New RA Drugs Show Promise

Pipeline Is Packed With New Rheumatoid Arthritis Treatments

From the WebMD Archives

June 15, 2007 (Barcelona, Spain) --The pipeline is bursting with promising new treatments for rheumatoid arthritis (RA), say researchers.

RA is an autoimmune disease in which the body attacks its own joints, resulting in pain and inflammation.

Though the advent of medications known as biologic agents have revolutionized the treatment of RA, the next generation also may have a lot to offer the 2.1 million people who live with rheumatoid arthritis, according to experts speaking here at the annual meeting of the European League Against Rheumatism (EULAR) in Barcelona, Spain.

Biologic agents such as Enbrel, Humira, Kineret, and Remicade reduce inflammation by blocking substances that cause or worsen joint inflammation in RA. They copy the effects of chemicals made by the immune system, which block inflammatory substances such as TNF (tumor necrosis factor).

“The pipeline is rich and there are a lot of new possibilities,” Iain McInnes, MRCP, PhD, a professor of experimental medicine and rheumatology at the University of Glasgow in Scotland, tells WebMD. “The challenge is to work out which ones to use and when.”

New Rheumatoid Arthritis Drugs

Cimzia. In people with RA who do not respond well to treatment with an older drug called methotrexate, adding the experimental TNF-blocker Cimzia may do the trick, says Edward Keystone, MD, a rheumatologist at the University of Toronto in Ontario.

People in the study who took the Cimzia with methotrexate were more likely to feel better than those who took methotrexate alone. What’s more, people taking Cimzia improved quicker than what has traditionally been seen with the other TNF-blockers on the market such as Enbrel, Remicade, or Humira.

This drug has a different chemical structure than the currently available anti-TNF drugs, which allows it to remain active in the body for longer periods of time and may allow it to go directly to the inflamed joint.

Among other potential perks, it may be cheaper to manufacture than other TNF-blockers. It also works faster and appears to be safer for women of childbearing age, which could put it ahead of the pack, he says.


Denosumab. This drug works differently than TNF-blockers. Denosumab targets a protein involved in the destruction of joints known as RANK ligand. But it doesn’t have any effect on the symptoms of RA.

“It is just affecting RANK ligand, and RANK ligand is involved in the bony erosions, not the overall process that leads to signs and symptoms,” explains Desiree van der Heijde, MD, a rheumatologist at the Leiden University Medical Center in the Netherlands.

Ofatamumab (HuMax-CD20). Another new agent, ofatamumab, targets B-cells, which are cells of the immune system that are believed to play a role in causing inflammation in rheumatoid arthritis. This drug binds to the surface of B-cells, effectively killing them off.

New research presented here shows that people with RA who received the drug did better than those who received a placebo or dummy pill. People with RA who were also taking methotrexate in combination with ofatamumab responded better than those taking the ofatamumab alone, says researcher Mikkel Ostergaard, MD, of Copenhagen University Hospital in Denmark.

Tocilizumab. This drug blocks another inflammatory chemical known as interleukin-6 (IL-6). New research presented here showed that it significantly reduces inflammation in RA within about two weeks' time. When given at the highest dose used in the study, it normalized levels of C-reactive protein, which is an indicator of inflammation in the body.

There were some side effects, however, including infections and an increase in levels of blood cholesterol and liver enzymes, reports Josef Smolen, MD, a rheumatologist at the Medical University of Vienna in Austria.

But “there was a rapid and significant improvement in the signs and symptoms of RA,” he says.

WebMD Health News Reviewed by Brunilda Nazario, MD on June 15, 2007


SOURCES: 2007 annual meeting of the European League Against Rheumatism (EULAR), Barcelona, Spain, June 13-16, 2007. Iain McInnes, MRCP, PhD, professor of experimental medicine and rheumatology, University of Glasgow, Scotland. Edward Keystone, MD, rheumatologist, University of Toronto, Canada. Desiree van der Heijde, MD, rheumatologist, Leiden University Medical Center, Netherlands. Mikkel Ostergaard, MD, Copenhagen University Hospital, Denmark. Josef Smolen, MD, rheumatologist, Medical University of Vienna, Austria.

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