DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claims 21-39 are pending and under examination in the instant application.
Information Disclosure Statement
The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claim(s) 21-30, 33-34, and 36-39 are rejected under 35 U.S.C. 103 as being unpatentable over Kar et al. (US20210024591A1, filed on 05/22/2020, and published on 01/28/2021), in view of Alberts, et al. (Alberts, et al. "Molecular Biology of the Cell, Fifth Edition". New York:Garland Science, 2008. pages 1-3 and 367).
Regarding claims 21, 22, and 38, Kar et al. teaches a prophylactic method for blocking neurogenerative disease associated with axon degeneration comprising treating a cell with a cell permeable polypeptide preventing induced and mediated neurotoxicity; wherein the cell permeable peptide disassembles aggregates of stress granules and neurodegeneration-associated RNA binding proteins along axons, and wherein the polypeptide is a G3BP1 peptide has the amino acid sequence of SEQ ID NO: 2 (please see below a screenshot of the amino acid sequence of SEQ ID NO: 2) (claims 1, 3, and 10 of Kar et al.)
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However, Kar et al. fails to teach the nucleic acid sequence encoding the amino acid sequence of SEQ ID NO: 2.
However, Alberts et al. teaches that the nucleotide sequence of a gene, through the intermediary of mRNA, is translated into the amino acid sequence of a protein by rules that are known as the genetic code (paragraph 3, page 367, lines 6-8) (please see below a screenshot of the query match of 100% between the nucleotide sequence of instant SEQ ID NO:1 and the nucleotide sequence encoding amino acid sequence of SEQ ID NO: 2 of Kar et al.).
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Therefore, based on well-known genetic code and the teachings of Kar et al. of the amino acid sequence of SEQ ID NO: 2 of the G3BP1 peptide, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to make the nucleic acid encoding Kar et al.’s amino acid sequence of the G3BP1 protein (SEQ ID NO: 2) with a reasonable expectation of success. One would have been motivated to have done so as the selection of the sequence of these nucleotide sequences represents nothing more than choosing from a finite number of identified, predictable solutions.
Regarding claim 23: Following discussion of claim 21 above, Kar et al. further teaches that the nervous system disease is a peripherical nervous system disease (paragraph 0164).
Regarding claim 24: Following discussion of claim 21 above, Kar et al. further teaches that the nervous system disease is a neurodegenerative disease (Abstract and paragraph 0003).
Regarding claim 25: Following discussion of claim 21 above, Kar et al. further teaches examples of nervous system diseases that are movement disorders, such as Parkinson's Disease and Amyotrophic Lateral Sclerosis (paragraph 0011).
Regarding claim 26-28: Following discussion of claim 24 above, Kar et al. further teaches examples of neurodegenerative diseases that are polyglutamine diseases that are positively influenced by the control of protein aggregation, such as Huntington's disease, spinocerebellar ataxia that are caused by an expansion in the polyglutamine segment of affected proteins (paragraphs 0005 and 0008).
Regarding claim 29: Following discussion of claim 26 above, Kar et al. further teaches that the polyglutamine disease is Huntington's disease (HD) or spinocerebellar ataxia (paragraphs 0005 and 0008).
Regarding claim 30: Following discussion of claim 29 above, Kar et al. further teaches that the polyglutamine repeat spinocerebellar ataxia is Spinocerebellar ataxia type 2 (Ataxin-2) (paragraph 0008).
Regarding claim 33: Following discussion of claim 21 above, Kar et al. further teaches that the polypeptide is a part of a vector (paragraphs 0176-0177).
Regarding claim 34: Following discussion of claim 33 above, Kar et al. further teaches that the vector is adenovirus (paragraphs 0176-0177).
Regarding claim 36: Following discussion of claim 33 above, Kar et al. further teaches that the vector is an AAV vector (paragraph 0177).
Regarding claim 37: Following discussion of claim 33 above, Kar et al. further teaches that the vector or construct is a host cell (paragraph 0012 and claim 10 of Kar et al.).
Regarding claim 39: Following discussion of claim 21 above, Kar et al. further teaches that the polypeptide is a part of a pharmaceutical composition (paragraph 0204).
Claim(s) 21-39 are rejected under 35 U.S.C. 103 as being unpatentable over Kar et al. (US20210024591A1, filed on 05/22/2020, and published on 01/28/2021), in view of Alberts, et al. (Alberts, et al. "Molecular Biology of the Cell, Fifth Edition". New York:Garland Science, 2008. pages 1-3 and 367) as applied to claims 21-30, 33-34, and 36-39 above, and further in view of Humbel et al. (Humbel et al., “Maximizing lentiviral vector gene transfer in the CNS”. Gene Ther 28, 75–88, published on 07/06/2020).
Regarding claims 21-30, 33-34, and 36-39, the teachings of Kar et al. and Alberts et al. are set forth in detail above.
Regarding claims 31-32 and 35: Following discussion of claim 21 above, Kar et al. further teaches that the AAV5 was injected into the proximal sciatic nerve of the mice.
However, Kar et al. fails to teach that the injection was directly into the brain of the subject or into the spinal cord of the subject by means like intravascular, intravenous, intranasal, intraventricular or intrathecal injection. Kar et al. further fails to teach that the vector is a lentiviral vector.
However, Humbel et al. teaches using lentiviral vector gene transfer in treating diseases in the central nervous system (Abstract). Humbel et al. further teaches using lentiviral vectors (LVs) to target neurons and astrocytes, neuronal connectome, and the retrograde transport properties of LV-FuG/B2 following injection into a highly interconnected area of the brain to increase transduction efficiency, enhance gene transfer, resulting in a widespread distribution of the vector in large areas of the brain following intrastriatal injection.
Given the teaching of Kar et al. of injecting AAV5 into the proximal sciatic nerve of the mice to treat neurogenerative diseases and the teachings of Humbel et al. of using lentiviral vector gene transfer in treating diseases in the central nervous system and the direct intrastriatal injection into the brain to increase transduction efficiency, enhance gene transfer in treating nerve system diseases, it would have been prima facie obvious to one of the ordinary skills in the art before the effective filing date of the claimed invention to have modified the treatment method of Kar et al. and substituted the AAV injection with the lentiviral injection of the G3BP1 protein directly into the brain of the subject for the purpose of enhancing gene transfer in treating neurogenerative diseases with predictable results.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to HANAN ISAM ABUZEINEH whose telephone number is (571)272-9596. The examiner can normally be reached Mon- Fri 8:30-5:00.
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Hanan Isam Abuzeineh
/H.I.A./Examiner, Art Unit 1633
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633