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Updated: Nov 6, 2025

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

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Breaking Oncogene Addiction: Getting RTK/RAS-Mutated Cancers off the SOS

Erin Sheffels1, Robert L Kortum1

  • 1Department of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, United States.

Journal of Medicinal Chemistry
|May 7, 2021
PubMed

Insights

A new SOS1 inhibitor, BI-3406, targets rebound receptor tyrosine kinase (RTK) activation in RTK/RAS-mutated cancers. This broad inhibition of RTK signaling may overcome therapeutic resistance and improve patient outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Therapeutic resistance in RTK/RAS-mutated cancers is often driven by the reactivation of multiple RTKs.
  • Broad inhibition of RTK signaling presents a potential strategy to delay resistance in a significant patient population.

Purpose of the Study:

  • To evaluate the efficacy of a novel SOS1 inhibitor, BI-3406, in targeting proximal RTK signaling.
  • To assess the potential of BI-3406 to overcome therapeutic resistance in RTK/RAS-mutated cancers.

Main Methods:

  • Utilized BI-3406, a novel SOS1 inhibitor.
  • Focused on inhibiting proximal RTK signaling pathways.
  • Investigated the impact on RTK/RAS-mutated cancer models.

Main Results:

  • BI-3406 demonstrated broad inhibition of proximal RTK signaling.
  • The inhibitor showed potential in addressing rebound RTK activation, a key resistance mechanism.

Conclusions:

  • BI-3406 broadly inhibits proximal RTK signaling, offering a promising therapeutic approach.
  • This SOS1 inhibitor may significantly enhance the efficacy of existing therapies for RTK/RAS-mutated cancers.

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