Amonafide 69408-81-7

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Molecular Weight:

283.33 Amonafide produces protein-associated DNA-strand breaks through a topoisomerase II-mediated reaction, but does not produce topoisomerase I-mediated DNA cleavage. Phase 3.

Biological Activity

Through a topoisomerase II-mediated reaction, Amonafide treatment
produces DNA single-strand breaks (SSB), double-strand breaks (DSB), and
DNA-protein cross-links in human myeloid leukemia cells. Amonafide
treatment inhibits conlony formation of the leukemic cell lines and the
normal human bone marrow GM-CFC in a dose-dependent manner.


Amonafide
does not produce topoisomerase I-mediated DNA cleavage even at 100 μM.
The m-AMSA-resistant line is less than 2-fold resistant to Amonafide Amonafide interferes with the DNA breakage-reunion activity of
mammalian DNA topoisomerase II resulting in DNA cleavage stimulation.


Compared with those of other antitumor drugs, Amonafide-stimulated
cleavage intensity patterns are markedly different. Amonafide highly
prefers a cytosine, and excludes guanines and thymines instead, at
position -1, with lower preference for an adenine at position +1. Topoisomerase II-mediated DNA cleavage induced by Amonafide is affected
only slightly (less than 3-fold) by 1 mM ATP, suggeting that Amonafide
is an ATP-insensitive topoisomerase II inhibitor in contrast to
doxorubicin, etoposide, and mitoxantrone.


Amonafide
significantly inhibits the growth of HT-29, HeLa, and PC3 cells with
IC50 of 4.67 μM, 2.73 μM, and 6.38 μM, respectively. Amonafide is unaffected by P-glycoprotein-mediated efflux, unlike those
of the classical topoisomerase II Inhibitors (daunorubicin, doxorubicin,
idarubicin, etoposide, and mitoxantrone).

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