL, are there any specific trial readouts or datasets that you are waiting in near future that would impact your development decisions?

[Vincent Milano:]

Thanks for the question Boris. Joanna?

[Joanna Horobin:]

Well, I think some efforts that we do in at the moment, although they are designed as Phase 1 dose finding studies, also looking at readouts of clinical activity, that is really going to be the thing that will define what we do going forward. And as we've already reported in Waldenstrom, we've already seen evidence of clinical activity which we believe is really meaningful. So not just looking at the serological effect but looking at hemoglobin in particular, which is, of course, why patients actually come in to these studies because why they get treatment, because they've got fatigue related to the anemia.

[Boris Peaker:]

And what about - sorry go ahead.

[Joanna Horobin:]

So that's really the read out we're looking for. We are - you're looking for symptomatic benefit, we're looking for maintenance of that symptomatic benefits as well. And the other thing just to point out is it to our knowledge there are no other competitors at this moment who are specifically targeting the MYD88 patient population.

[Boris Peaker:]

Okay. That was part of my question in terms of competitive landscape if there is anything that you're specifically focused on but it sounds like there isn't anything, any particular competitive study?

[Joanna Horobin:]

Not at this point.

[Boris Peaker:]

Got you. And maybe my last question here is for Vin, maybe greater strategic question. You certainly have enough number of programs ongoing and there is always a process of optimizing priorities and put one on hold in DMD. I'm just curious in a context perhaps capital constraints, I mean what are the programs would you consider putting on ICE until maybe a partner would prioritize?

[Vincent Milano:]

So that question - I think contingency planning is an obligation of all management team, and I guess I'm not - I'm going to be a father here too, I'm not going to say which one of my kids are not going to fund our education for the moment because we actually had a major decision, we do go through this exercise and have gone through this exercise periodically during the year but obviously if situation doesn't improve and the market continue to be the way they are - we'll have to make hard choices about which way we go. And in some cases we only have data to help inform them, in other cases we may have just make hard choices. But at this point Boris, I don't have a good answer to your question because we haven't chosen one.

[Boris Peaker:]

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

[Vincent Milano:]

Thank you, Boris.

[Operator:]

Thank you. And I'm showing no further questions at this time. I would now like to turn the call back over to Mr. Vin Milano for closing remarks.

[Vincent Milano:]

Thank you. And again, I want to thank everyone for taking the time out this afternoon to join us today and listen to this update. Hopefully, we conveyed to you the excitement that we have for the things going on here at Idera and we look very much forward to keep you up to date on the things we're doing. And we look forward to seeing you in the weeks and months to come. Thanks again.

[Operator:]

Thank you for your participation in today's conference. This concludes the presentation. You may now disconnect.