TG Therapeutics, Inc. (TGTX) Q4 2015 Earnings Report, Transcript and Summary

Greetings, and welcome to the TG Therapeutics' Inc. Fourth Quarter Conference Call. At this time all participants are in a listen-only-mode. A question-and-answer session will follow the formal presentation. [Operator Instructions] As a reminder this conference is being recorded. I’d now like to turn the conference over to your host, Ms. Jenna Bosco. Thank you. Ms. Bosco, you may begin.

Thank you. Good afternoon and welcome to our conference call regarding TG Therapeutics fourth quarter 2015 financial results and business update. I’m 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 an 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’d 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 Web site, 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’d like to turn the call over to Sean Power, our Chief Financial Officer to briefly discuss the financial results for the fourth 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 afternoon and can be viewed on the Investors and Media section of our Web site at www.tgtherapeutics.com. I’d like to begin by providing an update on our cash position, followed by a brief discussion of our financial results for the full-year and fourth quarter. We ended 2015 in a strong financial position with cash, cash equivalents, investment securities and interest receivable of $102.1 million. During the first eight months of 2015, we sold approximately 4.1 million shares of common stock under our ATM facility for a aggregate gross proceeds of approximately 68.2 million at an average selling price of $16.66 per share. With our current cash position, we feel we’re well positioned to execute our current development plans and our featured growth strategies. Moving on to the results of operations. Our consolidated net loss for the year ended December 31, 2015, excluding non-cash items, was $47.3 million, including other R&D expenses of $43.4 million of which $23.4 million related to manufacturing and CMC expenses in preparation for Phase 3 clinical trials and potential commercialization. The consolidated net loss for the year ended December 31, 2015, inclusive of non-cash items, was $63 million or $1.38 per diluted share, compared to a net loss of $55.8 million for the year ended December 31, 2014. The increase in consolidated net loss during 2015 was driven by increases in R&D expenses for both TG-1101 and TGR-1202 as a result of manufacturing and clinical trial costs related to ongoing and planned future Phase 3 registration programs, as well as launch preparation activities. The increase in R&D expenses was partially offset by expenses reported during 2014 in conjunction with our licensing agreements for TGR-1202 and the IRAK4 program, and a decrease in non-cash compensation expense over the comparable period in 2014. Our consolidated net loss for the fourth quarter of 2015, excluding non-cash items, was $14.8 million, including other R&D expenses of $13.7 million, of which $7.4 million related to manufacturing and CMC expenses in preparation for Phase 3 clinical trials and potential commercialization. The consolidated net loss for the fourth quarter of 2015, inclusive of non-cash items, was $17.6 million, or $0.37 per diluted share, compared to a consolidated net loss of $18.8 million during the fourth quarter of 2014. The decrease in consolidated net loss during the fourth quarter of 2015 was the result of a decrease in non-cash compensation expense over the comparable period in 2014, partially offset by a modest increase in other R&D expenses related to TGR-1202, which was driven by clinical trial expenses related to ongoing and planned future Phase 3 registration programs. With that, I will now turn the call over to Mike Weiss, our Executive Chairman and Interim CEO.

