Appeal No. 2003-0554 Page 3
Application No. 09/575,554
Initially, we note that appellants’ composition claims, claims 7-10, depend
from, and further limit claim 1 to include, inter alia, a modified oligonucleotide
backbone, or a pharmaceutically acceptable carrier. In addition, appellants’
method claims, claims 10-20, all require “an effective amount of an
oligonucleotide of claim 1.” As set forth above, claim 1 is drawn to an
oligonucleotide that is 8 to 30 nucleotides in length, which is capable of inhibiting
Ki-ras expression, and comprises at least an 8 nucleotide portion of SEQ ID NO:
20, 21, 22, 26, 28, 31, 32 or 33.2
THE REJECTION UNDER 35 U.S.C. § 103:
According to the examiner (Answer, bridging paragraph, pages 5-6), Bos
discloses antisense oligonucleotides to human H-ras and Ki-ras and to regions of
the ras genes corresponding to codons 12 and 61. According to the examiner
(id.), these oligonucleotides may be used in methods to detect the activated
forms of ras, by either hybridizing to single-stranded genomic DNA fragments or
to RNA. The examiner finds (Answer, page 6), “Hall teaches the sequence of N-
ras from which the specific antisense molecules are derived as well as the
importance of the mutations at codons 12 and 61….” As we understand the
examiner’s statement, Hall describes specific antisense molecules derived from
the sequence of N-ras. In addition, the examiner finds (id.), both Daaka and
Saison-Behmoaras teach oligonucleotides derived from H-ras that are capable of
inhibiting H-ras expression. The examiner relies on Uhlmann, Inoue, Agrawal
and Smith to teach modified oligonucleotide molecules. Answer, pages 6-7.
2 We agree with the examiner (Answer, page 17), “when the claims are drawn to a[n] ‘8
nucleobase portion’, then only 8 nucleobases of the SEQ ID NO[.] must be present.”
Page: Previous 1 2 3 4 5 6 7 Next
Last modified: November 3, 2007