Related Experiment Video

Updated: May 14, 2026

Evaluating In Vitro DNA Damage Using Comet Assay
10:43

Evaluating In Vitro DNA Damage Using Comet Assay

Published on: October 11, 2017

A review of iniparib in ovarian cancer

Ivy Wilkinson-Ryan1, David Mutch

  • 1Washington University in St Louis, Campus Box 8064, 4th floor maternity, 4911 Barnes Jewish Hospital Plaza, St Louis, MO 63110, USA. ivywilkry@gmail.com

Expert Opinion on Investigational Drugs
|February 12, 2013
PubMed
Abstract

Insights

Iniparib shows promise for treating ovarian cancer, with early trials indicating improved survival. Further research is needed to clarify its mechanism of action for personalized cancer therapy.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Metastatic ovarian cancer has high recurrence rates and morbidity.
  • Standard treatments for ovarian cancer are insufficient.
  • There is a need for novel, tumor-specific agents.

Purpose of the Study:

  • To review the mechanistic and clinical data on iniparib in ovarian cancer.
  • To assess the current understanding of iniparib's mechanism of action.
  • To evaluate the therapeutic potential of iniparib in ovarian cancer treatment.

Main Methods:

  • Literature review of mechanistic and clinical studies on iniparib.
  • Analysis of iniparib's interaction with PARP proteins.
  • Evaluation of safety and preliminary efficacy data from Phase I and II trials.

Main Results:

  • Iniparib's interaction with PARP-1 is non-specific; its exact mechanism remains unclear.
  • Iniparib is well-tolerated in Phase I studies.
  • Phase II studies suggest improved survival in recurrent ovarian cancer patients compared to historical controls.

Conclusions:

  • Iniparib demonstrates potential in early-stage ovarian cancer trials.
  • Understanding iniparib's cytotoxicity pathways is crucial for individualized cancer therapy.

More Related Videos

Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays04:07

Visualizing DNA Damage Repair Proteins in Patient-Derived Ovarian Cancer Organoids via Immunofluorescence Assays

Published on: February 24, 2023

In vivo Imaging and Therapeutic Treatments in an Orthotopic Mouse Model of Ovarian Cancer07:46

In vivo Imaging and Therapeutic Treatments in an Orthotopic Mouse Model of Ovarian Cancer

Published on: August 17, 2010

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...