I would like to extend a special thanks to everyone joining us today for an update on our clinical programs and many of the exciting developments at Precigen. Before we begin, I would like to remind you that during today's call, we will make various forward-looking statements. Investors are cautioned that our forward-looking statements are based on current expectations and are subject to risks and uncertainties that could cause actual results or outcomes to differ materially from those indicated by our forward-looking statements. Please read the safe harbor statement contained in this presentation, as well as risk factors contained in Precigen's most recent SEC filings for a more complete discussion of these risks and uncertainties. I am pleased to be joined today by Dr. Helen Sabzevari, President and CEO of Precigen, Dr. David Sallman, Assistant Member in the Department of Malignant Hematology at the H. Lee Moffitt Cancer Center and Research Institute, and the lead investigator for the PRGN-3006 study. Dr. Nora Disis, a Professor of Medicine and Director of the University of Washington Center for Translational Medicine, and Professor in the Clinical Research Division at Fred Hutch, and one of the lead investigators for the Precigen PRGN-3005 clinical study. Dr. Clint Allen, Principal Investigator with the Section on Translational Tumor Immunology at the NIH, and lead investigator for PRGN2012 clinical study. Dr. James Gulley, Branch Chief and Director of the Medical Oncology Service at the NIH, and lead investigator for PRGN2009 study. During this update call, we will focus on two of our technology platforms. First, the UltraCAR-T platform represented by the PRGN-3006, PRGN-3005, and PRGN-3007 UltraCAR-T trials. Second, we will provide updates on the AdenoVerse platform represented by the PRGN-2012 and PRGN-2009 trials. Following our prepared remarks, we will open the call to Q&A with our lead investigators. I will now turn the discussion over to Dr. Sabzevari. Helen? Thank you, Steve. I would like to first of all welcome everyone that are joining us for the clinical update in 2021. Since the December of 2020 that we had our last update, we have made a tremendous amount of progress. Before we start, first and foremost, I like to really thank all of the Precigen team for the outstanding job that they have done to advancement of both pre-clinical and clinical portfolio, and especially during a very challenging time of COVID. Also, I would like to thank all of our investigators. Their dedication really to advance these programs for the patients has been outstanding, and we are grateful to them on behalf of the patients and Precigen. With that in mind, today we will be focusing on two major platforms for Precigen, our Ultra CAR platform, as well as our AdenoVerse platform. In the first half, the Ultra CAR, we would show you a video that actually in a very short but effective manner describes how the Ultra CAR works and why it's differentiated from all the other platforms. With that, we will go to the video first and then followed by a presentation by Dr. Sallman on PRGN-3006, and Dr. Disis on PRGN-3005, and finally with the short presentation on our newest Ultra CAR, PRGN-3007. Can we show the video please? Chimeric antigen receptor, or CAR-T cell therapy, is an emerging weapon in the fight against cancer. Yet patient access to this potentially life-saving treatment remains limited because of the high costs of conventional CAR-Ts, which use viral vectors and lengthy T-cell manufacturing times, leading to the rapid exhaustion and short therapeutic lifespan of these agents in patients. The impact can be devastating, especially for patients with advanced stages of cancer, where every day is crucial. Precigen's UltraCAR-T platform represents a novel approach to autologous CAR-T therapy that addresses these challenges by use of non-viral vectors and an overnight manufacturing process at the cancer center or hospital and lowers the manufacturing cost and dramatically reduces vein-to-vein time. T-cells are modified using Precigen's UltraPorator electroporation system, an automated, commercially scalable, high-throughput system capable of processing billions of T-cells in under 12 minutes for manufacturing UltraCAR-T therapies at the medical center where the patient is treated. UltraPorator applies specialized electrical pulses to deliver our non-viral plasmids into the nucleus of a T cell in an overnight manufacturing process. With UltraCAR-T, a patient's own T-cells are modified using Precigen's proprietary UltraVector technology, delivering three or more effector genes using a single non-viral plasmid for a personalized, powerful, homogeneous drug product. UltraCAR-T cells express an antigen-targeting CAR, capable of attacking specific tumor cells, a membrane-bound IL-15, increasing persistence and survival of UltraCAR-T cells, and a kill switch as a safeguard against toxicity. Plus, UltraVector technology offers the potential to add three or more effector genes to the T-cell, such as checkpoint inhibitors. UltraCAR-T cells are manufactured without ex vivo activation or T-cell expansion and infused back into the patient only one day after manufacturing a patient's personalized UltraCAR-T. After reinfusion, UltraCAR-T cells survive inside the patient's body and kill cancer cells when they recognize the tumor-associated antigen expressed by the tumor and start to expand and persist within the body. Precigen is developing a library of non-viral plasmids to target tumor-associated antigens across various cancer types. Based on the patient's cancer indication and biomarker profile, one or more of the non-viral plasmids can be selected from our library to build a personalized treatment. After initial treatment, this approach has the potential for redosing of UltraCAR-T, targeting the same or new tumor-associated antigens based on the treatment response and the changes in the antigen expression of the patient's tumor. Precigen is working to empower medical centers to deliver personalized autologous UltraCAR-T treatment with overnight manufacturing to any cancer patient, enabled by design and manufacturing advantages of UltraCAR-T, coupled with the capabilities of the UltraPorator system. Precigen's UltraCAR-T and UltraPorator technologies have the potential to reshape the CAR T landscape, delivering a new generation of personalized CAR T therapies for solid and hematological tumors with rapid patient access and the ability to redose in a cost-effective manner, offering a powerful treatment option that can improve outcomes for cancer patients and their families. Precigen, advancing medicine with precision, advancing personalized UltraCAR-T therapy. Thank you, Helen. We will now turn the call over to Dr. David Sallman, lead investigator for the PRGN-3006 UltraCAR-T study in AML. Dr. Sallman? Hello, my name is David Sallman from Moffitt Cancer Center in Tampa, Florida. It's really, you know, a pleasure to be with you virtually. Wish I could definitely be there in person, but I think this is an exciting time in the evaluation of PRGN-3006 UltraCAR-T cells. I've been fortunate to be actually working, you know, with the company from an investigator perspective for multiple years now. It's taken a lot of time and hard work from multiple groups. We're really excited to present a little bit of the data, and then ideally really looking forward to the formal ASH presentation where you'll be able to see everything in significant detail. Just, you know, what is the unmet need for patients? Clearly despite a lot of improvements, a lot of changes in standard of care, if we focus first on AML patients, particularly older patients over the age of 60 years-65 years of age, you could see very low rates of long-term survival, and especially once patients have failed standard of care therapy or let's say have failed an HMA-venetoclax-based combination, the opportunities for additional therapy are limited. Without the subset of patients that may have molecular targetable mutation, even those patients, pretty much everybody will relapse, and again, still a very significant unmet need. The needs even further in myelodysplastic syndrome, there are lots of therapies trying to change the frontline therapy, but essentially unless you get to allogeneic stem cell transplant, all patients will eventually relapse. After HMA failure therapy, there is really no standard of care therapy. Unfortunately, this group of patients does not have targetable mutations. Including if you think about patients post-allogeneic stem cell transplant, which happens in at least half of all patients, both in MDS and AML, again, it's a very refractory group with a very limited selection of potential treatment options. With all of this, again, there is a significant unmet need, and unfortunately, traditional immune therapy