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Related Experiment Video

Updated: Jul 8, 2026

Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors

Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors

Published on: October 17, 2025

Tipifarnib in acute myeloid leukemia.

Alan K Burnett¹, Jonathan Kell

¹Department of Haematology, School of Medicine, Cardiff University, Cardiff, UK. BurnettAK@Cardiff.ac.uk

Drugs of Today (Barcelona, Spain : 1998)

|January 5, 2008

Summary

Tipifarnib, a farnesyltransferase inhibitor, shows promise for treating acute myeloid leukemia (AML) in older adults, including those unfit for intensive therapy. This novel AML treatment was generally well-tolerated and achieved remissions in some patient groups.

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Last Updated: Jul 8, 2026

Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors

Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors

Published on: October 17, 2025

Area of Science:

Hematology
Oncology
Molecular Biology

Background:

Acute myeloid leukemia (AML) treatment in older adults presents significant challenges, with limited improvement in outcomes from conventional intensive therapies.
A substantial portion of AML patients are ineligible for intensive treatment, facing limited therapeutic options.
Understanding AML's molecular mechanisms offers potential therapeutic targets.

Purpose of the Study:

To evaluate the efficacy and tolerability of tipifarnib, a farnesyltransferase inhibitor (FTI), as a treatment for acute myeloid leukemia (AML).
To explore tipifarnib's potential in both relapsed and untreated elderly AML patients, including those not fit for intensive chemotherapy.

Main Methods:

Clinical assessment of tipifarnib, the first farnesyltransferase inhibitor (FTI) evaluated in AML.
Observation of treatment response rates, including complete remission, in relapsed and untreated elderly AML patient cohorts.
Evaluation of treatment tolerability and assessment of responses irrespective of RAS protein mutation status.

Main Results:

Tipifarnib achieved complete remission in 4% of relapsed AML patients and 15% of untreated elderly AML patients.
Treatment responses were observed in patients regardless of RAS protein mutations.
Tipifarnib was generally well-tolerated by the patient population studied.

Conclusions:

Tipifarnib demonstrates activity in older adult AML patients, including those with limited treatment options.
The farnesyltransferase inhibitor tipifarnib represents a potential new therapeutic strategy for AML.
Ongoing and planned clinical trials will further define tipifarnib's role in AML treatment regimens.