TG Therapeutics, Inc. (TGTX) Q3 2015 Earnings Report, Transcript and Summary

Greetings, and welcome to the TG Therapeutics' Inc. Third Quarter 2015 Earnings Conference Call. At this time all participants are in a listen-only-mode. A brief question-and-answer session will follow the formal presentation. [Operator Instructions]. As a reminder this conference is being recorded. It is now my pleasure to introduce your host, Jenna Bosco, Director of Investor Relations. Thank you, you may begin.

Thank you. Good morning and welcome to our conference call regarding TG Therapeutics third quarter 2015 financial results and business update. I am Jenna Bosco, TG's Director of Investor Relations and I welcome you to our conference call today. Following our Safe Harbor statement, Sean Power, TG’s Chief Financial Officer, will provide a brief overview of our financial results and then turn the call over to Michael Weiss, the Company’s Executive Chairman and Interim Chief Executive Officer, who will provide an update on the ongoing development of our novel glycoengineered anti-CD20 monoclonal antibody, TG-1101, our novel once-daily PI3K delta inhibitor, TGR-1202, as well as a review of our preclinical program. Before we begin I would like to remind everyone that various remarks that we make about our future expectations, plans and prospects constitute forward-looking statements for purposes of the Safe Harbor provisions under the Private Securities Litigation Reform Act of 1995. TG cautions that these forward-looking statements are subject to risks and uncertainties that may cause our actual results to differ materially from those indicated. Factors that may affect TG Therapeutics’ operations include various risk factors and uncertainties that can be found in our SEC filings. This conference call is being recorded for audio rebroadcast on TG’s website, www.tgtherapeutics.com, where it will be available for the next 30 days. All participants on this call will be on a listen-only mode. Now, I would like to turn the call over to Sean Power, our Chief Financial Officer to briefly discuss the financial results for the third quarter of 2015 as well as the company’s overall financial conditions.

Thank you, Jenna. And thanks, everyone for joining us. As you may be aware, our financial results were released this morning and can be viewed on the Investors and Media section of our website at www.tgtherapeutics.com. I’d like to begin by providing an update on our cash position. At September 30, 2015, we had cash, cash equivalents, investment securities and interest receivable of $115.4 million, as compared to $78.9 million at December 31, 2014. Turning to the financial results for the quarter; our consolidated net loss for the third quarter ended September 30, 2015, excluding non-cash items, was approximately $12.4 million which included approximately $6.9 million of manufacturing and CMC expenses in preparation for Phase 3 clinical trials and potential commercialization. The consolidated net loss for the third quarter ended September 30, 2015, inclusive of non-cash items, was $13.7 million or $0.28 per diluted share, compared to a consolidated net loss of $17.5 million during the comparable quarter in 2014, representing a decrease in consolidated net loss of $3.8 million. The decrease in consolidated net loss was primarily the result of $8.1 million of expense, $4.1 million of which was non-cash recorded during the 2014 period in conjunction with our licensing agreement for TGR-1202 and a $2.9 million decrease in non-cash compensation expense related to equity incentive grants over Q3, 2014. Partially offsetting the aforementioned decreases, other R&D expenses related to TG-1101 and TGR-1202 increased $4.8 million and $2.1 million respectively over the comparable period in 2014. Our consolidated net loss for the nine months ended September 30, 2015, excluding non-cash items was approximately $32.5 million, which included approximately $16 million of manufacturing and CMC expenses in preparation for Phase 3 clinical trials and potential commercialization. The consolidated net loss for the nine months ended September 30, 2015, inclusive of non-cash items was $45.3 million or $1.01 per diluted share compared to a consolidated net loss of $37 million during the comparable period in 2014, representing an increase in consolidated net loss of $8.3 million. The increase in consolidated net loss during the nine months ended September 30, 2015 was primarily the result of other research and development expenses for TG-1101 and TGR-1202 increasing approximately $14.6 million and $4.5 million respectively over the comparable period in 2014. This was offset by $9.3 million of expense, $5.3 million of which was non-cash expense recorded in conjunction with our licensing agreements for TGR-1202 and IRAK4 inhibitors program during 2014 and a decrease of $3.2 million in non-cash compensation expense related to equity incentive grants over the comparable period in 2014. I will now turn the call over to Mike Weiss, our Executive Chairman and Interim CEO.

