Jenna Bosco - Director, IR Sean Power - CFO Mike Weiss - Interim CEO.

Joe Pantginis - ROTH Capital Partners Matt Kaplan - Ladenburg Thalmann Jonathan Aschoff - Brean Capital.

Greetings and welcome to the TG Therapeutics Second Quarter 2014 Earnings Call. At this time all participants are in a listen only mode. A brief question-and-answer session will follow the formal presentation. (Operator Instructions). It is now my pleasure to introduce your host, Jenna Bosco, Director of Investor Relations for TG Therapeutics.

Thank you, Ms. Bosco. You may begin..

Thank you. Good morning and welcome to our conference call regarding TG Therapeutics' second 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 and review the first data presentation if our proprietary combination of TG-1101, our novel glycoengineered anti-CD20 monoclonal antibody and TGR-1202, our novel once-daily PI3K delta inhibitor, reported last night at the 2014 Pan-Pacific Lymphoma Conference in Hawaii.

A copy of the posted presentation is available on our Web site. You can find it by following the publications tab contained under the heading Products Pipeline.

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 Web site, www.tgtherapuetics.com, where it will be available for the next 30 days. All participants on this call will be on 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 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 Web site at www.tgtherapeutics.com.

As of June 30, 2014 we had cash, cash equivalents, investment securities and interest receivable of $51.2 million as compared to $45.4 million at December 31, 2013.

The consolidated net loss for the second quarter ended June 30, 2014 was $12 million or $0.36 per diluted share, compared to a consolidated net loss of $6.6 million during the second quarter of 2013, representing an increase in consolidated net loss of $5.4 million.

The increase in consolidated net loss during the 2014 period was primarily the result of a $6.4 million increase in non-cash compensation expense related to equity incentive grants and $1.2 million of non-cash stock expense recorded in conjunction with the common stock issued to Ligand Pharmaceuticals for the license to the IRAK-4 inhibitors program.

These increases were partially offset by a decrease in research and development expenses of $2.3 million during the quarter ended June 30, 2014, principally related to the timing of manufacturing expenses incurred for TG-1101.

The consolidated net loss for the six months ended June 30, 2014 was $19.5 million, or $0.62 per diluted share, compared to a consolidated net loss of $10.3 million during the comparable period in 2013, representing an increase in consolidated net loss of $9.3 million.

The increase in consolidated net loss during the six months ended June 30, 2014 was primarily the result of an $8.7 million increase in non-cash compensation expense related to equity incentive grants, and $1.2 million in non-cash stock expense recorded in conjunction with the common stock issued to for the license to the IRAK-4 inhibitors program.

These increases were partially offset by a decrease in research and development expenses of $1 million during the six months ended June 30, 2014, principally related to the timing of manufacturing expenses incurred for TG-1101.

While other research and development expenses in total decreased during both the three and six months, primarily as a result of manufacturing costs incurred during 2013, clinical R&D costs for both of our programs increased over the comparable periods in 2013. I will now turn the call over to Mike Weiss our Executive Chairman and Interim CEO. .

Thanks Sean and thanks all of you for joining us on this call today. First let me say that we are all very excited about the data presented yesterday at the Pan-Pacific Conference on our proprietary combination and in just a moment I will review the data in some detail.

However, before I do, I’d like to say that the last few months have been extremely gratifying for me.

The team has worked very hard in advancing our programs with great speed and diligence, resulting in encouraging single-agent data presentation at ASCO for both 1101 and 1202 and very promising data at EHA for the combination of 1101 and Ibrutinib, and now, as reported yesterday, on a proprietary combination.

With these encouraging preliminary results, we look forward to a more mature and expanded data before year end we continue be extremely focused on commencing at least one Phase III trial for either TG-1101 or TGR-1202 or possibly both before year end. Now I’d like to review the data released yesterday afternoon at the Pan-Pacific Lymphoma Conference.

From our Phase 1/2 study of our proprietary combination of 1101 plus 1202 in patients with relapsed/refractory chronic lymphocytic leukemia, also referred to as CLL and non-Hodgkin’s lymphoma, also referred to as NHL being led by doctors Susan O’Brien and Dr. Nathan Fowler from MD Anderson.

