Greetings and welcome to the TG Therapeutics third quarter 2014 earnings call. (Operator Instructions) It is now my pleasure to introduce your host, Jenna Bosco. Please go ahead.

Thank you. Good morning, and welcome to our conference call regarding TG Therapeutics third quarter 2014 financial results and business update. I am Jenna Bosco, TG's Director of Investor Relations, and I welcome you to our conference call today. Following our Safe Harbor statement, Sean Power, TG's Chief Financial Officer, will provide a brief overview of our financial results; and then turn the call over to Michael Weiss, the company's Executive Chairman and Interim Chief Executive Officer, who will provide an update on the ongoing development of our product candidates. 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.tgtherapuetics.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 discuss the financial results for the third quarter of 2014 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 yesterday evening and can be viewed on the Investors and Media section of our website at www.tgtherapeutics.com. First I wanted to provide an update on our cash position. During the quarter, we took advantage of favorable market conditions and enhanced our cash position through stock sales under our at-the-market or ATM facility. Accordingly, at September 30, 2014, we had cash, cash equivalents, investment securities and interest receivable of $67.3 million as compared to $45.4 million at December 31, 2013. Additionally, subsequent to the third quarter, we received an additional $26.1 million of net proceeds from the ATM facility, giving us the pro forma cash, cash equivalents, investment securities and interest receivable balance as of September 30, 2014, of approximately $93.4 million. With the proceeds raised during and subsequent to the end of the quarter, we fully utilized the available capacity under the ATM program. And accordingly, no further sales can or will be made under the existing facility. We were quite pleased with the execution of the facility and believed it was an efficient way for us to raise capital at an average price over the period as opposed to trying to time the market with an offering. In the end, we raised approximately $50 million at an average sales price of $10.31 per share, which was approximately equal to the volume average weighted price or VWAP during the period of sales of $10.36, and in excess of the VWAP for Q3 of $9.63. With that, I'll turn to the financial results. Our consolidated net loss for the third quarter ended September 30, 2014, excluding non-cash items and a one-time upfront cash milestone payment, was approximately $5.2 million. The consolidated net…

Thank you, Sean, and thanks to all of you for joining us on this call today. Third quarter has been a truly transformational time for TG, and I'm proud of the work our team has done in advancing our clinical programs. As most of you are now aware, in September, we were thrilled to announce the granting of a Special Protocol Assessment or SPA for short, by the FDA for our first pivotal trial for TG-1101 in combination with ibrutinib, which has a brand name Imbruvica. We believe by designing a clear regulatory pathway for TG-1101, we have significantly changed the profile of the company, making our value proposition to both patients and investors very clear. As stated on prior update calls, our goal is to commence at least one registration trial before the end of 2014, and we're happy to be on track to accomplish that goal, with the expected kick-off of the TG-1101 Phase 2 trial expected in the coming weeks. In addition to the Phase 3 launch, we are also very excited to present updated data on all three of our ongoing priority studies at the upcoming American Society of Hematology or ASH Meeting in December. Before discussing ASH, I'd like to spend just a few minutes discussing the SPA and the highlights of the Phase 3 clinical trial design. This Phase 3 clinical trial is a randomized controlled trial, evaluating the combination of TG-1101 plus ibrutinib versus ibrutinib alone in patients with previously treated high-risk chronic lymphocytic leukemia or CLL, including patients with at least one high-risk cytogenetic abnormality. The presence of any abnormality is widely accepted to predict will response to the standard therapies and appear to predict earlier progression on ibrutinib. The trial will enroll a target of 330 patients, with 200 patients included…

(Operator Instructions) Our first question today is coming from Jonathan Aschoff of Brean Capital

Given the TGR-1202 and design of the trial, I was wondering what are your plans for the trial and what can you say at this point, given the moment in the results about toxicity from that combo regimen?

