Brickell Biotech Inc (BBI) 2011 Q3 法說會逐字稿

Good day. Welcome, ladies and gentlemen, to the Vical Incorporated financial results conference call. At this time, I would like to inform you that the conference is being recorded, and that all participants are in a listen-only mode. At the request of the Company, we will open the conference up for questions and answers from the invited participants after the presentation. I would now like to turn the conference over to Mr. Alan Engbring, Executive Director of Investor Relations. Please go ahead, sir.

Hello, everyone. Welcome to our third-quarter 2011 financial results conference call. Participating on the call today are Vical's President and Chief Executive Officer, Mr. Vijay Samant, and Vical's Chief Financial Officer, Ms. Jill Broadfoot. I will begin with a brief notice concerning projections and forecasts. This call includes forward-looking statements, including financial expectations and projections of progress in our research and development programs, that are subject to risks and uncertainties that could cause actual results to differ materially from those projected, including the risks set forth in Vical's annual report on Form 10-K and quarterly reports on Form 10-Q filed with the Securities and Exchange Commission, as well as the specific risks and uncertainties noted in Vical's news release on third-quarter 2011 financial results.

These forward-looking statements represent the Company's judgment as of today. The Company disclaims, however, any intent or obligation to update these forward-looking statements. Now I would like to introduce Vical's President and Chief Executive Officer, Mr. Vijay Samant.

Thank you, Alan, and welcome. We have made terrific progress in our key development programs during the third quarter, and the momentum is continuing as we approach year-end. I will provide an update on these programs today; but first let me pass on to our CFO, Jill Broadfoot, who will start the call with a review of the third-quarter financial results.

Thank you, Vijay. Our TransVax license agreement with Astellas drove financial results for the third quarter, and is expected to have a continued impact. As we recorded earlier today, third-quarter 2011 revenues were $26.6 million, compared with $2.3 million for the third quarter of 2010, which was primarily the result of the initial upfront payment recognized under the TransVax license. With relatively flat operating expenses quarter over quarter, the increase in revenues resulted in a net income of $16.4 million for the third quarter of 2011, compared with a net loss of $6.8 million for the third quarter last year.

We ended the third quarter with cash and investments of approximately $62 million, and we expect to end the year with cash and investments of $53 million to $56 million. As we advance through the development of TransVax over the next few years, we expect to receive ongoing reimbursement by Astellas of our costs for TransVax-related activities, which should offset a portion of our operating expenses. We will provide net cash burn guidance for 2012 when we announce year-end 2011 financial results in February. With that, I will turn the call back to Vijay.

Thank you, Jill. I will start today with our lead program, Allovectin, for metastatic melanoma. As we approach completion of our pivotal trial, the excitement around [this small] immunotherapy is increasing, and we are starting to get frequent questions on some common topics, and these occur in our one-on-one questions or our face-to-face presentations. I wanted to take this opportunity to address all those questions in a single forum, so everybody has the same answers.

The first question is -- what is the efficacy potential of Allovectin? Let me remind you that in our Phase 2 trial, we focused on 2 efficacy endpoints -- response rate and survival. We had 15 responders out of 127 patients, for an overall response rate of about 12%. The median duration of response was 13.8 months. Overall survival in our Phase 2 trial was 18.8 months, compared to a typical chemotherapy survival range of 6 to 11 months. So, our numbers look good in Phase 2. But let me explain why we expect our results in Phase 3 to be even better.

First, we wanted to select patients in our Phase 3 trial who had the best chance of living long enough for Allovectin-7 to work. Chemotherapy takes a toll on overall health, and especially in the immune system, so chemo-naive patients have a healthier constitution. In our Phase 2 trial, the majority of our responders were chemo-naive. In fact, patients who were chemo-naive had a response rate almost twice the rate as patients who had prior chemotherapy. So, Allovectin simply works better in chemo-naive patients; we therefore enroll only chemo-naive patients in Phase 3.

We have also enrolled healthier patients, with no brain or liver [meth] and normal LDH, which will help us to acknowledge we are the first Company to use LDH as a marker for recruitment in a melanoma trial. In addition, we measured LDH at a central lab to eliminate site-to-site variability in testing. For patients in our Phase 2 trial who met all the Phase 3 eligibility criteria, the response rate could have been about 17%.

