Geron Corp (GERN) 2016 Q3 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the Q3 2016 Geron Earnings Conference Call. (Operator Instructions)

I would like to introduce your host for today's conference, Anna Krassowska, you may begin.

Thank you. Good afternoon, everyone, and thank you for joining us for the Geron third quarter of 2016 earnings call. With me this afternoon are Dr. John Scarlett, our President and Chief Executive Officer; and Olivia Bloom, our Executive Vice President, Finance and Chief Financial Officer.

Today, we issued a press release that reported results for the third quarter ended September 30, 2016. This release can be found on our website at www.geron.com. Today's call is also being webcast live on our website and will be available for replay through December 3.

Before we begin, please note that except for statements of historical facts, the statements during this conference call are forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. These include, without limitation, statements regarding the timelines, milestones, prospects and plans for imetelstat, including the timing and occurrence of additional data reviews and the outcome of those reviews related to IMbark and IMerge, health authority and IRB approvals of a protocol amendment for IMbark; the therapeutic potential and safety of imetelstat; Geron's desire to diversify patent coverage, potential payments under the Janssen collaboration agreement and financial and operating projections or requirements.

These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. These risks and uncertainties include, without limitation, that imetelstat is safe and efficacious in IMbark and IMerge whether IMbark and IMerge continue to proceed without any delays caused by health authorities or IRBs or any other factors; or that one or both of the trials discontinued; Geron's is able to timely collect the requisite data from IMbark and IMerge; imetelstat will overcome clinical safety and efficacy technicals, scientific manufacturing and regulatory challenges; Geron's patents maintain their validity and whether Geron will actually receive continuation milestone and royalty payments from Janssen.

Additional information and factors that could cause actual results to differ materially from those in the forward-looking statements are contained in Geron's periodic reports filed with the Securities and Exchange Commission under the heading Risk Factors, including Geron's quarterly report on Form 10-Q for the quarter ending September 30, 2016.

Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, and the facts and assumptions underlying these forward-looking statements may change. Except as required by law, Geron disclaims any obligation to update these forward-looking statements to reflect future information, events or circumstances.

We'll begin today's call with a summary of the 2016 third quarter operating results from Olivia, and then Chip will review recent events and discuss ongoing activities with the imetelstat's clinical trials being conducted by Janssen. Olivia?

Thanks, Anna. Good afternoon. For the third quarter of 2016, the company reported a net loss of $3.6 million or $0.02 per share compared to net income for the third quarter of 2015 of $27.2 million or $0.17 per share. Net loss for the first nine months of 2016 was $21.1 million or $0.13 per share compared to net income for the first nine months of 2015 of $8.5 million or $0.05 per share.

Revenues for the three and nine months ended September 30, 2016 were $5.1 million and $6.1 million respectively compared to $35.4 million and $36.2 million for the comparable 2015 period. Revenues for the three- and nine-month period ending September 30, 2016 included licensing revenue of $5 million, which represents an upfront payment due under our license agreement with Janssen Pharmaceuticals, Inc., which is an affiliate of Johnson & Johnson that is separate from Janssen Biotech, Inc, the entity that is collaborating with Geron on the imetelstat program in hematologic malignancies.

Areas of focus for Janssen Pharmaceuticals include neurological and infectious diseases. The license agreement with Janssen Pharmaceuticals was signed and became effective in September 2016. The license grants certain rights to our specialized oligonucleotides backbone chemistry and novel amidates and excludes any right to imetelstat or telomerase inhibition.

Revenue recognition criteria for the upfront payment was met in September 2016. Revenues for the three and nine months period ending September 30, 2015 included the full recognition of the $35 million upfront payment from Janssen Biotech as collaboration revenue upon the revenue recognition criteria related to the upfront payment being met in the third quarter of 2015. This upfront payment was received in December 2014 in connection with the effectiveness of the imetelstat collaboration agreement with Janssen Biotech.

