Cachexia is a debilitating, progressive muscle wasting condition manifested by unintentional weight loss, muscle weakness, anemia, fatigue, and death. In advanced cancer patients the prevalence of cachexia increases from 50% at diagnosis to more than 80% prior to death. There is currently no FDA-approved therapy for treating cancer cachexia.

Early stages of cancer cachexia are largely driven by the factors that inhibit adequate nutrition (anorexia-cachexia). In contrast, later stages of cachexia are largely driven by severe inflammation and not responsive to increased nutrition including intravenous supplied nutrients (hypercatabolic-cachexia). In a few select cancers, cachexia may also be driven by treatment or cancer induced hormonal imbalances, such with testosterone suppression in hormone-sensitive prostate cancer or by inactivity-induced muscle atrophy.

Cachexia is a particularly serious problem for over 100,000 patients in the United States who exhibit hypercatabolic-cachexia associated with advanced solid-tumor cancer. Currently there are no FDA approved drugs for the treatment of cancer cachexia. It is estimated that the size of this market in the US exceeds $1 billion for all stages of cachexia and exceeds $250 million for hypercatabolic-cachexia associated with severe inflammation and advanced cancer.

Based on its initial indication for the treatment of cachexia in patients with advanced non small cell lung cancer, upper GI cancer or Head and Neck cancers, VT122 will address a US market of more than 100,000 patients with revenue potential of over $250 million. Achieving broader claims for the treatment of cachexia associated with other cancers, Vicus expects US revenue could exceed $250.

VT-122 is an oral, multi-targeted, chrono-modulated, fixed dose combination of propranolol, a non-selective beta adrenergic receptor blocker, and etodolac, a balanced COX1 and COX2 enzyme inhibitor. We chose the constituent drugs based on the results of our cancer cachexia disease model that predicted blocking systemic inflammation would reverse the wasting process. While etodolac targets key inflammatory pathways in the tumor, liver and immune system, propranolol suppresses autonomic nervous system activation and excess catecholamine release.

We designed the chrono-modulated dosing regimen to address known safety risks associated with etodolac and propranolol. Investigator-led trials were completed in 2006 and 2007 in weight losing subjects with stage IV cancer. These trials demonstrated reversal of rapid weight loss in seven of nine subjects. No treatment related adverse events were reported