Appeal No. 2005-0317 Page 2
Application No. 09/962,352
The examiner relies on the following reference:
Physicians Desk Reference (PDR), 43rd ed., pp. 2355-2358 (1989)
Claims 13-30 stand rejected under 35 U.S.C. § 103 as obvious in view of the
PDR. We reverse.
Background
“Estrogens have been shown to play an important role in the modulation of
estrogen receptor positive breast carcinoma. Binding of endogenous estrogens, in
particular 17β-estradiol (E2), to the estrogen receptor has been linked to proliferation of
the carcinoma cells.” Specification, paragraph [001]. “Current trends in the treatment of
estrogen receptor positive breast carcinoma are focused on the use of anti-estrogenic
agents that prevent the binding of E2 to the estrogen receptor.” Paragraph [002]. One
such anti-estrogen is tamoxifen. Id.
The specification discloses a method of treating estrogen receptor-positive
carcinoma by administration of 17α-dihydroequilin. See, e.g., paragraph [006]. The
specification discloses that 17α-dihydroequilin blocked the proliferative effect of
17β-estradiol in an in vitro assay, similar to tamoxifen. See paragraphs [010] to [013].
The specification also discloses that treatment with 17α-dihydroequilin in vivo caused a
reduction in the size of tumors induced in rats. See paragraphs [014] to [015].
Discussion
The claims are directed to a “method of treating an estrogen receptor positive
carcinoma . . . which comprises administering . . . an effective antineoplastic amount of
17α-dihydroequilin . . . in substantially purified form.”
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