IMV Inc.
Q3 2020 Earnings Call Transcript

Published: 12 Nov 2020

[Operator:]

Good morning, ladies and gentlemen, and welcome to the IMV's Presentation of Data on Relapsed Refractory DLBCL Treated with DPX-Survivac, Low Dose Cyclophosphamide and Pembrolizumab, which will be combined with the presentation of IMV third-quarter results and highlights. At this time, all lines are in a listen-only mode. After each presentation, there will be a question and answer session and instructions will be provided at that time in order to queue up for questions. I would now like to turn the meeting over to Mr. Pierre Labbé, Chief Financial Officer of IMV. Please, go ahead, Mr. Labbé.

[Pierre Labbé:]

Thank you, Julie. Good morning, ladies and gentlemen. My name is Pierre Labbé and I'm CFO at IMV. I'm pleased to welcome you to our presentation on the biomarkers associated with Oxford's clinical responses in patients with relapsed refractory diffuse large B-cell lymphoma and treated with IMVC cell therapy in combination with Keytruda. This presentation will be followed by our third quarter 2020 results presentation. We have the pleasure today to be joined by Dr. Neil Berinstein, Hematologist and Affiliate Scientist at the Sunnybrook Institute and Principal Investigator of this SPiReL Study. Dr. Berinstein We'll be presenting findings outlined in the abstract and post-presentation made this week at the SITC Conference. From IMV, you will also have Fred Ors, our CEO; Joanne Schindler, our Chief Medical Officer; Stephan Fiset, our VP Clinical Research and our newly appointed Chief Business Officer, Andrew Hall. The call will be divided into two parts. And in the first part, we will present and explain the CT data, and it will be followed by a dedicated Q&A Session. Afterwards, we will proceed with a review of our third quarter highlights that will also be followed by a Q&A session. Before we begin, I would like to remind you that except for historical information, this audio presentation and webcast contains forward-looking statements, which reflects IMV's current expectations about future events. These forward-looking statements involve known and unknown risks and uncertainties that could cause IMV's actual results to differ materially from these statements. These risks and uncertainties include, but are not limited to our ability to access capital, successful and timely completion of clinical trials, the receipt of all regulatory approvals, and other risks detailed from time-to-time in our ongoing quarterly filings and in our annual information form. The forward-looking statements made on this call are based on several assumptions which may prove incorrect and they represent views only as at the date of this call and are presented for the purpose of assisting potential investors in understanding IMV's business and may not be appropriate for other purposes. IMV does not undertake to update forward-looking statements, whether written or oral, that may be made from time to time by or on its behalf except as required under applicable securities law. Investors are cautioned not to rely on these forward-looking statements and are encouraged to read IMV's continuous disclosure documents, including its current annual information form as well as its annual financial statements which are available on SEDAR and on EDGAR.

[Frederic Ors:]

Thank you, Pierre, and good morning, everyone. I hope you and your families are all doing well. Welcome to the first section of this call where Dr. Berinstein and Dr. Schindler will present the results of biomarker analysis and dictating the SPiReL study in diffuse large B-cell lymphoma. We are extremely happy with these results. This was an important goal of our clinical development strategy as we believe that understanding of the mechanism of action and being able to precisely define the target population is the key for the success of late-stage clinical trials in oncology. PD-L1 is a well-recognized biomarker, it's approved for multiple cancer indication, and we believe - excuse me, that this finding is really bringing us closer to an excellent best to market in DLBCL. Before I turn the conference to Neil to present these key findings, I would really like to take this opportunity to congratulate him and his team at the Sunnybrook Institute for the great work and the commitment to the success of the study, which has already met its primary endpoint, as we announced earlier this year. Without further delay, I will turn the conference over to him. But please take note that due to other commitments, Dr. Berinstein won't be able to stay for the question period. Neil?