In summary, by following these specific inclusion and exclusion criteria, we are narrowing the very heterogeneous [oron] melanoma population and selecting a very homogeneous group of patients most likely to respond to Allovectin. Second, we wanted to keep these patients in Phase 3 trial on Allovectin long enough for it to work. Under standard [RECIST] criteria, patients must be withdrawn from the study if they develop any new lesions -- even small, clinically [ineligible] lesions. We lost almost 62% of the patients in our Phase 2 trial due to withdrawals during the first 8 weeks of the cycle of treatment.

In Phase 3, we have modified the RECIST criteria under an SPA agreement. That allows the patients to remain on study through at least 2 cycles, or 16 weeks, even if they develop new lesions, as long as their physician assesses that the treatment was providing clinical benefit. In addition, we have demonstrated a strong positive correlation with the Allovectin between response and survival. Despite the high dropout rate during the first cycle of treatment, our overall median survival in Phase 2 was an impressive 18.8 months. For responders, it was even impressive 22.5 months. If we can increase the response rate, we should also have a corresponding impact on survival; so, we believe the potential for achieving the efficacy goals of Allovectin is excellent.

The second common question is -- why do you inject a single lesion? Cancer cells can grow and replicate only if they can successfully evade the immune system. One way they do this is by changing the way tumor-specific antigens are displaced in the cell -- cancer-cell surface. Allovectin has multiple mechanisms that work together. The repeated injection of a cationic lipid complex draws the immune system resources to the tumor; that is the first step. The HLA [defemen] antigen makes the tumor look like a foreign tissue to the immune system, and the beta-2 microglobulin restores the normal display of tumor-specific antigens.

The result is that T cells can then find and destroy similar tumor cells throughout the body. So, Allovectin works by breaking the immune system's tolerance for the melanoma cancer cells. We inject the same lesion repeatedly to keep the immune system focused on a single lesion until the tolerance is broken. Some patients respond more quickly than others, so we try to keep all of the patients on treatment long enough to break this tolerance that I just mentioned. We have designed the trial to keep as many patients as possible on treatment through at least week 16 -- that is 4 months, guys. We have tested the concept of single versus multiple lesion injection in our Phase 2 trial, and found that the single-lesion injections indeed work best.

The third common question is -- what evidence do we have that Allovectin provides a systemic effect? In Phase 2 study, we have documented in multiple patients that uninjected tumors responded to the treatment -- in several cases, even completely disappearing from the distant parts of the body. So, for example, injection into lesion on the arm can cause the immune system to destroy a tumor in the lung. We also documented cases of vitiligo among the responding patients. Vitiligo is a condition that appears as light patches on the skin. It is caused by the immune system's attack on the melanocytes, the pigment-bearing cells of the skin, which are the same cells affected by melanoma. So, vitiligo provides the clear evidence of systemic immune effect.

The fourth common question is -- what is the safety profile of Allovectin-7? Of the 127 patients in the high-dose Phase 2 trial, we had zero patients withdraw from the study because of side effects. A typical melanoma treatment's withdrawal rates due to side effects can be 10% or more. We also had zero -- and I repeat, zero, Grade 3 or Grade 4 drug-related adverse events. This is an exceptional result, as typical melanoma treatment cause Grade 3 or Grade 4 adverse events in 10% to 15% of the patients, and even cause death in 1% to 2% of the patients. We are highly encouraged by the excellent tolerability of Allovectin-7 demonstrated in this high-dose trial. We have completed multiple interim safety reviews in the Phase 2 trial without any issues.

The fifth common question is -- can you summarize what have you done to improve the chances of success in the Phase 3 trial? Of course, as I mentioned earlier, we need to enroll the right patients -- those that can live long enough to benefit from our treatment, as in Phase 2. The enrolling patients with Stage III or IV metastatic melanoma with no brain or liver [met]. As in Phase 2, we are enrolling only patients with normal or better LDH, which is a good indicator of the overall patient health. Unlike Phase 2, we are only enrolling chemo-naive patients in Phase 3, because they are more likely to respond to Allovectin.

Second, also, as I mentioned earlier, we need to keep patients in the study long enough for Allovectin-7 to break the immune system's tolerance. We are doing that in Phase 3 by modifying the RECIST criteria to allow patients to remain on study through at least 2 cycles of 16 weeks, or 4 months of their treatment -- and at their physician's discretion, of course. So, we optimized the design of our Phase 3 trial to highlight the long-term response and survival characteristics of immunotherapy, that chemotherapy has demonstrated historically poor results.

And the final question -- if approved, how might Allovectin be used in the marketplace? Let me begin by describing the encouraging advancement approval of multiple new treatments for metastatic melanoma for most people -- there is still no cure. That means patients will likely to pursue new treatments to find what works best for them. The unique mechanism of Allovectin and its excellent safety profile should make it an attractive component of such combinations.

