Key result
LCZ696 did not change CSF levels of aggregable Aβ 1-42 compared with placebo in healthy volunteers.
Why the study?
Does sacubitril/valsartan alter cerebrospinal fluid concentrations of amyloid-beta isoforms in healthy subjects?
RCT (n=43)
Double-blind
parallel group
Does sacubitril/valsartan alter cerebrospinal fluid concentrations of amyloid-beta isoforms in healthy subjects?
Sacubitril/valsartan does not increase CSF levels of aggregable amyloid-beta isoforms (1-42 and 1-40) in healthy subjects, alleviating concerns about potential amyloid accumulation due to neprilysin inhibition.
Answers are grounded in this paper and cite their sources.
Reassures on short-term amyloid safety of LCZ696; challenges neprilysin inhibition concerns for CSF Aβ42 in humans.
AIMS: LCZ696 (angiotensin receptor neprilysin inhibitor) is a novel drug developed for the treatment of heart failure with reduced ejection fraction. Neprilysin is one of multiple enzymes degrading amyloid-β (Aβ). Its inhibition may increase Aβ levels. The potential exists that treatment of LCZ696, through the inhibition of neprilysin by LBQ657 (an LCZ696 metabolite), may result in accumulation of Aβ. The aim of this study was to assess the blood-brain-barrier penetration of LBQ657 and the potential effects of LCZ696 on cerebrospinal fluid (CSF) concentrations of Aβ isoforms in healthy human volunteers. METHODS: In a double-blind, randomized, parallel group, placebo-controlled study, healthy subjects received once daily LCZ696 (400 mg, n = 21) or placebo (n = 22) for 14 days. RESULTS: LCZ696 had no significant effect on CSF AUEC(0,36 h) of the aggregable Aβ species 1-42 or 1-40 compared with placebo (estimated treatment ratios 0.98 [95% CI 0.73, 1.34; P = 0.919] and 1.05 [95% CI 0.82, 1.34; P = 0.702], respectively). A 42% increase in CSF AUEC(0,36 h) of soluble Aβ 1-38 was observed (estimated treatment ratio 1.42 [95% CI 1.05, 1.91; P = 0.023]). CSF levels of LBQ657 and CSF Aβ 1-42, 1-40, and 1-38 concentrations were not related (r(2) values 0.022, 0.010, and 0.008, respectively). CONCLUSIONS: LCZ696 did not cause changes in CSF levels of aggregable Aβ isoforms (1-42 and 1-40) compared with placebo, despite achieving CSF concentrations of LBQ657 sufficient to inhibit neprilysin. The clinical relevance of the increase in soluble CSF Aβ 1-38 is currently unknown.
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Langenickel et al. (2015) conducted an RCT in Healthy subjects (n=43). LCZ696 vs. Placebo was evaluated on CSF AUEC(0,36 h) of aggregable Aβ species 1-42 (Treatment ratio 0.98, 95% CI 0.73, 1.34, p=0.919). LCZ696 did not change CSF levels of aggregable Aβ 1-42 compared with placebo in healthy volunteers.
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