Greetings, and welcome to the TG Therapeutics Inc. Third 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. It is now my pleasure to introduce your host, Ms. Jenna Bosco, Vice President of Investor Relations. Thank you. You may begin.

Thank you. Good morning, and welcome to our conference call regarding TG Therapeutics third quarter 2016 financial results and business update. I’m Jenna Bosco, TG's VP of Investor Relations, and I welcome you to our call today. Following our Safe Harbor statement, Sean Power, our 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 recent achievements and upcoming milestones. 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 third quarter of 2016, as well as the company's overall financial condition.

Thank you, Jenna, and thanks everyone for joining. As you may be aware, our financial results were released this morning and can be viewed on the Investors & Media section of our Web site at www.tgtherapeutics.com. At September 30, 2016, we had cash, cash equivalents, investment securities and interest receivable of 60.7 million, which we believe will be sufficient to fund our operations into the first half of 2018. Our net loss for the third quarter of 2016, excluding non-cash items, was approximately 22 million, including 10.2 million of manufacturing and CMC expenses for Phase 3 clinical trials and in preparation for potential commercialization, of which approximately 5.6 million was paid in prior quarters and was expensed through our income statement this quarter. The GAAP net loss for the third quarter of 2016, inclusive of non-cash items, was 24.8 million, or $0.50 per share, compared to a net loss of 13.7 million, or $0.28 per share, during the comparable quarter in 2015. Cash used during the quarter was approximately 15 million. Our net loss for the nine months ended September 30, 2016, excluding non-cash items, was approximately 48.4 million, including approximately 17.9 million of manufacturing and CMC expenses for Phase 3 clinical trials and in preparation for commercialization, of which approximately 7 million was paid in prior periods and expensed through our income statement this year. The GAAP net loss for the nine months ended September 30, 2016, inclusive of non-cash items, was 54.6 million, or $1.11 per share, compared to a net loss of 45.3 million, or $1.01 per share, during the comparable period in 2015. The increase in R&D expenses and net loss for both the three and nine months ended September 30, 2016, is primarily due to the ongoing clinical development programs and related manufacturing costs for TG-1101 and TGR-1202. I will now turn the call over to Mike Weiss, our Executive Chairman and Interim CEO.

Thanks, Sean, and thank you, Jenna, and thank you all for joining us this morning. I’d like to start the call by reminding everyone of the great progress we’ve made so far this year, including some highlights, which I’ll do in chronological order. In the first quarter, we announced the launch of our Phase 3 UNITY-CLL study, which is a large multinational Phase 3 study under special protocol assessment. Also in the first quarter, we solidified our patent portfolio by announcing the issuance of Composition and Matter Patents in the U.S. for both 1101 and 1202 providing protection through 2029 and 2033, respectively, exclusive of any patent term extensions. In May, we expanded our preclinical pipeline with the addition of a portfolio of BET inhibitors that we believe may be important to future combinations in non-Hodgkin's lymphoma, especially c-Myc-driven Diffuse Large B-Cell. In June, we presented data at ASCO and EHA which included safety and efficacy data from 165 patients treated with 1202 alone or in combination with TG-1101, the combination recall we refer to sometimes as TG-1303, and we’ve followed those patients for up to and beyond three years which demonstrated a unique and favorable safety profile for TGR-1202. Also in June, we were excited to announce we enrolled the first patient in our registration-directed UNITY Diffuse Large B-Cell Phase 2b clinical study evaluating TG-1101 and TGR-1202 as a combination compared to TGR-1202 as a single agent in patients with advanced relapsed/refractory Diffuse Large B-Cell. In August, we received orphan drug designation for TGR-1202 for the treatment of CLL and also orphan drug designation for TG-1101 for the treatment of neuromyelitis optica, NMO. In September, we presented clinical data from our first autoimmune study of TG-1101 in patients with NMO at the ECTRIMS conference with TG-1101 demonstrating a rapid…

Thank you. The floor is now open for questions. [Operator Instructions]. Our first question is coming from Joe Pantginis of ROTH Capital Partners. Please proceed with your question.

Hi, guys. Good morning. Thanks for taking the question.

Good morning.

Wanted to focus first on your recent blood article. Obviously, the author, you guys and many of us are very excited by the data that are in it. So I was wondering if you can provide any feedback from, say, KOLs beyond the author with regard to the impact on c-Myc and the data that point to the structural differences of 1202 which appear to be responsible for the differentiation against other PI3Ks?