During the third quarter, we also presented results from a study in an accepted melanoma mouse model, combining Allovectin with an anti-CTLA-4 antibody, which is used -- which is the mouse equivalent of (inaudible). Highlights of the study included the following -- combination of the 2 treatments provided a synergistic reduction of tumor growth, compared with either treatment alone. The benefits of combination therapy became evident about 12 days after the treatment initiation, suggesting a possible 2-step process in which Allovectin [flowed] direct T cells to the target melanoma tumor, and the anti-CTLA-4 antibody then maximally activates these T cells.

The combination provides a positive trend in survival, compared to either treatment alone. Allovectin alone significantly reduced tumor growth and significantly increased survival time, compared with the anti-CTLA-4 antibody alone, and compared with no treatment or treatment with placebo. We look forward to exploring additional combinations in clinical studies after approval. Allovectin's safety profile should also make it attractive to all the patients who cannot tolerate the side effects of other [flu] treatments. The median age of patients in our Phase 2 trial was 60, and the range was up to 98. Once we have the efficacy and safety data from Phase 3, we should be better able to establish commercialization specifics. We are obviously working on those.

I complete my discussion on Allovectin by doing the timeline, as updated last quarter. We expected to complete treatment and follow-up for the primary endpoint, which is response rate by February 2012, and to continue monitoring for the secondary endpoint, overall survival, up to the release of top-line data, which we expect to occur in the second quarter of 2012. I will note today that we have completed a planned sweep of sites to bring the survivor database as up to date as possible; and after that sweep, we are still lagging in the expected detriment rate for the study. Since we provided all the details around this timeline on our last call, I will not repeat them today but we will be happy to answer any questions. We will confirm the update and the guidance as needed in our call next [year].

Let me now move on to TransVax. We announced the TransVax license agreement with Astellas early in the third quarter, and reviewed the details in our last call. Since then, we have collected initial upfront payment of $25 million, and finalization of the Phase 3 trial design, which took another $10 million payment. We have made significant progress in collaboration with Astellas, and remain on track for the plan initiation of our Phase 3 trial in the first half of 2012; and the Phase 2 trial for solid organ transplant recipients is also expected to begin again in the same timeframe.

Let me now move to our herpes simplex 2 program. This is a therapeutic vaccine for herpes simplex 2. It represents a large potential market opportunity, which is conservatively estimated at more than $1 billion. The prevalence in the US alone is estimated at around 15 million people, with about 20% or 10 million people, suffering from periodic outbreaks of genital warts. The other 80% are asymptomatic, but can still shed the virus and transfer it to their sexual partners.

Since our last call, we presented new data at a scientific conference from our latest studies of our therapeutic vaccine and the standard guinea pig herpes model. Our Vaxfectin-formulated vaccine against HSV-2 provided complete protection in guinea pigs against both primary and recurrent HSV-2 disease. The vaccine also significantly reduced genital lesion recurrence and viral shedding, as well as latent infection in the central nervous system.

Collective results from our preclinical studies include the following -- prophylactic vaccines in coating glycoprotein D plus or minus to herpes virus (inaudible) proteins provided complete protection from both primary and recurrent disease. The prophylactic vaccines also significantly reduced viral replication at primary infection site, as well as detectable virus at the latent site. [Herpetic] vaccines and coating glycoprotein D plus, the two (inaudible) proteins significantly reduced the frequency of genital lesion outbreaks in animals with pre-established HSV-2 infections. The therapeutic vaccine also significantly reduced the frequency of genital viral shedding.

These are superb results, and we are working now to complete preclinical development and prepare a plan to advance the therapeutic vaccine into human clinical testing. We believe a relatively small and quick Phase [1-2] study should be conducted in infected volunteers to provide initial human safety and proof of concept data. The program is high on our priority list, and we look forward to defining a path forward in the near future. We expect continued progress in our independent and [partner] programs through the year in 2012 -- into 2012. In our Phase 3 trial for Allovectin, we expect to complete treatment and [follow-up] for the primary endpoint by February of 2012 -- that is a 2-year follow-up; and to release top-line data from both primary and secondary endpoints in the second quarter of 2012.

In our TransVax vaccine program, we expect Astellas to initiate a Phase 3 trial in stem cell transplant recipients, and a Phase 2 trial in solid organ transplant recipients in the first half of 2012. Our Japanese partner, AnGes, has recently updated its guidance and now expect to initiate a multinational Phase 3 clinical trial of its Collategene angiogenesis product in 2012. We expect to end the year with cash and investments of $53 million to $56 million.

