Thank you, and good afternoon. My name is Jörn Aldag. I'm the Chief Executive Officer of HOOKIPA Pharma. With me in the room here are Igor Matushansky, our Global Head of Research and Development, Reinhard Kandera, the Chief Financial Officer, Christine Baker, our Chief Business Officer, and Matt Beck, Executive Director for Investor Relations. Thanks for joining us today. The purpose of this meeting is to provide an update and share our enthusiasm on the progress made across our clinical pipeline, in particular, the exciting data we generated in immune oncology. Next slide. This is our safe harbor statement. Next slide. Before getting into the data in greater detail, let me briefly set the stage on the value of our novel approach. In short, we see a world in which cancers can be chronically managed or even eradicated. We're using our novel arenavirus-based antigen delivery system to develop life-saving therapies. Our strategic focus is T cells, the ultimate tumor killing cells. This is where our arenavirus approach really differentiates from others. We develop products which activate and expand T cells to precisely kill tumor cells. We want to be best at priming tumor killing T cells systemically, and we demonstrate with our data that we are. We can do this on our own, and we can combine with other therapies when needed to maximize benefit for our patients. Next slide. Vectorized arenaviruses are particularly strong at priming and activating tumor target specific CD8 T cells. Every immune therapy needs T cells to do their job, and often immune therapies do not work because they lack T cells at the tumor site. Arenaviruses differ from other approaches in that they specifically home in on immune cells, not directly on cancer cells. The immune cells will then reprogram and expand naturally occurring T cells, and with that, direct a massive and very specific attack against the tumor target. With our clinical data, we have shown that this mechanism actually works. To our knowledge, there is no other systemic in vivo technology able to activate T cells as potently as arenaviruses do. Our clinical data also show that this massive attack leads to antitumor activity in many patients. Let's have a look at the key clinical learnings in our phase I study to date. Slide five. There's increasing evidence of the strength of our T-cell mechanism. The clinical data is consistently confirming that we generate T cell levels that are clearly differentiating. We see the T cells migrating into the tumor tissue TILs in half of the biopsied patients. We can increase the T cell responses. Indeed, the two-vector approach of HB-202/HB-201 shows more outliers and reaches antigen-specific T cell levels up to 40% of all T cells in circulation. Our data show antitumor activity as a monotherapy, a remarkable achievement for active immunization in advanced, heavily pre-treated metastatic cancer patients. Remarkable means as measured against any other approach we know of that attempts to treat heavily pre-treated HPV16-positive head and neck squamous cell carcinoma patients in monotherapy. In numbers, in more than 50% of our patients, we see tumor shrinkage. A 75% disease control rate is higher than what any other approach has shown in this particular patient population. Since ASCO, we've added one additional unconfirmed partial response and another near partial response that shows a 29% tumor shrinkage. We're also seeing that with HB-202/HB-201, we're now able to shrink large soft tissue lesions, not only lymph nodes. While we are proud of our monotherapy antitumor activity, we will work on optimizing clinical responses in combination with checkpoint inhibitors. We have selected the recommended phase II dose based on the fact that the highest dose tested for HB-201 is safe, without a further significant increase in T cells. As Igor will later show, there's early evidence that combining HB-200 with pembrolizumab is also feasible without any additional safety concerns. We have shown that it works in patients who have progressed on pembrolizumab and demonstrated that it can be synergistic with checkpoint inhibitors. Merck & Co. has agreed to a clinical collaboration to test the combination of HB-200 with checkpoint inhibitor pembro. In summary, we have moved HB-201 into phase II as we have met all our study objectives. Based on our clinical trial data, we believe that our technology gives a lot of hope to cancer patients in the head and neck cancer space and beyond head and neck cancer, across many other cancer indications. Over to Igor for a more detailed discussion of the data. Thank you, Jörn. Let's go to the next slide. To remind everyone, our HB-200 program focuses on the development of our HB-201 asset alone, which is a vectorized version of the LCMV arenavirus encoding E6, E7, the dominant antigen of HPV-16 positive tumors, as well as in combination with a second vectorized arenavirus, Pichinde, also encoding the same HPV-16 positive E6, E7 antigen. Preclinically, we have seen that alternating the two arenavirus vectors while keeping the target antigen the same results in higher tumor antigen specific CD8 T cell responses, as high as 50% compared to one vector approaches, and with that we saw increased efficacy. This phase I/II trial was designed to assess dose escalation, route of administration, tumor type selection, and schedule determination of our HB-200 assets. At ASCO, we presented data that led us to conclude that intravenous administration and Q3W dosing is preferable over other routes and schedules tested. Since then, we have focused our accruals on intravenous HB-201 and alternating intravenous HB-202/ HB-201 in advanced locally recurrent unresectable and/or metastatic HPV-16 positive solid tumors, with an emphasis on head and neck squamous cell carcinomas. Since ASCO, we have dosed an additional 24 patients. The primary study endpoint was a determination for recommended phase II dose. Secondary endpoints included safety, tolerability, anti-tumor activity. Exploratory endpoints included immunogenicity and pharmacodynamic markers. We will be discussing all these today. Next slide. As of the data cut-off listed, 62 patients have been dosed. 