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spk00: Good morning and welcome to the Finch Therapeutics Corporate Update conference call. At this time, all participants are on a listen-only mode. After this speaker's presentation, there will be a question and answer session. To ask a question at that time, please press star followed by 1 on your touchtone telephone. If anyone has difficulty hearing the conference call, please press star 0 for operator assistance. I would now like to turn the conference call over to Stephen Jasper of Gilmartin Group. Please go ahead.
spk02: Thank you, Operator. Good morning, everyone, and thank you for joining today's call. As a reminder, this call is being recorded, and the replay will be available later today on the Investors & News section of the Finch Therapeutics website at www.finchtherapeutics.com. This morning, Finch issued a press release providing a corporate update as well as financial results for the first quarter of 2022. You may access the release under the Investors & News section of the Finch website. On today's call, I'll be joined by Dr. Mark Smith, Chief Executive Officer of Finch, and Dr. Howard Franklin, our newly appointed Interim Chief Medical Officer. Dr. Smith and Dr. Franklin will be providing updates regarding Finch's development programs and other business highlights. Joe Battiglio, Chief Business and Legal Officer, and Mark Blaustein, Chief Operating Officer and Principal Financial Officer, will be available for the question and answer session following today's remarks. Before we begin, I'd like to remind everyone that various remarks made about companies' future expectations, plans, and prospects constitute forward-looking statements. We will discuss Finch's expectations regarding its clinical development programs, platform, and runway. These forward-looking views are subject to risks and uncertainties, and our actual results could differ materially from the views expressed today. These risks and uncertainties include those described in the earnings release we furnished to the SEC on Form 8K, our annual report on Form 10K, and our other filings with the SEC. These forward-looking statements speak only as of today's date, and we undertake no obligation to update or revise any of these statements. I'll now turn the call over to Finch's CEO, Dr. Mark Smith. Mark.
spk01: Thank you, Steven, and thank you to everyone for joining the call this morning. Following the resolution of the clinical hold on our IND for CP101, we are excited to take this opportunity to provide updates on our development programs. On today's call, we will briefly review our strategy here at Finch and then discuss the next steps for our CP101 program in recurrent C. difficile infection, or CDI, and the next steps for our FIN211 program in autism spectrum disorder, or ASD, At the conclusion of our prepared remarks, we'll open up the floor to questions where I will be joined by Howard, Joe, and Mark from our executive team. Moving down to slide four, before I dive into the updates, I thought it would be helpful to remind everyone about the platform that we're building here at Finch and share broader context on how we think about this new modality. The microbiome consists of a community of tens of trillions of bacteria that live on and inside of us. and are responsible for many aspects of human health, ranging from modulation of our immune system to shaping our metabolism and even the production of key neurotransmitters. What is fascinating to me is that while we're all born with roughly 20,000 genes that we get from our parents, we have nearly 20 million that we get from our microbiome. We see the microbiome as a new organ system that comprises the majority of our genetic repertoire, and at Finch, We're focused on developing tools to engineer the microbiome to transform human health. Moving to slide five, our human first discovery platform is designed to enable capital efficient data generation to support our development programs. Our approach starts with clinical proof of concept data. There are more than 300 registered clinical trials right now exploring microbiota transplantation across a number of academic centers around the world. This research spans a diverse range of therapeutic areas, And we've established strong partnerships with many of the largest providers of microbiota transplantation in the world that enable us to use clinical data to evaluate new opportunities for engineering the microbiome before we make significant investments in a new program. As the field continues to mature and our collaborators generate ever more clinical data, we feel this approach which is the first stage of our human-first discovery process, will continue to differentiate Finch and provide us with capital-efficient entry points into new therapeutic areas. We believe having proof-of-concept clinical data before we initiate development is a key advantage to our approach, and we see it as a necessary but not sufficient step before we initiate a new program. The second element that we look for is having mechanistic insights, To gain these, we mine clinical data to identify the specific microbes and metabolic pathways that are driving the promising outcomes we see in early proof-of-concept studies. Once we have met both of these criteria with clinical data and mechanistic insights in hand, that's when we deploy our product development platform, which I will review in more detail on slide 6. Our product development platform is designed to enable us to tailor our products based on what we learn from the clinical data and our mechanistic insights, providing everything from full microbial ecosystems down to individual microbes. With our