agents have not been successful. CAR T has changed the paradigm in hematologic malignancy. I think we're gonna talk about some of the significant challenges in myeloid development, which hopefully the PRGN cells can overcome. What is PRGN-3006, and how does it differentiate from some other CAR T therapies? It targets CD33, which I would say is one of the two main targets being looked at for myeloid leukemia patients. CD33 is importantly overexpressed in the vast majority of patients, both with high-risk MDS as well as AML. It's expressed both on bulk blast as well as leukemic stem cell populations. Again, the very high percentage, probably as high if not higher than any other bulk target, including things such as CD123. It's nice in that it has very minimal expression outside of the hematopoietic system, so we would not really expect for on-target off-tumor toxicity, with the exception that CD33 can be expressed on normal hematopoietic cells. This has been shown by Saar Gill's group and others, and thus could there be a potential for ablation of the bone marrow that could also have its advantages in that potentially a bridge to transplant is an important consideration. The amount of CD33 may be significantly increased on blast populations versus normal, so that may open up a little bit of a therapeutic window in addition to that. In AML patients, they often can very rapidly be progressive, and treating the patient at the right time can be really critical. Patients may not be able to have the standard three-week or longer manufacturing process, and thus anything that is more rapid is an advantage for our patients. With PRGN-3006 cells, again, this is a very different procedure. Patients are leukapheresis with isolation of T cells, and really, in an overnight process, or you could consider from apheresis to infusion, really only takes two days in detail. The process is through electroporation with the Sleeping Beauty DNA plasmid. Again, this is what ultimately leads to the production of the UltraCAR-T cells that can then be infused into the patient. Importantly, with the rapid manufacturing, you know, cytokine support may be really critical for in vivo expansion and potentially persistence of cells. This CAR has built into its membrane-bound IL-15, which has been shown by this group and others to be a very critical cytokine. Additionally, we spoke a little bit that potentially, you know, ablation of the bone marrow could occur, or again, if there was any other unique toxicity, having a potential kill switch to rapidly eliminate the CAR-T cells is of a significant advantage and has been incorporated into this product as well. As far as what is the design of the clinical trial, this schema has been presented previously at last year's ASH, but it is eligible for relapse refractory AML patients, higher risk MDS patients, as well as really an orphan disease of chronic myelomonocytic leukemia, as long as they have greater than 5% blast. CD33 positivity is required. This is just done by standard flow cytometry. We do require an absolute lymphocyte count of 200 cells per microliter. Potentially we could go lower, but we thought this cutoff, especially with the rapid manufacturing, would be needed. Again, most patients do have a lymphocyte count, although some patients would be excluded based on having lower counts. Importantly, we do allow prior allogeneic stem cell transplant as long as there's no active graft versus host disease and they're off of immunosuppressive therapy, really otherwise standard eligibility. There's two cohorts, cohort one being a non-lymphodepleted cohort and cohort two being a lymphodepleted cohort, so again, post-apheresis. The only therapies that were used for potential bridging was hydroxyurea. It was discontinued either 72 hours prior to apheresis or prior to infusion of the cell product. Patients are then given the cells and then followed very closely, of course, for the traditional toxicity. Patients are inpatient for two weeks and in our area for 30 days, which is really a standard for entry for any cellular therapy. Of course, the primary endpoint of the study is overall for safety and to determine the maximum tolerated dose and ultimately the recommended expansion dose. Then of course, we're looking for activity and then really critical, especially in early myeloid development, is looking at expansion, persistence, kinetics in blood and bone marrow, and a lot of this will be presented at ASH in greater detail as well. Disease responses per standard criteria ELN for AML, IWG for MDS. This just looks at the clinical characteristics of the patients. We do separate this based on the non-lymphodepleted and the lymphodepleted cohort. Again, for safety, because again, these cells are made over again a very rapid, you know, really 24-hour process or again, two days from apheresis to the actual infusion of the patient. We thought it safest to test first in the non-lymphodepleted cohort. Once that cohort clears, we can then go at the same dose level for patients in the lymphodepleted cohort. You can see the median age of 63 years, pretty common, although we treated patients up to the age of 77 years, a relatively equal male-female disposition. These patients were heavily relapsed refractory, which is not unexpected, but again, these are kind of as sick as you can be for a relapsed refractory group with a median number of therapies of four. All patients having failed prior HMA venetoclax. Just to think about what the survival is, multiple groups have now published on that with really a median OS of two to six months, and again, no standard care therapies in that patient group. The majority of patients being refractory to chemotherapy and a third being post-allogeneic stem cell transplant relapse. All patients having either intermediate or adverse, with the majority being adverse. These are summarized in the ASH abstract, but if we look at just overall toxicity, cytokine release syndrome did occur in four patients, with only one patient having a transient grade three cytokine release syndrome that reversed in less than 24 hours with the use of tocilizumab. Importantly, no neurotoxicity to date, and you can see the doses that were administered across this cohort. Overall, well-tolerated with really additional detailed treatment data to be presented in the future. When we look at the number of cells, of course, we want to see as dose level goes up, as expected, we do see improved peak expansion in the blood. There'll be much more additional data to be presented at ASH in detail. In patients without lymphodepletion, no patient had an objective response, although several patients did have persistent stable disease and did have relevant bone marrow blast reduction. When we now look at cohort two, so this is with a standard fludarabine cyclophosphamide lymphodepletion. Overall clinical characteristics, you know, somewhat similar. Median age is a little bit less, but again, an N of six patients. There was a female predominance in this group. Again, very heavily relapsed refractory, and that most patients have had HMA venetoclax and a high percentage with intensive chemo, and actually half of patients being allogeneic stem cell transplant relapse. Still, all patients to date have been treated have had acute myeloid leukemia. The toxicity profile is overall quite similar, but notably, we had no grade three cytokine release syndrome or need of tocilizumab, although half of patients did have some degree of cytokine release syndrome. Again, no neurotoxicity. When we look at the response rates, notably one out of the three patients in dose level one and two out of three patients in dose level two responded. Or overall, half of our patients that have been treated with lymphodepletion, followed by PRGN-3006 cells have obtained an objective response. The response will actually go into some detail in the case examples which are described in the abstract as well. You can see the swimmer's plots as far as the follow-up of patients, including one patient still in remission, post being bridged to allogeneic stem cell transplant. I'll go into a little bit more detail on subsequent slides. Now if we look at the lymphodepletion cohort, again, as we go up in dose level, the peak expansion in the blood does increase, which is as expected. Importantly, when we look at the absolute value of this, we do see significant increased expansion in the patients in lymphodepleted versus non-lymphodepleted. Again, additional data with kinetics and ultimately other translational data will be presented at ASH. Again, in summary, we have seen dose-dependent expansion in all of the patients. We have seen persistence in up to three months post-infusion in the lymphodepletion cohort and even six months in the non-lymphodepleted cohort. Overall, a higher peak expansion again when we