Appeal No. 2001-1294 Page 5
Application No. 08/473,667
Chemical Co., 837 F.2d 469, 473, 5 USPQ2d 1529, 1531 (Fed. Cir. 1988).
According to appellants (Brief, page 10), Tu “recognizes anabaseine and
DMAB-anabaseine as a toxin. … Based on in vitro studies on frog skeletal
muscle, the reference concludes that the functional role of anabaseine is one of
paralysis on the muscle.” In addition, appellants point out (id.), Meyer “failed to
observe nicotine induced acetylcholine release with anabaseine. This contrasts
with appellants’ observation that pharmaceutical compositions of anabaseine of
DMAB-anabaseine stimulate brain cholinergic neurocortical receptors.” In this
regard we note, Meyer teach (page 1761, bridging paragraph, columns 1 and 2),
It was necessary to use minces which presumably contain intact
cholinergic interneurons to observe nicotine-induced [3H]ACh
release, and this effect was still not observed with THP or
anabaseine. These two compounds have been shown recently to
display high-affinity binding to rat brain nicotinic receptors….
Further, very high concentrations of nicotine were necessary to
release ACh. … The lack of effect of anabaseine and THP on ACh
release, even at high concentrations that activate peripheral
nicotinic receptors, suggests that more than one population of
nicotinic receptors exists in the rat brain.
Therefore, we cannot agree with the examiner’s position “that anabaseine and
nicotine are functionally equivalent in brain….” Answer, page 8.
We remind the examiner that as required by the claimed invention the
pharmaceutical composition must comprise a brain cholinergic neurocortical
stimulating amount of anabaseine or DMAB-anabaseine. We recognize the
examiner’s argument (Answer, page 9), that the discovery of a new property of
an old product is not sufficient, by itself, to support the patentability of the old
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