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PI3K inhibitor D-116883 is effective in in vitro models of ovarian cancer

A Honig1, J C Hahne, S Meyer

  • 1Department of Gynecology and Obstetrics, Medical University of Würzburg, Josef Schneider Str. 4, 97080 Würzburg, Germany. Arnd_Hoenig@hotmail.com

Anticancer Research
|May 18, 2012
PubMed
Abstract

Insights

The phosphatidylinositol 3-kinase (PI3K) inhibitor D-116883 demonstrates significant cytotoxic effects in ovarian cancer models. This drug effectively inhibits tumor cell growth and induces apoptosis, showing promise for further research.

Area of Science:

  • Oncology
  • Pharmacology

Background:

  • The PI3K/AKT pathway is crucial in ovarian cancer development.
  • PTEN loss often activates this pathway, driving tumorigenesis.
  • D-116883 is an oral PI3K inhibitor developed by Aeterna Zentaris GmbH.

Purpose of the Study:

  • To evaluate the cytostatic and cytotoxic effects of D-116883 in ovarian cancer.
  • To analyze the impact of D-116883 on programmed cell death in ovarian cancer cell lines.

Main Methods:

  • Assessed D-116883 potency in four ovarian carcinoma cell lines using crystal-violet and MTT assays.
  • Evaluated anchorage-independent growth using soft agar assays.
  • Performed cell cycle analysis via fluorescence-activated cell sorting (FACS), with and without specific inhibitors.

Main Results:

  • D-116883 exhibited significant growth inhibition across all tested cell lines (IC50 < 1 μM).
  • The drug reduced anchorage-independent growth, a key characteristic of tumor cells.
  • Cell cycle analysis revealed a dose-dependent increase in apoptosis, unaffected by zVAD or necrostatin.

Conclusions:

  • D-116883 displays substantial cytotoxic activity against ovarian cancer in vitro.
  • These findings position D-116883 as a promising candidate for further ovarian cancer investigation, including in vivo studies.

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