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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's third quarter results and highlights. [Operator Instructions]I would now like to turn the meeting over to Mr. Pierre Labbe, Chief Financial Officer of IMV. Please go ahead, Mr. Labbe.
Thank you, Julie. Good morning, ladies and gentlemen. My name is Pierre Labbe and I'm CFO at IMV. I'm pleased to welcome you to our presentation of the biomarkers associated with observed clinical responses in patients with relapsed/refractory diffuse large B-cell lymphoma and treated with IMV's T-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 the SPiReL study. Dr. Berinstein will be presenting findings outlined in the abstract and poster 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 of Clinical Research; and our newly appointed Chief Business Officer, Andrew Hall.The call will be divided into 2 parts. And in the first part, we will present and explain the SITC data and it will be followed by a dedicated Q&A session. Afterwards, we will proceed with the 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 contain 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, the successful and timely completion of clinical trials, the receipt of all regulatory approval, 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 of 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.The press release, the MD&A, the consolidated financial statement, the abstract and poster presentation referred to on this call are all posted on IMV's website at imv-inc.com. If you wish to receive a copy of either of these documents, please do not hesitate to contact us.And finally, take note that we will take questions only from sell-side analysts. Doctors and other interested scientific parties are invited to listen to Dr. Berinstein's poster Q&A session through the SITC web platform. The poster number is 356 and will be presented later today from 04:50 to 05:20 P.M. Eastern Time and also on Saturday from 01:00 to 01:30 P.M. Eastern Time.I will now turn the call over to Fred. Fred?
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 conducted in 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 that this finding is really bringing us closer to an accelerated path to market in DLBCL.Before I turn the conference to Neil to present his 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 this 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?
Well, thank you very much, Fred. As the principal investigator of the SPiReL study, it is my honor to present to 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.Next slide, please. A single agent checkpoint inhibitors have limited activity and have not been approved in the relapsed and refractory diffuse large B-cell lymphoma population. And we have tested a novel combination immune therapy that includes DPX-Survivac, a novel T-cell activating therapy that generates targeted immune responses against the survivin tumor-associated antigen, pembrolizumab, a humanized monoclonal antibody checkpoint inhibitor binding to PD-1, and intermittent, metronomic low dose cyclophosphamide, an inhibitor of regulatory T-cells.Study treatment includes administering subcutaneous doses of DPX-Survivac, 0.5 ml doses 3 weeks apart, then 0.1 ml doses every 8 weeks. Subjects also received intermittent, low dose cyclophosphamide 50 milligrams twice daily for 7 days on and then 7 days off as an immune modulator. Pembrolizumab was administered as 200 milligrams intravenously every 3 weeks. Tumor biopsies were obtained pretreatment and once on treatment.Next slide, please. Subjects with relapsed and refractory and incurable diffuse large B-cell lymphoma with survivin expression are eligible for participation in the study. The primary endpoint is to document the objective response rate using modified chasm criteria for the combination treatment, looking for a minimum objective response rate of 6 of 25 patients or 25%. Secondary objectives and exploratory endpoints included T-cell response, tumor immune cell infiltration and biomarker identification. To-date, 24 of 25 subjects have been enrolled and the first 22 are described in this poster. The patient characteristics of the enrolled population is shown in this table, 6 have transformed disease, 7 refractory, they had a median of 2 previous treatments and 4 had previous autologous stem cell transplant.Next slide, please. As of the data cutoff for this abstract, 22 patients have been enrolled. 18 subjects with complete biomarker information have been included in the analysis for this presentation, 11 of whom are evaluable based upon the per protocol criteria having received 3 doses of DPX-Survivac, 4 doses of pembrolizumab and having completed the first on-treatment imaging assessment. The SPiReL study has reached its primary endpoint and we now have 7 subjects that have achieved an objective response; 3 of them with a complete response and 4 with a partial response.In addition, 3 other subjects have achieved stable disease. In all, subjects have demonstrated clinical benefit. We observed minimal toxicity with the majority of Grade 1 and Grade 2 adverse events related to the site of injection of DPX-Survivac, whereas most nonresponders with progressive disease progressed quickly and were not evaluable for protocol. We evaluated diverse biomarkers and immune infiltrates to potentially identify patients who are most likely to respond to this novel immune therapy.Next slide, please. We have performed analysis of baseline tumor biopsies with 18 of 19 subjects having a baseline sample available for