Greetings, and welcome to the TG Therapeutics Inc. Second Quarter 2016 Earnings 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 second quarter 2016 financial results and business update. I am Jenna Bosco, TG's VP of Investor Relations, and I welcome you to our conference call today. Following our Safe Harbor statement, Sean Power, our 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 recent achievements and upcoming milestones. 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 second quarter of 2016, as well as the company's overall financial condition.

Thank you, Jenna, and thanks everyone for joining us. As you may be aware, our financial results were released earlier this morning and can be viewed on the Investors & Media section of our website at www.tgtherapeutics.com. At June 30, 2016 we had cash, cash equivalents, investment securities and interest receivable of $75.8 million, which we believe will be sufficient to fund our operations into the second quarter of 2018. Our net loss for the second quarter ended June 30, 2016, excluding non-cash items, was approximately $14.3 million, which included $3.4 million of manufacturing and CMC expenses for Phase 3 clinical trials and in preparation for potential commercialization. The GAAP net loss for the second quarter ended June 30, 2016, inclusive of non-cash items, was $15.9 million, or $0.33 per share, compared to a net loss of $17.1 million or $0.38 per share during the comparable quarter in 2015. The decrease in net loss during the second quarter of 2016 was the result of a decrease in non-cash compensation expense related to equity incentive grants over the 2015 period, partially offset by an increase in clinical trial expenses related to ongoing and planned clinical registration programs. Our net loss for the six months ended June 30, 2016, excluding non-cash items was approximately $26.4 million, which included $7.7 million of manufacturing and CMC expenses for Phase 3 clinical trials and in preparation for commercialization. We do expect that these manufacturing and CMC expenses will decrease in the second half of 2016. The GAAP net loss for the six months ended June 30, 2016, inclusive of non-cash items, was $29.7 million, or $0.61 per share, compared to a net loss of $31.7 million or $0.73 per share during the comparable period in 2015. The decrease in net loss during the 2016 period was the result of a decrease in non-cash compensation expense over the comparable period in 2015, partially offset by an increase in clinical trial expenses related to ongoing and planned clinical 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, and thanks everyone for joining us this morning. While 2016 continues to be a very challenging year for our stock price, which many of you I am sure are keenly aware. Fundamentally we believe the company is stronger than ever with a lot of great progress made in the first half of 2016. Some of those highlights included the issuance of Composition and Matter Patents in the US for both TG-1101 and TGR-1202, providing protection through 2029 for TG-1101 and 2033 for TGR-1202. In both cases, plus up to an additional five years under the rules of patent term extension. At the American Association for Cancer Research (AACR) Annual Meeting scientists from the Moffitt Cancer Center presented preclinical data describing the differential regulation of human T-cells by TGR-1202 as compared to other PI3K-delta inhibitors and close to presentation that may partially explain why we are not seeing the same autoimmune like effect with TGR-1202 as seen with other PI3K-deltas. We also announced the commencement of the company’s first clinical trial of TG-1101 in multiple sclerosis, opening an entirely new area of potential value for the company. We also entered into a global collaboration to develop and commercialize novel BET inhibitors for the treatment of hematological malignancies. We also enrolled our first patient in our registration-directed UNITY Diffuse Large B Cell Phase 2b clinical study, and finally we presented an integrated safety and efficacy analysis of 165 patients treated with TGR-1202 both alone and in combination with TG-1101 at the American Society of Clinical Oncology (OTC:ASCO) Annual Meeting as well as at the European Hematology Association (EHA) Annual Congress. Some highlights from this presentation included that TGR-1202 alone and in combination with TG-1101 continued to demonstrate a favorable safety profile. Discontinuations due to TGR-1202 adverse events…

[Operator Instructions] :

Thank you. Hi guys. Good morning and nice to see the clinical progress and the continued 1202 differentiation.

Thank you.

I wanted to ask how the recent pivotal results in diffuse large B-cell impacts your thinking regarding TG-1101 in that indication?

