Greetings. And welcome to the Inovio Pharmaceuticals Incorporated Third Quarter 2017 Financial Results Conference Call. At this time, all participants are in a listen-only-mode. A question-and-answer session will follow the formal presentation. [Operator Instructions] As a reminder, this conference is being recorded. I would now like to turn the conference over to your host, Mr. Jeff Richardson. Thank you, Mr. Richardson. You may now begin.

Good afternoon. Today’s call may contain certain forward-looking statements relating to our business, including our plans to develop DNA immunotherapies and electroporation-based delivery technologies, products and product candidates, as well as our capital resources, all of which involve certain assumptions, risks and uncertainties that are beyond our control, and could cause actual results to differ materially from these statements. A description of these risks can be found in our latest SEC disclosure documents and recent press releases. These statements speak only as of today’s date and we undertake no duty to update or revise them. Presenting for you today are Dr. J. Joseph Kim, Inovio’s President and CEO; and Peter Kies, our Chief Financial Officer. Now, Dr. Kim.

Thank you, Jeff. Good afternoon, everyone. Before talking about our operations and financial results, I want to remind you of the path we’re travelling and the milestones we have passed, because I think that underscores the reason why we’re so confident about achieving our goals. What are these goals? My vision for Inovio is to become the leader in the following three critical areas. First, we will be the company that transformed the treatment of HPV-associated disease with the first immunotherapy to treat both pre-cancer and cancer caused by this common infection. Second, in the field the immuno-oncology, our T cell activating immunotherapies will be considered the go-to combination therapy with checkpoint inhibitors. Third, through public private alliances, Inovio will become the leader in rapid vaccine development to combat emerging infectious diseases and biodefense threat. I’ll take each one of these goals briefly and show you how far along the path we are in achieving our objective. First, Inovio will be recognized as a leader in HPV-caused disease. Overall, Inovio is well-position to comprehensively treat HPV-associated diseases across the continuum of HPV infections from pre-cancerous conditions through to cancer in both women and men with VGX-3100, already the most advanced product for treating these diseases. In June of this year, Inovio commenced the Phase 3 clinical program to evaluate the efficacy of VGX-3100 to treat cervical dysplasia caused by HPV. The pivotal data from this program will support the licensure application of VGX-3100. And I’m proud to point out, this product will be the first immunotherapy and the first non-surgical therapy for this disease. In a little over three months since Phase 3 initiation, Inovio has already opened nearly 35 U.S. sites and now initiated several sites internationally, all recruiting and ready to dose patients. By the end of the…

Thanks, Joseph. Total revenue was $2.6 million for the three months ended September 30, 2017 compared to $12.5 million for the same period in 2016. Operating expenses were $31.8 million for the current year quarter compared to $32.7 million for the prior year quarter. The net loss attributed to common stockholders for the quarter ended September 30, 2017 was $34.1 million or $0.39 per share compared to $20.8 million or $0.28 per share for the quarter ended September 30, 2016. The increase in net loss for the quarter resulted primarily from lower revenue recognized from our DARPA Ebola grant and a higher non-cash accounting expense related to the change in the fair value of the investment in our affiliated entity. The decrease in revenue was primarily due to nearing of successful completion of our DARPA Ebola grant. Research and development expenses for the third quarter of 2017 were $25.5 million compared to $27 million for the third quarter of 2016. The decrease in R&D expenses was primarily related to less expenses incurred related to our DARPA Ebola program. General and administrative expenses were $6.3 million for the third quarter of 2017 versus $5.8 million for the third quarter of 2016, a slight increase from our increase in headcount. On July 25th of this year, we closed an underwritten public offering of 12.5 million shares of our common stock, raising $75 million. Looking at the big picture, this raise nearly doubles Inovio’s cash position. It will strongly support advancement of our Phase 3 trial and four Phase 2 immuno-oncology trials and other pipeline advancements. And the financing brought in new investors -- new institutional investors into the stock. We also amended our partnership with the ApolloBio such that Inovio would receive $15 million in upfront payment and $35 million in equity investment with a share price of $7.22, in return for ApolloBio attaining a license and commercial rights to VGX-3100 in the Greater China region. The agreement will become affect of upon approval by ApolloBio shareholders and the Chinese government, which could occur by year-end. Finally, our financial position remains very solid with total cash and cash equivalents and short-term investments of $141.9 million as of September 30, 2017. At quarter end, the Company had 90.3 million shares outstanding and 99.7 million shares outstanding on a fully diluted basis. Joseph, back to you.

