0
Interference No. 104,522 Paper108
Nichols v. Tabakoff Page 49
constitute or explain a claim limitation."' Bristol-Myers Squibb Co. v. Ben Venue Labs.,
Inc., 246 F.3d 1368, 1373-74, 58 USPQ2d 1508, 1512 (Fed. Cir. 2001) (quoting Pitne
Bowes, Inc. v. Hewlett-Packard Co., 182 F.3d 1298, 1305, 51 USPQ2d 1161, 1166
(Fed. Cir. 1999)).
103. During prosecution of the Tabakoff application, the examiner stated that
"[c]ompounds having diphenylureido group have been used to inhibit the voltage
sensitive sodium channels ... [and djerivatives of kynurenic acid as antagonists of
strychinine insensitive glycine binding at the NIVIDA receptor have been described."
The examiner further stated that the "high degree of unpredictability in the NIVIDA
receptor antagonist art and the voltage dependent sodium channel inhibitor art is well
known. A slight change in the structure of the compound would drastically change its
biological activity." Thus, according to the examiner, "generic claims ... [having] high
affinity for both strychinine-insensitive glycine binding site on NMDA receptor and
voltage dependent sodium channels ... [is] not commensurate in scope with the
objective enablement, especially in view of the high degree of unpredictability ......
[Office action mailed August 27, 1999 (Paper 4) in Tabakoff '697, pp. 3-4, 7 4, copy
attached.]
Here, we conclude that the preamble of Tabakoff claim 12, i.e., a compound "for
treating withdrawal syndromes manifested in a patient suffering withdrawal symptoms
and/or withdrawal-induced brain damage," sets out a material claim limitation in that it
provides a specific structural limitation requiring a kynurenic acid derivative that inhibits
both voltage sensitive sodium channels and NMDA receptor function, specifically
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