Total operating expenses for the three and nine months ended September 30, 2016 were $9 million and $27.9 million, respectively. Compared to $8.3 million and $28.1 million for the comparable 2015 period. Research and development expenses for the three and nine months ended September 30, 2016 were $4.3 million and $13.9 million respectively compared to $4.1 million and $13.8 million for the comparable 2015 period.

General and administrative expenses for the three and nine months ended September 30, 2016 were $4.7 million and $14 million respectively compared to $4.3 million and $12.9 million for the comparable 2015 period.

Year-to-date operating expenses for 2015 also included restructuring charges of $1.3 million in connection with the company's organizational resizing announced in March 2015.

The increase in research and development expenses for the three and nine months periods ending September 30, 2016 compared to the same periods in 2015, primarily reflected the net result of higher cost for Geron's proportionate share of clinical development expenses under the imetelstat collaboration with Janssen Biotech partially offset by reduced personnel related costs resulting from the March 2015 organizational resizing and lower cost for the manufacturing of imetelstat drug product. We expect overall research and development expenses to be higher in 2016 compared to 2015 as the clinical development of imetelstat continues in collaboration with Janssen Biotech.

The increase in general and administrative expenses for the three and nine months periods ending September 30, 2016 compared to the same periods in 2015 primarily reflected higher non-cash stock-based compensation expense and an increased allocation of facilities and other overhead costs to general and administrative activities.

We ended the third quarter of 2016 with $129.8 million in cash and investments. We have not incurred any impairment charges on our marketable securities portfolio.

I will now turn the call over to chip to review recent company events. Chip?

Thanks, Olivia. Good afternoon, everyone, and thank you for joining. I'd like to begin with a brief overview of the imetelstat related abstracts that have been accepted for presentation at the American Society of Hematology or ASH annual meeting in December. As a reminder, Janssen and Geron did not submit any abstract to ASH related to imetelstat clinical data this year. However, as part of the translational research program for imetelstat, Janssen has been sponsoring numerous preclinical studies to explore the effects of imetelstat in other hematologic myeloid malignancies. There will be three nonclinical presentations at ASH, which describe data from such ongoing work.

The abstracts related to these presentations are available online on the ASH website, and information regarding presentation times is also contained in the press release we issued this morning. In compliance with the embargo policies of ASH, on this call, I will limit my comments to the topics for each of the abstracts.

First in an oral session Dr. Steve Lane from the University of Queensland Australia will present data on the activity of imetelstat in a nonclinical model of AML. Dr. Lane and his colleagues have been continuing their exploratory work to understand the potential clinical efficacy of imetelstat in AML by using preclinical models derived from patient samples.

Second, during the post-recession, scientists from University of California and San Diego and Janssen R&D will present data from nonclinical models of chronic myeloid leukemia and blast crisis. This work provides further support to the potential impact of imetelstat on leukemic stem cells.

Third, scientist from the University of Bern in Switzerland in collaboration with clinical investigators of the prior Phase 2 study in patients with essential thrombocythemia and Geron will present a poster describing the dynamics of telomere length in patients with ET who are treated with imetelstat. These data extend the clinical evidence that imetelstat treatment in ET patients may suppress the neoplastic clones underlying the disease.

Lastly, a poster presentation will be available from the Janssen commercial team that reviews treatment patterns and outcomes of patient with myelofibrosis from United States medical claims database. Although, this poster does not contain imetelstat data, it is relevant to the imetelstat program. The analysis support published observations by others that suggests that median overall survival is greatly reduced once patients with MF fail or discontinue ruxolitinib, the only approved drug for MF today. These data further underscore the unmet medical need in MF in this patient population, which is currently being tested in the ongoing imetelstat MF trial being conducted by Janssen.

Next, I'd like to briefly summarize the outcomes of the planned internal data reviews conducted by Janssen during the third quarter and highlight the recent actions taken by them related to the two ongoing imetelstat studies, IMbark and IMerge.

I will start with IMbark. This Phase 2 trial was originally designed to evaluate two different dose levels of imetelstat in patients with intermediate-2 or high-risk myelofibrosis who are refractory to or have relapsed after treating with a JAK inhibitor.