Great. Thanks, John and good morning everybody. The third quarter of 2015 was an exciting time for us as we were able to check off some additional key milestones from our list of goals for 2015 obtaining a Special Protocol Assessment for our UNITY-CLL trial, in patients with front-line as well as relapsed/refractory CLL, it was an extremely important and exciting milestone for us as it represents our first pivotal trial for the combination of TG-1101 plus TGR-1202 what we call TG-1303 or simply 1303. If successful, this trial should provide 1303 with a broad approval in CLL offering patients in both front-line and relapsed/refractory setting, a novel, chemo free treatment option. It also will allow us to use 1303 as a base for future triple and possibly quad combination therapies. Another important achievement for the quarter was the initiation of a Phase 1/2 study evaluating the use of TG-1101 plus TGR-1202, plus pembrolizumab, the anti-PD-1 immune checkpoint inhibitor, in relapsed/refractory CLL patients. This study marks the first clinical trial evaluating the safety and tolerability of combining a PI3K delta, an anti-CD20 monoclonal antibody and an anti-PD-1 checkpoint inhibitor as we continue to break new ground and lead the field in novel combinations. We are excited about the progress we made during the third quarter and have been working tirelessly towards accomplishing remaining goals on our 2015 list. With the two phase 3 programs established in CLL, we are looking forward to expanding our registration program into Non-Hodgkin's lymphoma as soon as possible. Before taking a deeper look into our oncology programs and the upcoming ASH presentations, I wanted to briefly touch on an area I think will start to capture broader investor interest next year and manage [ph] our expansion into autoimmune disease, an area where B-cell targeted therapies have proven to be highly efficacious. Our goal is to launch our first trial in Multiple Sclerosis in the near-term. I won’t say in much more today on the autoimmune applications in terms of strategy or trial design but investors should get ready as the next year this area can really heat upcross. I will say since Roche announced their successful Phase 3 study for their anti-CD20 monoclonal antibody NMS and Novartis paid almost $1 billion in upfront of milestone payments for obinutuzumab we have seen considerable interest in our B-cell targeting agents from larger players in the space. We plan to move forward in autoimmune as aggressively as we move to the oncology programs and believe it may be possible to launch a phase 3 trial late next year. Moving back to oncology, I’d like to start by reviewing our current phase 3 programs. First, the GENUINE Phase 3 trial which is evaluating TG-1101 in combination with ibrutinib, in patients with high risk chronic lymphocytic leukaemia, or CLL which now has nearly 140 sites participating in the study. Enrolment into this trial is of the utmost importance to us and the number of sites we’ve been able to bring on board is a great accomplishment and a testament to the appeal of the 1101 or ibrutinib regimen among clinicians. Enrolment is moving along on pace and we are still targeting to complete enrolment into this study and analyze the overall response end point by the end of 2016. Moving along to our recently announced UNITY-CLL study, this is a phase 3 clinical trial of TG-1101 plus TGR-1202 or again referred to as a 1303 combination in front-line and previously treated patients with CLL which is also being run for CMC and SPA. The basis study design is a randomized controlled clinical trial that includes two key objectives. First, to demonstrate the contribution in each agent in the 1303 regimen and second to demonstrate superiority in progression free survival over the standard care to support for submission for full approval of the combination. The study will randomize patients with the four treatment arms 1101, plus 1202 or 1303, 1101 alone, 1202 alone and an active control on obinutuzumab which is commercially known as Gazyva plus chlorambucil. In each interim analysis, we’ll access contribution of each single agent in the 1303 combination regimen and which if successful will allow early termination of both single agent owners, a second interim analysis will be conducted on total enrolment into the study which if positive we plan to utilize for accelerated approval assuming an early termination of the 1101 and 1202 single agent arms the study will enrol approximately 450 patients. This study is being led by Dr. John Gribben, Professor of Medicine and the Gordon Hamilton Fairley Chair of Medical Oncology at St. Bartholomew's Hospital, at the Barts Cancer Institute in London, England. As mentioned earlier, we are very excited about this study and the related SPA. If successful, this trial should lead to a very broad label in the treatment of CLL and position 1303 as a backbone for further proprietary combination therapies as it continues to drive for better patient outcomes and ideally for secure [ph]. Now, let me read some of the data continued in our ASH abstracts, which were released last week. Please be aware that the ASH abstracts were submitted only about two months after our ASCO and Lugano presentations and thus do not contain all the patient data that will be presented at ASH. Turning to the abstracts, which I’ll review in the order in which they will be presented. The first presentation which will occur during the Saturday post recession will be an update to the 1101 plus 1202 combination or our 1303 study. Some highlights from this abstract include of the 56 patients enrolled in evaluable for safety, the only grade 3 for adverse events reported in greater than 5% of patients was Neutropenia. On the efficacy side, of the 37 evaluable patients treated at the higher doses of TGR-1202, five or seven patients with CLL, SLL responded to treatment. Of the two patients not responding, one patient remains on study as a stable disease creating further assessment and the other patient ibrutinib refractory 70p delete [ph] patients achieved stable disease that eventually