This concludes our prepared comments, Operator. We are now ready to open the call to questions from our invited participants.

Thank you, Mr. Samant. (Operator Instructions) George Farmer, Canaccord.

Vijay, do you have any evidence as to how many patients, if any, in either the Phase 2 or the Phase 3 trial went on to subsequent Yervoy therapy after disease progression?

Let me walk you -- first of all, in Phase 2, there was [to an extent] almost 7-plus years ago, there was no Yervoy in existence at that time. It was probably in a pre-clinical state. So, to acknowledge a [non] -- because the study was completed very long time ago. Let's talk about our Phase 3 study. When our Phase 3 study was conducted, obviously the front-line therapy for Yervoy was being conducted.

The second line therapy for Yervoy was been conducted, and also, the Roche-Lexicon drug front-line therapy was also being conducted in the same time. Our study started in January of 2007, approximately. Both of those front-line studies for the Roche drug and Yervoy required treatment-naive patients. So, during the conduct of those studies, neither of our patients in either of the arms -- the chemo arm or the Allovectin arm, were progressed into those studies, because they were for treatment-naive patients. Got it?

Yes.

So, the first time anybody could have got Yervoy in the United States was sometime in the April-May timeframe, when it was formally approved. And then, in Europe, much later is approved a second-line therapy, and you just heard about the [Nice] issue. So, I don't know what -- how widespread usage is. It was allowed in the April-September timeframe -- that is 4 years after the start of our study.

Okay. Sorry, Vijay. I thought that the Yervoy entry criteria stipulated that patients had to be chemo-naive.

No, treatment-naive. Look up the New England Journal of Medicine article. I'll send you the article. Both the studies, both the Roche-Lexicon drug was treatment-naive, and their study was treatment-naive.

Okay.

And the second-line therapy for Yervoy, which was for chemo-[refractive] patients, had a specific clause that patients who were enrolled in other studies where survival was the endpoint were not eligible to enter into those studies. So, neither of our chemotherapy drug or the Allovectin [on] from our study could have gotten in until after these drugs were approved. And those drugs were approved in April in the United States; September, October in Europe. Yervoy was only approved second-line therapy in Europe. So, that is 4 years after our study started. Remember, our last patient was recruited in the study in -- that's 2010. That means these drugs were approved almost 15 months after our last patient was recruited.

Okay.

And if you assume -- let me finish. Now you got me going here. Now, if you assume that the chemo patients die very quickly in the chemotherapy arm, and our study started in January 2007 -- so, a lot of our patients had progressed way before these drugs are approved, and went on to other therapies, okay? We don't have specific patient-by-patient determination of who got what.

Okay.

Does that answer your question?

Yes, thanks. And regarding your timelines, you mentioned that the OS event rate was lagging behind your expectations. Is it possible you could unblind the trial and give us the response rate data, while keeping the OS data blinded?

No, I don't think that's what is in the plans right now. Because remember, we -- our two-year follow-up on the response rate data completes in February of 2012, then we need a couple of months to clean up the data, then we have to adjudicate it. And that kind of brings you -- the adjudicated data is what you guys want to hear about -- and that brings you towards the end of second quarter. And we hope that at that point in time to have the survivor data also in hand, so we will announce them at the -- both of them at the same time. There is really no upside of announcing either of the data independently, because it leaves a lot of questions open. Okay? And plus, you don't want anybody to accuse us that we, by announcing data either way, that it's influencing our ability to wait longer for the survival data. So, we're going to be blinded from the data ourselves; that's our goal.

Okay. So, you could still provide us with OS data prior to hitting any -- the requisite number of events?

No, no. We will wait for the requisite number of events. We will not unblind the data until the requisite events -- and we will give you an idea in our February call, because -- though we are lagging behind, you don't know -- maybe it will catch up. And if it doesn't catch up, then we will have to give you our revised guidance at that point in time.

Okay, very good. 1 more quick question before I hop back. Do you have to prove to FDA that you are demonstrating expression of HLA-B7 or beta-2 microglobulin at all? Is that required?

We have done a lot of pre-clinical studies before, in animal models, where we have demonstrated that the [expression] levels have been proven. We have tumor (inaudible), we will be doing a mechanism study. But the FDA is not requiring it. But the mechanism study always helps. So, we have -- we'll be running all kinds of panels of the bloodwork where the patients are consented.

