Estrogen receptor-&bgr; ligands

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Having -c- – wherein x is chalcogen – bonded directly to...

Reexamination Certificate

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C514S456000, C514S457000

Reexamination Certificate

active

06518301

ABSTRACT:

TECHNICAL FIELD
The present invention is directed to a series of ligands, and more particularly to estrogen receptor-&bgr; ligands which have better selectivity than estrogen for the estrogen receptor-&bgr; over the estrogen receptor-&agr;, as well as to methods for their production and use in the treatment of diseases related to the estrogen receptor-&bgr;, specifically. Alzheimer's disease, anxiety disorders, depressive disorders, osteoporosis, cardiovascular disease, rheumatoid arthritis, or prostate cancer.
BACKGROUND
Estrogen-replacement therapy (“ERT”) reduces the incidence of Alzheimer's disease and improves cognitive function in Alzheimer's disease patients (Nikolov et al. Drugs of Today, 34(11), 927-933 (1998)). ERT also exhibits beneficial effects in osteoporosis and cardiovascular disease, and may have anxiolytic and anti-depressant therapeutic properties. However, ERT shows detrimental uterine and breast side effects that limit its use.
The beneficial effects of ERT in post-menopausal human women is echoed by beneficial effects of estrogen in models relevant to cognitive function, anxiety, depression, bone loss, and cardiovascular damage in ovariectomized rats. Estrogen also produces uterine and breast hypertrophy in animal models reminiscent of its mitogenic effects on these tissues in humans.
The beneficial effects of ERT in post-menopausal human women is echoed by beneficial effects of estrogen in models relevant to cognitive function, anxiety, depression, bone loss, and cardiovascular damage in ovariectomized rats. Specifically, experimental studies have demonstrated that estrogen effects the central nervous system (“CNS”) by increasing cholinergic function, increasing neurotrophin
eurotrophin receptor expression, altering amyloid precursor protein processing, providing neuroprotection against a variety of insults, and increasing glutamatergic synaptic transmission, among other effects. The overall CNS profile of estrogen effects in pre-clinical studies is consistent with its clinical utility in improving cognitive function and delaying Alzheimer's disease progression. Estrogen also produces mitogenic effects in uterine and breast tissue indicative of its detrimental side effects on these tissues in humans.
The estrogen receptor (“ER”) in humans, rats, and mice exists as two subtypes. ER-&agr; and ER-&bgr;, which share about a 50% identity in the ligand-binding domain (Kuiper et al. Endocrinology 139(10) 4252-4263 (1998)). The difference in the identity of the subtypes accounts for the fact that some small compounds have been shown to bind preferentially to one subtype over the other (Kuiper et al.).
In rats. ER-&bgr; is strongly expressed in brain, bone and vascular epithelium, but weakly expressed in uterus and breast, relative to ER-&agr;. Furthermore, ER-&agr; knockout (ERKO-&agr;) mice are sterile and exhibit little or no evidence of hormone responsiveness of reproductive tissues. In contrast, ER-&bgr; knockout (ERKO-&bgr;) mice are fertile, and exhibit normal development and function of breast and uterine tissue. These observations suggest that selectively targeting ER-&bgr; over ER-&agr; could confer beneficial effects in several important human diseases, such as Alzheimer's disease, anxiety disorders, depressive disorders, osteoporosis, and cardiovascular disease without the liability of reproductive system side effects. Selective effects on ER-&bgr;-expressing tissues (CNS, bone, etc.) over uterus and breast could be achieved by agents that selectively interact with ER-&bgr; over ER-&agr;.
It is a purpose of this invention to identify ER-&bgr;-selective ligands that are useful in treating diseases in which ERT has therapeutic benefits.
It is another purpose of this invention to identify ER-&bgr;-selective ligands that mimic the beneficial effects of ERT on brain, bone and cardiovascular function.
