Rheumatoid Arthritis Drugs in the Pipeline

What Does the Future Hold for RA Treatment?

RA Drug Pipeline
sturti/Getty Images.

A drug pipeline is a set of drugs that are under discovery and/or in development by drug manufacturers. Drug pipelines offer promise in improving the outlook and quality of life for people with a variety of health conditions, including rheumatoid arthritis (RA).

The introduction of biologics in the late 1990s has revolutionized the treatment of RA. And since then researchers have uncovered a wealth of information about disease progression, symptom improvement, and how working towards new therapies can improve the quality of life for people with this very debilitating condition.

What RA Treatment Currently Looks Like

There is no known cure for RA. To date, treatment goals in RA include reducing joint pain and inflammation, increasing joint function, and preventing joint damage. Early and aggressive treatment is important in improving patient outcomes and preventing disability. Numerous therapies can prove to be successful and are available in a variety of forms. The most aggressive treatments include DMARDs, biologics and JAK inhibitors.

Disease-modifying anti-rheumatic (DMARDs) block inflammation to preserve joints. Without DMARDs, such as methotrexate, leflunomide, hydroxychloroquine, and sulfasalazine, inflammation would slowly destroy joints and cause them to become damaged and disfigured.

Biologics, also known as biologic response modifiers, are designed to reduce or prevent the joint-damaging inflammation RA is known for. Biologics target molecules in the cells of the immune system and joints, which are responsible for inflammation and joint damage. There are several different types of biologics that target different molecules, including tumor necrosis factor, interleukin-1, and cell surface molecules on T and B lymphocytes. Brand name biologics include Cimizia, Humira, Orencia, Remicade and Simponi. Some of these drugs must be given by self-injection while others require intravenous infusion in a doctor’s office or hospital setting. These medications are also very expensive and may not be covered by insurance. 

Janus Kinase (JAK) inhibitors, such a Tofacitinib (Xeljanz), filgotinib and baricitinib, are the newest RA drugs. JAK inhibitors work by hindering the activity of one or more of the Janus Kinase enzymes. These enzymes are responsible for the cell signaling that causes inflammation and immune responses seen in RA.

Researchers are currently working towards creating RA drugs that are less expensive and available in pill form.

What's in the Pipeline?

RA treatments have traditionally focused on targeting inflammation pathways and responses. However, newer research is now focusing on the management of additional components that cause RA progression and immune system malfunction. 

Below are some of the newest drugs in the RA pipeline that may potentially reduce RA’s effects, and in some cases, even reverse the disease’s progression.


Initially, Johnson & Johnson’s sirukumab was rejected by the FDA. More recent research indicates sirukumab can reduce clinical signs and symptoms of RA and reduce damage over two years in comparison to DMARDs. In September 2017, the FDA’s position was that there was an “imbalance” in the number of deaths for people taking the drugs versus the number taking the placebo. A 2018 RMD Open report notes the safety profile of sirukumab is as expected for an anti-IL agent, with no new signals noted.

If eventually approved, sirukumab will compete with two other Il-6 inhibitors, Actemera and Kevzara. Kevzara was approved by the FDA in May of 2017, while Actemera has been on the market for many years.


ART-I02 is currently being investigated by the biopharmaceutical company, Athrogen. It is a gene therapy medication that may reduce interferon-beta (IFN-β), a protein that produces other proteins that promote the development of RA. Pre-clinical studies have found that one single injection of ART-I02 in animal subjections is beneficial to managing the symptoms of RA and other types of arthritis, including osteoarthritis. 

Researchers are now looking at the effect ART-102 has on humans.


A 2018 study reported in the Journal of Experimental Medicine finds CDD-45 can reduce the damage associated with RA. A protein called p38 MAPK, when working correctly, can help tissue to remain healthy. However, when p38 MAPK is switched off, it may cause the body to attack its own healthy tissues. CDD-450 is designed to halt inflammation and may be effective in reducing the damage associated with inflammatory autoimmune diseases, including RA.

The current research has looked at animal subjects and human cells and finds CDD-450 can reduce inflammation-promoting molecules. The researchers suggest reducing inflammation will prevent the destruction of bones and joints. They have been able to demonstrate this evidence in rat models.

The new drug does not have the same negative effects biologics do. Biologics need to be injected in the bloodstream, which makes them expensive and unpopular with patients. Another downside of biologics is the body’s immune system may see them as foreign invaders and reject them. CDD-450 would be available as a pill and should not have the same negative effect on the immune system.


In a 2018 study reported in the Journal of Pharmacology and Experimental Therapeutics, scientists discovered that components in scorpion venom can potentially reduce the severity of RA in animal models, and in some cases, even reverse damage. Moreover, this study shows iberiotoxin may have fewer side effects than other types of RA medications.

Researchers treated rodents with iberiotoxin and found a reduction in disease activity and, in some instances, a reversal of signs and symptoms. The researchers suggest iberiotoxin could block fibroblast-like synoviocytes (FLS) potassium channels to reduce RA severity in rat models. Researchers believe FLS plays a role in RA because it may secrete compounds into the joints that cause damage and attack immune cells that promote joint inflammation and pain.

A Word From Verywell

The current research on RA drugs in the pipeline is ongoing with scientists all over the globe exploring new ways to prevent and diagnose RA, design clinical trials, measure treatment outcomes, and deliver treatments that are effective and less costly. The hope is to make huge strides to allow people living with RA to live pain-free and good quality lives. The future for people with RA is bright, and the best is yet to come. 

Was this page helpful?

Article Sources

Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial policy to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
  • Arthritis Foundation. Rheumatoid Arthritis Treatment.

  • Clinical Trials. A Single Dose Clinical Trial to Study the Safety of ART-I02 in Patients With Arthritis. Updated November 14, 2018.

  • FDA Briefing Document. Arthritis Advisory Committee Meeting. Published August 2, 2017.

  • Gelar J. Medical News Bulletin. New gene therapy drug for rheumatoid arthritis undergoes phase 1 trial. Published May 1, 2018.

  • Qiang G, Wang Y, Xu, D, et al. Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies. Bone Res. 2018; 6: 15. DOI: 10.1038/s41413-018-0016-9.

  • Tanner MR, Pennington MW, Chamberlain BH, et al. Targeting KCa1.1 Channels with a Scorpion Venom Peptide for the Therapy of Rat Models of Rheumatoid Arthritis. J Pharmacol Exp Ther. 2018 May; 365(2):227-236. DOI: 10.1124/jpet.117.245118.

  • Thorne C, Takeuchi T, Karpouzas GA, et al. Investigating sirukumab for rheumatoid arthritis: 2-year results from the phase III SIRROUND-D study. RMD Open 2018;4:e000731. DOI: 10.1136/rmdopen-2018-000731.

  • Wang C, Hockerman S, Jacobsen EJ, et al. Selective inhibition of the p38α MAPK–MK2 axis inhibits inflammatory cues including inflammasome priming signals. Journal of Experimental Medicine May 2018, 215 (5) 1315-1325; DOI: 10.1084/jem.20172063.