complete consortia product candidates, we have the ability to deliver entire intact microbial communities derived from rigorously screened healthy human donors. On the other end of the spectrum, our targeted consortia product candidates deliver individual organisms grown in pure culture from master cell banks. And then we have a third approach, our enriched consortia product strategy, which combines the first two approaches. For enriched consortia products, we use a complete consortia scaffold and then add individual strains that hit specific pathways of interest on top of that scaffold. All of these product candidates are orally administered And because we are able to deliver full communities, we can let the biology guide our development, rather than being limited by our technology to delivering narrow subsets of the microbiome. We believe that our ability to tap large clinical datasets, mine them for mechanistic insights, and then translate them into differentiated products uniquely positions Finch to lead the next chapter of this field as we look to build on our promising clinical data in CDI and bring this emerging modality into the many conditions that are closely linked to the microbiome. Slide seven shows how we are executing against our strategy to first demonstrate the power of our platform in CDI and then extend into new areas of significant unmet need that are linked to the microbiome through interventional clinical data. Our lead program in CDI is in phase three development And Howard will share more on the data we have generated to date and our plans for this program going forward in just a few moments. We also have a partnership with Takeda focused on inflammatory bowel diseases. We have handed off development responsibility for TAC524, the first product candidate to emerge from this collaboration with Takeda, and we are leading discovery efforts in FIN525 for Crohn's disease. Separately, we are also developing FIN211 for autism. focusing initially on the roughly one-third of autistic children that have significant GI symptoms. We see this as a transformational opportunity, and I'll provide additional detail on our plans for this program after Howard wraps up his discussion of CDI. Today, all of the programs we have prioritized for development target gastrointestinal effects as a component of their target product profile, a logical starting point given the physical proximity for our GI-targeted therapies and one which we hope to build on over time. I'll now turn it over to Howard to share more about our exciting work developing CP101 in recurrent CDI.
spk04: Thank you, Mark, and good morning, everyone. With many years practicing as a general surgeon before I entered the biopharmaceutical industry 20 years ago, I've treated many recurrent C. difficile patients who are fighting for their lives. I have a firsthand understanding of the horrific impact that C. difficile can have on patients and their families and the tremendous need for therapeutics that can prevent recurrent CDI. It's a privilege to be in a position to work towards delivering much-needed innovation to this community. Turning to slide nine, I'd like to briefly review the enormous human and economic burden of recurrent CDI. There are nearly 200,000 cases of recurrent CDI every year in the U.S. and an estimated 44,000 deaths are attributable to CDI each year in the U.S. CDI is believed to result in approximately $5 billion in direct treatment costs per year in the U.S., and despite this spending, tens of thousands of people die each year from CDI. CP101 has the potential to break the cycle of recurrence that so many patients suffer from. and prevent patients from going back into the hospital setting again and again with recurrent disease. Given the high cost of this disease, I'm struck by the potential value that we can deliver with a product candidate that we believe can change the course of disease by restoring a diverse microbial community that can effectively outcompete C. difficile. For example, pharmacoeconomic studies have found cost savings of $25,000 to $30,000 per patient with the use of microbiota, transplantation. Moving to slide 10, we have completed PRISM-3, a phase two randomized placebo-controlled trial that highlights the potential for CP101, a complete consortia product candidate in CDI. PRISM-3 was designed to demonstrate the superiority of CP101 plus standard of care antibiotics over placebos. plus standard of care antibiotics for the prevention of recurrent CDI. It's important to note that we are not trying to compete with or displace antibiotic therapy. Antibiotics play a critical role in stopping an active CDI infection, but antibiotics can also significantly disrupt the microbiome and leave patients vulnerable to CDI recurrence. Rather than displacing antibiotics, our objective is to deliver CP101 after an antibiotic treatment and restore a diverse, healthy microbiome that can protect against future recurrences and prevent the significant morbidity and mortality associated with recurrent CDI. The primary efficacy endpoint in the PRISM-3 trial was the proportion of participants without CDI recurrence through eight weeks. Participants were followed up to 24 weeks for long-term safety and efficacy. PRISM-3 enrolled participants with all stages of recurrent CDI, including first CDI recurrent, and we accepted all guideline-recommended methods of CDI diagnosis at study entry, two distinguishing features of the PRISM-3 trial that we believe will be important for supporting our potential label and market access in the future. On the next slide, I will briefly recap the top-line results from PRISM-3. The results of PRISM-3 are really exciting. As shown on the