TG Therapeutics Inc (TGTX) 2016 Q3 法說會逐字稿

Greetings and welcome to the TG Therapeutics, Inc. third-quarter conference call.

(Operator Instructions)

As a reminder, this conference is being recorded. It is now my pleasure to introduce your host Miss 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, 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 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 and 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 in 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 and media section of our website 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 at $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 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 will 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 of matter patents in the US for both 1101 and 1202 providing protection through 2029 and 2033 respectively exclusive of any patent term extension.

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 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 rapid and profound B-cell depletion with a single 450 milligram dose. In October we were excited, although apparently we were the only ones excited, to announce the revisions to the GENUINE Phase 3 clinical trial. With the modifications we expect enrollment to be completed before year-end 2016 and top-line data to be available in the first half of 2017.

More recently, we announced the publication in Blood describing the novel complementary mechanism of CK1 epsilon inhibition by TGR-1202 which potentially offers a mechanism for the clinical activity of TGR-1202 observed in aggressive lymphomas. Based on that research, we launched a Phase 1/2 study of TGR-1202 and carfilzomib in patients with relapsed or refractory lymphoma in collaboration with Columbia University Medical Center.

And last, but not least, we announced upcoming data presentations at the ASH meeting next month for TGR-1202 and TG-1101 which include three oral presentations and three poster presentations. As you can see, we have been busy driving hard towards achieving our 2016 goals and objectives.

With that, I'd like to briefly touch on the recent amendments to the GENUINE trial as announced last month. Given the movement in the stock price following the announcement I can only wonder if perhaps there was some misunderstanding regarding the changes and the impact on our registration path for TG-1101.

First, let me remind everyone of the two substantive changes that we made. First, part two of the original GENUINE study was eliminated and accordingly the revised study's sole primary endpoint is now overall response. The second change was to reduce targeted enrollment to approximately 120 randomized patients.

So why were these changes necessary and why are we excited about them? As we shared with investors starting as early in the year as January we were facing enrollment challenges with GENUINE. By August when we had our last quarterly conference call we noted that GENUINE's slow enrollment was diminishing its original purpose of a fast-to-market strategy and indicated that all possible options were on the table for the study including shutting down the study.

So with the enrollment challenges as they were we had two options: shut down the program entirely or try to find an approvable use for the data we could obtain. For us we were very excited to be able to amend the protocol and still leave open the possibility to discuss the results with the FDA. Given the context of our FDA interactions, we believe the FDA could have taken a negative position regarding our ability to use the revised GENUINE study to support a BLA filing for accelerated approval but they did not.

And they did agree that we could seek a pre-BLA meeting to discuss a filing for accelerated approval based on the results. Again, I think some shareholders misunderstood these interactions.

Importantly, the revised GENUINE study still has a 90% power to show a statistically significant improvement in overall response with a minimal detectable absolute difference between the two arms of approximately 20%. Patients will be followed until progression but the study will no longer be powered for PFS. We believe the expected data set from the revised GENUINE study is now in line with the overall response data sets provided to the FDA to support the first accelerated approval of ibrutinib, idelalisib and venetoclax, none of which were conducted pursuant to a special protocol assessment.

Now with the amendments in place we are projecting full enrollment in GENUINE to occur by the end of this year and we expect to have top-line data available in the May/June time frame of 2017. These changes put us back on track with our original enrollment guidance and also are expected to save us approximately $10 million over the next two years.

I also wanted to note that the changes to the GENUINE study in no way affect the UNITY-CLL trial which is being conducted pursuant to an SPA. The UNITY-CLL trial, as many of you know, is a randomized controlled clinical trial that is designed to support full approval for both TG-1101 and TGR-1202 with a potentially broad label for the treatment of both front line and relapsed/refractory CLL.

As mentioned, enrollment to the UNITY-CLL study began in February of this year and we are pleased with the early enrollment trends observed to date. We now have over 80 sites open for enrollment in the US and we should have over 100 sites open before the end of the year.

