Good day ladies and gentlemen and welcome to the November 12 Conference Call. [Operator Instructions] As a reminder this conference call may be recorded. I would now like to turn the conference over to David Connolly, Vice President of Corporate Communications and Investor Relations at ZIOPHARM Oncology. You may begin.

Thank you. On November 9, we filed our 10-Q for the third quarter of 2018. And this morning we announced a private placement and a new collaboration with Regeneron. The From 10-Q and both of these press releases are available on our website. During today's call, representatives of the company will make a number of statements that are forward-looking, including statements regarding the potential of therapeutic candidates in our development pipeline. Forward-looking statements are subject to numerous risks and uncertainties, many of which are beyond our control, including the risks and uncertainties described in our SEC filings. On today's call are Dr. Laurence Cooper, CEO and Director of Ziopharm Oncology; and Dr. David Mauney, Executive Vice President, Chief Business Officer, Interim Chief Operating Officer. And we’ll take questions at the end of the call. Dr. Cooper?

Thank you all for joining us today. We’re about one month into the new ZIOPHARM and during this short time we have already secured financing, formed a new collaboration with Regeneron, and have an ongoing dialogue surrounding a business development initiative, which is now in advanced stages. We last spoke with investors on October 9. On the heels of the announcement that as of October 5, 2018, we dissolved the original collaboration known as the Exclusive Channel Collaboration or ECC with Intrexon and replaced it with a new licensing agreement. As of early October, Ziopharm is a different company. And with the support of our new Board, we can now move forward, unencumbered operationally and clinically. The financing is expected to close on November 13. As it closes, we have much to look forward to with capital for some of our largest, most supportive and deep pocketed investors to execute our clinical development and corporate development plans. Our patients and investors will be rewarded as we are solving today's big issues facing immuno-oncology, namely we are attacking cancer with the patients’ own immune system using cost effective, safe and scalable technologies, and increasingly aligning these treatments for solid tumors. We believe we have two best-in-class therapeutic platforms with the controlled IL-12 gene therapy based on our tunable switch and non-viral Sleeping Beauty gene transfer to produce TCRT and CAR-T therapies. As we promised, 2018 is a transformational year for ZIOPHARM. A lot has transpired in the few weeks since we last held a conference call and we will focus on those updates. With that I'll turn the call over to David for additional details.

Thank you, Lawrence and thanks everybody for being on the call today. We're obviously very excited. Looking backwards, I joined Ziopharm just over a year ago. I consider this a tremendous opportunity for me personally and as a scientific platform was then and is today rock solid, it's frankly getting better every day. To capitalize on this opportunity though, we had to become an independent company. Prior to our announcements last month, we were faced with many issues. We had a number of encumbrances that held us back as a result of the original ECC agreement with Intrexon. For example, we were inefficient in our drug development activities in large part due to joint governance and shared decision making and development responsibilities. The intellectual property provisions in the contract restricted the production, protection and continued use of IP developed by Ziopharm. The ECC’s sub-licensing provisions and the potential for de factor veto rights showed the interest and the ability for Ziopharm to attract and execute sub-licensing arrangements. And our balance sheet and financing viability was severely limited by the preferred stock being issued to Intrexon. Finally there were times, at times misalignment between the companies that absolutely needed to be resolved. We knew we had to create a new way of doing business and we knew the preferred stock had to go away. But we did not stop there. In fact, we succeeded across the Board and then some – and we did so on great terms. ZIOPHARM management and our Board initiated and drove a vigorous process throughout the entire course of 2018, that took us the better part of this year because we were unrelenting in our believes and our desires and we did not stop until we got the deal that we wanted and deserved. If it…

Thank you, David. We greatly appreciate all your efforts. It is indeed a bright new day. Since we recently updated the investment community, I'm going to be fairly brief regarding our clinical programs. Controlled IL-12 with the RheoSwitch to regulate IL-12 production is being evaluated in adult and pediatric brain tumor trials as a monotherapy and is currently being tested in combination with PD-1 inhibitors for patients with recurrent glioblastoma. Enrollment in our expanded monotherapy trial is progressing. This trial seeks to increase the number of adults with recurrent GBM, who receive what we believe to be the ideal dose of veledimex, which is 20 milligrams. And we have already dosed 12 new patients on our way to 25 in this trial. We expect this study to complete enrollments in the first quarter of next year. Previously, we have shown a median overall survival of 12.7 months at a mean follow-up at 12.9 months, which favorably compares to historical controls. Indeed, as a reminder, these controls show us the patients with recurrent glioblastoma live on average only five to eight months after recurrence despite all available therapies. Our data further reveals that patient on low dose steroids may have an additional benefit in terms of overall survival. And we're testing this in the expansion cohort. We know IL-12 makes cold tumors hot, specifically the brain tumor biopsies before an IL-12 – before and after IL-12. Demonstration of this cytokine recruits CD8 expressing T cells. These killer T cells are likely the reason patients with recurrent GBM appear to be living longer after IL-12 as monotherapy. We've also seen that these invading T cells increased PD-1 checkpoint expression within the tumor. This helps convince us that combining with an immune checkpoint inhibitor against PD1 will further improve the antitumor effect we…

Thank you. [Operator Instructions] Our first question comes from the line of Reni Benjamin of Raymond James. Your line is now open.