Yes, that is a good question Jonathan. So that study particularly we thought was the one study of that registration program and their [rituxan replacement program] was the most likely to be negative. This is front line patients with aggressive diffuse large B-cell lymphoma. You would expect, one should rituxan perform quite well in a frontline patient population, where there is high expression of CD20. So the ability to differentiate the difference between those two drugs I think is and clearly was a challenge. So we really I think all along though that that was the toughest place for them to demonstrate that they could show that [Indiscernible] was better than rituxan in that front line patient population, and was absolutely zero. There is no question that in a head to head basis they have proven it twice now, both in follicular and CLL that glycoengineered CD20s are better than non- glycoengineered CD20s or rituxan. So I think it is just one of those situations where the trial design was set up that was very challenging and probably [failure] from the very beginning but I think they had to try as part of their replacement. It seems like they will probably be R-CHOP or remain diffuse large B-cell, but they will be able to replace rituxan across indolent lymphomas and CLL.

Okay, thanks and I guess that it is simply too difficult to presently estimate genuine trial time, and I guess, since you have the coverage from UNITY for both drugs you almost don’t care?

I would say almost – I wouldn’t say exactly, again I think we are still working with GENUINE. We think it is an important study design. We think it is important to show the benefit of ibrutinib, but yes, there is some sense that with the UNITY-CLL study enrolling quite nicely and a lot of – most of our major academic sites are not yet open in the US and we have a lot of interesting and exciting sites in Europe, both Western and Eastern Europe where there has been a lot of enrollment in these studies. I think the big CLL 11 study, which was the Gazyva CLL study, I think almost of the enrollment came from Eastern Europe or a lot of it. It was the major enrollers, and we have a lot of those sites ready to get them involved in hopefully by the end of year have them up and running. So, enrollment right now is strong. We still have the major academic centers to get up and running in all of Europe. So, yes, I think we are feeling very optimistic and that obviously will set us up for approval for both drugs, but again we do think having data from the combination of TG-1101 plus ibrutinib is still important. We still think it would be great if we can figure out how we can make that happen fast enough, so that it gets done before we get any further with UNITY-CLL.

Great. Thank you very much.

Thank you.

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

Good morning guys.

Good morning.

Thanks for the update in terms of the profile for 1202 and breaking up I guess the Phase 3 [plus too], I guess given the differentiation of 1202 versus idelalisib and duvelisib, one of the things that we heard at ASCO and ASH was excitement from investigators in terms of combining it, can you update us on your plans for additional doublets and triplets with 1101 and 1202, and also 1303 and then also the ongoing combos?

You kind of lost me in there a little bit Matt, but I will say that our hope is that we will have some really nice presentation at ASH this year for some of the triple combination work we have been doing both with TG-1101 and TGR-1202 plus ibrutinib, which has been conducted in CLL and NHL. We also have 1101, 1202, and 1303 plus [Indiscernible], which we are studying in lymphomas. And I think there is a few other novel combinations that we are looking at 1202 plus ibrutinib as an oral, and I think there is one another oral combo that we are looking at as well. So, we are hoping that at ASH we will have some pretty interesting data on some of those next-generation combinations.

Okay, great. And then with the MS for 1101, the Phase 2 ongoing, what are you looking to share I guess in that study and then what do you think I guess at this point the Phase 3 could look like?

Well, in terms of what we want to show from the Phase 2 study, the most important information that we are trying to get so that we can move on to Phase 3 is really just the B-Cell depletion information. We just want to get comfortable that at those doses we are looking at, we are depleting the B-Cells in sufficient quantities. We are pretty confident we are going to do that, but until you actually do it you still don't know with certainty. So that is the big part of the program. We will continue to follow patients over a two-year period to look at certain aspects of MS efficacy, including GAG lesion reductions but that kind of information would not hold us up to start the Phase 3 program and that will be data that will come out nicely during the conduct of our Phase 3 trial. So first is the B-Cell depletion data. The other part that is important to us is our ability to show we can infuse in shorter time frames. Right now I believe [Indiscernible] is a three to four hour infusion every six months. We would like to see our infusion come down closer to one hour. As you know, on the cancer side, after the first one or two doses we are able to get 900 mg into a patient in an hour and a half, and our anticipation is that the Phase 3 dose for MS will be less than 900 mg. So that is what we are looking for both B-Cell depletion and infusion times data, and then in terms of what a Phase 3 design should look like, I think if you look at OPERA I and OPERA II, which were the Phase 3 trials run by OPERA, I…

Great, thanks for the [indiscernible].