[Neil Berinstein:]

Well, thank you very much, Fred. As the principal investigator of the SPiReL study, it is my honor to present you the poster that is being presented this week during the SITC Annual Meeting. I'm starting off on Slide 5, which shows that relapsed and refractory diffuse large B-cell lymphoma is an unmet medical need. CAR-T cells are promising, but this treatment is not easily accessible and cannot be considered for many patients because of its toxicity profile and because of the comorbid illnesses of many of these patients. Novel approaches to control this clinical dilemma are required to fill this medical gap.

[Joanne Schindler:]

Thank you, Dr. Berinstein for walking us through the data. I'd also like to extend my thanks to your great research staff at Sunnybrook, as well as the entire SPiReL team. In the next few minutes, I would like to provide some additional context to the data that Dr. Berinstein has nicely presented and outline IMV's next step in DLBCL. Next slide, please. To begin, this trial was initiated based on a positive that there was a significant unmet need in this patient population. And preliminary studies indicated that neither Keytruda nor DPX-Survivac treatment alone would likely be sufficient to achieve the strong clinical responses urgently required in the population. As shown here, checkpoint inhibitors have limited activity in relapsed refractory DLBCL. We also know from these reported studies that there does not seem to be a correlation with PD-L1 expression and response. In the SPiReL study, patients were chosen based on the expression of survivin within the tumors. Clinically, what we've seen is that more subjects have a significant clinical benefit to the combination treatment than we would expect, which is exactly what we had hypothesized. Next slide. Additionally, a key goal of our development program is to identify biomarkers that might help us to better understand how to optimize clinical activity. In this case, we've identified PD-L1 as a potential biomarker response to the combination of DPX-Survivac, low dose cyclophosphamide and Pembrolizumab. PD-L1 is a well-known biomarker that uses companion diagnostics and multiple indications. When we focus on the subject with PD-L1 positive tumors, we observe an objective response rate of 86%, which is in stark contrast to the lack of responses observed in the PD-L1 negative subsets, suggesting that selecting subjects based on PD-L1 status might enrich the clinical responses to this immuno-oncology treatment regimen.

[Frederic Ors:]

Thank you, operator. We'll now continue with a review of our Q3 financial results and other ongoing clinical activities. Before I continue, I first would like to welcome to IMV two new members. We're sure their experience and network will surely have tremendous value to our existing team. At the Board level, I'll start by welcoming Michael Bailey who currently serves as President and Chief Executive Officer at Aveo Oncology, another NASDAQ listed company seeking to advance targeted medicine for oncology and other unmet medical needs. Michael brings more than 20 years of experience in the industry, including business development, product launch, sales and strategy planning. And I also welcome to IMV's management team Andrew Hall, who will act as the new Chief Business Officer and be responsible for all business development and commercial initiatives for IMV's pipeline. Andrew joins us with more than 20 years of executive experience in biopharma and licenses. His carrier has been focused on corporate and portfolio strategy, business development and commercial operations, with industry leaders such as Celgene, Merck, Schering-Plough and Bristol Myers Squibb. Since we already covered DLBCL extensively in the first portion of the call, I will only review our other recent corporate milestones. /let me start first with our Phase 2 DeCidE1 study in advanced ovarian cancer. We will be presenting subline data in KOL event, scheduled for December 3. We'll shortly issue a press release providing the details and you will be able to register for the webcast through IMV's website. With respect to the development of our COVID-19 vaccine candidate, we continue to make progress to our plan to initiate a combined Phase 1 and 2 clinical trial in Canada by the end of the year. And we have so far secured up to $10 million to farm the entire program and development efforts. And we've also applied for the non-diluted funding request to continue to be funded for the further clinical development that we anticipate for the vaccine. On the manufacturing front, we've entered collaboration with a global partner and initiated transfer and scale up activities. And this collaboration has the potential to bring two additional production sites on top of what we have, with capacity to produce several hundred million dollars of DPX-COVID-19. In the context of recent advancement and the global landscape in COVID-19 vaccines, we continue to believe our approach is highly differentiated and has the potential to improve the duration of protection, and protection in the elderly and other more vulnerable populations. Finally, on our Phase 2 Basket trial, in multiple advanced metastatic solid tumors, as of October 30, we had enrolled a total of 106 patients out of the planned 184. And that's across all the five indication. And we have 19 different clinical sites in Canada in the US. Unfortunately, the COVID-19 pandemic has continued to impact the speed of enrollment. And we now project - reporting the results in Q1 2021. On a final note, as the results of recent financial initiatives, we finished the quarter in a very strong financial position which Pierre will further expand later on the call. We are grateful for the extraordinary work and commitment of our employees and the continued support to our shareholders and partners. We look forward to working closely with them as we continue to deliver on our great opportunities. And this concludes my comments. I will now turn the conference over to Pierre for a review of our financials.