Hey, good morning guys. Thanks for taking the questions and congratulations on the continued transformation and investments. I guess I have a couple of questions. Maybe starting off of with maybe at a 10,000-foot view question, there are a lot of learnings that have been coming out over the last month between ESMO and just this weekend at SITC, really trying to hone in on the issues that's impacting the cell therapy space and especially in solid tumors. So while watching the hurdles that the first movers hit, obviously fast followers can, utilize those learnings and really try to navigate around them. So can you talk maybe a little bit about what you were seeing? Persistence is one of the big issues that hits me. But what are you seeing and how do you think the platform might be able to overcome these issues?

Yes it’s a great question. So the first is that it's necessary to be able to deliver a product, right? Many folks are interested in targeting solid tumors, whether that be through a vaccine approach, which we could get into. Or importantly, I think, most significantly by administering T cells. So unless you are a company that could administer T cells, you can't address any of the other downstream questions that you're getting into in terms of solid tumors. So Ziopharm has that key to unlock the door. We have the technology where we can make patient-by-patient TCR-modified T cells to get to solid tumors. And that's going to be, I think, the first gating principle. The rest is noise. Unless you can make the T cells on a cost-effective patient-by-patient basis, you can't even address the second question. Then the second question is though are essentially de-risked for us, because we are using the technology at the NCI, which has already been shown to work. Let's not forget that there are major papers, whether they be in science, New England Journal of Medicine, and so on that show that the manufacturing process of the NCI to generate the T cells, in other words, the TIL the tumor-infiltrating lymphocytes that are grown up and are infused, those result in dramatic anti tumor effects for patients with solid tumors. The issue is that it doesn't work all the time because they are not using genetically and modified cells they are using T cells from the tumor that had been essentially exhausted in many cases. The Sleeping Beauty system is the link to take those T cell receptors, which we know have worked in the past to have using that programming or using that technology at the NCI and then insert them into these fresh, younger T sells. So for Ziopharm we're in great shape. We have the gating technology to be able to go after it. And we have the essentially the manufacturing solution through the NCI, which has already been proven to work.

Yes, this is David. I would also add that for the headwinds we're seeing in the CAR space, where you're going after a single CAR target, it all comes down to commercial viability. And we're already seeing the headwinds for commercial viability even with decent science. We expect those headwinds to be magnified when we think about multiple TCRs on an individualized patient basis. And so whether you're in bioinformatics or sequencing or anything else, if you can't deliver a commercially viable product, you're stuck. And we think we enable that capability.

So just to expand on, on one comment that Lawrence had made regarding those fresh cells, can you just remind us what were the cells that you will be transitioning using the Sleeping Beauty are coming from?

Yes, it's from the peripheral blood. So in the mind's eye then technology is based on taking these neoantigen-specific TCRs, in other words that the TCRs that recognize the fundamental genetic lesion that given rise to the cancer. Those TCRs are then taken and put into the Sleeping Bed cassette system, which is really like lego blocks you can just insert one TCR after another into the plasmid backbone. And then the Sleeping Beauty system is used to insert the TCRs into fresh T-cells that are swimming in the circulation in the peripheral blood.

Got it. Okay. And can you just remind me, have we ever seen clinical data from clinical data from cells that have utilized the Sleeping Beauty system? I thought that the original CD19 program was suppose to provide that bridging data, but maybe just remembering incorrectly.

Sure, so we have several updates. So one is that we have a paper out in JCI, that talks about the survival of patients who received, Sleeping Beauty-modified T cells expressing CAR, targeting CD19, then we updated at ASH showing essentially, I think, it was something up to four years of survival and up to four-year persistence of those CAR-modified T cells in subsets of patients, then we updated on the second generation Sleeping Beauty trial. And we had a press release out showing, for instance patient entering into a complete remission, the PET imaging, I think, we showed that point, showed the tumor going away, and so forth. So the Sleeping Beauty has a lot of clinical rhythm to it. There's additional work ongoing at M.D. Anderson, where we are essentially preparing for this very rapid manufacturing solution, shortening, the time essentially between vein to vein. That trial has a number of updates that we will give over the coming months to year associated with that clinical data. And then last of course, is that the NCI is rapidly using the Sleeping Beauty system and there in essentially their ramp-up phase for submitting the IND there.

