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 .
Election/Restriction
Applicant’s election without traverse of Group 1, claims 1-7 and 9-20 in the reply filed on 08 December 2025 is acknowledged.
Claim 26 is withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 08 December 2025.
Claim Status
Claims 5-6 and 17 have been amended, claims 8, 21-25, and 27-30 have been cancelled, claim 26 is withdrawn, and claims 1-7 and 9-20 have been considered on their merits.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 16 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 16 recites the phrase “GT2A_VI (SEQ ID NO: 21) or GT2A_V2 (SEQ ID NO: 22)”, which renders the claim indefinite because it is unclear whether the limitation in parentheses are part of the claimed invention. MPEP § 2173.05(d) states, description of examples or preferences is properly set forth in the specification rather than the claims. If stated in the claims, examples and preferences may lead to confusion over the intended scope of a claim. Therefore, it is unclear whether the information in parentheses is exemplary or a limitation of the claim.
Amending the claim to include, for example, The viral vector of claim 9, further comprising a 2A linker selected from GT2A_V1 or GT2A_V2, wherein the sequence encoding the 2A linker is SEQ ID NO: 21 or SEQ ID NO: 22, may obviate the rejection.
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 1-3, 6, and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Kwiatkowski et al., (WO 2020/053815 A1, published 19 March 2020) in view of Hinderer et al. (WO 2017/024198 A1, published 09 February 2017, IDS ref.).
Regarding claim 1, Kwiatkowski et al. teach conjugates of a glucagon-like-peptide (GLP), for example, a glucagon-like-peptide 1 (GLP-1) polypeptide or analogs thereof (Abstract). Kwiatkowski et al. teach SEQ ID NO: 11, Dulaglutide (LY2189265, TRULICITY®), which is a molecule consisting of two identical, disulfide-linked chains, each containing a human GLP-1 analog sequence covalently linked to a modified human immunoglobulin G4 (IgG4) heavy chain fragment (Fc) by a small peptide linker (p. 63 lines 16-19). Kwiatkowski et al. teach the GLP-1 analog sequence, SEQ ID NO:8, which is identical to instant SEQ ID NO: 3; the IgG4 Fc sequence, SEQ ID NO: 9, which is identical to instant SEQ ID NO: 11; and the small peptide linker, SEQ ID NO: 10, which is identical to instant SEQ ID NO: 13 (pp. 63-64). Kwiatkowski et al. teach the sequence of one monomer of Dulaglutide, SEQ ID NO: 11, which consists of instant SEQ ID NOs: 3, 10, and 11. See alignment of SEQ ID NO: 11 and instant SEQ ID NO: 14 below:
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Kwiatkowski et al. teach does not teach a viral vector comprising said sequence or a human thrombin leader sequence prior to the GLP-1 analog.
However, Hinderer et al. teach viral vectors comprising nucleic acid molecules comprising a sequence encoding a propeptide and the active portion of GLP-1, wherein, when expressed, the N-terminal amino acid of GLP-1 immediately follows the C-terminal amino acid of the propeptide (Abstract). Hinderer et al. teach this approach could provide a convenient and effective therapy for type II diabetes (T2DM) in both humans and other species affected by the
disease (para. [0003]). Hinderer et al. teach anticoagulant factor II is also called prothrombin, also known as factor II which is used interchangeably with prothrombin and thrombin (para. [00057]). Hinderer et al. teach in one embodiment, the propeptide sequence is a factor II leader sequence (para. [00057]). Hinderer et al. teach the amino acid sequence of human Factor II is known and the propeptide sequence is amino acids 1-43 of SEQ ID NO: 28 (para. [00057]). SEQ ID NO: 28 is identical to instant SEQ ID NO: 7.
Therefore, it would have been obvious to one of ordinary skill in the art to utilize the sequence of Dulaglutide of Kwiatkowski et al. with the human propeptide and viral vector of Hinderer et al. with a reasonable expectation of success because Hinderer et al. teach GLP-1 expression constructs have been developed for use in subjects including companion animals and humans, in which the leader propeptide is derived from proteins endogenous to the species of the veterinary or human patient (para. [00024]). Additionally, viral vectors could provide long-lasting expression of GLP-1 because delivering the fusion peptide via viral vector would enable a patient's own cells to produce the GLP-1 receptor agonist, rather than relying on periodic injections. One would be motivated to utilize the sequence of Dulaglutide of Kwiatkowski et al. with the human propeptide and viral vector of Hinderer et al. because Hinderer et al. teach GLP-1 cannot be expressed in its native form from a gene therapy vector due to the need for cell-specific proteases to release the active peptide from the precursor polypeptide (para. [0004]). Additionally, Hinderer et al. teach, in mice, thrombin propeptide produced more active GLP-1 than other propeptide constructs (para. [00099]). While Hinderer et al. focus is directed towards animal studies, the success of the thrombin propeptide would provide motivation to try in human patients and the propeptide is required to be derived from proteins endogenous to the species.
