Actelion Ltd and Oxford GlycoSciences Plc announced that a licence agreement has been signed extending the parties' existing European marketing relationship and granting Actelion worldwide marketing rights to Zavesca (miglustat), with the exception of Israel. Zavesca is a small molecule developed by OGS for the treatment of patients with mild to moderate type 1 Gaucher disease for whom Enzyme Replacement Therapy (ERT) is unsuitable.

Under the terms of this agreement, which is for an initial five years, Actelion will be the marketing licence holder and will be responsible for all regulatory and marketing activities and for booking sales of Zavesca. OGS will be paid a share of the product's net revenues. The financial terms of the agreement are not disclosed.

David Ebsworth, Chief Executive Officer of OGS, commented: "With Actelion's experience in marketing on a global basis, with the product Tracleer, it was a logical decision to extend our relationship beyond Europe. This extension moves OGS another step closer to meeting its strategic objective of making its Inherited Storage Disorders business unit profitable by the end of 2005. It will also assist in reducing the Company's cash burn."

In the European Union, Zavesca has received marketing authorisation under exceptional circumstances (see today's separate release) and the drug is expected to be launched during spring 2003.

Following recent discussions with the U.S. Food and Drug Administration (FDA), the companies intend to submit an amendment to the New Drug Application (NDA) for Zavesca next year. This follows the End-of-Review Conference on Zavesca with the FDA. In addition to the United States, Actelion intends to file for registration of Zavesca in Japan and will evaluate opportunities in other territories, as appropriate.

The two companies, through a joint steering committee, will evaluate further potential uses of the product in other diseases, such as type 3 Gaucher disease, Niemann-Pick type C and late onset Tay-Sachs disease.

Gaucher disease is a rare genetic disorder, which results from reduced activity of glucocerebrosidase, an enzyme responsible for glycosphingolipid (GSL - a subclass of fats) metabolism. Symptoms include enlargement of spleen and liver, bone disease and anaemia.