The preliminary data from the Phase 1 portion of this study was presented by Dr. Matthew Lunning of the University Of Nebraska Medical Center.

The poster presentation includes data from patients with advanced CLL including 17p and 11q [indiscernible] patients and a patient with Richter’s Transformation as well has heavily pre-treated relapsed and/or refractory patients with Diffuse Large B-cell Lymphoma, referred to as DLBCL and Follicular Lymphoma.

As of the data cut-off date for the presentation, 21 patients were evaluable for safety with 15 evaluable for efficacy. 6 patients were too early for assessment. Prior to discussing the data, let me elaborate on our goals for the study.

First and foremost at the Phase 1 study we want to make sure we can dose the two drugs safely together and to better understand the side effect profile of the combination. Second, we want to confirm the activity of the combination in CLL.

As we’ve seen very nice activity from both drugs in CLL, we wanted to confirm that collectively we will see a high level of activity. And finally, we designed the study to be signal finding, ideally to identify an unmet medical need that could benefit from a proprietary combination.

Accordingly the study permits enrollment of heavily pre-treated and high risk patients, excluding those with aggressive lymphomas and Richter’s transformation with no limit on prior therapies, including patients relapsed from or refractory to prior treatment with other PI3K delta and PTK inhibitors.

As I review the data below you will see why even at the early stages of this study, we believe we’ve already achieved each of these objectives. Regarding our first goal, from the safety standpoint, the combination appears to be well tolerated in the 21 patients evaluable for safety.

Day one infusion related reactions, also referred to as IRRs were the most frequently reported adverse events. All IRRs were manageable without dose reduction and all but 1 IRR was grade 1 or 2 severity.

Other observed adverse events included neutropenia, nausea and diarrhea with neutropenia being the only breakthrough for adverse event reporting greater than 10% of the patients.

One CLL patient required a several day dose delay for neutropenia in cycle 1, which met the criteria for dose limiting toxicity, necessitating additional patients to be enrolled into the CLL Cohort 1.

No additional dose limiting toxicities have been observed, with full enrollment completed in Cohorts 1 and 2 and accordingly, dose escalation continues.

Consistent with the data observed to date in the ongoing TGR-1202 single agent Phase 1 study, no drug related events of AST/ALT elevations were observed among the 21 patients treated to date in this combination study with TG-1101. Additionally, there were no reported cases of colitis.

From an activity standpoint, referring to our second objective of confirming activity in CLL, of the 8 CLL/SLL patients enrolled to date, five were evaluable for efficacy while three were too early to assess. Of the five evaluable patients, four achieved a partial response at the first efficacy assessment.

Remaining patient, a CLL patient with both 17p and 11q deletions achieved stable disease with a 44% nodal reduction at first assessment and a greater than 50% reduction in ALC and remains on study pending further efficacy assessments.

Additionally, consistent with our prior experience with single agent 1101, all 5 CLL/SLL patients were peripheral responders, with one patient achieving normalization of ALC and the other four patients achieving greater than 80% reduction in Blood Lymphocyte Count by the first efficacy assessment.

We believe these early data confirm the activity of the combination in patients with CLL and are consistent with our projections. We look forward to enrolling more patients and following these patients longer, so we can better characterize the activity profile in patients with CLL.

As per our third objective, signal finding outside of CLL, while early, we are very intrigued by the activity of the combination of patients with Diffuse Large B-cell Lymphoma. DLBCL is a very aggressive form of lymphoma. For patients that fail first and second line therapy, there are very few treatment options.

Diffuse Large B-cell Lymphoma can be further sub-divided into ABC and GCB subtypes. While ibrutinib has recently shown interesting activity in ABC subtype, GCB seems generally non-responsive to ibrutinib. In our study of the five DLBCL patients evaluable for efficacy, two responded to the combination.

Both were heavily pre-treated and one was a refractory GCB subtype, who had received three prior lines of Rituxan based therapy. Another patient with a GCB subtype also saw approximately 30% reduction in tumor mass at first assessment.

