Switching from adalimumab to upadacitinib demonstrates clinical improvement for patients with RA
Click Here to Manage Email Alerts
PHILADELPHIA — An early switch from adalimumab to upadacitinib due to non-response demonstrated clinical improvement among patients with rheumatoid arthritis, according to data presented at ACR Convergence 2022.
“A small proportion of patients switched treatments from adalimumab to upadacitnib and from upadacitinib to adalimumab within weeks 14 to 22 due to non-response to initial therapy,” Iain McInnes, PhD, FRCP, Muirhead professor of medicine, versus arthritis professor of rheumatology, and vice principal and head of college of medical veterinary and life sciences at the University of Glasgow, said during a presentation. “Although both switches showed improved efficacy, a higher proportion of patients rescued from adalimumab to upadacitinib achieved CDAI-low disease activity at 6 months post switch than patients rescued from upadacitinib to adalimumab.”
The analysis was made up of a randomly selected subset of patients with RA from the SELECT-COMPARE trial, which included 100 patients receiving placebo, 100 receiving upadacitinib, and 100 receiving adalimumab.
Of the patients on adalimumab who switched to upadacitinib, 36% achieved a Clinical Disease Activity Index score of 10 or less at week 26 compared with 17% of patients on upadacitinib who switched to adalimumab, according to the poster.
The researchers evaluated the levels of 181 inflammation-related protein biomarkers and of these, ten, which included CCL7, CCL8, CHI3L1, CSF1, IL6, MMP1, SLAMF1, TNFRSF9, TNFSF14, and VEGFA, demonstrated different modulation when comparing patients with a response to adalimumab and those with a non-response. Moreover, at week 26, these levels significantly decreased when switched to upadacitinib. Similar responses were seen with a different group of 13 biomarkers which included CCL13, CCL19, CCL23, FGF21, IL18, IL10RA, IL18BP, IL1R1, IL2RA, MMP3, TNFSF11, TNFSF13B, TNFRSF1A.
At week 8, the first 10 biomarkers were the same when comparing patients with a response to upadacitinib and those with a non-response.
“Notably, the baseline levels of nine out of 10 of these biomarkers were correlated with DAS28 at baseline, suggesting a potential relationship these biomarkers and the pathophysiology of RA,” McInnes said.
He and colleagues found that while the levels of the second group of 13 biomarkers was similar between patients with a response to upadacitinib and those with a non-response, this excluded FGF21. Furthermore, when patients were switched to adalimumab, the levels of CCL13, CCL19, CCL23, IL10RA, IL1R1, IL2RA, and TNFSF11 increased at week 26.
“Patients who switched treatment with adalimumab to upadacitinib due to early non-response demonstrated favorable clinical improvement and robust inhibition of biomarkers associated with the adaptive and innate immune responses,” McInnes said. “Patients who switched from upadacitinib to adalimumab experienced lower clinical improvement than patients who switched from adalimumab to upadacitinib and demonstrated only marginal changes in these biomarkers. This suggests, and is consistent with, the broader mechanistic inhibition achieved with upadacitinib as compared to the cytokine receptor discreet TNF inhibition by adalimumab.”
Collapse
McInnes I, et al. Abstract 0304. Presented at: ACR Convergence 2022; November 11-14, 2022; Philadelphia (hybrid meeting).
Read more about
Click Here to Manage Email Alerts