40 patients were dosed in the head and neck squamous cell carcinoma Q3W schedule. An additional 22 patients were dosed in cohorts dedicated to exploring other schedules, including every two weeks and/or intratumoral dosing and/or non-head and neck squamous cell carcinoma subtypes, and those will not be further discussed today. Of the 40 patients who were head and neck squamous cell carcinoma dosed in a Q3W schedule, 20 patients were treated with HB-201 alone, and 20 patients were treated with HB-202/HB-201 in an alternating manner. Of the 20 patients treated with HB-201 alone, 14 patients had at least one scan, and six of the 14 are still ongoing treatment at the time of the cut-off. Similarly, of the 20 patients treated with HB-202/HB-201 in alternating manner, 14 patients had at least one scan and seven patients are ongoing at time of the cut-off. As a reminder, all patients were generally heavily pre-treated with multiple prior metastatic lines of therapy, a median of three to be exact, and 88% had received a checkpoint inhibitor at least once during their treatment history. Next slide. Jörn already told you that we are a CD8 T cell company. Let us first focus our attention on the CD8 T cells. Next slide. Arenaviruses potently activate T cells, which are the backbone of cancer immunotherapy. As we all know, immunotherapy cannot work without functional antigen-specific T cells. An arenavirus technology drives these unprecedented T cell levels in order to kill tumor cells. Advance. HOOKIPA's T cell therapies can also be safely combined to enhance anti-tumor immune activity across a spectrum of tumor killing mechanisms. None of these other therapies can work if there is not adequate tumor antigen-specific CD8 T cells to start with, and that's what we do. Next slide. Let's get to the data. In terms of immunogenicity, we see that nearly all of our patients are able to mount a potent and rapid tumor antigen-specific T cell response following administration of our therapies. Furthermore, as you can see on the right, some of our patients are able to reach a maximum of 40% tumor antigen-specific response. This means that almost half of all of their CD8 T cells have been reprogrammed to focus on eradicating the tumor. If you look carefully at the majority of our patients, you can see that the majority are indeed attaining levels greater than 1%. For decades, it has been theorized that if a technology could ever consistently get patients to mount a CD8 T cell response that is this high, that should correspond to efficacy. However, no technology has ever been able to do this on a consistent basis before, perhaps until now. Next slide. Furthermore, while we are seeing this peripheral tumor antigen-specific CD8 T cells are not just high in the periphery, they're indeed able to penetrate into the tumor. Arguably, the best prognostic factor in the antigen-specific CD8 T cell space is the presence of tumor-infiltrating lymphocytes. We can see clearly how devoid of CD8 T cells these pretreatment biopsies are, as seen in the top panels, and how CD8 T cells are seen in purple not only infiltrate the tumor, as seen in the bottom histopathology pics, but wherever they do infiltrate, little tumor can be detected. This is very apparent on patient three, which is a core needle biopsy and shown at low magnification, so that the outline of the tumor can be seen and it's obvious how much little of the tumor remains and how the CD8 T cells just dominate the picture. We are seeing this clearly in 50% of all of our biopsies. Next slide. We believe that our arenaviral platform leads the field by a large distance in the CD8 T cell space. We do not make the statement lightly. We have performed an in-depth analysis comparing ourselves to other so-called CD8 T cell technologies and to the best of our abilities to compare often diverse data sets on the following five parameters. Immune response after first injection, percent antigen-specific T cells, resulting T cell polyfunctionality, T cell responses with no prior stimulation via ELISpot, and monotherapy efficacy. We conclude that our data is truly unprecedented. I will not belabor the slide, but encourage everyone to look at the data as referenced at the bottom of the slide and make their own conclusions. Next slide. Let us now speak to our safety data. Next slide. Overall, the HB-200 program exhibits a favorable safety profile. The vast majority, that is 92% of the patients that had less than grade 3 events, were either grade 1 or 2 and can broadly be characterized as low-grade fevers, malaise, fatigue, usually occurring 2 or 3 days after first administration and resolving shortly thereafter. In fact, there were only five non-grade 1 or 2 AEs, five grade 3 or higher AEs, in the entire 62 patients treated to date. There were three grade 3 AEs and two grade 4 events reported. One grade 3 anemia, one grade 3 arthritis reported, for which both were present at baseline prior to treatment. One grade 3 rash was reported, resulting in a dose reduction and rapid resolution of the rash. One grade 4 encephalopathy was reported, resulting in dose discontinuation. This case was further complicated by recent pembrolizumab administration, as well as concurrent hypercalcemia and pneumonia without laboratory evidence of viremia. Finally, one grade four elevated AST liver enzymes were reported concurrently with a grade three febrile neutropenia in a patient with known metastatic liver disease, which may actually suggest antitumor activity. Of note, no maximum tolerable dose has been reached for either HB-201 or HB-202/HB-201. Next slide. Turning our attention now to the efficacy data. Next slide. I remind you that we are going to focus on the 40 head and neck squamous cell carcinoma patients who received either HB-201, denoted by blue coloring, or HB-202, alternating with HB-201, denoted by red coloring throughout intravenously every three weeks. These patients have progressed, as I said before, in a median of three prior lines of therapy, including platinum and checkpoint inhibitors, and for the most part, have widespread metastatic disease and were actively progressing on their current treatments when they started HB-200 therapy. Focusing first on the 20-patient HB-201 data set, of which 14 patients had at least one scan. Next slide. This is the HB-201 data set. On the left, we see the swimmer's plot showing all 20 patients dosed. six patients are shown in grayed out bars as they either did not or have not as of yet reached a time point for efficacy evaluation. Of the 14 patients that are evaluable, we could see, comparing the lighter blue colors to the darker blue colors, which represent increasing dose levels, the higher dose levels, for which we have sufficient maturity, appear to stay on therapy longer. Looking at the right on the waterfall plot, we see that we have one confirmed PR, one unconfirmed PR, and an overall 71% disease control rate, with 50% of these advanced metastatic patients who have progressed on all standard of care treatments actually showing target tumor shrinkage. Next slide. Now I would like to focus on HB-202/HB-201 data set. Here we also have 20 patients dosed and 14 evaluable. This is the HB-202/HB-201 data. On the left, we see the swimmer's plot showing all 20 patients dosed. Again, six patients are shown in grayed out bars as they either did not or have not as of yet reached a time point for efficacy evaluation. Of the 14 patients evaluable, we could see comparing the lighter red colors to the darker red colors, which represent increasing dose levels, again, the higher dose levels to which we have sufficient maturity appear to stay on therapy longer. Looking at the right on the waterfall plot, we see that we have one near PR at 29% and still ongoing, with one unconfirmed PR at 31%. That patient is also ongoing. Overall, we see a 78% disease control rate with 57% of these advanced metastatic patients who have