The co-primary endpoints of IMbark, which are spleen volume reduction and total symptoms response will be assessed in a 24-week time point. As you'll recall, the first internal data review of IMbark was conducted as planned after 20 patients from each dosing arm have been followed for at least 12 weeks.

Outcomes determined by Janssen from this first internal review included the following. First, the safety profile at both doses was consistent with the prior clinical studies imetelstat in hematologic malignancies and did not identify any new safety signals. Second, lower starting dose of 4.7 mg/kg did not show sufficient activity among the first 20 patients assessed at the early 12-week time point nor did the data suggest that additional time on drug would result in an adequate response to 24 weeks. Thus, the 4.7 mg/kg dosing arm did not warrant further investigation and has been closed to further enrollment. Third, the higher starting dose of 9.4 mg/kg showed encouraging trends in efficacy among the first 20 patients and warranted further investigation with patients being allowed to continue to receive imetelstat. However because not enough patients in this trial met a predefined 12-week interim criteria to declare the dose adequate, new patient enrollment is being suspended while 24-week data can be collected and analyzed.

Janssen has informed us that as of today over a 100 patients have been enrolled in IMbark across both dosing arms compared to over 90 patients that were enrolled when the enrollment suspension was announced in September. The reason for the increase in enrollment from over 90 to over 100 is because there were a number of patients who were already in screening for the trial. And investigators were allowed to enroll those patients in the 9.4 mg/kg dosing arms.

Since the first IMbark internal data review, Janssen has submitted to health authorities for review and clearance a protocol amendment that includes allowing investigators to increase the dose of eligible patients in the 4.7 mg/kg dosing arm to 9.4 mg/kg.

Prior to being implemented, this protocol amendment must also be reviewed and approved by each clinical sites institutional review board or ethics committee. Until that time, investigators can continue to treat those patients with imetelstat using 4.7 mg/kg dose.

By the end of the second quarter of 2017, Janssen plans to conduct a second internal data review for IMbark, including patients who were enrolled with the 9.4 mg/kg starting dose and have been followed for at least 24 weeks. This timing also allows some of the more recently enrolled patients at the 9.4 mg/kg starting dose to reach the 24-week time point for inclusion in the second review.

There are a number of possible outcomes following the second review. Enrollment in the 9.4 mg/kg dosing arm could be resumed. A new dosing arm could be added, or the trial could be closed. If enrollment resumes, the primary analysis is projected to occur after all patients planned to be approximately100 patients enrolled and treated in the 9.4 mg/kg arm as a starting dose has been followed for at least 24 weeks. Therefore, because the enrollment is currently suspended, the timing of the primary analysis is uncertain.

A separate analysis is planned for patients who are enrolled in the 4.7 mg/kg arm, whether or not their dose was subsequently increased to 9.4 mg/kg.

Moving on to IMerge. This study is a Phase 2/3 trial evaluating imetelstat in patients with low or intermediate-1 risk myelodysplastic syndromes, who are transfusion dependence and have relapsed after or are refractory to treatment with an erythropoiesis-stimulating agent.

IMerge has two parts. Part 1 is a Phase 2 open label single arm design in up to 30 patients. Part 2 of the study is a Phase 3 randomized placebo controlled trial of up to 170 patients. With Part 1 being fully enrolled, no further patient enrollment is occurring as originally designed. The primary endpoint in IMerge is red blood cell transfusion independence for a consecutive eight-week period, with 24-week red blood cell transfusion independence as a key secondary endpoint.

In the third quarter, Janssen conducted an internal data review for IMerge for a subset of patients from Part 1. Based on this review, Janssen determined that emerging safety and efficacy appears to be consistent with the data reported from the MDS patients in the Mayo Clinic pilot study. We are encouraged by these preliminary data, and the trial currently continues unmodified.

