New Pathway for Reducing the Severity of Rheumatoid Arthritis Symptoms


Compound shows promise in reducing a precursor to RA.

Compound shows promise in reducing a precursor to RA.

Researchers have identified a novel chemical compound that can reduce the severity of rheumatoid arthritis (RA), according to a study published in the Journal of Pharmacology and Experimental Therapeutics (JPET).

Researchers from Montana State University built on prior studies which had identified the chemical compound, called IQ 1S, in order to evaluate its effects on RA. The Montana research team had identified the compound, as well as the independent discoveries elsewhere.

Biologics, types of drugs that treat RA, are developed from genetically engineered proteins or antibodies that can act on substances in the immune system. When these biologics, such as Enbrel and Humira, are used in the treatment of RA, the university press release explained, they are designed to interrupt inflammatory processes that are the hallmark of RA.

“There is a real need to develop new kinds of drugs that are different,” senior author Mark Quinn, PhD, explained in the statement.

He also mentioned that other problems with biologics include their cost and the fact that sometimes a patient will only respond to the biologics for a short period of time, then stop responding.

“They could be combined with other available drugs or replace drugs that aren’t working for patients," Dr. Quinn added.

The researchers observed the chemical compound’s ability to reduce the severity of collagen-induced arthritis, which is a precursor to RA. The compound also demonstrated a capability to inhibit the destruction of cartilage and bone.

The investigators wrote that the compound was effective because it targeted kinase proteins that release activation signals to destructive and inflammatory cells. The IQ 1S compound inhibited the kinase activities, which limited inflammation in joint tissue and lymph node cells, the authors explained.

“IQ 1S can reduce inflammation and cartilage loss associated with collagen induced arthritis and can serve as a small molecule modulator for mechanistic studies of c Jun N terminal kinases function in RA,” the authors concluded.

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