compare lymphodepleted versus non-lymphodepleted. Just a couple of case examples. This is the, you know, case images that you'll see in the ASH abstract as well, where we had a 53-year-old patient that had extramedullary acute myeloid leukemia, actually with seven lines of prior therapy, including allogeneic stem cell transplant. Really had widespread and innumerable cutaneous lesions. You can see on the PET scan a lot of PET avid lesions, that you can see. The patient was treated on dose level two with lymphodepletion and actually was very well tolerated with no cytokine release syndrome in that patient. You could see nice expansion, early on. In this patient on serial PET scans, actually nearly all lesions were gone with really some residual PET activity, and the scalp lesion was even more impressive on cutaneous exam, where nearly, you know, all the lesions were now absent, again, outside of this one scalp lesion. This did persist through several additional PET scans until the patient did ultimately have progressive disease around day 90, and that patient continues to be followed. Looking at another case example for a patient on the same dose level treated with lymphodepletion was a relapsed refractory AML patient that was again treated with multiple lines of prior therapy, including HMA venetoclax and induction chemotherapy. Again, we see very nice and actually very impressive expansion, which again, I think this is really a key finding when we look at myeloid patients. Whether or not this occurs in the setting of CAR T, I think is a really critical question. Notably, if you look at the flow cytometry data based on the peripheral blood, that actually nearly 10% of the CD3 cells were actually the CAR T- cells. Quite robust expansion you can see out to day 2- 14. Overall, this patient tolerated treatment well, did have a grade one cytokine release syndrome. Notably, as the patient was entering into remission and actually really full donor chimerism, this was a post-allogeneic stem cell transplant relapse, did have a significant what we would say is grade two graft-versus-host disease, although it was rapidly reversible with corticosteroid therapy and completely resolved. The patient did achieve a CRi at day 28 and actually had significant continued improvement of counts up to a CRh at day 60, although ultimately did have progressive disease at day 100. Lastly, we did even have a response in the first dose level with lymphodepletion, a patient that had overall lower blast disease, although status post two lines of intensive chemotherapy. Again, we see this nice expansion on the right. She also tolerated therapy very well without any significant treatment-related adverse events. Had clearance of blast, which then had continued count recovery actually very near a true complete remission, by the time of allogeneic stem cell transplant, and fortunately is still in remission post allo transplant, at least at data cut off for the ASH abstract. In conclusion, PRGN-3006 is overall very well tolerated, both with and without lymphodepletion. Importantly, no dose-limiting toxicities have been observed and really overall have had well manageable grade one, two cytokine release syndrome, again, with only one transient grade three event. Importantly, and this may be unique to myeloid malignancies or to this therapy that there have been no neurotoxicity observed, which I think is very important. Again, this manufacturing process is quite unique with a really overnight decentralized manufacturing process, you know, done at our center and again, really can go from apheresis to infusion of patients in two days. This really will allow for, you know, rapid treatment of patients and ideally at the right time. Of course, the first step is to evaluate the safety of a therapy and the tolerability and the manufacturing ability up to certain dose levels. Then ultimately, I think treating the patient at the right time, you know, can be a very key consideration. Again, this processing may better allow for us to do that. We have seen nice dose-dependent expansion and persistence, that's even improved as expected, in the lymphodepleted cohort. Although numbers are small, excited based on low dose levels of having a 50% objective response rate in the lymphodepleted cohort. Just thinking about where we're going, of course, looking forward to the official and complete data presentation at ASH. Again, what are the next steps? Of course, to complete the dose escalation in both cohorts. Then thinking about the future, of course, we need to go into dose expansion of the trial, truly identify what the overall efficacy is of the drug. Are there patient subgroups that may better or worse respond to therapy? Given the rapid manufacturing ability, the ability to repeat dosing is a possibility, and it's gonna be considered in future study with PRGN-3006 cells. Of course, thinking about what could registration strategies be. The bar is very low in, you know, particularly HMA-venetoclax, HMA failure, MDS, AML, or really any relapse refractory patient. If we can ultimately have durable outcomes, you know, 20%, 30% in this setting that can even last for 4-6 months or ideally longer, that's probably a key consideration. Again, I think these early data are exciting and proof of principle efficacy as far as targeting CD33, and again, this technology is rapidly adaptable, which may be very important as I think myeloid malignancies has a lot of complexities differentiating it from other hematologic malignancies. Really with that, I look forward to the discussion session and really look forward to the official last presentation as well. Thank you for listening to this. Thank you, Dr. Sallman. We will now turn the call over to Dr. Nora Disis, lead investigator for the PRGN-3005 UltraCAR-T study in ovarian cancer. Dr. Disis. Hello, my name is Dr. Nora Disis from the University of Washington Fred Hutchinson Cancer Research Center, and this is an update on a clinical trial that we're running of Precigen 3005 UltraCAR-T. The UltraCAR-T is its first in class of an investigational therapy that we're testing in ovarian cancer. Why ovarian cancer? It's the most lethal of all the gynecologic malignancies. There's a high unmet need as the majority of patients are diagnosed with stage three and stage four disease, and survival long-term is as low as about 20%. Even though it's not a very common cancer, we still have 22,000 cases diagnosed each year in the United States and 300,000 cases worldwide. As I said before, the majority of patients who are diagnosed with ovarian cancer will succumb to the disease. The current standard of care for ovarian cancer is surgery followed by chemotherapy with a combination of platinum agents and taxanes. Recurrence of the disease occurs in most patients after the initial treatment within 3 years-5 years. This results in a cycle of repeated surgeries and additional rounds of chemotherapy. An anti-PD-1 treatment has been used in ovarian cancer because the disease has been identified as immunogenic. Unfortunately, with either anti-PD-1 or anti-PD-L1, there's been a low overall response rate, about 10%, with few, if none, complete responses. This is a disease that's really crying out for a new therapy. The CAR T-cell that we are testing is targeting MUC16. MUC16 is expressed in over 80% of ovarian cancer patients, very commonly expressed. It's also found in multiple other diseases. Over 60% of pancreatic cancer, lung cancer, about 50% of breast cancer, and 75% of endometrial cancer. It's a very ubiquitously expressed target. PRGN-3005 targets the unshed portion of MUC16, and that's important because even though it's overexpressed on greater than 80% of ovarian cancer tumors, much of the protein is shed and can be measured in the sera. That's one of the ways that we monitor disease burden. The unshed portion of MUC16 is retained in the tumor and limited expression is found on healthy tissues. It really makes an ideal target for advanced stage platinum-resistant ovarian cancer. The CAR-T cell has a multigenic design. It's a non-viral system. It simultaneously expresses MUC16 CAR, but also IL-15 to propagate persistence of the CAR in vivo, as well as a kill switch to prepare for any untoward toxicity we would be able to immediately treat and eliminate the CAR. I think one of the most unusual things about PRGN-3005 compared to other CAR-T cells that we've used is that it has a very easy manufacturing process. Literally, we leukapheresis the patients. There's an overnight electroporation, which is fully automated, and then UltraCAR-T cell infusion can take place the next day. Unlike other CAR-T cell products that can take weeks to generate, this is a very easy autologous system. The clinical trial is a phase I/IB trial design. We're really looking to answer a couple of questions. It's a