analysis. The bar graph shown here demonstrates the baseline expression of different tumor immune cell infiltrates, CD8 positive cells, CD4 positive cells, PD-L1 positive cells and FoxP3 regulatory cells categorized based upon their clinical response, the lymphoma subtypes and the response status shown below the bar graph.In the figure, we can see the variation of PD-L1 expression in the pink or magenta bars in subjects with various clinical responses and a clear observation of the increased presence of PD-L1 in patients with a complete or partial response shown left of the red vertical dashed lines. Below the bar graph, we show photomicrographs of the actual multiplex IHC slides. You can see greater intensity of PD-L1 expression in the 3 samples on the right, all of which had clinical benefit or response from the treatment compared to the absent PD-L1 expression seen from the patient on the left who had progressive disease.Next slide, please. Interestingly and importantly, there is a statistically significant correlation documented between baseline PD-L1 expression assessed by multiplex IHC and clinical response as demonstrated here. All analyzed subjects who achieved a complete response or partial response on study expressed PD-L1 using a cutoff of greater than 10% by multiplex IHC analysis, making PD-L1 a possible predictive response using this combination immune therapy. Showing our results for PD-L1 expression on CD20 B-cells, figure A and B, and show PD-L1 for all cells in the tumor microenvironment, figure C and D. You can see the percent PD-L1 positive cells or a percent PD-L1 positive cells in total is significantly greater in patients with clinical response.Next slide, please. We have also demonstrated a statistically significant increase in survivin-specific T-cell responses when compared to baseline response with the best on-treatment response. As highlighted in Panel B, DPX-Survivac induced survivin-specific T-cell responses are observed in 100% of subjects with a complete response and 75% of subjects with a partial response, supporting the mechanism of action of DPX-Survivac.Next slide, please. In conclusion, the combination of immunotherapy with DPX-Survivac, pembrolizumab and low-dose cyclophosphamide induced clinical response and disease control in patients with relapsed and refractory diffuse large B-cell lymphoma. Clinical responses are associated with a higher baseline expression of PD-L1 and DPX-Survivac induced survivin-specific T-cell responses. The higher baseline expression of PD-L1 in tumors support PD-L1 as a potential predictor of response to this novel immunotherapy combination in relapsed and refractory diffuse large B-cell lymphoma. The association between PD-L1 expression on B-cells and induction of survivin-specific T-cellsurvivin-specific T-cell responses suggest a novel and important interactive immune mechanism of action.I'd like to thank you for your attention. I now turn the call over to Joanne.
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 so nicely presented and I'd outline IMV's next step in DLBCL.Next slide, please. To begin, this trial was initiated based on a hypothesis 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 this population. As shown here, checkpoint inhibitors have limited activity in relapsed/refractory DLBCL. We also know from these reported studies, that they do 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 have 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 in multiple indications. When we focus on the subject with PD-L1 positive tumors, we observed an objective response rate of 86%, which is in stark contrast to the lack of responses observed in the PD-L1 negative subset, suggesting that selecting subjects based on PD-L1 status might enrich for clinical responses to the senior oncology treatment regimen.Next slide, please. This figure has already been presented, but I think it's important to highlight it again. On the last slide, we showed the clinical responses correlated with baseline levels of PD-L1 and thus is supportive of the role of Keytruda as it has been demonstrated as a biomarker on other tumor types. However, the clinical responses also correlate to DPX-Survivac and survivin-specific T-cells, indicating that the induction of these cells is also a key component to the clinical responses that have been observed.On the next slide, we summarize in the top 3 rows of this table, recently approved therapies in DLBCL and their associated response rates. These response rates range from 30% to 63%, but these agents also demonstrated high rates of serious adverse events as well as discontinuations due to adverse events, hinting that the ongoing need for highly active, better tolerated therapies. For DPX-Survivac, cyclophosphamide and pembrolizumab, we have provided a range for objective response rates based on the larger intent-to-treat population with a response rate of 37% as well as the PD-L1 positive subset of that population with an objective response rate of 86%. Also noteworthy is the generally well-tolerated safety profile, which we believe will be a significant asset, especially in this older heavily treated population.Next slide, please. In summary, our data supports our hypothesis and our clinical path forward using this treatment combination. It's long been hypothesized by others that induction of tumor-specific T-cells would act in concert with PD-1 inhibition and that has been shown in multiple preclinical models, including our own. Now we have early clinical data indicating that a T-cell specific therapy in PD-1 inhibition can deliver on