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
Election without traverse to Group I, drawn to claims 1-16, in the reply filed 18 May 2026 is acknowledged.
Claims 17-21 are withdrawn from consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed 18 May 2026.
Claims 1-16 are under consideration.
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 Objections
Claims 2 and 7 are objected to because of the following informalities:
Regarding claim 2, the correction, "a lentivirus, or an SV40 viral vector" is recommended.
Regarding claim 7, the correction, "a VP1 capsid protein [in] comprising a 7 to 11 amino acid long insertion peptide [is] inserted in the GH loop..." is recommended.
Appropriate correction is required.
Claim Interpretation
To promote compact prosecution, the following interpretations are made for the purpose of examination:
Claim 8 is interpreted to depend from claim 3 and to recite the open-ended language "comprises" rather than "comprises or consists of".
Claim 12 is interpreted to depend from claim 11 to correct for lack of antecedent basis.
Claim Rejections - 35 USC § 112(b)
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.
Claims 5, 8, 12, and 13-15 are rejected under 35 U.S.C. § 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor regards as the invention.
Claim 5 recites "in particular a pMNTC expression cassette". 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. See MPEP § 2173.05(d). The claim is indefinite because it is unclear as to whether the pMNTC expression cassette is merely exemplary of a minimal M-opsin promoter, and therefore not required, or a required feature of the claim.
Claim 5 recites "a GRK promoter or truncated version thereof" as an alternative for a cone-specific promoter. However, rhodopsin kinase (GRK) promoters are not cone-specific (S.C. Khani, et al., Invest Opthamol Vis Sci, 2007). Therefore, the metes and bounds of the claim are indefinite because it is unclear whether the scope of the claim is limited to cone-specific promoters or include non-specific promoters.
Claim 8 recites the limitation "said insertion peptide". There is insufficient antecedent basis for this limitation in the claim.
The phrase "comprises or consists of" recited in claim 8 renders the claim indefinite. These transitional phrases define the scope of the claim with regard to what is included or excluded from the claim. The term "comprises" is open-ended and allows for additional elements to present in the invention, whereas the phrase "consists of" is closed language that excludes additional elements. It is therefore unclear whether the claim is limited to SEQ ID NO: 10, 11, and 12 or the claim includes other insertion peptides. See MPEP § 2111.03.
Claim 12 recites the limitations "the vector comprising a nucleotide sequence encoding a mammalian cone opsin" in lines 9-10 and "the mammalian cone opsin" in line 21. There is insufficient antecedent basis for these limitations in the claim.
Claim 13 contains the trademark/trade name Lipoplex. Where a trademark or trade name is used in a claim as a limitation to identify or describe a particular material or product, the claim does not comply with the requirements of 35 U.S.C. § 112(b). See Ex parte Simpson, 218 USPQ 1020 (Bd. App. 1982). The claim scope is uncertain since the trademark or trade name cannot be used properly to identify any particular material or product. A trademark or trade name is used to identify a source of goods, and not the goods themselves. Thus, a trademark or trade name does not identify or describe the goods associated with the trademark or trade name. In the present case, the trademark/trade name is used to identify/describe a cationic lipid vector and, accordingly, the identification/description is indefinite.
Claim 14 recites the limitation "the mammalian cone opsin". There is insufficient antecedent basis for this limitation in the claim.
Claim 15 recites the limitation "with or without a pharmaceutically acceptable carrier, with a diluent or excipient." It is unclear whether the limitation "with a diluent or excipient" is a required claim limitation. The specification does not provide a definition for which the inventor regards "a pharmaceutically acceptable carrier", and under broadest reasonable interpretation, pharmaceutically acceptable carriers include diluents and excipients. Therefore, it is unclear whether diluents and excipients are merely exemplary of pharmaceutically acceptable carriers and would be included in the negative limitation, or whether a diluent or excipient is required regardless of the presence or absence of other pharmaceutically acceptable carriers.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. § 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
Claims 4-5 are rejected under 35 U.S.C. § 112(a) as failing to comply with the written description requirement. The claims contain subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, at the time the application was filed, had possession of the claimed invention.
