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Effect of the antihepcidin Spiegelmer lexaptepid on inflammation-induced decrease in serum iron in humans.
Lucas T van Eijk1, Aaron S E John1, Frank Schwoebel2
1Department of Intensive Care Medicine, and Radboud Institute for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands;
Blood
|August 29, 2014
Summary
Lexaptepid, an anti-hepcidin oligonucleotide, effectively prevented a drop in serum iron during experimental inflammation. This demonstrates its potential for treating anemia of inflammation.
Area of Science:
- Biochemistry
- Pharmacology
- Clinical Medicine
Background:
- Anemia of inflammation is characterized by increased hepcidin production.
- Hepcidin plays a crucial role in regulating iron metabolism.
- Targeting hepcidin offers a potential therapeutic strategy for anemia of inflammation.
Purpose of the Study:
- To investigate the efficacy of lexaptepid, an anti-hepcidin l-oligoribonucleotide, in preventing serum iron decrease during experimental human endotoxemia.
- To establish proof of concept for lexaptepid as a treatment for anemia of inflammation.
Main Methods:
- A randomized, double-blind, placebo-controlled trial involving 24 healthy males.
- Administration of Escherichia coli lipopolysaccharide to induce endotoxemia.
- Intravenous injection of lexaptepid or placebo.
Main Results:
- The lipopolysaccharide-induced inflammatory response was comparable between lexaptepid and placebo groups.
- Serum iron increased by 15.9 ± 9.8 µmol/L from baseline in the lexaptepid group at 9 hours.
- Serum iron decreased by 8.3 ± 9.0 µmol/L from baseline in the placebo group (P < .0001).
Conclusions:
- Lexaptepid effectively inhibits hepcidin, leading to increased serum iron levels.
- This study provides proof of concept for lexaptepid in treating anemia of inflammation.
- Further investigations into lexaptepid for anemia of inflammation are warranted.