This patient was also refactored at prior therapy, had seen six prior lines with three prior lines Rituxan based therapy. Interestingly this patient and both of the responders were treated at the higher dose of TGR-1202. Only one of the GCB subtype patients progressed at first hand and that patient was treated at the lower dose.

It is also worth noting that in our Phase 1 study of TGR-1202 as a single agent, a patient with GCB subtype DLBCL had a greater than 40% reduction in tumor mass and was stable on single agent 1202 for over six months.

So in terms of our third goal we’re excited by the signals seen in patients with Diffuse Large B-cell Lymphoma, particularly GCB subtype and we’ll continue to enroll patients with this disease to better define the activity of the combination in this patient population, which we do believe would represent an unmet medical need.

We will also continue to look for additional signals in other lymphoma subtypes, including other aggressive forms but also in indolent forms like follicular lymphoma, where we expect to see activity that have not focused today. In this study we have treated only a handful of very heavily pretreated patients with follicular lymphoma.

While we have not seen any responses in this group yet, all patients were stable at first assessment and all had seen a reduction in their tumor mass. In fact the median reduction was about 30% with one patient near response of about approximately 45% reduction in tumor mass.

We’re quite pleased with this early activity in this particularly sick population of patients that were heavily pretreated with a minimum six prior lines of therapy, half of which were refractory to prior therapy and all had seen Rituxan no less than three times and up to seven prior Rituxan based treatments.

Overall we and the clinical investigators have been very impressed with the level of activity seen with the combination to date across multiple B-cell malignancies and are excited to continue enrolling patients and expanding the trial.

Now let me do a quick review of the other key data reported this quarter as it’s been a quite busy quarter for us in terms of data presentation. Let me start with the data presented last month at EHA, the combination of 1101 with ibrutinib in patients previously treated with CLL and mantle cell lymphoma. That study is being led by Dr.

Jeff Sharman at the U.S. Oncology Network. The data included 28 patients with a relapse and/or refractory CLL or mantle cell lymphoma of which at the time of the data cut off, 10 patients were evaluable for response, 17 were too early to assess and one patient had discontinued prior to first assessment for ibrutinib related diarrhea.

From a safety standpoint, the combination of 1101 and ibrutinib appeared to be well tolerated with few Grade 3/4 events reported and day one infusion related reactions being the most frequently reported adverse event for TG-1101 and diarrhea and rash being the most prevalent for ibrutinib, which is consistent with their product label.

And for the clinical activity of the 10 evaluable patients at the first planned efficacy assessment, the overall response rate was 90%. One patient with CLL was stable at first assessment with a 40% nodal reduction coupled with a greater than 50% reduction in ALC.

In other words, that patient was nearing a response but had not quite gotten there by the first assessment. I am pleased to report today that as of the second assessment, that patient is also now a responder. Accordingly the updated overall response rate for the first 10 evaluable patients from the EHA presentation is 100%.

While still early, we believe these rapid and high response rates compare very favorably to the ibrutinib published data and data presented in their product label where response rates of approximately 60% to 70% have been reported, with many of those responses taking months or even years in some cases to occur.

We look forward to presenting data on additional patients towards the end of the year. Let me now briefly update the data presented from our single agent studies of 1101 and 1202 during the quarter, beginning with the data at both ASCO and EHA for single agent 1101 in patients with Rituxan, relapsed and/or refractory B-cell malignancies led by Dr.

Owen O'Connor from Columbia University Medical Center. From a safety standpoint TG-1101 appeared to be well tolerated with all dose levels tested with day one infusion related reactions being the most frequently reported adverse events. All IRRs were great one or two in severity, were manageable and occurred more frequently in patients with CLL.

In terms of the clinical activity, the overall response rate for the 30 patients evaluable for efficacy was 43%, 30% PRs and 13% CRs including patients refractory to Rituxan. In the CLL subset, four of six patients or 67% responded to single agent 1101. Enrollment into the study is now complete.

Also presented in ASCO and updated EHA was data from our single agent study of TGR-1202 in patients with relapsed or refractory hematologic malignancies being led by Dr. Howard Burris from the Sarah Cannon Research Institute. From a safety standpoint, TGR-1202 appears to be well tolerated with no dose related trends and adverse events reported.