left of the slide, CP101 achieved its primary efficacy endpoint with a 33.8% relative risk reduction over placebo for CDI recurrence through week eight. As shown on the right of the slide, we observed that participants treated with CP101 had a lower risk of CDI recurrence through week 24 as well. We also saw that CP101 had safety profile similar to placebo with no treatment-related serious adverse events in the CP101 arm. On slide 12, I will briefly recap the top-line results from our Phase II open-label trial of CP101 for the prevention of recurrent CDI. PRISM extension was an open-label trial which enrolled 132 participants with recurrent CDI. Like PRISM-3, PRISM extension participants received standard of care antibiotics prior to receiving CP101. As shown on the left of the slide, we observed that 80% of participants were without CDI recurrence through eight weeks, and we saw that this result was sustained over time with 78% of participants not experiencing a CDI recurrence through week 24. In a post hoc analysis of participants who received up to two doses of CP101 in PRISM-3 and PRISM extension, an aggregate 88% did not experience CDI recurrence through eight weeks following their last dose. These data give us visibility into how this drug may behave when patients are given up to two doses in a real-world setting. These data led us to launch PRISM-4, our phase three trial of CP101. As shown on slide 13, PRISM-4 has a very similar design to our PRISM-3 trial with a couple of key features that I will highlight. We have extended the antibiotic washout period, which we believe will support a more robust engraftment We increased the sample size and we have moved to a two to one randomization ratio to make the trial more attractive to patients that may want to enroll. Finally, we have also included ex-US sites to bolster enrollment and support marketing authorization outside the US down the road. Now that our hold has been released, we are deeply focused on preparing ourselves to begin serving patients again later this year. Ahead of being able to do so, we have additional manufacturing and quality activities we need to complete, along with submitting additional materials for FDA review, including a PRISM IV protocol amendment. With these activities completed, we expect to be in a position to proceed with enrollment in the second half of this year, and we are excited to build on the success observed in PRISM III and PRISM Extension. I'll turn it back to Mark to share updates on our work in FIN 211 for autism.
spk01: Thank you, Howard. I'm excited to share updates on our plans to develop FIN 211 for autism. Let's start off on slide 15 by talking about the unmet need here. There are more than 4 million individuals with autism in the U.S., and roughly a third of them suffer from significant GI symptoms. There are currently no approved therapies for the core symptoms of autism. And instead, many of these families rely on intensive behavioral therapy, which requires many hours of one-on-one engagement each day. This is incredibly costly care to deliver, as the US spends approximately $100 billion every year supporting individuals with autism. Despite these high costs, outcomes are still very poor for many individuals. Moving down to slide 16, we believe FIN 211 could be a transformational opportunity for this community. offering the potential to address both behavioral and GI symptoms based on clinical data from more than 200 individuals treated with microbiota transplantation in third-party clinical studies. FIN211 is an orally administered enriched consortia product candidate. This means that it includes both a donor-derived complete consortia component and bacteria grown in pure culture from a master cell bank, which together are designed to engage three mechanisms, neuroinflammation, barrier function, and oxytocin induction. On neuroinflammation, children with autism often exhibit elevated systemic inflammation, decreased blood-brain barrier integrity, and increased neuroinflammation, which can interfere with typical neural activity and development. As an example, one study found that children with autism have more than three-fold higher TNF-alpha positive lymphocytes than neurotypical children, and even had similar levels to children with Crohn's disease. Improved gut barrier function is a second target mechanism for FIN211, potentially addressing GI symptoms while preventing neuroactive microbial toxins from entering circulation and interfering with neurological function. Children with ASD and GI comorbidities experience increased levels of neuroactive microbial toxins, which are reduced following microbiota transplantation. Both inflammation and gut barrier function are mechanisms that we have spent years focused on modulating and measuring through our work in IBD, positioning us to leverage our platform capabilities now in autism. A third mechanism that we have focused on is induction of oxytocin, a neuropeptide responsible for regulating sociality and bonding. Extensive preclinical work has shown that microbes can address autistic behaviors in an oxytocin-dependent manner, while clinical data have shown that children with autism can exhibit lower levels of oxytocin than their neurotypical peers. We're excited to bring this enriched consortia product candidate designed to impact neuroinflammation, barrier function, and oxytocin expression into the clinic, and on slide 17, I'll review our key objectives in early development for FIN211. We have three primary objectives in early development of Fin211. First, as always, it is critical for us to establish safety and tolerability for this product candidate. Second, we need to identify the optimal treatment