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Precision Targeted Therapy with BLU-667 for RET-Driven Cancers.

Vivek Subbiah1, Justin F Gainor2, Rami Rahal3

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Cancer Discovery
|April 17, 2018
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A new drug, BLU-667, shows promise for treating cancers driven by rearranged during transfection (RET) gene alterations. This selective RET inhibitor is more potent and less toxic than current treatments, offering hope for patients with RET-driven non-small cell lung and thyroid cancers.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Development

Background:

  • Receptor tyrosine kinase (RET) alterations drive various cancers, including non-small cell lung cancer (NSCLC) and thyroid cancer.
  • Current treatments rely on multikinase inhibitors (MKIs) with limited efficacy and significant off-target toxicities.
  • There is a critical need for targeted therapies specifically designed to inhibit RET.

Purpose of the Study:

  • To evaluate the preclinical and clinical efficacy of BLU-667, a novel selective RET inhibitor.
  • To assess BLU-667's potency and selectivity against oncogenic RET variants and resistance mutations.
  • To validate selective RET inhibition as a therapeutic strategy in RET-driven cancers.

Main Methods:

  • In vitro assays were used to compare BLU-667's potency against RET variants and resistance mutants relative to approved MKIs.
  • In vivo studies involved NSCLC and thyroid cancer xenografts driven by RET alterations to assess BLU-667's anti-tumor activity and selectivity (VEGFR2 inhibition).
  • First-in-human clinical trials evaluated BLU-667's safety, tolerability, RET signaling inhibition, and clinical response in patients with RET-altered NSCLC and MTC.

Main Results:

  • BLU-667 demonstrated at least 10-fold greater potency than approved MKIs against oncogenic RET variants and resistance mutants in vitro.
  • BLU-667 effectively inhibited the growth of RET-driven NSCLC and thyroid cancer xenografts in vivo without affecting VEGFR2.
  • First-in-human trials showed significant RET signaling inhibition and durable clinical responses in patients with RET-altered NSCLC and MTC, with minimal off-target toxicity.

Conclusions:

  • BLU-667 is a potent and selective RET inhibitor with demonstrated efficacy in preclinical models of RET-driven cancers.
  • Clinical studies validate BLU-667's ability to inhibit RET signaling and induce durable responses in patients with RET-altered NSCLC and MTC.
  • Selective RET inhibition represents a clinically validated and effective therapeutic strategy for patients with RET-driven malignancies.