No MTD has been reached to-date and limited grade 3 events have been observed. It is important to note of the 40 patients evaluable for safety, no drug related athletic or liver toxicity or colitis has been observed with several patients on daily TGR-1202 for one year. Recall those toxicities have been problematic for other PI3K delta inhibitors.

In terms of clinical activity, 100% on evaluable CLL patients treated 800 milligrams or higher exhibited significant nodal reductions with eight of the nine or 89% achieving a nodal response, of which four patients have now achieved a true partial response.

The one patient that did not achieve a nodal response continues to have stable disease with greater than 40% reduction in nodal size. Dose escalation into the single agent study of TGR-1202 continues at 400 milligrams once per day of the micronized formulation in the fed-state.

You may recall over the last six months we completed exploratory studies in healthy volunteers to determine the effect on absorption and exposure of micronizing the particle size of TGR-1202 as well as the effect of dosing 1202 with food, as opposed to in the fasting state as was currently being done in the Phase 1 study.

Both of those efforts were quite successful and we believe these modifications will provide exposures approximately three to four fold greater than those seen with equivalent doses of the previous formulation dosed in the fasting state.

Overall, we’ve been very impressed by the single agent activity of 1101 and 1202 and believe that both drugs exhibit potentially best in class attributes, setting up for what could be a best in class combination.

The preliminary data presented at Pan-Pacific supports that potential and we excited to treat more patients for longer durations to fully explore the activity and safety profile of the combination.

Finally, let me mention that in addition to the clinical progress we have made thus far we were also excited to announce this quarter that we expanded our portfolio through an agreement with Ligand Pharmaceuticals to license the exclusive global rights to develop and commercialize their IRAK-4 inhibitor research program.

Preclinical models suggest inhibition of IRAK-4 could provide therapeutic benefit in patients with certain B-cell malignancies and look forward to advancing this program.

Program is currently in preclinical development and while it’s still early, we believe the addition complements our existing portfolio and demonstrates our commitment to identifying important mechanisms in the treatment of B-cell diseases with the goal of creating future best in class combinations.

Additionally, as you may have noticed, we also filed an 8-K last night regarding the implementation of a shareholders’ rights plan, typically referred to as a poison pill. We did not implement the plan in response to any specific threats for the Company, but instead as part of an overall review of our corporate governance.

Certain changes were also made to our bylaws, which was the subject of another 8-K last night.

We believe strongly in the value of our long term strategic vision and do not want opportunistic hostile suitors or short term focus investors to drive our process at a price that we do not believe takes into account the long term value of the Company, which of course we don’t believe is reflected in the current stock price.

To close, let me highlight some of our second quarter and recent accomplishments.

As discussed today, we presented the first data from our proprietary combination study of TG-1101 plus TGR-1202 at the Pan-Pacific Lymphoma Conference currently ongoing in Hawaii confirming early activity in CLL and presenting potentially a new opportunity in Diffuse large B cell lymphoma.

We presented compelling data for TG-1101 in combination with ibrutinib, the first data presentation of a glycoengineered CD20 in combination with ibrutinib at the EHA Meeting held in Milan last month and as updated today all 10 evaluable patients presented at the conference have now responded to the combination.

And at both ASCO and EHA we presented single agent data for TGR-1202 and 1101, and finally in addition to the data presentations, we also are excited to announce the licensing of the IRAK-4 inhibitor program from Ligand Pharmaceuticals.

With that I’d like to turn the call back over to the conference operator for the Q&A session, following which I will return to provide some concluding remarks..

Thank you. (Operator Instructions) Our first question is from the line of Joe Pantginis with ROTH Capital. Please proceed with your question..

A couple of questions if you don’t mind. First let me ask something about a specific patient from last night’s data, kind of a bit intriguing. It’s the fourth patient that’s listed of the overall efficacy that had FCR Rituxan and then intriguingly [indiscernible] PTK. It didn’t appear that this patient had high risk cytogenetics.

So I was just wondering if you had any specific commentary about this patient, about what led to relapse or what you saw with this person?.

