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J. SteroidBiochem. Molec. Biol. Vol. 60, No. 1-2, pp. 131 136, 1997
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Non-steroidal L-245,976 Acts as a Classical
Antiandrogen In Vitro
Jeffrey H. Toney, 1. Yuli Chen, 2 Sue-Jane Rutledge, 3
Azriel Schmidt 3 and Alex Elbrecht 2
'Department of Biochemistry, Merck Research Laboratories, Rahway, NJ, U.S.A.; 2Department of Molecular
Endocrinology, Merck Research Laboratories, Rahway, NJ, U.S.A. and SDepartment of Bone Biology and
Osteoporosis Research, Merck Research Laboratories, West Point, PA, U.S.A.
Non-steroidal antiandrogens have been employed in the management of prostate cancer, but the
mechanism of action is unclear due to a lack of good tissue culture models. The growth of a hamster
ductus deferens cell line (DDT1) is highly dependent upon the addition of 10 nM testosterone to syn-
thetic serum-free media. We describe a non-steroidal compound N-(4-chlorophenyl)-(Z,Z)-2,3-bis(-
cyclopropylmethylene) cyclopentanecarboxamide (L-245976) which antagonizes the action of
testosterone on DDT1 cells at 10 pM but exhibits little or no effect on cell growth by itself. This com-
pound also blocks the binding of 3H-dihydrotestosterone (DHT) to the human androgen receptor
(AR) with an ICs0 of ~28 pM. In addition, L-245976 was found to antagonize DHT-dependent trans-
activation of the AR via the probasin gene promoter at comparable doses with no agonist activity.
Copyright © 1997 Elsevier Science Ltd.
J. Steroid Biochem. Molec. Biol., Vol. 60, No. 1-2, pp. 131-136, 1997
INTRODUCTION
Non-steroidal antiandrogens such as ICI-176344
(Casodex) or (hydro~r)flutamide (Scheme 1) have
been employed in the management of prostate can-
cer ([1] and references therein) with modest success.
Although extensive clinical data is available on these
compounds, the mechanism of action has been diffi-
cult to elucidate due to a paucity of androgen-depen-
dent cell lines. Stirrmlation of cell growth by
androgens was reported 20 years ago using the
human breast cancer cell line MCF-7 in serum-free
media [2] and was inhibited by antiandrogens such as
cyproterone acetate. Hydroxyflutamide has also been
shown to inhibit androgen-stimulated growth of the
breast cancer cell line EVSA-T [3]. The human pro-
static carcinoma cell line LNCaP has been well stu-
died [4-12], and is known to contain a point
mutation of the androgen receptor (AR) within the
ligand binding domain [8, 10]. Thus agents such as
hydroxyflutamide can act aberrantly and can promote
*Correspondence to Dr J. Toney, Department of Biochemistry,
Building 80M-136, P.O. Box 2000, Merck Research
Laboratories, Rahway, NJ 07065-0900, U.S.A. Fax: +1(908)
594 3664.
Received 15 Apr. 1996; accepted 29 Jul. 1996.
cell growth of LNCaP cells instead of acting as an
antiandrogen [11, 12]. In addition, the maintenance
of LNCaP in serum-free media is difficult [4]. Other
human prostatic cell lines such as DU145 and PC3
have been employed to study the effect of antiandro-
gens [13]. However, these cell lines have been
reported to be both hormone-sensitive and hormone=
insensitive depending upon growth conditions, and
cannot be maintained in synthetic media. An andro-
gen-dependent hamster ductus deferens cell line
(DDT1) has been described that can be maintained
in serum-free synthetic media in which proliferation is
highly dependent upon the addition of testosterone
[14]. The DDT1 cell line thus presents a good model
for studying the biological action of putative andro-
genic/antiandrogenic agents.
We describe a 96-well colorimetric assay for cell
proliferation using the DDT1 cells in the presence of
androgens which led to the identification of the non-
steroidal compound N-(4-chlorophenyl)-(Z,Z)-2,3-
bis (cyclopropylmethylene) cyclopentanecarboxamide
(L-245976; see Fig. 1). An assay for androgen-depen-
dent transactivation of the AR using the rat probasin
gene promoter [15] is also described to allow dis-
crimination between agonists and antagonists. Taken
together, these assays should prove useful for the
131