Good day, ladies and gentlemen. And thank you for standing by. Welcome to the ZIOPHARM Oncology Incorporated Second Quarter 2016 Financial Results Conference Call. All this time all participants are in a listen-only mode. Later we will conduct a question-and-answer session and instructions will follow at that time. [Operator Instructions] I would now turn to introduce your host for today's presentation Dr. Laurence Cooper, Chief Executive Officer of ZIOPHARM. Sir, please begin.

Thank you very much and good afternoon and good day to everybody. Joining me today is Caesar Belbel, our Chief Operating Officer and Francois Lebel, our Chief Medical Officer. And if we could now all together just turn to slide two. Before we begin, let me remind you that during today's conference call we'll be making forward-looking statements to represent the company's intentions, expectations or belief concerning future events. These forward-looking statements are qualified by important factors set forth in today's press release and the company's filing with the SEC, which could actual results to differ materially from those in such forward-looking statements. Information discussed on today's call is accurate as of today and we do not intend to update. So with that disclosure out of the way. Let's get into the meeting of the presentation on slide three. This is ZIOPHARM's pipeline. It’s been really shown throughout the year and for the purposes of orientation I am going to give a brief overview and then we'll go through each program in depth. The top, in bold print is the Ad-RTS-IL12, these our words to describe AD for adenovirus. So this is an Adenovirus based product. The RTS is the RheoSwitch which is a set control systems that I will be explaining at length. And then IL12 is an important cytokine that in our estimation is the master regulator in terms of controlling in the immune response. This adenoviral genetically engineered virus has been now been deployed in two ongoing trials that we'll discuss in an update format in this presentation. And additionally I'll be giving some guidance to the listeners regarding our interest in a pediatric indication, as well as the first combination trial, in which we're combining this adenovirus with the checkpoint inhibitor. Turning from the viral program…

[Operator Instructions] Our first question or comment comes from the line of Keith Markey from Griffin Securities. Your line is open.

Good afternoon. I was just wondering if you could tell us what your impressions are about the Veledimex and the RheoSwitch for regulating the CAR expression, is the half life of Veledimex and the recurrent of the cells short enough?

Yes, sure. So I think these are – so Keith is important question, it really goes to that idea of how it is that the transcriptional on of weight of CAR expression we honor and hear the biology really –is really in development and we'll be working on that. So I think you know the issue I want to share with you is that its clearly working now, that you can turn on and off CAR expression and this essentially is really I think first in class biology that been out pressure tested in the human.

Thank you. And one other question, I was just wondering when you go into GBM trial with IL-12 will you be using overall survival as the endpoint even with the anti-PD-1 molecule is that’s the way you choose to go?

Yes, Keith, so absolutely. The primary endpoint that the FDA [ph] want to use for any brain tumor study is overall survival, obviously we would collect additional information and with the combination we clearly – there is going to be dose-escalation and we need to focus on toxicity of the combined regimen at different doses. So you know, dose-escalation initially identifying the correct dose, but all the way obviously we're attracting survival.

Okay. Thank you.

Thank you. Our next or comment comes from the line of Reni Benjamin from Raymond James. Your line is open.

Hi. Good afternoon, guys. Thanks for taking the questions. Maybe just starting off with the Adenovirus program, can you – finally it was a great presentation, really very thoughtful and so this is sort of – so these are just maybe some specific questions. But starting off with some of the preclinical work, can you tell us what the half life of eh IL-12 mRNA is and I guess where I am going with this is once you stop taking Veledimex how long does it take to the IL-12 protein expression to actually go down in the body?

Right, so in the brain tumor patients you know, we don’t have that opportunity to kind of give really example of the brain, so what we do have obviously is two important guide points. One is that sitting in Boston, Dr. Lebel can control the gene expression at patients in Los Angeles. And therefore we can advice the clinician and he or she will call us and say oh look, the patient has a fever, they are behaving this and that and we can guide that patient in real time, now the doctor in real time to dose adjust to Veledimex. And so one way to answer that question is its clinical, in other words, we follow these patients clinically and can make real time adjustments to what's going on. And the second of course is the biomarker which is the amount of IL-12 in circulation and I'll let Francois just comment on that.

Yes, the Veledimex half life is dose-dependent to some degree but its roughly 14 hours, so once we stop the Veledimex, it will get cleared and but clinically when we look at targeted side affects, depending on the nature of the side affect, but if you look at cytokine related side affects, they will abate within 24, 36 hours. So as long it’s indicated and we can track along that. The level of cytokine, so there is a direct correlation between the targeted side affect and the measure cytokine level at the periphery.

Got it. And when we talk about overall survival in this disease indication, I guess, I am curious to try to figure what other treatments for these patients getting, so for example, you mentioned that these patients do recur, do they undergo further surgical resection each time, have the patients been dosed further with injections of the Adenovirus and do you have any PSS results that might more directly give us a sense as to – as to what the therapeutic affect - immediate affect of the Adenoviral Vector might be?

Sure. So if you look at the slide seven, where we showing you the overall survival and you will notice the green [indiscernible] and that indicates the time at which by imaging, by MRI imaging, the tumor size is changing and at that point it can either reflect or represent for progression or sudo progression and its then important to understand at that point if our therapy worked your first image that it works which show that the tumor size could increase simply because you are eliciting an inflammatory response immune cells, NK cells, cytotoxic T cell, our in cell treating to tumor and we have evidence of that as well. So that tells you that. In terms of the – we know that it doesn’t necessary correlate with overall survival and the PSS that is and that is why the FDA, especially for immune therapy want to get the data in the primary endpoints on studies is overall survival because PSS does not correlate directly and the prime example is Avastin. So you're asking what other therapy are being used, so various calculating agents like CCNU, Temodar, so in other words the patient that has failed Temodar in first line could – you know patient later on could be given Temodar again. There is a paucity of agent to be used that have been shown to be effective and some have shown improvement in PSS, but none have really shown improvement in overall survival, especially after a patient has failed Temodar and Avastin.