We also recently began to open sites in Europe and believe we will enter 2017 with a full complement of worldwide sites up and running and fully engaged. We expect to see robust enrollment in 2017, building on the positive enrollment trends we are already seeing for the UNITY-CLL study.

I'd also like to highlight our UNITY diffuse large B-cell registration-directed Phase 2b study evaluating TG-1101 in combination with TGR-1202 as well as TGR-1202 alone in patients with previously treated diffuse large B-cell lymphoma. This study is being led by Dr. Owen O'Connor at Columbia University Medical Center.

The primary goal of this study is to assess the efficacy as measured by overall response rate of the combination of 1303 as compared to 1202 alone with the goal of dropping the single agent 1202 arm after approximately 20 to 40 patients. Given the strong responses seen in the recently released ASH abstract for the combination of TG-1303 plus bendamustine, when the 1202 arm is complete, again we are hoping to drop that after approximately 20 to 40 patients, we plan to replace that arm with 1303 plus benda permitting us to compare 1303 to 1303 plus benda.

Assuming positive results after approximately 200 patients are enrolled, we would like to transition the study into a Phase 3 trial and ideally follow 1303 alone and/or in combination with benda for accelerated approval. We are highly encouraged by the early data in diffuse large B-cell from our Phase 1 and 2 studies for TGR-1202, TG-1303 and the 1303 plus benda triplet and believe we are working to an important new treatment option for patients with diffuse large B-cell where there is currently no approved treatment for relapsed refractory patients.

With that let me provide an update on our MS program. As many of you are aware, B-cell depletion therapy has already proven to be highly efficacious in treating relapsing and progressive forms of MS. Based on that data, earlier this year we launched our MS program for the Phase 2 study designed to find the optimal dosing regimen for TG-1101 in MS.

In this study we are evaluating B-cell depletion and other established MS efficacy endpoints as well as the overall safety profile of TG-1101 in MS patients and the safety and tolerability of accelerated dosing regimens designed to reduce infusion times. Enrollment is moving along nicely and we anticipate complete enrollment by year-end in the pre-specified cohorts with expansion cohorts continuing to enroll into early next year. We plan to use the data from this Phase 2 study to commence a Phase 3 registration program in MS in the first half of 2017.

We are highly confident from our experience on the cancer side and from early data from our ongoing NMO and MS studies that TG-1101 is a potent B-cell depleting agent. We have already begun communicating with the FDA and the EMA to understand their expectations for our Phase 3 program and we look forward to providing an update on this in the first half of next year. Having said that, we do believe given what we know about the efficacy of other anti-CD20 antibodies in MS that our Phase 3 program will be much smaller than the 1,600-plus patients in the ocrelizumab Phase 3 trials.

Finally, I want to touch briefly on the upcoming ASH conference. With three oral presentations and three poster presentations we are looking forward to a very positive conference.

It's worth noting that all of the clinical presentations include TGR-1202 in combination with other agents. We and investigators continue to believe that TGR-12 at two is a best-in-class PI3K delta inhibitor which based on its differentiated safety profile can be safely combined with multiple agents: BTK inhibitors, now JAK inhibitors, monoclonal antibodies and even chemotherapy whether in doublet or triplet combinations. We are very excited for the upcoming ASH conference and are looking forward to providing you with expanded data sets for each of the abstracts released last week.

In addition to the formal ASH presentations we will be hosting an investor reception with a distinguished panel of leading experts in CLL and NHL on Monday, December 5 at 8 p.m. at the Marriott Gaslamp in San Diego, California. And we welcome and encourage all of you to join us. We are planning a great event this year and hope to provide attendees the opportunity to hear some fresh perspectives on TG-1101 and TGR-1202.

Let me finish my prepared remarks by reminding everyone how far we've come to achieving our goal of creating best-in-class combination therapies across a broad range of B-cell malignancies. With GENUINE expected to read out in the first half of next year and our UNITY program kicking into high gear we believe we are on track to create significant value for our shareholders in 2017. And while pharmaceutical pricing controversies have damaged the entire industry and brought us down with it, unlike many other companies we see our value proposition rising as these concerns grow.