Thank you, Peter. Let me close with this message. There are two attributes I want you to remember when you think of Inovio. First, relentless innovation; and second, executional excellence. Inovio is innovation, advancing a broad pipeline of activation in immunotherapies and vaccines for people in need. And we continue to innovate with new immunotherapies and DNA-based monoclonal antibodies, targeting new disease areas in new ways. Inovio is also executional excellence, that is we do what we say we’re going to do and we do it with efficiency, speed and quality, and we hold a recent track record to prove it. We started a pivotal Phase 3 and four Phase 2 trials for important pre-cancers and cancers. We forged cancer immunotherapy partnerships and collaboration with top-tier pharma companies like MedImmune, Genentech and Regeneron, and we supported global public health advancing clinical vaccine initiatives in HIV, Ebola and Zika, all advanced with third-party funding with demonstrated consistent 90% to 100% response rate across all studies. For a company that really began with a 2009 merger, I’m proud of our accomplishments, which gives me great confidence in our meeting our three major goals. We always remember that patients are waiting. Thank you for your attention. I’m pleased to address your questions and comments.

Thank you. At this time, we will be conducting a question-and-answer session. [Operator Instructions] Our first question comes from the line of Charles Duncan of Piper Jaffray. Please proceed with your question.

Hi, guys. Congrats on the progress in the quarter and thanks for taking my questions.

Thank you, Charles.

Joseph, let me ask you about the cervical dysplasia trial or the REVEAL program, I guess, there are two trials. Do you have any operational goals in terms of that which you’d like to share for with us? And then, in terms of the visibility we may have on that trial over the course of say the next 18 months for 2018, let’s call it…

Yes, absolutely. So, as you know, each of our REVEAL trials enroll 198 patients across the globe. About approximately half or slightly less than that will from the United States, the rest will come from Europe, Asia and even a site in South Africa. So, we’re very excited to get this launched. And as you know, we got held up a bit with the device related hold. But we were able to overcome that. So, our team, our highly dedicated and efficient team members are dedicated to keep our heads down, get the sites open. As I mentioned, over almost 50 sites in six different countries, those sites will be opened and operating to recruit patients are rapidly as possible. And that will continue on, we will add additional sites in 2018 as well. So, really, it’s all about executing the site openings and utilizing those sites to recruit the patients. So, REVEAL 1, just to talk about, the timeline is the last patient and plus nine months on drug plus 12 months follow-up. So, it’s a total of 88-week study. REVEAL 2 in contrast is nine months on drug and with the one month follow-up; so, it’s a total of 40-week study. So, we’re still targeting enrolling all almost 400 patients across the two trials, landing the un-blinded data in 2020 from both REVEAL 1 and REVEAL 2. And there is nothing that I see that we cannot achieve those objectives. So, we’re very excited about the progress we’re making. And you know and I know, we were just time to go from our clinical hold. So, we have a team that’s truly dedicated and executing with excellence, as I mentioned in the enrolling of these patients.

And I know that IRB, Institutional Review Boards are proving to be more challenging than in the past for a whole host of companies. But, your excitement over the progress is related to perhaps a few sites being open and maybe even available for enrolling patients. Would you anticipate being able to give some incremental updates over the course for next 12 months on site initiations and patient enrollment?

Yes, we -- thank you. First part of what you said, IRBs in our experience have not been the limiting stuff for Inovio. Our products have -- fortunately have extremely strong record of safety across our platform programs. We’ve dosed to-date 1,500 patients across all of pipeline products over 5,000 different administration with stellar safety records. So, we haven’t had any, knock on wood, IRB issues, just both in the United States and overseas. So, we will continue to execute. And really, I don’t want us to give a, like a play-by-play of the enrollments rates. Rather, I like us to provide the guidance on how we’re tracking compared to what I said. And our goal is to have the un-blinded including safety data of the results from REVEAL 1 and 2 by 2020.

