Virulizin, Lorus’ lead anticancer drug candidate, has demonstrated favorable safety and efficacy in phase I and II clinical trials by stimulating the immune system to attack and destroy tumor cells. Scientists at Lorus have continued to identify the cellular components of the immune system involved in the mechanism by which Virulizin acts as a novel biological response modifier.
Previously published results demonstrate that macrophages and NK cells, essential parts of the innate immune response, are important components in the antitumor mechanism of Virulizin.
To further understand how Virulizin acts on the molecular level, Lorus initiated studies to identify cytokines that may be involved in transmitting the stimulatory effects of Virulizin.
Given that Virulizin induces IL-17E expression, this leads to the possibility that Virulizin recruits pro-inflammatory cells to the tumor site which may function in parallel and/or in synergy with macrophages and NK cells in mediating tumor destruction.
Virulizin is currently being studied in a fully enrolled pivotal phase III clinical trial for the treatment of pancreatic cancer.