With that, let me now turn the call over to the conference operator to begin the Q&A session, following which I will return to make some concluding remarks as well as reiterate our goals for the remainder of the year.

(Operator Instructions) Joe Pantginis, ROTH Capital Partners.

Hey guys, good morning. Thanks for taking the question. I wanted to focus first on your recent Blood article.

Obviously, the authors, 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 authors 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 IW NHL conference to I think a standing ovation when he got finished or close thereto.

But, yes, very well received. Following that presentation actually we got a lot of inbound interest from KOLs wanting 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 the response has been incredible. I think people are really impressed by the science and how they've interrogated the molecule. And we've been, I think we've been on the receiving end of the benefit of that good science.

That's great. I guess I would look forward a little bit, are there other ways you could potentially take advantage of targeting c-Myc beyond the Kyprolis combo study?

Yes. We are super excited about potentially bringing in our BET inhibitor.

That one in particular has activity in c-Myc. So fingers crossed, we are hoping that we'll get compounded to the clinic in the first half of next year and we will be able to start to evaluate it both as a single agent in lymphomas, I think diffuse large B-cell and follicular there's been activity of the class, and then particularly looking at the combination with 1202 and even 1202 plus carfilzomib plus BET inhibition to see if we can't 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 expand us into some solid tumor areas as well. Triple negative breast cancer is one that's well known to be a c-Myc-driven solid tumor.

That's great. Thanks.

Maybe 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 are expecting them to scale down a little bit in the early part of next year, but certainly not done. I don't know if that is helpful.

No, no, it is. It definitely is. Thanks a lot, guys.

Matt Kaplan, Ladenburg Thalmann.

Hey guys, congrats on the progress. 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 and what we are 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 that 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 are 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 would like to see c-Myc inhibition.

I think once we have confirmation and hopefully we will 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 is a theory that one could re-sensitize patients to chemotherapy or turn a c-Myc, challenging c-Myc-driven patient who is very challenging to treat with chemotherapy basically convert them back to a normal risk patient where the results of diffuse large B-cell with R-CHOP in the front line 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 to understanding what that means in and of itself, does 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 PS3K delta inhibitor.

So for us we are excited to see across multiple applications both with new targeted agents as well as with chemotherapy the compounds continue to do well from a safety standpoint. So that's one.

Obviously, we are intrigued by combinations with ibrutinib. The benda combination is intriguing to us. I think you heard we're excited enough that we are probably going to build a cohort into our UNITY diffuse large B-cell study to explore that further.

The novel combinations with brentuximab and ruxolitinib are also intriguing to us. I think the re-sensitization of some of those Hodgkin's patients who are refractory to brentuximab is also intriguing. So there is a lot of kernels 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 will have our core registration approvals. And then this kind of experimentation is nice to see and leads to ultimately compendia listing and continued use in lots of different applications.

So we are 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.

And I think the PS3K delta class is deemed to be more promising in a lot of ways than BTK and even BTL2 across the broader lymphoma category. And I think we are sitting on the only PS3K delta that is easy to use and people like to combine.

So we feel like we are sitting in a desirable position from that standpoint. And, again, I think for us looking, circling 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.

Great, 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?

So we are targeting conferences in the first half of 2017 to present the first data. It will primarily be B-cell depletion data. It's possible by the second half of next year.

But more likely it would be the first half of 2018 where we'd have, our Phase 3 would be up and running but we'd start to present more of the hard MS endpoints. So GAD lesion 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 second half and maybe 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.

Ren Benjamin, Raymond James.

Good morning guys. Thanks for taking the questions. Just very quickly, I guess on GENUINE, and I apologize if this has been 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 a similar 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 target is 120 randomized patients. So that is the target.

In terms of the data, the original study was powered for 80% overall response rate for the combination arm versus 60% response rate for the ibrutinib arm. Basically we've 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, the 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 a 95% response rate for the high risk patients.

We've always assumed that as you go larger and you end up seeing some sort of lowering of that response rate we've been targeting success somewhere between 80% and 85% we think would 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 are 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 would just love to hear your thoughts.

