Vical's CEO Presents at Bank of America Merrill Lynch Health Care Conference Call (Transcript)

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Vical Inc. (NASDAQ:VICL) Bank of America Merrill Lynch Health Care Conference Call May 15, 2012 1:00 PM ET


Vijay B. Samant – President and Chief Executive Officer


Rachel Mcminn – Bank of America Merrill Lynch

Rachel Mcminn – Bank of America Merrill Lynch

Okay, thanks very much everybody for joining us for our next presentation. My name is Rachel McMinn, I’m one of the biotech analyst here at Bank of America Merrill Lynch. It’s my pleasure to introduce our next speaker Vijay Samant, President and CEO of Vical and he’s been at Vical for 10 years, 10 years so long time I look forward to hearing the latest on the company.

Vijay B. Samant

Thank you, Rachel and thank you to Bank of America for inviting us to this conference. Before I begin my formal presentation, please refer to our Safe Harbor, I may be making some forward-looking statements. And please refer to our Q’s and K’s to fully understand the risk associated in investing in Vical.

For the members of the audience who don’t have a full understanding of Vical, Vical is a development stage drug company with strong pipeline a lead program is for treatment of Allovectin, treatment of melanoma. Allovectin is the lead program, we have a substantial franchise for treating CMV disease we have partnered that with Astellas.

And then we have an exciting preclinical program for Herpes Simplex 2, where nothing is really going on, but one out of three people in the U.S. are HSV-2 positive. We have number of partnerships with major pharma companies. We are one of the few companies in Southern California, which has a biological manufacturing facility and we have a strong balance sheet, plenty of cash and no debt.

So Allovectin-7 something that we’ve been working for very long time, we’re pretty excited the pivotal data from this program will be coming out by the end of this year. It’s a systemic immunotherapy, but the beauty of it, it’s given locally. So the fact that it’s given locally, but works systemically does not have the side effects of traditional systemic drugs.

We have treated about 900 patients in variety of cancer applications, its well tolerated. Let me give an example of how it’s given, it’s given in the outpatient setting one injection per week into the lesion and you repeat every week for six weeks in a row followed by two week of observation period.

So one cycle of treatment is about eight weeks, in eight weeks you get six injections. Most patients start showing benefit of the drug after about two cycles of treatment, which is 16 weeks or four months. So, the key thing that you need to understand as you walk through my presentation that in immunotherapy the patients need to live long enough to benefit from immunotherapy.

It has a unique mechanism of action, I’m not going to spend a lot of time talking about it, you can go to our website and look at it. But, I think the most important thing it has potential synergies with currently approved new therapies for melanoma, it has an orphan drug status or fast-track status. With all the U.S. and EU commercial rights and we have an SP or a Special Protocol assessment with the agency.

Our people ask, what’s the melanoma market now that the new two drugs have been approved. There is plenty of room for melanoma. Melanoma is not been cured, the two drugs have benefits, but they have their own toxicity. These kind of patients we’re treating in our Phase 3 trial will represent about third of the vulvar melanoma patients. The current drugs have been priced at $60,000 to $120,000 per therapy, so plenty of room a huge commercial opportunity for a company for our size.

So without getting into how the mechanism works I think the key thing is it’s a unique mechanism and the unique mechanism is such a way that you treat the tumour to teach the immune system to recognize what’s wrong with the cancer and UE use the lesion while you inject Allovectin as a classroom and that classroom is really teaching the immune system. Some immune systems learn very quickly, some immune systems take about 8, 10, 12 months before they learn. And that learning of the immune system is breaking of tolerance or teaching the immune system to recognize what’s wrong with that tumor getting it to recognize the markers that the cancer cell presents on the surface telling the immune system kill me, okay.

The most important thing is the newly approved drug therapy, immunotherapy Yervoy which is known as CTLA mAb. In animal studies we’ve shown that we’ve synergy with our therapy, a combination of Allovectin and CTLA mAb actually did better than CTLA mAb alone, so if this translates into human our drug that immunotherapy should have synergistic affects. So Vijay what’s the data.

