Evidence map›Paper›PMID 40875177›Full record

ArticleMolecular diagnosis & therapy2025

Prademagene Zamikeracel: First Approval.

Arnold Lee

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular diagnosis & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

1 author.

Arnold LeeSpringer Nature, Private Bag 65901, Mairangi Bay, Auckland, 0754, New Zealand. mdt@adis.com.ORCID 0000-0002-6519-7831

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prademagene zamikeracel (ZEVASKYN™) is an autologous cell sheet-based gene therapy developed by Abeona Therapeutics Inc. for the treatment of wounds in patients with recessive dystrophic epidermolysis bullosa. Prademagene zamikeracel contains the patient's own genetically modified cells with functional copies of the COL7A1 gene, as patients lacking functional copies of this gene may develop chronic open wounds caused by the separation of dermal layers. This article summarizes the milestones in the development of prademagene zamikeracel leading to this first approval for treatment of wounds in adult and paediatric patients with recessive dystrophic epidermolysis bullosa.

Indexed as

Collagen Type VIIEpidermolysis Bullosa DystrophicaGene Therapy AgentsGenetic TherapyAdultChildHumansCOL7A1 protein, humanCollagen Type VIIprademagene zamikeracel

Identifiers

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.