Okay. Thanks very much.

Nathan Cali, Noble Financial.

Just a quick question on the patient group in the Phase 3 study. You indicated that the overall survivor for these type patients is 7 to 11 months. Would it be that the profile of these patients being at healthier profile without the [HCL would remiss] and so forth? Compared to the Phase 2, it would have a higher rate of survival, on average. Could you talk about that a little bit?

We don't know -- if you look at all the -- this was a full disclosure on what data is out there. But if you look, the majority of the literature, it is between about 8 and 9 months. I don't know where -- I think it's the [Chapman] study -- I can send you the recently published data. We believe that 8 or 9 months is what chemo gets, and you would add about 2 plus months to it, it will be in the 11-month range for the kind of patients we are dealing with. That is our guess, and that is the assumption that we have made in our statistical calculations for our survival endpoint. But as you know, there is no specific data available for our patient population.

Okay. Thanks a lot for taking the question.

Ren Benjamin, Rodman & Renshaw.

Congratulations on the progress. Just a couple of quick questions. 1 is -- can you talk to us a little bit about the release specs for Allovectin? Is there a immunogenicity assay that is in place? And kind of talk a little bit about what that is?

There is always a potency assay, where to make sure -- what is known as the expression assay, to make sure that the genes that you are encoding are actually expressed. It's a cell-based assay that we have been doing for a number of years, to make sure the (inaudible).

Have you ever encountered an issue where you have had to throw away batches? Or where the process that you have gone through, just given vaccines that aren't as potent? And do you have any idea of what that percentage might be?

I think we -- let me explain to you -- first of all, that is one of the beauty of [plasmid] manufacturing. [To be reproducible.] The lots are reproducible from lot to lot. We have not had any problems, to my knowledge, of us throwing out lots. We don't [share] big lots or anything like that, if that's what your question is. The potency assay has always worked, the expression of the plasmid in the transgene is a matter of routine.

Got it. Okay. And very quickly, for TransVax, have you gotten any more details regarding what the design of the Phase 3 might be? And how, either for the transplantations or the solid organs, what the design would be and how long it could take?

I think -- all I can tell you at this stage is that we are very intimately involved in active discussions with the agency in these weeks, as we are talking right now. And anything I would say would undermine the tone of our conversation, which has been very collaborative and productive at this stage.

Okay. And then, 1 final question. Any progress or thoughts on next steps for the influenza program?

Well, I don't know if you saw the article in the New York Times magazine section over the weekend on the anthrax program. If you have not read it, it's an interesting article that you can get. And also, Forbes has an article on the anthrax program, talking about companies who have depended on government contribution to take [a new] program or an anthrax program, going forward. That is not a win-win situation for a company. But investors are putting money, because really, there is not much money in the flu business.

And the only money in the flu business is if you can develop a vaccine where you can demonstrate efficacy, which is superior to the existing vaccines in people who are aged 60 and older. The problem is there is no regulatory pathway for doing it. And until there is such a regulatory pathway defined by the agency, we're not going to put our shareholders' money in jumping in a genetic flu business market, because not [only] are we going after [borrowed] money or Department of Defense money, because it 's a loss proposition.

So, we shouldn't be expecting anything more from this program. It seems --

Unless there is a big outbreak of bird flu or something, and the government decides they want to really now engage in new technologies and take the risk on their own mantle, as opposed to companies taking the risk -- I don't think at the present time, the program would be status quo. But remember, 1 of the goals of us doing the program was simply allowing us to get real human experience in 2 clinical trials, with Vaxfectin adjuvant, to make sure it's safe, well-tolerated, and that it enhances the expression levels that we see in humans. And that we have accomplished.

Okay. 1 last question for Vaxfectin. Clearly, the -- we've heard some very good news out there regarding GSK's malaria vaccine. Any thoughts regarding partnering, or moving that [vaccine] into much bigger indications?

The answer to that question is yes. We are working with a number of people right now. But as it turns out, every new company that wants to work on it wants to make sure it works in their models, in a long-term study, better than the old mousetrap that they have tested it against. And this takes a long time. In the development path, there's torches. But 1 of these days, this is going to come to fruition. I've always been saying that people have forgotten that this could be a very important value driver for the Company. Having said that, adjuvants are not approved. It's the product that is approved. So, Vaxfectin cannot be approved on its own; it has to be approved in combination with an antigen.

Right, right. Okay. Well, great. Thank you very much, and good luck.

Nicholas Bishop, Cowen and Company.