Well Phase 2 trial which we did on 127 patients it’s a single-arm open-label study pretty large for a single-arm open-label study. 50% of the patients where stage 3, 50 % of those patients were stage 4, the key thing is the patients did not have brain mets and liver mets why? Because patients with brain mets and liver mets die very quickly and immunotherapy in order for the patient to benefit, they need to live long enough. What did we accomplish in that study we demonstrated first of all the drug was safe and efficacious, that’s key.

There were no withdrawals for toxicity or adverse events if we look at the two approved drugs you’ll see why that benefit is very important. There were no great three or four drug related adverse events. The objective response rate was 12% and the median overall survivals about 19 months, 18.8. are you going to say well Vijay the objective response rate looks slow but look at that (inaudible) only you can see it, but we lost almost 60% of the subjects without completing one cycle of treatment why, because under standard RECIST criteria, patients who are metastatic melanoma if they present a new lesion the doctors force to take them off the therapy.

What we have done in the Phase 3 studies, we have actually modified that RECIST criteria an agreement with the agency so that patients can stay on the study for up to two cycles or 16 weeks or four months as long as the doctors sees that the patient is benefiting from the therapy, even if a new lesion shows up. So we should expect that dropout rate of 16% to drop substantially and more Allovectin you give to the patients, it should benefit both response rate and survival.

This is a beautiful curve. This came out after we started the Phase 3 study. The dotted line represents the intent to treat patient, and that’s this curve here. And the median survival for all the patients is about 18.8 months, despite losing 60% of the patients without completing one cycle.

But I think the more interesting curve is the blue curve, these are the responders, patients who responded to the drug, they had not reached median survivals even after seven, eight years after the study. So it’s a good correlation between patients who respond, who gone to live longer. And as I told you, we believe that patients who get more Allovectin, it should impact that survival number, and I’ll talk more about that in a minute.

So what’s the quality of life? And obviously, this has to translate in Phase 3 and we’re comparing apples and oranges, but if you look at the Allovectin data from Phase 2 versus the Yervoy data from Phase 3, our drug was given an outpatient setting, there was no hydration, no premedication, no withdrawals for toxicity at adverse events, no grade 3 or 4 drug-related adverse events.

Take a look at the Yervoy, 10% to 15% at GI autoimmunity issues, 2% deaths, this is published in the New England Journal of Medicine, I’m not making this upper cycle go along. So, we can maintain this kind of profile in Phase 3, and if we can show efficacy, it should be a new paradigm shift in treatment of melanoma.

So what are we done in the Phase 3 study to improve the outcome from the Phase 2 study? I mean that’s really the key. First thing we have done is, as I told you, we pick healthy patients, healthier the patients, the better off then treatment of immunotherapy. We also use important mark on this LDH and we use patients with normal LDH. LDH is a market on Lactate Dehydrogenase, this is an enzymatic market that tells you how long the patients generally live is the prognosis of their immune system.

And then finally, I told you, we modified that in RECIST criteria, so that the patients gets down to cycle for up to two weeks. Even if a new lesion shows up as long as the doc believes that the patient is benefiting good therapy, that we will give more Allovectin 70 patients. And finally, the primary endpoint, which is a response rate, which is this reduction in the size of the tumors by standard RECIST criteria, we’re measuring reduction six months after randomization anybody you’d respond for six months is not counted, why? Because in chemotherapy most patients respond in the first six months and they progress immunotherapy, you start reaching peak after six months. So we’ve setup that comparator at a point where we will have maximum difference between both arms.

So where does this study start. The study was – it’s an SP approved Phase 3 pivotal study. It recruited stage 3 and 4 melanoma patients, no liver mets and brain mets. The study started in Jan of 2007. Recruitments completed in Feb of 2010 about three years, half of the patients were recruited in the first two years and the remaining half are recruited in the last year. The trial sites are in U.S., Europe, Brazil and Israel. Israel we have partnered the drug with Teva already.

The patients have no or chemo-naïve and chemo-naïve is an important determination because patients who are chemo-refractory, the immune systems are battered. We learn from our Phase 2 study that chemo-naïve patients were the majority for responders. The study is randomized 2:2:1 twice the number of patients get Allovectin-7, so there will be about 260 patients getting Allovectin-7 and about 130 getting Dacarbazine.