Thus, the teachings of Kwiatkowski et al. in view of Hinderer et al. render obvious the limitations of claim 1, to include instant SEQ ID NO: 14.
Regarding claim 2, Kwiatkowski et al. in view of Hinderer et al. render obvious SEQ ID NO: 14, thus, also render obvious the at least 75% identical to nucleic acid sequence encoding the fusion protein, SEQ ID NO: 15.
Regarding claim 3, Hinderer et al. teach an expression cassette comprises a nucleic acid molecule comprising the GLP-1 construct coding sequence, promoter, other regulatory sequences and packaged into the capsid of a viral vector (para. [00064]). Hinderer et al. teach the expression cassette for generating a viral vector contains the GLP-1 construct sequences flanked by packaging signals of the viral genome and other expression control sequences (para. [00064]).
Hinderer et al. teach the minimal sequences required to package the expression cassette into an AAV viral particle are the AAV 5' and 3' ITRs (para. [00068]).
Regarding claim 6, Hinderer et al. teach the ITR sequences are from AAV2 and an
expression cassette for an AAV vector comprises an AAV 5' ITR, the propeptide-GLP-1
active peptide coding sequences and any regulatory sequences, and an AAV 3' ITR (para. [00068]).
Regarding claim 20, the limitation directed to the composition being suitable for use in treating a metabolic disease, is an intended use statement which is not limiting because it does not add structure to the composition. Therefore, the claim reads as an aqueous liquid and the viral vector of claim 1. Kwiatkowski et al. teach pharmaceutical compositions comprising administration as a solution or a suspension in an aqueous liquid (p. 92, line 18) and Hinderer et al. teach the rAAV is preferably suspended in a physiologically compatible carrier, to include saline (para. [00079]). Thus, the teachings of Kwiatkowski et al. and Hinderer et al. render obvious the limitations of the claim to include a pharmaceutical composition comprising an aqueous solution and the viral vector of claim 1.
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.
Claim 4 is rejected under 35 U.S.C. 103 as being obvious over Kwiatkowski et al., (WO 2020/053815 A1, published 19 March 2020) in view of Hinderer et al. (WO 2017/024198 A1, published 09 February 2017, IDS ref.) as applied to claims 1-3, 6, and 20 above, and further in view of Wilson et al. (US 2022/0389457 A1, priority to provisional application 62/924,970, filed on 23 October 2019).
The applied reference has a common inventor with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2).
Regarding claim 4, Hinderer et al. teach the rAAV has a capsid selected from AAV8, AAVrh64Rl, AAV9, AAVhu37 or AAVrh10 (para. [00011]). Kwiatkowski et al. in view of Hinderer et al. do not teach wherein the viral vector is an rAAV having the AAV capsid of AAVrh91.
Wilson et al. teach recombinant AAV (rAAV) comprising an AAV capsid having packaged therein a vector genome, wherein, in certain embodiments the rAAV capsid is AAV9, AAVhu68, or AAVrh91 (para. [0007]).
Therefore, it would have been obvious to one of ordinary skill in the art to substitute the AAVrh91 capsid of Wilson et al. with the capsid of Hinderer et al. because Wilson et al. and Hinderer et al. both teach AAV9 as an exemplary capsid which suggests these capsids are suitable alternatives. One would be motivated to substitute the AAVrh91 capsid of Wilson et al. with the capsid of Hinderer et al. in order to avoid potential hepatotoxicity which AAV9 capsid is known to cause at high doses and to avoid potential pre-existing immunity to AAV9 capsid which would limit efficacy.
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.
This rejection under 35 U.S.C. 103 might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C.102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B); or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement. See generally MPEP § 717.02.
Claims 5, 9, 11-15, 17, and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Kwiatkowski et al., (WO 2020/053815 A1, published 19 March 2020) in view of Hinderer et al. (WO 2017/024198 A1, published 09 February 2017, IDS ref.) as applied to claims 1-3, 6, and 20 above, and further in view of Chen et al. (Human Gene Therapy Methods 24, August 2013, IDS ref.).
