Krystal Biotech Announces EMA Validation of Marketing Authorization Application for VYJUVEK for the Treatment of Dystrophic Epidermolysis Bullosa

• If approved, ~3,000 people with DEB in the European Union could receive VYJUVEK to treat the underlying cause of the disease for the first time
  
  
• VYJUVEK received Orphan Drug Designation and PRIME designation from the EMA

PITTSBURGH, Nov. 27, 2023 (GLOBE NEWSWIRE) -- Krystal Biotech, Inc. (the “Company”) (NASDAQ: KRYS), a commercial-stage biotechnology company focused on the discovery, development and commercialization of genetic medicines to treat diseases with high unmet medical needs, today announced that the Company’s Marketing Authorization Application (MAA) to the European Medicines Agency’s (EMA) Committee for Medicinal Products for Human Use (CHMP) for VYJUVEK (beremagene geperpavec-svdt, also known as B-VEC) for the treatment of dystrophic epidermolysis bullosa (DEB) has been validated and is now under CHMP review. A CHMP opinion is anticipated in the second half of 2024.

“The validation of our MAA for review by CHMP is an important step toward our goal to bring VYJUVEK to patients in the EU who are living with DEB,” said Suma Krishnan, President, Research & Development, Krystal Biotech, Inc. “We look forward to working closely with EMA through the MAA review process, as VYJUVEK has the potential to fulfil an unmet medical need for DEB patients and their families.”

In September 2023, Krystal Biotech received a positive opinion from the EMA Pediatric Committee on the Pediatric Investigation Plan for VYJUVEK for the treatment of DEB. Based on this positive opinion, the Company would be eligible for up to an additional two years of marketing exclusivity in the EU, on top of the ten-year EU market exclusivity after market approval in the EU. Previously, VYJUVEK received Orphan Drug Designation and PRIority Medicines (PRIME) eligibility from the EMA.

About Dystrophic Epidermolysis Bullosa (DEB)
DEB is a rare and severe disease that affects the skin and mucosal tissues. It is caused by one or more mutations in a gene called COL7A1, which is responsible for the production of the protein type VII collagen (COL7) that forms anchoring fibrils that bind the dermis (inner layer of the skin) to the epidermis (outer layer of the skin). The lack of functional anchoring fibrils in DEB patients leads to extremely fragile skin that blisters and tears from minor friction or trauma. DEB patients suffer from open wounds, which leads to skin infections, fibrosis which can cause fusion of fingers and toes, and ultimately an increased risk of developing an aggressive form of squamous cell carcinoma which, in severe cases, can be fatal.