Investigational Therapies and Research for Ankylosing Spondylitis
Current research is focused on several areas to better understand what causes ankylosing spondylitis and how to treat it.
Research has demonstrated that there are genetic factors that play a role in the development of AS. Having family members with the disease increases your risk of developing it, and research suggests that over 90% of the risk of AS relies on a person’s genes. One of the most well-known genetic markers is HLA-B27. However, HLA-B27 only accounts for about 20% of the genetic risk. Other genetic factors that have been identified include ERAP 1, IL-12, IL-17, and IL-23.1,2 One gene – TLR7 – seems to be a marker for susceptibility in males but has a protective effect in females.1 More research is needed to understand all the genetic factors and how they react to different environmental factors.
The microbiome is the collection of different microorganisms, like bacteria, fungi, and viruses, that are naturally a part of the human body. The microbiome plays many important roles, including the function of the immune system. Alterations in the microbiome can lead to dysfunction in the immune system and have been linked to several autoimmune diseases.3
An estimated 70% of people with AS have inflammation in the gut, which may be related to a dysbiosis (imbalance) in the gut microbiome. Researchers have demonstrated that the gut microbiome is altered in people with AS, and this imbalance in the microbiome may be actively involved in the disease process of AS.4 It is not yet known whether certain genetic factors influence the microbiome, or whether changes to the microbiome, such as due to an infection, trigger other processes that lead to the development of AS.1 The microbiome continues to be an area of research, as scientists uncover which microorganisms are critical for health and how best to rebalance a microbiome that is altered.
There are several new treatments under investigation for AS. Some of these new treatments may be available to certain patients through clinical trials. Clinical trials are a type of medical research in which new treatments are studied in groups of patients. Through the clinical trial process, new treatments can be tested to find more effective treatments.
One of the types of biologic treatments that are under investigation for AS are interleukin inhibitors. Interleukins (IL) are chemical messengers that are involved in the inflammatory process in the body. People with inflammatory arthritis conditions like AS have abnormally high levels of some of these interleukins, and certain biologics can block specific interleukins. Several of these IL therapies are currently in clinical trials for various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, and AS.1
Janus kinases (JAKs) are a group of enzymes that work within the immune system and other cells to transmit signals that influence certain cell functions, including promoting inflammation. JAK inhibitors block these enzymes and are currently approved for other inflammatory conditions like rheumatoid arthritis. JAK inhibitors are being studied in people with AS to see if they help with the inflammation and other symptoms of AS.1
Biosimilars are a type of biologic therapy that are highly similar to an already approved biological product. While they are not generic versions of the approved products, they do provide another option and may be less expensive to patients. Several biosimilars are already available for the treatment of AS and more are being developed and investigated.
Stem cells are immature cells that can develop into other cells in the body. While they are well-known as being present in embryonic tissue, stem cells are also present in adult bodies. While current biologic treatments target the inflammatory processes that occur in AS, these therapies do not affect the abnormal bone formation and damage that occurs. Researchers are investigating whether stem cell transplants may offer a way to regenerate healthy bone tissue in people with AS.