Okay. That’s fair. I appreciate the added color. And then, as you look at 2018 and 2019, what is your -- what’s the thing that you’re looking forward to, in terms of turning over card or whatever that could further enhance your conviction in the technology and growth prospects for Inovio?

Yes. We’re going to continue to add new trial data. We have couple of very exciting posters and at CEPI this weekend, both our hTERT vaccine, INO-1400 as well as MEDI0457 updates from our Phase 1 with some signal of efficacy. So, we’re very excited about additional data that will be coming out from all of our oncology infectious disease program. And staying on infectious disease, we expect to have additional or data from our hepatitis B immunotherapy, INO-1800 in the first quarter -- first half of 2018, along with additional Zika vaccine data from our Puerto Rica trial that’s got the signal of clinical efficacy built in to a typical immune response and safety vaccine study with 160 persons participating in Puerto Rico that we’ll report in 2018, among other things. And we always like to have some positive surprises. So, we expect data and other business development progress in the coming year. Now, I also just -- since I’ve mentioned Puerto Rico trial, you may be wondering because of the hurricane and so on. So, we were able to dose all 160 participants prior to the hurricane devastation. And there is a one year follow-up. So we’re in that one year follow-up stage from this summer on. So, I’m pleased to say we expect minimal impact to our Puerto Rican Zika vaccine trial. I mean that’s not to say that we may find additional impact as we go. But so far the sites are up and running. So, we are very encouraged by that.

Very good. Well, I appreciate you taking my questions. And I’ll hop back in the queue.

Thanks you, Charles.

Our next question comes from the line of Joel Beatty of Citi. Please proceed with your question.

Hi, guys. This is Sean [ph] calling in for Joel. Thank you so much for taking our questions today. My first question…

Yes. Hi, Sean.

How are you? My first question is with the goal of your primary corporate goal of kind of becoming the go-to HPV pre-cancer therapy. Is the goal to kind of receive a broad HPV label there? And if so, what signals do you think are most important to get you there from your REVEAL and vulvar and anal neoplasia studies?

So, thank you for the question. We’re going to block and tackle each indication one at a time because of the differential in timing. Obviously, we’re going to get to send cervical data first from REVEAL 1 and 2. Our primary endpoint for our REVEAL 1 and 2 are similar to our VIN Phase 2 endpoint, and will be similar to our AIN study that we’ll launch in early 2018. These are both the histologic trends of the lesions. So, the actual clearance of the lesion or the regression, and the clearance of the virus HPV in the tissue which caused the problem in the first place. So, that’s the primary endpoint for our cervical dysplasia study as well as our VIN study. So, really, I think based on our VIN Phase 2b data, we believe we will be able to demonstrate tremendous impact on both the lesion regression and the clearance of the virus. Because ultimately, if you can clear the virus, you can remain -- you can provide long-lasting therapeutic impact to these patients. And that’s what we’re going for.

Great, that’s very helpful. And I just have two quick questions on your hTERT program coming up the heels of CEPI abstract. First one was, hTERT kind of being a very common and ubiquitous tumor antigen, can you comment on what path forward could look like in that AIN neo adjuvant setting there?

Yes. So, the current Phase 1 study was actually enabling study looking at nine different solid tumors with our hTERT antigen therapy alone. But now, based on our early promising data, we’ve placed hTERT antigen as the anchor antigen for INO-5401 along with PSMA and WT1. So, we’re not planning to develop hTERT as a monotherapy. Rather, we have added two other brother antigens that can provide in a similar way a pan, a very broad universal cancer treatment using these three pan cancer antigens hTERT, PSMA and WT1. So, in our poster, we’re showing safety, because these are cancer antigens, we want to see that we can deliver this in a safe way, answer is yes. And we will -- we are showing some immune responses to hTERT in the early look at these patients, so quite excited about the progress. To stay on the topic, we’ve already shown that anti-PSMA immune responses in our prostate cancer study. So, we know the PSMA and hTERT are generating specific T cell responses in cancer patients. And we have pretty good indication from preclinical data that WT1 is also an excellent generator of T cell. So, why am I so excited about INO-5401 is that we have a pan -- potentially “pan cancer” immunotherapy that can generate specific CD8 positive T cell and we’re going to hit -- we’re going to combine -- we are combining with Genentech TECENTRIQ, PD-L1 for bladder cancer and Regeneron’s REGN2810, recently declare breakthrough therapy for -- as a PD-1 inhibitor for our glioblastoma trial. So, we have two shots on goal there, with 5401, very excited about that. Our third shot on goal for PD-1 combination is with MEDI0457. And we’re going to show some exciting data at CEPI in the poster session, . So, please stay tuned.