Janssen plans to conduct a second internal review for IMerge by the end of the second quarter of 2017 including longer follow-up for all Part 1 patients. We expect Janssen to assess the benefit risk profile with imetelstat in Part 1 as well as data from the imetelstat program as a whole, and regulatory review before deciding whether to move forward to Part 2 of IMerge. If Janssen moves forward with Part 2, we expect the Phase 3 portion of the trial to be open for enrollment in mid-2017. We expect Janssen to submit data from Part 1 of IMerge to be considered for presentation in a medical conference in the future. We and Janssen continue to be committed to advancing the development of this very novel drug.

Before we open the call to questions, I will also note that our search and evaluation process to identify and evaluate oncology products, programs or companies for potential acquisition continues, but we have not yet identified such candidate.

Thanks very much for your attention. We would be pleased to answer questions in the time we have remaining. With that Operator, let's open the call to questions, please.

(Operator Instructions) Our first question comes from the line of Roy Buchanan from Janney Montgomery. Your line is open.

My first question is actually something John just said discussing IMerge evaluation by Janssen that should happen in 2Q. You mentioned regulatory review. Can you describe precisely what that means? Is that the prior review of the clinical hold for imetelstat or is that something else?

We plan to submit information as you would expect to regulators and I think that's what that implies.

So we're going to wait for that feedback to come back from the FDA and?

I don't think we will comment -- make any comments further about any regulatory matters, Roy.

So my next question is and I think maybe the last poster that you mentioned or presentation at ASH that I haven't found yet might speak to this, but the patient population for IMbark, how do we think about or maybe help us think about maybe the relapsed refractory population. So about 50% of the Mayo myelofibrosis patients where prior JAK patients. Can you help us, maybe point us in the right direction of how to think of the relapsed refractory population, how to think of the potential outcome?

Yes, happy to do so. So the relapsed refractory population as we've described on previous calls and presentations, Roy, is as far as I know and as far as I think we've been able to identify, this the only time this patient population has been really fully addressed. So these are not just JAK in the IMbark study, these patients are not just patients who have been previously exposed to or treated with a JAK inhibitor, but actually they are patients who have -- who are actually -- did not respond initially to a JAK inhibitor that's the, obviously, the refractory and -- or they are patients who have had deterioration or progression of their symptoms, both symptoms and spleen volumes while on a JAK inhibitor. So this is quite a severely ill population and I think that it represents a more ill population than any that we studied previously and that as far as I know we have been studied by other drugs in the space, in the field.

Okay, great. So this last poster that you mentioned from Janssen, the drug treated population, does that speak to that population at all or?

Yes, it does actually. I mean within the confines of it not being a clinical, natural clinical study, it was a study of claims databases. It was pretty interesting. I mean they -- you can read the poster and we're not going to go into it in depth. But they recapitulated sort of the -- whether there was or was not a survival benefit associated with rux treatment and then they also calculated a mean survival in patients who would actually discontinued treatment with rux. I mean we don't know exactly why, but presumably because they were no longer responding and it was very substantial difference. So I think that it really did a nice job of recapitulating how quite ill these patients are.

Okay. Great, that's helpful, thanks. Last question will be a quick one. The CML poster presentation that you mentioned the abstract, I think this is going to be like getting blood from a stone, but they have a light at the end, a strong rationale for trials. Any comment on the potential for a CML trial?

I don't think we're ready to talk about CML or really any of the other indications that we have been chatting about. I will say that one of the benefits potentially or at least one of the rationale for studying imetelstat in hematologic myeloid malignancies are that many of these, if not all of them, of these types of malignancies appear to be associated with highly proliferative neoplastic clonal populations. And so one's tempted at least to think that there may be some opportunity beyond in multiple different heme malignancies beyond those that we've studied and we've talked about that in the past. But whether or not there is anything specific that's going to come out of for example this program or this abstract or any others, we're certainly not prepared to articulate anything beyond the studies that we started today.

Okay, great. And sorry, last one, do you guys have anything planned at ASH this year, Investor event?

We don't have an Investor event planned this year.

