Appeal No. 2000-0344
Application No. 08/718,408
10. The process of Claim 9 wherein the ruthenium sodium tungstate-
based catalyst is RuW11O39SiNa5.
The examiner relies on the following references:
Pearson et al. (Pearson), “A New Method for the Oxidation of Alkenes to Enones.
An Efficient Synthesis of ? 5 –7-Oxo Steroids,” J. Chem. Soc., Perkin Trans. I, pp.
267-273 (1985)
Muzart, “Synthesis of unsaturated carbonyl compounds via a chromium -mediated
allylic oxidation by 70% tert.butylhydroperoxide,” Tetrahedron Letters, Vol. 28,
No. 40, pp. 4665-4668 (1987)
Neumann et al. (Neumann), “Alkene Oxidation Catalyzed by a Ruthenium-
Substituted Heteropolyanion, SiRu(L)W11O39 : The Mechanism of the Periodate
Mediated Oxidative Cleavage,” J. Am. Chem. Soc., Vol. 112, pp. 6025-6031
(1990)
Claims 1-16 and 18-26 stand rejected under 35 U.S.C. § 103 as obvious
over Pearson and Neumann.
Claims 1-16 and 18-26 also stand rejected under 35 U.S.C. § 103 as
obvious over Muzart and Neumann.
We reverse.
Background
“The principal mediator of androgenic activity in some target organs, e.g.,
the prostate, is 5a–dihydrotestosterone (‘DHT’), formed locally in the target organ
by the action of 5a-reductase, which converts testosterone to DHT.” Specification,
page 1. Excessive accumulation of testosterone or DHT causes “undesirable
physiological manifestations” such as benign prostatic hyperplasia; “[i]nhibitors of
5a-reductase will serve to prevent or lessen symptoms of hyperandrogenic
stimulation.” Id.
2
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