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 .
Claim Status
Claims 1-69 are cancelled, claims 70-74 are new, and claims 70-74 have been considered on their merits.
Claim Interpretation
The wherein clause of claim 70, starting at the end of the second line of the claim, reads as an inherent result of the cells expressing the exogenous wild-type gene. Therefore, if the cell comprises the gene, it would necessarily possess these properties. Thus, the wherein clause of claim 70 is not considered limiting.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 70-71 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Nakagawa et al. (Proc. Natl. Acad. Sci., Vol. 92, published March 1995).
Regarding claim 70, Nakagawa et al. teach expression of recombinant protein AUH, utilizing the plasmid AUHp32 (p. 2052, 1st column). Nakagawa et al. teach the recombinant proteins were expressed in Escherichia coli (p. 2052, 1st column). The E. coli expressing recombinant AUH read as a cell comprising the wild-type AUH gene.
Regarding claim 70, the plasmid AUHp32, reads as an expressible nucleic acid comprising an AUH gene.
Thus, the reference anticipates the subject matter of claims 70 and 71.
Claims 70-71 and 74 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Baumgartner et al. (J Clin Invest. 2001, February 2001) as evidenced by Grünert et al. (Orphanet Journal of Rare Diseases 2012, published 29 May 2012).
Regarding claims 70-71 and 74, Baumgartner et al. teach the molecular basis of human 3-
methylcrotonyl-CoA carboxylase (MCC) deficiency (Abstract). Baumgartner et al. teach cloning of MCCA and MCCB cDNAs and the organization of their structural genes (Abstract). MCCA and MCCB were later renamed MCCC1 (formerly MCCA) and MCCC2 (formerly MCCB), as evidenced by Grünert et al. (Grünert et al. p. 1, Background). Baumgartner et al. teach cloning full-length human wild-type MCCA and MCCB cDNAs into pCR Blunt II TOPO (p. 497, Construction of wild-type and mutant human MCCA/B expression vectors). Baumgartner et al. teach transferring the wild-type and mutant MCCA and MCCB constructs into a mammalian expression vector, pTracer-CMV2 (claim 71) at the EcoR I site (p. 497, Construction of wild-type and mutant human MCCA/B expression vectors). Baumgartner et al. teach the human wild-type MCCA and MCCB cDNAs subclones were electroporated into a SV40T transformed reference CG2 or CG1 cell line to measure MCC activity (p. 501, Expression of MCCA and MCCB alleles). The CG2 or CG1 cells comprising the MCCA and MCCB cDNAs subclones read as cells comprising both MCCC1 and MCCC2 (claim 70 and 74). Baumgartner et al. teach wild-type MCCA and MCCB alleles restored MCC activity to 43% and 53% of untransfected control fibroblasts, respectively (p. 501, Expression of MCCA and MCCB alleles and Table 3).
Thus, the reference anticipates the subject matter of claims 70-71 and 74.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 70-73 are rejected under 35 U.S.C. 103 as being unpatentable over Kariko et al. (WO 2011/071931 A2, published 16 June 2011).
Regarding claim 70, Kariko et al. teach a method for inducing a mammalian cell to produce a recombinant protein, comprising contacting the mammalian cell with an in vitro-synthesized RNA molecule encoding the recombinant protein (p. 20, lines 3-5). Kariko et al. teach the encoded recombinant protein is MCCC1, MCCC2, or IVD, wherein, each recombinant protein represents a separate embodiment (p. 61, lines 15 and 27; p. 63, line 18; p. 65, lines 13-14).
Regarding claim 71, Kariko et al. teach transfections with EPO mRNA were performed with Lipofectin in the presence of phosphate buffer, an effective delivery method for in vitro cell expression (p. 108, lines 14-15). The EPO mRNA reads as an expressible nucleic acid, since Kariko et al. teach other embodiments wherein MCCC1 is expressed, the teachings of Kariko et al. read as an expressible nucleic acid comprising an MCCC1 gene.
Regarding claims 72-73, Kariko et al. evaluated the impact of unique UTRs on enhancement of ΨmRNA translational efficiency and compared both enhanced and not enhanced in vitro protein production using EPO mRNA (p. 108, lines 21-24). Kariko et al. teach the efficiency of protein production from each mRNA was assessed in multiple cell types to include the mammalian cell lines, HEK293 (claim 73) and CHO (claim 72) (p. 108, lines 26-26).
This protein expression example taught by Kariko et al. was utilizing EPO mRNA, however, it would have been obvious to one of ordinary skill in the art to substitute the encoded recombinant proteins MCCC1, MCCC2, or IVD into the same mammalian cell lines, HEK293 and CHO with a reasonable expectation of success because Kariko et al. teach separate embodiments wherein the recombinant proteins are MCCC1, MCCC2, or IVD. One would be motivated to utilize HEK or CHO cells for expressing exogenous proteins as both cell lines are very-well known in the art and widely used in the biopharmaceutical industry.
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Relevant prior art
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
Grünert et al. (Orphanet Journal of Rare Diseases 2012, published 29 May 2012).
Grünert et al. teach isolated 3-methylcrotonyl-CoA carboxylase (MCC) deficiency is an autosomal recessive disorder of leucine metabolism caused by mutations in MCCC1 or MCCC2 encoding the α and β subunit of MCC. Grünert et al. teach the MCCC1 (formerly MCCA) or the MCCC2 (formerly MCCB) gene coding for the α and β subunit, respectively. Grünert et al. teach transient expression in transformed MCCC1 and MCCC2 deficient fibroblasts of wild-type MCCC1 and MCCC2. Grünert et al. teach all nucleic acid constructs were transferred into the mammalian expression vector pTracer-CMV2.
Conclusion
No claims are allowed.
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/N.A.H./Examiner, Art Unit 1631
/LAURA SCHUBERG/Primary Examiner, Art Unit 1631