[Pierre Labbé:]

Thank you, Fred. As a reminder, all the numbers that we'll be discussing are in Canadian dollars. So as of September 30 2020, IMV's cash and cash equivalents of CAD54.7 million, and the working cap of CAD55.9 million is the best cash position the company has ever had. So, it compares to CAD14.1 million cash at the end of 2019, and the working cap at that time of CAD13.2 million. The increase in cash since the end of June is mainly explained by the gross proceeds of $24.5 million US or CAR33.2 million from the At-The-Market facility and also by or CAD2.3 million. So based on our current plan, we expect that the current cash position will be sufficient on the operation for more than the next fund . And for the third quarter, we incurred a net incomprehensive loss of CAD8.3 million or CAD0.13 per share, which compares to a net loss and comprehensive loss of CAD7.9 million or CAD0.16 cents per share for the quarter ended September 30, 2019. This is mainly explained by the CAD889,000 increase in R&D expenses for the quarter ended September 30, 2020, compared to 2019. Increase in R&D expenses reflects costs for preclinical development for DPX-COVID-19 vaccine candidate, which is offset by an increase in government assistance towards approaching. To a lesser extent the increase in R&D cost is also attributable to higher personnel costs due to an increase in that gap. The increase in R&D expenses was partly offset by a decrease in travel and DPX development costs, as well as cost related to the DeCidE1 trial in patients with evidence-recurrent ovarian cancer. The G&A expenses increased by CAD1.1 million for the quarter ended September 30, 2020, compared to 2019. And the increase is mostly explained by higher insurance premiums. And for the first nine months of the 2020, our cash burn rate, which is defined as the net loss for the period adjusted for operations not involving cash, was CAD23.6 million. So as of November 11, 2020, 67.1 million shares were issued, and a total of 4.5 million stock options units and warrants were outstanding. Finally, please note that our non-audited financial statements for the three- and nine-months period ended September 30, 2020, and the related MD&A are available on SEDAR and EDGAR. Thanks for your attention. And I will now turn the call back over to Fred Ors for his closing comments before the Q&A session.

[Frederic Ors:]

Thank you, Pierre. As you can appreciate, we've recently made significant progress validating your platform, advancing your critical assets and controlling our balance sheet. We are especially excited we have found a potential predictive biomarker associated with a very high level of clinical efficacy in patients with relapsed refractory DLBCL. We believe our approach in treatment provides superior advantages with respect to efficacy, tolerability, toxicity profile and custom ease of patient care in this disease. It could also address an important unmet medical need for patients who have failed or have negligible to palsy treatments. With respect to other clinical programs in oncology, we're looking forward to providing top line data from Phase 2 monotherapy in recurrent ovarian cancer next December, and about our ongoing Basket trial with Merck in the first quarter of 2021. Before the end of the year, we also expect to initiate with Phase 1, 2 clinical trial for our vaccine candidates against COVID-19. And we continue making progress in our quest to deliver a new class of immunotherapy which improves outcomes for patients. We are grateful for the continued support of all stakeholders, doctors, shareholders and employees. And thank you for your attention. Operator, we are now ready to take questions.

[Operator:]

Thank you. And your first question comes from the line of Jim Birchenough with Wells Fargo. Please go ahead.