progressed. We’ve also seen a high level of activity in Indulin [ph] lymphomas and diffused large B-cell lymphomas including 16 responses out of 28 patients which includes a Richter's patient that responded to the combination. The next presentation will be during the Sunday post recession and will give the combination of 1202 plus obinutuzumab and chlorambucil. This is an interesting study, which was designed as a backup registration strategy and we’ve been unable to establish a regulatory pathway for 1303 which now has been accomplished for the UNITY-CLL study. Nevertheless, we believe this study provides you interesting data points and helps in foremost about what we may expect to see in the front line setting with 1303. Some highlights from the abstracts include, of the 14 valuable frontline patients, 13 or 14 responded with the remaining patient exhibiting a 48% reduction in the novel size and a further efficacy assessment. Of these frontline patients 43% were MRG negative following treatment. Interestingly, there were only three previously treated patients on this study, all three would be [Indiscernible] of which two or three responded to the combination with the third patient experiencing a significant no reduction ending further assessments. Moving to Monday, we will have three additional presentations. The first is for the combination of 1101 plus ibrutinib in patients with mantle cell lymphoma. As you may recall, this is the second cohort of the 1101 plus ibrutinib study for which we’ve previously reported results for CLL patients. Some highlights from this abstract include of the 15 evaluable patients 87% responded with 33% out of 15 having a complete response. This compares very favourably to the ibrutinib label that showed a 66% overall response rate with just 17% complete responses. We believe these data further confirm the activity seen in the CLL cohort with the 1101 plus ibrutinib combination where we see higher response rate in deeper responses by adding 1101 on top of ibrutinib and this gives us additional confidence in the possible positive outcome for GENUINE Phase 3 study. The next presentation during Monday’s post recession will be an update to our single agent TGR-1202 Phase 1 study. Highlights from this abstract include of the 75 patients with a variety of relapsed refractory B-cell malignancies treated with single agent TGR-1202 no grade 3 or greater AEs were observed in greater than 10% of the patients. Notably with single agent 1202 hepatic toxicity remains limited and we have yet to observe a case of colitis with some patients now on this study for over two and a half years. From an efficacy standpoint, 94% or 15 of 16 of the CLL patients achieved a notable response including 63% that have a true partial response by the Hallek criteria. In the Indolent NHL cohort, of the 16 evaluable patients, 14 or 88% have achieved reductions in tumor [ph] burden with six patients on study for over 12 cycles which is approximately 12 months and some patients on therapy over two years with five of 12 follicular patients achieving an objective response with many still on study pending further efficacy assessments. Finally, TGR-1202 demonstrated activities of diffused large B-cell as a single agent with three of eleven evaluable patients responding to therapies. And last, but not least on Monday Dr. Dang [ph] from Columbia University will give an oral presentation for some very exciting preclinical work which identified a novel mechanism of action with TGR-1202 as distinguished from other PI3K delta inhibitors. Through this new mechanism, TGR-1202 synergised with Brentuximab [ph] the produce inhibitor [Indiscernible] now AMGEN to the previously very challenging target. This research could have important implications in the treatment of aggressive lymphomas and potentially from solid tumors. We are very excited for the upcoming ASH conference and are looking forward to providing you with extended data sets for the abstracts we just reviewed. We will also be hosting an investor reception with the distinguished panel of leading experts in CLL and NHL on Monday December 07, at 7:45 PM at the Hyatt Regency in Orlando, Florida. And we welcome and encourage all of you to join us. We are planning a great event this year and hope to provide attendees the opportunity to hear some fresh perspective. As always, this event will be live webcast on our website at www.tgtherapeutics.com and for those of you who cannot listen into the live event, a replay will also be available on our website. With that, I’d like to wrap up today’s call by reviewing the key golden objectives remaining for 2015. We will continuously aggressively recruit into the GENUINE Phase 3 clinical trial of 1101 in combination with ibrutinib with the goal of completing enrolment and analyzing the overall response endpoint in the second half of next year. We look forward to enrolling the first patient by year and our UNITY-CLL Phase 3 clinical trial of the combination of 1303 and front line and relapsed/refractory CLL, our second Phase 3 clinical program under SPA. We also hope to announce our next registration file, evaluating 1303 in patients with NHL. We will continue to recruit into a triple combination cohort of 1303 plus ibrutinib as well as the triple combination study of 1303 plus pembrolizumab as well as seek to evaluate additional novel triple combinations of interest. We look forward to expanding into auto immune disease with diverse trial, a Phase 3 trial on Multiple Sclerosis to start in the near future. We will continue to advance our preclinical compounds including IRAK4, anti-PD-L1 and anti-GITR in the clinic and towards clinical development as an update we had hoped to have IRAK4 in the clinic before yearend, however we are still reviewing the two lead candidate and we are now targeting the first half of next year. And finally, we will continue to seek additional drug candidates to further compliment our current portfolio. With that, let me turn the call back over to the conference operator to begin the Q&A session, following which I will return to make some concluding remarks.