Thank you. Your next question is coming from Joe Pantginis of Roth Capital Partners, please proceed with your question.

Hi guys, good morning, thanks for taking the question. Michael, can you provide a little color with regard to your earlier prepared comments on 1202 with regard to efforts that you’re going through right now with regard to the broader physician population and I guess the way you put it was painting the PI3Ks with the broad stroke as, they’re all the same versus the safety call filing, efficacy profile that you’ve provided?

Yes, I mean, anyone has ever touched that drug doesn’t see it that way and we’ll take we’ve one investigator and we’ve a lot of investigators now that touch that drug and talking about hundreds who have purchased – anyone has ever given the drug to the patient and has also given one of the other drugs to the patient, feels the same in terms of their tower zoning safety profile there – but it’s a big country, it’s a big world and is so as of others, you’re not – I’ve always felt and believe that any physician who has in touch to drug to – actually touched the drug it’s negative until they use it. And we do have a pretty effort onto expand the user base of the drug 1202, like I said unit you’ll study, the 60 site that are currently opened only handful of those are major academic centers and the next 40 without a good number of major academic centers that will be opening as part of that next tranche they take as you know six to nine months to a launch of a large academic center into clinical trials of, this is why they're in the second half of this year, but the more people that can touch [indiscernible] the more people are going to be believers, you just have to keep getting more people involved, so we have an active effort to get them into the UNITY-CLL study, and we have active efforts to get them into UNITY-DLBCL, and we'll continue to actively try to get them into molecular studies. We've been talking to them about even anyone who is -- some of the major academic, kind of who want to do their own things, so we've even have an outreach program, and more offering sites to do trials and demos interested in. And I think we'll hear about a few more of those over the next few quarters. So I think, our goal, we have to get more people to cut drugs and I think we will do that through UNITY program.

It’s very helpful. Thank you. And then my next two questions are relatively brief. I was just curious with regard to MS Program, are you still looking to present B-cell depletion data by yearend. And second, what is the status of the IRAK-4 program?

So in terms of B-cell depletion data, we'll certainly have plenty of B-cell depletion data before yearend, just the question is what the appropriate venue for disseminating that information. The way we end that conferences go out, as ACTRIMS, is big ones in September. Clearly, we won't have any a net data there. We will have [indiscernible] data there. And then the next major conference I think is actually AAN, which is in April, so I think in between those two time points, we'll come up with certainly present some of the information, possibly with corporate presentations, that I don't think we're going to just throw a PR out there with some random B-cell depletion data, but we will have plenty of B-cell depletion data long before the end of the year for sure.

Okay. Great. And IRAK-4?

IRAK-4, we're still trying to figure out exactly what we want to do with that program. It has a pre-clinically as a tight therapeutic window and we're just not sure if given all the other activities we have ongoing in the preclinical with both PD-L1, GITR, now we have BET in house. We're looking at some other agents as well, we're just trying to prioritize and see where it makes the most sense. It could be in a position to put it into the clinic if we wanted to, probably within the six month period once we turn the system to do it, though I just said, I think preclinical has been a pretty tight therapeutic window and we're just trying to figure it out.

Okay. Great. Thanks a lot.

Your next question is coming from Yatin Suneja of SunTrust Robinson Humphrey. Please proceed with your question.

Hi guys, congrats on all the progress and thank you for taking my question. Just a couple of questions on UNITY CLL. Could you remind us when you might be able to complete enrollment and how many patients per center are you guys targeting for that trial?

