Appeal No. 1997-3122
Application No. 08/082,848
phosphorylation of NOS by FK-506 diminishes functional NO activity in neuronal cultures
(Example 3).
Based on these examples, appellants conclude that “immunophilin-binding drugs,
by inhibiting calcineurin, cause the enhanced phosphorylation of NOS, thereby leading to
lowered nitric oxide production” and that “immunophilin-binding, calcineurin-inhibiting
drugs may be used therapeutically to treat neurotoxicity mediated through NMDA-type
glutamate receptors.” Specification, page 13.
Enablement
In its broadest aspect, the present invention is directed to inhibiting glutamate- and
NMDA receptor-mediated neurotoxicity in vascular stroke and neurodegenerative disease
patients by administering a drug which binds to an immunophilin and inhibits calcineurin, in
an amount effective to inhibit glutamate-mediated neurotoxicity or to inhibit calcineurin
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(e.g., claims 1 and 17). According to the examiner, however, “the disclosure is enabling
only for claims limited to methods for blocking glutamate-mediated neurotoxicity mediated
by N-methyl-D-aspartate (NMDA) receptors in cortical neurons by administering FK506.”
Examiner’s Answer, page 5.
If we can summarize the examiner’s position, it is that the amount of direction or
guidance supplied by the specification, including the working examples discussed above,
4According to the specification, neurodegenerative diseases include Huntington’s
disease, Alzheimer’s disease and Parkinson’s disease (page 5).
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