When we think about the anti-CD20, 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 come back and start to say it's a crowded space or it's a class that's no longer functioning well. And when we 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 docs versus institutional docs, it seems to us that there is a market for the second or third CD20 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 can 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 are looking at CLL, diffuse large B-cell and follicular, CLL is clearly the most going on. But as you describe, it's not as complicated as people think.

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 starts to set up a different dynamic in terms of competitive landscape even for CLL. When you move into NHL and follicular, diffuse large B-cell in 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 are going to see it's a pretty large greenfield for us. And the only competition is really idelalisib and the toxicity profile there we think is just not compatible with broad application and broad use.

But circling back to CLL, which is again our lead indication, when you look at community-based practices, and for better or for worse we've focused for the last 20 years on community-based practices and they are different in how they treat patients and academic centers. In this particular case, probably the biggest difference is going to be where venetoclax fits into the treatment paradigm. In most community settings, including big networks like US oncology, venetoclax will not be used in their CLL patients.

So the thought of bringing a patient into the ICU and the potential for that patient to get very sick is just not attractive. In fact, I think people in the community have the perception that venetoclax is dangerous and can be very dangerous and I don't think they are that far off. I think it can be in certain settings quite dangerous and you have to be ultra careful.

So if you look at community oncologists what are they going to look for to treat their patients? They are going to look for the highest activity with the lowest toxicity. And so what their choices are going to be, if you are not eligible for FCR, which is again probably 70% of the patients are not eligible for FCR, their front-line choice is going to be either a BTK plus CD20, and I don't care which BTK you choose, that's not our problem, or they are going to choose our PI3K delta plus our CD20. So those are your two options.

If you are in the community and your front-line patient that does not -- is not eligible for FCR, you have two choices. You can go with a BTK plus a CD20 or you can go with 1303.

We think that people are -- people today believe that the market is going to be completely dominated. In fact, I feel people are giving us the probability that we will have zero uptake in that front-line marketplace and I think that's completely inaccurate. I think even if you just look at in the community the 10%, 15%-plus of the patients who will not tolerate BTK therapy for whatever reason will be candidates for our drug in the front line. That market alone far exceeds our valuation today.

And then on top of that you can layer in what is the impact of the perception that it is extremely hard to treat an ibrutinib failure patient and you don't need to rush into BTK therapy, that you could save it for second line. We do think that's going to drive patients to our PI3K delta 1101 combination.

And then the last piece of it is pricing. Front-line patients are going to be on a drug for up to five years, maybe more. The question is going to be who's going to pay for it? And if we can come in with a discounted price, it's not just a one-year discount, it's a five-year discount and we think that's going to be material.

So I think people are going to be quite surprised how well we do in front-line CLL. And, again, that's the most competitive marketplace. And I think we are going to do great there.

Having said that, if you're in the community and you did get a BTK-based treatment first, luckily for us we've designed our UNITY trial to both capture front-line and relapsed/refractory patients, so our label is expected to be for both. We will be on-label for patients who come off of BTK CD20 therapy in the front line and we will be ready to treat those patients and we will provide great value to those patients with very little toxicity.

So yes, the second-line setting is not as robust and it you won't be on the drug as long but it's a great market for us, as well. And we think we are going to have a nice blend of both first-line and second-line patients in the community. We will get utilization in the academic settings, but admittedly it's a little bit more complicated there when you start to add in how people are going to use venetoclax.

Now you have three options to choose from and how people sequence those will be up to time will tell. But, again, I think for us we are going to do great in our core market. I think, unfortunately, investors spend way too much time talking to KOLs and not enough talking to community oncologists.

And I think if you come to our Analyst Day you will have an opportunity to talk to some community oncologists and hear where most of the patients are being treated first and second you will hear how they are looking at the world. And it's quite different than the skewed view people get from talking to just a handful of academics.

Got it. And then just one final one for me regarding MS.

Just help me understand, I think you mentioned that the market that you are going after is relapsed remitting. And I thought through one of the key opinion leaders talks that we had attended that the primary relapsed 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, so the primary progressive, there is nothing approved today for primary progressive. Ocrelizumab ran a large study, came up with a p-value of 0.04 and change in the primary progressive, so it's the first time ever anything has been positive, which is amazing.