Thanks, Sean, and thanks, Jenna. I want to thank all of you for joining us this afternoon. 2015 was a busy and exciting year for us. As we solidified the foundation of the Company by announcing our second Phase 3 clinical trial to UNITY-CLL trial for the proprietary combination of TG-1101, plus TGR-1202, or as we refer to the combination TG-1303. This trial marks a major set forward for our Company, and if successful, should provide 1303 with a broad label for the treatment of CLL. 1303 become only a few -- only one of a few novel non-chemotherapy doublet combination therapies approved for CLL and positions us as a leader in the future development of wholly owned novel triple and quad combination therapies, which has been our vision from the beginning of TG and brings us closer to the goal of developing in short for CLL. 2015 also provide us the opportunity to expand our clinical development programs to include new triple combination therapies, broaden our disease focus into Non-Hodgkin's lymphoma and autoimmune diseases, expand our product portfolio and strengthen our balance sheet for the prudent and well executed use of our ATM facility. Primarily some of the notable achievements in 2015. In the first quarter, we expanded our product portfolio through a global collaboration with Checkpoint Therapeutics to develop and commercialize anti-PD-L1 and anti-GITR antibody research programs from Dana Farber Cancer Institute and hematological malignancies. Also in the first quarter, we commenced enrollment into the GENUINE Phase 3 clinical trial, which is now opened at over a 150 sites throughout the U.S. In the second quarter, we presented the first data from the triple combination study of TG-1101, plus TGR-1202, plus ibrutinib. So not only the combination was well tolerated, but produced 100% overall response in patients with high risk, CLL and SLL and a 75% overall response in Indolent Non-Hodge lymphoma. In the third quarter, we obtained an SPA UNITY-CLL Phase 3 clinical trial and in the fourth quarter we announced key data updates at ASH, which I will review shortly. We also launched a new Phase 1/2 triple therapy study of TG-1101 plus TGR-1202 plus the PD-1 checkpoint inhibitor pembrolizumab, which is the first clinical trial to evaluate the safety and efficacy of the triple combination of a PI3K delta inhibitor with an anti-CD20 monoclonal antibody and an anti-PD-1 checkpoint inhibitor. With that, I’d like to provide some brief highlights from the data presented during the ASH conference this past December. We presented four clinical posters and one preclinical oral presentation. Some of the highlights included a 94% overall response rate for TGR-1202 in CLL, including both PRs and PRs with lymphocytosis was reported. In those -- in that study, 94% represents again both PRs and PRs with lymphocytosis, which as many of you’re aware now most of our competitors report their data in that way. We typically only report that data as true partial responses. In this study, we reported at the conference, if 59% overall response rate for the iwCLL 2008 criteria. Additionally, we observed a 24-month median progression for survival with single agent 1202 and patients were relapse/refractory CLL. Next we presented updated data on our TG-1303 combination which showed an 80% overall response rate in patients with CLL and SLL, all responses again by iwCLL and the case of lymphomas Cheson criteria, including one CR and seven PRs. In addition, the 35% overall response rate was observed in patients with Diffuse Large B-Cell and Richter's transformation, including three patients who achieved a complete response. TG-1303 showed a median progression free survival that had not been reached for both the CLL and Indolent non-Hodgkin lymphoma patients with follow-up now beyond 20 months. We also presented final data from the Phase 3 trial of TG-1101 in combination with ibrutinib, in patients with Mantle Cell Lymphoma which showed an 87% overall response rate, including 33% complete response rate, which compares favorably to historical [indiscernible] ibrutinib data, which has shown a 66% overall response rate and a 17% complete response rate. And then our final clinical update. We presented data from the Phase 1 trial of TGR-1202 in combination with obinutuzumab commercially known as Gazyva plus chlorambucil which showed a 100% overall response rate in treatment of naïve CLL patients with a 33% complete response rate and 47% of the patients achieving minimum residual disease negativity. For these front line patients, a PR test has not been reached with the longest patient on study almost two years. We believe this study set the stage for what we might expect to see in front line patients taking 1303 in our UNITY Phase 3 trial. And lastly, we finished up ASH -- the ASH conference with an oral presentation delivered by Dr. Deng from Columbia University, which reviewed some very exciting preclinical research, identifying novel mechanism of TGR-1202 which was distinct from other PI3K delta inhibitors and might indicate a senior targeting mechanism of TGR-1202. We’re highly encouraged by the data we’ve seen thus far from our trials and are particularly enthusiastic about the efficacy and safety given TGR-1202 as a single agent and the TGR-1303 combination. As of December 2015 ASH update, in studies of TGR-1202 as a single agent or in combination with TGR-1101 or TGR-1202 in combination with Gazyva plus chlorambucil, we had more than 80 patients