[JimBirchenough:]

Hi, guys. Congrats on the data. I guess the quest - a few questions from me. Just first, in terms of those patients that didn't achieve the three doses of DPX-Survivac and the four doses of pembro, what was the distribution between patients that didn't get adequate DPX-Survivac versus adequate pembro and what was the reason that these patients weren't able to complete the doses?

[Frederic Ors:]

Joanne? You want to answer this one?

[JoanneSchindler:]

Yes. Hi, Jim. Thanks for the question. So in general, I think as Neil had presented, most of those patients had a more rapidly progressive disease. And this was anticipated by the SPiReL team, which is why they were very careful about defining an invaluable population in this first exploratory study. I think, as you know, with the CAR-T therapies, therapies are often used for the very rapid progressive disease. But I'd also highlight here that with those subjects that we've now found to be the PD-L1 positive, it obviously controlled the disease quite readily. And there's where we're seeing that high positive rate of response.

[JimBirchenough:]

And so that sort of leads into my second question, and when you talk to FDA, would you bring up the topic of having a bridging therapy before initiating DPX-Survivac or some way to handle the rapid progressors? Or would you would you screen those patients out? Or perhaps deal with it with less advanced patients with less prior treatments?

[JoanneSchindler:]

Great question. And those are all the things that we're thinking about now as we're putting that design together. So we will have that - we do plan to have that conversation with FDA.

[JimBirchenough:]

And then just one final question, what - what's the go-forward plan with Merck and getting supply locked up for a pivotal or maybe getting more than that in terms of their contribution? Have you shared the results with them? And any sense of where that relationship might go?

[Frederic Ors:]

Sure, Jim, we, obviously, as we are planning to propose a design to the FDA very soon, we had to anticipate that and have started, some time ago, discussion with Merck, so we're quite advance into those discussions. And we'll update the market when we reach a point where we can talk about it.

[JimBirchenough:]

Terrific. Well, congrats again on the data.

[Frederic Ors:]

Thank you.

[Operator:]

Your next question comes from the line of Tom Shrader with BTIG. Please go ahead.

[TomShrader:]

Thank you, everybody. It's just fascinating data. It's a lot of fun to think about. As you think of this - and I guess this is for Dr. Berinstein. As you think about this response, do you think PD-L1 is a marker for the - for tumors where there's time for DPX-Survivin to work, or is it part of the mechanism? Is there any data to tease that out?

[Frederic Ors:]

Hi, Tom. Sorry, Dr. Berinstein had another commitment at SITC and could not wait for the question. But I'll stop and we'll invite Joanne to summarize the discussions we had with him on this very positive, but also fascinating and kind of surprising results - result that we have based on the literature that is out there on checkpoint inhibitors where they didn't find really any strong correlation with expression of PD-L1. If you look at the checkpoint inhibitors globally in different indications, I think there's about - the median level of response in PD-L1 positive patient is 30 to 40 person. So it's not like PD-L1 is an absolute biomarker, even though it's the target. It's certainly a very good biomarker to enrich the responses. But there is still a significant number of patients that are PD-L1 positive but are not responding. So there's something missing here. And what we believe that is missing, like Joanne was highlighting. Is that the T-cells are also required; not only PD-L1 inhibition, but you actually need the T-cells. And in some patients, for some reasons, T-cells are not the way they are. And by generating those T-cells, those survivin specific T-cells, we overcome that limitation and make PD-L1 bring those PD-1 patient into categories of patients that have both PD-L1 inhibition and T-cells so they can see responses. That being said, this is definitely something we want to dig out more because we believe that there's an opportunity here with a better understanding of what's really happening to bring the combination of T-cell with checkpoint to another level in terms of understanding where it should be applied, what are the best patients and the best indication. So we have a plan to really go deeper and deeper on your explanation of what's happening. Joanne, I don't know if you want to add something.

