Researchers identify potential new RA pathway

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Researchers identify potential new RA pathway

15/08/2006 - Biogen has revealed details of a potential new pathway

in rheumatoid arthritis (RA) that could provide unique insights into

the disease process and eventually a new approach to developing RA

therapies.

RA affects approximately 0.5 to one per cent of the adult population

worldwide and about twice as many women as men suffer from the

disease. Currently, Enbrel (etanercept) and Remicade (infliximab)

dominate the US and European RA markets, accounting for more than 80

per cent of value sales.

Studies conducted by Biogen and University of Geneva scientists have

revealed that inhibiting the TWEAK molecule may interrupt the disease

through a series of multiple mechanisms.

" Despite considerable progress, many rheumatoid arthritis patients do

not adequately respond to current treatments, indicating that other

pathways are involved in this complex disease, " said Zheng,

senior scientist, molecular discovery at Biogen.

" Our investigative research suggests the TWEAK pathway may also

represent a new set of opportunities for treatment. "

TWEAK belongs to a family of molecules called tumour necrosis factor

(TNF) that plays an important role in normal immune system and

inflammatory responses.

TNF-inhibiting therapies are currently used to treat a number of

diseases including RA, a chronic, autoimmune disease that causes

inflammation and swelling of the joints and the surrounding synovial

tissue, resulting in progressive damage to the cartilage and bone.

TWEAK stimulates blood vessel growth (angiogenesis) and production of

inflammatory proteins called cytokines and chemokines.

The published studies found that TWEAK promotes a number of events

that are hallmarks of RA, including joint inflammation and synovial

angiogenesis (blood vessel growth in joints).

Specifically, Biogen researchers found that TWEAK promotes joint

inflammation by stimulating the production of several types of

inflammatory proteins, triggers joint damage by stimulating the

production of damaging metalloprotease enzymes and promoting bone

breakdown, and contributes to joint tissue disease by directly

promoting angiogenesis in synovial tissue.

The studies also suggest that TWEAK may impede normal bone repair

mechanisms.

" Our research is part of a broader effort to identify the role of the

TWEAK pathway in several autoimmune diseases, " added Burkly,

the TWEAK program leader at Biogen.

Current treatments for RA are varied with local steroid injections,

joint replacements used to treat the symptoms. Seldom did the

therapies make the pain go away completely or for very long, nor did

they affect the underlying joint damage.

However, much progress has been with drugs called biologic response

modifiers or biologics. This group of drugs include, Enbrel, Humira,

Kineret, Remicade, Rituxan and Orencia.

Enbrel, Humira, and Remicade inhibit a cytokine called tumor necrosis

factor or TNF. Kineret blocks the cytokine interleukin-1 (or IL-1).

Rituxan selectively targets immune cells known as CD20-positive B cells.

http://www.drugresearcher.com/news/ng.asp?n=69860-biogen-rheumatoid-

arthritis-tweak