Our next question comes from the line of Matthew Eckler of RBC Capital Markets. Please state with your question.

So, Joseph, just to kind of follow up a little bit on the upcoming CEPI data. I know, we’ll see a poster presentation on MEDI plus nivolumab in the single head and neck cancer patient who has given the two drug sequentially. So, I guess thinking a little bit about, one, what data we might see, as well as any read through to the logic and potential outcomes from the ongoing combo study being run by MedImmune, maybe if we could just start there?

Yes. So, it looks you’ve read the abstract. So, thank you for pointing that out. This is a very exciting data. Because we know we had 22-patient Phase 1 study with MEDI0457. It’s a monotherapy trial. We were able to generate very -- in significant percentage of these patients very strong T cell immune responses measured, both in the blood and T cell infiltrating in the tumor issues in the head and neck in some of these patients. So, we’ve shown that data. What’s exciting about this is, one of the patients who had modest level of T cell immune responses started to progress at month 11. And so, this person -- this patient was subsequently taken out of our trial. And then, the oncologist provided PD-1, nivolumab in this case, inhibitor. And just within four doses, the patient completely -- had a complete response, and the patient remains through 16 months disease-free of the cancer. So, now, you have to tamper this with this being just in one. But it’s only one person that subsequently had checkpoint therapy, post dosing with MEDI0457. So, what does this mean for MEDI0457 plus [ph] study, the PD-L1 inhibitor from MedImmune. Very excited, I think it’s a metastatic head and neck cancer patient setting, 50 total patients. So, it’s not a small study. ORR typically in this level is less than -- significantly less than 20% with checkpoint alone. So, our goal is to see ORR of higher percentage than that. And we’re very optimistic, we’re very bullish on this because we know we can generate anti-HPV anti-tumor T cells from our Phase 1 study. And what is doubly exciting here is we’re dosing PD-L1 inhibitor at the same time as the dosing of MEDI0457. So, it’s a true one-two punch and we can’t be any more excited about any study because of the potential of what we found in the earlier Phase 1 study results that is being presented at CEPI.

Okay, great. Thanks very helpful there. And then, maybe shifting gears a little bit thinking about the VGX-3100 studies in vulvar and anal. So, based on the timelines you’ve discussed, we’ll very likely see that data ahead of the Phase 3 CIN readout. So, maybe just talk a little bit about what you see as the threshold for go no-go decision in terms of moving either of those indications forward?

It’s an open label study and unlike cervix, vulvar and anal areas [ph] are more determinable throughout the study period. And there are very little spontaneous regressions. So, the placebo was not needed. And we don’t want to give what the threshold is, because it’s a highly unmet medical need indications where surgery is the only option and god, those surgeries have tremendously negative impact to these patients and they recur. Even after a successful surgery, over 50% of these patients recur. So, they have to undergo another painful surgery and sometimes in the same year, and those recurrence is devastating. And what we want to do is to not only treat the lesions, which is a great goal, but also clear the virus that caused it. And we we’re heartened by the fact that we saw that in our cervical dysplasia Phase 2 studies. And we’ll look forward to showing that in our REVEAL 1 and 2 study. So, what do we expect, we expect to see similar results with some tampering because it’s first time we’re going to vulvar tissues and it’s first time we’re going to anal tissues. And all tissues are not the same, not all organs are the same. But we think we have immunotherapy that leverages the CD8 killer T cells targeted against HPV antigens are present in all of these lesions. I like our chances.

And is REVEAL 2 still on track to initiate by year-end?

Actually, because of the timing and so on, and I just alluded to the FDA agreed in having the follow-up period, the safety follow-up period for REVEAL 2 to be limited to one month after the efficacy readout, unlike the REVEAL 1. That gives us a little lower leverage. So, we probably will start later than that. But, our goal is to end and land two planes at the same time. Two planes are taking off at a different time and we know we need to enroll a total of 400 patients. So, it really doesn’t matter what sequence we do. Although, because REVEAL 1 has 11 months longer follow-up time, it behooves us to start that first. So that’s why we’re focusing on first. But, we are still on track with our timeline that I gave, previously.

