Proceeds to support the advancement of lead candidate through the final stages of clinical development for recurrent C. difficile infection, and the advancement into the clinic of programs for autism spectrum disorder and chronic hepatitis B
Sep 17, 2020
Somerville, MA, September 17, 2020 – Finch Therapeutics Group, Inc. (“Finch”), a clinical-stage microbiome drug development company, announced today a $90 million Series D financing. New investors in the round include Baupost Group, Humboldt Fund, MSD Capital, MSD Partners, Octave Group, and OMX Ventures, along with support from existing investors, including Avenir Growth Capital, OCV Partners, Shumway Capital, SIG, SymBiosis, TPTF, and Willett Advisors.
“We are delighted to have the support of this strong syndicate to advance our platform and pipeline,” said Mark Smith, PhD, Chief Executive Officer of Finch Therapeutics. “The microbiome field is at an exciting inflection point, with recent positive clinical data from our trial in recurrent C. difficile and other clinical data suggesting that microbiome drugs may become the next major therapeutic class to transform patient care.”
“This additional funding positions us well for our next stage of development,” said Greg Perry, Chief Financial Officer of Finch Therapeutics. “In addition to advancing our lead candidate CP101 for recurrent C. difficile, we look forward to rapidly evaluating CP101 for the many other conditions linked to microbiome disruption, starting with a trial in chronic hepatitis B.”
Finch will use the proceeds from the financing to advance CP101 through the final stages of clinical development and regulatory submission in recurrent C. difficile infection (CDI), and to advance its platform and pipeline, including the initiation of Phase 1b studies evaluating FIN-211 for autism spectrum disorder (ASD) and CP101 for chronic hepatitis B (HBV).
“By starting their discovery process with insights mined from clinical data, Finch is pioneering a new and very promising approach to drug discovery,” said Nick Haft, Managing Director of OMX Ventures. “Recurrent C. difficile is only the tip of the iceberg, with dozens of proof-of-concept human microbiota transplantation studies demonstrating the potential of this approach for a wide variety of indications. With their platform, Finch is uniquely positioned to translate many of these exciting insights into promising new microbiome therapies.”
The financing builds on recent progress by Finch, with its lead candidate CP101, an investigational oral microbiome drug designed to deliver the full diversity of a healthy gut microbiome, meeting its primary efficacy endpoint for the prevention of recurrent CDI in a large, placebo-controlled trial earlier this year. Finch also recently announced the initiation of a program to evaluate CP101 for the treatment of chronic HBV, building off pre-clinical and clinical studies suggesting that delivery of a complete microbiome may drive viral clearance through stimulation of the innate immune response (1-4). Finch’s proprietary pipeline also includes FIN-211, an investigational oral microbiome drug initially targeting the treatment of children with ASD that suffer from serious gastrointestinal (GI) symptoms. FIN-211 is designed to re-establish a normal microbiome composition and function, building off pre-clinical and clinical studies suggesting that GI and behavioral symptoms may be linked to a disrupted microbiome (5-8). In partnership with Takeda Pharmaceuticals, Finch is also developing investigational oral microbiome drugs composed of rationally-selected strains designed to target specific mechanisms underlying the pathogenesis of inflammatory bowel disease. Finch’s first program with Takeda is focused on the development of FIN-524 for ulcerative colitis. After achieving key pre-clinical milestones with FIN-524, Finch and Takeda expanded their partnership to include the development of FIN-525 for Crohn’s disease.
Finch Therapeutics is developing novel microbiome drugs to serve patients with serious unmet medical needs. Finch’s Human-First Discovery® platform enables reverse translation from clinical data to engineer the composition of the microbiome based on disease-modifying mechanisms. Finch’s platform uniquely enables development of both complete microbiome communities and rationally selected consortia to restore microbiome functionality and resolve conditions driven by dysbiosis, or disruption of the microbiome. Finch’s lead program, CP101, is an investigational microbiome drug with Fast Track and Breakthrough Therapy designation from the U.S. Food and Drug Administration (FDA) for the prevention of recurrent C. difficile infection. The company is also developing FIN-211 for the treatment of children with autism spectrum disorder and CP101 for the treatment of chronic hepatitis B. The company has a strategic partnership with Takeda Pharmaceuticals focused on the development of microbiome drugs for inflammatory bowel diseases.
1. Ren et al. Fecal microbiota transplantation induces hepatitis B virus e‐antigen (HBeAg) clearance in patients with positive HBeAg after long‐term antiviral therapy. Hepatology 2017.
2. Xie et al. Faecal microbiota transplantation induced HBSAG decline in HBEAG negative chronic hepatitis B patients after long-term antiviral therapy. Gut 2018.
3. Chauhan et al. Fecal microbiota transplantation in hepatitis b e antigen-positive chronic hepatitis b patients: a pilot study. Dig Dis Sci 2020.
4. Chou et al. Age-related immune clearance of hepatitis B virus infection requires the establishment of gut microbiota. PNAS 2015.
5. Kang et al. Microbiota transfer therapy alters gut ecosystem and improves gastrointestinal and autism symptoms: an open-label study. Microbiome 2017.
6. Kang et al. Long-term benefit of microbiota transfer therapy on autism symptoms and gut microbiota. Scientific Reports 2019.
7. Ning et al. Efficacy analysis of fecal microbiota transplantation in the treatment of 2010 patients with intestinal disorders. China J Gastrointest Surg 2019.
8. Sgritta et al. Mechanisms underlying microbial-mediated changes in social behavior in mouse models of autism spectrum disorder. Neuron 2018.