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CHANGE THE COURSE OF HF CARE
Proven risk reduction
KERENDIA is proven to reduce CV death, HF hospitalization, and urgent HF visits in adults with HF LVEF ≥40%
Clinical results
Established safety
KERENDIA was generally well-tolerated in patients with HF LVEF ≥40%
Safety
Addresses key drivers
KERENDIA blocks MR overactivation thought to contribute to sodium and fluid retention, inflammation, fibrosis, and cardiac hyperthrophy
MOA
For your adult patients with HF LVEF ≥40%
KERENDIA helps protect your patients’ hearts by reducing the risk of CV death, hospitalization for HF, and urgent HF visits
ON TOP OF BACKGROUND HF THERAPIES
PRIMARY COMPOSITE ENDPOINT1,3
16% RRR
vs placebo
RR=0.84 (95% CI: 0.74-0.95)
P=0.007
Sensitivity analysis1,15*
Time to first HF event† or CV death at 36 months
ARR=3.5%; NNT=29 (95% CI: 17-91)
Secondary composite endpoint
HF hospitalizations and urgent HF visits were reduced by 18% in patients receiving KERENDIA vs placebo†
*In a prespecified sensitivity analysis, the time to first HF event or CV death was evaluated at month 36 to calculate NNT and ARR, as determined by the FINEARTS-HF Steering Committee (RR=0.84 [95% CI: 0.76-0.94]). †Total HF events: 18% RRR vs placebo (RR=0.92 [95% CI 0.71-0.94]; P=0.006).
ARR=absolute risk reduction; CI=confidence interval; CV=cardiovascular; HF=heart failure; HF LVEF=heart failure with left ventricular ejection fraction; NNT=number needed to treat; RR=relative reduction; RRR=relative risk reduction.
FINEARTS-HF evaluated ~6000 adult patients with HF LVEF ≥40% taking KERENDIA or placebo
KERENDIA has a generally well-tolerated safety profile
Adverse reactions reported in ≥1% of patients on KERENDIA and more frequently than placebo1,3,4
Permanent discontinuations due to adverse events were similar between KERENDIA and placebo (3.2% vs 2.8%, respectively).
Adverse reactions related to worsening renal function were reported more frequently in the KERENDIA group (18%) vs placebo (12%) in FINEARTS-HF. The most frequently reported adverse reactions included renal impairment (7% vs 4%), eGFR decreased (5% vs 4%), acute kidney injury (4% vs 2%), and renal failure (3% vs 2%). The majority of events were reported to be mild to moderate. These events led to dose modifications in 9% receiving KERENDIA vs 4% receiving placebo. Hospitalization due to events related to worsening of renal function for the KERENDIA group was 2.0% vs 1.3% with placebo.
Initiation of KERENDIA may cause an initial small increase in blood creatinine levels (mean change <0.1 mg/dL) and a small decrease in eGFR (mean change 2 to 3 mL/min) that occurs within the first 4 weeks of starting therapy and then stabilizes. These changes were reversible after treatment discontinuation. Initiation of KERENDIA may also cause a small increase in serum uric acid. This increase appears to attenuate over time.
eGFR=estimated glomerular filtration rate; HF=heart failure; HF LVEF=heart failure with left ventricular ejection fraction; LVEF=left ventricular ejection fraction.
Taking aim at HF LVEF ≥40% from a different angle
KERENDIA addresses critical drivers of disease by targeting the mineralocorticoid receptor pathway
The FDA has categorized KERENDIA in its own drug class as a nonsteroidal MRA
HF LVEF=heart failure with left ventricular ejection fraction; MOA=mechanism of action; MR=mineralocorticoid receptor; MRA=mineralocorticoid receptor antagonist.