Corbus Pharmaceuticals Holdings, Inc., a company focused on the development and commercialization of new therapies for rare, chronic, serious inflammatory and fibrotic diseases, recently announced that its President and Chief Scientific Officer Dr. Mark A. Tepper is presenting a poster (June 1-2) at the 2015 Cystic Fibrosis Foundation Research Conference: Pushing the Frontiers, in Chantilly, Virginia, revealing promising data on the efficacy of Resunab(™) in a mouse model of cystic fibrosis (CF). The poster is entitled “Resunab Benefits in The Murine Model of CF Lung Infection and Inflammation without Jeopardizing Resolution of Pseudomonas Aeruginosa (PA) Colonization in the Lung.”
CF is a life-threatening genetic disease in which a defective gene called cystic fibrosis transmembrane conductance regulator (CFTR) induces a salt imbalance, causing the body to form unusually thick, sticky mucus that can obstruct the airways, promoting dangerous bacterial lung infections and causing ineffective inflammatory responses that can lead to lung damage and scarring (fibrosis). Cystic Fibrosis patients often experience serious respiratory and gastrointestinal manifestations, and the majority of deaths associated with the disease are due to respiratory failure. There is no cure for the disease and it is estimated that almost 70,000 individuals worldwide and 30,000 in the United States suffer from CF.
Resunab is a new synthetic oral drug designed to resolve chronic inflammation and halt fibrosis. Resunab binds to the CB2 receptor in immune cells leading to their activation and subsequent induction of pathways that can resolve inflammation and fibrotic processes (tissue scarring) without causing immunosuppression. The drug is able to reduce the number of immune cells in the affected tissues and induce an increased production of anti-inflammatory factors and “specialized pro-resolving lipid mediators of inflammation.” Resunab was found to be safe and well-tolerated in pre-clinical and Phase 1 trials, and showed promising results in pre-clinical models of inflammation and fibrosis.
Using a CFRT-deficient mouse model infected with Pseudomonas aeruginosa, a serious bacterial infection for CF patients, the team found that Resunab was able to improve mice survival, to decrease their weight loss, reduce the number of white blood cells in the lungs and to improve the animal’s ability to resolve the pulmonary infection.
The team concluded that Resunab can be considered a potential effective therapy for resolving lung inflammation in CF patients and to improve the body’s ability to overcome pulmonary bacterial infections, ultimately resulting in an improved survival.
“This study provides additional preclinical confirmation of the potential for Resunab via its novel inflammation-resolving mechanism of action to treat diseases like CF in which chronic inflammation and infection contribute to disease progression,” said Dr. Tepper in a news release. “As shown in previous preclinical and Phase 1 studies, Resunab was well tolerated and demonstrated a satisfactory safety profile with no evidence of immune suppression. Data showing that Resunab improved overall health in CFTR-deficient mice and reduced bacterial bioburden is encouraging as we prepare to commence our CF Phase 2 clinical study over the next 90 days.”
“The results with Resunab in this model are truly encouraging with respect to the potential of Resunab to treat CF through its novel mechanism of inflammatory resolution,” added Dr. Tracey L. Bonfield at Case Western Reserve University in Cleveland, Ohio, who conducted the study in collaboration with Corbus Pharmaceuticals. “I look forward to adding to these studies with additional data on the mechanism of action of Resunab in CF.”