[JoanneSchindler:]

Thanks, Fred. I think it touched upon the key points, is, we're continuing to look at this data set to better understand it and to dig deeper into that. And that would definitely be our plan moving forward to continue to better understand the mechanistic rationale behind this. It's - but as he said, it's really very intriguing and it's obviously showing a great deal of clinical benefit in a subset of patients.

[TomShrader:]

If I guess, one quick follow up. So there are some responses with just PD-1 and DLBCL, do you find your responses are slower to develop because you have the 10 days to re-educate the immune system? Or is that - it's just not enough data to make that differentiation yet?

[Frederic Ors:]

Well, I think, what we were expecting, and as you know, we are paying a lot of attention actually, to the pharmacokinetic. We do believe it's an important factor that has not been always studied in previous clinical trials with cancer vaccines and equivalent technology. So we really believe it's an important factor, and we pay a lot of attention to that. Our hypothesis when we went into DLBCL was that in blood cancer, the pharmacokinetics could be slightly different than what it is from solid tumors, just because not only the time to generate the T-cells, but the - to reach out tumor bed and go through the tumor microenvironment and get to those tumor cells. Plus simply the distribution of the tumors that are not in the blood, but to be different. So, we were expecting that DLBCL, we're hoping actually, that the immunotherapy would show a faster response pattern and we are seeing, if you look ovarian versus DLBCL, we - most of the responses, most of the tumor shrinkage is really happening early on the study for the patients that make it to the first scan. And why in ovarian it could take six months, even more sometime. So, there is really a difference. Nonetheless, all that being said, I think the - it was a challenge. We knew from the beginning that DLBCL is a very fast progressive disease, so - and we knew that CAR-T we were using bridging chemotherapy. So the question that we had was; I would be able to incorporate that in developing a target population for DLBCL. And it looks like PD-L1 is a marker. Is a marker because they are slowly progressing or it's just, it makes the product act faster in the tumor? I think those are questions we will try to answer.

[TomShrader:]

All right, fantastic. Thank you for answering some long-winded questions. Appreciate it.

[Frederic Ors:]

Thanks, Tom.

[Operator:]

Your next question comes from the line of Ted Tenthoff with Piper Sandler. Please go ahead.

[TedTenthoff:]

Good morning and thank you very much for the data, it was really interesting. I wanted to kind of get a sense for what next steps are, and really how this could be applied in the real world. Also, just kind of wondering if maybe even we get to a point where a fast progressor would maybe be someone who would move on to alternative therapy, but just trying to get a sense for how this would be applied to real world. And, again, congrats on the data.

[Frederic Ors:]

Thanks, Ted. So clearly, we - like I said at the beginning, we are very happy with the results because we believe it gives us a potential first pass to market for this technology. As you know, we have a platform. I won't go back into the details of the mechanism of action that we have, but it's a new mechanism of action. And in our business plan we really want to get first approval to validate the platform, and then use that as a foundation to really extend so this is a top priority for us. So in terms of next step we want to design trial, like Joanne was saying that we hope will be designed in a way that could support an extra approval. There's a lot of precedent - recent precedent in DLBCL, so we think it's an achievable goal. So we'll do that, fast as we can when we have feedback from the FDA and we have an agreement with them. In the first quarter of 2021, we will report back on the design of the trial, and I think it's going to give a lot of clarity for the company on this path to market, the size of the trial, the design, what's going to be the primary and secondary endpoints. And, really, it's going to be an important focus going forward, to find ways to make sure we can enroll patients quickly and get to the endpoint as fast as we can.

[Ted Tenthoff:]

I think that all makes a lot of sense. And again, the relative ease and safety of this regimen really makes a lot of sense. One last quick one, if I may, and this may be obvious, but what are the implications for the solid tumor basket study? And I have to imagine that you're looking at this there, as well. Have you seen any correlation into solid tumors? Thanks.