Obviously, the TGR-1202 design was not a core trial for us. We did set it up as a backup trial, so that we have options depending on what happen with TG-1101 plus TGR-1202. So we set up originally as a back up plan. I think in the end it's given us a lot of good information, competitive intelligence in our ways, what other people might expect when they combine PI3K-deltas with Gazyva. Particularly, we have the ability to compare that information internally versus TG-1101 plus TGR-1202. I can't say too much, because it hasn't been published and it is pretty early to say. I mean we don't have that many patients on that trial, but we do have enough to feel very good about the profile overall of TG-1101 plus TGR-1202 versus Gazyva-1202. So I think we're excited anywhere more or so when we get to look at both sides of the equation. We get to see the performance of both antibodies, the tolerability of the antibodies in combination with the delta. I would say this is probably worth keeping a close eye on, other trials that use deltas and Gazyva to take a look at the toxicity profile, I think they'll see things that, I mean, that are probably expected. If you look at what you're seeing with single agent rather the other delta in terms of liver tox, neutropenia, those things are likely to be aggravated. You can look at the Gazyva label and see that they already have reasonable levels of both liver tox on their own and also high levels of neutropenia. So it will be interesting to see how well those combinations go together. Again, like I said from our standpoint, we get to see both sets of data and we're pretty comfortable with that. TG-1101 and TGR-1202 is a very nice regimen, both from a safety and efficacy standpoint.

When might we be able to see the results of TGR-1202 and Gazyva, would that be ASCO '15 or afterwards?

I guess that's probably the reasonable timeframe. It won't be at ASCO this year, so probably would be in after.

By the way, what does the $50 million ATM that's been exhausted, what does that mean for cash runway if you make the following two presumptions, that now you have two SPAs and you start the trials roughly at about the same time?

We're estimating that our base run, including one Phase 3 trial is still going to be about $4 million to $6 million per quarter. And then each Phase 3 trial is still going to be about $46 million per quarter. And then each Phase 3 trial, we assume again approximately a $15 million cost per trial; up to $20 million would be on a high-end. But I think we're actually more at like $10 million to $15 million, $15 million in the middle of the cost, divide that over two to three-year period, even if it's over a three-year period, its $5 million per year. You add another $1.5 million to $2 million per quarter, if it's over 2.5 years. So every Phase 3 trial we add, we could probably add about $2 million to that $4 million to $6 million burn because it will come out again over time. Does that make sense?

Totally.

Our next question today is coming from Matt Kaplan from Ladenburg Thalmann.

Just some follow-up question in terms of toxicity and what you expect. I guess, given some of the recent failures of the combinations that we've seen, specifically for instance like data, the trial which was stopped for the toxicity. What do you expect and are there any concerns that you have around the ibrutinib delta combination?

So I think it's a good question. We've been hearing that from folks that there is a generalized level of concern about combining the ibrutinib plus PI3K-delta inhibitors. Obviously, we're clearly the first folks to do it. We're going to only have a handful of patients available for the conference, so we're still learning ourselves. But again, I think given the general safety profile that we're seeing thus far with TG-1101, TGR-1202, we're feeling okay about and pretty good about the profile, so it's pretty early, but we do feel like we have from an overlapping toxicity perspective, we wouldn't necessarily expect to have too much, other than the fact they hit the pathway together, the toxicity profiles of the three agents don't seem to have a lot of overlapping toxicity. So the theory of worry comes from originally from the Gilead study, where they tried idelalisib plus our Syk inhibitor. They put the two piece together, they had very high-levels of liver-tox. They have a baseline high-level of liver-tox with idelalisib to begin with. This Syk inhibitor I don't think it's mechanistic. So again I think just from clinical property standpoint, I don't think it is the fact that they're walking with B-cell receptor pathway from two ways that they had aggregated liver-tox. Again, each drug and each chemical is different. And I am sure there's also been, obviously there is new concerns that were raised when I guess they just presented some triple data in abstract form on idelalisib, Rituxan plus lenalidomide Revlimid, that too was highly toxic. I think three patients ended up in the ICU. There were four DLTs in the first day patients, so they discontinued that triple therapy. So again, I think that finding the right triple therapy is a little bit of challenge, and it's partially the mechanisms and partially it's going to be the actual agents themselves and their underlying toxicity profile that's off-target. And again, thus far with TG-1101, TGR-1202, we've seen a very nice profile. We think it's a great backbone for additional triple therapy. Again, first information will be with the ibrutinib, where based on everything today, we feel like that's a tolerable regimen and shouldn't have some extreme toxicity as far as we know today. And again based on the mechanism, this shouldn't have really an overlapping toxicity profile what we've seen from these individual agents as well, we won't expect to have any major toxicities when combining the three agents.