The study is not blinded to the doctors and the patients. It’s blinded to us, so every doctor and patient in his own clinical setting knows how the patients are doing. The FDA knows it. It’s part of our SPA. The primary goal is response rate at 24 weeks. Secondary goal is overall survival. The beauty of this the entire study was funded by Japanese company AnGes, you are saying well wait a minute. You still have U.S. and European rights how did you get the study be funded. We get them head and neck cancer rights for Asia excluding Australia, New Zealand and India. So it’s a very sweet hot deal for us and we still have commercial rights for this drug in the U.S. and Europe.

So what are the statistical parameters on this trial has been designed. There are two endpoints, objective response rate and survival. Under the objective response rate, we have to show a 10% absolute difference between both arms. We believe that the number that we expect in the control arm at six months and beyond in the chemotherapy arm will be less than 4%, and the secondary endpoint is survival. And here the control arm assumption is 11 months. The historical data that has been published for this patient population treating the (Inaudible) is anywhere from six to nine months.

We have used the upper end of that number to take into account the healthier patients of 11 months. Our upper bound for the treatment arm is about 18 months. And it’s power to detect about 90% part to detect that survival difference between both arms. We expect the median number for the treatment arm to be more than 22 months based on our Phase 2 data. So there is a plenty of room even the control arm does slightly better, but I am going to talk more about that in a minute.

So the question comes up, let me backup for a second. The study is now almost five plus years, by the end of 2012 will be six years right. Am I right, Alan, you are six years. That’s 72 months and we still have not reached the target inventory that we are talking. So the patients are living longer. Why the patients living longer because may be the treatment arm is living longer, maybe the control arm living longer. I want to get a little more into it because people repeat asking me questions regarding that. So could the control arm be living longer? Dacrabazine as I told you historical data, you can look at the Chapman article it’s on our website it’s 6 to 9 months, okay we have used a median survival of 11 months, does it have any synergy that new therapies the answer is no, chemotherapy and new immunotherapy has no synergies.

Our patients going on getting new immunotherapy after they progress, the likelihood is no body even if they did, that could impact survival in that arm. Remember those drugs were approved, the Yervoy was approved in the United States in May 2011 and Zelboraf is approved in September 2011, long after our study started. So there would be number of control arm patients progressing in getting that drugs is very small, but let’s assume indeed they are getting it and that could impact the control arm survival. So fair enough, that could be an impact on the control arm.

Now let’s look at the treatment arm. The original number that we showed the mean was 18 months but those patients were chemo-naïve, chemo-refractory, bio-refractory as you know we’re using only chemo-naïve patients in the phase III study. If you take just the chemo-naïve in the Phase II the number is about 22.5 months. Now superimposed on that the fact that we have modified RECIST criteria that patients will getting at least two cycle of the treatment, more Allovectin should impact that survival. So that should move that number 22.5 months further north. And then we’ve shown at least in animal models that CTLA ipilimumab synergies with Allovectin-7 that should further impact that number. So the number could be greater than 22.5 months.

So the likelihood of why we are not getting the event rate is probably but the control arm is living longer, as well as the treatment arm is living longer. So where do we stand on the timeline? So we will be closing or locking data, we split the database for response rate and survival. And the reason we have split the database for response rate and survival simply is because we can clean up the response rate database so that we can adjudicate the data, the data is adjudicated independently by a panel of radiologist and oncologists to come with the response rate in a blinded fashion. And that’s a long process and a very detail RTO’s process which is starting right now.

And as that process is going on, we expect that process to complete somewhere and the fourth quarter will continue to collect survival data, hopefully we will reach our target events by the end of the year and our goal is announce both the end point simultaneously. We are pretty excited about how this trial has gone. We believe that if this therapies approved it will be a create a paradigm shift in treatment of melanoma. And I would remind people here in the audience that there is applications for this drug and other solid tumors such as head and neck cancer, where we have done all the studies that could be the logically pathway to take this drug into other critical trials.

Quickly on our infectious disease franchise, CMV is a nasty herpes family bug, nobody knows about it. People understand Chickenpox, people understand herpes simplex, but this is the nastier of that herpes family. Most of us are positive and when you are positive, it hides in a synergistic balance in your body, but when your immune system is compromised, it comes and attacks everything inside.