Our next question comes from the line of Yi Chen of H.C. Wainwright. Please proceed with your question.

Regarding the three collaboration therapies in immunotherapy space, could you give us some idea when we can likely see some updates or data readout for those three trials?

So, do you mean immuno-oncology study, the combo study?

Yes.

Yes. So, I mean, I have to speak less on MEDI-run studies, because they control it; we’re just a passenger in that trial; they’re the drivers. But, INO-5401 studies, we’re the driver. And these are open-label and we’ll be tracking the progress. So, I think I estimate it by 2019 will be significant amount of data. We might see early indications in 2018. We have our fingers crossed, but that’s only by 2019, we hope to have significant elucidated efficacy results. So, we’re -- we want to -- these are very exciting data -- studies, and we definitely want to get to efficacy readout as rapidly as possible. And they are powered and they’re sized to be significant. So, bladder is 80 patients, 60 of them are going to be enrolled from the PD-1 refractory patient population with very little other treatment options ahead of them. So, we hope to recruit these patients very quickly. And glioblastoma, the newly diagnosed glioblastoma, again very dire prognosis going forward; it’s the same indication that Senator John McCain has been diagnosed with this year, and we also want to know those patients and provide some avenues potentially with 5401.

Assuming the results from these two trials, with 5401 are positive, is Inovio considering a further development for those two indications by yourself or you have other strategies planned for these two indications?

It’s either or both have moderate level of efficacy above what’s been seen. I think you’ll have to beat the potential partners away with this. In other words, PD-1 alone -- or PD-L1 are in less than mid-single digit in ORR, maybe even less than that. Most companies don’t even quote what their efficacy levels are for GBM. That’s a high bar or low bar in terms of showing efficacy to move forward into pivotal and licensure. So, we should be that lucky and we hope to be there in the near term. And then, bladder, one of the most immune responsive tumor, but still over 80% of the checkpoint therapies, these patients are refractory. So, we’re drawing from a large population. And if we can turn their PD-1, PD-L1 non-responsive status to responsive status even in a moderate level of percentages, we think that’s a homerun. So, in those cases, I think we would have a plenty of potential partners including the ones that we’re collaborating with currently along with others who are just watching enviously I think with this progress from these studies. And not to mention what we expect exciting data from MEDI0457. Obviously that’s already spoken for to MedImmune. But I think there will be a great indicator of what’s to come.

Got it. Thank you.

Our next question comes from the line of Jason McCarthy of Maxim Group. Please proceed with your question..

Hi. My name is Joanne and I’m calling for Jason McCarthy. The first question he had was if you could walk us through the glioblastoma trial design, in particular, the enrollment criteria for the patients. Will patients be stratified based on MGMT status? And in addition, since the checkpoint will be used in the study, will you have a biomarker data from the patients receptive tumor profiling, the level of PD-L1 expression?

Last question first. We’re going to look at those biomarkers and PD-L1 and so on. And the first question, yes, we will enroll both MGMT positive as well as negative or unknown, and they’ll be stratified, so total of 50 patients. And post surgery and radiation along with temozolomide. So, really these GBM patients are going to be treated with standard therapy, which still -- and we’ll be dosing them with 5401 and Regeneron’s PD-1 inhibitor, post that. And typically, they have pretty low, 15 months median survival, with five-year survival rate of less than 3%. So, we’re hoping to see the change in overall survival, as well as other biomarkers including immune responses to these antigens, as well as other -- the markers that we’ll be tracking. So, this going to be highly informative and hopefully -- with efficacy endpoint. So, it’s a very ambitious, but should be highly informative study for the power and the impact of 5401 with checkpoint in addition.

Could you also give us an update on the DNA-based monoclonal antibodies and plans to move candidates and other infectious disease and oncology into the clinic?

