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Experimental Cystic Fibrosis Drug Could Pose Challenge to Kalydeco

Resunab targets lung inflammation

Resunab (Corbus Pharmaceuticals), an experimental drug for cystic fibrosis (CF), could pose a challenge to rival Kalydeco (ivacaftor, Vertex Pharmaceuticals), according to a report from Reuters.

Corbus received $5 million from the Cystic Fibrosis Foundation in April to develop the drug and expects to begin a mid-stage study shortly.

The company hopes Resunab will treat all patients with CF, in contrast to Kalydeco, which is approved only for a small subset of patients with certain underlying genetic mutations. Rather than focusing on the genetic aspects of CF, Resunab aims to manage the lung inflammation that the disease causes.

Kayldeco was approved by the FDA in 2012 and had sales of approximately $464 million in 2014.

CF affects 30,000 people in the U.S. and 70,000 people worldwide. The chronic, life-threatening disease is caused by a defective or missing CF transmembrane conductance regulator (CFTR) protein resulting from mutations in the CFTR gene. The abnormal protein causes the buildup of thick, sticky mucus in the lungs, which, in turn, leads to recurrent bacterial infections. Importantly, individuals with CF also have an ineffective innate immune response that compounds the inflammation and lung damage caused by the infections. The outcome is constant, harmful inflammation leading to progressive lung damage and failure.

Resunab –– a first-in-class, synthetic, oral anti-inflammatory drug –– is designed to trigger the resolution of chronic inflammation by binding to and activating CB2 receptors on immune cells. Phase I clinical studies in a total of 123 subjects have shown that the drug has a favorable safety profile coupled with promising potency in preclinical models of inflammation and fibrosis, according to Corbus.

In preclinical studies, Resunab demonstrated a reduction in immune-mediated inflammation and tissue injury by acting on and influencing cellular immunity (i.e., inducing apoptosis of T-lymphocytes); inhibiting leukocyte migration; reducing the secretion of cytokines (interleukin [IL]-1beta, IL-6, and IL-8), inhibiting the production of matrix metalloproteinases (MMP-1, -3, and -9); reducing levels of pro-inflammatory eicosanoids (prostaglandin E2 and leukotriene B4); and increasing the production of non-inflammatory eicosanoids (prostaglandin J2 and lipoxin A4). The combined pharmacologic effects of Resunab influence the balance of pro- and anti-inflammatory cytokines, eicosanoids, and metalloproteinases, resulting in the resolution of inflammation.

In addition, Resunab stops the influx of new inflammatory cells into tissue and can act directly on fibroblasts to reduce their production of collagen, which promotes fibrosis.

Resunab is also being tested to treat scleroderma.

Sources: Reuters; May 5, 2015; Corbus Pharmaceuticals; May 2015; and Corbus Pharmaceuticals; April 22, 2015.

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