Sure. I’d have to say we’ve had really unbelievable response. I know that Owen has presented it at a number of conferences I believe a month or two ago, he presented at the iwNHL conference to I think a standing ovation when he got finished or closed thereto. But yes, very well received. Following that presentation actually we got a lot of inbound interest from KOLs who wanted to join the UNITY Diffuse Large B-Cell study. A number of folks that we had actually tried to contact previously who were hard to reach actually reached out to us. So yes, the response has been incredible. I think people are really impressed by the science and how they’ve interrogated the molecule and yes, I think we’ve been on the receiving end of the benefit of that good science.

That’s great. And I guess I would sort of look forward a little bit, are there other ways you could potentially take advantage of targeting c-Myc beyond the carfilzomib [ph] combo study?

Yes, we’re super excited about potentially bringing in our BET inhibitor. That one in particular has the activity in c-Myc, so we’re – fingers crossed, we’re hoping that we’ll get that compounded into the clinic in the first half of next year and we’ll be able to start to evaluate it both as a single agent in lymphomas, I think Diffuse Large B-Cell and follicular there has been activity of the class, and then particularly looking at the combination with 1202 and even 1202 plus ublituximab plus BET inhibition to see if we can really knock out c-Myc. And obviously that’s important in Diffuse Large B-Cell, it’s important in some follicular patients but it does extend I think to some solid tumor areas as well. Triple negative breast cancer is one that’s well known to be c-Myc driven solid tumor.

That’s great. Thanks. And maybe just a quick and final question for Sean. Is there any potential other CMC expenses we could anticipate at this point that might be outliers, or are we pretty much done?

I wouldn’t say we’re pretty much done. I think we’re expecting them to certainly scale down a little bit in the early part of next year; but certainly not done. I don’t know if it’s helpful.

No, it definitely is. Okay. Thanks a lot, guys.

Thanks, Joe.

Thank you. Our next question is coming from Matt Kaplan of Ladenburg Thalmann. Please proceed with your question.

Hi, guys. Congrats on the progress.

Thanks, Matt.

Just following up on Joe’s question, maybe zeroing in a little bit more on the TGR-1202 plus carfilzomib study. Can you help us understand what your goals are for the study, what we’re looking for?

I think probably the early key is to see if we can silence c-Myc. So I think the correlates with the study are quite robust to get to the answer and to see if we can match the clinical data to the preclinical data. Of course, if we can silence c-Myc, we’d like to see what that actually translates into in terms of response rates and durability of response. So I think it’s a classic Phase 1/2. We’re going to be dose escalating the carfilzomib, so the early cohorts we wouldn’t expect to see full c-Myc inhibition and whatever that translates into in treating human cancers. But I do think that once we get to the target dose, like I said it’s a very fulsome study on the scientific correlates and we’ll like to see c-Myc inhibition. I think once we have confirmation and hopefully we’ll have some sort of pharmacokinetics of that c-Myc inhibition, so how we’d like to see – I personally would like to see how that looks over time. I think there’s a potential strategy to use that c-Myc inhibition in combination with chemotherapy. There are some tumors that are resistant to chemotherapy because of c-Myc activation and there’s a theory that one could re-sensitize patients to chemotherapy or turn a c-Myc driven patient who’s very challenging to treat with chemotherapy basically convert them back to a normal risk patient where the results of Diffuse Large B-Cell [indiscernible] in frontline are quite impressive. So I think there’s a number of applications. Once we understand if we are in fact silencing c-Myc, one is just understanding what that means in and of itself; the silencing c-Myc translate into clinical responses, and then leveraging that c-Myc silencing to look at combinations with chemotherapy and re-sensitization to chemotherapy.

Great. Thanks for the detail. And just turning to ASH, it looks like you have a robust presence there. Could you highlight a little bit for us what we should be looking for I guess at ASH?