(Operator Instructions) And our next question comes from the line of Alex Schwartz from Stifel. Your line is open.

Congrats on your continued progress. Just two questions if I may. How will the interim analysis of the 2Q myelofibrosis and MDS be communicated? Will it be in a press release similar to September interim analysis or if a call afterwards or are you kind of somewhat captive to your partner's wishes, if you could elaborate on any of that, that would be excellent.

Great question. If it gets my usual answer, it depends. What we've always said Alex is that, if there were changes made in the program and/or any of the studies that we would then report on those changes. The change that was made to the dosing arms in the IMbark and the MF study clearly qualified for that, so that's why we went ahead and have press release and actually a conference call surrounding that. And at the same time, it seemed churlish not to note that the MDS study was continuing unchanged.

I think it is highly likely that there will be some information available especially from the MDS study since we have effectively finished the -- and we will have pretty much fulsome data on Part 1. I think it would not be unreasonable to expect that we would have some information around that. But we're not promising anything [with specificity].

Right.

So that's pretty much what I would say today if there are changes in the program then we will make an announcement and we're pretty disclosive -- pretty quickly disclosive about those kinds of things.

Yes, absolutely. Well, the additional color definitely helps. The other question I had is congrats on the up coming ASH presentations. You've produced some interesting preclinical data with imetelstat in AML, when can we expect to see clinical development in that indication as much as you can talk about it and what might be some relevant competitive therapies or where do you kind of see it fitting into the treatment landscape?

Yes, that's a great question. Thanks. Well, first of all, I think both we and Janssen have always been intrigued by potential in AML. Although Dr. Tefferi never actually as far as I recall never actually presented the results, it was extremely early single agent activity. We've always said that there was anti-leukemic activity that was observed in those patients, and you will recall that those were the patients with the blast phase of MF, which is a particularly difficult secondary form of AML to treat and most of those patients die very quickly unfortunately. But we did see anti-leukemic activity and we've also stated before that it would be necessary in our, I believe, also Janssen's view to actually treat patients with combination therapy.

With regard to other therapies, I think all I can say about that is that, and with regard to sort of where you might aim, I think our biggest challenge, which is a common challenge in the treatment of AML is that many of the existing therapies do have significant cytopenias associated with them. If you look at the hypomethylating agents, there's no question about that, right. And so they're -- and they're quite toxic. And so on one hand one would like -- you probably going to need to do some form of induction therapy because imetelstat takes a little bit longer to get going and get acting at least in other indications.

But with regard to the exact type of drugs and/or the exact nature of those combination drugs, that's actually under consideration at the moment. I don't really have anything to announce or give you any specifics around AML, but I can tell you we continue to remain very interested.

And our next question comes from the line of Charles Duncan with Piper Jaffray. Your line is open.

This is Sarah on for Charles. So glad to hear the progress from you guys today. I have two questions. First one, can you help us to understand why it might take 24 weeks to show an impact from imetelstat and its mechanism in MF?

Sure. I would remind everyone that the standard length of time in most studies of MF even amongst the JAK inhibitors is actually most of the primary endpoints are 24 weeks, that was COMFORT-1, the ruxolitinib. COMFORT-1,which was the initial study used to support an approval was actually had a primary analysis of 24 weeks. I don't believe we've ever seen a 12-week data actually from that study or any other studies for that matter that I am aware of in JAK inhibitors.

COMFORT-2, the second study, was as I recall a 48-week time point. So these diseases and other studies done by other manufacturers with other JAK inhibitors in the space have all required fairly lengthy periods of time before they read them out. And I think that, that's not so much a reflection necessarily of the mechanism of action, but I think it is actually a reflection of the fact that these patients developed most of their anatomic abnormalities including bone marrow fibrosis, including splenomegaly and many of the bony changes that you see and other changes you see as a result of MF over some period of time. And just getting reversal of those does take a fairly lengthy period of time.

So, I think it's better safe than sorry and we don't actually -- this is an experiment in patients with IMbark as to a more severely ill patient population. So we don't really know exactly how long it would take, so 24 weeks seems to be a very reasonable timeframe based on prior experiences with other drugs.