two-arm design. Arm one is an intraperitoneal infusion. We chose not to do a lymphodepletion because the theory was the IL-15 would allow expansion of the T-cells in vivo. Arm two is an IV infusion, again with no lymphodepletion. The question here is whether IV infusion would be more effective for metastatic disease, which is found in ovarian cancer. Eligibility is advanced-stage ovarian, fallopian or primary peritoneal cancer. We're looking for disease that's measurable by RECIST and CA-125 levels that are greater than the upper limit of normal. There's no stratification based on biomarker MUC16 expression that's built into the trial to look at the end of the trial. This makes sense since most of the patients will end up expressing MUC16 in their tumor. The trial is really designed as a safety trial. We're looking at standard battery for adverse events, with particular focus on whether cytokine release syndrome develops or whether there's neurotoxicity to very significant toxicities that are seen with most CAR T-cell products. The disease responses by RECIST, as I said before, but we're also measuring iRECIST, and we'll be looking at many correlatives. The most important are the persistence and expansion of the CAR T-cell in vivo, the immune phenotype of the tumor, and expression of several biomarkers, including MUC16. The patients are apheresed, they're treated with the CAR T-cell. We observe them inpatient, and then we follow them up for 12 months. The primary endpoint again is safety and to determine the maximal tolerated dose of Precigen 3005 delivered either by IP or IV infusion. The secondary objective is to evaluate the in vivo persistence and get some preliminary data on antitumor activity of PRGN-3005. We've been able to enroll 10 patients so far, all on the IP cohort. Again, heavily pretreated ovarian cancer patients. I'd like to talk a bit about the patient characteristics, the doses that we're able to achieve and the safety. The median age of the patients is about 60, which is kind of the common age of patients diagnosed with ovarian cancer. 100% of the patients have high-grade serous carcinoma, the most common subtype of ovarian cancer. 30% of them have ascites, 60% have locally advanced disease that has spread just within the peritoneum, and 40% actually have distant metastases. They are heavily pretreated, with many of them receiving multiple lines of previous chemotherapy after their adjuvant treatment. Here you can see 64%, including adjuvant therapy, had between 6-9 lines of chemotherapy. You can see these are really platinum-resistant ovarian cancer patients that are heavily pretreated with aggressive disease, and they have a very high target tumor burden. What do we know about the safety of the product? We did not see any evidence of cytokine release syndrome, any grade, not even grade one. We didn't have to use tocilizumab in any of the patients. We also did not see any evidence of neurotoxicity of any grade in any of the patients. There was an excellent safety profile really across all the dose levels studied in the IP cohort so far. No incidents of CRS, no incidents of neurotoxicity. The majority of the adverse events attributed to the CAR product itself were really low-grade toxicities. Here in the bottom of the slide, you can see the dose levels that we're aiming for, and the total UltraCAR-T- cell dose administered between 6-7 million cells, 12-21 million cells, and 321 million cells. This is a lot of product that's being able to be delivered and we haven't had a problem reaching these dose levels in these heavily pretreated patients. What are we seeing in terms of any change in the tumor? Here on the far left-hand side of the slide, you can see the percent change in target lesions, the sum of the diameters of target lesions from baseline. Colors are dose level one, purple, dose level two, blue, dose level three. As you can see, the major response is in stable disease, which can really last in some patients quite a few days post-infusion. Similar to other types of immunotherapy, we do see mixed responses. I'm showing you on the right-hand side of the slide responses that represent changes that we've seen in individual target lesions. This is a patient administered low dose. This is dose level two Precigen 3005 via intraperitoneal administration. Again, we're not using lymphodepletion. This at baseline is in the box, a bladder cancer tumor. A bladder tumor. So the ovarian cancer metastases. Here you see the lesion is about four centimeters long. After she was infused with the CAR T-cell, we see a significant decrease of more than a centimeter in this bladder lesion. This is evidence that even with infusion of CAR T-cell intraperitoneally, we are seeing changes in disease in parenchymal lesions that are not located in the peritoneum. Were we able to get expansion of PRGN-3005 in the blood? In the far left-hand side, you see a graph, again, dose level one in the green, dose level two in the purple, and dose level three in the blue of monitoring CAR T-cell in the blood. Again, you can see there was some expansion and persistence in each of the dose levels. That expansion and persistence really appears to be dose-dependent because as you can see, we achieved the highest levels that persisted the longest in dose level three. On the right-hand side of the slide, just to remind you, this is about 6 million cells, 12 million cells, and 33 million cells infused. This is very good evidence that along with no evidence of toxicity, we did get significant expansion and persistence of the CAR T-cell at the highest dose levels. What's next for PRGN-3005 in this clinical trial? What is our road ahead? We're on the verge of completing the dose escalation in the intraperitoneal arm, and we're poised to complete the dose escalation, start and complete in the intravenous arm. We have already asked for approval to incorporate lymphodepletion prior to the CAR T-cell infusion. In fact, FDA clearance has already been received to see whether giving lymphodepletion will result in higher levels of proliferation of the CAR T-cells in vivo and greater persistence. Because of the excellent safety profile we have with the CAR T-cell, we're looking to evaluate repeat dosing based on this excellent safety profile. It may be that we could use these CAR T-cells on a chronic basis. Since we're able to generate the cells so easily, you might envision an apheresis being taken place, freezing back the cells, and then being able to use CAR T-cells that are generated from frozen cells for many lines of CAR T-cell therapy. With that, this is the summary of where we stand to date in terms of our phase I clinical trial of MUC16 CAR T-cells in patients with advanced stage ovarian cancer. Thank you, Dr. Disis. We will now turn the call back to Helen for an overview of our newest UltraCAR-T clinical candidate, PRGN-3007 in ROR1-positive hematological and solid tumors, followed by an intro to our industry-leading AdenoVerse platform. Helen? Now I would like to discuss our newest member of UltraCAR-T platform, which is our PRGN-3007, which recently cleared the FDA IND from the FDA. This UltraCAR-T, as we consider the next generation, it not only has all the elements that we had seen in prior UltraCAR-T, which is a CAR target, in this case, ROR1, a safety switch, and a membrane-bound IL-15. Now we have introduced a mechanism that intrinsically it downregulates the PD-1 and blocks that in these cells. First of all, the ROR1, it is a very exciting target. Its expression is highly regulated on tumor cells, both on hematological as well as solid tumors. We see it in CLL, ALL, and MCLs. We also see it in a number of solid tumors in triple-negative breast cancer cells, pancreatic cancer, ovarian, and lung adenocarcinomas. What is to remember about this target is that on the normal tissue, there is a minimal expression of this ROR1. One other specific thing that I would like to mention, the UltraCAR PRGN-3007 uses the exact same manufacturing that we are using for PRGN-3005, 3006, and now in this case, 3007, which is overnight. If we look at the next slide, this is a snapshot of the data from what we have submitted to the FDA. In December, in the ASH presentation, obviously, you will see a much more significant amount of data. Here as a highlight, this is one of our in vivo models that expresses the hematological tumors. I want to get your attention to that red line. What you see there, this is the survival of the animals that they have been treated with the PRGN-3007, which is highly significant even over the regular ROR1 UltraCAR-T that does not have the PD-1 downregulation mechanism. This is important because it addresses some of the challenges that the CAR-Ts in general experience in a tumor microenvironment by upregulating the PD-1. What is very specific about our PRGN-3007 is