exposed to TGR-1202 for over six months and another 42 patients on drug for more than one-year with no cases of colitis being reported. As I’ve stated in the past, I think the take home message here is not that we will never see colitis, but that specifically speaking the conference intervals around 0% colitis reported at that time with that many patients treated, it is the high-level of comfort that the rate of colitis will be significantly less than reported with other PI3K deltas. Additionally, grade 3/4 liver tox remains minimal with less than 4% being observed with TGR-1202 and a single agent and in combination with TG-1101. With that, let me quickly review our current Phase 3 clinical trial. I will begin with the GENUINE Phase 3 trial, which is evaluating TG-1101 in combination with ibrutinib in patients with high-risk CLL which now has over 150 sites participating in the study. I’d like to first thank my team for their extraordinary effort in launching the study. This is a large U.S only study and they’ve worked tirelessly identifying and enlisting both academic and major community centers around the country. Starting trials is hard enough, but starting the Company’s first major Phase 3 program is always -- it’s a little more challenging. But the team rose to the occasion and in 2015 we built a fantastic network of clinical collaborators which we believe will pay significant dividends not only just for the GENUINE study, but as we expand into our UNITY program across CLL and NHL. And beyond that to our triple and quad registration trials that we hope to follow. With 2015 spend building our trial site network, 2016 is a year of enrollment for us. We’ve been pleased by the early adapters into the GENUINE study, including several major academic centers as well as the few large community networks. In the broader community, we found that testing for high risk CLL was not routinely done and since few front line patients have high risk features, many patients at the time of relapsed were not being receptive. We are in the process of launching a separate screening protocol that will enable sites to more easily screen all relapsing patients. As expected, we’re finding that about half of the patients that are screened, few have high risk features, which is consistent with our projections. Again, we believe the screening protocol that we’re launching now will certainly streamline the process and accelerate enrollment. With so many great sites on board, we believe we’re nearing that key inflection point where these types of studies accelerate dramatically. When that occurs, we will be able to provide more clear guidance as to when the study will be completed, but until then we’re continuing to target the end of year to complete enrollment with data in early ’17. Moving on to the UNITY CLL study, our Phase 3 clinical trial of TG-1101 plus TGR-1202, again as we [indiscernible] referred to as 1303, combination in front line and importantly in previously treated patients with CLL, which is also being run pursuant through a special protocol assessment. We are excited to announce that we’ve now enrolled our first patient in the study. From a site engagement perspective, its still early days. We’ve currently -- have eight sites opened in the U.S with a goal of having over 50 up and running by the end of May and over a 150 sites internationally by year-end. Early on we’re targeting sites for the study that are also participating in the GENUINE study and are also opening the newly discussed screening protocol. These types provide us incredible operating efficiencies. They’re easier to engage, because of our existing trial agreements. They’re easy to monitor, because we’re already visiting those sites for the GENUINE study. And most importantly and excitingly, is that the power of the screening protocol to ensure that every relapsing patient that they screen is captured into one of our two protocols. Though the 50% of the patients that screen is high-risk will of course continue to go into GENUINE and those that don’t won't be loss as they are today but then go into UNITY. We believe this approach will enhance enrollment into both studies. Finally before wrapping up today’s call, I want to mention how excited we’re about moving forward with our autoimmune disease program, and we expect to launch our first trial in multiple sclerosis in the next 30 to 60 days. Our first study will be a Phase 2 dose finding study. For this study, we planned out 8 to 10 sites and enroll up to 24 patients in several cohorts with flexibility for additional cohorts to optimize dosing a schedule. Given the reasonably straightforward path established in this area, but others develop -- developing B-cell target therapies for MS, we believe we can move rapidly, through this program and into Phase 3 sometime next year. For us understanding the B-cell depletion effect of TG-1101 at different doses and schedules is our goal prior to moving forward into Phase 3. We believe, B-cell depletion is highly correlated with GAG [ph] lesion reduction, which in turn is highly correlated with the Phase 3 endpoint of annual relapse rate. We will have B-cell depletion data before the end of 2016. Our plans to open-up a dialogue with the FDA relatively early in the process to better understand their Phase 3 expectation. With that, let me now turn the call over to the conference operator, to begin the Q&A session, following which I’ll return to make some concluding remarks.

