Celyad Oncology SA

Greetings, and welcome to the Cellulite Oncology Year-End 2020 Earnings Call. At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. I'll now turn the conference over to your host, Filippo Petti, Chief Executive Officer of Cellulite Oncology. Thank you. You may begin.

Thank you, Operator, and thank you, everyone, for joining us today for our 2020 Financial Results Call. Joining me from the management team is our Chief Scientific Officer, Dr. David Gillum, our Vice President of Global Clinical Development and Medical Affairs, Dr. Frederick Lehman, and our Chief Business Officer, Dr. Stephen Rubino. We will start today's call with an operational and clinical update, followed by an overview of our financials, And then we'll then outline the expected key milestones for the company over the next several months. We'll then open the line for your questions. As we look back over the past 12 months, two key themes shape Cellulite Oncology. On a macro level, there is a COVID-19 pandemic that has impacted everyone within our organization and worldwide to varying degrees. We're thankful for our team's hard work this past year amid challenging times and their overall steadfast dedication to our mission to bring innovative CAR T therapies to cancer patients with unmet medical needs. On a company level, 2020 marked a significant period in our history as we announced a rebrand to reflect our experience and expertise more accurately in the oncology space, along with prioritizing our pipeline to develop our allogeneic CAR T therapies. This streamlined strategy allows us to focus our resources more efficiently and advance our allogeneic portfolio and technology platforms. Today, we are excited to announce preliminary safety clinical data from our lead SHRNA-based allogeneic CAR-T candidate, CIAD211, from the Immunity 1 trial, a Phase 1 study for the treatment of multiple myeloma, in which we initiated late last year. In addition, at the beginning of this year, during ASCO GI, we announced updated data from our CIAT 101 program for the treatment of advanced metastatic colorectal cancer. We believe the progress made over this past year is a strong example of how cellulite oncology is leading the field in CAR-T development and creating novel therapies for cancer patients. The past two years have been one of steady progress, strategically focusing on establishing a foundation for the organization to build upon for future success. One of our key goals has been to highlight our differentiated outlook to allogeneic CAR-T development by showcasing the advantages of our platform, including our non-gene edited technologies and our all-in-one vector approach, as well as to advance our clinical candidates. I feel that we have made great strides in strategically positioning the company for future success within the dynamic CAR-T landscape. Let me stop here and turn the call over to Dr. David Gillen, our Chief Scientific Officer, to provide more detail into our progress. David?

Thank you, Filippo, and thank you everyone again for joining us today. As Filippo just discussed, in 2020, we have thoroughly evaluated our portfolio and underlying technologies. Now, back in 2017, we started working clinically with the NKG2D receptor as a novel CAR T-cell therapy approach. Our clinical trial activity has definitively demonstrated the safety of this approach with promising evidence of clinical activity in both solid tumor indications and hematological malignancies. It certainly seems to me that the explosion of interest around NKG2D at the moment is in no small part thanks to our groundbreaking clinical work with this receptor. Behind the scenes, cellular oncology has been highly active working on practical solutions and forward-looking programs. The NKG-UD-CAR-T clinical program has been delivered thanks to our pioneering efforts to generate highly robust and reliable clinical cell manufacturing. We have subsequently built our first non-gene-edited allogeneic cell therapy, combining this innovation around clinical cell manufacture with our novel peptide-based technology, referred to as TIM, to produce the highly differentiated CIAD101, our allogeneic NKG2D CAR T-cell therapy. As Frederick will describe, this is now in an expansion cohort in our Phase I allostring trial after initial encouraging results from the dose escalation segment. Given this differentiated, non-gene-edited approach to allogeneic CAR-T, over the last two years or so, we have been working hard using a different technology referred to as short hairpin RNA or SH RNA that we feel brings significant possibilities to the field beyond that offered by other technologies in the CAR-T space and as a platform can be used for any chimeric antigen receptor strategy. Within two years of starting to work on this technology, we have taken CIAD2-11, our first-generation single hairpin BCMA-targeted allogeneic CAR-T, into the clinic. Frederick will discuss this trial in detail momentarily. But to recap, CIAD2-11 has been developed using a single shRNA to target CD3-Zeta, It results in knockdown of cell surface T cell receptor expression with no detectable evidence of graft-versus-host disease in our preclinical models. But, interestingly, leads to increased persistence of T cells as compared to T cells with a comparable gene-edited CD3Z2 knockout. We expect the ImmuneC1 Phase I trial to firmly establish that allogeneic CAR T cells using shRNA technology can generate clinical benefit without inducing graft-versus-host disease. We have not stood still with the development of CIAD211. While we demonstrate the shRNA allogeneic platform at the clinical level, it is important to remember that we have also shown in our autologous CIAD02 candidate that shRNA can be used to refine and enhance the therapeutic activity of clinical candidates. At ASCO last year, we showed that multiplexing shRNA is feasible in the preclinical setting, where multiple shRNA can be expressed from a single vector. Over the last year, we have worked further on our second generation multiplexed shRNA platform, which we believe has advantages when using our first generation multiplexing system. Going forward, we will leverage our multiplexed shRNA platform with our all-in-one vector-based approach, to underpin our future allogeneic CAR-T candidates, including several programs which are in a discovery phase of development. We are very excited about these latest advancements and look forward to providing more details on the platform and these new candidates in the future. With that, I now turn over the call to Frederick Lehmer, Cellular Oncology's Vice President of Clinical Development. Frederick?