On March 2016 BioInvent International (BINV) reported that the European Patent Office, EPO, has decided to grant the company’s patent EP 1 960 432, relating to the immune-oncology antibody BI-505 (Press release, BioInvent, MAR 16, 2016, View Source [SID:1234509596]). BioInvent plans to shortly initiate a Phase II trial with BI-505 in patients with multiple myeloma, with the aim to prevent or significantly delay relapse of this serious form of hematologic cancer. Schedule your 30 min Free 1stOncology Demo! The European patent for BI-505 will enter into force on 6 April 2016 and will expire in 2026. Corresponding patents have already been granted in the US, Japan, Australia, China, South Korea and Russia, among other countries.
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"The extended geographical patent protection for BI-505 increases the value of our project and underlines BioInvent’s ability to develop innovative and unique antibodies against severe cancer diseases", says Michael Oredsson, CEO of BioInvent.
During 2016, the start of clinical studies for three of BioInvent’s clinical phase drug projects are planned. In addition to the study mentioned above with BI-505, clinical studies are also expected to be initiated with BI-1206 in patients with non-Hodgkin lymphoma and chronic lymphatic leukaemia, and with TB-403 for treatment of rare but serious types of cancer in children.
About BI-505
BI-505 is a human antibody against ICAM-1 developed by BioInvent, which will be clinically tested in cooperation with researchers at Penn Medicine as an immuno-oncological therapy to prevent or delay relapse in patients with multiple myeloma (a form of bone marrow cancer) undergoing stem-cell transplantation. Preclinical data indicates improved activity against myeloma when BI-505 is administered in combination with Velcade or Revlimid. BI-505’s favourable safety profile has been demonstrated in a previous phase I trial. This and the unique mechanism of action, "flagging" remaining myeloma cells for elimination by actively recruited macrophages, as well as the potential to inhibit ICAM-1 dependent survival signals between myeloma cells and tumour stroma, indicate a unique possibility of improving the therapeutic effect of stem-cell transplantation.