Thank you. We will now be conducting a question-and-answer session. [Operator Instructions]. Our first question comes from the line of Joe Pantginis with ROTH Capital. Please proceed with your question.

Hey guys, good morning thanks for taking the call. A question on -- Mike in one of the under studies going right now, it appears there’s been deliberate talks in the accomplished study between design or and [Indiscernible] so just wondering if you can just -- you might have seen today or not seen today with regard to your CD20? Thanks a lot.

Yes, thanks Joe. Yes, I think I need to go back and look at some data of our CD20 alone, but in terms of 1101 plus 1202, again I think we reported a compilation of data at ASCO and [Indiscernible] of the data and I’m recalling it somewhere below 3% or 4% of how the toxicity we have seen with both single agent and the combination with CD20. So it does appear to be very different than what we’ve seen with obinutuzumab and chlorambucil. The other thing I’ve noted about that, that toxicity that we’ve seen in that combination study, one, we are adding chemotherapy into the mix. Two, the obinutuzumab plus chlorambucil toxicity profile does have about a 30 % incidence of liver tox on its own. It does not appear that adding 1202 increase the incidence of liver tox, it does appear that perhaps it’s moved some patients that were grade 1/2 liver tox from the obinutuzumab kind of cell to grade 3. So looks like there might have been just some shifting when you add the third drug on top, but again you know we are working with chemotherapy, the responses were great, I mean the patients all seem to tolerate the therapy and stay on therapy, so it wasn’t an actual issue in terms of patient management. But I think anytime you are using chemotherapy, in combination with anything you might expect to see additional toxicity.

Thanks Mike.

Our next question comes from the line of Matthew Kaplan with Ladenburg Thalmann. Please proceed with your question.

Hey guys, good morning.

Good morning, Matt.

A couple of questions, first I guess focussing on your monotherapy in combination. Could you talk a little bit about how you designate responders or PRs, I think you know using the Hallek criteria and the impact of lymphocytosis in patients you are designating PRs.

Yes, sure Matt. So you know it’s interesting and kind of larger process up. I mean we have seen a movement among some other companies to sort of lump together as responders PRs and PRs with lymphocytosis. The Hallek criteria is quite clear that the PR is a PR and it does not include a PR with lymphocytosis, but I think a lot of companies will post a very large number and include those patients with lymphocytosis. We always, we refer to patients who could lymphocytosis as those that are -- in nodal response but not a true response, and so, when you look at the single-agent therapy we just reported we had – with the nodal response we had 94% of the patients. Technically we could say that we had an overall response of 94% which include true response of 53% another 31% of the patients who had PR with lymphocytosis and got a larger number of 94%. I think it a – it's just a different way that people try to present data. We try to keep it as strict as possible to the Hallek criteria and what's generally acceptable in the CLL community. But I do thing that if you look at our data on an apples-to-apples basis the 94% PR, plus PR plus lymphocytosis, it’s as good if not better than any BTK data that’s ever been presented and certainly is good if not better than any PI3K delta data that’s been presented. Now, I would also caution that regard to smaller number and across study comparisons are always dangerous, but I do feel that we present in a way that strict to the Hallek criteria and I would just say that, we do believe our PI3K delta has shown data that is as good as the best data that's been seen out there and we're certainly confident that's an active PI3K delta and in active agent-CLL.