And then in terms of your Phase 3 study that's about to kick off, congrats on a big win with respect to getting the SPA there for over response rate. How do you expect that combination to potentially use in the future, assuming that that trial leads positive, as kind of expect it to do based on the Phase 2 data you've seen so far. How would that be used in treatments setting?

I mean we think that the combination of TG-1101 plus ibrutinib could be the most attractive doubling in relapsed/refractory settings. We know that ibrutinib is getting great traction, it is a great drug. But it's not curing patients and everyone does relapse eventually. So we do think we can improve upon that and can improve upon in a relatively low toxic way, and in a way that patients can get immediate benefit. They can feel better, much more quickly. We've heard a lot of anecdotes about patients feeling better very rapidly by using the combination. So again, we think that, one, we're going to obviously improve the overall response rate; we think we're going to improve the outcome of these patients. And it's a very easy combination to use, again the toxicity appears to be quite low, relative certainly to any other regimens that we've seen, reports of any combination regimen thus far. It's going to be the only labeled CD20 with ibrutinib alone. It will be a label for ibrutinib plus bendamustine/Rituxan. Bendamustine will add toxicity. I think if you want, you could look at some of the 199 plus bendamustine/Rituxan data, there you'll see that there is definitely more toxicity, if we start combining in the chemotherapy. So it's a great regimen. Again, we think it's going to be, the response rates seem to be quite high in the 90 to 90-plus range. We think from an activity standpoint and safety standpoint, it's a very attractive regimen. And again, super easy to use, so particularly if you think about what patients maybe most suitable for this kind of therapy, it will be for any patient in the community, where doctors don't want to deal with toxicity profile or something like a 199, or even the toxicity profile of Gazyva, and of course that they can eliminate bendamustine, that's a positive without any degradation effect. So I think community where most of these patients will be seen, ibrutinib is being used heavily in the community, because it's easy to use and it's early into relapsed something that community docs can easily use. This is a great add-on in the community. And again, most of these patients are being seen in the community. So again, our impression is this will be the leading regimen in the community, and probably in academic center as well. But as the field evolves, academic centers won't see the patients unless you're in academic center. Until these patients have multiple relapses, and then they'll end up at the academic centers, because of the long duration of effect of ibrutinib alone and plus TG-1101, these patients are all going to be seen in the community, before they end up in a double or triple relapse into the academic centers. So yes, we're feeling extremely good about our position in the marketplace. It will be very attractive treatment option without a question.

And then final question, in terms of bigger picture, in terms of clinical development plans in oncology and part of unifications for TG-1101 and TGR-1202, and potentially TG-1101 plus TGR-1202 in oncology. First, maybe you could comment on, as we saw with data at Pan Pacific some very interesting data that you read out there in combination with the DLBCL indication. I guess what are your plans going forward with respect to that and then autoimmune as well?

