Key takeaways

• Inflammation is increasingly recognised as an important contributor to cardiovascular disease.

• Pacibekitug is a long-acting monoclonal antibody that targets interleukin-6, a known mediator of inflammation.

• In the TRANQUILITY trial, pacibekitug produced sustained reductions in inflammatory markers, with no clear dose-related safety signals identified.

• The findings support further investigations with pacibekitug to assess whether these effects translate into improved cardiovascular outcomes for patients.

Munich, Germany – 29 August 2026: The interleukin-6 (IL-6) antibody, pacibekitug, produced sustained reductions in inflammatory biomarkers in patients with chronic kidney disease at high inflammatory risk, according to results from the phase II TRANQUILITY trial presented in a Hot Line session today at ESC Congress 2026.¹

Addressing hypertension, smoking, diabetes, high cholesterol levels and obesity is known to reduce cardiovascular risk, but these factors only account for around half of the global burden of cardiovascular disease.²

Inflammation is increasingly recognised as an important contributor to cardiovascular disease. Despite standard therapies, around 30% of patients with atherosclerotic cardiovascular disease and around 40% of those with concomitant chronic kidney disease are at high inflammatory risk, based on elevated levels of the marker, high-sensitivity C-reactive protein (hs-CRP).³

“A growing body of genetic, epidemiological and clinical evidence suggests that IL-6 mediates a key inflammatory pathway linked to cardiovascular risk,” explained Principal Investigator, Professor Deepak Bhatt from the Icahn School of Medicine at Mount Sinai, New York City, USA. “We evaluated the long-acting monoclonal antibody against IL-6, pacibekitug, in patients with chronic kidney disease and elevated levels of hs-CRP in the TRANQUILITY trial,” he continued.

This was a placebo-controlled phase II study conducted at 49 centres in the US. A total of 143 patients with chronic kidney disease (stage 3–4) and elevated hs-CRP (2 to <15 mg/L) were included. Participants were randomised (1:1:1:1) to receive subcutaneous pacibekitug 25 mg or 50 mg every 90 days, 15 mg every 30 days or placebo for six months. The mean age of the study population was 69 years, 64% were women, 72% received statins and 59% had diabetes.

Pacibekitug treatment resulted in dose-dependent decreases in hs-CRP by day 30, which were sustained to day 180. Median time-averaged change from baseline in hs-CRP through day 180 was +7% with placebo, −76% with pacibekitug 25 mg every 90 days, −85% with pacibekitug 50 mg every 90 days and −89% with pacibekitug 15 mg every 30 days (all p<0.0001 vs. placebo).

Sustained reductions in other inflammatory markers, as well as fibrinogen and lipoprotein(a), were also observed across pacibekitug groups vs. placebo.

Pacibekitug was well tolerated with few discontinuations (1.9%) and no clear dose-related safety signals.

“Results from the TRANQUILITY study demonstrate that the IL-6 pathway can be durably suppressed with infrequent dosing and no new safety signals,” summarised Professor Bhatt. “The next step is to determine whether the biomarker effects observed in TRANQUILITY translate into improved cardiovascular outcomes for patients in a larger, longer-term phase III trial,” he concluded.

ENDS