progressed on standard of care actually showing target tumor shrinkage. Next slide. Looking at this data strictly by the numbers, we see the following. An overall response rate of 14% for HB-201. Currently an overall response rate of 7% for HB-202, with patients ongoing and likely to convert and probably become a 14% shortly. Without further splitting the data for the moment, what we see is a blended disease control rate of 75% and a median progression-free survival of three and a half months. Let me again remind you, these patients have progressed on a median of three prior lines of therapy, including platinum and checkpoint inhibitors, and for the most part, have widespread metastatic disease who are progressing on all previous treatments. When you look at these numbers, it is important to put them in context. The response rate for nivolumab and pembrolizumab in earlier head and neck squamous cell carcinoma settings is 13% to18%. The median progression-free survival is two months. The fact that we are seeing objective responses as monotherapy in a post-CPI space with a median progression-free survival that appears to be longer than the median progression-free survival of checkpoint inhibitors in the earlier second line is quite telling of the strength of our data. Finally, not only is 75% disease control rate an extremely strong response in late-line solid tumor phase I programs, it is also quite unique in the HPV-16 positive immunotherapy space. Next slide. Again, we have looked carefully at the current HPV-16 literature. There are 35 trials targeting HPV-16 positive tumors in all stages, accounting for 32 therapeutic agents. 22 of these are in the metastatic setting. Of these 22, only 10 have ever released monotherapy data of any kind, which is a statement in and of itself. Six of the 10 that have released antitumor data, and four of the six actually included HPV-16 positive head and neck squamous cell carcinoma in their datasets. Likely, the other clinical trials that did not release data also included HPV-16 positive head and neck squamous cell carcinoma, but that data was never released. Looking more closely at the four that did release data and characterize them by technology, the list should not surprise you. As before, I will not belabor this comparison, but allow you to make your own conclusions. I will only say that for a long time, we have been saying that we are generating the kinds of tumor antigen specific CD8 T cell levels that have previously been only possible with TCR and never with active immunization. Well, now we feel that we are also beginning to show the kind of antitumor activity, especially when you look at the disease control rate, that is comparable to TCRs as well. Next slide. We have spent a lot of time talking about CD8 T cells and separately efficacy. Yes, we believe that we are attaining tumor antigen-specific CD8 T cell levels that were previously unattainable with active immunization and at which monotherapy efficacy was theorized to occur. Yes, we are seeing antitumor activity as evidenced by tumor shrinkage and objective response rates. However, is there a relationship between T cells and antitumor activity? The short answer is yes. However, it is not a simple yes. Currently, what I can say is that it is the kind of loose relationship that checkpoint inhibitors, specifically PD-L1 inhibitors like nivolumab and pembrolizumab, have with their intended target, PD-L1. We knew from the beginning, and now even more so, that the more PD-L1 is expressed on the tumor, the better checkpoint inhibitors have in terms of efficacy. The exact cut-off is not always straightforward, and a perfect linear relationship does not exist. Same here. We have enough confidence in our data to similarly conclude that more tumor antigen-specific CD8 T cells are preferable over lesser amounts for tumor control. It is not a perfect linear relationship. Our platform and its ability to generate these levels of antigen-specific CD8 T cells, as for the first time in the field, will begin to answer these questions. Next slide. Having looked at our data collectively, I would like to briefly reexamine the data for HB-201 and HB-202, alternating with HB-201 separately. If the 29% near PR who continues on therapy converts to a formal PR in the HB-202/HB-201, then the two datasets will look almost identical. However, the numbers may not do justice to the qualitative differences between these two assets. Next slide. Looking at the T cell data separately for HB-201 versus HB-202/HB-201, we see that on the whole, patients who receive HB-202 with HB-201 mount higher tumor antigen-specific CD8 T cell responses than HB-201 alone. This is something we predicted based on our preclinical modeling and something that we are now beginning to see clinically. I remind you, HB-202/HB-201 is still in dose escalation. Next slide. Furthermore, the quality of the responses we are seeing in patients treated with HB-201 versus HB-202 alternating with HB-201 are different. Looking at the left, we are showing you patients we have previously shown before, which demonstrate objective responses in target lesions in patients treated with HB-201. Note that while the percentage reductions are fairly large, the tumors being measured are in lymph nodes and are themselves relatively small. However, when looking at more recent data from patients treated with HB-202/HB-201, we see these patients are having reductions in large soft tissue lung metastases. This patient shown on the top had a baseball-sized mass in his lungs, which has now become a golf ball after one cycle of HB-202/HB-201 and is still ongoing. This other patient shown below had a golf ball-sized mass in his chest that has now become a marble following two cycles of HB-202/HB-201, and this patient is also still ongoing. These kinds of soft tissue responses were not observed in any HB-201 treated patients. These observations go along very nicely with the overall higher CD8 T cells being observed in the HB-202/HB-201 treated patients I showed you a moment ago. Again, HB-202/HB-201 is still in dose escalation. Now, these two patients are also important for other reasons on the right, and I'd like to spend a little bit more time discussing them in detail. Next slide, please. We are often asked about how previous usage of checkpoint inhibitors affects our responsiveness. In short, we have examined our data in relationship to previous usage of CPIs, time on CPIs, time in between CPIs, and starting our therapy, whether patients were primary refractory or became resistant to checkpoint inhibitors. In short, we see no obvious pattern. Take this patient as an example. After progressing quickly on pembrolizumab and then platinum-based chemotherapy, the patient was placed on a trial of pembrolizumab and another immunotherapy. On this pembrolizumab combination clinical trial, the patient actually had stable disease for 19 months until the multiple metastases in his lungs began to rapidly grow. One such rapidly progressing lesion is shown here on your left, circled in