Thank you. At this time, we will be conducting a question-and-answer session. [Operator Instructions] Our first question comes from Jonathan Aschoff with Brean Capital. Please state your question.

Thanks. Good afternoon, guys.

Hey, good afternoon, Jonathan.

I was curious is that less than 4% liver tox with 1202. Is that a little higher than reported at ASH or is that the same?

I believe that’s pretty consistent with what was referred at ASH. I don’t think it’s higher.

Okay. And I was wondering with about a year under your belt and you did that Checkpoint deal, any sense of IND filing or Phase 1 timing with either GITR or PDL1 antibody?

Yes. So, we’re definitely moving forward pretty rapidly with the PDL1 program. We’ve again been targeting right again to the clinic before the end of the year. I’d say that it’s going to be a bit of a challenge, but early next year it should be definitely on the table. Part of the reason is we’re spending a good amount of time to signing on the ultimate manifestation of that product. And we’ve at least two antibodies that we’re targeting forward even right now. But one thing that I think is important for us when we spend a bit of extra time upfront, optimizing the antibody to make sure we had really best-in-class or comparable to best-in-class binding, potency of that antibody. And then the other thing that we’ve been quite keen on is understanding if in fact it’s better to not just leave the FC function and its natural state which would imply that, the antibody would have some level of ADCC. But to actually consistent with our -- with ublituximab look at glycoengineered version of this PDL1 and new something that actually has a high level of ADCC. So the interesting part of that PDL1 as a target versus PD-1, PDL1 fits primarily on tumor cells, PD1 sits on T-cells. So the ability to target not only the tumor cell, with PDL-1 antibody for a recognition by T-cells, but it also have some direct anti-tumor effect. We think it’s quite interesting and really what set as part is the only glycoengineered Anti-PDL1. So because of that I think we’ve taken a little bit extra time here now to make that kind of determination. But it’s a long answer to a very short question, which is we’re still looking at the end of the year, but more likely it will be sometime in the first quarter we get again to the clinic with that antibody. But I think we’re excited about the profile we’re developing and we do think that we will be able to differentiate it from what seems like a crowded area. But when you narrow down to PD1 versus PDL1 and when you look at the class of PDL-1, there is only one PDL-1 that’s the Pfizer, Merck Serono product that did not engineer out SD function. And they’ve seen some very interesting and positive data and we think we maybe able to either just be -- will certainly because [indiscernible] SD function in, but we may go a step further and optimize it for even a higher level of ADCC.

Right. Could you focus only on the few costs, the presence, the amount of [indiscernible] costs or you will go beyond that?

We are targeted on the [indiscernible] level of that similar to how we view ublituximab.

Okay. And the last two are just, can I have maybe some timing for the large cell trial and which would be consistent with the whole SPA process for this third trial and that was one question. The last is maybe specifically what we’d expect to see at ASCO with the patient on regeneration [ph] of therapy in such?

Yes, so the second question, I’d say I don’t have that information at my fingertips. But I know that we will just -- we continue to update at the end. The focus has really shifted away from some of those earlier trials. I don’t know how much additional enrollment we’ve for the update, but we’re -- we will definitely try to present with wherever we’ve available. With respect to diffused large B-cell, the current plan is to look at more of a Phase 2b type study, taking advantage of component of what we learned in our SPA discussions with the FDA relating to the UNITY studies and the NGCLL study. I think we’re probably going to do to the diffused large B-cell in two steps whereas in the UNITY CLL, we took one giant step and put the whole thing in one study. We’ve a slightly different approach that we’re looking forward into diffused large B-cell where we’re going to look at contribution earlier. We decided to do that, because we did see some interesting signals with respect to the difference in activity between GCBs, and ABCs. Our result was prudent to maybe take a step, I won't say decided, but just take this in steps versus doing it all at once. We get a lot more information. We don’t think from a timing standpoint, it will be much longer in terms of overall timeframe to get to a pivotal trial or to an execution with pivotal trial. In fact, we believe that there is a component of the first part of our trial, the Phase 2b that we can use for registration. But it wouldn’t be something that we would seek in SPA on. So, I think we’re going to do this one probably in two stages. First stage, hopefully it will be opened up shortly in the next several months. And that will give us a lot of good information on the activity level of 1303 particularly as it may be differential at ABC versus GCB or is that just a -- an early signal that’s not real. And then that will be just directly, I think pieces of that we maybe will have to file for approval, and will lead us into our randomized follow-on approach.

Great. Thank you very much for that clarity.

Thanks, Jonathan.

Our next question comes from Matt Kaplan with Ladenburg Thalmann. Please state your question.

Hi. Good afternoon, guys.

Hi, Matt. How are you?

Doing great. Thanks.

Just a follow-up on the GENUINE Phase 3, from your prepared remarks in terms of commuting patients for the screening relapsing patients for risk factors, where are you now in terms of implementing that change or standardizing that protocol in terms of putting that into action of state?