regimen, including dosing and whether there is a need for pretreatment antibiotics. Third, we will want to generate early proof of concept data that can be used to support the key design elements like power calculations that we'll need for later stages of development. We previously planned to address the first two objectives in our initial clinical study before moving on to an early proof of concept study with a placebo comparator in the future. As a great example of our human first discovery platform in action, over the past several months, we've analyzed new clinical data with microbiota transplantation in ASD. Specifically, we have additional information on dosing and outcomes without pretreatment antibiotics. These data informed our decision to simplify our clinical development strategy, moving directly into an early proof-of-concept study with a placebo comparator. On the next few slides, I'll briefly walk through some of the third-party clinical data that are supporting our development strategy. On slide 18, we've summarized one of the first studies in the field which evaluated microbiota transplantation in 18 children with ASD and significant GI symptoms following vancomycin and bowel prep conditioning. Participants were evaluated at baseline eight weeks after cessation of therapy and then followed up to two years post-therapy. There is significant improvement in GI symptoms at eight weeks, which continued over time. The behavioral data, though, is what I find particularly striking about this study. Again, as with the GI scores, the study found a statistically significant improvement in the behavioral scores at eight weeks, but what is remarkable to me is that these outcomes continue to improve over time, with a third of the participants no longer meeting the criteria for diagnosis of autism at the end of the study period. These are exceptional findings in a small, open-label clinical study, and so a logical follow-up is to see if the core observations hold up in a larger, controlled study. On slide 19, we see that they did. This separate study evaluated 45 individuals who were randomized to either receive behavioral therapy alone or behavioral therapy plus microbiota transplantation without antibiotic preconditioning. Again, the study showed significant improvements in both GI and behavioral outcomes, and these were matched with shifts in the microbiome composition, which we believe support the view that vancomycin pretreatment may not be necessary to engraft a new microbiome in this population. On slide 20, we see results from a third, 40-participant study that evaluated microbiota transplantation in autistic children with significant GI symptoms. This study found that both GI and behavioral endpoints improved significantly eight weeks after cessation of therapy. This study also did not rely on pretreatment antibiotics. On slide 21, we summarized data from more than 200 individuals treated with microbiota therapy across six third-party studies. These studies show consistent improvements in both GI and behavioral endpoints with or without pretreatment antibiotics. We have re-evaluated our development strategy in light of some of these new clinical data that have emerged since we originally designed Aspire. We believe these clinical and translational data are sufficient to inform a dosing regimen that does not include antibiotic pretreatment. As a result, we plan to focus Aspire on dreading safety as well as early proof-of-concept data. Building on these insights, we've updated our study design for ASPIRE, which I'll review on slide 22. In the ASPIRE trial, we plan to evaluate 36 children between the ages of 5 and 17 with autism and significant GI symptoms. Participants will be randomized 2 to 1 between FIN211 and a placebo after completing a bowel prep. Our primary endpoints will be safety and tolerability. In addition to evaluating safety and tolerability, this study is designed to provide early visibility into the impact of FIN-211 on GI and behavioral endpoints to inform the design and power calculations for larger studies in later stages of development. As we work to complete additional manufacturing activities to support this new study design, including the production of a placebo product, we anticipate filing our IND in Q4 of this year. By leveraging our human-first discovery platform to inform our dosing regimen, we believe this approach will enable us to deliver early proof of concept for this program earlier than originally anticipated and exciting development for us and the community that we aspire to serve. I'll wrap up by briefly recapping our portfolio on slide 23. We have a phase three asset in CDI, and we anticipate that we will proceed with enrollment in our PRISM-IV trial later this year. We have a collaboration with Cicada in IBD, which is advancing our targeted consortia product platform. And finally, we have a potentially transformational opportunity in autism, which we plan to advance into a placebo-controlled study to establish both safety and tolerability, as well as early proof of concept. Furthermore, with the financing we announced earlier this morning with our new partner, Hercules Capital, together with Cash on Hand, and anticipated non-dilutive sources of additional cash, as described on slide 23, we anticipate cash runway into the second quarter of 2024. Importantly, we believe our cash runway will support us through clinical milestones in both C. difficile and autism programs. We believe our focused portfolio, coupled with our human-first discovery platform, leave Finch well-positioned to lead this field through the next chapter in its development. And with that, operator, we can open up the line for questions.