yellow. This patient was taken off the pembrolizumab combination clinical trial and started on our trial. We could see clearly that this baseball-sized lesion that progressed on pembrolizumab combination previously responded very quickly to just HB-202/HB-201. This patient is ongoing and demonstrates that lesions that do not respond to pembrolizumab respond quite quickly to our assets. Next slide. This next patient makes the previous point even more strongly. Here we see a patient who presented with metastatic lesions, with two lesions, one in his right lung, one in his left. Similarly to the previous patient, he started on a pembrolizumab-based clinical trial, a different one than previous patient. As could be seen, this lesion circled in green responds very nicely to the pembrolizumab combination clinical trial. The lesion circled in yellow progresses right through pembrolizumab, and the patient is taken off this pembrolizumab clinical trial and started our trial below. We can clearly see below in the two scans that this lesion in yellow that never responded to pembrolizumab combination clinical trial responds very quickly to HB-202/HB-201. Of course, at this point, we could only theorize what might have happened if our HB-202/HB-201 asset was given concurrently to this patient with pembrolizumab from the beginning. Next slide. What do we know about combining HB-201 and/or HB-202/HB-201 with pembrolizumab? At ESMO, we presented a case series of three patients from our ongoing clinical trial who were either clinically suspected and/or radiologically shown to progress on the HB-200 program and to whom investigators added pembrolizumab while still maintaining either HB-201 or HB-202/HB-201. As shown on the left, the addition of pembrolizumab while maintaining HB-201 and/or HB-202/HB-201 did not lead to any additional safety issues. In fact, in two patients, additional antitumor activity was seen. One such patient is shown here on the right. We could see that while overall the patient's tumor was stabilized on HB-201, comparing the baseline to the second scan, we could see that the patient was having skin breakdown at the tumor site. This patient had progressed twice previously before on pembrolizumab. However, now adding pembrolizumab on top of HB-201, as you'll clearly see, resulted in rapid tumor shrinkage and obvious clinical improvement. Next slide. Before going forward, let us please summarize what we have learned from our phase I data set. I remind you, we were in the recurrent metastatic population, patients having a median of three lines of prior therapy. What we saw in terms of safety and tolerability was a favorable tolerability profile with an overall low rate of treatment-related adverse events. No maximum tolerable dose was achieved for either HB-201 or HB-202. In terms of T-cell immunogenicity, overall, we showed that we are able to mount a very large unprecedented tumor antigen-specific CD8 T-cell response in all of our patients. The T cells that were induced are polyfunctional, which means they are fit to kill and are not exhausted. Furthermore, we clearly demonstrated that these CD8 T cells from the periphery are able to actually infiltrate the tumors, and when they do, show clear evidence of the fact they're able to kill those tumors. In terms of antitumor activity for the HB-201 asset, we showed a 71% disease control rate and 50% tumor shrinkage. For the HB-202/201, we showed a 78% disease control rate and 57% tumor shrinkage. Since ASCO, we have shown additional unconfirmed PR and additional near PR for the 202/201 group. Prior to ASCO, as presented at ASCO, we had three PRs and additional combination of a PR with pembrolizumab. Qualitatively, I think we've also shown you today that the responses we're seeing with HB-202 and HB-201 are better in terms of they are able to shrink soft tissue lesions as opposed to small lymph nodes with just HB-201. With that, we are seeing higher T cells in the HB-202/HB-201 group. With that, we are happy to announce that we are now progressing into phase II for the HB-201 asset. The recommended phase II dose for HB-201 has been determined. It will be dose level 3, given intravenously on a Q3W only basis. That decision was based on a combination of safety, efficacy, and CD8 T-cell levels, and also based on the fact that it's currently the highest dose that we are able to feasibly deliver to patients. Additionally, we have shown safety and combination antitumor activity with checkpoint inhibitors. Currently, as we are continuing following up on the efficacy of patients in dose level 3 for HB-201, we will be entering the phase II portion, and we'll continue dose escalation of HB-202/HB-201 for several more dose levels and make a recommended phase II dose for that grouping in the next several months. Once doing that, we are also gonna enter phase II with that group. Next slide. Well, based on everything I've said to date, we are indeed entering the phase II portion of our trial. Currently, we are entering just with HB-201 alone, since we haven't determined the recommended phase II dose. As HB-202/HB-201 completes its dose escalation, we will enter the phase II. If the data continues to be as strong for HB-202/HB-201 as it already is, and we're still in dose escalation, HB-202/HB-201 may supplant HB-201's position as the preferred pembrolizumab partner, but that is to be determined. Currently, however, we are opening both first line combinations and second line combinations with HB-201 and pembrolizumab alone or HB-201 and pembrolizumab plus chemotherapy, depending on the CPS. That is the PD-L1 levels in these patients in both the first line and the second line setting as indicated on the slide. We are also preparing for monotherapy in the more advanced head and neck squamous cell carcinoma settings, but we'll await the termination of the determination of the recommended phase II dose of HB-202/HB-201 before opening those groups. Please keep in mind, the response rate in the first line to pembrolizumab alone is only 22%, which means that 78% will not respond at all. There is a lot of room for improvement, and based on the quantity and quality of the antitumor activity we are seeing in the advanced setting, we are confident that we will be able to improve on it in the first line as well. Next slide, please. Well, we're not the only ones that are excited by this. As you know, Merck & Co have entered in a collaboration with us to run a large 280-patient randomized clinical trial of HPV-16-positive head and neck squamous cell carcinoma in the frontline, comparing pembrolizumab versus pembrolizumab and either HB-201 or HB-202/HB-201. The choice as to which asset to take forward in this trial is ours, and we'll make that determination in 2022 based on our ongoing phase II data in the frontline, with intent to start this randomized trial in early 2023. Next slide. Well, so far we have been very focused on our HPV-16, HB-200 program and for obvious reasons. However, building on HB-200 success, and I define that success as showing tumor antigen