Thanks. That's helpful. Look forward to those results. And then second question. So I notice there's an ASH abstract with data from imetelstat in essential thrombocythemia, where you see the increase telomere length with decreased driver mutation burden. Is that new data this year and does that support what we think the mechanism of this drug is?

Well, to take the latter first, yes, I think it does strongly support it. Again, I don't want to go into great detail about the specifics of the data in the abstract, but I'll just simply say that at a high level certainly telomere length is often been thought to be associated with -- shorter telomere length is often been -- thought to be associated with very rapidly dividing malignant cells. And we know that there were a variety of different things in the past that have been talked about in The New England Journal paper and so on of the -- in these ET patients that when they had strong clinical responses, there was also a decrease in mutational burden, an allelic burden in the blood and so forth. Now this extends some of those observations specifically to telomere length, which is probably we think closely associated with the mechanism of action of the drug.

So, overall, I think that this was an important additional observation made in a group of patients -- from patient materials and patients themselves, who have been followed for an awful long period of time on the drug and who have very well characterized clinical observation. So I applaud Gabriela Baerlocher and her colleagues who have continued to -- to really get the most out of this patient data set and really understanding even further that how the drug probably works, which is all associated with suppression of malignant progenitor cell clones.

And our next question come from the line of Ling Wang from be BTIG LLC. Your line is open.

Chip, I just wanted to clarify for the IMbark study, the primary analysis will be based on 100 patients or 200 patients received imetelstat for 24 weeks?

Yes, so it's now 100 patients in the 9.4 mg/kg arm. Since we've dropped the enrollment -- stopped enrollment in the 4.7 mg/kg arm, Ling, obviously there -- you had to pick a number of patients and the original number of patients in the 9.4 mg/kg was expected to be 100. So that was -- that's the number that is currently being expected for the primary analysis.

So but the trial will only enroll 100 patients with the lower dose drug?

No, there will have been however many patients that were already enrolled in the lower dose arm will -- they weren't stopped, they continue on. And then there were -- then all of the new patients that -- well, there were number of patients that were in screening and we've said that those patients were put onto 9.4 mg/kg.

Now enrollment today is suspended in the 9.4 mg/kg arm and so we don't know today whether we'll ever get to a 100 patients in that arm. If the study is restarted, it would be with the expectation we would get there. If it's not restarted and something else is done, then we won't.

So if it is the enrollment restart and then you will enroll a total of 100 patients for the 9.4 mg/kg dose plus whatever number of patients already in the 4.7 mg/kg dose, is that right way?

That's correct with one minor additional comment. The 100 patients for the primary analysis is actually those patients who were started, a 100 patients who were started at 9.4 mg/kg as the starting dose. So the patients who get changed to 9.4 mg/kg from 4.7 mg/kg, they don't count for that 100. Just to make it all the more confusing.

I see. Exactly. It's good. So I understand it now. So the lower dose -- patients started with lower dose, just keep there. Once the amendment is completed, they will receive higher dose, but they're not included in the primary analysis.

That's right. There will be a separate analysis for the low dose patients or patients for that matter started at low dose and went to a higher dose.

And our next question comes from the line of Thomas Yip from FBR & Company. Your line is open.

I guess, first, I just want to learn more about IMbark specifically regarding the protocol amendment and progress. What should we expect to be the main focus of the review, would it be more weighted on safety or more weighted on efficacy?

There's a good question. I usually, resolutely, don't try to predict what regulatory authorities or health authorities will focus on. We obviously are giving them all the necessary information. I certainly -- if I understood your question right, which was what will they focus on. Now, so Olivia is shaking her head at me and saying I may have misunderstood your question, maybe you could restate your question.

I mean that was primarily my point is that so they have the data so far for [both] final dose imetelstat. So, in the process of approving the patients in the low dose arm to be given high dose in the future. Would they be looked at -- I mean I mean they will look at data from both doses, but would they be focused primarily on the safety of those two doses or at the efficacy of those two doses.

