Shire has signed an agreement to acquire Lotus Tissue Repair, Inc., a biotechnology company developing the first and only protein replacement therapy for the orphan disease, dystrophic epidermolysis bullosa (DEB). The acquisition is subject to customary government approvals. Shire will purchase Lotus Tissue Repair an upfront payment and contingent payments based on the achievement of certain safety and development milestones.
The Human Genetic Therapies team at Shire will further develop Lotus Tissue Repair's lead product candidate, a proprietary recombinant form of human collagen type VII (rC7), for the treatment of DEB. This intravenous protein replacement therapy is currently in late-stage preclinical development.
DEB is a genetic disorder, characterized by extremely fragile skin and recurrent blister formation resulting from minor mechanical friction or trauma. Severe cases of disease may include internal blistering of the mouth, esophagus, lower gastrointestinal tract, upper airway and genitourinary tract.
"DEB is one the most devastating orphan diseases, severely impacting the lives of patients and their families, many of whom have few or no treatment options other than palliative care," Dr. Philip J. Vickers, global head of R&D at Shire Human Genetic Therapies in a press release. "rC7 protein replacement therapy has the potential to provide a first-in-class disease-modifying treatment for these children. We plan to apply our proven ability to develop protein replacement therapies for rare genetic diseases to progress rC7 as a possible groundbreaking treatment that offers hope to patients with DEB."
"This acquisition of Lotus Tissue Repair by Shire further underscores the potential of this proprietary rC7 technology to dramatically change the treatment landscape for DEB patients and their families," said Dr. Mark de Souza, founding CEO of Lotus Tissue Repair. "We are thrilled that this program will become part of the innovative pipeline at Shire and the company's growing commitment to this patient community."