specific CD8 T cells at unprecedented levels with objective response rates in large soft tissue lesions, we are pushing forward to other immuno-oncology indications. Next slide. Specifically, for both self-antigens like PSA, PSMA, PAP of prostate cancer, as well as mutant antigens like mutant KRAS of colorectal, pancreatic, and lung cancer, we are pre-clinically generating similar extremely high levels of antigen-specific CD8 T cells, as we did for HB-200 program. With that, we are quite confident that our preclinical data will translate directly to patients, just like it did for the HB-200 program. The IND for the prostate program is scheduled for the second half of 2023. Next slide. With that, I would like now to turn this over back to Jörn for a brief summary and outlook. You have seen that indeed our oncology data are remarkable and things are falling in place. Because of the strength of this data, we decided to prioritize oncology and move forward our infectious disease programs only in partnership. Let me briefly summarize the second preliminary CMV data update and our conclusions. The CMV trial was a small randomized phase II program testing the efficacy of our CMV vaccine, HB-101, to prevent viremia in high-risk living donor kidney transplant patients when given prior to transplantation in comparison to placebo. Enrollment completed in June 2021. The final study report will be available in 2022 after completion of all 12 months patient follow-ups. Our second round of preliminary CMV data is consistent with the previous data, an acceptable safety and tolerability profile, strong immunogenicity, and a trend towards reductions in post-transplant viremia and the use of antivirals in patients who have received three doses. Given the many high-value opportunities we see in immuno-oncology, we decided to focus on oncology projects and to seek a partnership for further development of HB-101. Both Gilead programs, HPV and HIV, have successfully completed all preclinical activities. This is strong validation of our technology again. The HPV program passed the second request for development milestone recently and will move into the clinic late 2022 as a two-vector construct. Despite the successful conclusion of the preclinical research for the program, Gilead informed us that they plan not to progress the HIV program internally. We're currently in ongoing discussions with them over a revised collaboration agreement. Next slide. Going forward, we will focus our technology on therapeutic applications where the strength of our T-cell mechanism is most needed, in the cancer setting. Here's a look at our oncology pipeline. We will advance our ongoing head and neck cancer program with multiple readouts in 2022, first line and second line. We will get ready to initiate a randomized study in our collaboration with Merck & Co with pembro as a comparator. We will push our prostate cancer program to an IND in Q3 2022 and expand our pipeline to include HB-700, a new program targeting KRAS-mutated colorectal, pancreatic, and lung cancers. Next slide. To finish off our highlights, we have a clear focus on a validated novel platform that drives unmatched T-cell responses, many of which infiltrate tumors and are called TILs. TILs has often been called the holy grail of immunotherapy. We show antitumor activity as a monotherapy, a remarkable achievement for active immunization in advanced, heavily pretreated metastatic cancer patients. As we initiate combinations in phase II, the outlook for our combinatorial results is very strong, given the complementary mechanisms of action and our established monotherapy activity. We look forward to updating you on our combination data, showing a tolerable therapy with additive, if not synergistic efficacy. Thank you for participating in this. We'd be very happy to answer any questions that you have. Over to you. Thank you. As a reminder, to ask a question, you will need to press star one on your telephone. To withdraw your question, please press the pound key. Please stand by while we compile the Q&A roster. Your first question comes from the line of Vikram Purohit. Please ask your question. Good afternoon. This is Gospel on for Vikram. We have two questions. Regarding your oncology program, could you clarify that evaluation of HB-200 moving forward will only focus on combination use with a checkpoint inhibitor? In regard to the infectious disease program, could you clarify that your work with HB-101 has been paused now until you find a partner? Thank you. Igor. Yeah. Sorry. As you look, as I think a slide I showed where I talked about the phase II plans, I was quite clear that we will have a monotherapy in the third line, slide 32. The only question is, will it be HB202/201 or HB201 alone? We'll make that decision once we complete the dose escalation of HB202 and HB-201. As for the CMV, we are completing our phase II trial. It is not paused at all. The trial is completing its follow-up, and we'll complete that trial to the end. While that trial is being completed to its end, we will try to find appropriate partnership for this program. Thank you very much. Thank you. Your next question comes from the line of Brian Abrahams from RBC Capital Markets. Please ask your question. Hi. Good afternoon, and thank you for taking my questions, and thanks for the very comprehensive and complete update on the programs. A couple of questions from me on the 200 program. I guess, first off, I'm interested to learn more about what you're looking for from the evolving data set to guide your decision of whether to go forward with the HB-201/ HB-202 alternating versus HB-201 alone. I guess it looked like immunogenicity and disease control rate was maybe modestly better for the combination. At this point, so far, it looks like PFS, with the additional HB-201/ HB-202 patients, looks to continue to be around the three and a half-month time point. Is PFS going to be the primary driver, or are you looking for a wider delta on some of those measures? What are gonna be the key guiding things? I think it's clearly not one parameter we're looking at. We're looking at all the parameters, and we're trying to optimize all the parameters if we're making a formal decision as to absolutely what to take forward. I think I would. If you're asking me, you know, what are we looking for? We're looking to take our best asset forward, and we're trying to make a determination with a sufficient amount of data, which includes not just objective response rates, but durability and follow-up, as to what that is. I would say the data on HB-202/HB-201 is quote-unquote looking better, but that data, I would say, is less mature than HB-201 is. That program is about nine months behind the HB-201 program since it entered the clinic after HB-201. I guess I'm trying to say is, and I was pretty specific about this, that I'd like to wait till we actually have a recommended phase II dose for HB-202 and HB-201, and then compare the full dose escalation data set for HB-201 versus the full dose escalation set for HB-202/HB-201 