Synspira’s inhaled SNSP113 candidate therapy against bacterial biofilms in the lungs of patients with cystic fibrosis (CF) has received orphan drug status by the U.S. Food and Drug Administration (FDA).
The buildup of mucus in CF patients’ organs, including the lungs, promotes the development of bacterial biofilms — aggregates of bacteria that adhere to the lungs’ surface. Biofilms make it harder for antibiotics to reach the bacteria, rendering them less efficient.
SNSP113, a complex sugar polymer called polycationic glycopolymerpoly acetyl arginyl glucosamine or PAAG15A, is a modified sugar molecule that enhances mucus clearance and biofilm decomposition.
Specifically, the therapy has a dual action: it interacts with components of bacteria in biofilms, breaking them apart; and with components of mucus, making it less sticky. SNSP113’s ultimate purpose is to improve lung function in CF patients.
The orphan drug status aims to encourage the development of therapies for rare and serious diseases, through benefits such as seven years of market exclusivity and exemption from FDA application fees.
“The orphan designation granted for PAAG15A by the FDA reflects the need for new treatment options for patients living with cystic fibrosis, and in particular for those patients with relentless and antibiotic-resistant bacterial infections such as Burkholderia and non-tuberculous Mycobacteria,” Shenda Baker, PhD, chief executive officer of Synspira, said in a press release.
SNSP113 was originally developed by Synedgen using its glycomics technology platform, which is now exclusively licensed to Synspira to develop inhaled therapies for CF, chronic obstructive pulmonary disease (COPD), and pneumonia.
Once-daily treatment with SNSP113 (previously known as SYGN113) was shown to lead to a significant decrease in biofilms of nontuberculosis mycobacteria (NTM) Mycobacterium abscessus isolated from CF patients.
More recently, SNSP113 showed the capacity to eliminate antibiotic-resistant Pseudomonas aeruginosa bacteria, a major cause of lung disease in CF patients. Within two to four hours after treatment, the bacteria numbers decreased by 1 million to 10 million, and elimination was seen within 24 hours after treatment.
“We are developing SNSP113 to treat pulmonary infection and airway congestion in cystic fibrosis patients to improve pulmonary health. Because SNSP113 treats the drivers of pulmonary decline rather than the underlying CFTR mutation [the mutation causing CF], it has the potential to treat a broad population of CF patients regardless of genetic mutation,” Baker said.
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