I don’t -- we can check. I don’t know that we have much further information on the prior care, other than what’s listed here. We can probably get some more anecdotal information from the investigator. But clearly the patient was heavily pre-treated, seen a few lines of therapy. They definitely were on a PTK inhibitor.

Presumably, they stayed on the inhibitor until they failed, but we will try to figure out more and get more information back to you. .

Okay.

And then with regard to the responses that you are seeing, are these currently investigator confirmed responses and how often will you be testing for responses again?.

So I think we test every two months early on and then I think it moves to every three months and these are all investigator confirmed responses. .

And then maybe this one last one if you don’t mind. Just wanted to get a sense from the feedback you’ve been getting from investigators and as you talk to others in the field.

A, the safety of the combination and B the safety of the monotherapies of these products, especially 1202 with the lack of say the liver enzymes that you have been seeing relative to the competition and also the importance of the ALC data that you've been seeing as well as the patient or as docs evaluate the landscape here?.

So the feedback we’ve gotten from investigators has been great. I think from -- starting with the activity side, I think they are quite impressed with the combination. They are seeing reactions in patients that they were not expecting to see reactions in. So that’s quite positive.

And we’ve had very good feedback from the investigators on the single agent safety profile of both drugs and the combination profile looks quite inline, no unexpected toxicities, patients seem to be tolerating both drugs quite well.

Again we’ve now -- you combine single agent and combination 1202, you’ve got almost 60 patients of data without seeing any effects on liver tox that we’ve seen with some of the other PI3K delta inhibitors. I do think that’s a real issue. I do think investigators care.

I think that if you had your choice of one drug you have to think about that issue and not, you would go for the drug that you don’t have to think about it and that flows through the combination.

So again, I don’t think many PI3K deltas are going to be used as single agents, but you’re going to choose your combination regimen based on the aggregated safety and tolerability profile and I think this one stacks up pretty darn well against the competition and in particular against the other delta combinations that will come through. .

Our next question comes from the line of Matt Kaplan with Ladenburg Thalmann. Please proceed with your question. .

So congrats on the initial data you are seeing in the combination studies, 1101 plus 1202.

Can you talk about -- a little about the initial responses you're observing I guess in the two combination studies and with specific focus on the different tumor sub-types and what this means with respect to your thinking for potential pivotal studies in Phase III studies that you hope to embark on later this year? And I have a couple of other questions as well.

.

No, only one question Matt. So in terms of the combinations and the different sub-types, we're certainly in an exploratory phase of development. We know we have active -- I’ll say regimens. Clearly Ibrutinib is more straight forward, right? They have two labeled approvals, CLL and mantle cell lymphoma.

In both of those sub-types, we are seeing very nice results with the combination. They’ve got approval. They see very nice results with single agent.

I think we're seeing again -- it’s early but I think we’re seeing something over and above what one might expect to see with Ibrutinib alone and so I think that both CLL and mantle cell are potential opportunities for us for registration trials and when we look over it, our combination trial, certainly CLL is a focus.

Again we know both drugs work quite well in CLL and combination seems to be doing exactly what we would have expected it to do. So that’s all inline and perfectly sets us up for potentially a CLL registration pathway.

I think as we look at the data in the other sub-types, follicular again I think it’s a little bit early to say too much about follicular but I think we know that CD20 has very nice activity in follicular, we know that the delta’s have very nice activity.

So we’re pretty confident that we will find nice a registration pathway in follicular or more to the matter into lymphomas generally, which would include sub-types like marginal zone, which we know we’ve had an excellent activity whether our CD20 as well. So we think there is always going to be an opportunity for us in follicular.

We think the drugs will perform quite well in that area. Again I think at this early snapshot, a little bit hard to discern it but again I think we’ve seen some very nice reductions in all of those patients with the follicular subtype basically responding to the drug with tumor reduction all stable.

So I think we’re looking at that a little bit early, given the sickness of those patients. And then the most exciting to me, which is news because again follicular is known. It’s an area where deltas [indiscernible].

Our combination -- it will be shocking to me if it doesn’t work well in follicular when we pick the right patient population and we go for a proper study in that area. But the real interesting area and new is Diffuse Large B-cell Lymphoma, which is very aggressive. It’s not an area where the other deltas are currently going.

