Appeal No. 2002-0253
Application No. 09/093,450
The rejection of claim 15 under 35 U.S.C. § 112, first and second paragraphs,
has been withdrawn. Answer, p. 2.
Having carefully considered the record before us which includes, inter alia, the
specification, the appellants’ Brief (Paper No. 16), the examiner’s Answer (Paper No.
19) and the declaration of Dr. Marc Feldmann (Paper No. 12), we affirm each of the
examiner’s rejections.
Background
Tumor necrosis factor " (TNF") and tumor necrosis factor $ (TNF$) are
cytokines which are said to be produced by monocytes and macrophages in response
to endotoxins or other stimuli. Le, col. 1, lines 28-31. Prior to the present invention, it
was known in the art that TNFs cause inflammatory actions which result in tissue injury,
and that they are associated with infections, immune disorders and other pathologies.
Id., col. 1, lines 46-47 and lines 55-57. TNF-related pathologies were known to include,
inter alia, “acute and chronic immune and autoimmune pathologies, such as systemic
lupus erythematosus (SLE) rheumatoid arthritis, thryoidosis, graft versus host disease,
scleroderma, diabetes mellitus, [and] Graves’ disease.” Id., col. 34, lines 7-13. It had
been the goal of researchers in the field to devise methods of treating or inhibiting such
disorders using compounds which inhibit or neutralize the effects of TNF" and TNF$.
Id., col. 9, lines 46-50; Aggarwal, the abstract. Such compounds, known as TNF
antagonists, include anti-TNF" and anti-TNF$ antibodies (i.e., “polyclonal antibodies,
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