spk00: Thank you. Ladies and gentlemen, if you'd like to ask a question at this time, you will need to press the start and the one key on your touchtone telephone. Please stand by while we compile the Q&A roster. And we have a question coming from the lineup. Jason Gerberry with Bank of America. Your line is open.
spk03: Hey, guys. Good morning, and thanks for the update. I guess first, just with the autism update and trial, Can you speak to a level of FDA with their FDA interaction that helped inform your thought process on this design update going forward? And I presume that your enrollment criteria would be CARS baseline scores kind of in the 35 to 40 range, just trying to get your sense in terms of given patient level heterogeneity on the behavioral component, how you guys look to try to manage that in the context of trial. And then I guess lastly on CP101, the data timeline update, as we think about eventually a data timeline here, can you add sites? Are there any other levers you can pull to just sort of increase the pace of enrollment to keep with the original timeline for data? Thanks.
spk01: Wonderful. Well, thank you, Jason. Thanks for those questions, and I'll try to tick those off in order. So The first question around the autism study and our engagement with the agency as we've prepared for this updated design. So we did have a pre-IND meeting with the agency and we've used some insights from that pre-IND meeting to inform the design that we're proceeding with with the ASPIRE program. And your second question around some of the baseline criteria that we're using in order to manage heterogeneity. As we get closer to filing the IND, we'll likely provide some additional updates on some of those key inclusion-exclusion criteria. But we will be characterizing both the GI and behavioral scores, including CARS, at baseline and provide some updates on what the entry criteria will look like as we get closer to initiating enrollment in that. And the third question that I caught around levers that we have at our disposal in order to accelerate the timeline, as you note, we'll look forward to providing some additional guidance around the timeline to top line data. as we get into the clinic and start to see our rates of accrual. We've taken a number of steps in order to position this study for success, including the use of a two-to-one randomization ratio, which Howard previously noted, in order to make this as attractive as possible for patients to enroll. We've also ensured that there's a an open-label extension opportunity for patients who may have received placebo or otherwise failed to achieve a response in the main portion of the study, and we feel that that's a really attractive element as well. And then finally, we are working with sites around the world, so additional XUS sites, in order to provide access in other geographies and to diversify the geographic basis that we're using for enrolling patients in the study. So a number of steps underway and more to come in order to deliver this data at high quality and as expeditiously as possible. So thank you for the questions, Jason, and feel free to follow up if you have any others that I missed there.
spk03: Great. Thanks, guys.
spk00: Ladies and gentlemen, if you'd like to ask a question, please press star 1. And I am showing no further questions at this time. I would now like to turn the call back over to Dr. Marks-Smith for any closing remarks.
spk01: Fantastic. Thank you, operator, and thank you all for your participation in today's call. We're really excited about the opportunities that lie ahead for us and look forward to sharing updates as we continue to pioneer this new field of medicine. Have a great day.
spk00: Ladies and gentlemen, that does end our conference for today. Thank you for your participation. You may now disconnect.
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