and make that decision on the collective data set. I agree with your assessment. For the moment, HB-202/HB-201 looks better, but I'd like to have a little bit more maturity of that data set and make it upon completion of the HB-202/HB-201 dose escalation part of the trial. That decision will be round about January, February of 2022. Got it. That's really helpful. Bigger picture, I'm curious what you think is gonna be most important going forward to unlock even better antitumor activity and based on the high levels of polyfunctional antigen-specific T cells that you're seeing? Do you think maybe an earlier stage population may have less tumor fibrosis? A pembro combination may help further break tolerance. Might HPV antigen expression in the tumors themselves be a factor? I guess along those lines, I'm curious. I think you mentioned that patients the T cell levels loosely correlated to activity. Did patients with better tumor infiltration of those cells have better disease control versus those who did not? I would say that, you know, we have six paired biopsies. Out of the six paired biopsies, I would say the majority of those patients had stable disease. Given the fact that the majority of those patients had stable disease, it's hard for me to correlate whether or not there were responses based on the depth of infiltration. They were all radiologically stable. Okay. Got it. Just maybe one more quick one from me. In terms of the new unconfirmed response that you reported, when might we expect to see an update there? I guess what are the gating factors to a confirmation of that response? I'll hop back in the queue. Thanks again. I think publicly, we'll probably update the market, probably as to the status of the phase I program in mid-2022. At the update of the entire phase I program, which we do believe will be in mid-2022, as shown, I would say on slide 28. That is when you can expect 28. But that was our last slide, not 38. I'm sorry. The last slide of the deck. When we do the update on the kind of we call the monotherapy part in mid-2022 is when we'll be able to do a formal update on all of the patients in the phase I. That's when we'll update, not only this, but all the ongoing patients at the time. Great. Thanks again for taking my questions. Your next question comes from the line of Alec Stranahan from Bank of America. Please ask your question. Hey, guys. Thanks for taking our questions. A couple from me. First, could you just talk a bit more about the phase II dose selection for the KEYTRUDA combo study? I'm wondering if you had any additional comments around dose level 3 activity given you have the one patient from the phase I who had the PR after the combo as a reference point, but I think they were at dose level 1. So any other color there? As a follow-up to that, is your plan to make the larger randomized phase II registrational and maybe ORR or PFS? Although I believe you said it is open label, just trying to put an earmark on path to market for the asset. Yes, thank you. Matt, can you please go to the swimmer's plot? In the swimmer's plot, go to the blue right there. You can actually see, Alex, that we actually have shown which patients actually were combined with pembrolizumab by showing you the hatched marks. You can see that the two patients that got pembrolizumab in combination with HB-201 were actually at dose level 2. Although the monotherapy dose level for recommended phase II dose will be dose level 3, we will do a run-in at dose level 2. We start the combination with pembrolizumab, and if there are no safety concerns with the formal run-in of six patients, we'll go to dose level 3. Okay. Just on the registration intent of the Yeah. Sorry, the registration intent. Sorry, if you can go to that trial. That trial is formally not, I would say, presented as a registrational trial. It's got a combined endpoint of ORR with the ability to basically actually transfer the power of the ORR to the OS. In discussion with the FDA on this point, they said that this design is acceptable, that an ORR could be transferred to an OS. In which case, you know, if the data is there, we could potentially try to make it registrational, but that would depend on the strength of the data. Formally speaking, this trial is not intended as a registration trial. Okay. That's helpful. One more, if I may. Sort of on the time to response you're seeing with the HB-201, HB-202, I think the PR took about 150 days to occur, whereas I think the PRs with HB-201 alone occurred around day 90. Just curious as to sort of the slope of tumor reduction you're seeing, whether this matches, I guess what you'd expect given the preclinical and clinical observations to date? Thanks. Sorry, one second. Matt, can you go to the 221 for a second? You know, when you look at the responses, I would say, comparing you know, the two responders, you know, new responders to the HB-201, the unconfirmed PR occurs on the third scan. The 29% reduction occurs on the second scan. I would say that, you know, to the extent that I can compare HB-202/HB-201 to HB-201 alone, this does match the kinetics seen in the mice, in the sense that when we introduce the second vector, we need actually to get the boost in CD8 T cells. What you tend to see basically is that you have to wait till that second boost comes in from the CD8 T cells. It is possible that there is potentially a shift out by one cycle treatment in terms of the efficacy responses, but I wouldn't want to make too much out of two and two. In other words, what I'm trying to say is the numbers are really too small to make these comparisons here at the moment. It's something that I would watch, but I would not overread the initial data. Okay. Thanks, Igor. Very helpful. Your next question comes from the line of Asthika Goonewardene. Please ask your question. Hey, guys. Thanks for taking my question. A quick one to start us off, please. Apologies if I missed it. Can you tell us how many patients are you planning to recruit into each cohort of these phase II studies? I have a couple of follow-ups. Twenty. Lovely. Thank you. Can you sort of talk to us a little bit about yeah, I find the data where you've given patients pembro after the monotherapy to be quite interesting, as well as with the HB-200. Can you tell us a little bit about what drove the decision to give those patients the pembro? Maybe how you're planning on giving pembro to patients that are still on study that haven't progressed yet, particularly at DL 3 and DL 4 for HB-200, and then you have still a few more patients left on DL 3 on HB-201. The clinical trial has a provision in it that says patients who are either clinically or radiologically progressing on our HB-200 program, of course, clinical is a determination by the investigator, can basically continue HB-200 and add pembrolizumab on top. Those patients are no longer factored into any of our safety or efficacy analyses, but they are allowed in the protocol to be treated sort of as like one-offs, basically. If an investigator feels that there is, you