Interference No. 104,436 Paper 98
Shyamala v. ffillman Page 8
[54] In deciding Hillman Preliminary Motion 2, the Board determined that Shyarnala had not
identified a utility for MIP, other than its interaction with MKK3, in its two provisional
applications.
[55] The filing for Shyarnala's involved 572 application and theaccorded benefit date for Shyamala is
I July 1997.
[561 Its provisional applications were filed in 1996.
The state of the art at and after Shyantala's filing d
[57] The Herlaar review article [1004] was published 0 ctober 1999.
[58] Herlaar confirms that, at least in 1999, that the p38 MAPK signaling pathway is one of many
pathways of clinical interest because of their relation to inflammatory diseases [ 1004 at 439:0].
[59] Herlaar identifies MKK3 to be one of four kinases; that activate p38 MAPK [1004 at 440:Fig. 1].
[60] Herlaar confirms that "protein kinases have become important targets for drug therapy" [1004
at 445:L], but focuses on synthetic inhibitors of p38 MAPK itself rather than a protein targeting
an intermediate kinase [1004 at 445:L-446:Ll.
[61] In the concluding remarks, HerIaar focuses on the continuing uncertainty in understanding
inflammatory pathways generally, and p38 MAPK' pathways in human cell lines in particular
[ 1004 at 446:Ll.
.[62] Herlaar offers five "outstanding questions" [ 1004 at 446:L]:
5 E. Herlaar & Z Brown, "p38 MAPK signalling cascades in inflammatory disease", 5 Mol. Med. Today 439
(OCL 1999) (Herlaar). The authors are affiliated with Novartis Horsham Research Centre.
6 Page:columm, in this case left column.
7 Among other complications, the paper discusses five separate isoformis for "p38 MAPK". The p3ga isoform
is one of three isoforms activated by MKK3.
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