A Phase II Trial of the WEE1 Inhibitor Adavosertib in SETD2-Altered Advanced Solid Tumor Malignancies (NCI 10170)

Cancer Res Commun. 2024 Jul 1;4(7):1793-1801. doi: 10.1158/2767-9764.CRC-24-0213.

Abstract

We sought to evaluate the efficacy of WEE1 inhibitor adavosertib in patients with solid tumor malignancies (cohort A) and clear cell renal cell carcinoma (ccRCC; cohort B). NCT03284385 was a parallel cohort, Simon two-stage, phase II study of adavosertib (300 mg QDAY by mouth on days 1-5 and 8-12 of each 21-day cycle) in patients with solid tumor malignancies harboring a pathogenic SETD2 mutation. The primary endpoint was the objective response rate. Correlative assays evaluated the loss of H3K36me3 by IHC, a downstream consequence of SETD2 loss, in archival tumor tissue. Eighteen patients were enrolled (9/cohort). The median age was 60 years (range 45-74). The median duration of treatment was 1.28 months (range 0-24+). No objective responses were observed in either cohort; accrual was halted following stage 1. Minor tumor regressions were observed in 4/18 (22%) evaluable patients. Stable disease (SD) was the best overall response in 10/18 (56%) patients, including three patients with SD > 4 months. One patient with ccRCC remains on treatment for >24 months. The most common adverse events of any grade were nausea (59%), anemia (41%), diarrhea (41%), and neutropenia (41%). Nine patients (50%) experienced a Grade ≥3 adverse event. Of eight evaluable archival tissue samples, six (75%) had a loss of H3K36me3 by IHC. Adavosertib failed to exhibit objective responses in SETD2-altered ccRCC and other solid tumor malignancies although prolonged SD was observed in a subset of patients. Combination approaches may yield greater depth of tumor response.

Significance: WEE1 inhibition with adavosertib monotherapy demonstrated limited clinical activity in patients with SETD2-altered solid tumors despite compelling preclinical data indicating a synthetic lethal effect, which did not translate into robust tumor regression. Loss of the H3K36me3 trimethylation mark caused by SETD2-deficiency was confirmed in the majority of evaluable tumors. A subset of patients derived clinical benefit as manifested by minor tumor regressions and prolonged SD.

Publication types

  • Clinical Trial, Phase II

MeSH terms

  • Aged
  • Carcinoma, Renal Cell / drug therapy
  • Carcinoma, Renal Cell / genetics
  • Carcinoma, Renal Cell / pathology
  • Cell Cycle Proteins* / antagonists & inhibitors
  • Cell Cycle Proteins* / genetics
  • Female
  • Histone-Lysine N-Methyltransferase* / genetics
  • Humans
  • Kidney Neoplasms / drug therapy
  • Kidney Neoplasms / genetics
  • Kidney Neoplasms / pathology
  • Male
  • Middle Aged
  • Mutation
  • Neoplasms / drug therapy
  • Neoplasms / genetics
  • Neoplasms / pathology
  • Protein-Tyrosine Kinases* / antagonists & inhibitors
  • Protein-Tyrosine Kinases* / genetics
  • Pyrazoles* / adverse effects
  • Pyrazoles* / pharmacology
  • Pyrazoles* / therapeutic use
  • Pyrimidinones / administration & dosage
  • Pyrimidinones / pharmacology
  • Pyrimidinones / therapeutic use

Substances

  • adavosertib
  • Histone-Lysine N-Methyltransferase
  • WEE1 protein, human
  • Protein-Tyrosine Kinases
  • SETD2 protein, human
  • Cell Cycle Proteins
  • Pyrazoles
  • Pyrimidinones