clinical benefit in a patient population.With that in mind, we're planning an IND sponsored Phase 2 study in relapsed/refractory DLBCL. We intend to use one of the approved companion diagnostics to select subjects with higher levels of PD-L1 expression in order to enrich for response. Based on our current data set, we anticipate that almost all of the subjects will be survivin positive, and around 30%, 40% will be classified as PD-L1 positive. We intend to focus on the smaller patient subset. This study will be designed to try to take advantage of an accelerated approval path, but we'd like to discuss such opportunities with the FDA. Therefore, we expect to have more details on the design in early 2021.In conclusion, we believe that DPX-Survivac will be demonstrated to have clinically meaningful activity in combination with cyclophosphamide and pembrolizumab and a PD-L1 positive population. And though our focus today has been on the promising SPiReL data, I'd also highlight that DPX-Survivac is a novel mechanism of action with unique target. Its well-tolerated safety profile, ease of care and lack of anticipated drug interactions, additional combinations are readily possible.So with that, I'd like to thank everyone for their attention and I'm going to turn the call over to Fred. Thank you.
Thank you very much, Neil and Joanne. Operator, we'll now take questions from the analysts.
[Operator Instructions] And your first question comes from the line of Jim Birchenough with Wells Fargo.
Congrats on the data. I guess a few questions for me. Just first, in terms of those patients that didn't achieve the 3 doses of DPX-Survivac and the 4 doses of pembro, what was the distribution between patients that did get adequate DPX-Survivac versus adequate pembro? And what was the reason that these patients weren't able to complete the doses?
Joanne, you want to answer this one?
Yes. Jim, thanks for the question. So in general, I think as Neil had presented, most of those patients had a more rapidly progressive disease. This was anticipated by the SPiReL team, which is why they were very careful about defining an evaluable population in this first exploratory study. I think, as you know, with the CAR-T therapies, bridging 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.
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 screen those patients out or perhaps deal with it with less advanced patients with less prior treatments?
Great question. And those are all those things that we are thinking about now as we're putting that design together. So we will have that. We do plan to have that conversation with FDA.
Okay. And then just one final question. What's the go-forward plan with Merck in 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?
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, discussions with Merck. So we're quite advanced in to those discussions and we'll update the market when we reach a point where we can talk about it.
And your next question comes from the line of Tom Shrader with BTIG.
Just fascinating data, is 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 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?
Tom, sorry, Dr. Berinstein had another commitment at Citi and couldn't stay for the question. But I'll start and will invite Joanne to summarize the discussion we had with him on this very positive, but also fascinating kind of surprising results 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 it is about -- the median level of response in PD-L1 positive patients is 30% to 40%. 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 they're 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 a way there. And by generating those T-cells -- those survivin-specific T-cells, we overcome that limitation and make PD-L1, bringing those PD-1 patients into categories of patients that have both PD-L1 inhibition and T-cells, so they can see responses.That being said, this is definitely is 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 the explanation of what's happening.Joanne, I don't know if you want to add something?
I think you touched upon the key points. 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. But as you said, it's really very intriguing and it's obviously showing great deal of clinical benefit in this subset of patients.
If I could ask one just 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 reeducate the immune system? Or is that -- is there just not enough data to make that differentiation yet?
Well, I think what we were expecting, and as you know, we are paying a lot of attention actually to the pharmacokinetic. We 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 pharmacokinetic could be slightly different than what it is from solid tumors, just because not only the time to generate the T-cells, but as you know, to reach out the tumor bed and go through the tumor macro environment and get to those tumor cells plus simply the distribution of the tumors are not in the blood. So it's a bit 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 shrinkages are really happening early on the study for the patients that make it to the first scan. And while in ovarian, it could take 6 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-Ts were using bridging chemotherapy. So the question that we had was how would we be able to incorporate that in developing a target population for DLBCL?And it looks like PD-L1 is a marker. Is it a marker because they are slowly progressing? Or if it's just -- it makes the product act faster in the tumor? I think those are questions we will try to answer.
And your next question comes from the line of Ted Tenthoff with Piper Sandler.
I wanted to try to 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 of how this would be applied in real world. And again, congrats on the data.
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 path 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 expand. So this is a top priority for us. So in terms of next step, we want to design this trial, like Joanne was saying, that we hope will be designed in a way that could support an extended approval. There's a lot of precedent, recent precedent in DLBCL. So we think it's an achievable goal.So we'll do that as fast as we can. When we have feedback from the FDA and we have agreements with them in the first quarter of '21, 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, again, as fast as we can.
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?
It's a good question. I will repeat what we said earlier. This is pretty recent data. So yes for sure. This is something that we believe has implications beyond DLBCL and how -- what we are finding in the blood cancer will translate into solid tumor and white differences might be there. This is actually something we are working on to look at what kind of learning we can have and what implication it has for the basket trial.
And your next question comes from the line of David Novak with Raymond James.
I'll echo everybody else, really interesting data here and we look forward to seeing how this plays out in a future prospective trial. I guess just on the current SPiReL study, a 2-parter question for you. We came across the 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 with an OR of 36% in a relatively larger sample set. And I guess, based on this, Merck is currently running its own Phase 2 evaluating pembro monotherapy in PD-L and amplified DLBCL patients.So looking at your data and seeing how the analysis here is post hoc and only includes a fairly small 7 patients in the PD-L1 positive cohort, what gives you guys the confidence that the result you're seeing here isn't entirely related to pembro alone? And further, are you all concerned with the lack of activity seen in the PD-L1 negative cohort, which I guess some could potentially interpret to suggest that DPX-Survivac may or not be conferring benefit by itself?
Just as a reminder, it's -- the study 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 high level of responses that we have combined to the fact that there are no responses without PD-L1 is statistically significant and different from what they have seen and what their plan are currently.On the PD-L1 negative nonresponders, we -- there's 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 1 in extensively described mutation in DLBCL, there are a number of patients that are -- that have 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 checkpoint 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 in DLBCL, there are more patients that have PD-1 over-expression coming from inflammatory condition in the tumor than from alteration because the level of alteration in DLBCL is very low.If you have a copy gain or amplification, it's a very small subset of patients that have that. But there's another important percentage of those patients that do have other expression coming from an inflammatory status. And so again, we are not looking at this data just timely, but there's a partner walking on this with us that have a lot of information around PD-L1 and the interpretation of the results.I don't know, Joanne, if you want to add something on this?
Yes. Thanks, Fred. Thanks for the question. I think I just want to also highlight, we do see the DPX-Survivac induced survivin-specific T-cells. 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 over-expression as compared to the gene amplification that's observed in DLBCL. So there seems to be something that is happening by providing these 2 therapies together. So 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 are each contributing to that response.
And your next question comes from the line of Joseph Pantginis with H.C. Wainwright.
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 patients that are PD-L1 positive that you don't see -- you seem to have survivin-specific T-cells, but you don't see responses. I was wondering, is there a threshold that you identified or you are looking to identify foreseeing responses.
Joanne, do you want to answer it now?
I'm sorry, Fred. So 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?
Yes.
Response -- a clinical response.
Yes, clinical response.
Okay. 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 PBMCs or the tumor biopsy. So ongoing research on that aspect of the equation.
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?
Yes. That one is, to me, sort of a little bit of a harder research question because this is one point in time, right, 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.
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 with your antibody, you have a positivity of around 39%, 40%. I was wondering if you have tested other antibodies. There is also companion diagnostics specific for Keytruda. And are you planning to use this clone moving forward?
So, yes, we are going to be looking at that so that we can do that bridging for ourselves.
Okay. So you -- just so I understand correctly, you are planning to use the one -- the antibody you have been using so far or the companion diagnostic for Keytruda?
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 2 so that we have a better understanding of how to choose that cutoff and threshold.
And there are no further questions at this time.
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 2 new members who with their experience and network will surely add 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 medicines 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 a 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 life sciences. His career 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 option of the call, I will only review our other recent corporate milestones. Let me start first with our Phase II, DeCidE1 study in advanced ovarian cancer. We will be presenting top line data in a KOL event scheduled for December 3rd. 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 through our plan to initiate a combined Phase 1/2 clinical trial in Canada by the end of the year. And we have so far secured up to CAD 10 million to fund the entire program and development efforts. And we've also applied for other non-dilutive funding request to continue to be funded for the further clinical development that we anticipate for this vaccine.On the manufacturing front, we've entered a collaboration with a global partner, and initiated transfer and scale up activities, and this collaboration has the potential to bring 2 additional production sites on top of what we have with capacity to produce several hundred million doses 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 30th, we had enrolled a total of 106 patients out of the planned 184. And that's across all the 5 indication. And we have different -- 19 different clinical sites in Canada, in the U.S. Unfortunately, the COVID-19 pandemic has continued to impact the speed of enrollment and we now project reporting the result in Q1 2021.On a final note, as a result of recent financial initiatives, we finished the quarter in a very strong financial position, which Pierre will further expand on later on the call. We are grateful for the extraordinary work and commitment of our employees and the continued support of our shareholders and partners. We look forward 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.
Thank you, Fred. As a reminder, all the numbers I will be discussing are in Canadian dollars. So as of September 30, 2020, IMV had cash and cash equivalents of CAD 54.7 million and a working cap of CAD 55.9 million. It is the best cash position the company has ever had. So it compares to CAD 14.1 million of cash at the end of 2019 and a working cap at that time of CAD 13.2 million. The increase in cash since the end of June is mainly explained by the gross proceeds of USD 24.5 million or CAD 33.2 million from the -- at the market facility and also by the exercise of warrants for CAD 2.3 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 12 months.And for the third quarter, we incurred a net and comprehensive loss of CAD 8.3 million or CAD 0.13 per share, which compares to a net loss and comprehensive loss of CAD 7.9 million or CAD 0.16 per share for the quarter ended September 30, 2019. This is mainly explained by the CAD 889,000 increase in R&D expenses for the quarter ended September 30, 2020 compared to 2019.The increase in R&D expenses reflects cost for preclinical development for the DPX-COVID-19 vaccine candidate, which is offset by an increase in government assessment towards the project. To a lesser extent, the increase in R&D cost is also attributable to higher personnel costs due to an increase in headcount. The increase in R&D expenses was partly offset by a decrease in travel and DPX-SurMAGE preclinical development costs as well as costs related to the DeCidE1 trial in patient with advanced recurrent ovarian cancer.The G&A expenses increased by CAD 1.1 million for the quarter ended September 30, 2020, compared to 2019. And the increase is mostly explained by higher insurance premium. And for the first 9 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 CAD 23.6 million. So as of November 11, 2020, 67.1 million shares were issued and a total of 4.5 million stock option, DSUs and warrants were outstanding.Finally, please note that our unaudited financial statement for the 3 and 9 months period ended September 30, 2020 and the related MD&A are available on SEDAR and on EDGAR.Thanks for your attention and I will now turn the call back over to Fred for his closing comments before the Q&A session.
Thank you, Pierre. As you can appreciate, we've recently made significant progress validating our platform, advancing our clinical assets and strengthening our balance sheet. We are especially excited. We have found that potential predictive biomarker associated with a very high level of clinical efficacy in patients with relapsed/refractory DLBCL. We believe our approach and treatment provides superior advantages with respect to efficacy, tolerability, toxicity profile and cost of means of patient care in this disease. It could also address an important unmet medical need for patients who have failed or are ineligible to clarity treatments.With respect to other clinical programs in oncology. We are looking forward to providing top line data from a Phase 2 monotherapy, beta stage ovarian cancer next December 3 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 our Phase 1/2 clinical trial for our vaccine candidates against COVID-19.As we continue making progress in our quest to deliver a new class of immunotherapy with improved 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 Instructions]. And your first question comes from the line of Jim Birchenough with Wells Fargo.
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 I guess the second part is just what's gating at this point in starting the Phase 1/2? And is it further discussions with Health Canada? And I guess, what's your level of insight into how timely that process will be?
So to answer the last part of your question, we are just completing the 2 studies that are required in Canada to initiate any clinical trial for COVID-19 vaccine, 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 those studies back in August. So we are very close to be completing those studies when we have all the documentation and the results will be to complete the package that we had with Health Canada and hopefully get a quick approval and then initiate the clinical study.As we'll be doing that, we'll also be completing the publication that -- of the preclinical results, including the results of the challenge study in particular study as part of the publication of what led the development of this vaccine into a clinical trial.
And so, Fred, do you request a formal meeting, presumably, virtually, but is there a formal meeting with Health Canada?
No, it's really been -- I have to say, the bar may be higher in Canada, but it's been a very cooperative process with them. It's a rolling process, really an ongoing discussions on their requirements. And so it's a bit less formal than, I would say, usual type of IND or CTA where we are in constant discussion and completing the file as we go. So there is no formal meeting before we can start just completing the file.
And then just maybe obvious, but I'd be interested in your thoughts on the Pfizer biotech data, the 90%, at least preliminary efficacy. A 90% reduction in risk of infections seems quite impressive. How do you view that in terms of implications for you guys? Would that ultimately help you size a smaller study on assuming a similar effect size? Does that create a barrier for you guys? How do you think about that?
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, is are the antibody levels in the blood a good correlates for protection. I think from what we are seeing from Pfizer result is even though its interim data, it seems to indicate that, yes, every vaccine in the world that 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 are 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 RV is that it's -- this prolonged exposition is closer to a natural infection and provide you a protection that could be much longer than what you had when you have a short exposure. So we're really focusing the clinical development and repeating the same data asset that we generated in RV, where we have more than one year of PIK antibody levels in the blood of patients. And I -- honestly, I have still yet to see another publication that's even close to that in terms of antibody levels in the blood.And we still strongly believe that if we repeat that data set, that the vaccine -- that this vaccine 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 a 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 are 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 others are doing. When they publish the full data set 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 think of things we couldn't do in our home clinical trials to highlight the differences. Sorry, it was a very long answer.
[Operator Instructions]. And your next question comes from the line of Eduardo Garcia with National Bank Financial.
Yes, I just wanted to have an idea how is the recruiting process evolving? Do you see like any improvement in particular for basket trial?
Well, it has been quite challenging to project the enrollment just because over the summer, there was -- I think we all have for a moment hope that COVID-19 would not -- I mean, there was an expectation that there might be a second wave, but the level of the second wave in the U.S., as you are all aware, I think it's way beyond -- in any way, it's way beyond what we were expecting. So the impact on the clinical site is quite significant. It's on a specific site. It could be different from one site 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.There's a lot of things that -- and we reported that before that we've put in place to make sure we could keep the full quality of the data set, very important for us. We want to make sure that when we reach a conclusion on the trial, there's nothing that was not done by the book because of the situation. So we've put in place a lot of ways to do a lot of the quality checks and all of that remotely, which is really the focus for us at this point.
Okay. And building on that, given all these headwinds faced while data collection and verification, do you expect like to redo any work? Do you think the data integrity has been impacted at all?
No, not really. This is where we -- and thanks to our clinical team. They are doing an amazing job. I think that's the most important part. You want to -- our 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 trials.
Okay. And one more question. Is there going to be any hold up with the data in terms of like with Health Canada if Health Canada will allow to release the information right away? Or how is that process going to be?
You mean related to COVID-19 to -- the COVID-19 vaccine?
Yes, sorry, yes, regarding the COVID-19 data.
Are you talking about the preclinical data or the clinical data?
The preclinical.
No, no, they don't know -- there's no reason for them to do that. So it's really for us to get the final complete results from those 2 studies and finalize the paper and submit it.
And there are no further questions at this time. I will turn the call back over to the presenters.
Thank you. Well, I just thank you all again for your time this morning. All the good questions, really appreciate it, and wish you a good day.
This concludes today's conference call. You may now disconnect.