But for us from a regulatory standpoint that study shows us that they were reasonably powered but 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 and MS.

On the other hand, their study, their OPERA I and II study was wildly positive in relapsing MS. The p-value 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 that's significantly or study or studies that combined would be significantly smaller than the OPERA I and OPERA II programs.

So from a regulatory standpoint the path through relapsing MS is quite straightforward and that is the regulatory strategy we are going through. We do believe that given the value proposition we will 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.

Edward White, FBR.

Hi guys, thanks for taking my questions. So just on a timing standpoint, did you say that you were 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 2017, so in the first half of 2017.

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 hope to convert to a Phase 3 for 1303 versus 1303 plus benda also in 2017, was that correct?

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 is randomized, but it's two single arm and trials running randomized together.

Each one basically has, well, it's the same hurdle rate to get through. And the goal is that hopefully within the first two checkpoints of approximately 20 and approximately 40 patients at one of those two checkpoints we will 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, at the point at 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 will replace that arm with 1303 plus benda. Again assuming that we are going to a full 100 patients for 1303 alone that would imply that somewhere between 60 and 80 patients will go on to a 1303 plus benda arm which we think is a pretty good number of patients to compare versus the 1303 alone arm.

So we will have to comparisons. We will have 1202 to 1303 and then if all goes well we will also have a 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 if we can show that 30% to 35% response rate with that number of patients that that's a package that is filable. We will, obviously, in advance of that I think once we get around the 50 to 60 patient mark we will start to dialogue with the FDA, make sure they are on board with the concept of continuing to enroll and also potentially bringing that data down for a discussion.

Assuming all is going well, I guess I would hope that sometime before the end of 2017, although we haven't fully given guidance on this so I'm 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 could convert into a Phase 3. But I think that's soft guidance right now and we will have to figure that out.

Okay great. Thanks, Mike.

David Fang, SunTrust Robinson Humphrey.

Hey guys, thanks for taking my question. I just want to follow up on Joe's question. As you guys are getting a bevy of data on TGR-1202, let's 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 registrational trials in CLL and DLBCL?

I think in terms of some of these other indications where we are looking at data in Hodgkin's disease with rituximab and myelofibrosis 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 more of a compendia listing types of studies.

So I wouldn't say that these are would rapidly become priority studies for us. The priority is get our hopefully two approvals in CLL, both for 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 the 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. Again, we talked about 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 are 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 indolent lymphoma program. When might we get an update on the timing for that?

Yes, that's a great question. We are going to be having an advisory board at ASH, so we are bringing together I think now if the group keeps growing which is nice, how many?

17.

17. So we are up to 17 KOLs who 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 will have also at ASH.

So we've got a big group coming together. But at the more intimate 17 person KOL advisory board we are 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 are working toward it.

Hopefully early next year we will be able to launch. We are considering looking at similar strategies the way we are doing the UNITY diffuse large B-cell. The data that we are presenting at 1303 plus benda is both in diffuse large B-cell and follicular at ASH, so I think we will see some, again, the early response rates look quite good and we will see some more data.

So, again, I think we are leaning toward, we are vetting some ideas at this advisory board. So I think the long-winded way of saying probably early next year we should be able to nail down what we are going to deal with our UNITY indolent program.

Great, thanks. I just had one quick question, so you mentioned maybe in the previous call that the anti-PD-L1 antibody program might insert clinical development sometime in 2017. Is that still the case?

Yes. Right now we are still on target to get into the clinic in the first half of 2017.

Great, thank you for taking my questions.

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 Phase2b trial. We expect to complete initial enrollment in the MS Phase 2 trial by year-end and the first half of next year present preliminary Phase 2 clinical trial results and start our Phase 3 program.

Finally, we look forward to a very impactful ASH meeting next month. We will further expand on the abstracts mentioned in the conference call and also look forward to our analyst and investor event where we will 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 patients as well as our shareholders for their continued support. Thanks again for joining us and have a great day.