The published findings demonstrate how pre-treatment with IdeS in tumour animal models can increase the efficacy of currently available antibody based cancer therapies.

Christian Kjellman, Senior Vice President R&D at Hansa Medical, said: “We are very encouraged by this data, which demonstrate the potential of IdeS as a pre-treatment for cancer patients. Removing inhibiting IgG antibodies prior to dosing the patient with a therapeutic antibody could potentially stimulate a stronger immune response thereby increasing the efficacy of the given treatment.”

IgG antibodies are one of the most abundant proteins in the body. They play an important role in the immune system, protecting against bacterial and viral infections by targeting the pathogen and attaching it to immune cells. The target-specific elimination capacity of IgG has been utilized in the development of a number of anticancer therapeutic antibodies currently in clinical use.

However, high levels of IgG antibodies have been shown to limit the efficacy of these anticancer therapies, as they can saturate the receptors of the patient’s immune cells preventing them from efficiently killing the tumour cells.

IdeS is an enzyme that depletes IgG antibodies fast and effectively. The article entitled “Enzymatic inactivation of endogenous IgG by IdeS enhances therapeutic antibody efficacy” show that IdeS is a potent tool to reboot the human antibody repertoire and to generate a window to preferentially load therapeutic antibodies onto effector cells. 

Pre-treatment with IdeS could be a potential new treatment to unblock the receptors of immune cells thereby enabling the full potential of the therapeutic antibodies. Hansa Medical is investigating applications of IdeS in cancer immunotherapy under the project name EnzE – Enzyme based antibody Enhancement. The company is currently evaluating options for initiating a clinical study.

The information in this press release is disclosed pursuant to the EU Market Abuse Regulation. The information was released for public disclosure through the agency of the contact person stated below on May 23 2017 at 08.00 CET.