Yes, so our plan is to broadly rollout registration trials of TG-1101 plus TGR-1202 in CLL, in NHL, so that would be follicular, and diffuse large B-cell, so we're working on those study designs now. And as each one percolates over through their system and ideally gets sign-off from the FDA, we'll be announcing those studies. So we're working on them. I think that's something I'm trying to say definitively, but the plan is absolutely to rollout the doubling of TG-1101 and TGR-1202 across CLL and follicular and diffuse large B-cell, I think we have a good design and we believe that drives our, as a combination, a viable and important new treatment options for patients across all of those disease states. And then once you've rolled, and then beyond that, as you described and we mentioned in our prepared statements, and we've been talking about for sometime, autoimmune disease is an area of great interest for these drugs and for us. We need all that interfering in autoimmune disease with Rituxan and CD20 inhibitor has efficacy, it's approved in rheumatoid arthritis, it's used in other autoimmune diseases. So we think the proof-of-principle for B-cell depletion, B-cell intervention exist. The [ph] anti-glyc treatment originally from human genome was approved in lupus again targeting the B-cell. So would you know that the proof-of-concept exist that interfering with the B-cell can improve a number of autoimmune diseases, so we think that we can bring the same kind of combination approach into the treatment of autoimmune disease, and we think that will be the first time that anyone has really focused on rationally build combinations in those disease states.

And I guess, is your strong cash position likely to accelerate that timeline at all or in terms of entering those patients?

We have a pretty aggressive timeline to begin with. I don't know that we can accelerate it too much, but we want to make sure we deal it in a measured fashion; quickly, but measured. So I think it simply gives us the financial flexibility to be comfortable in doing those activities that we need to do to, one, prepare for those trials, and as you conduct those trials without completing the resources that people turn around and get nervous about, where our cash is vis-à-vis our timelines on our approval studies.

Our next question today is coming from Joe Pantginis from ROTH Capital Partners.

I'd like to dive in a little bit to the science aspect here, when you link some preclinical data versus clinical data. And specifically what I mean is when you look at the mechanism of action by ibrutinib, there has been some preclinical data that has suggested what appears to be antagonism between ibrutinib and ADCC activity, but when you look at your clinical data, obviously the data suggests otherwise, so I guess maybe if you can comment on that. And then also in general, how you can or cannot monitor for increased ADCC activity with TG-1101?

I'm sure you've received a few inbound questions on that yourself and we've certainly received inbound questions about that research. I don't know what to say about it to be quite honest. I mean, when you look at it, it's certainly seems that there has been a few labs who has identified this potential antagonism. Now, this is all occurring in a test tube, right. And so when you look at it, sure it sounds interesting from a scientific standpoint, but as you mentioned, we already have human clinical experience demonstrating that there is no antagonism and certainly no antagonism that would be noticeable in terms of how humans react to these two agents together. Response rates are very high, 98%-plus thus far. So I guess, its one of the situation that if this research had come out five years ago, it is possible that we would not have tested TG-1101 plus ibrutinib, and Rituxan plus ibrutinib, and we would have only used, I guess ofatumumab or perhaps we're looking for a BTK inhibitor that perhaps didn't antagonized, but we know that at this point its completely discredited research. It has no validity other than its interesting in a test tube, but we already know that in humans it has no validity, which I find interesting. And most of the questions that do come in, Joe, are from Ph.D.s. Most other folks kind of ignore it and you would think Ph.D.s would know the best that most things don't come to test tube, don't translate into humans. And so that to try to put so much weight on an experiment in the test tube, and try to glean what CD20 should use of ibrutinib or what BTK should try to use with the other CD20s, seems a bit foolhardy at this point. And so I know you're getting inbound calls, we get them too. And I think I guess if you're Ph.D. and you do lab research, you apply a lot of weight to lab research, even though intuitively know that most of the stuff, it never really translates into human experience. But again, we do the question, glad you asked it, but again I think the research, if it had happened five years ago, we might not have tried it, but have been tried it, we would have then said, well, we completely discredited that research. I think we can feel we've completely discredited that research with the human experience.

Our next question today is coming from Ren Benjamin from H.C. Wainwright.

Just a couple of questions. I guess, starting off with the Phase 3 trial, could you give us some sense as to is there any interim or futility analyses built in, what are your baseline assumptions and what sort of delta are you looking for, from both the overall response rate perspective as well as PFS perspective and the power and when do you think the data or the trial could conclude?