know, progression, either clinical or radiological, they have the option, of course, of taking the patient off our trial and putting them on a different trial or give them a different treatment, or they could continue this patient on HB-200 and add pembrolizumab on top. This is an option for all of our patients, and to date, three patients have exercised that option. Igor, just related. Do you think that with the ongoing patients, given that this data's been presented now, that we're likely to see more of this, the more of these clinicians opting to give the combination on progression? I don't know. We've had the option open for quite a while. I would say I certainly hope so. You know, one of the things we are interested in studying is, you know, do patients who progress on our vectors get benefit if pembrolizumab is added? Vice versa, do patients who are progressing on pembrolizumab get benefit if we're added on top while pembrolizumab is continued? I would say I'm certainly hopeful that investigators will take the opportunity to exercise that option more often. Got it. Just very quickly, on the six patients where you do have paired biopsies, were you able to get biopsies on progression as well? And if so, wondering what you saw in terms of what the tumors expressed. I'm just wondering what might have been turning. I, uh- Helping turn these polyfunctional T cells off. Yes, that's a great question. Unfortunately, no. All the patients we were able to obtain are patients who were at least at stable disease. You know, if you look at our spider plots. We're not showing spider plots here, but if you look at our spider plots, the patients who progress, you know, we don't have many of them. We have a lot of stable disease for a prolonged period of time. True progressers, we don't have a lot of. You know, there were only a handful of patients that really progressed, you know, between, you know, at around the first scan. Many patients have stable disease. If they progress at the first scan, we don't even have the chance to get a biopsy because the biopsy happens afterwards. We don't have any data on patients who progress, just basically on patients who had stable disease. Got it. Thanks, guys. I'll jump back in the queue. Your next question comes from the line of Roy Buchanan from JMP Securities. Please ask your question. Hey, great. Thanks for taking the questions. I guess to start on the HB-200 again, just wanna make sure I'm totally clear on the phase II study design. So you've got the patients starting the HB-201 and pembro, et cetera. Then the green arrows go into the combo HB-202/HB-201 plus pembro. Are those the same patients starting on HB-201 then going to 202? No. Okay. Yeah, no. Great. Well, let me clarify. What I'm trying to say there is that we're gonna start HB-201 plus pembro now. Yeah. Sites are open. We're starting that now. You know, we're gonna get in the next couple of months, I would say, some safety and, you know, efficacy data for that combination. Yeah. Let's say in the next couple of months, you know, as you've heard the conversation goes, HB-202/HB-201 and monotherapy continues to look better and better. Yeah. What I'm gonna do is just basically add HB-202 on top. In other words, the next thing, I'm gonna stop recruiting into the HB-201 plus pembro alone and recruit only into the HB-202/HB-201 plus pembro. Yeah. what I'm trying to say is I'm gonna transition. Now it'll be different patients, but that box will transition. Right. Okay, that's what I thought. Just wanted to make sure. Back to the prior question, I guess. Is that gonna be 20 patients per the combined HB-201, HB-202. HB-201 is gonna be 20 patients, then 20 patients HB-201 and HB-202. To answer your question, I don't have a hard number on here there. We're looking at about 20 patients. I'd say if HB-202/HB-201 doesn't indeed look better at, you know, when the dose escalation is HB-201, we'll transition it and we may, you know, we'll. If we have five patients at that point who already got HB-201 pembro, we probably won't accrue any more. So it'll be somewhere in the ballpark of, you know, 20 patients, and we'll probably be preferential as to who we think the winner is. Okay, great. Back to the dose determination. You know, you guys have mentioned multiple variables, including the amount of virus that you can give and the T cell levels. I guess, what's the reason? So it looks like you can give PICV at 1 × 10^8, LCMV at half that. Is there a reason that PICV can be given at higher viral loads? And then the T cell, you know, you guys have gotten up to 40% CD8 T cells specific for HPV. Do you think you can go above that? Do you want to go above that? Thanks. I have some follow-ups. Let's answer the first question is easier. I would say a Pichinde grows easier or faster than LCMV, easier to get to higher titers. Okay, great. Yes, yeah. It's not something to do with the volume that you're giving, it's just. No, the volume. manufacturing feasibility. No, no. Yes and no, remember. Yes, we can. The higher the titer means, the smaller the volume I can give it in. Yeah. I can give, you know, for example, LCMV at a dose of 5 × 10^8, but that means I have to give a liter of it. Yeah. It's more for concentration effect, right? If it grows better, it's easier to concentrate. If it doesn't, I have some more volume. Yes, we can give more volume, but that's why I said in the talk, it becomes a feasible feasibility issue more than anything else. I'm not sure we're getting a benefit in terms of other parameters such as T cells. Okay. To your second question, does it matter if I go above 40%? I think that's what I tried to comment, you know, in my relationship slide. You know, we are seeing a relationship between the more CD8 T cells, the better. Is it a perfect linear relationship? As I said, I'm afraid not, but it's also not a perfect linear relationship for checkpoint inhibitors and PD-L1 expression. I think we're trying to figure out if there are indeed levels, just like, you know, the PD-L1, the checkpoint inhibitor field is trying to figure out if there are thresholds for, you know, PD-L1 levels by CPS, and is that tumor type specific or across the board? I would say we had an ad board with about 10 very prominent international KOLs in the immuno-oncology space where we kind of asked that same question. You know, the answer was probably you're reaching the kinds of levels where probably more than 40%, you know, more than half, you know, is already at levels, to quote one KOL, that are at ludicrous amounts of tumor antigen specific CD8 T cells. I don't think at this point, more is the answer. Let's put it this way. All right. I think we're at levels that should be sufficient. More than 40% I don't think is the answer, as to how to get better efficacy. Can we? Maybe. Should we? Not so sure. Okay, great. I'm moving on to the infectious disease programs. I guess first question on the hepatitis B, you said it's gonna be a two-vector. Is that gonna be replicating or non-replicating? And then, what are the specific antigens? Does it go