Release issued 12th October 2001

The new data was presented Friday October 12, 2001 at the ASBMR's (American Society of Bone and Mineral Research) 23rd Annual Meeting in Phoenix, Arizona. Drs. Takuo Juji and Sakae Tanaka of the University of Tokyo have together with scientists from Pharmexa used Pharmexa's proprietary AutoVac technology to vaccinate against RANKL, a self protein known to be involved in the balance between bone formation and bone absorption.

RANKL and its role in bone absorption/loss In osteoporosis and other diseases characterised by bone loss, the body produces too much of a protein, called RANKL, which advances the loss of bone. Pharmexa's AutoVac approach is through vaccination to stimulate the patient's immune system to treat themselves by removing the excess RANKL. Abnormal bone loss is seen in several disease conditions, including osteoporosis, rheumatoid arthritis and bone metastases.

Drs. Juji and Tanaka of the University of Tokyo tested Pharmexa's AutoVac therapy in several pre-clinical bone disease models. The aim was to induce a specific therapeutic immune response in the form of antibodies against RANKL. Several important conclusions can be drawn from the studies:

AutoVac therapeutic vaccination against RANKL induced significant protection against osteoporosis

AutoVac RANKL therapeutic vaccination significantly reduced bone loss in a mouse model of postmenopausal osteoporosis. The group of mice with osteoporosis showed a 16% reduction on average in bone mineral density, a measure of bone preservation. In contrast, mice treated with AutoVac RANKL showed only insignificant reductions in bone mineral density. Thus, treated mice were significantly protected against bone loss. The osteoporotic mice had a 2.3 times increase in the number of osteoclasts, which are special cells associated with bone absorption. AutoVac RANKL treated mice had normal osteoclast counts.

In another disease model of rheumatoid arthritis AutoVac RANKL treated mice were also significantly protected from common signs of this disease, such as bone destruction and inflammation

The level of inflammation in the joints of AutoVac RANKL treated mice was reduced by 40% compared to the control group. Similarly, in the AutoVac RANKL treated mice the number of osteoclasts was reduced by more than 60% compared to the control group. Most importantly however, the level of bone destruction associated with rheumatoid arthritis was reduced by more than 80% in the AutoVac RANKL treated mice. Particularly, the destruction of bone makes advanced rheumatoid arthritis a severely crippling disease, and the ability to prevent this bone destruction would therefore be a highly desirable feature in any new therapy.

Together, these findings suggest that an AutoVac pharmaccine against RANKL is an effective treatment candidate for bone-related disorders characterised by bone degradation, such as osteoporosis, rheumatoid arthritis and bone metastases.

When will Pharmexa start phase I/II studies in the RANKL programme? Pharmexa's AutoVac RANKL programme is currently in the early pre-clinical phase. Pharmexa expects to submit an application to initiate phase I/II studies in 2003. The primary objective of these studies will be to evaluate the safety of Pharmexa's therapeutic vaccine. Other objectives will be to observe if RANKL specific antibodies can be induced by the AutoVac RANKL product, and finally to evaluate on a preliminary basis the efficacy of the treatment. Pharmexa currently owns all rights to the RANKL programme.

Brief description of osteoporosis, rheumatoid arthritis and bone metastases Osteoporosis is a major health concern affecting more than 40 million women over the age of 50 in the US, EU and Japan combined (The International Osteoporosis Foundation). It is sometimes called the silent disease because it can progress painlessly until a bone fracture occurs. In osteoporosis the normal process of maintaining bone strength is imbalanced resulting in weakened bones that are more likely to break. Unfortunately, the incidence of osteoporosis is increasing and safer and more effective therapeutics are urgently needed. In 1999 alone the total costs related to osteoporosis reached an estimated 52 billion USD in the US, EU and Japan combined (WHO). With the predicted rise in the number of osteoporotic patients and the overall aging in the world population, osteoporosis will continue to be a major health concern in the coming many years unless a new effective treatment is developed.

Rheumatoid arthritis is one of the most widespread chronic inflammatory diseases in the developed world. It is estimated that approximately 2.1 million people in the US suffer from rheumatoid arthritis (Arthritis Foundation). The disease leads to the destruction of cartilage, connective tissue and bone, resulting in destruction and deformity of synovial joints. Patients with advanced rheumatoid arthritis experience pain, are unable to partake in almost any normal physical activity and have a reduced life expectancy in the order of 3 to 7 years. As is the case with osteoporosis, there is a great need for new and better therapeutics.

Every year, millions of new patients around the world are diagnosed with cancer. Unfortunately, for many of these patients, the cancer will eventually spread to other locations in the body as metastases and very often to the bones. It is estimated that 65-75% of breast cancer and 95-100% of multiple myeloma patients develop bone metastases during the course of their disease, leading to severe pain and bone fractures. Skeletal complications are expensive for the healthcare systems, accounting for up to 60% of hospital costs in one study of advanced breast cancer patients (Coleman RE. Skeletal complications of malignancy. Cancer. 1997;80 1588-1594). The very limited number of current treatment options for bone metastases are hampered by severe side effects and there is a great need for new and better therapeutics.

Hørsholm, October 12, 2001

Søren Mouritsen Chief Executive Officer

Additional information: Søren Mouritsen, chief executive officer, telephone +45 21 45 62 44 Jakob Schmidt, chief financial officer, telephone +45 20 22 68 60

Note to editors: Pharmexa A/S (CSE: PHARMX) is a leading company in the field of therapeutic vaccines for the treatment of serious chronic diseases. Pharmexa´s proprietary AutoVac pharmaccine technology platform is broadly applicable, but the company currently focuses its resources on a number of cancer forms and chronic inflammatory diseases. Pharmexa´s research and development programs are targeted towards breast cancer, rheumatoid arthritis, Crohn's disease, asthma, osteoporosis, allergy and prostate cancer.

Pharmexa has entered into collaborative agreements with Ferring, Schering-Plough, H. Lundbeck and NeuroSearch. The company was founded in 1990 and has 110 employees, of which more than 90 are engaged in research and development. Pharmexa also owns 84% of Inoxell, a drug development company based on post-genomics technology.

Pharmexa's approach in osteoporosis and other diseases characterised by bone loss is to stimulate the patient's own immune response to participate in the treatment of the disease. This is achieved with the company's proprietary AutoVacä technology. With the AutoVac technology it is possible to point out to the immune system a certain protein called RANKL, which is known to be important to the progression of the disease in such a way that this protein is now fought by the immune system.

To learn more about Pharmexa please visit our homepage at www.pharmexa.com.

Important notice: This press release may contain forward- looking statements, which are subject to considerable uncertainty. We would like to caution you that actual results might differ materially from those projected in any forward- looking statements made herein.

(17th December 2001) Pharmexa in AutoVac cancer license option

(14th December 2001) Pharmexa subsidiary Inoxell announces achievement of first milestone in a collaboration with AstraZeneca

(9th July 2001) Pharmexa initiates phase I/II trials in breast cancer in Denmark