Related Experiment Video

Updated: Aug 10, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

Farnesyltransferase inhibitors versus Ras inhibitors

J B Gibbs1, S L Graham, G D Hartman

  • 1Merck Research Laboratories, West Point, PA 19486, USA. jay_gibbs@merck.com

Current Opinion in Chemical Biology
|August 1, 1997
PubMed

Insights

Farnesyl-protein transferase (FPTase) inhibitors show promise as anticancer agents. Their antiproliferative effects extend beyond ras-driven tumors by inhibiting the farnesylation of various proteins.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Farnesyl-protein transferase (FPTase) inhibitors have emerged as potential anticancer agents.
  • Initial research focused on their efficacy against ras-transformed cells and tumors.
  • Emerging evidence suggests broader applications beyond ras-dependent cancers.

Purpose of the Study:

  • To explore the antiproliferative and antitumor potential of FPTase inhibitors.
  • To investigate the mechanisms underlying the efficacy of FPTase inhibitors.
  • To determine if FPTase inhibitors are effective against non-ras-driven tumors.

Main Methods:

  • In vitro studies using cultured cells.
  • In vivo studies using rodent cancer models.
  • Analysis of protein farnesylation pathways.

Main Results:

  • FPTase inhibitors demonstrated antiproliferative effects in cell cultures and rodent models.
  • The efficacy of FPTase inhibitors was observed in cancers beyond those driven by Ras.
  • Inhibition of farnesylation of non-Ras proteins contributes to the antitumor activity.

Conclusions:

  • FPTase inhibitors represent a promising class of anticancer therapeutics.
  • The therapeutic potential of FPTase inhibitors is not limited to Ras-mediated cancers.
  • Targeting protein farnesylation offers a versatile strategy for cancer treatment.

More Related Videos

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein07:08

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein

Published on: January 16, 2020

Quantitative Structure-Activity Relationship, Activity Prediction, and Molecular Dynamics of Non-nucleotide Reverse Transcriptase Inhibitors10:29

Quantitative Structure-Activity Relationship, Activity Prediction, and Molecular Dynamics of Non-nucleotide Reverse Transcriptase Inhibitors

Published on: May 9, 2025

Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
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...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
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...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...