It’s an area where ibrutinib has been tested. I think the only study that they did or one of the few studies that they did, they showed about 40% single agent response rate in the ABC subtype but about 5% response rate in the GCB subtype. So again it’s reasonably Greenfield for us to go after.

Once you get past second line, it's clearly an unmet medical need. These patients are relapsing very quickly. In this study a lot of them were refractory to their prior therapies. So to me that's probably -- of all the news -- my expectation with CLL was great. My expectation is follicular will be -- will work very well.

And then the new information to me today is we have an opportunity now to explore Diffuse Large B-cell, where again no one else is going. No one else can really run the combinations in this area the way we can with our delta and our CD20. So we’re feeling pretty good.

Again I don’t think, if you look at these patients with the prior lines of Rituxan, it would be interesting I am sure for someone to run Rituxan plus, which is approved plus one of the other deltas. But I think they wouldn’t see much success.

So again we’re the only ones who have a CD20 that could possibly provide some value in the setting and the delta to work with it. So again I think that was always our initial intent; to go into areas where no one else could really logistically or practically go and demonstrate activity. Again very early. We only have five patients.

Two out of five responded. That’s pretty good in my book and I think you are on site there in Hawaii, Matthew. You should talk to the investigator. I think one of those patients is his patient. He’s a very, very sick patient.

I think they were very surprised that the patient had such a remarkable reaction to the combination, but you can confirm that on site. So I think again when you look at all of these, we have a lot of opportunities in front of us. What we’ve told folks is we’re not staking a claim to what exact indication and what setting we’re going to go forward in.

Today we have -- in house, we have five, 10 or more protocol designs that we’re working on in the various subtypes. And we’re going to start to work closely with the FDA and the ones that we think make the most sense that they are amenable to us running stays in, over the areas that we move forward.

And so we really can’t say too much about what the registration path is going to be. But I think we can see registration paths in all of these subtypes today..

And then going back to the safety tolerability you are observing so far, I guess with both molecules but initially focusing on 1202. I guess -- now that you’re using a micronized dose and assuasive state, how does this compare with the mono therapy trial testing? And I guess what’s impressive is you’re still not seeing any liver-tox.

So give us a sense in terms of what dose you’re actually at and where you are especially in the combination study and now in the mono therapy study as well, using the micronized dose and how would you compare that to the mono therapy?.

So we’re now using the 400 milligram once per day micronized dose with food in all of our studies. So in the single agent study, I think we’ve just about completed that dose cohort and we’re probably going to be dose escalating shortly to the 800 milligram dose.

But that dose is being used in the single agent as well as now we've just moved that into the combination. So that dose is probably equivalent to approximately 1,200 milligrams, maybe up to 1,600 milligrams of pre-micronized fasted dosing. And so again we had anticipated that’s an active dose.

Everything above 800, we’ve seen very nice activity above 800. We went 800 fasted, 1,200 fasted, 800 fed, 1,200 fed, no DLTs, no liver-tox. So the 400 dose we think is probably equivalent to about the 1,200 fasted or also approximately the 800 fed..

And when did -- in comparison to some of the other Pi3 kinase delta inhibitors, when did they see the liver-tox start to develop in there in the entire course of their treatment?.

The liver-tox is a relatively early event, and say it's seen -- if -- it's going to be seen usually in the first two months of treatment..

Okay, great. And then in terms of the initial responses and this in little bit of follow up to Joe’s question; initial responses and the criteria using the highlight criteria to define a PR; are you -- you’re doing scans to define the responses in these patients.

Is that correct?.

Yes, all these patients were responders through scans..

Okay, great. And I guess the question a Sean and then I’ll jump back in the queue.

When you take out the non-cash charges, what you expect I guess the cash burn to be in the second half of this year?.

Matt, we expect the cash burn in the second half to be consistent with what we’ve guided, which has been approximately $4 million to $6 million. If you look at it for the second quarter, it went from roughly 54.5 to 51. So certainly on the low side of that from the cash perspective. So I would say our guidance remains consistent..

Our next question comes from the line of [indiscernible] of MLV. Please proceed with your question..

