Targeting inerleukin-6 for renoprotection.

Sterile inflammation has been increasingly recognized as a hallmark of non-infectious kidney diseases. Induction of pro-inflammatory cytokines in injured kidney tissue promotes infiltration of immune cells serving to clear cell debris and facilitate tissue repair. However, excessive or prolonged inflammatory response has been associated with immune-mediated tissue damage, nephron loss, and development of renal fibrosis.

Interleukin-1 Blockade With RPH-104 (Goflikicept) in Patients With ST-Segment Elevation Myocardial Infarction: Secondary End Points From an International, Double-Blind, Randomized, Placebo-Controlled, Phase 2a Study.

In a randomized double-blinded clinical trial of patients with ST segment elevation myocardial infarction (STEMI), goflikicept, an interleukin-1 blocker, significantly reduced systemic inflammation, measured as the area under the curve (AUC) for high-sensitivity C reactive protein at 14 days. We report secondary analyses of biomarkers at 28 days, and cardiac function and clinical end points at 1 year. Patients received a single administration of goflikicept 80 mg (n = 34), goflikicept 160 mg (n = 34), or placebo (n = 34).

[Long-term goflkicept therapy for patients with idiopathic recurrent pericarditis: results of the interim analysis of an ongoing open-label extension study].

Aim: To evaluate the long-term safety and efficacy of goflkicept treatment in patients with idiopathic recurrent pericarditis (IRP).

Materials And Methods: This report presents the interim analysis of an ongoing open-label extension (OLE) clinical trial of goflkicept in patients with IRP (NCT05673902), as a continuation of the core study (NCT04692766). The study assessed the frequency of pericarditis recurrence, time to recurrence after 12 and 60 weeks of goflkicept therapy, changes in C-reactive protein level, chest pain intensity, pericardial effusion size, and adverse events (AEs).

Inflammation-mediated drug interactions of olokizumab and cytochrome P450 activities in patients with rheumatoid arthritis.

Aims: In patients with rheumatoid arthritis (RA), interleukin (IL)-6 affects the activity of cytochrome P450 (CYP) enzymes. Treatment with anti-IL-6 therapy can reverse the IL-6-mediated downregulation of CYP enzymes, resulting in changes in plasma levels of CYP substrates. The primary objective of this study was to evaluate the impact of the IL-6 inhibitor olokizumab on the pharmacokinetics of CYP probe substrates in subjects with active RA.