Yes. So first, I’ll just add on top of what I said in the prepared remarks. It was -- its interesting to us, when we -- when we did the Phase 2 trial, we didn’t have to screen patients in advance. We basically took the patients as they were, and we basically just screened them afterwards instead of saying, these are high risk and these are not high risk. When we went out to the field and we started doing the trial, we hadn’t even thought about the fact that a lot of sites just do not in fact -- not just a lot, most sites in the community are not prescreening for high risk features. So at the suggestion of U.S. Oncology obviously our lead center and Jeff Sharman were in the study. They suggested implementing a screening protocol, basic streamlining and then -- and get everyone on the same page on how we -- how you want people screened. And this has been a major effort independent of us. Jeff Sharman has been patting the table for community physicians, community oncologists to prescreening all of their relapsed patients. So it’s been sort of a combined effort that this has been a program for Jeff independent of the trial, and now we’ve actually implemented as part of the trial. So the screening protocol is open. It makes it a lot easier to screen patients when you -- if you think about, we’ve always known that about half the patients would not qualify the study. Logistically what that translates into, is the site has to actually go through the effort of consenting a patient. They could spend upwards of two, three hours discussing the trial with the patient, and then they screen them and half of the patients are not going to qualify. So it’s not easy to do that. A screening protocol basically enables them to probably spend five or ten minutes with the patient asking for their blood. And on the other side of that, they can basically then talk to them specifically about the trial that they qualified for. The beauty of the screening protocol in collaboration with the GENUINE study and now the UNITY study is that package becomes very powerful, and something we’ve been thinking about for a while of how we present GUINUINE and UNITY to a particular site and the screening protocol really had it altogether for us. So we’re super excited about getting that up and running. We think its going to not only just accelerate what's going on with GENUINE, but its going to really ramp up dramatically our ability to enroll into the UNITY study. So for us its one of our core focuses for the next month or two to get that fully launched, engaged in the site. And again coupling that with the UNITY study into those already existing 150 GENUINE sites, we’re not going to get all of them. But I think our goal is at least to get 60%, 70%, 80% of those existing GENUINE sites open with both the screening protocol and the UNITY study. And again, I’ll give all credit to our Head of Clinical who is -- genius was asking and discussing with the FDA the ability to put not only frontline patients into the UNITY study, but to also include relapsed/refractory patients. And again one thing that’s probably also worth mentioning is, this study is designed to accept either frontline or relapsed/refractory patients in terms of the overall timing of progression free survival endpoint. The higher the percentage of patients that have -- that are previously treated is shorter the PFS time is going to be overall which makes the study just a shorter time study. So we think it’s a more interesting probably more balanced study between frontline and relapsed/refractory, and this package of screening protocol plus GENUINE immunity really helps to balance and give us a nice group of patients who have relapsed/refractory disease as well.

Great. Now thanks for the detail. And then, in terms of your MS program, it seems like, a steady new endeavor from the Company. Can you talk a little bit more about that program and what you, I guess, specifically hope to show or hope to accomplish or demonstrate in the Phase 2 trial that you’re planning?