Claims 4-5 are drawn to a cone-specific control of expression of the vector of claim 3, and claim 5 is further drawn to alternatives for the cone-specific promoter. However, the claims encompass alternatives that a skilled artisan would not recognize as promoters with cone cell-specific activation that would lead to cone-specific expression of the vector. The specification provides examples of cone-specific promoters, including "pR1.7 or a functional variant thereof", "a minimal M-opsin promoter, in particular a pMNTC expression cassette" (p. 11 lines 26-29). The specification provides no description that a rhodopsin kinase (GRK) promoter or any truncated version is cone-specific, although claim 5 includes GRK as an option for a cone-specific promoter.
The disclosure of only one species encompassed within a genus adequately describes a claim directed to that genus only if the disclosure “indicates that the patentee has invented species sufficient to constitute the gen[us].” See Enzo Biochem, 323 F.3d at 966, 63 USPQ2d at 1615; Noelle v. Lederman, 355 F.3d 1343, 1350, 69 USPQ2d 1508, 1514 (Fed. Cir. 2004) (Fed. Cir. 2004) (“[A] patentee of a biotechnological invention cannot necessarily claim a genus after only describing a limited number of species because there may be unpredictability in the results obtained from species other than those specifically enumerated.”). The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, such as physical and/or chemical properties, functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show that the inventor was in possession of the claimed genus. See MPEP § 2163(II)(A).
Regarding pR1.7 promoter and functional variants thereof, Ye (G.J. Ye, et al., Hum Gen Ther, 2016) teaches variants of the pR2.1 promoter, including pR1.7 (Abstract and Introduction p. 73). Ye further teaches that of the four variants tested (pR2.1, pR1.7, pR1.5, and pR1.1), "all except the PR1.7 promoter also directed expression in retinal pigment epithelium (RPE) cells" (Results p. 76 and Fig. 2). Therefore, it is known in the art that functional variants of pR1.7 are not all cone-specific promoters. Furthermore, it is unclear what structural features must be present or absent in a pR1.7 promoter to maintain specificity to cone cells and maintain functional equivalence to pR1.7.
Regarding minimal M-opsin promoters, the specification does not provide a definition for the inventor or joint inventor regards as "minimal". The specification further points to Neitz (WO 2015142941 A1, 2015) for examples of minimal M-opsin promoters. However, Neitz also does not provide a definition or sufficient examples for an M-opsin promoter by which a skilled artisan could understand what structural features are required or dispensable for an M-opsin promoter.
Regarding GRK promoter and truncated versions thereof, Khani (S.C. Khani, et al., Invest Opthamol Vis Sci, 2007) teaches that the GRK promoter is "a promoter of choice for somatic gene transfer and gene therapy targeting rods and cones" (Abstract). Therefore, the GRK promoter is not recognized in the art as a cone-specific promoter. Khani further teaches several truncated versions of the GRK promoter, but does not evaluate cell specificity (Results p. 3956 and Fig. 1A). It is not taught in the art what structural features of the GRK promoter must be truncated to achieve a cone-specific promoter.
Claims 9, 11-12, 14, and 16 are rejected under 35 U.S.C. § 112(a) as failing to comply with the written description requirement. The claims contain subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, at the time the application was filed, had possession of the claimed invention.
Claims 9, 11-12, 14, and 16 encompass a nucleotide sequence encoding a mammalian cone opsin. The specification contemplates short wavelength and long wavelength cone opsins from mouse (Mus musculus) and human (p. 6 lines 24-26 and p. 8 lines 4-11). Claim 14 specifically recites a mammalian short wavelength cone opsin.