Yes. Yes, Thomas, they will. I think everyone -- whether you were a sponsor or regulator, I think that you would look at the same things, which are fundamentally, is there a meaningful difference in safety or risk profile or risk-benefit profile in one arm versus another. We obviously made the conclusion that there was a difference in the low dose in that the efficacy was not adequate and that's by definition a change in the risk benefit profile.

And I guess we've stated our point of view, which is or Janssen stated their point of view that by offering an amendment to increase patients to the 9.4 mg/kg that they feel comfortable that patients who would move from 4.7 mg/kg and 9.4 mg/kg would enjoy at least as good, if not better, presumably a better benefit risk profile than at the 4.7 mg/kg. I think beyond that, it's pretty hard to read everybody's mind, but I think all of that will be taken into consideration.

Janssen, certainly, by offering up that amendment, I think made it clear that their point of view and I would concur with it, is that they -- is that that would be a reasonable thing for people to do, to go to the higher dose.

Sure. That makes sense. Thanks for the explanation. And also following the protocol amendment, I mean I know you just say, "Can we read their minds," but is it possible for them to recommend another dose that is other than 4.7 mg/kg or 9.4 mg/kg?

Who is them in this case, Thomas, just so I'm clear?

I'm guessing mostly, you mentioned regulatory agencies, I'm assuming the FDA and perhaps the EMA?

Well, usually in protocol amendments one puts forward a protocol amendment and if it is agreed upon, it goes forward. If not, there's a conversation of some nature. And I suppose it is entirely possible within that conversation that they could say they would not be comfortable with that. But clearly the sponsor in this case has said that they are and usually the sponsor has the most data and so might be asked to justify it or what have you, but that would be the general gist of things would be kind of makes sense.

We don't have -- I mean let me be very clear, we don't -- we have very, very limited data in MF or for that matter really most diseases. But in MF in particular or any of the heme malignancies at lower doses intermediate between 4.7 mg/kg and 9.4 mg/kg other than the MDS, which is obviously 7.5 mg/kg. But in MF, the majority of our information is that -- is at the -- at these two doses now. So it would be -- it's possible someone could ask for information or speculate on what might happen, but it would be hard for us to know our priority. So that's, I think, we've made our best. We've put our best foot forward for the 9.4 mg/kg.

Sure. That's reasonable. One final question, can you please remind us what should we expect at the second internal review of both IMbark and IMerge trials that's expected in second quarter 2017?

Well with regard to IMerge, the MDS study, the design in that study is that there is a Part 1, which was the open label sort of lead-in, if you will, hoping to recapitulate some of the types of responses seen in the open label study that Ayalew Tefferi conducted in a much smaller number of patients. And so we should be in a position or Janssen should be in a position to determine at some point after seeing the results from the Part 1 whether or not to proceed to Part 2, which as you may recall is already part of the protocol and is a randomized placebo-controlled study of imetelstat in MDS. And is intended to be a Phase 3 study. So at some point, there will have to be some decisions made whether to proceed or not with that.

With regard to IMbark, we've commented that there are couple different things that could happen. The first one is that the study could be restarted at 9.4 mg/kg and continued on and as we talked about in the previous discussion with Ling, that would go presumably to 100 patients for the primary analysis, 100 patients would be started on 9.4 mg/kg in total. Another possibility is that arm could be dropped, I guess another could be substituted, it's possible, but could be dropped or the study -- that trial could be stopped altogether. Those are kind of the things that we've laid out and I think that after this interim analysis one, our interim review, I think we should be in a position to hopefully make some of these decisions.

Thank you. And that completes today's question and answer session. I would like to turn the call back over to Dr. John Scarlett for closing remarks.

Well, I'd just like to thank everyone for joining and following the company. We look forward to communicating future results in future conference calls. Everybody, have a good day. Bye.

Ladies and gentlemen, thank you for your participation in today's conference. This does conclude the program, and you may now disconnect.