Regarding claims 5, 9, and 12, Kwiatkowski et al. in view of Hinderer et al. teach a vector comprising a regulatable promoter (claim 9d) (Hinderer et al., para. [00065]), the sequence encoding the fusion protein, and a polyadenylation signal (Hinderer et al., para. [00066]); however, are silent to an inducible gene expression system.
Chen et al. teach adeno-associated virus (AAV)-based vector with tissue-specific gene regulation (p. 270, Introduction). Chen et al. teach a nucleic acid constructs comprising FRB p65, the activation domain comprising the FRB (FKBP12-rapamycin binding) domain of human FRAP (FKBP12-rapamycin-associated protein) (claim 9a) fused to a portion of human NF-KB p65 (claim 12); ZFHD1 3x FKBP fusion (claim 9b), hGH poly A; and the vector comprising twelve ZFHD sites followed by a minimal IL2 promoter (claim 9c) and reporter gene (see Fig. 1 below).
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Chen et al. teach gene regulation is achieved by reconstituting two split domains for DNA binding and transcription activation of a transcription factor using a dimerizing inducer, rapamycin, an orally bioavailable drug (p. 273, Results). Chen et al. teach the rapamycin-induced system combines extremely low basal expression with highly inducible, dose dependent expression in order to achieve pharmacological control over the levels and kinetics of therapeutic gene expression (p. 270, 2nd column). The rapamycin-induced system of Chen et al. reads as wherein the presence of an effective amount of a rapamycin induces expression of the transgene in a host cell.
Therefore, it would have been obvious to one of ordinary skill in the art to utilize the inducible expression system of Chen et al. with the expression cassette of Kwiatkowski et al. in view of Hinderer et al. because Chen et al. teach the usefulness of viral vector-mediated gene transfer for therapeutic applications would be greatly enhanced if the expression of the transgene could be regulated with respect to both the timing and level of gene expression (p. 270, 2nd column). Additionally, inducible gene expression systems offer control for gene therapy, facilitating precise regulation of therapeutic genes, adjusting expression levels, and manage side effects by minimizing leaky expression and enabling rapid shutdown. One would be motivated to utilize the inducible expression system of Chen et al. with the expression cassette of Kwiatkowski et al. in view of Hinderer et al. because Chen et al. teach the inducible expression system provided reversible, reproducible, and dose-dependent gene regulation (Abstract and p. 275, 2nd column).
Regarding claim 11, Chen et al. teach a vector comprising FKBP (Fig. 1A and Fig. 2B, E, and F). Chen et al. does not disclose any mutant variants of the FKBP, which suggests native FKBP was utilized, absent evidence to the contrary.
Regarding claim 13 and 14, Chen et al. teach a CMV promoter (claim 14), which is a constitutive promoter (claim 13). Chen et al. teach a rapamycin-induced system, therefore, the CMV promoter is considered part of this regulatable system, thus, a regulatable promoter.
Regarding claim 15, Chen et al. teach the viral vector comprises IRES and T2A (Fig. 1).
Regarding claim 17, Chen et al. teach 12 copies of the binding site for ZFHD (Fig. 1).
Regarding claim 19, Chen et al. teach a viral vector comprising the p65 transactivation domain, FRAP, a DNA binding domain comprising a ZFHD, three FKBP subunit genes, and 12 copies of the ZFHD (which comprises 8 copies) (Fig. 1). Chen et al. does not teach a sequence encoding a fusion protein comprising a GLP-1 analog and a human IgG4 Fc. Kwiatkowski et al. in view of Hinderer et al. teach the sequence encoding a fusion protein comprising a GLP-1 analog and a human IgG4 Fc. Therefore, Kwiatkowski et al. in view of Hinderer et al. and Chen et al. teach all of the limitations of the claim.
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.
Claims 7 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Kwiatkowski et al., (WO 2020/053815 A1, published 19 March 2020) in view of Hinderer et al. (WO 2017/024198 A1, published 09 February 2017, IDS ref.) and Chen et al. (Human Gene Therapy Methods 24, August 2013, IDS ref.) as applied to claims 5, 9, 11-15, 17, and 19 above, and further in view of Buck et al. (Int. J. Mol. Sci. 2020, published 12 June 2020).
Regarding claim 7, Kwiatkowski et al. in view of Hinderer et al. and Chen et al. render obvious the viral vector of claim 5. Hinderer et al. teach vectors comprising a CB7 promoter (para. [00065]). Hinderer et al. teach expression cassettes may contain other processing signals such as polyadenylation (poly A) signals (para. [00066]).