And so it’s a big problem in transplant patients who are CMV positive, particularly in bone marrow transplant patients, where when their bone marrow is white dot, you take the immunity of the learning process of fighting CMV that’s hiding in the body and the new bone marrow that comes in, the immune memory in there does not have the knowledge of finding the CMV.

So the goal of our vaccine is to teach this new bone marrow or the new immune memory, how to fight CMV the first hundred days, because these guys get first reactivation day 100 and another reactivation in about six months time and those are massive severe reactivations, which again lead to graph rejection or complications. And we have been working on this for quite sometime along with Sanofi, which is the other company, which owns a lot of intellectual property. We own a lot of intellectual property. We have published a lot on this. We have done a variety of clinical trials, but Phase 2 double-blinded efficacy study, which was presented at ACAG few years ago.

You can look at the date on our website, which led to a partnership with Astellas. But there are two segments of the market, TransVax, which is for the treatment of transplant patients reactivation, but the big opportunity CyMVectin, which is prevention of CMV infection in females of childbearing age, and I’ll cover that in a minute. That’s like the next holy grail of vaccinology. So we did a great deal with Astellas recently.

We got a commercial deal with about a $130 million of each $25 million were paid initially, we got a $10 million milestone when we agreed in the conceptual endpoints with the agency, we had double-digit royalties from day one, we have option to co-promote, this is about a $0.5 dollar market in U.S and Europe.

Astellas [only] bearing the entire expense of running the clinical trials, which will be the pivotal Phase 3 trial for hematopoietic cell transplant patients, as well as the solid organ transplant patients will be providing services, including manufactured goods, it will impact our bone rate, I told you our bone rate next year is going to about $17 million to $20 million and the reason it’s slow is most of our expenses are being funnel through Astellas and some of our other programs. And with Vical, we will be providing preclinical regulatory support to this activity. So we are very excited, c is a great partner, because Astellas is Prograf, which is a leading transplant drug, and so they understand the transplant setting.

CyMVectin, this is the last big commercial target, females who get infected during CMV, during their pregnancy, the first trimester is a leading cause of birth defects by an infectious agent, go to YouTube; you can see parents with kids born with CMV. The biology of protection is well understood, the FDA recently had a workshop with Big Pharma and Vical about five companies to define surrogate endpoints for doing the clinical study, we have an IND approved. We are ready to go into the clinic but until those surrogate markers are defined, we’ll not proceed on it and we have a lot on our plate right now. So this could be a program that we’re going to actively explain (inaudible) opportunities.

Herpes simplex, not to scare you, massive out break worldwide, one out of three, one out of four people are positive, almost large 80% of the people are asymptomatic means they are infected, they don’t get lesions but they pass on, most people who had lesions get 6 to 12 recurrences every year, big opportunity, nothing going on, this will be a therapeutic vaccine.

We published terrific clinical data probably one of the best preclinical data that you’ve seen, okay. So I’m not going to go with the data sterilizing immunity in mice prevention of recurrence of lesions. but the concept here is to go into people who get large outbreak of lesions, divide them into two groups, give one group placebo, one group vaccine but before you get the vaccine and placebo first 90 days you actually measure the shedding through the lesions.

So each patient will be its own control, they need to do a 90 day vaccination period and then a 90 day post vaccination period, you look at shedding reduction across both groups, as a group as well as individual patients. And that’s really the key surrogate marker of seeing whether this vaccine works or not. So we’re pretty excited. We have a lot of important scientific advisers working with us, this strong can be recruited in a matter of days that’s how eager patients are to get into this study.

Very quickly financially we’re in great shape, we ended the quarter with about $96 million in cash. We received another 10 million post that quarter which is not in our cash balance I said our projected born rate is about $70 million to $22 million. We have no debts, no warrants, we had a well managed company which if you can look at our born rate in the last six years, it’s been surgically managed, we have a good management team who understands drug development, we have filed almost 15 INDs with the agency in the last 10 years that’s one head off in the biological space, we have a great relationship with the agency.

So in terms of upcoming milestones, we’ll have top line data from Allovectin 7 in the fourth quarter of this year response rate and survival will be simultaneously allowed. We’re very excited about how this program has gone for us so far. Astellas will deliver the clinical material in the second half of this year and they’ll start their pivotal study in bone marrow transplant patient in the second half of this year followed by solid organ transplant study. We should start the Herpes Simplex 2 study sometime next year, and we are looking for marketing opportunities for CyMVectin.

