Related Experiment Video

Updated: Jun 24, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
07:25

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

Development of a second-generation antiandrogen for treatment of advanced prostate cancer

Chris Tran1, Samedy Ouk, Nicola J Clegg

  • 1Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.

Science (New York, N.Y.)
|April 11, 2009
PubMed

Insights

New antiandrogen compounds, RD162 and MDV3100, effectively treat advanced prostate cancer. They target castration-resistant prostate cancer by inhibiting androgen receptor activity, showing promising results in preclinical and early clinical studies.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Metastatic prostate cancer treatment often fails due to resistance mechanisms.
  • Castration-resistant prostate cancer (CRPC) is driven by elevated androgen receptor (AR) expression.
  • Existing anti-androgen therapies become ineffective against CRPC.

Purpose of the Study:

  • To characterize novel nonsteroidal anti-androgens, RD162 and MDV3100.
  • To evaluate their efficacy in preclinical models of CRPC.
  • To assess their safety and preliminary efficacy in a Phase I/II clinical trial.

Main Methods:

  • Compounds RD162 and MDV3100 were optimized from a screen for nonsteroidal anti-androgens.
  • AR binding affinity, nuclear translocation, DNA binding, and coactivator recruitment were assessed.
  • In vivo efficacy was tested in mouse models of CRPC.
  • A Phase I/II clinical trial was conducted to evaluate MDV3100 in patients with advanced prostate cancer.

Main Results:

  • RD162 and MDV3100 demonstrated higher AR binding affinity than bicalutamide.
  • Both compounds inhibited AR nuclear translocation, DNA binding, and coactivator recruitment.
  • RD162 and MDV3100 induced tumor regression in CRPC mouse models.
  • In the clinical trial, 43% of patients treated with MDV3100 showed significant prostate-specific antigen (PSA) declines.

Conclusions:

  • RD162 and MDV3100 are potent nonsteroidal anti-androgens active against CRPC.
  • These compounds represent promising therapeutic candidates for advanced prostate cancer.
  • MDV3100 warrants further investigation in larger clinical trials for CRPC treatment.

More Related Videos

A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance05:19

A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance

Published on: November 7, 2025

Related Concept Videos

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...
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...
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...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...