Appeal No. 2006-2644 Page 4
Application No. 10/047,945
administering a peptide comprising at least the sequence Leu-Lys-Ala-Met to the
patient.
2. Enablement
The examiner rejected claims 9-18 under 35 U.S.C. § 112, first paragraph, for
lack of enablement. The examiner reasoned that Appellants’ “US Patent numbers
5,576,297 and 5,744,449 [disclose] that a peptide identical to SEQ ID NO:2, as well as
peptides comprising at least 3 amino acids of this sequence, have the biological
property of inhibiting the lethal effects of venom from poisonous snakes. . . . As such,
the prior art clearly demonstrates that the peptide of SEQ ID NO:2 as well as fragments
of SEQ ID NO:2 were known to be inhibitors of metalloproteinases found in snake
venom.” Examiner’s Answer, pages 5-6.
The examiner noted the experiments described in the specification that
purportedly show that LT-10 reduces IgE levels, but concluded that the data do not
support that conclusion:
SEQ ID NO:1 [LT-10] is a metalloproteinase inhibitor that is 10 amino
acids in length. It is not an enzyme, so it would not be expected to have
degraded the IgE present in the solution. . . . Since the epitope
recognized by the anti-IgE antibody used by appellant is not specified, the
only logical way that peptide binding to IgE could render the IgE
undetectable is if the peptide masks the epitope on IgE recognized by the
anti-IgE antibody. If this is so, peptide binding does not reduce IgE levels
since IgE would still be detectable if an anti-IgE polyclonal sera or an anti-
IgE antibody that recognizes a different epitope is used in the detection
assay.
Id., pages 7-8. The examiner concluded that the data in Table 4 suffers from the same
problem. He concluded that undue experimentation would be required to reduce IgE
levels via the claimed method.
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