I had a -- I was intrigued by the comments you made about, as you track the patients longer that you’re getting some of the stable diseases converting and looking at your combination data, it looks like there is multiple patients that are kind of right up that cusp and I'm wondering -- obviously this is the first response.

But looking at I guess what kind of timeframe do you think some of these will take to convert? And as well, if it’s a dosing issue that you might -- versus a dosing issue I guess?.

Yes, so very good question. We definitely do not know the answer to that question, which is whether higher doses will make the responses occur faster.

But typically with these drugs and we saw with the ibrutinib study too where there's always going to be one or two patients that just don’t get there at the first go around and if you look at ibrutinib alone, it could take six to 12 months to get the patients through to responses.

And then clearing up the cytosis takes you longer but we don’t have that issue when we combine with CD20. But when -- so when we look at it, we’re not really sure what the time frame is. I can’t say that I expect by the second everyone should be responder and to be honest we can't expect that everyone is going to respond to both combinations.

Even though we’re now at 100% with ibrutinib, I can’t imagine we’re going to maintain a 100% response rate. Obviously that would be amazing, but somewhat unrealistic because there is always going to be a challenging patient out there. And there is always going to be a handful when you go into a larger study.

Having said that, I think that we are seeing a very accelerated pattern of responses already and again my expectation is that most of the patients that -- not all but most of the patients that do not respond at the first assessment will ultimately become responders.

Again, not all but most and I can’t really -- today we don’t have enough information to predict exactly the time frame..

Okay.

And then maybe as a follow up, what kind of data can we expect at ASH this year? Are you going to update all of these trials or maybe hold off on some of them to get longer duration follow up?.

No, I think we feel comfortable that we’re going to present whatever we have available for all three of these studies, the two combinations and with the continued dosing in our single agent. So we’ll present updated data in both of those, not all three of those studies.

In terms of longer term follow up, we’ll continue to follow patients in the single agent study. We continue to follow patients in our proprietary combination study. In the combination was ibrutinib, that study was designed as an early response rate trial, not for long term follow up. So we only actually follow those patients for six months.

Part of the reason for that is that we could follow those patients for two years and the expectation is we’re not going to see a lot of progressions based on the ibrutinib data and so I'm not sure what we would learn by following those patients longer in that particular setting.

And there is obviously a great cost associated with following those patients for that long, but really very little expectation of change and variables to compare it to. So again for us that study was designed. We wanted the goal of that study and I think we’re already feeling pretty good about it.

One very simply -- one safety of the combination is when we’re talking about ibrutinib, I talked about three goals of the combination -- of our proprietary combination. I say the ibrutinib one really has two goals, because it wasn’t really signal finding. We knew that CLL [indiscernible] should be active. So that wasn’t, there was no challenge there.

So we only had two objectives there. One was make sure we can safely dose the two drugs together. It looks like that’s what we're seeing. Again we will have a lot more patients for safety evaluable and available for ASH.

And two, really our goal was to see if we can get very high response rates relatively early on in the process, within six months basically versus waiting up to two years for Ibrutinib responses and ideally again taking that response rate which is potentially 60% or 70% over two years, not only accelerating it to within the first six months but also driving it closer to 85%, 90%, 95%..

Thank you. Our final question today will be from the line of Jonathan Aschoff of Brean Capital. Please proceed with your question..

Congrats on the data and I just had a one, which was for the Diffuse Large-Cell, the GCB subtype.

What is the prevalence in incident [ph] to that?.

Yes, very good question. I don’t have it off the top of my head but it’s a -- it’s a very prevalent form of the disease. I can get you those statistics but it’s almost as common, if not more common than follicular..

Thank you. At this time I will turn the floor back over to Mr. Michael Weiss for 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 us and we plan to continue to aggressively push forward our clinical development programs and ongoing clinical trials with the goal of commencing one or more registration trials prior to year end.

Along the way, we plan to present updated data throughout the rest of the year. On behalf of all of us at TG Therapeutics, I’d like to thank all of our investigators, their patients and all of our shareholders and investors for their continued support. Thanks again for joining us and have a great day..

This concludes today’s teleconference. You may disconnect your lines at this time and we thank you for your participation..