Evidence map›Paper›PMID 35099769›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2022

IDP-410: a Novel Therapeutic Peptide that Alters N-MYC Stability and Reduces Angiogenesis and Tumor Progression in Glioblastomas.

Ricardo Gargini, Berta Segura-Collar, María Garranzo-Asensio, Rafael Hortigüela, Patricia Iglesias-Hernández, Daniel Lobato-Alonso, Miguel Moreno-Raja, Santiago Esteban-Martin, Juan M Sepúlveda-Sánchez, Laura Nevola and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

11 authors at 3 institutions in 1 country.

Ricardo Gargini *Neurooncology Unit, Instituto de Salud Carlos III-UFIEC, Madrid, Spain. ricgargini@gmail.com.
Berta Segura-Collar *Neurooncology Unit, Instituto de Salud Carlos III-UFIEC, Madrid, Spain.
María Garranzo-AsensioNeurooncology Unit, Instituto de Salud Carlos III-UFIEC, Madrid, Spain.
Rafael HortigüelaNeurooncology Unit, Instituto de Salud Carlos III-UFIEC, Madrid, Spain.
Patricia Iglesias-HernándezNeurooncology Unit, Instituto de Salud Carlos III-UFIEC, Madrid, Spain.
Daniel Lobato-AlonsoNeurooncology Unit, Instituto de Salud Carlos III-UFIEC, Madrid, Spain.
Miguel Moreno-RajaIDP Discovery Pharma S.L, Barcelona, Spain.
Santiago Esteban-MartinIDP Discovery Pharma S.L, Barcelona, Spain.
Juan M Sepúlveda-SánchezInstituto de Investigaciones Biomédicas I+12, Hospital 12 de Octubre, Madrid, Spain.
Laura NevolaIDP Discovery Pharma S.L, Barcelona, Spain. l.nevola@idp-pharma.com.
Pilar Sánchez-GómezNeurooncology Unit, Instituto de Salud Carlos III-UFIEC, Madrid, Spain. psanchezg@isciii.es.ORCID 0000-0002-0709-4973
Instituto de Salud Carlos III · ESLight Prescriptions Innovators (Spain) · ESResearch Institute Hospital 12 de Octubre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastomas (GBMs) are the most frequent and highly aggressive brain tumors, being resistant to all cytotoxic and molecularly targeted agents tested so far. There is, therefore, an urgent need to find novel therapeutic approaches and/or alternative targets to bring treatment options to patients. Here, we first show that GBMs express high levels of N-MYC protein, a transcription factor involved in normal brain development. A novel stapled peptide designed to specifically target N-MYC protein monomer, IDP-410, is able to impair the formation of N-MYC/MAX complex and reduce the stability of N-MYC itself. As a result, the viability of GBM cells is compromised. Moreover, the efficacy is found dependent on the levels of expression of N-MYC. Finally, we demonstrate that IDP-410 reduces GBM growth in vivo when administered systemically, both in subcutaneous and intracranial xenografts, reducing the vascularization of the tumors, highlighting a potential relationship between the function of N-MYC and the expression of mesenchymal/angiogenic genes. Overall, our results strengthen the view of N-MYC as a therapeutic target in GBM and strongly suggest that IDP-410 could be further developed to become a first-in-class inhibitor of N-MYC protein, affecting not only tumor cell proliferation and survival, but also the interplay between GBM cells and their microenvironment.

Indexed as

Brain NeoplasmsGlioblastomaCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansNeovascularization, PathologicN-Myc Proto-Oncogene ProteinPeptidesTumor MicroenvironmentN-Myc Proto-Oncogene ProteinPeptidesAngiogenesisGlioblastomaGliomaN-MYCPeptide inhibitorsProtein stabilityTumor microenvironment

Identifiers

PMID35099769
PMCPMC9130446
OpenAlexW4210502843

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.