The disclosure of only one species encompassed within a genus adequately describes a claim directed to that genus only if the disclosure “indicates that the patentee has invented species sufficient to constitute the gen[us].” See Enzo Biochem, 323 F.3d at 966, 63 USPQ2d at 1615; Noelle v. Lederman, 355 F.3d 1343, 1350, 69 USPQ2d 1508, 1514 (Fed. Cir. 2004) (Fed. Cir. 2004) (“[A] patentee of a biotechnological invention cannot necessarily claim a genus after only describing a limited number of species because there may be unpredictability in the results obtained from species other than those specifically enumerated.”). The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, such as physical and/or chemical properties, functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show that the inventor was in possession of the claimed genus. See MPEP § 2163(II)(A).
Mammalia comprises thousands of extant species and numerous cone opsin genes. Mouse and human cone opsin represent only a small number of genes in this broad genus. Jacobs (G.H. Jacobs, Phil Trans R Soc B, 2009) teaches that ultraviolet (UV), short wavelength (SW), medium wavelength (MW), and long wavelength (LW) opsins are largely shared across divergent mammalian orders (Fig. 3). Jacobs further teaches divergences in mammalian cone opsin genes, including loss of function mutations in SW opsins (p. 2959) and shifts in spectral positioning (p. 2961). Jacobs notes that a single nucleotide mutation can shift the spectral properties of an opsin protein (p. 2963). Taken together, the art teaches structural and functional divergences in mammalian cone opsins. The specification does not contemplate what structural or functional characteristics are shared between mouse and human cone opsins that sufficiently identify other mammalian cone opsins.
Claim Rejections - 35 USC § 102
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 1, 10, and 15 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Vivaudou (M. Vivaudou, et al. J Biol Chem, 1997) as evidenced by Chan.
Vivaudou discloses a plasmid vector comprising a nucleotide encoding G-protein-gated inwardly rectifying potassium channel 4 (GIRK4) with the point mutation S143T (GIRK4 S143T) (claim 1) (Abstract and Experimental Procedures p. 31554). The plasmid is administered to Xenopus oocytes by microinjection in a solution comprising calcium chloride and HEPES-buffered saline (Vivaudou Experimental Procedures p. 31554 with reference to Chan Materials and Methods p. 383). The specification does not provide a definition by which the inventor or joint inventor regards as a pharmaceutically acceptable carrier. Therefore, any substance used as an inactive ingredient in any pharmaceutical composition is considered to be a pharmaceutically acceptable carrier. The solution comprising calcium chloride and HEPES-buffered saline disclosed by Vivaudou is a pharmaceutically acceptable carrier, a diluent, and an excipient (claims 10 and 15).
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.
Claims 1-2 and 9-16 are rejected under 35 U.S.C. § 103 as being unpatentable over Isacoff (US 10,745,453 B2) in view of Vivaudou (M. Vivaudou, et al. J Biol Chem, 1997).
Isacoff teaches administration of a vector comprising nucleotide sequence encoding a medium wavelength cone opsin (MW-opsin) packaged in an adeno-associated virus 2 (AAV2) capsid to treat loss of light sensitivity in mouse retinas (Example 1, col. 27 lines 53-67 and col. 28 lines 20-35). Expression of MW-opsin was controlled by a synapsin promoter (Isacoff Example 1, col. 28 lines 28-31).
Isacoff further teaches transfection of MW-opsin into HEK293T cells comprising G-protein-gated inwardly rectifying potassium channel 1 (GIRK1) with the point mutation F137S (GIRK1 F137S) (col. 33 lines 37-42). GIRK1 F137S is capable of homotetramerization, whereas wild-type (WT) GIRK1 requires other GIRK family proteins to form tetramers (Isacoff col. 33 lines 37-42 and Vivaudou Introduction p. 31553).
Regarding claims 2 and 12, Isacoff teaches packaging the nucleotide sequence encoding an opsin into an adeno-associated virus 2 (AAV2) capsid (Example 1 col. 28 lines 27-35).
Regarding claim 9, Isacoff teaches that the cone opsin may be human (mammalian) (col. 4 lines 45-50 and SEQ ID NO: 1).
Regarding claims 10-11, Isacoff teaches that the viral vector (pharmaceutically acceptable carrier) comprising MW-opsin is delivered in vivo (Example 1, col. 28 lines 20-35). Note that the specification of the immediate application does not provide a definition by which the inventor or joint inventors regard as a "pharmaceutically acceptable carrier". Therefore, any substance used as an inactive ingredient in any pharmaceutical composition is considered to be a pharmaceutically acceptable carrier.