I think for us it’s the totality of the data that’s most important. So I think if you look across all the studies using TGR-1202, I think the safety profile continues to shine and that’s something that we continue to hear questions, is it truly differentiated? Again, I think the pieces are coming together both scientifically and clinically to show that this is a differentiated PI3K delta inhibitor. So for us, we’re excited to see across multiple applications both with new targeted agents as well as chemotherapy the compound continues to do well from a safety standpoint. So that’s one. Obviously we’re intrigued by combinations with ibrutinib, the benda combination is intriguing to us. I think you heard we’re excited enough that we’re probably going to build the cohort into our UNITY Diffuse Large B-Cell study to explore that further. The novel combinations with ublituximab and ruxolitinib are also intriguing to us. I think the re-sensitization of some of those Hodgkin patients who were refractory to ublituximab is also intriguing. So there’s a lot of cornels of really exciting long-term potential and I think again, some of these things will ultimately – could ultimately become registration strategies for us. But longer term we’ll have our core registration approvals. And then this kind of experimentation is nice to see and leads to ultimately companion listing and continue to use in lots of different applications. So we’re excited to see the expansion of the program. Most of those studies have come from investigator interest. We continue to see a lot of investigator interest. Then I think the PI3K delta class is deemed to be more promising in a lot of ways than BTKs and even BCL2 across the broader lymphoma category. And I think we’re sitting on the only PI3K delta that is easy to use and people like to combine. So we feel like we’re sitting in a desired position from that standpoint. And again I think for us looking certainly back to your question, for us ASH is about continuing to demonstrate the utility and safety of TGR-1202 across multiple applications with multiple combinations.

All right. And last question shifting gears a little bit to your autoimmune MS study that’s ongoing. When could we potentially see some data from that study?

Yes, so we’re targeting conferences in the first half of 2017 to present the first data. It would primarily be B-cell depletion data. It’s possible by the second half of next year but more like would be the first half of '18 where we’d have – our Phase 3 would be up and running but we’d start to present more of the hard MS endpoints [indiscernible] reduction I think is probably the primary more MS specific endpoint that we’d be able to show. And again I think that’s early as second half and maybe even next year but B-cell depletion data which we think is the primary surrogate endpoint for determining dose we’ll have in the first half of this year.

Great. Thanks a lot.

Yes.

Thank you. Our next question is coming from Reni Benjamin of Raymond James. Please proceed with your question.

Hi. Good morning, guys. Thanks for taking the questions.

Good morning.

Hello. Just very quickly I guess on GENUINE, and I apologize if this was answered. I jumped on the call a little late. On the GENUINE study you mentioned completing enrollment by the end of the year. About how many patients should we be expecting for that study? And in terms of what we’ve seen from the abstract at ASH in combination with ibrutinib, are we looking for sort of response for it to be successful or how should we be thinking about it when the data finally comes out?

Yes, so the revised protocol targets 120 randomized patients, so that’s the target. In terms of the data, the original study we powered for 80% overall response rate for the combination arm versus 60% response rate for the ibrutinib arm. Basically we powered the amended protocol such that the minimal detectable difference is that same 20%. So the powering is probably mid-50s versus 80 but again minimal detectable difference is still that same 20%. It’s hard to know – again, we described in that Phase 2 with 40 patients we had about an 88% overall response rate for that trial with the 95% response rate for the high risk patients. We’ve always kind of assumed that as you go larger and you end up seeing some sort of lowering of that response rate, we’ve been targeting success on reaching 80% and 85% we think could be highly successful. We know that in the HELIOS study, ibrutinib plus Rituxan plus bendamustine had an 83% response rate. So again I think if we’re within the 80% to 85% response rate without having to use toxic chemotherapy, we should have the most desirable combination with ibrutinib in relapsed/refractory patients.

Okay. And then I guess just a high level question that I’m sure you guys think a lot about and we’d just love to kind of hear your thoughts. When we think about the anti CD 20 space, when we think about the PI3K delta space; on the one hand, validated targets with approved agents that are out there. On the other hand, people and investors kind of come back and start to say, it’s a crowded space, right, or it’s a class that’s no longer functioning well. And when we kind of take the totality of the data, like you were talking about with ASH, and then we also take into account the differences in treatment regimens between, let’s say, community boxes versus institutional box, it seems to us that there is a market for the second or third CD 20 that’s out there, or a more gentler PI3K delta inhibitor. But how should we be thinking about these drugs that you guys are moving forward and the advantages that they could have from what’s already out there?