[FredericOrs:]

A good question. I will repeat what we said earlier, this is pretty recent data. So, for sure, this is something that we believe adds implication beyond DLBCL. And what we are finding in the blood cancer was translating to a solid tumor and what differences might be there, we can't say something, we are walking on to look at what kind of learning we can have, and what implications it has for the for the Basket trial.

[Ted Tenthoff:]

Great, excellent. Thanks.

[Operator:]

And your next question comes from the line of David Novak with Raymond James, please go ahead.

[DavidNovak:]

Good morning, and thanks for taking my questions. I'll echo everybody else, really interesting data here and we look forward to seeing how this plays out in a future prospective trial. And I guess just on the current SPiReL study, a two-part question for you. We came across a study published in JCO, which suggests that DLBCL patients with PD-L1 gene amplification seems to actually respond fairly good to PD-1, specifically opdivo monotherapy within ORR 36% in a relatively larger sample set. I guess based on this Merck is currently running its own Phase 2 evaluating pembro-monotherapy in PD-L gene amplified DLBCL patients. So, looking at your data and seeing how the analysis here is post hoc, it only includes a fairly small seven patients in the PD-L1 positive cohort, what gives you the confidence that the result you're seeing here isn't entirely related to pembro alone? And further, are you at all concerned with the lack of activities seen in the PD-L1 negative cohort, which I guess some could potentially interpret to suggest that DPX-Survivac may not be conferring benefit by itself?

[FredericOrs:]

Thanks, David. Just as a reminder, the studies is done in collaboration with Merck. So, we are not making decisions alone on the interpretation of the results. And, obviously, Merck has a lot more information than what is published and that we have access to in terms of PD-L1 correlation in DLBCL. And so, we are very confident that the highest level of responses that we have combined with the fact that there are no responses without PD-L1 is statistically significant and different from what they have seen and what their plans are currently. On the PD-L1 negative non-responders, we did a lot of science around immune evasion and immune escape, and there's been a lot of studies around those things. And things like MHC Class I in extensively described mutation in DLBCL. There are a number of patients that are having an immune condition in the tumor that makes immunotherapy impossible to work with. And so, the results that we have are not surprising at all. PD-L1 is a biomarker not only for checkpoint inhibitors, but it's the most important check-pointing inhibitor of our immune system, generally speaking. It's a marker of an immune activity. And it's not only - it's not always only a question of genomic alteration in the PD-L1 receptor, but there's also actually DLBCL. There are more patients that have PD-L1 overexpression coming from inflammatory condition in the tumor than from alteration, which is the level of adoration in DLBCL is very low. If you have copy, gain or amplification, it's a very small subset of patients that have that. But there's another important percentage of the patients that do have overexpression coming from an inflammatory status. So, again, we are not looking at this data just timely, but there's a partner walking on these rivets that have a lot of inflammation around PD-L1 and the interpretation of the results. I don't know, Joanne, if you want to add something to this?

[JoanneSchindler:]

Yes. Thanks for the question. I think I just want to also highlight, we do see the DPX-Survivac induced survivin-specific T-cell. So we definitely do believe that DPX-Survivac is bringing that added effect, which is what we believe is changing the results that have been seen previously in terms of the PD-L1 overexpression, as compared to the gene amplification that's observed in DLBCL. So there seems to be something that is happening by providing these two therapies together. I think that's why we have confidence in this data set. We've identified a population of patients that respond quite well, and it seems to involve the individual components of each contributing to that response.

[DavidNovak:]

Great, thank you very much, folks. I'll hop back in the queue.

[Operator:]

And your next question comes from the line of Joe Pantginis with H.C. Wainwright, please go ahead.

[Unidentified Analyst:]

Good morning. This is actually Emanuela calling for Joe. Well, congratulations on the results, these are very exciting. I guess you answered partially to one of my questions. But I wonder if you can tell us a little bit more about those stations that are PD-L1 positive that you don't see - you seem to have survivin-specific T-cells, but you didn't see responses. I was wondering, is there a threshold that you identified or you're looking to identify for seeing responses? I just wanted to clarify the question. Are you referring to individual patients who might have had the T-cell response and didn't see a clinical response?