beyond just the S protein or are you gonna look at the whole virus? And then as far as the HIV program, you said Gilead's not gonna advance it themselves. Did they give any color as to why they chose to do that? Thanks. Yeah, we're unfortunately not in a position to comment on this because Gilead is driving the collaboration, and they're responsible for any communication to public markets. We cannot say anything about the HPV program and what it's set up is. On HIV, we have a good relationship with Gilead, and we're currently talking with them about a potential alternative to progress it. But the decision is not made, and we will see what will happen. Okay, thank you. Thank you. Your final question comes from the line of RK from H.C. Wainwright. Please ask your question. Thank you. Yeah, good afternoon, folks. A couple of quick questions. I know we talked a lot about percentages of T-cells this afternoon, but I just wanna see if within these patients that you've been looking at, is there some sort of a T-cell percent cut-off that you feel you need, you know, to even start seeing some sort of an activity in terms of tumor reduction? Yeah, it's a great question. I would say this is a question that the field has been struggling with, I would say, for decades. You know, the question has been, you know, the magic question has been, is there a threshold, is there a magic number that if only it could be reached, has been, you know, an ongoing, I would say, unknown in the field for a long time. People have always theorized based on adaptive cell therapy experiments back in the kind of, you know, in the 1990s, that, you know, if single percentage kind of numbers could be reached by active immunization, then theoretically, efficacy should be observed. Those numbers were extrapolated from adaptive cell transfer experiments that were themselves done by, you know, transferring CD8 T cells in a background that was first conditioned. We actually had an educational advisory board session several months ago, which is on our website, that we encourage everyone to look at it. We actually spent quite a bit of time generally just talking about this issue in order to better understand. I think the consensus in the field is that, you know, if you're able to get to single- digit percentages, you're already kind of, you know, got a home run as far as what's achievable with the space. And with that should come efficacy. However, to date, as I've said, no one has consistently ever been able to generate single digit percentage, you know, tumor specific CD8 T cells. And as a result, no one has seen efficacy. This is because it's almost become like a catch-22. You don't see efficacy if you don't get high enough T cells, and you never get high enough T cells to see efficacy, so how can you ever establish a relationship? Mm-hmm. I think we are, for the first time, in a position to really answer this question with the kind of data that we're showing. Perfect. Last question from me. You know, looking at your phase II design, I'm just trying to understand the rationale for starting off with HB-201 and then, you know, because your combination, the HB-202/HB-201 combination is coming up, you know. Yeah. Within three months or four months from here. Why go into this study? Yeah. You know, with, without waiting? You know, I'm just trying to u nderstand the rationale behind it. Yep. Right. Let's take a second on that. You see in the third line, right, we are waiting. I said we're gonna wait for the monotherapy in the third line before choosing one. Why am I not waiting to choose one for the first line? Because the first line is different. These patients are, you know, newly diagnosed metastatic. This is first line standard of care. Before we introduce, you know, two different arenavirus vectors in them, I'd like to de-risk safety concerns in the first line setting. Although we have some safety data in the advanced setting for both, you know, HB-201 along with pembro as well as HB-202 plus HB-201 plus pembro, these are patients who have seen pembrolizumab before and have, you know, tolerated side effects. Pembrolizumab itself, as I'm sure we all know, has a very significant side effect profile. Before I introduce two replication-competent arenavirus vectors into first-line combinations, I'd like to make sure that there are no surprises from a safety perspective. Because of that, we're starting with HB-201 plus pembro first. Make sure there are no safety concerns. Then, introduce HB-202 and HB-201 on top. It's a different patient population. It's first-line and safety here is very, very important. Perfect. That logic makes sense. Okay, thank you very much. You have a question from the line of Christopher Louie. Please ask your question. Hey, guys, this is Chris on for Andy from SVB Leerink. Just wanted to get your thoughts on a potential accelerated approval. Is that still a path forward, or are you thinking that you might have to do a phase III study? I think that the accelerated approval still depends on how good monotherapy efficacy is in the advanced setting. I think I've been consistent in my messaging here, that if monotherapy data in the third line looks as good as monotherapy data in the second line, then I think we have a chance at monotherapy approval. I remain consistent with that. I think this is a conversation we will have at the end of the recommended phase II dose of HB-202 and HB-201, where we collectively look at these monotherapy datasets. Got it. I guess just rephrasing it a bit, based on the data you have today, do you think it would be possible to have an accelerated approval? If you did have to run a phase III, what would that study potentially look like? Right. I think, you know, looking at the data, I would say the data suggests that we have, I would say, several parameters, where we are indeed showing superiority over second-line therapy. I think I remain optimistic that we do indeed have the opportunity to be able to do accelerated approval in the third plus line as a monotherapy. Again, to be discussed, to be confirmed by the data at the end of the phase I, but I remain quite optimistic. In terms of your second question, if I had to do a randomized trial, what would it be? I mean, you know, head and neck cancer is complicated. There is no second-line approved therapy, and clearly there is no even third-line approved therapy. The last randomized trial run in the second line space, nivolumab ran it against methotrexate as a comparator, for which methotrexate showed in the second line 8% response rate with a median progression-free survival of also two months. I think if we had to run it in the third line, it would probably be something similar to a methotrexate as a historical comparator used in the second line against nivolumab. Got it. Thank you very much. There are no further questions. Please continue. If there are no further questions, we thank you very much for participating in this call and wish you a good afternoon or a good night for those who are in Europe. Thanks a lot and take care. Bye-bye.