that we have not knocked out the PD-1, but we have knocked down or downregulated the PD-1 expression, which now allows the T-cells to stay more active and not become exhausted rapidly. You see that actually on the right-hand side, the red diagram shows downregulation of the PD-1 as opposed to a normal ROR1 CAR-T or our ultra ROR1 CAR-T. With that in mind, I think what I would like to address is the clinical trials that will be at Moffitt Cancer Center with two arms, hematologic malignancy as well as solid tumors, addressing a number of indications in both. It is starting with the patients that they will receive apheresis followed by a lymphodepletion, and then their T- cells overnight will be manufactured with our UltraVector PRGN-3007, and next morning, I should say they receive those cells back, their own autologous T- cells. We are very excited about this trial. Why? It's for this reason. I have spoken to you previously about our vision for the UltraCAR-T library that would eventually allow the patients to walk into a cancer center or a hospital, and upon the diagnosis, then make a tailor-made autologous UltraCAR-T for them overnight, and the next day, they receive their own autologous UltraCAR-T. This, while introducing PRGN-3007, now we are getting a step closer to that vision. With that, you can see that we can have number of the UltraCAR-T now in sitting and being ready for addressing different indications. Now you have different CARs in case that there are mutations in the tumor that in the case of, for instance, ovarian tumor, if there is a MUC16 and then there is a heterogeneity, now you can also use a ROR1 PRGN-3007 and combine it. Similarly for hematological, we believe this is the only platform that allows this kind of flexibility with the rapid manufacturing overnight, significant decrease in the cost, and the possibility of redosing number of times as well as redosing with different CARs. This is what is so exciting, and as we are clearing these INDs, we are moving forward with. In the next part of our update, we will be discussing our AdenoVerse immunotherapy platform. Our AdenoVerse platform is basically a library of gorilla vectors that we have. Then they have the large genetic payload capacity. They are obviously off the shelf. What is very interesting and differentiated about them is the ability for repeated administration of them, unlike all the other adenoviruses, retroviruses, and others. They have a durable antigen, a specific immune responses, which we will be speaking to some of this. Importantly, for the safety, they are non-replicating adenoviruses. We also have advanced the manufacturing processes around these adenoviruses, which has become highly productive, that can be easily scalable for commercial viability. Thank you, Helen. We will now turn the call over to Dr. Clint Allen, lead investigator for the PRGN-2012 AdenoVerse trial in RRP. Dr. Allen? Well, good morning, everyone. My name is Clint. I'm an investigator at the National Institutes of Health. I have a basic science and a clinical research program that focuses on the study of immunotherapies for different head and neck disorders, such as head and neck cancer. What I'm going to talk to you about today is recurrent respiratory papillomatosis. I've had the opportunity to collaborate for the last few years with Precigen, and we're going to talk about this new molecule called PRGN-2012, which is a therapeutic vaccine for patients with diseases related to chronic HPV 6 and HPV 11 infection. Let's dive right in. Recurrent respiratory papillomatosis is caused by chronic infection with either HPV 6 or HPV 11. It's a fundamental problem where the immune system is not clearing a chronic infection, and we do not understand why most patients clear HPV 6 and HPV 11 totally fine, and we're all exposed to it, and while other people's immune system allows that persistent infection. Essentially, what happens is there's a chronic infection of either HPV 6 or HPV 11 in the upper aerodigestive tract, including the throat, voice box, and windpipe. This leads to development of papillomas, or essentially warts, throughout those areas. When you have warts on your voice box and in your windpipe, it can devastate your voice. If the papillomas get big enough, they can lead to airway obstruction. Rarely, people do die from this disease, primarily related to airway obstruction, or if the papillomas go down into the small bronchioles of the lungs, they can block off parts of the lungs. Here on the right side of the screen is an example of a normal trachea. This is a view we get in the operating room, and this is an example of a trachea from a patient with RRP who's really filled up with, we would call this trachea carpeted with papilloma. This is a coronal cut of a CT scan that shows normal lungs on the left-hand side, and this is an example of a patient with really severe RRP, where the lower airways have been completely blocked off by papilloma, and subsequently, this left lung has just filled up with fluid and infection. The incidence of this disorder is somewhere in the realm of 2-3,000 new cases a year. As opposed to cancer, patients with RRP don't die right away, so the prevalence of the disease builds up. While the incidence is only 2-3,000 cases a year, it's difficult for us to know how many people actually have this disease in the U.S., probably in the tens of thousands. I would argue just as important is that HPV-6 and HPV-11 chronic infection can lead to RRP, but it's the same viruses that cause other disorders such as anogenital condyloma, and there are millions of new cases of anogenital condyloma every year in the U.S., and this is an especially troublesome population and troublesome disease in the immunosuppressed population. Patients with HIV, it's a bad problem. There's a really high unmet need for a therapeutic for these diseases caused by chronic infection with HPV 6 and HPV 11. Just to give you a better sense of the disease, on the left-hand side here, this is a clinic endoscopy exam in the ENT clinic where we put a scope through the nose and we go down the back of the nose into the throat, and we're looking around the throat and the voice box. This is normal. This is what my throat hopefully would look like. This is a normal voice box. These are the vocal cords. That hole going down through the vocal cords goes down the windpipe and leads to the lungs. By contrast, here's a patient with pretty severe RRP. We see all those nice, smooth mucosal surfaces that we see on the left have all these papillomatous growth. All these lesions that are sticking out that have these pock-like appearances, this is all the papilloma. You can see it's really covering the top of the voice box, and the inside part of the vocal cords is covered in papilloma. This patient's voice is gonna be destroyed. This patient is not gonna be able to hold a job because they can't talk to their colleagues. This patient's spouse is constantly going to be mad at them because they're constantly having to repeat themselves. I mean, it's difficult to describe the degree to which severe voice disturbance like this can really destroy these people's lives. The standard of care treatment that everyone does is repeat surgery. That's really all we have. We take these patients back when the papillomas grow to the degree that they cause significant voice and breathing disruption, and we use different tools in the OR, and we mow the weeds, essentially. We take down the papillomas, and we know the treatment isn't curative because we're not addressing the underlying problem, which is the chronic HPV infection. We can do as much surgery as we can, but we really try to be minimally destructive to not disrupt the normal tissues because we know the papilloma is just gonna grow right back. Believe it or not, it is not uncommon for patients with RRP to require hundreds of lifetime surgeries. We have one patient we've been taking care of here at the NIH who's had over 800 lifetime surgeries, which is just incredible and really unhealthy for patients. Our focus is really to try to develop new adjuvant therapies. In other words, can we use surgery to keep someone's disease burden low and give them something that either prevents the papilloma from coming back or ideally activates the immune system and cures the infection? What you see here is a figure from a review article that we just recently published, which kinda describes the three main categories of adjuvant treatments that currently are being explored for RRP. One is simply the use of antiviral drugs such as cidofovir. I'll keep a long story nice and short by saying many, many people have studied cidofovir over several decades in retrospective large case series, and it doesn't work. If it worked, we'd all be using it. There's lots of reasons why it doesn't work, which we cover in