That’s in a nutshell my presentation. Rachel, you have a few questions, so we’ll leave about nine minutes for Q and A.

Question-and-Answer Session

Rachel Mcminn – Bank of America Merrill Lynch

Sure, great, thanks very much. And are there any questions from the audience?

I’ll get things off. So, maybe if we can just go back to Allovectin Phase III. You’ve had some patients on for quite a long time, you’ve talked a little bit about the event rates and why they’ve been slower, probably both the control and drug arm. I guess, remind us if you have had any interim looks over the study?

And I guess in a way like, even if the event rates were somewhat slower, the kind of difference that you’ve pointed out for Phase II suggests that you should already have such an extremely large p-value, I mean and let’s say, that rate is still so low. But just given where you’re today, only maybe six more months to go, just what do you know about the event rate and the study and how it looks?

Vijay B. Samant

So the first question is have we taken an interim look? Unfortunately, there is no interim look in the study. So the only interim look has been at safety and we have gone through about five or six safety reviews, and those safety reviews have gone well. And the Safety Board has told us that we should continue with the study.

We’re pretty pleased with the event rate. The event rate that comes to us, comes in a blinded fashion, so we don’t know what the event rate in each of the arms. But we have the ability to model in a variety of ways to see what control arm behaviors will still satisfy and give us pretty exciting p-values. And our modeling has pleased us so far, but in the end, the data is the data. But I think everything has gone according the way we planned. Obviously, as the event rate start plateauing out, then there’s no incremental advantage here for continuing to collect the data, even though we don’t reach the target event rate.

But I think right now, the rate controlling stuff for us is really getting our adjudication done, which will occur in the fourth quarter. So, nothing is going to happen till we finish our adjudication that delves upon blinding the data.

Rachel Mcminn – Bank of America Merrill Lynch

But in terms of the actual event rate, I guess maybe if you just take a big step back, when you first started the study, how long have you planned the study to go? And where are you versus that initial estimate?

Vijay B. Samant

Well, it’s a great question. And the original game plan and Alain will correct me if I make a mistake. It was the middle of 2011 when we talked we’ll have the data, then we postponed it to the end of 2011, then it was again postponed to the middle of 2012, and now saying it’s the end of 2012. So it’s almost a 18 to 24 months of postponement from the original target.

Rachel Mcminn – Bank of America Merrill Lynch

And I guess what is there other than telling you that patients are living longer. Do you have a sense of what the progression rates look like or response rates in the study?

Vijay B. Samant

No, we have no idea what the progression and response rates. All we have also anecdotally we have is that we do ship Allovectin so we have general idea of how Allovectin shipped out, but we don’t have any ideas patients specific usage.

We know one of the most interesting things is that, since the study finished recruiting the last patient in Feb 2010 and the maximum follow-up for the patient is about two years. The follow-up of the patient would have been Feb 2012. Our expectation was that by September, October most of the patients would have progressed, unfortunately it was not the case.

We had patients all the way to Feb 2012, so we couldn’t, that tells you that patients are on treatment till the very end, okay. Obviously we are blinded to what arm they are in, but I doubt that dacarbazine patients stay on dacarbazine for two years.

Rachel Mcminn – Bank of America Merrill Lynch

And I guess just based on again its May, you are hoping for the adjudication date on 4Q and how solid is that is there a potential for this sweeper shot for another…?

Vijay B. Samant

No, I think the adjudication is solid because it’s a well laid out process. We are already well into it, the survival data also is moving reasonably well and as I told you before even if we don’t reach the target event if we reach a plateau then I think that should be sufficient confidence to un-blind the data, okay.

Now all the modeling that we have done is assumes that both the curves are not going to separate but the reality if Allovectin-7 is working the curves will indeed separate, so we should get additional benefit form it okay.

Rachel Mcminn – Bank of America Merrill Lynch

And just going back to the big picture mechanism, you’ve mentioned at the very beginning of your talk that this was a drug that is injected locally, but acts systematically. So how do I guess take that statement and then interpret your other remarks where you could have somebody’s lesion that shrinking, but then another new lesion pops up. So maybe you can just talk about the time that it takes to new mechanism on a lesion versus preventing new lesions from popping out?