So in terms of the overall response rate endpoint, there is no interim analysis, so there is no true futility analysis. I guess that DSMB has the right to look at the data and I think that it's futile they can do anything they want, but there is no formal futility or stopping rules for efficacy. The study is designed to look at approximately what we've seen in the expansion of ibrutinib alone, so we'd expect approximately 60% or so response rate with ibrutinib. It could be low as 55% as high as 65% or even close to 70%, which I think will be super high, that it could be. And we're looking at our drug at 90% give or take. So it could 85% to 95%, our working assumptions. And the study is basically 100 patients in each arm for overall response, its well powered for any of those comparisons, even at the highest ranges of ibrutinib and lowest ranges of our drug combination.

And then as far as timing, when do you think, I mean obviously I know you're about to start the study, and it all depends on enrollment, but given that ibrutinib is one of the components, it doesn't seem like enrollment would ever be an issue, so when do you think this might be available?

So we do agree with you that enrollment should be rapid to this trial, though there is always a recruitment curve, it always starts off slow, just because you got to get all the sites up and running and that takes time. And then it takes time for the sites to integrate it into their workflow. So there is always going to be that portion that is really unchangeable. But once it gets rolling, we do expect recruitment to be quite rapid. And so the only other reservation we have in terms of how rapid the recruitment can be in the final reservation, it's just we have to be thoughtful. It is restricted to the high-risk patients, which we estimate is probably 35% to 40%, maybe a little bit higher percent of the actual patients that walk in the door with relapsed/refractory CLL. So again, we think it's going to go rapidly. I think our target projections, I think if we got the study fully recruited in 18 months, we'd be quite thrilled, and probably closer to 24 months, but somewhere in that range I think would be the ideal target. And again it's possible we'll go faster, again depending how quickly we get the sites up and running. We do have an advantage working with U.S. Oncology. They're an unbelievably great organization to work with, and they can initiate sites we have one contract and they can initiate sites around the country quite rapidly. So it should help to minimize the upfront part of the recruitment curve. But I think that's kind of the way we're thinking about it. And this much close I can get you, so 18 to 24 is kind of the target range. We do feel that at the time we complete enrollment, we should be prepared or soon thereafter, I guess we'll get it done in 18 months. So we'll have to see exactly, but pretty close to at the time we finish recruitment, we'll be able to break the blind on the overall response rate endpoint.

And then just a question on TGR-1202. Is it true you're not seeing any hepatic toxicity or is just you're not seeing grade 3/4 hepatic toxicity? And if you're not, is there something unique about the chemistry of TGR-1202 or do you think it's just a dosing issue and you just haven't hit that maximum tolerated dose, where you may see a hepatotox. And I'm trying to understand, if you think it's more of a class effect or its molecule specific?

So we do not think it's a class effect based on everything we've seen to date, particularly with respect to the other members of this class. So we're pretty-to-highly confident that it is not a class effect. There is no evidence in a PI3K-delta knockout mouse-model that you would see the liver tox. And the other drugs are highly homologous in terms of their actual clinical structure. Our drug is not. And it's of a completely different backbone. And we're just not seeing the liver toxicity. We've not seen any grade 3/4, liver tox. I think the only thing we did see was maybe a grade 1 that was so transient than reported by the investigator cannot be associated with the drug. I don't know what else is going out with the patient at the time, but basically it's been non-existent. It's not just grade 3/4, it's pretty much been non-existent.

Has there been any work on the company's part to identify those patients that are more likely to response? So any biomarker work that's ongoing, that you might be thinking of. And in the ongoing studies have you seen any development of resistance, because you've had several patients obviously that have been on therapy for years, just wanted to get a sense?

I'd have to get back to you. I don't think we've identified any particular mechanism of resistance. We've said that we don't know that we've actually looked for it. So if there are, I'll double-check and try to get to an answer on that. The front-end to that question was related to, what was it?