Yes. So we’re -- the more I spend working on MS, the more excited we get about it. We’ve been engaging KOLs around the country, and also large community practices. We’re having another big advisory board meeting in the next week or two, where we have a great group of KOLs coming into the city. And the enthusiasm seems great for a novel CD20 in this space obinutuzumab has really generated a lot of enthusiasm in the medical community for targeting B-cells. So, I think overall, we’re getting more and more excited. The nice part about MS is it’s not as from a B-cell [ph] targeting site. It’s not a very crowded or complicated field. Obviously, there’s obinutuzumab, there is obinutuzumab and there will soon be ublituximab. So we think from that standpoint it’s a pretty clear playing field in terms of targeting B-cells. And the endpoint is interesting, slightly different from treating leukemias and lymphomas. B-cell depletion certainly peripheral B-cell depletion is not as perfectly correlated with response as you’ll see in MS. And what the others have shown is that if you get good B-cell depletion, you’re going to get the effect that you’re looking for which ultimately is the Phase 3 endpoint of our reduction and an angle of relapsed rate. So when we think about B-cell depletion, our drug in cancer patients has a very, very robust, even the first day effect. We see major declines in B-cells, in patients that have highly elevated B-cells. So when we start to go into MS patients they have normal levels of B-cells. There is something aberrant going on with those B-cells are part of a -- have the genesis process for MS, but otherwise are not elevating and they’re certainly not elevating the way you’re seeing the patient with CLL. So we’re highly confident that with reasonably low doses of our CD20 that we can see very robust levels of B-cell depletion, and that answer is not for Phase 3 and for MS you have to wait two years to see what the annual relapsed rate was. B-cell depletion is probably less than two weeks, I mean, the fact it literally can be one or two days and you can see complete eradication of B-cell. So it’s a very short-term endpoint. Our study is designed to look at a few doses, but we’re not looking at a large group of doses. But we’re also looking to take the time in which we give our infusion down to one hour. So as you know on the cancer side after the either second or probably the third or fourth infusion we can give a 900ml dose in 90 minutes. So our expectation is that, we’ll be using doses half of the [indiscernible] maybe 33% less. But we do believe that, wherever that dose is and it could be even, it could even be lower, that we can certainly deliver that in an hour. So that’s part of our trial is basically getting that infusion time down. We see that as an -- and a very nice advantage over [indiscernible] which has a three and half to four hour fusion time. We can take it down to close to an hour. So we do think that gives us a very interesting competitive advantage. And then we’ve talked about in the past that we are quite keen on looking at even lower dosing strategies which is more nuance. I don’t think we’re going to slow our development program. We think the, the very basic program of an infusion a reasonably good dose, but low dose compared to cancer will give us really nice B-cell depletion which will carry us for a six month dosing regimen and that we can look at more nuance lower -- even lower dose approaches.

Great. That’s very helpful. And, I guess, one question especially for Sean. Even though your manufacturing costs during 2015 were a large portion of your R&D, almost 50%. What are your expected manufacturing cost in 2016?

Sure, Matt. So we think those will remain relatively consistent between ’15 and ’16. Obviously there’s been timing issues as to the quarter that it will fluctuate between the quarters that, I think we may get to the end of 2016, it will be relatively consistent with what we saw over ’15.

Okay, thanks. That’s helpful.

Our next question comes from Reni Benjamin with Raymond James. Please state your question.

Hi, good afternoon guys. Thanks for taking the questions. I guess, just -- if going back to the timing question of GENUINE. Can you just give us any more color as to, I know you mentioned that you have a 150 sites ongoing, and that you’re hoping that enrollment will complete by the end of this year, and then data by the early part of 2017. But I would have thought that, you could have gotten that response data from enough patients, maybe even without enrollment completing. I’m assuming that you would interim, but maybe with enough patients. But I might not be thinking about it correctly. So how should I be thinking about this timing and the reporting of that data?

Yes. So the important part to note and again to nuance that we’ve talked about, but maybe not fully clear is that. We can't open up the overall response rate endpoint until we have 100% enrollment complete. So we’ve talked about that in the past. I think most people are familiar with that, but [indiscernible] isn’t clear and we should be very clear that part of the deal on the assay is that, even though we might have the overall response information earlier, we can't actually open it up until we have complete enrollment.

Got it. Okay. And then just related to that, when do you think now that you have the 150 sites up and running; you mentioned that we’re getting near that, that point where you should be able to get a good sense as to how enrollment is coming along. How much longer you think that might be, is the vast majority of sites just kind of come onboard, so it will still take a little bit of time or you think this will be relatively quick for you to get a good obsession?

Yes, I mean look, we always hope the answers will come relatively quick. It’s just -- it’s hard to know. I mean your studies always are -- they’re always a mystery until they’re very clear, and they always end up coming together rapidly. And when they do so, again a lot of sites were basically -- I said we completed really site initiation visits into the third and fourth quarter of last year. So we’re two months into this year. There is -- as I’ve been involved in a lot of clinical trials, I’ve seen how this works. And again, its -- its going at a good clip, but you don’t see that real inflection until sometime when all the sites are up and running and then you’ve got them -- and you’ve got to get back in there to those sites, and just getting the sites initiated is one thing, getting them actively enrolling is another. And it just requires effort and being there and coaching and following up. I think for us the screening protocol to me is the glue that brings the whole thing together. It is not -- as much as we’d like to say well its no big deal to have, we know in advance 50% of patients are screen failures. There are some sites that could get discouraged. When you’re flipping a coin, you could still go four heads in a row or four tails lets say in this particular case. That could be discouraging. So the nice part about having the screening protocol really simplifies everything for everybody and avoids that kind of discouragement when you do have a screen failure. So I think, all the pieces are coming together which I’m excited about. And now we’ve got the sites and they’re all in place and we’ve got -- we’ve been not having to visit them and to get them more engaged in the screening protocol again just really provides the glue to get that going. So I wish, I had a better idea of when that would happen and so enrolling at the end, because in the last two months you have twice the enrollment of the -- of even the prior nine months. It just really happens fast. So again, I’m hoping give us another two, three months, lets look at it again and hopefully we’ll really get that part of the curve and then we can give a pretty clear projection on timing. But these studies are always kind of a mystery in that way.

