Evidence map›Paper›PMID 26101137›Full record

ReviewImmunobiology2016

Therapeutic control of complement activation at the level of the central component C3.

Daniel Ricklin, John D Lambris

Registry-linked trialAbstract readReview
In one paragraph

Review in Immunobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03316521 (Safety, Tolerability, Pharmacokinetics), which is not on this map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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.

NCT03316521 phase1completednot on this mapstarted 2017, after this paper: background citation

Safety, Tolerability, Pharmacokinetics (PK) and Pharmacodynamics (PD) of a Single Ascending Dose (SAD) and a Multiple Dose (MD) of the Complement Inhibitor AMY-101. A Prospective, Single-center, Open-label, First-In-Human (FIH) Clinical Study in Healthy Male Volunteers

TypeinterventionalSponsorAmyndas Pharmaceuticals S.A.Ran2017 to 2017Enrolled50ConditionsComplement Mediated DiseasesArmsAMY-101
3 · Its place in the literature

Who cites it

32 citing papers in PubMed.

  1. Article
  2. Observational
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Complementing the Cancer-Immunity Cycle.Frontiers in immunology · 2019
    Review
  15. Article
  16. Article
  17. The renaissance of complement therapeutics.Nature reviews. Nephrology · 2018
    Review
  18. Article
  19. Article
  20. Article
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

2 authors.

Daniel RicklinDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, USA. Electronic address: ricklin@upenn.edu.
John D LambrisDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, USA.

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
STRUCTURE-FUNCTION ANALYSIS OF DIFFERENT C3 SPECIESR01AI030040 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 1993 to 2016
$4.1M
Complement in AMD: Mechanisms and Therapeutic InterventionR01EY020633 · NEI · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2011 to 2013
$1.8M
A novel approach for assessing dynamic events in the human complement systemR21AI097805 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI RICKLIN, DANIEL · 2012 to 2013
$426k
VIRAL RESPIRATORY PATHOGENS RESEARCH UNIT /VRPRU/-266030040-266030040N01AI030040 · NIAID · UNIVERSITY OF IOWA · PI APICELLA, MICHAEL A. · 2003 to 2006
–
NEI NIH HHS R01 EY020633NIAID NIH HHS N01 AI030040NIAID NIH HHS P01 AI068730NIAID NIH HHS R01 AI030040NIAID NIH HHS R21 AI097805
6 · The paper itself

Abstract

The increasing recognition of the complement system's association with diseases of the inflammatory spectrum and with biomaterial and transplant-related complications has generated growing interest in the therapeutic modulation of this innate immune cascade. As a central functional hub that largely drives the activation, amplification, and effector generation of the complement response, the plasma protein C3 has long been recognized as an attractive target. While pharmacological modulation of C3 activation may offer a powerful opportunity to interfere with or even prevent complement-driven pathologies, the development of C3 inhibitors has often been accompanied by concerns regarding the safety and feasibility of this approach. Although no C3-targeted inhibitors have thus far been approved for clinical use, several promising concepts and candidates have emerged in recent years. At the same time, experiences from preclinical development and clinical trials are slowly providing a more detailed picture of therapeutic complement inhibition at the level of C3. This review highlights the current therapeutic strategies to control C3 activation and discusses the possibilities and challenges on the road to bringing C3-targeted therapeutics to the clinic.

Indexed as

Complement ActivationAnimalsClinical Trials as TopicComplement C3HumansImmunity, InnateImmunomodulationInflammationMolecular Targeted TherapyComplement C3Alternative pathwayC3ComplementConvertaseTherapeutics

Identifiers

PMID26101137
PMCPMC4675703

What OpenQuestion holds

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Registered trials

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 OpenQuestion graph.