[JoanneSchindler:]

Just wanted to make sure I was answering the right question. I think in those cases, what we do know there are other factors that are involved in response. So we do see that response, but we need to better understand in that case why there might be some resistance. So that's ongoing work that we are doing, whether it be looking at PBMC or the tumor biopsy, so ongoing research on that aspect of the equation.

[Unidentified Analyst:]

Got it. And do you think there is a threshold you have to see of survivin-specific T-cells in order to be able to see clinical responses?

[JoanneSchindler:]

That one is, to me, a little bit of a harder research question, because this is one point in time that we take those samples. So, it would be very hard, I think, to dive into that, but it is certainly something we will look at. I just believe because you only take those samples at certain time points, it will be harder to necessarily see that.

[Unidentified Analyst:]

Got it, and also another question about the PD-L1 expression. So you also reported that there is a high variability in the literature regarding the reported PD-L1 expression in DLBCL, and this is possibly due to the variabilities in the clones that are used for detection, so, in your population and your antibody you have a positivity of around 39%, 40%. I was wondering if you have tested other antibodies, the results of companion diagnostics specific for Keytruda and are you planning to use these clones moving forward?

[JoanneSchindler:]

Yes. We are going to be looking at that, so that we can do that bridging for ourselves.

[Unidentified Analyst:]

Just so I understand correctly, you are planning to the antibody you have been using so far or the companion diagnostics?

[JoanneSchindler:]

No. Sorry, let me clarify, we plan on looking at both. So we anticipate that we'll move forward with one of the companion diagnostics that is already out there. So, we will look to compare the two, so that we have a better understanding of how to choose that cut-off and threshold.

[Unidentified Analyst:]

Thank you very much.

[Operator:]

And your first question comes online of Jim Birchenough with Wells Fargo. Please go ahead.

[JimBirchenough:]

Hi, thanks for taking the questions. So I guess a few on DPX-COVID-19, on the vaccine for COVID-19. Could you maybe give us an update on where you're at with publishing preclinical data, when you'll have a complete preclinical data set, including challenge study? And when we might all see that data? And then the second part is, what's gating at this point of starting the Phase 1/2, and with further discussions with Health Canada, and what's your level of insight into how timely that process will be?

[FredericOrs:]

Thank you, Jim. To answer the last part of your question, we are just completing the two studies that are required in Canada to initiate any clinical trial for COVID-19 vaccines, which are the typical studies that you would anticipate to have to complete for the development of a vaccine, which are toxicology studies and a challenge study. Like we said in an earlier release, we started the study back in August, so we're very close to be completing those studies, when we have all the documentation and the results will be to complete the package that we have with Health Canada, and optimally, get a quick approval and then initiate the clinical study. As we'll be doing that, we'll also be completing the publication of the preclinical results, including the results of the challenge study as part of the publication of what led the development of the vaccine into a clinical trial.

[JimBirchenough:]

And, Fred, you request a formal meeting, presumably, virtually, but is it a formal meeting in Canada?

[FredericOrs:]

No, it's really been - I have to say, the bar may be higher in Canada, but been a very cooperative process with them. It's a rolling process really, an ongoing discussion on the requirements. And so it's a bit less formal than I would say, a usual type of IND or CTA, where we are in constant discussion and completing the file as we go. So there's no formal meeting before we can start just completing the file.

[JimBirchenough:]

And then maybe obvious, but I'd be interested in your thoughts on the Pfizer biotech fate at the 90%, at least preliminary efficacy, a 90% reduction in risk of infection seems quite impressive. How do you view that in terms of implications for you, does that ultimately help you size a smaller study on assuming a similar effect size? Does that create a barrier for you? How do you think about that?