some of our review articles, and I encourage you to look at those. Local injection of cidofovir doesn't work. The other approach is to kill the blood supply of the papilloma by binding and inhibiting the signals that induce the new blood vessel formation, namely VEGF-A, and we do that with bevacizumab. The trade name is Avastin, but bevacizumab is the drug name, and it does just what I described. It basically binds VEGF-A, and it prevents the papilloma from sending out those signals to induce new blood supply. Myself and many other investigators and physicians who take care of RRP have seen dramatic regression of disease with use of systemic, so IV-injected bevacizumab. The problem is that you can't stay on it forever. Like any other targeted therapy for cancer, for example, it works while you're getting the drug, but you can't stay on the drug forever because it's renal toxic. It will make people's creatinines go up slowly over time. When you stop the drug, you get rebound of RRP, and sometimes the RRP is even worse after the rebound. While this is a temporary measure that many people across the United States are receiving, systemic bevacizumab, it's not the long-term answer. I would make the argument that the only thing that is the long-term answer, the only thing that is the cure for RRP, is activating the immune response against the HPV infection. We know that T- cells are the only immune cell that can detect and kill a cell within the, you know, lining of the throat or voice box that's already infected with a virus that's inside the cell. Gardasil, which is a preventative vaccine, induces a strong antibody response, but antibodies can't do anything once the virus is already inside the cell. An intracellular virus like HPV, antibodies probably don't do you much good. You need that strong T- cell response. That really forms the rationale for an HPV six and eleven therapeutic vaccine. We need to activate those HPV-specific T- cells, which, as this figure illustrates, has the ability to detect and kill cells that already have virus in the intracellular compartment on the inside. To address this need, we worked with Precigen on initially the preclinical and now the clinical development of the PRGN 2012 molecule, which is a gorilla adenovirus that encodes a very specific mixture of antigens derived from HPV 6 and HPV 11. We were lucky enough to be granted orphan drug designation by the FDA, which I think is an important step for this rare disease. We published the totality of this preclinical development of PRGN 2012, which again, we did here at the NIH along with collaboration with Precigen. We published this in npj Vaccines, which is a Nature group vaccine, a nice journal. What this figure is illustrating is that administration of PRGN 2012 to mice with normal immune systems induces strong HPV specific immune responses, which is exactly what we're going for. This is just kind of proof that the vaccine in mice in the preclinical setting does what it's supposed to do. After really validating that it works in the preclinical setting, we've now undertaken this clinical study. This is the first in-human clinical study of PRGN 2012. This is occurring here at the NIH. I'm kind of the lead clinical investigator who's involved with managing the patients and doing some of the science on these samples. Dr. Scott Norberg is the medical oncologist here who's the PI of the study. This is for adult patients who have a diagnosis of RRP and have required two or more clinically indicated interventions in the past 12 months. They have to be healthy and functional as evidenced by the ECOG status. We're evaluating for safety, or evaluating for recommended phase II dosing. The design of this is to be used just like we talked about as an adjuvant. We would identify these people, bring them into the NIH. I would do a baseline surgery to clean out as much of their papilloma as I can and get down to minimal residual disease, and then we start with the vaccinations. They get their first therapeutic vaccination the same day as that surgery, actually, that afternoon, we give it to them. We bring them back two weeks later. We make sure they're doing okay from a safety standpoint. We give them their second dose. They come back four weeks after that, so now six weeks after the initial surgery. We check them out in clinic. If they've had any papilloma that started to regrow, we take them back to the OR, and we clean them out 'cause we wanna maintain that state of minimal residual disease throughout this whole process as much as possible. They get their third dose on day 43. They come back six weeks after that, so now it's 12 weeks after the first dose, and it's the same thing as day 43. We check them out in clinic. If they have disease, I clean them out. If not, they just get the fourth vaccination. It's a phase I study, so of course, the primary outcome measure is safety and tolerability and determining that RP2D. Of course, we're looking for clinical signals. We have enrolled and treated and started treatment on 14 patients. We enrolled our 15th patient yesterday, and I took him to the OR this morning and cleaned him out. FDA and IRB approval for what we have for this first clinical study is a maximum of 15 patients. We are officially done with accrual of that part of the study as of right now. The 14 patients that we accumulated data on for this table, a mean age of 50, relatively equal mix of male and females. These are patients that are typically adult onset, average 15 years since being originally diagnosed, and this number is right. The average number of surgeries that these 14 patients have had for their RRP is over 50. We have one, this one patient who's had over 800 surgeries. This is incredible and devastating. There's two dose levels. We've treated the first three patients with dose level one, which is 1 x 10^11 viral particles. After verifying that these three patients did fine, and they did, we've now been treating everyone at dose level two, which is 5 x 10^11. This is a neutralizing antibody assay performed by Precigen that explores whether or not patients receiving either dose level one or dose level two are developing systemic antibodies against the vaccine itself. What I can tell you from past experience is that these antibody titers, while measurable, are quite low. This is really important because this is probably one of the advantages of Precigen, this adeno vector vaccine, is that we can redose. One of the initial rationales of using, even using the gorilla adenovirus is that people did not have pre-existing antibody responses like they would have had to almost any human adenovirus based vaccine platform. This is really encouraging news. Safety summary. So far, we have had zero grade three or four adverse events. They've essentially all been grade one. We've had a couple grade twos. All adverse events have been self-limiting. We do not even give these people pain medicine after the vaccine. We just tell them, you know, if they're having fever and chills to, you know, to take Tylenol. The typical course of what happens is patients get the shot. They almost always have a local injection site reaction. This is a photograph of an injection on the back of the arm. This is a photograph of an injection on the side of the right leg. These are both about 24 hours after the injection. The clinical trial is designed where when we give them the vaccines, we rotate each limb. So for the four shots, it goes from left arm to left leg to right leg to right arm. That's why you see some pictures of arm and some pictures of leg. A very typical course after injection is they'll have 2 days-3 days of a reaction like this, where at the injection site, there's redness, swelling, tenderness. Most patients develop 1-2 days of feeling like they have a low-grade fever, chills, fatigue. It has all been self-limited, and the most intense local and systemic reactions typically occur with the first shot. Shots two, three, and four tend to have much less intense side effects. Overall, we're very pleased with this adverse event profile, again, with no grade three or grade four adverse events. Let's go over a few case series of the patients that we've treated so far, a few case studies. This is a 60-year-old male. He's a former retired firefighter. He ran into the Pentagon when the plane flew into it on 9/11, was pulling generals out of the Pentagon. He's an incredible person. This is his baseline endoscopic exam. You can see both of his true vocal cords are just completely covered with papilloma, a big bulky thing here in the epiglottis. This is He went through the whole three-month regimen where he had his three protocol indicated surgeries and his four vaccinations. This is six weeks after his last vaccination, and this is incredible because this is a patient who had been having surgery