Regarding claim 13, Isacoff teaches that the nucleotide sequence encoding an opsin may be formulated in a liposome (col. 13 lines 1-4).
Regarding claim 14, Isacoff teaches that the cone opsin may be a human (mammalian) short wavelength cone opsin (SW-opsin) (Col. 6 lines 39-43 and SEQ ID NO: 5).
Regarding claims 15-16, Isacoff teaches that the nucleotide sequence encoding an opsin may be present in buffered saline (pharmaceutically acceptable carrier, diluent, and excipient) (col. 13 lines 27-31).
Isacoff does not teach delivery of a mammalian cone opsin in the same vector as a nucleotide encoding G-protein-gated inwardly rectifying potassium channel 1 (GIRK4) with the point mutation S143T (GIRK1 S143T) as required by claims 1-2 and 9-16.
However, Vivaudou teaches a plasmid vector comprising G-protein-gated inwardly rectifying potassium channel 4 (GIRK4) with the point mutation S143T (GIRK4 S143T) (Abstract and Experimental Procedures p. 31554) as discussed in the rejection of claims 1, 10, and 15 under 35 U.S.C. § 103 above. Vivaudou further teaches that wild-type GIRK1 and GIRK4 are homologous proteins that complex to form heteromeric potassium channels (Introduction p. 31553). Vivaudou further teaches that F137S mutation in GIRK1 and S143T mutation in GIRK4 allows for the mutant GIRK proteins to form homomeric potassium channels, each with activity comparable to wild-type heteromeric channels (Conclusions p. 31559).
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to combine the AAV2 vector comprising a nucleotide encoding a mammalian SW-opsin operably linked to a cone-specific promoter as taught by Isacoff with a nucleotide encoding GIRK4 S143T as taught by Vivaudou to arrive at the claimed invention. One would be motivated to make such a combination as Isacoff teaches co-expression of an opsin with a GIRK protein that capable of forming homomeric channels. One would have a reasonable expectation of success in making the combination as Vivaudou teaches that GIRK1 and GIRK4 are homologous proteins and that GIRK1 F137S and GIRK4 S143T both form homomeric potassium channels that are functionally equivalent to each other and to wild-type heteromeric potassium channels.
Claims 3-5 and 8 are rejected under 35 U.S.C. § 103 as being unpatentable over Isacoff (US 10,745,453 B2) in view of Vivaudou (M. Vivaudou, et al. J Biol Chem, 1997) as applied to claims 1-2 and 9-16 above, and in further view of Khabou 2016 (H. Khabou, et al., Biotech & Bioeng, 2016).
Isacoff and Vivaudou teach an adeno-associated virus 2 (AAV2) vector comprising a nucleotide encoding a mammalian short wavelength cone opsin (SW-opsin) and a nucleotide encoding G-protein-gated inwardly rectifying potassium channel 4 (GIRK4) with the point mutation S143T (GIRK4 S143T) operably linked to a cone-specific promoter or rhodopsin kinase promoter (GRK promoter) for improving light sensitivity in mice as discussed in the rejection of claims 1-2 and 9-16 under 35 U.S.C. § 103 above.
Isacoff further teaches that the AAV vector may comprise a variant capsid protein that "confers infectivity of a retinal cell and/or the ability to cross the inner limiting membrane (ILM) in the eye" (col. 10 lines 45-52).
Isacoff does not teach a 7 to 11 amino acid long insertion peptide in the GH loop of the VP1 capsid protein comprising the sequence LGETTRP (SEQ ID NO: 5) as required by claim 3 or the sequences AALGETTRPA (SEQ ID NO: 10), LALGETTRPA (SEQ ID NO: 11), or GLGETTRPA (SEQ ID NO: 12) as required by claim 8.
