Breaking Oncogene Addiction: Getting RTK/RAS-Mutated Cancers off the SOS.
Drug Resistance, Neoplasm
/ drug effects
Humans
Mutation
Neoplasms
/ drug therapy
Protein Kinase Inhibitors
/ chemistry
Protein Tyrosine Phosphatase, Non-Receptor Type 11
/ antagonists & inhibitors
Receptor Protein-Tyrosine Kinases
/ antagonists & inhibitors
SOS1 Protein
/ antagonists & inhibitors
Signal Transduction
/ drug effects
ras Proteins
/ antagonists & inhibitors
Journal
Journal of medicinal chemistry
ISSN: 1520-4804
Titre abrégé: J Med Chem
Pays: United States
ID NLM: 9716531
Informations de publication
Date de publication:
27 05 2021
27 05 2021
Historique:
pubmed:
8
5
2021
medline:
22
6
2021
entrez:
7
5
2021
Statut:
ppublish
Résumé
In RTK/RAS-mutated cancers, therapeutic resistance is driven by rebound activation of multiple RTKs; broad inhibition of RTK signaling can potentially delay therapeutic resistance for a majority of patients. A new SOS1 inhibitor, BI-3406, broadly inhibits proximal RTK signaling will greatly expand the efficacy of therapies used to treat RTK/RAS-mutated cancers.
Identifiants
pubmed: 33961431
doi: 10.1021/acs.jmedchem.1c00698
doi:
Substances chimiques
Protein Kinase Inhibitors
0
SOS1 Protein
0
Receptor Protein-Tyrosine Kinases
EC 2.7.10.1
Protein Tyrosine Phosphatase, Non-Receptor Type 11
EC 3.1.3.48
ras Proteins
EC 3.6.5.2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM