Evidence map›Paper›PMID 23028738›Full record

ArticlePloS one2012

NVX-412, a new oncology drug candidate, induces S-phase arrest and DNA damage in cancer cells in a p53-independent manner.

Alexandra Hebar, Barbara C Rütgen, Edgar Selzer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 48% of its field
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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

3 authors at 2 institutions in 1 country.

Alexandra HebarDepartment of Radiation Oncology, Medical University of Vienna, Vienna, Austria.
Barbara C Rütgen
Edgar Selzer
Medical University of Vienna · ATUniversity of Veterinary Medicine Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The new molecular entity quinoxalinhydrazide derivative NVX-412 was identified as a promising drug candidate for the treatment of various cancer types due to its strong cytotoxic activity and relative specificity. Here, we provide first data about the mechanisms of action of NVX-412. We show that NVX-412 exerts its anti-neoplastic activity in a p53-independent manner and induces S-phase arrest and DNA damage as assessed by γH2AX staining. We suggest a bi-modal (dose-dependent) mode of action of NVX-412, being primarily cytostatic at lower and predominantly cytotoxic at higher concentrations. Based on the broad and consistent anti-neoplastic activity observed, NVX-412 holds promise as an effective drug candidate for the treatment of various cancer types, especially for hematological malignancies with highly unmet medical need.

Indexed as

DNA DamageAntineoplastic AgentsBiomarkers, TumorCell Line, TumorCell ShapeCell SizeDNA ReplicationDrug Screening Assays, AntitumorHumansHydrazinesInhibitory Concentration 50NeoplasmsPhosphorylationQuinoxalinesS Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Antineoplastic AgentsBiomarkers, TumorHydrazinespyrazine-2-carboxylic acid N'- (7-fluoropyrrolo(1,2-a)quinoxalin-4-yl)-hydrazideQuinoxalinesTumor Suppressor Protein p53

Identifiers

PMID23028738
PMCPMC3441706
OpenAlexW2028986505

What OpenQuestion 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 OpenQuestion graph.