That's helpful when you're comparing across different studies, which is obviously impossible to do.

Yes.

But I guess in term so few of you some of the triple combos study that you have ongoing. And then also some plans that you have. Notice recently you initiated, there was a study in solid tumors, any plans there as well?

Yes. With respect to the triples, the main triple therapy studies are the combination with ibrutinib 1303 plus ibrutinib. And just to be clear on that particular study is a sub-cohort of our 1303 doublet study. So what’s seem -- we definitely were hopeful to have additional triple data available for this conference. But as it turn we really need to focus our recruitment on the doublet, so we can start our Phase 3 trials for the doublet, so we did deemphasize recruitment into the triple cohort of that study, and these are same site, face the same patients, so we have to devote in priority direction, so we did that to complete the doublet cohort and we'll recircle back and start to emphasize the triplet, so 1303 plus ibrutinib cohort going forward. The other combination which is a separate study is our combination with the PD-1 inhibitor that's been conducted at Pem [ph] so that's going along so far quite nicely. We're obviously super excited about that study. There is going to be some data of PD-1 in CLL patients just coming up at ASH, so think that will interesting and exciting information, because we have that maybe to layer into our 1303 combination. And then, in terms of solid tumors we – I'd say, we've seen preclinical some signals. We've definitely review the literature and seen some potential for exciting translation of science, PI3K deltas in solid tumors. So, I would call this first study highly exploratory as we continue to just expand potentially utilization of our compounds.

Great. And then, another question, shifting gears a little bit to autoimmune setting, you mentioned in your prepared remarks that you see some interest on the partnering guidance. From a business point of view what's your strategy in MF and would be considering partnering I guess, some of those assets there?

Yes. Obviously it's super early for us. We’ve just literally starting to rotate into autoimmune, but maybe because of that, we probably more willing to consider partnership opportunities on the autoimmune side. And we have definitely seen some interest in that area. So I think very early days and that's why I said sometime next year we should see things heating up a bit as we get our clinical program up and running. But in contrast to the oncology side where we've been quite resistant to seek partners because we see it as a complicated metrics as we're interested in achieving in terms of these combinations and trying to identify partner that may share our vision, our very long-term vision just did not make it interesting for us to explore opportunities on that side. I think on the autoimmune side it’s a little bit more straightforward. We do think we actually come to the table with a unique package of opportunities and a way to enable B-Cell therapy to be different than what is currently available with the two antibodies that are working their way through the clinic one obviously is about to be filed and one is about to enter Phase 3. So we do think we provide a very interesting approach where we have the CD20, but we also have PI3K delta and we do think there's a wait of combine those – that's rational and that could really achieve the face of treating autoimmune disease with B-Cell targeted therapy. So we are excited about the area where we're doing a lot of work of cells. We see some great interest in this area. So I think from strategic standpoint we're definitely probably more open to opportunities in the autoimmune side, but clearly we're not in a super rush to do it. If the deals are not on terms that would make us excited, we'll push forward. We really do think we have a very intriguing value proposition for patients.

Thanks for taking questions and congrats on the progress.

Thanks, Matt.

Our next question comes from the line of Jonathan Aschoff with Green Capital. Please proceed with your questions.

Thank you. Good morning, guys.

Hey, Jonathan.

You know I was bouncing [ph] around a few 8.30 a.m. calls, I'm sorry if any of this is covered, but given the very positive Roche MS data, what is sort of your early data go, no go kind of – do you want to be active is a better of mandated wear or you maybe making the decision for the next trial after the first one?

Yes. So, we have a strong believe that B-cell depletion data will guide us in terms of – actually B-cell and some repletion data or recovery data will be the guide, so we don't need to do it very large study before we move into Phase 3. We're highly confident that our CD20 should work as well if not better than the Roche CD20. So, we're going to enter Phase 2 dose ranging trial. We're going to look at just a few different doses and schedules for the MS protocol. And assuming we see the level of B-cell depletion as comparable to what is seen with of the other CD20 antibodies, we'll be prepare to move directly into Phase 3. We don't see any reason to wait around to see – the effect of these drugs is for B-cell depletion. I would say the changes in the lesions and other outcomes are consistent with B-cells depletion effects. So, it’s a really strong target for us. And that's would be the plan moving forward. So that's why we do believe that is possible to get into a Phase 3 sometime in the later second half of the next year.