Yes, so I think to a certain extent fairly, so investors have focused on CLL which – again, since we have two registration trials in CLL that’s a fair place to start. And of all the indications that we’re looking at; CLL, Diffuse Large B-Cell and follicular, CLL is clearly the most going on. But as you described, it’s not as complicated as people think. And when you start to look at the market dynamics and separate out the academic world from the community and our estimate is somewhere between 60% and 70% of all patients will be treated by first and second line in the community. It’s also sort of a different dynamic in terms of the competitive landscape even for CLL. When you move into NHL and Diffuse Large B-Cell and follicular, the competition dwindles quite dramatically and quite quickly where again in the bigger indications outside of mantle cell, you don’t really see BTK inhibitors and even venetoclax is not as promising as people once had hoped outside of mantle cell as well. So I think if we look at the lymphoma side of it, I think when people start to look over there, they’re going to see it’s a pretty large greenfield for us and the only competition is really [indiscernible] and the toxicity profile there we think is just not compatible with broad application and broad views. But circling back to CLL which is again our lead indication, when you look at community base practices and we for better, for worse we have focused the last 20 years on community base practices and they are different in how they treat patients than academic centers. In this particular case, probably the biggest difference is going to be where venetoclax fits into the treatment paradigm. In most…

Got it. And then just one final one from me regarding MS. Just help me understand, I think you mentioned that the market that you’re going to after has relapsed remitting [ph]. And I thought through one of their key opinion leader talks that we had attended that the primary relapse MS market seems to be an area that’s a lot more open and a lot less competitive. I guess it’s a long-winded way of asking how should we be thinking about the MS market as it pertains to you guys?

Yes. Look, primary and progressive – there’s nothing to prove today for primary/progressive. Ublituximab ran a large study, came up with a P value of 0.04 in change in the primary/progressive. So it’s a first time ever anything has been positive, which is amazing. But for us from a regulatory standpoint that study shows us that there were reasonably powered by we probably would need to even be more strongly powered given the 0.04 P value. And it’s probably not a study that we want to embark on as a first regulatory strategy in MS. On the other hand, their study there, the OPERA I and II was widely positive in relapsing MS. The P value had three to four zeros in them before you even hit a number. And again the implication there is that they were well overpowered and thus as we have described we believe that we can do a study or studies that combined would be significantly smaller than the OPERA I and OPERA II program. So from a regulatory standpoint, the path through relapsing MS is quite straightforward and that is the regulatory strategy we’re going through, we do believe that given the value proposition we’ll be bringing into MS including a more convenient infusion time plus a lower price point that we should receive insurance coverage across the treatment of all MS. And we could do probably some interesting studies in progressive MS to help build out the insurance coverage.

Great. Thanks, guys.

You’re welcome.

Thank you. Our next question is coming from Edward White of FBR. Please proceed with your question.

Hi, guys. Thanks for taking my question. So just on a timing standpoint, did you say that you think you could start Phase 3 enrollment in MS in 2017?

Yes. So the goal is to get it up and running before the end of the first half of '17, so in the first half of '17.

Okay. And then on the second question as far as the UNITY DLBCL, can you just review the timelines on that again as well, because I think you had said that you hoped to convert to a Phase 3 for 1303 versus 1303 plus benda also in 2017, was that correct?

That I don’t think we gave specific timeline guidance on that. So the goal of the study is first and foremost to compare 1303 to 1202 and basically it’s – essentially it’s randomized but it’s two single arm trials running randomized together. Each one basically has the same hurdle rate to get through and the goal is that hopefully within the first two checkpoints, so approximately 20 and approximately 40 patients, one of those two checkpoints we’ll be able to stop 1202 as being good but not good enough in our opinion to move it forward, which will leave 1303 which we believe will be showing activity ideally around what we’ve seen in the Phase 2 which was in the 30% to 35% range of overall response. At that point – the point in which we drop 1202 and I think again our hope is that sometime in the first half, we should have at least the first checkpoint. And again, if it drops off there or not – when it does drop out, again assuming it does drop out, we’ll replace that arm with 1303 plus benda again assuming that we’re going to a full 100 patients for 1303 alone that would imply that somewhere between 60 and 80 patients will go onto a 1303 plus benda arm, which we think is a pretty good number of patients to compare versus the 1303 alone arm. So we’ll have two comparisons. We’ll have 1202 to 1303 and then if all goes well, we’ll also have the 1303 plus benda to 1303. And then at that point, once we get through – again our target is about 100 patients on 1303. We believe again if we can show that 30% to 35% response rate with that number of patients that that’s a package that is fillable [ph]. We’re obviously in advance of that. I think once we get around the 50 to 60 patient mark, we’ll start the dialogue with the FDA, make sure they’re on board with the concept of continuing to enroll and also potentially bringing that data down for a discussion. Assuming all this is going well, I guess I will hope that sometime before the end of '17, although we haven’t fully given guidance on this, so I’m sort of jumping ahead and my team will probably get very angry with me. But I would hope sometime before the end of 2017, if all goes well, we can convert into a Phase 3. But I think that’s soft guidance right now and we’ll have to figure that out.