Mine is about R&D, looking forward. You've had some time now to digest the revised financial position through the new partnership. But I was wondering if you have any commentary on what your R&D plans in 2012 might be? You mentioned potentially an early clinical trial of HSV-2; is that what we should be thinking about? Or are there other programs you might work on?

We have 3 choices, which I have outlined. We haven't actually formally decided which one we will take; but we are leaning towards is HSV-2, obviously, because the data is pretty spectacular. But CyMVectin is another program which we are examining very carefully and debating internally, because the advantage of CyMVectin obviously is what? They are IND approved, ready to go. But with HSV, we'll have to do more pre-clinical work to get that IND filed and get it approved; so there are timing issues. However, the trial is a much more complex trial; so, we need to make sure that the target endpoints are properly defined. But if it's HSV-2, the endpoints are much easily achievable, or -- whether they are achievable, but they can be easily demonstrated.

The third option that we have is really embarking and taking an early risk and moving into head and neck cancer with Allovectin, which we have done or at least studied, which has shown some early [clinical] efficacy. And we can quickly go into the clinic with a program like that. So, those are the 3 programs we are looking at, and we, hopefully, in the coming months will tell you what our pathway is. But it is an excellent question.

Okay. And then, 1 second question -- I guess, financially, about the remaining milestones you have prior to commercial launch with that Astellas partnership -- the $95 million or so potential milestones. Just kind of, for modeling purposes, I wonder if you could give a little color on what events might lead to your realizing those milestones. For example, if TransVax were to be approved by the FDA between now and then, about what fraction of those milestones might you achieve, would you expect?

Well, these -- it's a great question, but some of those milestones, as to when they occur (inaudible) agreements. But logically, these milestones are spread over a variety of events, such as regulatory filing, regulatory approval -- those are the kinds that those milestones are. It would be unfair to give granularity, because of our confidential relationship with Astellas on those matter. So, you need to make some judgment calls on those.

Okay. Fair enough. Thank you very much.

Boris Peaker, Oppenheimer.

I just wanted to ask a question on some of the commercial perspective on Allovectin-7 -- specifically, as we look at your Phase 3 recruiting criteria, how do you believe that may impact the label, particularly the brain and liver [met] contraindication?

Obviously, the label would exclude patients with brain [mets] and liver mets when it's initially approved, unless we decide later on to go into a small study, which includes brain mets and liver mets, whether it's a Phase 2 study, and show that this drug indeed can make -- is some impact on its own, in combination with another drug. But the label definitely will include brain mets and liver mets patients.

I want to follow up in terms of epidemiology of melanoma, then -- what fraction of patients would that exclude?

I would say that of all the melanoma patients, about 30 to 35 patients would have a characteristic outlined in our study. Let me go the other way. So, about 65% of the patients would be excluded.

Okay, got it.

But it's still a huge number.

Got it. In terms of clinical practice, do you think physicians would inject only 1 lesion, or multiple lesions? And do you anticipate that to be -- a single-lesion injection to be a part of the labeling requirement, as well?

I think so. It will be. And I think physicians report to injecting a lesion, because it takes the guesswork out. Because remember, it is a 2 mg, 1 mg dose -- if they are going to start spreading injection between multiple lesions, you really have no idea what you will inject in each lesion. And if you start injecting more than 2 mg in multiple lesions, than you will pay a lot more money. So, they really -- the physicians generally like to pick a easily injectable target lesion, which they can access easily, and inject that.

So, I don't think, to my knowledge, unless we do a study to demonstrate that there is some advantage of injecting 2 mg or higher dose in multiple individual lesions has any benefit -- I think initially we inject it into single lesions. That's the feedback we are getting right now. But obviously, we are doing a market research study, which will continue to give us some more feedback in the coming months.

And if we look at the study where you have looked at single- versus multiple-lesion injections, where you decided to go with a single lesion with a single injection going forward, did you look at the mutational profile of the multiple-lesion injections to see if maybe the ones that -- where it did work -- or the one where it didn't work very well, both tumors were the same, or whether they were different?

I don't know the answer to that question. You are asking a very important technical question. I will ask Alan Engbring to go through the paper, to our oncologist, [Dmitry], and get back to you on that, okay?

Okay. Well, congratulations on the progress, and thank you for taking my questions.

At this time, we have no further questions. I would like to turn the call back over to Mr. Samant for any closing remarks.

Thank you for joining us on this call this morning. We look forward to seeing all of you in the near future. Thank you again.

Ladies and gentlemen, this concludes our conference for today. You may now disconnect.