Kwiatkowski et al. in view of Hinderer et al. and Chen et al. are silent to a rabbit globin poly A.
However, Buck et al. teach polyadenylation sequences in rAAV-gene cassettes for efficient pre-mRNA processing (p. 16). Buck et al. teach several examples of poly A sequences utilized in rAAV gene cassettes, to include SV40, hGH polyA, and rabbit poly A (Table 5).
Therefore, it would have been obvious to substitute a rabbit poly A taught by Buck et al. for the SV40 or hGH polyA utilized by Chen et al. with a reasonable expectation of success because SV40, hGH polyA, and rabbit poly A are all known as commonly used poly A signals in viral vector systems for gene expression and one would have had a reasonable expectation they would have worked in the same manner. One would be motivated to substitute a rabbit poly A taught by Buck et al. for the SV40 or hGH polyA utilized by Chen et al. because rabbit poly A sequence is significantly shorter than the alternatives, thus, making it ideal for maximizing the limited packaging capacity of AAV vectors.
Additionally, substitution of one known element for another known element, the elements having equivalent effect, is considered to be obvious, absent a showing that the result of the substitution yields more than predictable results. See MPEP 2143(I).
Regarding claim 18, SEQ ID NO: 16 is not known in the prior art, however, Kwiatkowski et al. in view of Hinderer et al., Chen et al., and Buck et al. render obvious all of the components of the vector genome. The instant specification states at p. 31, “The vector genome (or rAAV genome) comprises 5' and 3' AAV inverted terminal repeats (ITRs), the polynucleotide sequence encoding the fusion protein, and regulatory sequences which direct insertion of the polynucleotide sequence encoding the fusion protein to the genome of a host cell.” As indicated in the rejection of claims 1, 7, and 9, the sequence of the polynucleotide sequence encoding the fusion protein is obvious, as are the ITRs and regulatory sequences. This suggests it would have been obvious to combine the sequences of these vector genome components to arrive at a sequence at least 70% identical to SEQ ID NO: 16 with a reasonable expectation of success because all of the components of the vector genome were known in the art according to the teachings of Kwiatkowski et al. in view of Hinderer et al., Chen et al., and Buck et al. One would be motivated to combine the sequences of these vector genome components to arrive at a sequence at least 70% identical to SEQ ID NO: 16 because to utilize the inducible expression system of Chen et al. with the expression cassette of Kwiatkowski et al. in view of Hinderer et al. because Chen et al. teach the inducible expression system provided reversible, reproducible, and dose-dependent gene regulation (Abstract and p. 275, 2nd column).
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.
Claim 10 is rejected under 35 U.S.C. 103 as being unpatentable over Kwiatkowski et al., (WO 2020/053815 A1, published 19 March 2020) in view of Hinderer et al. (WO 2017/024198 A1, published 09 February 2017, IDS ref.) and Chen et al. (Human Gene Therapy Methods 24, August 2013, IDS ref.) as applied to claims 5, 9, 11-15, 17, and 19 above, and further in view of Tong et al. (Curr Mol Pharmacol. 2015).
Regarding claim 10, Kwiatkowski et al. in view of Hinderer et al. and Chen et al. are silent to the FKBP subunit gene sequences sharing less than about 85% identity with each other.
However, Tong et al. teach FKBP subunits, such as FKBP12 and FKBP12.6 share 83% identity (p. 1, Introduction). Tong et al. teach FKBP12 and FKBP12.6 are the smallest subunits and both comprise one PPIase domain (p. 1, Introduction and Fig. 1). Tong et al. teach the PPIase domain is involved in mediating protein-protein interaction (p. 16, Conclusion). Tong et al. teach FKBP12 and FKBP12.6 preferentially associate with different molecules (p. 3, Section 2.1.2), which suggests a potential for differential regulation.
Therefore, it would have been obvious to one of ordinary skill in the art to combine the heterogeneous FKBP12 subunits taught by Tong et al. with the viral vector system of Kwiatkowski et al. in view of Hinderer et al. and Chen et al. with a reasonable expectation of success because the teachings of Tong et al. suggest a potential for differential regulation and in a viral vector system for chemically induced dimerization (CID), this could facilitate precise control over protein interactions and incorporating both FKBP12 and FKBP12.6 in a viral vector system could allow for differential regulation. One would be motivated to combine the heterogeneous FKBP12 subunits taught by Tong et al. with the viral vector system of Kwiatkowski et al. in view of Hinderer et al. and Chen et al. because a system using both FKBP12 and FKBP12.6, with their variations in binding affinity, could allow for more precise binding.
