Appeal No. 1999-0197
Application 08/054,970
44. A method for preventing or treating a disease caused by tumor necrosis factor,
comprising administering a molecule identifiable by the process of claim 43 in a manner
by which said molecule can come into contact with the portion of the p55-TNF-R (SEQ ID
NO:2) which includes Ser197 or amino acids 405-415, or the corresponding amino acids
of human p75-TNF-R, in an amount effective to prevent or treat said disease.
60. A method for modulating the cleavage of the soluble form of TNF-R from TNF-
R, comprising:
obtaining an antibody that binds to the human p55-TNF-R in the region of amino
acids 170-174, 175-179 or 170-179 of human p55-TNF-R (SEQ ID NO:2) in a manner
such that cleavage of the soluble form of TNF-R from the TNF-R is inhibited; and
bringing said antibody into contact with the portion of said TNF-R to which said
antibody is specific.
The examiner does not rely upon prior art in rejecting the claims in the Examiner’s
Answer.
Claims 34 through 38, 40, 42 through 44, 47 through 52, 54, 56, 57, and 60 stand
rejected under 35 U.S.C. § 112, first paragraph (enablement). We reverse and raise other
issues for the examiner and appellants to consider.
Background
The claimed invention involves tumor necrosis factor receptors. As explained in the
second full paragraph of page 1 of the specification:
TNF, a pro-inflammatory cytokine produced primarily by macrophages,
contributes to the defense of the host against pathogens as well as to
various detrimental manifestations of inflammation through a variety of
different effects on cell function (Old, 1990; Beutler and Cerami, 1989).
These effects are initiated by the binding of TNF to specific, high affinity cell
surface receptors (TNF-Rs), expressed on most kinds of cells (Baglioni et
al., 1985; Beutler et al., 1985; Kull et al., 1985; Tsujimoto et al., 1985;
Aggarwal et al., 1985; Israel et al., 1986). The receptors provide the
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