every six weeks for years because his disease looked like this. To be at this point, six weeks after finishing the clinical trial, is a home run in and of itself. At 12 weeks, he started to get a little papilloma right at the very front of the vocal cords that we call the anterior commissure. I actually offered him a clinically indicated procedure here at the NIH at the 12-week mark even though he did not have disease anywhere near where he had when he started the trial because it was the anniversary of 9/11. He was giving, like, USA Today interviews and all this stuff, so he had very, very high voice demand. Even this little bit of papilloma in the front of his vocal cords was enough that he could tell it was altering his voice. This is another case report of a 30-year-old male. This is a young guy from Minneapolis who has two small kids at home. His baseline disease was really bad. He had big bulky papilloma on top of his voice box, and you can see his vocal cords almost don't even look like vocal cords. They're just covered with papilloma. He also had been having surgery about every six weeks for years prior to enrolling in the study. This is what he looks like six weeks after completing the study. This is actually 12 weeks since his last surgery because at the 12-week mark of the study, he had no detectable disease. We didn't take him to the OR to do a clean-out, and he just had his fourth vaccination. For him to be 12 weeks out and have essentially no detectable disease is unheard of. I've never seen anything like this, and this is beyond even what we see with systemic Avastin. The final case that I'll tell you about is a 60-year-old who he has a job that's a very high voice demand. He was having surgery every 2-3 months for this disease that you see. Not real bulky disease, but again, really carpets the inner edge of both true vocal cords, which is how we make voice. He had baseline surgery and had no disease at his six week mark, so we didn't take him to the OR. He came back for his 12-week, didn't have much disease, but he actually tested positive for COVID. He was asymptomatic, so his 12-week assessment and that fourth vaccine got bumped by four weeks because of the COVID. What you're seeing here is his 16-week exam. Again, 16 weeks since he's had surgery. This is basically the morning before he would get his fourth vaccination, and he has absolutely no disease. These are actually his videos, and I wanted to show you these just 'cause I think it's so incredible. Let me kind of fast-forward this, and I'll pause it when we've got a good view of his true vocal cords. Again, here's that kind of, moderately bulky bilateral true vocal cord disease. This is his exam at the 12-week mark. I mean, literally no papilloma anywhere. I'm sorry, the 16 mark. He's now 16 weeks out here. This is great. This is a home run. Obviously, he's very happy because correspondingly, his voice is gonna be fantastic. I'm gonna stop here and to summarize what I've told you, and again, I'm looking forward to the Q&A session 'cause that tends to be when the best questions or the best details come up. Repeat administration of PRGN with four doses, we've seen no serious adverse events, no grade three, grade four, almost all just grade one that are self-limiting. Neutralizing antibody data really supports that we can repeat administer, repeat dose this vaccine platform, which is fantastic. We're very encouraged about the initial. Again, everything here is about durability, so if all of our data that we have right now looks the same six months from now, we'll be really excited. Right now, we're very excited about these early clinical responses. We're in the process of doing all the correlative studies on the blood and the tissue, and that's one of the real advantages of this study, is because I'm the investigator and I care about the science. I'm the one taking these people to the OR. We have loads and loads of papilloma to study, really where the action's at. We should be able to definitively answer mechanistic questions like, "Does the vaccine do what it's supposed to do? Does it induce HPV specific T-cells that traffic into the papilloma? We can answer all those questions that we're in process. Phase IB expansion cohort is now finishing enrollment, and I think we're going to talk about larger expansion cohorts that we have planned. That's it for me. Thank you for your attention and happy to answer any questions. Thank you, Dr. Allen. For our final update, we will now turn the call over to Dr. James Gulley, lead investigator for the PRGN-2009 AdenoVerse trial in HPV-positive cancers. Dr. Gulley? Hello, this is James Gulley. I am the Chief of the Genitourinary Malignancies Branch and Director of the Medical Oncology Service, as well as serve as the Deputy Director of the Center for Cancer Research in the National Cancer Institute. I'm gonna be talking to you today about PRGN- 2009. PRGN- 2009 is a first-in-class investigational therapy for HPV-associated cancers. It's comprised of a gorilla adenoviral vector that has the genes for E1, E3, and E4 deleted to decrease the ability to replicate. In addition, it has HPV antigen expression cassette added in. This encodes for HPV E5, E6, and E7 for HPV-16 and for HPV-18. HPV-associated cancers account for about 5% of all cancers. Globally, 690,000 new cancer cases are attributable to HPV infections each year. You can see this is led by cervical cancer, as well as head and neck cancer. Multiple other cancers are present too. The clinical trial design that I'm gonna tell you about today, done at the National Cancer Institute, is a first-in-human study evaluating the safety and preliminary clinical activity of PRGN-2009 as monotherapy and in combination with immune checkpoint inhibitors. Patients that are 18 years of age or older that have recurrent or refractory HPV-associated cancers and disease progression following standard of care and had at least one measurable lesion by RECIST 1.1 were enrolled into two sequential arms. The first arm is a dose escalation of just the vaccine alone, and it had a 28-day dose-limiting toxicity observation period. In the second arm, the vaccine was given with M7824 or bintrafusp alfa. This is an anti-PD-L1 agent that has the ability to also sequester TGF-β. The safety monitoring plan included physical exam, vitals, clinical labs, and electrocardiogram, as well as disease response assessment with RECIST 1.1 and correlative analysis of immune response and neutralizing antibodies. Primary objective of this study was to evaluate the safety and recommended phase II dose of PRGN-2009, as well as to look at the objective response rate, duration of response, progression-free survival, and overall survival. I wanna first talk about the vaccine monotherapy arm. You can see the patient characteristics. All of these patients were female. You can see half of the patients had cervical cancer. There were two patients with anal cancer and one patient with vaginal cancer. All of the patients had prior systemic therapies with a median of 2.5 prior therapies, range 1-3 prior therapies. All of the patients also had prior PD-1 or PD-L1 inhibitors. Median number of doses was five, with anywhere between 3-16 doses given. You can see here the safety summary. You can see very well tolerated. There were injection site reactions in five out of the six patients. However, this was grade one or grade two, and you can see that the rest of the symptoms, the flu-like symptoms, the fatigue, and the rash, were all grade one or grade two, seen in a minority of patients. I just want to remind you of the dosing schedule here. This is dosed every two weeks up front and then dosed every month. What you can see here is the neutralizing antibody response. You don't see a continued increase in the neutralizing antibody response over time with subsequent additional vaccinations. This slide depicts the change in tumor burden following PRGN-2009 treatments in the monotherapy arm. As you can see here, none of the patients had an objective response. However, there was one patient that had quite a prolonged stable disease, patient number two, which we'll talk about in a little bit. You can see here the waterfall plots of these same patients. This slide depicts scans from patient number two, the subject with durable stable disease for over a year, who has received 16 PRGN-2009 vaccinations. You can see at baseline the lesion in the lung and follow-up three months later really had not changed at all in size. In addition, here you can see a lesion in the pelvis, again, really did not change at all in size, and there were no new lesions. This patient with cervical cancer continues to receive monthly vaccinations and has had durable stable disease. We also looked at her HPV-specific T-cell response by flow cytometry with intracellular cytokine staining. You