Got it. And then, I guess, just maybe related to that, do you think you have enough employees to kind of manage the process or do you think it would fallout or that SG&A might go up this year to run, 1, 2, like three large Phase 3 studies probably by the end of 2016?

Yes, so we’re adding people almost say everyday, that we’re adding people. And yes, I think you’re right, we are continuing. As we add more studies we’re going to go international shortly for the UNITY study. Yes, so we continue to add. Will the SG&A run go up? I’m sure will go up. I don’t know how dramatically, but it will certainly go up. I think Sean; maybe he’ll provide a little guidance …

And can you remind me how many people are at the Company right now, and maybe how much you can probably grow to by the end of the year?

Yes. So, I mean, we have somewhere between 40 and 50 employees. My guess is, it will grow internally by another potentially 10 to 20 employees. But as we go -- again the one thing I’d say is, we do -- we have and we continue to do most of the things internally. But as we go internationally, we’ll end up -- we will have some employees overseas. But we’ll end up using CROs more over there in terms of following up on the sites and that kind of stuff. So it will be much more of a mixed -- once we have those international sites, we’ll have more of a mixed profile of employees plus CROs.

Got it. Okay. And just one final question for me, I guess, [indiscernible] issued some guidance recommending against these ibrutinib like three CLL patients were not just for chemotherapy but also CLL patients who have had prior lines of therapy. And I guess, and it’s a big level question, but have you thought at all about how that might impact the commercial outlook for lets say 1101, which is being used in combination with ibrutinib or those -- does the combination, could the combination provide such benefits that [indiscernible] overlook that?

Yes. So I saw the press release on that and I was pretty damn excited about it. I think for us 1303 one from a clinical trial sampling starting there is a great option for frontline patients in the U.K. who don’t have access to ibrutinib. So they can really only get a novel therapy like ours on the clinical trial. So starting there, I think its great John Gribben is our PI, he’s in the U.K. He’ll bring in a lot of great sites in the U.K., and I think we’ll do quite well there. So I’m super excited about that part of that announcement. And I think that leads right into the benefit that we can provide at the right price with our drugs. So I think we can go in there with a two drug regimen that provides as much benefit as anything that’s probably available to those patients or anything that could available, and we have flexibility on price. So I do think that we can make a major impact with 1303 in the frontline in the U.K. with the right price point. So clinical trial wise it’s great for us. Opens up the U.K. for our study in a way that may or may not have existed before, but certainly for sure we don’t have to worry about it now. And I think commercially it really feeds into our goal of providing combination therapies at reasonable prices.

Got it. Thanks for taking the questions and good luck.

Thanks, Reni. I appreciate it.

There are no further questions at this time. I would like to turn the call back over to Mr. Weiss for closing remarks.

Thank you. So I’d like to wrap up today's call by reviewing the key goals and objectives for 2016. Our top priority for the year is to aggressively recruit into the GENUINE Phase 3 clinical trial. Next is to aggressively enroll into the UNITY-CLL Phase 3 clinical trial. Again as we discussed we’re also planning to convince our registration directed UNITY diffuse large B-cell Phase 2b clinical trial as well as a registration directed UNITY trial in the lymphomas. Also as you heard moments ago, we plan to initiate a Phase 2 clinical trial in Multiple Sclerosis. And finally as in the past, we’ll try to update our programs at the major Hematology, Oncology conferences during 2016. On behalf of all of us at TG Therapeutics, I’d like to thank our investigators and their patients as well as all of our shareholders for their continued support. Thank you again for joining us, and have a great evening.

Ladies and gentlemen, this concludes today's conference. Thank you for your participation. You may disconnect your lines at this time.