So the original guidance was that we figured it was about a 24 month enrollment period. The study got up and running March April of this year. So 24 months from now, sort of first half into first quarter and second quarter of 2018, but as I said in my prepared remarks, I think we can turn a neat work seal that time frame, which the way we're seeing it today. And in turns of patients per center, if we have globally about 150 sites up and running that would imply about three patients per site, so I think pretty modest. We're expecting -- I mean, as a study, there is 150 sites that's going to enroll at all, and there will sites, I don't know -- we already have many sites that are already above three enrolled patients at this point.

And then in terms of the end point, I think the PFS was the primary endpoint. If we had to push an accelerated approval, could you tell us that what the bar would be? And when can we see that data?

So basically the study is designed with, say, three checkpoints, the first is to remove the two single agents on, so we had a contribution interim analysis. And that will be after approximate 200 patients have been enrolled into the trial. Once we view that and hopefully we'll be able to turn move the two things, raise an ARM, the study will continue as a head-to-head. All the patients enrolled prior that will obviously maintain and be part of the study, and enroll as a one-to-one randomization [indiscernible] versus 1303. And then once we get to the end of enrollment there is another interim analysis for HRA approval with overall response rate. And we're now at the end of enrollment. And then we'll continue to file patients for PFS. I think the overall response was part of the minimum of six months of follow up since that's the time frame, which we give because I have [indiscernible] that's when we could do the overall response. My guess is that the PFS will probably be close to really lie it around the same time as [indiscernible], and we can't be completely 100% sure, but I think if we assume that somewhere between 25% to 30% of the patients are going to be also re-factoring and the remainder will be frontline, we're going to see some reduction in the overall PFS from the desire of the Phase III trial, which was I think past 26, 27 months. So we'll see what happens first. We're accepting very strong PSF curves from the study or setting the free ARM, but it’s kind of possibly, it’s a free option for us to have a little response, but maybe that the PFS difference is still great with the studies earlier.

And just maybe one more question on GENUINE. So the challenge that you are facing, is it because that the centers have not been screening patient appropriately or are we just overestimating the legible patients pool, because my guess would be like there should be a lot of patients out there who are refractory or who have already taken ibrutinib?

Well, I think it’s a combination of both, which is I think there are definitely lot of momentum and sites were not rescreening these patients, so I definitely I think broke some early some momentum there we're having. And then obviously went back and we've implemented the screening protocol, but we're still seeing that there is lot of patients that just don't qualify. So I think the incidence maybe slightly smaller than we expected. And then there is an always an efficient -- even if it were a 50% natural screening, meaning 50% of the patients will be high risk and 50% will not be, that's a relatively accurate estimate, which is obviously quite below. But then there is always some very potential reasons why patients won't qualify for trials, even if they know they're 10% or 15% degradation from there, so that definitely creates the challenge. When we talk to doctors about it, they say, yes, I mean, in their mind they view it as a real niche setting in terms of finding high risk patients, so I think it’s a combination of both. I think the incidence of high risk is probably slightly below the 50% projected target, and then you lay on top of that, just any other reasons why patients will fail to be eligible for trial or will openly decide not to enter the trial, there is always some reason that always comes up that, certainly if it is fused together, it’s definitely a lot more challenging than something like said, where it’s wide open. The only real restriction is having team desire to work around we saw previously. In the U.S., generally for [indiscernible], so that's not an issue. And for relapsed/refractory patients, not many of them that seen under this two drugs, so that has not been a challenge. We always deal with a more open design, easier to enroll to, and its clearly chosen to be the case.

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

Thanks for taking the question. First, can you talk a little bit how an anti-CD20 and a PI3K inhibitor kind of fit into this world where you have IVR, you have Venetoclax, where do you think this gets sort of relegated to and who are the docs that are ideally using it?