Okay, great. Thanks, Mike.

Thank you. Our next question is coming from David Fang of SunTrust Robinson Humphrey. Please proceed with your question.

Hi, guys. Thanks for taking my question. I just want to follow up on Joe’s question. As you guys are getting a belly [ph] of data on TGR-1202, I would say these trials with investigator sponsored trials and your own trials are successful. How would you go about prioritizing these indications going forward, given that you already have your core registration trials in CLL and DLBCL?

Yes. I think in terms of some of these other indications where we’re looking at data in Hodgkin’s disease with rituximab and myelofribrosis with ruxolitinib, I think we need to see that kind of data evolve I think if investigators want to push forward and we can build larger Phase 2 studies. But I think our core registration approach is still to get these larger indications approved and then help to build out behind that more of a companion listing types of studies. So I wouldn’t say that these are or would rapidly become priority studies for us. The priority is, let’s get our hopefully two approvals in CLL both our 1101 plus ibrutinib and then more importantly the 1303 combination across all of CLL; get 1303 approved in Diffuse Large B-Cell and also get 1303 approved in follicular lymphoma. Those are the big broad markets. And backfilling behind that I think looking at new combinations and new indications but also then our true mission still is to build on what we have on 1303 plus to create the best treatments across the bigger indications of CLL, Diffuse Large B-Cell and follicular. So again, we talked about the BET inhibitor. We haven’t spoken today at all about our PD-L1 program. So we have a lot of components at work here. Again, the more people want to work with our drug and identify interesting indications, we’re not going to get ourselves off our focal point but I do think longer term it’s how you build out a very robust market for this kind of a drug.

Great. Thanks. So maybe just an update on the lymphoma program, when might we get an update or a timing for that?

Yes, that’s a great question. We’re going to be having an advisory board at ASH, so we’re bringing together – I think now if the group keep growing, which is nice – how many? 17. So up to 17 KOLs will be joining us for our intimate advisory board. On top of that we have over 150 investigators and their staff expected for our investigator meeting that we’ll have also at ASH. So we’ve got a big group coming together. But at the more intimate 17-person KOL advisory board, we’re going to be trying to drill down and come up with our strategy for follicular. I don’t think it will come out of that meeting exactly. I won’t be able to walk around ASH saying we’ve got our strategy. But we’re working towards it. Hopefully early next year, we’ll be able to launch. We are considering looking at similar strategies the way we’re doing at UNITY Diffuse Large B-Cell. The data that we’re presenting at 1303 plus benda is both in Diffuse Large B-Cell and follicular at ASH, so I think we’ll see some – and again, the early response rates look quite good and we’ll see some more data. So, again, I think we’re leaning toward we’re vetting some ideas at this advisory board. So I think a long-winded way of saying probably early next year we should be able to nail down what we’re going to do with our UNITY DLBCL program.

All right, thanks. I just had one quick question. So you mentioned maybe in the previous call that anti-PD-L1 antibody program might enter clinical development some time in 2017, is that still the case?

Yes, right now we’re still on target to get into the clinic in the first half of '17.

Great. Thank you for taking my questions.

Thank you.

Thank you. At this time, I’d like to turn the floor back over to Mr. Weiss for any closing comments.

Great. Thank you very much. So I’d like to wrap up today’s call by reminding everyone of some of our key catalysts over the remainder of the year. We look forward to announcing the completion of enrollment into the GENUINE Phase 3 study by year end. We will continue to aggressively enroll into our Phase 3 UNITY CLL trial and our UNITY Diffuse Large B-Cell Phase 2b trial. We expect to complete initial enrollment in the MS Phase 2 trial by year end. And in the first half of next year present preliminary Phase 2 clinical trial results and start our Phase 3 program. And finally, we look forward to a very impactful ASH meeting next month where we’ll further expand on the abstracts mentioned in the conference call. And also look forward to our Analyst and Investor event where we’ll be able to add even a bit more color on top of what we can present at the conference. So 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, thank you for your participation. This concludes today’s teleconference. You may disconnect your lines at this time, and have a wonderful day.