And you think you would do all of that with relapsing forms only or will you start perhaps the more difficult to treat MS before you start a Phase 3 with relapsing?

The relapsing is the – I would say the most linear way to market, lowest hanging fruit, the primary progressive data Roche presented is incredible and that it was positive, but we need to do just little more work around the powering of the study and the sizing given the effect size was not as dramatic in the primary progressive, which is understandable. But given that the effect size was not as dramatic as it was in the relapsing remitting population, we just really need to think hard about what that study would look like. In the meantime, the relapsing remitting data was quite robust with 340s in the fee value before a number, which gives us a very good understanding of how to power our Phase 3 studies. So I think we have a lot of information now on how to power those studies and we think that we don't need to run as large pivotal study. Again, there'll be a function of how many patient exposures and for how long will be required and that will be further discussion with the agency. But in terms of surely powering a Phase 3 program to Phase 3 studies, we do that we will need significantly less patients from a powering standpoint, efficacy standpoint than Roche had used those studies, because we now have a better understanding of what the effect size ought to be. So, for us the Roche remitting is sort of the direct linear path, low hanging fruit. I think there is great interest in our side and attacking the primary progressive as well. I just think that will be on a slight stagger start from the last Roche remitting program.

Okay. Thanks. I was wondering how many patients are enrolled to-date in 1303 plus ibrutinib. Can you tell us that or anything else about how it's progressing given that we won't see it in the next month?

The 1303 plus ibrutinib triple therapy?

Right.

I have no idea. I have to go check with the guys. I just know that they were in a lot of new patients and the investigators wanted to instead of updating what they had they wanted to really push from nominal and into a bigger presentation later itself, so I actually don't have the number on hand, but I can check and back to you.

Okay. And Sean, what's the SG&A spend anomaly about. Is Sean there?

Yes. Sean is out remotely and so hopefully he can answer that question.

As just say, it was awfully low and I was just wondering what the reason was. Jonathan, can you hear me, okay.

I can hear you.

So you asked about the SG&A anomaly and what their uses are?

It was just low in the third quarter and I was just curious as to why?

We stop paying salaries Jonathan.

Take it easy.

I think Jonathan actually pull out the non-cash compensation, looked at just the regular SG&A you’ll find that it’s inline with prior period.

Okay. Thanks a lot. Thank you.

Thanks, Jonathan.

[Operator Instructions] Our next question comes from the line of Reni Benjamin with Raymond James. Please proceed with your questions.

Hey, good morning, guys. Thanks for taking the questions.

Hi, Reni.

Hey, Mike. Can you – I think you mentioned that there's a 140 sites that are onboard right now. Will you be expanding a further the number of sites and when you really comes on board will you have largely the same sites that are going to be enrolling for UNITY and if that's the case, how do you deal with potential cannibalization of the patients for both the trial?

Yes. Thanks, Reni. I think that we're coming to the end of the site enrolment period, so my guess is somewhere between 140 and 150 will be approximate where we end the push on the sites. We've done a very good job in covering the United States and we've taken on again lot of the best community centers. So yes, the goal would be to bring UNITY on as many of the sites as possible, that would really synergize our efforts in terms of our ability to monitor, the cost savings will be tremendous and also what we like most about having both UNITY and GENUINE at the same site is that we basically offer to the site a trial for every patient. So if you're screening a patient they should never move the patient to a screen -- again obviously let they have some extrusion criteria that's difference than the actual diseases but we basically through the two studies. We basically cover every possible patients that could come – every CLL patients that comes through the door. The GENUINE study is focused on – if you look at a metrics of four boxes, front line and relapse/refractory, high risk, low risk or high risk normal risk, the GENUINE study is only in one of the boxes which is the high risk relapsed/refractory patient. The UNITY study covers all four boxes. So we're not really worried about cannibalization, anyone who is the high risk relapsed/refractory patient in an overlapping site would go into the GENUINE study while it’s still open and again the anticipation of that study will close at some point during the condos of the UNITY study, but while its open anyone with high risk CLL relapsed/refractory CLL will go into the GENUINE study, the patients does with the other three buckets, so frontline, all frontline will go into UNITY and relapsed/refractory with normal site, GENUITY will go into UNITY until GENUINE enrolment is done and then all patients at those particular crossover site would be eligible to just going to UNITY.