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.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-4 and 6-7 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3-4, and 7-8 of copending Application No. 18/843,440 (reference application).
Although the claims at issue are not identical, they are not patentably distinct from each other because the reference claims anticipate the instant claims.
Regarding claims 1 and 3, reference claim 3 reads on all of the limitations of instant claims 1 and 3, to include SEQ ID NO: 14 of both applications being 100% identical. See alignment results below:
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Regarding claim 2, reference claim 3 discloses SEQ ID NO: 14 which is the amino acid sequence. The reference claims do not specifically disclose a viral vector comprising SEQ ID NO: 15, however, the coding sequence, SEQ ID NO: 14 would necessarily be at least 75% identical to SEQ ID NO: 15, as it is the nucleic acid sequence which encodes SEQ ID NO: 14
Regarding claim 4, reference claim 4 discloses wherein the viral vector comprises the AAV capsid of AAVrh91.
Regarding claim 6, reference claim 7 discloses all of the limitations of instant claim 6.
Regarding claim 7, reference claim 8 discloses all of the limitations of instant claim 7.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim 5 is provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1, 3-5, and 7-8 of copending Application No. 18/843,440 in view of Domenger et al. (Human Molecular Genetics, 2019).
The reference claims anticipate instant claims 1-4 and 6-7, therefore, also render them obvious.
Regarding claim 5, reference claim 5 discloses an inducible expression system, a regulatable promoter, and the sequence encoding the fusion protein.
However, the reference claim is silent to the composition comprising a viral vector and a polyadenylation signal. Domenger et al. teach components of a typical AAV expression vector comprise a polyadenylation signal, as this marks the end of the transcriptional cassette (Fig. 1).
Therefore, it would have been obvious to one of ordinary skill in the art to include a viral vector and polyadenylation signal to effectively express the composition comprising the expression cassette of the fusion protein of the reference claim with a reasonable expectation of success because this method of delivery is well known in the art. One would be motivated to include a viral vector and polyadenylation signal to effectively express the composition comprising the expression cassette of the fusion protein of the reference claim because Domenger et al. teach recombinant adeno-associated viruses (AAV) are under intensive investigation in numerous clinical trials after they have emerged as a highly promising vector for human gene therapy (Abstract).
This is a provisional nonstatutory double patenting rejection.
Claims 9, 12-15, 17, and 19-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3-5, 7-9, 12-17, and 21 of copending Application No. 18/843,440 in view of Domenger et al. (Human Molecular Genetics, 2019) and further in view of Chen et al., (Human Gene Therapy Methods, 2013, IDS ref.).
The reference claims anticipate instant claims 1-4 and 6-7, therefore, also render them obvious.
Regarding claim 9, reference claim 9 in view of Domenger et al. disclose all the limitations of the inducible gene expression system of instant claim 9, however, is silent to the specific minimal promoter.
Chen et al. teach a nucleic acid constructs comprising FRB p65, the activation domain composed of the FRB (FKBP12-rapamycin binding) domain of human FRAP (FKBP12-rapamycin-associated protein) fused to a portion of human NF-KB p65; hGH poly A and SV40 poly A, and a minimal IL-2 promoter (Fig. 1). Therefore, it would have been obvious to one of ordinary skill in the art to utilize the minimal IL-2 promoter in an expression cassette comprising the same elements as the reference claim because the minimal IL-2 promoter was known in the art as an effective promoter in this type of expression system. One would be motivated to utilize the minimal IL-2 promoter because the minimal IL-2 promoter is known in the art to create activation-inducible transgene expression.
Regarding claims 12-15, 17, and 19, reference claims 12-15, 16, and 17, respectively, in view of Domenger et al. and Chen et al. teach all of the limitations of instant claims 12-15, 17, and 19, as the reference claims are identical to the instant claims with the exception of the composition being a viral vector which has been made obvious by Domenger et al. and Chen et al., above.
Regarding claim 20, reference claim 21 discloses a composition formulated to be administered, which reads as a pharmaceutical composition which would comprise an aqueous liquid in order to achieve the appropriate dose and for administration purposes. Reference claim 21 refers to a composition, but is silent to the composition comprising a viral vector, which has been made obvious by Domenger et al and Chen et al., above.
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claims are allowed.
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/N.A.H./Examiner, Art Unit 1631
/LAURA SCHUBERG/Primary Examiner, Art Unit 1631