EQS-News

Relief and NeuroRx Announce Partnership for Global Commercialization of RLF-100(TM) and Selection of Commercial Partners - Seite 2

As part of their agreement, Relief and NeuroRx intend to pursue the issuance of trademarks on RLF-100. NeuroRx shall prosecute such trademarks in the U.S., Canada and Israel, while Relief shall prosecute trademarks in all other territories.

Raghuram (Ram) Selvaraju, Chairman of the Board of Relief, said: "We are pleased to reach this agreement with NeuroRx, a partner we believe is best suited to ensure rapid clinical development as well as timely and expedient interaction with regulatory authorities in what is likely to be the most important market for the drug, the United States. We are looking forward to collaboratively and productively working together in order to maximize the value of the overall franchise for our shareholders and get this potentially life-saving drug to patients as swiftly as possible."

Jonathan C. Javitt, Chief Executive Officer of NeuroRx, added: "As the global pandemic continues to devastate families and communities, our small team is encouraged by the early promise we have seen in Sami Said's scientific legacy and we are working around the clock to bring this drug to patients."

About VIP in Lung Injury
Vasoactive Intestinal Polypeptide (VIP) was first discovered by the late Dr. Sami Said in 1970. Although first identified in the intestinal tract, VIP is now known to be produced throughout the body and to be primarily concentrated in the lungs. VIP has been shown in more than 100 peer-reviewed studies to have potent anti-inflammatory/anti-cytokine activity in animal models of respiratory distress, acute lung injury, and inflammation. Most importantly, 70% of the VIP in the body is bound to a rare cell in the lung, the alveolar type 2 cell, that is critical to transmission of oxygen to the body. VIP has a 20-year history of safe use in humans in multiple human trials for sarcoidosis, pulmonary fibrosis, asthma/allergy, and pulmonary hypertension.

COVID-19-related death is primarily caused by Respiratory Failure. Before this acute phase, however, there is evidence of early viral infection of the alveolar type 2 cells. These cells are known to have angiotensin converting enzyme 2 (ACE2) receptors at high levels, which serve as the route of entry for the SARS-CoV-2 into the cells. Coronaviruses are shown to replicate in alveolar type 2 cells, but not in the more numerous type 1 cells. These same type 2 alveolar cells have high concentrations of VIP receptors on their cell surfaces giving rise to the hypothesis that VIP could specifically protect these cells from injury.