OXFORD BIOMEDICA

NOVEL MECHANISM IDENTIFIED FOR ANTI-CANCER GENE THERAPY

Scientists Demonstrate the Potential for Delivery of Gene-Based Therapeutics Utilising Tumour-Specific Hypoxia

Oxford BioMedica plc, a world leader in retroviral gene delivery technologies, is developing a novel anti-tumour gene therapy which is set to accelerate the Company's clinical strategy by approximately 12 months. The therapy is based on exploiting the unique conditions that exist in tumours compared with other regions of the body.

The Company's collaborators in teams led by Professor Adrian Harris, Professor Peter Ratcliffe and Professor Ian Stratford at the Institute of Molecular Medicine, Oxford, will publish in Nature Medicine tomorrow (1.5.97) the first results that demonstrate the potential use of the Company's therapeutic strategy. The data published demonstrate that a novel gene switch that responds to low levels of oxygen can be used to selectively target therapeutic genes to tumour cells. In particular the technology may provide therapeutic strategies against tumours that have developed resistance to drugs and radiotherapy.

This significant advance has potential application for both existing and future cancer treatments and may allow powerful anti-cancer drugs to be delivered without the harmful side-effects often associated with their use.

Within tumour masses, regions of reduced oxygen concentrations (hypoxic zones) develop, which for most current chemo- and radiotherapies, renders the cancer cells resistant to effective treatment; this is a major hindrance to such therapies. However, the control mechanism described by the research team has been designed to positively exploit this phenomenon to selectively target tumour cells with effective therapeutics.

This technology offers the potential to deliver a range of therapeutic genes to many different cancers, for example, breast, colorectal and ovarian cancers, for targeted tumour destruction.

'We began planning an anti-cancer strategy that exploits the selectivity of the hypoxia response and acquiring exclusive rights to the technology some time ago. This demonstration of proof of principle reported in Nature Medicine, combined with advances in our proprietary gene delivery technologies allow us to accelerate our clinical trial plans, bringing them forward by about 12 months,' commented Dr Sue Kingsman, Research Director at Oxford BioMedica. 'We anticipate that, although our first trial will be in breast cancer, the technology will be applicable to the treatment of a range of solid tumours.'

'We are very pleased to be working in collaboration with Professor Adrian Harris at the Institute of Molecular Medicine. It is our strategy to invest our resources to develop clinically relevant therapeutics, optimised for specific cancers, which can integrate with current and future cancer treatment regimes and his considerable clinical expertise and advice is invaluable.'

'I believe this technology offers a real opportunity to develop the significant potential inherent in gene therapy for the effective treatment of cancer. The next stage will be to optimise the clinical strategy and produce sufficient material to assess the potential of this development in patients,' stated Professor Harris, Professor of Clinical Oncology.

Notes to Editors

1. Oxford BioMedica is a gene therapy company, established in 1995, specialising in the development and commercialisation of novel customised gene delivery technologies for the treatment of cancer, AIDS, neurodegenerative disease and cystic fibrosis. The company was floated on the UK Alternative Investment Market of the London Stock Exchange in December 1996.

2. The Institute of Molecular Medicine (IMM) was established in 1989 in the Clinical School of the University of Oxford to carry out research in molecular and cell biology with direct application to the study of human disease. Professor Adrian Harris is Professor of Clinical Oncology at the IMM and is Director of the UK Imperial Cancer Research Fund (ICRF) Oncology Unit at the John Radcliffe Hospital, Oxford, UK.

3. This research published in Nature Medicine (1.5.97) was funded by the UK ICRF, Medical Research Council (MRC), Wellcome Trust and the US National Cancer Institute (NCI, Grant No. PO1-CA55165)

4. Additional information is available from the 30th April 1997 on the following websites: http://www.oxfordbiomedica.co.uk http://www.immwww.jr2.ox.ac.