Academic Journal
Complement Factor H-Based Therapeutics: A Comprehensive Overview.
| Τίτλος: | Complement Factor H-Based Therapeutics: A Comprehensive Overview. |
|---|---|
| Συγγραφείς: | Hamers SMWR; Sanquin Research, Landsteiner Laboratory of the Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.; Amsterdam Institute for Immunology and Infectious Diseases, Immunology, Amsterdam, the Netherlands., Buter EJ; Sanquin Research, Landsteiner Laboratory of the Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands., Pouw RB; Sanquin Research, Landsteiner Laboratory of the Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.; Amsterdam Institute for Immunology and Infectious Diseases, Immunology, Amsterdam, the Netherlands.; Department of Hematology, Amsterdam UMC Location VUmc, Amsterdam, the Netherlands. |
| Πηγή: | European journal of immunology [Eur J Immunol] 2026 Jul; Vol. 56 (7), pp. e70241. |
| Τύπος έκδοσης: | Journal Article; Review |
| Γλώσσα: | English |
| Στοιχεία περιοδικού: | Publisher: Wiley-VCH Country of Publication: Germany NLM ID: 1273201 Publication Model: Print Cited Medium: Internet ISSN: 1521-4141 (Electronic) Linking ISSN: 00142980 NLM ISO Abbreviation: Eur J Immunol Subsets: MEDLINE |
| Imprint Name(s): | Publication: <2005->: Weinheim : Wiley-VCH Original Publication: Weinheim, Verlag Chemie GmbH. |
| Ιατρικοί όροι (MeSH): | Complement Factor H*/immunology , Complement Factor H*/therapeutic use, Complement Activation/drug effects ; Complement Activation/immunology ; Complement Pathway, Alternative/drug effects ; Complement Pathway, Alternative/immunology ; Humans ; Animals |
| Περίληψη: | The complement system is a key component of innate immunity, modulating immunological processes to maintain proper homeostasis. However, dysregulation of the complement can lead to severe pathologies. Complement therapeutics strive to reduce and lower the risk of breakthrough complement activation, and the field has been growing steadily since the first complement-regulating compound was introduced to the clinic in 2007, with many complement-regulating strategies currently under development. This review focuses on therapeutic developments surrounding factor H (FH), which is a critical and native regulator of complement. FH is a complement inhibitor that controls the self-amplifying alternative pathway (AP). It functions by destabilizing C3 and C5 AP convertases through decay-accelerating activity, mainly via competition with factor B for binding to C3b. Additionally, FH acts as a cofactor for factor I, which cleaves C3b into iC3b. The classical and lectin pathways converge at the C3 level, triggering the AP self-amplification loop. Independently, the AP is triggered by a tick-over mechanism that is continuously activated. Both the amplification loop and the tick-over mechanism of the AP are controlled by FH. Consequently, enhancing FH function in a dysregulated system represents a promising therapeutic approach. FH-driven therapeutic strategies include replenishing FH via plasma-derived or recombinantly produced full-length FH. On top of that, protein-engineered constructs that contain FH fragments both with and without targeting mechanisms are under development, as well as modulating moieties such as antibodies and peptides that bind and potentiate FH. In this review, we provide an extensive overview of these developments, discuss the underlying rationale of each strategy, and evaluate their status in the therapeutic pipeline. (© 2026 The Author(s). European Journal of Immunology published by Wiley‐VCH GmbH.) |
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| Substance Nomenclature: | 80295-65-4 (Complement Factor H) |
| Entry Date(s): | Date Created: 20260722 Date Completed: 20260722 Latest Revision: 20260906 |
| Update Code: | 20260906 |
| PubMed Central ID: | PMC13390659 |
| DOI: | 10.1002/eji.70241 |
| PMID: | 42484484 |
| Βάση Δεδομένων: | MEDLINE |
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