AstraZeneca's Anifrolumab Shows Benefit for Skin, Joint Symptoms of Lupus

Anifrolumab is consistently associated with improvements in both skin rash and arthritis across three different disease measures in patients with moderate to severe systemic lupus erythematosus (SLE), results of a new post-hoc analysis of pooled data from the TULIP phase 3 clinical trials show. The data were presented at the annual European Congress of Rheumatology (EULAR 2021).

Anifrolumab is a potential first-in-class type I interferon inhibitor in development by AstraZeneca.

For skin rash, the difference in response rates for anifrolumab versus placebo at week 52 were 13.5% SLE Disease Activity Index (SLEDAI), 15.5% British Isles Lupus Assessment Group index (BILAG) and 15.6% modified Cutaneous Lupus Erythematosus Disease Area and Severity Index (mCLASI). For arthritis, differences in response rates were 8.2% SLEDAI, 11.8% BILAG and 12.6% joint response.3

The most frequently reported adverse events for anifrolumab in the TULIP-1 and TULIP-2 trials were upper respiratory tract infection, bronchitis, infusion-related reactions and herpes zoster.

Joan Merrill, MD, Oklahoma Medical Research Foundation, Arthritis & Clinical Immunology Research Program, is optimistic about the data. “I've been in this business a long time and I have seen so many failed clinical trials. We're getting signals out of this one. Part of the reason is, probably, because there's something to it. There's something to this story,” she said in an interview with DermWire. 

“Lupus is a very complicated disease and it probably is multifactorial. It probably has a number of different immunologic pathways activated, but a majority of the patients, especially the more sick patients, have activation of type one interferon pathways...The type one interferons in individual people can play out in very complicated ways,” she says, noting that all type one interferon signals go through the interferon alpha/beta or IFNAR receptor. “Anifrolumab is an antagonist of that receptor. So it's really hitting all of the complexity of type one interferon signals.”