Sionna Therapeutics, a clinical-stage life sciences company focused on developing innovative treatments for cystic fibrosis (CF), has successfully closed a $182 million Series C financing round. The funding will support the advancement of novel small molecules aimed at fully restoring the function of the cystic fibrosis transmembrane conductance regulator (CFTR) protein by stabilizing the first nucleotide-binding domain (NBD1).
Led by Enavate Sciences, the oversubscribed Series C round also saw participation from new investors Viking Global Investors and Perceptive Advisors, alongside existing investors including RA Capital, OrbiMed, TPG’s The Rise Fund, Atlas Venture, the Cystic Fibrosis Foundation, T. Rowe Price Associates, Inc., and Q Healthcare Holdings, LLC.
Dr. Edd Fleming, Executive Vice President of Commercialization at Enavate Sciences, will join Sionna’s Board of Directors, bringing over 30 years of healthcare industry experience to the team.
Mike Cloonan, President and CEO of Sionna, expressed confidence in the company’s focus on developing small molecules targeting NBD1 and complementary modulators. The funding provides financial flexibility, allowing Sionna to execute its clinical development plan through 2026, with multiple anticipated clinical readouts.
Cystic fibrosis, a genetic disorder caused by mutations in the CFTR gene, results in impaired CFTR function. Sionna’s preclinical data, including results from human bronchial epithelial cell models, demonstrate the potential of its NBD1 stabilizers to restore CFTR function to wild-type levels when combined with complementary modulators.
Sionna’s Phase 1 clinical trial of its first clinical-stage NBD1 stabilizer, SION-638, has shown promising results, with identified safe doses and target exposure achieved at all levels.
The company plans to advance two additional NBD1 stabilizers, SION-451 and SION-719, pending results from ongoing toxicology studies. Furthermore, Sionna continues to develop compounds targeting complementary mechanisms, such as SION-109, which entered Phase 1 clinical trials in January 2024, targeting NBD1’s interface with the CFTR intracellular loop 4 (ICL4) region.
