Appeal No. 1997-3275
Application No. 07/963,329
drawn to a method of enhancing the survival of non-mitotic
cholinergic neuronal cells in a mammal, using IGF-I. . . . The
‘317 patent does not claim the method for photoreceptor
neurons in particular.
Ocrant is relied on as discussed in the previous rejection. The examiner relies on Leschey
as teaching that "an understanding of the factors that control retinal pigment epithelium
(RPE) cell proliferation may provide information that is relevant to normal and abnormal
ocular would [sic, wound] healing (p. 839, col. 1), and that several different growth factors,
including IGF-I, increase DNA synthesis and cell proliferation of human RPE cells in vitro."
(Answer, page 11). The examiner relies on Yorek as teaching that "IGF-I increases the
uptake of the neurotransmitter glycine in human Y79 retinoblastoma cells in vitro (e.g.,
abstract, p. 10986)." (Id.)
The examiner concludes that (id.):
it would have been prima facie obvious to one of ordinary skill
in the art at the time the invention was made to modify the
method of enhancing survival of nonmitotic, cholinergic
neurons with IGF-I in a mammal as taught by U.S. Patent No.
5,093,317 to treat photoreceptor neurons in particular to
promote their survival, because (i) Ocrant et al., Leschey et al.,
and Yorek et al. collectively teach that IGF-1 was known to
stimulate and bind the retina and to bind to the region of the
retina where photoreceptor cells are present in particular; (ii) a
specific receptor that binds IGF-1 was known
to be present in the region of the retina where photoreceptor
cells are present, as taught by Ocrant et al.; and, (iii)
photoreceptors are a type of neuron.
The examiner, further, urges that (id.):
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