Okay. Thanks for that clarification. But I guess just looking at UNITY; you mentioned kind of the key components of the study. And I guess trying to get a sense, when do you think we might see the results from that first portion where we can get the potential termination of the single ARM and what kind of delta should we be looking for, do you guys need to hit in order to move to the next component?

Yes. The study can move on the next component without hitting anything technically, I mean the goal is as an adaptive design is to get rid of those ARMs as early as possible. The actual analysis for contribution will occur at somewhere less than half of the patients. We're at 40% of the patients on approximately. But given a non-linear recruitment curve, I wouldn't say that it will happen 40% into the study, let's say it is approximate 40%, right. It’s going to happen somewhere forward into enrolments as the enrolment will go on a pretty flat trajectory and then starts rising typical recruitment curves down. So I don't know – we don't know actually when that will occur. We do – obviously we know how many patients we need and getting understand the recruitment curve, its we could try to make projection, but it won't be – it will probably more than halfway into enrolment before we're able to do that analysis in terms of enrolment time, even though its less than half the patients.

And if there the ability built in at that same time or not really.

Is there if utility for the overall study?

Yes. I mean, at that first component juncture when you're trying to let's say drop-off the single ARM, if there a utility for the entire study both in as well?

No, no. I would not think we have enough data at that point anyway to do a utility analysis. But there is no form of utility analysis built into the study, obviously the TSMB has their own ability to terminate study early for Utility [ph] but we do not have a [Indiscernible] analysis built in. So at that point what we do the contribution, I'd say the worst case scenario at that point is that we are unable to eliminate ARMs because they are working so well and we cannot eliminate them at that point. Then those ARMs would have continued on forward, the study would be larger. I do believe we have an approach that will ideally lead to the elimination of those ARMs, but it is possible that they would vulnerable to them; it has to be carried forward, because we could not eliminate them based on activity.

Got it. Okay. One final question, just regarding, I know the abstracts pressure that you'd highlighted some of the endpoints and you mentioned the evaluable patients in each of those abstracts, can you give us a sense when we get the ASH for each of the study about how many evaluable patients per study we would have because I know you mentioned, you deemphasize the normal in the triple combos how much data are we expected to see in the other trials?

I don't have that handy right now. Might as well get back to you to give some additional guidance. I assume that – what I’ve assumed overall, and having talked how much many input in the abstracts versus which will be pending presentation, but our assumption is that in each of the studies that we're been presenting we'll see from the last update the ASCO regarding to update we're seeing additional 10 to 15 patients in each one.

Got it. Thanks very much and congrats on the progress.

Thanks, Reni.

Mr. Weiss, we had no further questions at this time. I would now like to turn the floor back over to you for closing comments.

Great. Thank you very much. So just to finish off 2015 has been extremely productive and exciting year for our company and we look forward to reaching more of our goals before year end. Our company has rapidly evolved over the last few years into a leader in combination treatment for B-cell malignancies. Starting combination trials that had never been tried before and gaining approval on unique trial designs, utilizing novel novel agents as we did with the UNITY-CLL study. We are proud of the data we have generated to-date and we're excited for the launch of our second Phase 3 study, the UNITY-CLL study which will be our first pivotal study for the proprietary combination of 1101 plus 1202. With two Phase 3 oncology programs underway and the third and possibly a fourth in the wings, we plan to next explore the autoimmune space with the same drive that we continue to show on oncology. We believe the potential of our pipeline candidates in autoimmune diseases and anticipate commencing our first trial in multiple sclerosis in the near term. Of course, we will continue to aggressively recruit into the GENUINE Phase 3 trial and look forward to presenting topline data from the study in the second half of 2016. But lastly, from a financial perspective, with more than a 150 million in cash and investments on hand at the end of the quarter we believe we are well positioned to extend on our goals and continue to broaden both our pipeline and clinical programs. On behalf of all of us at TG Therapeutics', I'd like to thank our investigators and their patience as well as our shareholders for their continued support. Thanks again for joining us and have a great day.

Ladies and gentlemen, this does conclude today's teleconference. You may disconnect your lines at this time. Thank you for your participation and have a wonderful day.