Evidence map›Paper›PMID 38799460›Full record

ArticleFrontiers in immunology2024

Moss-produced human complement factor H with modified glycans has an extended half-life and improved biological activity.

Todor Tschongov, Swagata Konwar, Andreas Busch, Christian Sievert, Andrea Hartmann, Marina Noris, Sara Gastoldi, Sistiana Aiello, Andreas Schaaf, Jens Panse and 3 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Article
  2. Frontiers in immunology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Engineering the mossFrontiers in plant science · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Todor TschongovDepartment of Internal Medicine IV (Nephrology), Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Swagata KonwarDepartment of Internal Medicine IV (Nephrology), Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Andreas BuschEleva GmbH, Freiburg, Germany.
Christian SievertEleva GmbH, Freiburg, Germany.
Andrea HartmannDepartment of Infection Biology, Leibniz Insitute for Natural Product Research and Infection Biology, Jena, Germany.
Marina NorisCentro di Ricerche Cliniche per le Malattie Rare "Aldo e Cele Dacco", Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
Sara GastoldiCentro di Ricerche Cliniche per le Malattie Rare "Aldo e Cele Dacco", Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
Sistiana AielloCentro di Ricerche Cliniche per le Malattie Rare "Aldo e Cele Dacco", Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
Andreas SchaafEleva GmbH, Freiburg, Germany.
Jens PanseDepartment of Oncology, Hematology, Hemostaseology and Stem Cell Transplantation, University Hospital Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen, Aachen, Germany.
Peter F ZipfelDepartment of Infection Biology, Leibniz Insitute for Natural Product Research and Infection Biology, Jena, Germany.
Paulina Dabrowska-Schlepp *Eleva GmbH, Freiburg, Germany.
Karsten Häffner *Department of Internal Medicine IV (Nephrology), Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most drugs that target the complement system are designed to inhibit the complement pathway at either the proximal or terminal levels. The use of a natural complement regulator such as factor H (FH) could provide a superior treatment option by restoring the balance of an overactive complement system while preserving its normal physiological functions. Until now, the systemic treatment of complement-associated disorders with FH has been deemed unfeasible, primarily due to high production costs, risks related to FH purified from donors' blood, and the challenging expression of recombinant FH in different host systems. We recently demonstrated that a moss-based expression system can produce high yields of properly folded, fully functional, recombinant FH. However, the half-life of the initial variant (CPV-101) was relatively short. Here we show that the same polypeptide with modified glycosylation (CPV-104) achieves a pharmacokinetic profile comparable to that of native FH derived from human serum. The treatment of FH-deficient mice with CPV-104 significantly improved important efficacy parameters such as the normalization of serum C3 levels and the rapid degradation of C3 deposits in the kidney compared to treatment with CPV-101. Furthermore, CPV-104 showed comparable functionality to serum-derived FH

Indexed as

Complement Factor HAnimalsBryopsidaGlycosylationHalf-LifeHumansMaleMiceMice, Inbred C57BLMice, KnockoutPolysaccharidesRecombinant ProteinsCFH protein, humanComplement Factor HPolysaccharidesRecombinant ProteinsC3 glomerulopathyCFHcomplementcomplement-associated diseaseCPV-104recombinant factor H

Identifiers

PMID38799460
PMCPMC11117068

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.