Phase 2 study of LY3023414 in patients with advanced endometrial cancer harboring activating mutations in the PI3K pathway

Cancer. 2020 Mar 15;126(6):1274-1282. doi: 10.1002/cncr.32677. Epub 2019 Dec 27.

Abstract

Background: PI3K pathway activation is common in endometrial cancer. We evaluated the safety and efficacy of the dual PI3K/mTOR inhibitor, LY3023414, in patients with advanced endometrial cancer harboring activating mutations in the PI3K pathway.

Methods: We conducted a single-arm phase 2 study of monotherapy LY3023414. Eligible patients had advanced endometrial cancer of any grade, prior management with 1-4 cytotoxic lines, and PI3K pathway activation prospectively defined as a loss-of-function PTEN alteration or activating alteration in PIK3CA, AKT1, PIK3R1, PIK3R2, or MTOR. The primary objective was best overall response rate (ORR) per RECIST 1.1.

Results: Twenty-eight patients were treated; histologies included endometroid (39%), carcinosarcoma (25%), serous (21%), and mixed (14%). Patients were heavily pretreated, with a median of 2 prior cytotoxic lines (range, 1-3). The most common alterations involved PIK3CA (68%), PTEN (43%), and PIK3R1 (32%). In the 25 efficacy-evaluable patients, the ORR was 16% (90% CI, 7%-100%), and the clinical benefit rate was 28% (90% CI, 16%-100%). Four patients had a confirmed partial response, and 2 responses lasted for >9 months. The median progression-free survival and overall survival were 2.5 months (95% CI, 1.2-3.0) and 9.2 months (95% CI, 5.0-15.9), respectively. The most common all-grade treatment-related adverse events were anemia (71%), hyperglycemia (71%), hypoalbuminemia (68%), and hypophosphatemia (61%). No correlation between molecular alterations and response was observed.

Conclusion: In patients with heavily pretreated advanced endometrial cancer prospectively selected for tumors with activating PI3K pathway mutations, LY3023414 demonstrated modest single-agent activity and a manageable safety profile.

Keywords: LY3023414; PI3K pathway; advanced; dual PI3K/mTOR inhibitor; endometrial cancer.

Publication types

  • Clinical Trial, Phase II
  • Research Support, N.I.H., Extramural

MeSH terms

  • Aged
  • Class I Phosphatidylinositol 3-Kinases
  • Class Ia Phosphatidylinositol 3-Kinase / genetics
  • Endometrial Neoplasms / drug therapy*
  • Endometrial Neoplasms / genetics*
  • Endometrial Neoplasms / pathology
  • Enzyme Activation
  • Female
  • Humans
  • Hyperglycemia / chemically induced
  • Hypoalbuminemia / chemically induced
  • Hypophosphatemia / chemically induced
  • Middle Aged
  • Mutation*
  • PTEN Phosphohydrolase / genetics
  • Phosphatidylinositol 3-Kinases / genetics*
  • Progression-Free Survival
  • Proto-Oncogene Proteins c-akt / genetics
  • Pyridines / adverse effects
  • Pyridines / therapeutic use*
  • Quinolones / adverse effects
  • Quinolones / therapeutic use*
  • Signal Transduction
  • TOR Serine-Threonine Kinases
  • Treatment Outcome

Substances

  • LY3023414
  • Pyridines
  • Quinolones
  • PIK3R1 protein, human
  • phosphoinositol-3 kinase regulatory subunit 2, human
  • MTOR protein, human
  • Class I Phosphatidylinositol 3-Kinases
  • Class Ia Phosphatidylinositol 3-Kinase
  • PIK3CA protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • PTEN Phosphohydrolase
  • PTEN protein, human