CURRENT TREATMENTS FOR AUTOIMMUNE MYOSITIS

Timely escalation and more targeted treatment options are needed in autoimmune myositis

In autoimmune myositis (AIM), irreversible damage can accumulate across the muscles and organs involved, even when day-to-day symptoms can fluctuate, highlighting the importance of early effective treatment and prompt escalation when needed.1–3


Unfortunately, current treatment options have several limitations, and few are specifically approved for AIM, highlighting a need for new treatment options.2,4,5

Limitations of existing treatments

With a lack of targeted treatment options, clinicians have to rely on broad immunosuppressants including corticosteroids and conventional immunosuppressants, which for some patients are too toxic or intolerable.1,2,6

Blue and white ceramic IV bag ornament placed on a wooden surface.
Blue and white ceramic cloud figurine decorated with storm patterns, lightning bolts, and raindrops on a wooden surface.

Burden of current treatments

Current treatments involve time-intensive administration (e.g. infusions) and can have cumulative side effects, such as osteoporosis and diabetes. These effects can disrupt daily life and force ongoing lifestyle adjustments.3,6,7

Lack of targeted treatments

The inconsistent disease control commonly seen with current therapies highlights a need for treatments that target underlying disease drivers while preserving protective immunity.2,5,8

Blue and white ceramic medicine bottle with anatomical muscle-pattern decoration beside a blue-and-white capsule on a wooden surface.

Continue exploring AIM

Learn more about the subtypes of AIM, burden of disease, and current and emerging treatments.

What is AIM?

AIM is a rare autoimmune rheumatic disease spectrum, encompassing heterogeneous subtypes with diverse clinical presentations.2

Role of autoantibodies

Autoantibodies are a hallmark feature of AIM.5

Burden of disease

AIM can reshape the lives of patients and those around them.3

Abbreviations:
AIM, autoimmune myositis.



References:
1. Oldroyd A, et al. Clin Med (Lond). 2017;17(4):322–328; 2. Lundberg IE, et al. Nat Rev Dis Primers. 2021;7(1):86; 3. Oldroyd, et al. BMC Rheumatol. 2020;4:47; 4. Neves A, et al. Rheumatology. 2024;63:2938–2947; 5. Groener M, et al. Front Immunol. 2025;16:1581323; 6. Aggarwal R, et al. Clin Rheumatol. 2025;44:4169–4178; 7. Chérin P, et al. Medicine (Baltimore). 2020;99(7):e19012; 8. Campar A, et al. Autoimmune Rev. 2023;22(12):103455.