So I think that's a good question, Reni, because I think most people just believe that this space is very crowded, but if you really break it down it’s not as crowd as a space as one might think. And there is always room for a very good, well-tolerated treatment option, but again, let's assume all positive thoughts that UNITY-CLL is a positive outcome trial that we see benefit in both frontline and lots of refractory patient, and its approved across all of CLL, so we would have the first real utility regimen that could be used in basically almost any setting for CLL patients. And if you think about what line treatment does start, you're going to have, I don't know, 60%, 70% of the patients are going to be started in the community, the remainder will be started in academics center. And in the community, they're going to look for drugs that they can easily provide to the patients with the least amount of toxicity, and they're going to make a decision whether they want to start with BTK base first line treatment or they're going to start with a PI3K delta phase treatment and we'll be the only one of that class, so we will be competing with the BTK base treatment. There will be BTKs plus Gazyva, which are running through the clinic as we speak. There is going to be some portion of the patients that do not tolerate. Again, we'll start from the worst case scenario now, which is everyone believes that the BTK is a better and we're not going to be as competitive. But there'd still be 15% to 20% of the frontline patients that go on in BTK therapy and don’t tolerate it well and come off for some reason. So,…

And then do you guys have a program, maybe evaluating a triple combination with the NEDA IRAK, like here?

We haven’t announced anything but as part of our outreach to physicians that may not be interested I working on anything that we've developed but they have their own ideas. I'd say that is definitely in the work.

Got it. Just switching gears to GENUINE. Are there, at least when I look at both trials, I almost besides GENUINE being in my view the low hanging free trial and probably the most straightforward and easiest to succeed for a study. Are there any trial modification whether it's entry criteria that you might be able to institute and I guess just reading kind of the language in today's call. Is there at any points maybe this year or next year where you just look at the enrollment rates and you say what we have to call it and kind of fill the study for to conserve resources and the like.

Look. I think any and all of those are practical responses to what's going on and obviously if it's obvious to you, it's probably obvious to us that those are the things that we need to consider and are considering. So, yes, I think we're keeping our eyes wide open, we're watching the enrollment of both studies. We're trying to figure out what makes the most sense. Again I think we'd like to be able to continue to use GENUINE for accelerated approval of 1101. But we just have to see again whether you're right, whether there is something we can do with the inclusion exclusion criteria or whether we just in some way modify the study or terminate the study as you described again and save resources all those are on the table. Like I said as they're too intuitive to you as they're intuitive to us as well.

Got it. And just one final question. Can you give us a sense as to the Checkpoint program status and why you feel your checkpoint PD-L1 and GITR that's being developed is different than what's already out there. And I presume that’s part of your pre-clinical testing, you are testing at against other products that are being evaluated around the market. Could you just give us some color on that program?

Yes. So, I think in terms of the profile of the actual PD-L1 antibody for one and I think GITR probably we could say the same about is that we're looking for certainly best or near best-in-class in terms of potency, binding affinity, all those attributes, I mean, we're coming in with a very strong antibody products. We're confident of that. I think on the PD-L1 side, where they are lot on the market, I think the key differentiators for us will be we will maintain some level of ADCC in the first product and we are evaluating glycoengineered versions of our PD-L1 which would basically create the first and only dual action PD-L1 where we can engage both T-cells and NK cells. And so we do think that actually provides some interesting additional activity for PD-L1 as a class. So, that will be very novel and interesting. And again we've always felt that we wanted have a own products as that we can continue to build on those pricing advantages that we touched on briefly on 1303 as we continue to add antibodies on top, I think we can do it in a very cost effective manner and be able to come in with triple and quad therapies that are priced closer to what you pay for one half to two drugs that you have to buy in the open market. So, we do see a lot of advantage that again we're hopefully adding activity and not adding a lot of toxicity and a lot of cost. I think those that's kind of the goal of having these things internally. So, we definitely want to have comparable to best in class antibodies that come out of that program and we have a great team working on them. And then being able to use them efficiently in the clinical trials to create extra benefits for patients without adding extra toxicity and without adding extra cost. Or marginally extra toxicity and marginally extra cost, I mean, there's always going to be some level of toxicity that will come with new drugs.

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

Thanks, Reni.

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