Got it. And have these patients also gone through further receptions and have they've been dosed again with the Adenovirus agent?

We've not. In the animal data that we have suggest that one course is sufficient to activate the immune system and you will get the benefit as a result of that. And as the Lauren's had indicated, we've also now have data showing that in combination with the PD-1 inhibitor we can – we not only prolong survival, but we may actually be able to cure the disease. We've not done that in human yet, but certainly the data in animal is highly promising.

Got it. And just regarding that combination study with the PD-1 inhibitors, you mentioned you'd be hopefully starting that by the end of the year, can you let us know which PD-1 you are going to choose and is this something that make sense to be done in combination with a partner, to move forward with?

So we have not communicated which one it is. We know which one we want to use and we have discussed with potential partners going jointly in this efforts but discussion is ongoing.

Got it. Any update just sticking with Adenovirus, any update on the breast cancer program that’s ongoing or when we might see an update from that?

Yes, we will provide an update at ESMO, I believe in October in Copenhagen and we will be able to show you the clinical results, as well expanding on what we seen and presented at ASCO recently, as well as provide you various biomarkers.

Okay. Just switching gears to the CAR program real quick, I guess, one question is, should we be thinking about the sleeping beauty system now, given your presentation as primarily the go to system for the TCR franchise and tackling the solid tumors and the lengthy the viral system for more the homological malignancies?

Yes, that’s an excellent question and that’s where my brain is too. I mean, the company clearly has a valuable asset and that we have the gating technology to go after solid tumors now for the purposes of targeting new antigen. So the other way to say that is, you know, you can't use Adenovirus at situation. So the only way for it is a non-viral approach if you are interested in targeting T-Cells that are going after new antigens. So that’s a truth. The question is what's the better message regarding [indiscernible] and there I think we are in echo point in the company. We're going to look and see at our data from Adenovirus and we're going to continue to make process improvements in the CBD system, particularly its not the question – its really around efficacy, it works, the question is can I build a system which is one in which for instance limits the amount of time, I have to spend money in the DNT facility that allows me to build a program where I can treat many, many patients, but I don’t have essentially as to lag time of having to just make viral base sector. And that’s essentially within my field of view right now. So as I think about the CAR program, I am very interested about building the sleeping beauty to really be essentially disruptive to really if I can really do something special beyond essentially making CD19 CAR therapy.

Got it. And when will the real RheoSwitch control the CAR cells be in the clinic and I guess when I think about the switch, it seems to me that you would either want this switch on or off and that this might be a case where you definitely really don’t need a real or so dial it back sort of activity, I am thinking about that right or…

Yes, no, I mean, so exactly, I am just giving you one embodiments right now with the CAR and the control of RheoSwitch. But obviously I have a clinical program that’s controlling cytokine under a RheoSwitch, but you know, that just happens to be an Adenovirus. So I think you know, without giving away too much of our treasure, I think its reasonable to conjecture that we will start looking not only at CARs under RheoSwitch, but other types of biology under the RheoSwitch. Ones that maybe for instance quite useful for not just one, off, but on Rheostat off and so forth and so on. So the CAR is really just the tip of the iceberg.

Got it. And just one final question from me, on the NK platform, can you maybe just help us understand how this is different than let's say NaN Quest [ph] platform or you know, Jeff Miller's work at the university of – I think its Minnesota where he has NK cells in the clinic as well?

Yes, so let's do the bulk, so NaN Quest obviously delighted that they are in the field, but they have really put themselves firmly behind using a tumor cell line, NK 92 cells, which is an immortalized NK cell. And my read of – in that space is one of which there is a challenge and that challenge is that because if you've had to eradiate I think for the most path in cells they may have limited life span after their infusion. And therefore we have developed an alternative, and that alternative is using primary NK cells and these primary NK cells have full replicative capacity. They are not – they haven’t been irradiated, they are ready to propagate, they are ready to divide, just like CAR therapies divide in the human. So that’s a major difference between us for instance and our competitors who are using an immortalized product. And then your question to Jeff, who is superb, and I know I am well, University of Minnesota, he has developed an elegant approach where really don’t need any propethane [ph] you have a isle to activation set and then you put these cells on a magnet and you strip out all of the T-cells and you had a product that’s enriched for NK cells and you essentially then try and put in these NK cells for the purposes of therapy in the AML space. That is a potential solution, but in our estimation difficult to commercialize because it really is patient derived product, it requires some specialized bio processing, I am much more of mind guy about what I can do with primary NK cells just like Jeff, but one in which I can handle a campaign and make these NK cells in advanced that a patients need, so they are infused on demand, in other ways, the patients gets the NK cells when they are needed not necessarily when they are available such as using if you would the Miller approach.

Got it. Thank you very much for answer the questions and good luck going forward.

Sure. Thank you so much. Thank you.

Thank you. Showing no additional questions in the queue, I would like to the conference back over to Dr. Laurence Cooper for any closing remarks.

Okay, I just want to give everybody and thank you for listening and we wish everybody a good day and evening. Bye-bye now.