[FredericOrs:]

I don't think it creates a barrier with the information that's available at that stage. So one thing, I think one thing that's very encouraging, that was a big question in my mind, are the antibody levels in the blood a good correlates for protection? I think from what we're seeing considering those, even though it's interim data; it seems to indicate that, yes, every vaccine in the world that's in development can rely on that. So I think it is going to simplify, in a way, the clinical development of the other vaccines. What we're really focusing on is, because that's the fundamental value of this new technology that we have is prolonging the exposure of the antigen to the immune system. And what this does, what we have demonstrated with IV is that it's this prolonged exposition is closer to a natural infection and provides you a protection that could be much longer than what you have when you have a short exporter. So we really focusing the clinical development on repeating the same data set that we generated in IV where we have more than one year of peak antibody levels in the blood of patients. And, honestly, I've still yet to see another publication that see even close to that in terms of antibody levels in the blood. And we still strongly believe that it will repeat that data set, that the vaccine - that these vaccines will be uniquely positioned in terms of duration of protection. But the correlate of that is also the fact that, if you have a stronger and longer exposition, you can also improve the protection in the elderly, in patients with comorbidities, even in patients with cancer, for example, where we have a lot of data on the ability of the technology to generate strong immune responses. So, we're staying focused on the value of what we do, the differentiation of what we do, I would say independently at this stage of what the orders are doing, when the publishing of the fuller asset and we can take a look at the duration, because we don't have any idea of the duration yet. I think that's where we're going to be digging into this to maybe in our own clinical trials to highlight the differences.

[JimBirchenough:]

That's a very fulsome answer. Thanks, Fred.

[Operator:]

And your next question comes from the line of Eduardo Garcia with National Bank Financial, please go ahead.

[EduardoGarcia:]

Hi, thank you for taking my question. I just wanted to have an idea how is the recruiting process evolving, if you see any improvement particularly for Basket trial?

[FredericOrs:]

While it has been quite challenging to project the enrollment just because, over the summer there was - I think we all have for a moment hoped that COVID-19 would not - there was an expectation that there might be a second wave, but the level of the second wave in the US, as you are all aware, I think it's way beyond - it's way beyond what we were expecting. So, the impact on the clinical side is quite significant. It's on the specific side, it could be different from one side to the other, but generally speaking, some hospitals are very busy dealing with the influx of patients. So this is something we have to deal with, the things that --we reported that before what we put in place to make sure we could keep the full quality of the data set. It's very important for us, we want to make sure that whenever we reach conclusion on the trial, there's nothing that was not done by the book because of the situation. So we put in place a lot of ways to do a lot of the quality checks and all that remotely, which is really the focus for us at this point.

[EduardoGarcia:]

Okay, thank you for your answer. And building on that, even though all these headwinds, faithful data collection and verification, do you expect to redo any work, do you think the data integrity is being impacted at all?

[FredericOrs:]

Not really. This is where we - and thanks to our clinical team, they're doing an amazing job. I think that's the most important part, you want enrollment to be as fast as possible, of course, but nothing - it should not be at the cost of potentially creating a problem with the integrity of the data. So, again, everything we've put in place in the company was primarily focused on making sure we can maintain that level of quality and integrity of the clinical data across our clinical trial.

[EduardoGarcia:]

Okay. And one more question, is there going to be any holdup with the data in terms like we tell because then it will allow to release the information by the way or how is that process going to be?

[Frederic Ors:]

You mean related to COVID-19; to the COVID-19 vaccine?

[Eduardo Garcia:]

Yes, sorry. Regarding the COVID-19?

[Frederic Ors:]

Are you talking about the preclinical data or the clinical data?

[EduardoGarcia:]

The preclinical.

[FredericOrs:]

No, no, you know - they don't. There is no reason for them to do that. So they surely for us to get the final complete results from those two studies and finalize the paper and submit it.

[Eduardo Garcia:]

Okay, excellent. Thank you very much.

[Operator:]

And there are no further questions. At this time I will turn the call back over to the presenters.

[Frederic Ors:]

Thank you, all. I just - thank you, all, again for your time this morning. All the good…