Vijay B. Samant

Sounds good. Well, the mechanism was pretty straight forward. We encode into the plasmid, HLA-B7 which is rare in (inaudible) Caucasians so when that’s expressed on the surface is like a foreign tissue because HLA-B7 is rear in Caucasians, melanoma is a disease of Caucasians so when its expressed on the surface, the immune system goes buzzard and attacks that cancer cell, I mean when it attacks the cancer cell, it starts seeing the other abnormalities on the cell and it takes some time for the immune system to understand those cell bondages or human protein shouldn’t be there at this point in time and once that recognition of breaking of tolerance those activated T cells strengthen the lymph nodes and in some patients it takes time and even since it takes time in patients, the cancer continues to grow and that’s when you get new lesions.

So but once that occurs you, if you were good drainage to the lymph nodes you will get systematic reaction. We have shown them and it’s on our website where patients will be – by the way we inject the same lesion throughout the treatment, so it’s not like going through multiple lesions. And we’ve seen lesions, the lung going lesions distally shrinking so and we have seen some autoimmunity such as vitiligo and all those all the time in our studies.

Rachel Mcminn – Bank of America Merrill Lynch

And you mentioned Yervoy and just the control group there, I believe you put up a number of about a 11 months for survival in the Yervoy study. So maybe I have it wrong, but I just was curious if you can compare the entry criteria for your Phase 3 versus Yervoy, so we can get a sense of whether that would be too conservative?

Vijay B. Samant

So the Yervoy published in The New England Journal of Medicine used entry criteria, which is pretty much identical to us except that they had liver mets, okay. And then LDH markers, there was no normal LDH marker on it, and they had as median survival of nine months versus we using number of 11 months, okay. So that’s really the difference.

Rachel Mcminn – Bank of America Merrill Lynch


Vijay B. Samant

They did not have brain mets. Zelboraf study indeed had brain mets, so they are in a complete different category, because brain mets patient die very quickly.

Rachel Mcminn – Bank of America Merrill Lynch

And is there any data for the kind of patients that you have in your study to give us a sense of whether 11 months is the right number or maybe it should be 15 months. How do you get confidence throughout that number?

Vijay B. Samant

We have a lot of confidence. First of all, we have done an exhaustive review of the literature Rachel and first of all, there is no patient group, which mimics our patient population. Having said that, the best number that’s published and you guys can look at the data yourself is a number where there is a 13-month survival in the dacarbazine arm, but the LDH numbers like.8X or.9X and as you drop starting the LDH number, the survival indeed improves, but there are two data points, which we have not published, which gives us a lot of confidences.

The Phase 2 study we lost almost 60% of patients without completing one cycle, which is almost 72 patients and you plot the median of that, that gives us hope that we are not very far from the 11-month number. And the second which we have not published is, we did a low-dose Allovectin study in 200 patients, Allovectin plus dacarbazine versus Allovectin-7, their both arms at about 9 or 10 months median survival.

We have the ability to extract patients with normal LDH, which we have done, which we will publish in sometime in the future. This gives us confidence we are not far from the number.

Rachel Mcminn – Bank of America Merrill Lynch

And in terms of the retention in this study, do you have a sense of, I mean, presumably just giving your death rate being slow that you would have much better retention, do you know what it is?

Vijay B. Samant

We haven’t publicly pronounced it, but I think we are pretty good. And our retention made is very good, despite the fact the study was not blind, somebody gone into the dacarbazine arm could have walked out of this study, right, because they knew exactly what they are getting. So the drop out rate is very low in this study.

Rachel Mcminn – Bank of America Merrill Lynch

And even though for patients staying on past, the first two cycles that percentage is much lower than 60% where you have lost…

Vijay B. Samant

Absolutely, yes, so I think we haven’t revealed that number, but I think it pleasantly please that drop out rate is much less than 60% that we saw in the Phase 2 study.

Rachel Mcminn – Bank of America Merrill Lynch

Any questions from the audience? All right, if not, I think we’ll have to leave it there. Thanks very much.

Vijay B. Samant

Thank you. Thank you very much.

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