can see that when you combine the CD4 and CD8 responses together with these different intracellular cytokines, there was a substantial increase over baseline, and that increase continued to increase with subsequent vaccinations. This slide depicts the patient characteristics, safety summary, and neutralizing antibody response for the combination arm, that is, PRGN-2009 with bintrafusp alfa. As you can see, the median age again is 61. In this case, two out of the six patients were female. Oropharyngeal cancer was four out of the six cases, and cervical cancer, the remaining two. Prior number of systemic therapies, median was three, with 1-4 being the range, and all patients had prior PD-1 or PD-L1 inhibition. In addition, the patients got on average five doses of Precigen PRGN-2009. I want to turn your attention to the safety data. You can see very similar to the monotherapy, very limited side effects. We did see some side effects associated with the TGF-β component of the bintrafusp alfa with namely keratoacanthoma, as well as bleeding and anemia that often are associated with the bintrafusp alfa. However, when you look at the neutralizing antibody response, you can see there was no significant increase in the neutralizing antibody response over time. This slide depicts a change in tumor burden following combination therapy. In the panel on the left, I want to draw your attention to these two patients. Remember, all of these patients had progressed on prior PD-1 or PD-L1 therapy. These two patients had nice, deep and durable responses. You can see here in the waterfall plot a greater than 60% decrease in this patient with a deep partial response, and 100% decrease in this patient who had a complete response. You can see here both the monotherapy in maroon as well as the combination therapy in gray, the swimmer plots of these patients, and you can see the ongoing responses in patient number two as we talked about, patient number nine and 10. All of whom are on study and remain with stable disease or better with partial response and complete response, respectively. The disease control rate you can see from the monotherapy arm, three out of six patients had evidence of disease control at their first restaging and three out of five in the combination therapy arm. An objective response was also noted in two out of the five evaluable patients in the combination arm. I want to highlight one patient here, and that is patient number 10. This is the patient on the combination therapy arm who has an ongoing complete response. You can see here at baseline, this patient with cervical cancer had this lesion here that after two months became little bit less circumscribed and more diffuse. By four months really had shrunk significantly in size and by six months was completely gone. This patient did require the bintrafusp alfa and, Precigen 2009 to be held because of rash thought to be due to the bintrafusp alfa. However, the complete response remains in the most recent, imaging scan. You can see also here that her HPV specific T-cell response, much like the other patient we showed you, was substantially increased over time with vaccination. In conclusion, repeated administrations of Precigen 2009 were well tolerated, both as monotherapy and as combination therapy. No dose limiting toxicities were identified on study. Increases in HPV-16 and HPV-18 specific immune responses were seen with the administrations of Precigen 2009. Neutralizing antibody data support repeated administrations of gorilla adenovirus. Post-vaccine, we saw only low levels of neutralizing antibody that did not increase over time, and the immune responses appeared to increase over time. Although the data is early, it is encouraging to see that in the combination treatment arm in PD-L1 refractory patients, two out of five evaluable patients had an objective response, including a prolonged complete response. There is a phase II study in newly diagnosed oropharyngeal squamous cell cancer patients, which is ongoing. Thank you, Dr. Gulley. We will now turn the call back to Helen for a summary and thoughts on the road ahead at Precigen. Helen? First of all, I would like to thank all of our PIs for all the hard work that they have done as well as the presentation today. Also our patients for participating in this trial for advancement of the treatments for every patient in every corner of this world. We are grateful to all of them. With that in mind, if someone asks me, "Helen, what should we take from all of these presentations?" Which I can imagine it has been a lot of information and data at this point. On an UltraCAR platform side, what I would like to say is with presentation on PRGN-3006 and 3005, we clearly have shown excellent safety profile up to this point, both in hematological and solid cancers. We actually have shown the validation of overnight decentralized manufacturing, which truly has changed the paradigm for the CAR Ts in general and the cell therapy. This is probably the one of the most important changes in this field. We also have shown excellent in vivo expansion and long-term persistence of our UltraCAR-T, both in hematological as well as solid tumors. In the cases that Dr. Solomon spoke to for PRGN-3006, we have shown objective responses, preliminary objective responses, but very exciting ones in the cases of lymphodepleted cohort. In regard to 3005, we are advancing rapidly in our in vivo expansion arm, which will be addressing, for instance, the trafficking to the metastatic site. What is in the road ahead for us on the UltraCAR platform? As was mentioned before, we are expanding these both trials, PRGN-3005 and PRGN-3006, now to move toward the efficacy and expansion of the patient population. We also are very excited about the potential to pursue a rapid regulatory development path, for instance, as Dr. David Sallman mentioned in regard to the PRGN-3006, as there is really nothing in front for these patients. We also have an opportunity to evaluate now, once the dose is established for a repeat dosing. We are initiating our dosing in PRGN-3007 trials in the upcoming year. Also finally, the PRGN-3007, the innovation is not just strictly related to PD-1. This platform that we have introduced for the downregulation of a checkpoint, it can address a number of checkpoints in a variety of different tumor microenvironments, and we are very excited about that. In regard to our AdenoVerse platform, what we have shown is an excellent safety profile and what Dr. Allen and Dr. Gulley both spoke to in cancer and infectious disease setting. We have strong data that clearly shows you can repeat dosing this and use this AdenoVerse in a repeated fashion and still enhance the specific tumor immune responses, which is very unique. We also have shown strong preliminary clinical data with PRGN-2009 in combination with the checkpoint inhibitor. Initial data from our PRGN-2012 shows clinical responses in RRP, including the reduction of a surgical intervention, which is the only therapy that currently exists for this patient. What is the road ahead for us in that platform? We are going very rapidly toward the completion of our ongoing clinical trials. We have the ability and the potential to pursue a rapid regulatory development path for PRGN-2012, which is very, very exciting. Also we have attractive opportunity for combination of PRGN-2009 with the checkpoint inhibitors in multiple HPV-associated cancers with a high unmet need. This is quite exciting, and similarly we can have a rapid regulatory development path for these clinical trials. We also continue to obviously innovate with our AdenoVerse platform and advance this to other indications as well as other therapies. First of all, I wanna go back and thank all of our PIs for an incredible job that they have done through the years, especially during these past few years with the COVID challenges, but have kept this clinical trial going and really for making a difference for our patients. At the same token, I wanna thank all of our patients. Their participation in this clinical trial, it's absolutely has been so helpful because not only for themselves, but for all the other cancer patients across. This is how we move medicine forward. Finally, what I really wanna say is to my team at Precigen, I am indebted to them on behalf of the patients for what they have done, for all of the time that they have put in. I think this body of the data and the progress speaks to their dedication and the commitment for the advancement of this treatment for the patients. I think that is at the heart of Precigen, and we wanna make things happen for our patients. This is the most important thing, and I'm grateful for having such incredible team, both on a clinical side as well as our Precigen side. This is what makes it unique about Precigen. With that, I thank everyone.