Got it. And then just one final question from me, one of the programs that I don't see in your pipeline that I thought you guys had involved CAR NK cells. And so we got some interesting data from SITC, showing some pretty profound responses in indications like AML. And so I just – am I remembering wrong that you had a CAR NK program is that kind of gone away?

Yes it’s a good memory. So we had an NK cell program that we thought about for awhile, in terms of it being used in certain clinical scenarios, like for instance, off the shelf therapy. That program still exists for us. We can execute on that. We have a relationship with Precigen to move on that. But at the moment it's not part of our core set. We are essentially aligned behind what really is, I think, the very large opportunity in solid tumors. And CAR, in our mind, whether it's on an NK cell or T cell, is not going to get you into the solid tumor space. There's no target that the CAR target for solid tumors.

Got it, thanks very much and congratulations on the progress.

Thank you.

Thank you. Our next question comes from the line of Eric Joseph with JPMorgan. Your line is now open.

Hey guys, thanks for taking the question and congrats on the updates. I have a couple of – pipeline questions for me. First on the IL-12 program in GBM, I'm just looking for a little bit more color on the cemiplimab supply agreement and sort of what the particular rationale is to collaborate with Regeneron, given that you already have a Phase 1 on going with nivolumab? Is there something particular about their PD1 versus nivolumab, that’s particularly attractive or something in terms of resources that Regeneron is bringing to the clinic – bringing to you in terms of clinical development? And then I guess wondering if there are any additional economics beyond this supply that are tied to the IL-12 program? And then I have a follow-up.

Yes thank you for that. So were anxious to start a combination trial and nivo because that was approved. And that got us going. And a lot of learning is ongoing in that trial. That learning has guided us now to essentially go from a Phase 1 to a Phase 2 trial. And as we position that we discovered to our delight that Regeneron cemiplimab, their PD1 inhibitor was also going to be approved. So we transitioned the program from that Phase 1 to that Phase 2 trial with cemiplimab, with a supply agreement with Regeneron because essentially, we have alignment with them on targeting a recurrent GBM. They like us see recurrent GBM as a major opportunity. And I think that's a really a lot of the driver that got us excited about working with them.

I think also – this is David, I think, one of the interesting things about a company like Regeneron and with a new market, new player in the checkpoint inhibitor markets, they're very aggressively looking for new advantages, new opportunities. And so as a company with that mindset it puts us in a position to be excited to have multiple shots on goal. As far as your question on additional economics we can't give any guidance on that at this point.

Okay. And just on the TCRT program, I'm wondering whether the 70% cell viability threshold similarly applies to the TCRTs the way it has for the CAR-T point-of-care program? And if so, has that been demonstrated?

Yes, that's a great question. So yes, so really across the Board the FDA is asking for 70% viability. I mean you saw for instance, Novartis come out with a statement around the viability of their T cells that have been made using their viral approach. So in the CAR-T program, the goal is to essentially electroplate [ph] the cells into the Sleeping Beauty plasmas and then immediately infuse them. So there’s no possibility to grow out if you would healthy T cells. And so that puts stress on the system that we’re solving to essentially generate a process, the less than two-day process in which the cells come out of the technology 70% or greater viability, the NCI process with the TCR in bold propagating the cell after the gene modification. So you have time to essentially grow out the living cells, the viable cells. And I would add that's the same that's ongoing in our second generation CAR-T trial at M.D. Anderson. That trial for instance, regularly splits out cells that a greater than 70% percent viable. The viability is not an issue there. And similarly at the NCI, when you propagate the cells, the viability is not going to be an issue. It's really confined to this very rapid, less than two-day manufacturing. And essentially we're at the very limits essentially of next generation technology and that's part of the puzzle is cracking, is it providing a solution to crack that problem.

Got it. That's helpful. And did I hear correctly that you – that NCI expects to be in a clinic in mid-2019?

Correct.

That sounds like a bit of a delay, I guess from prior guidance of being in a clinic this quarter or…

No. No, it's essentially – we actually are tightening up the guidance. We said that in our guidance that it will be 2019 clinical program and we're actually narrowing it down and saying it's going to be mid-2019.

Got it.

For three patients.

Got it. Thanks for the clarification.

Sure.

Thanks for taking the questions.

Thank you. Great.

Thank you. I'm showing no further questions at this time. I like to handle it back over to Dr. Cooper for any closing remarks.

Great, thanks everyone. Look this is a really exciting time for us. We have the money, we have the technologies, we have the people, we have the Board to deliver on expectations and we are just delighted to come to work every day on behalf of shareholders and our patients. So thanks everyone.

Ladies and gentlemen, thank you for participating in today's conference. That does conclude today's program. You may all disconnect. Everyone have a great day.