It is another purpose of this invention to identify ER-&bgr;-selective ligands that increase cognitive function and delay Alzheimer's disease progression.
SUMMARY OF THE INVENTION
This present invention is directed to the use of compounds having the generic structure:
as ER-&bgr;-selective ligands, which mimic ERT, but lack undesirable side effects of ERT. These compounds particularly satisfy the formula:
(
K
i&agr;A
/K
i&bgr;A
)/(
K
i&agr;E
/K
i&bgr;E
)>1,
preferably:
(
K
i&agr;A
/K
i&bgr;A
)/(
K
i&agr;E
/K
i&bgr;E
)>30,
more preferably:
(
K
i&agr;A
/K
i&bgr;A
)(
K
i&agr;E
/K
i&bgr;E
)>100,
wherein K
i&agr;A
is the K
i
value for the ligand in ER-&agr;; K
i&bgr;A
is the Ki value for the ligand in ER-&agr;: K
i&agr;E
is the K
i
value for estrogen in ER-&agr;; and K
i&bgr;E
is the K
i
value for estrogen in ER-&bgr;.
DETAILED DESCRIPTION OF THE INVENTION
The instant invention involves a method for treating a disease associated with the estrogen receptor-&bgr;, comprising the step of administering a therapeutically-effective amount of a compound that satisfies the equation (K
i&agr;A
/K
i&bgr;A
)/(K
i&agr;E
/K
i&bgr;E
)>1, wherein K
i&agr;A
is the K
i
value for the agonist in ER-&agr;; K
i&bgr;A
is the K
i
value for the agonist in ER-&bgr;; K
i&agr;E
is the K
i
value for estrogen in ER-&agr;; and K
i&bgr;E
is the K
i
value for estrogen in ER-&bgr;. Preferably, the compound satisfies the equation (K
i&agr;A
/Ki
&agr;A
)/(K
i&agr;E
/K
i&bgr;E
)>100. Preferred diseases associated with the estrogen receptors &bgr; are selected from Alzheimer's disease, anxiety disorders, depressive disorders, osteoporosis, cardiovascular disease, rheumatoid arthritis and prostate cancer. More preferably, the diseases are Alzheimer's disease or depressive disorders.
The compounds of the instant invention are ER-&bgr;-selective ligands of the structure:
In this structure L
1
is —C(═O)—, ═C(R
6
)—, —CH(R
6
)—, O, S, or NR
a
, preferably —C(═O)—, ═C(R
6
)—, —CH(R
6
)—or O; L
2
is ═C—or —CH—; L
3
is ═C(R
6
)—, —CH(R
6
)—or —C(═O)—; and L
4
is —C(═O)—, CH
2
, O, S, or NR
a
, preferably —C(═O)—, CH
2
, or O, provided that when L
1
is —C(═O)—; L
4
is CH
2
, O, S, or NR
a
; when L
4
is —C(═O)—, L
1
is CH
2
, O, S, or NR
a
; and when L
3
is —C(═O)—, L
1
is ═C(R
6
)—or —CH(R
6
)—, and L
4
is O or NR
a
. Additionally, when L
1
is ═C(R
6
)—, L
2
is ═C—; when L
1
is —CH(R
6
)—, L
2
is —CH—; when L
3
is ═C(R
6
)—, L
2
is ═C—; and when L
3
is —CH(R
6
)—. L
2
is —CH—. ═ represents a single bond or double bond, depending upon the hybridization of L
1
-L
4
. The structures for L
2
show only three bonds because the fourth bond is a single bond to R
1
.
R
1
is attached via a single bond to L
2
, and is phenyl, substituted phenyl, Het, or substituted Het, as defined below. R
1
is preferably:
wherein: R
7
is H, Cl, or methyl; R
8
is Br, Cl, F, R
a
, OR
a
, or allyl; R
9
is H, OH, NH
2
, Br, Cl; and R
10
is H or methyl: or R
8
and R
9
may combine to be —OCH
2
O—, forming a secondary 5-membered ring structure exterior to the phenyl group; or R
1
is a substituted or unsubstituted heterocyclic substituent having the following structure:
more preferably unsubstituted
R
2
, R
3
, R
4
, and R
5
are each independently, —R
a
, —OR
a
, —SR
a
, —NR
a
R
a
, —NC(═O)R
a
, —NS(═O)R
a
, —NS(═O)
2
R
2
, halogen, cyano. —CF
3
, —CO
2
R
a
, —C(═O)R
a
, —C(═O)NHR
a
, nitro, —S(═O)R
a
, or —S(═O),R
a
, and is preferably R
a
, OR
a
, NR
2
a
, NC(═O)R
a
, CF
3
, or halogen, preferably, hydrogen, hydroxyl or methyl.
R
6
is R
a
, phenyl or CF
3
.
R
a
is, independently, at each occurrence, H or (C
1
-C
5
)alkyl.
When L
1
is —C(═O)—, and R
2
is hydroxy or hydrogen, and R
3
is hydrogen, and R
4
is hydroxy, and R
5
is hydrogen, and R
6
is hydrogen, then R
1
is not para-phenol.
For purposes of this invention, “substituted” when used to modify a phenyl or a heteroatomic ring means such a ring substituted at one or more positions, independently, with —R
a
, —OR
a
, —SR
a
, —NR
a
, R
a
, —NC(&

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