The biomarkers, any work on identifying patients, likely it sounds although you have such higher response rates that might not even be an issue?

I think that's the way we've kind of felt about it, Ren, is that the response rates are high. We don't really need a biomarker. I think the biomarker itself is a B-cell malignancy at this point.

One final question regarding drug supply agreements and larger partners. We saw Pharmacyclics enter into an agreement with Roche. What are you thoughts regarding these types of agreements? And I guess it's a roundabout way of me asking how any potential discussions, if any, are going?

Right. I think the ibrutinib arrangement to access Gazyva is a rational approach for them, given the fact that Gazyva is the approved agent on the market, and the only way to really test it without chlorambucil is to actually buy the Gazyva or to get it from Roche. And I think they smartly went out and got a deal from Roche, so they can get it for free. I think from Roche's perspective it's an interesting, I'd call it, probably for them a backup strategy. I think they'd like to be selling 199 and Gazyva together. My guess is that they are going to realize that may not be as wisely usable as they once hoped based on toxicity profile, and they'll be happy to ride at the back of ibrutinib, Gazyva in a frontline setting, as we are happy to ride at the back of ibrutinib in relapsed/refractory setting for now. So I think it was a rational play for both of those parties given the circumstance. Again for us, there is really not much out there that we need access to, right. We have the CD20 that we think is as powerful as Gazyva and we feel it has a very nice safety-tolerability profile and ease-of-use profile. And same goes for PI3K-delta side of it. And as far as accessing ibrutinib, it's just much easier to use the commercial supply, than to have wasting time with other folks negotiating protocols and it just didn't seem like a good use of our time from that standpoint. So in terms of drug supply arrangements, there's really not much that interest us. I mean I could say that there is certainly some other agents that have been used outside of malignancies that was trying to coming in versus the PD-1s could be interesting, and so we're thinking about those types of things, but in terms of the universe that's sitting in front of us, the basic universe, there's not much for us to really want to access.

Our final question today is coming from Arlinda Lee from MLV.

Thanks for taking my questions, I have couple of them. For housekeeping, what were your shares outstanding at the end of the quarter?

I'll hand it over to Sean.

So following the completion of the ATM facility, we'll have approximately 44 primary out, 48 fully dilutive.

And then I guess going back to the TG-1101 plus ibrutinib trial, within the FDA, is there any durability requirements and what kind of durability might we see at ASH from the association?

Yes. So the overall response rate, there is no durability requirement that will come out as part of the PFS analysis. And at ASH, similar to the actual Phase 3, we designed the study really as the six month overall response rate study, given it's a single arm study and ibrutinib already has a very high progression-free survival or duration of response, there really was no practical reason to follow patients in our study beyond six months. So basically there were two cycles in that study and release the patient basically to the commercial ibrutinib maintenance after that.

And then lastly, maybe on manufacturing. Can you give us an update on any manufacturing effort you have completed?

Sure. I think for both of the drugs we're in the process of finalizing at commercial scale and everything is on track.

We have reached at the end of our question-and-answer session. I will turn the floor back over to Mr. Weiss for any further or closing comments.

Great, thank you. So as I'm sure everyone can agree, so far 2014 has been a very exciting and productive year for TG Therapeutics. For a small company, we have accomplished much in a short period of time, champing best-in-class combinations to improve patient care and drive towards that ever-illusive cure. We plan to continue aggressively pushing forward our clinical development programs, including the launch of our first Phase 3 trial, as well as our ongoing clinical trials. In addition, we look forward to additional Phase 3 programs being announced in early 2015 for both TG-1101 and TGR-1202. Finally, we are excited to have strengthened our balance sheet during the quarter and believe we are sufficiently funded to execute on our strategic vision. On behalf of all of us at TG, I'd like to thank all of our investigators for their patience and all of our shareholders and investors for their continued support. Thanks again for joining us on the call and have a great day.

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