Dihydrofolate reductase mutant with exceptional resistance to methotrexate but not to trimetrexate

Pamela Pineda, Aaron Kanter, R. Scott McIvor, Stephen J. Benkovic, Andre Rosowsky, Carston R. Wagner

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Two double (F31A/F34A, I60A/L67G) and one quadruple (F31A/F34A/I60A/L67G) mutant murine dihydrofolate reductases were constructed and evaluated for their ability to impart antifolate resistance. Both I60A/L67G and F31A/F34A/I60A/L67G were found to be unstable and devoid of catalytic activity. The Ki values for F31A/F34A, methotrexate (MTX), bis-MTX, and PT-523 were found to be 10100-, 4410-, and 617-fold higher than the wild-type enzyme, respectively, but only 13.5-fold higher for trimetrexate (TMTX). These findings suggest that F31A/F34A could be used for gene therapy to render normal cells resistant to MTX but sensitive to TMTX.

Original languageEnglish (US)
Pages (from-to)2816-2818
Number of pages3
JournalJournal of medicinal chemistry
Volume46
Issue number14
DOIs
StatePublished - Jul 3 2003

Fingerprint

Dive into the research topics of 'Dihydrofolate reductase mutant with exceptional resistance to methotrexate but not to trimetrexate'. Together they form a unique fingerprint.

Cite this