Inflammatory Bowel Disease (IBD) affects 1.5 million people in the United States, with nearly half suffering from ulcerative colitis (UC). This condition is generally caused by a combination of genetic and environmental factors that lead to an over-reactive immune response in the large intestine. Current treatments (including infliximab and other tumor necrosis factor [TNF] inhibitors; corticosteroids; and antibiotics such as metronidazole, ampicillin, and ciprofloxacin) are aimed at suppressing the immune system or alleviating symptoms. Unfortunately, these therapies can have harsh side effects and are ineffective in 25% to 33% of patients. For these, colectomy may be the last option.
Ventria conducted a thorough research program that discovered a novel mechanism for the human milk protein, lactoferrin, (VEN120). This discovery revealed that VEN120 protects against tissue damage from proinflammatory cytokines by interacting with the immune system and skewing the immune response toward the immunomodulatory T regulatory phenotype. It was concluded that VEN 120 presents an attractive therapeutic strategy for the management of IBD with this novel mechanism by going beyond immunosuppression to balance the T cell populations in the gut and limit tissue damage from inflammation. In addition, Ventria’s research revealed that VEN120 had positive effects on the gut microbiota diversity and preferential species that may reduce gut inflammation.