Yes. So, we’ve published dMAb as a early technology program. We actually only started this two years ago, fresh as an application or a platform to generate monoclonal antibodies directly from our DNA, injected DNA sequences, we’re challenged by $54 million contract from DARPA across two grants, as well as additional funding from the NIH and the Gates Foundation. So, we’ve just in the last three months publish three impactful research publications in cancer immuno-oncology and as well as Nature Communications and so on. So, we published actually take papers into the last two years. Our plan is to take one or more of these candidates fund with grant funding into clinical studies in 2018, which we see as a -- that’s just a product development, but also as a platform validating clinical studies. So, behind all of our published dMAb work, we have some exciting other candidates. We have, our own version of Humira, which is a largest selling rheumatoid arthritis -- I think it is a highest grossing pharmaceutical product today over $10 billion in sales. We have our own dMAb version of that. We have our own dMAb version of PD-1, PDL-1 and other undisclosed checkpoint inhibitors. So, these are all preclinical, but we’re developing them in our very prolific research engine. So, we’re going to show some proof-of-concept or proof-of-principle with the early infectious disease targets to show that we can generate the level that are relevant clinically and people, and we look forward to starting down in 2018. Along the way, obviously, we’re going to show our expression in higher animal models like the non-human primates and so on, leading up to that. So, you should expect lot more publications on dMAb coming from our group as well as our collaborators, executing on our funded research from various places and certainly we are moving in lightening speed and transforming this one, say, just exciting thought into a clinical product to be evaluated starting next year.

We have a follow-up question from the line of Charles Duncan of Piper Jaffray. Please proceed with your question.

Hey, Charles. Hello? I think we lost Charles.

Sorry.

Charles, you’re still there?

Yes, still here, just talking to myself on mute, sorry for that. So, quick follow-up, thanks for taking it. Question that I’ve been asked by investors is relevant to the REVEAL program. When a person is being -- or actually the other two programs as well for VIN and AIN. When a person is being treated in those programs, how do you deal with the prospects of the potential re-infection or do you believe that the technology prevents that from getting traction as well?

So, first of all, I think that’s a great question. I’m not sure we have other than our follow-ups. And so, for instance, if it’s let’s say HPV type 16 and the new infection. Let’s say we cleared it and then the person gets re-infected from a partner or whatever with the same type of virus, we believe we can -- how the immune system works is the T cells existing in the patient’s body should clear the new invading virus with the same type. But, clinical trials -- we’re not -- it’s going to be very difficult to track whether that is a unfinished clear virus from originally or the person has been re-infected. In reality, in my knowledge of 25 years in T cell immunology is it shouldn’t matter. So, T cells don’t care whether it’s a virus from last year or 10 years ago or from today, as long as the T cell can recognize those specific viral antigens from the same virus type that will clear. So, that’s a long winded answer but that’s a very interesting question which will have -- which will be really difficult to prove one way or the other. But, all we care is during the study period, are we clearing the virus and clearing the lesion and during the follow-up. And we’re also planning to have post licensure Phase 4 follow-up, get the information and so on. And we have other efforts to investigate how long are the true timing, the long-term impact of this. And we could only evaluate that in the clinic. But, what I can tell you is in monkey -- and monkeys aren’t people and using HIV virus, vaccines, our collaborators have tracked up to 8 years at the NIH. I mean, the cost and the efforts in generating killer T cells that last for 8 plus year in preclinical study. So, we think potentially -- and this is how the immune system works. Once you have memory T-cells against an antigen, they should last for very, very long time. And potentially that’s what we would see and that -- but that’s going to be very hard to show in a short study but we will continue to -- we plan to continue to track them, even through licensing and having this product on the market.

That makes sense to me, certainly based on my rudimentary knowledge of immune system function. But, I’m wondering if you have any evidence from tracking patients from previous studies. It certainly, would make sense to me that if you bolster T-cell responses, you ought to do that till any further infection. But any data that you can rely on there?

Yes. And we should have a lot more preclinical and clinical studies, which could add insights to those through publications and more study reports. So, we’ll look forward to bringing you those and adding to that data set that we are starting to match in this area.

There are no further questions over the audio portion of the conference. I would now like to turn the conference back over to management for closing remarks.

Thank you very much for following up on our progress. Please stay tuned for the rest of the year and beyond. Thank you.

This concludes today’s conference. Thank you for your participation. You may disconnect your lines at this time. Have a wonderful rest of your day.