However, Khabou 2016 teaches an AAV9 insertion peptide LALGETTRPA (SEQ ID NO: 11, claim 8) comprising the heptamer LGETTRP (SEQ ID NO: 5, claim 3) (Introduction p. 2713). Khabou 2016 further teaches that the LALGETTRPA insertion peptide was inserted between amino acids 588 and 589 of the AAV2 capsid protein and the same modification in AAV9 (Introduction p. 2713). Khabou 2016 further teaches that the insertion peptide allows recombinant AAV9 to overcome limitations in diffusion through heparan sulfate proteoglycans abundant between the vitreous and the retina, thereby improving transfection to retinal cells (Introduction p. 2713, Results pp. 2716 and Fig. 3-5).
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to improve the wild-type AAV2 vector for gene delivery to mouse retinas taught by Isacoff and Vivaudou using the same improvement of including an LALGETTRPA insertion peptide within the AAV2 capsid protein as taught by Khabou 2016 to arrive at the claimed invention. One would be motivated to make the improvement as Isacoff teaches that a variant AAV capsid protein may improve transfection to retinal cells and as Khabou 2016 teaches that the insertion peptide allows AAV9 to overcome barriers to viral transfection of the retina. One would have a reasonable expectation of success in making the improvement as Khabou 2016 teaches that recombinant AAV9 comprising a LALGETTRPA insertion peptide has greater transfection efficiency in mouse retinas compared to wild-type AAV9 when administering a similar gene therapy vector.
Claim 7 is rejected under 35 U.S.C. § 103 as being unpatentable over Isacoff (US 10,745,453 B2) in view of Vivaudou (M. Vivaudou, et al. J Biol Chem, 1997) and Khabou 2016 (H. Khabou, et al., Biotech & Bioeng, 2016) as applied to claims 1-5 and 8-16 above, and in further view of Khabou 2018 (H. Khabou, JCI Insight, 2018).
Isacoff, Vivaudou, and Khabou 2016 teach a recombinant adeno-associated virus 9 (AAV9) comprising a LALGETTRPA insertion peptide comprising a nucleotide encoding a mammalian short wavelength cone opsin (SW-opsin) and a nucleotide encoding G-protein-gated inwardly rectifying potassium channel 4 (GIRK4) with the point mutation S143T (GIRK4 S143T) operably linked to a cone-specific promoter or rhodopsin kinase promoter (GRK promoter) as discussed in the rejection of claims 1-5 and 8-16 under 35 U.S.C. § 103 above.
Isacoff further teaches that optogenetic approaches are needed for the treatment of inherited retinal degenerative diseases (col. 1 lines 24-36). Isacoff further teaches that suitable promoters include a red cone opsin promoter (col. 10 lines 14-15).
Isacoff does not teach a pR1.7 promoter as required by claim 7.
However, Khabou 2018 teaches an AAV2 vector comprising a gene under the control of a pR1.7 promoter (Results p. 2). The pR1.7 promoter is a synthetic promoter based on the human red opsin gene enhancer and promoter sequences (Khabou 2018, Results p. 2). Khabou 2018 teaches that cone cells in the fovea are the primary targets for gene therapy for the treatment of inherited retinal diseases (Introduction p. 1). Khabou 2018 teaches that the pR1.7 promoter leads to highly specific expression in cone cells compared to another synthetic red cone opsin promoter (Results p. 2 and Fig 1). Khabou 2018 further teaches that nonspecific expression in other cell types is unsuitable for optogenetic approaches as nonspecific expression dampens downstream neuronal response from cone cells (Discussion p. 10).
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to substitute the red cone opsin promoter controlling expression of a nucleotide sequence encoding GIRK4 S143T packaged in a recombinant AAV9 vector comprising a LALGETTRPA insertion peptide as taught by Isacoff, Vivaudou, and Khabou 2016 with a pR1.7 promoter as taught by Khabou 2018 to arrive at the claimed invention. One would be motivated to make the substitution as Khabou 2018 teaches that the pR1.7 promoter leads to highly specific expression of an AAV-delivered gene therapy in cone cells, which are the major target for optogenetic approaches to treating inherited retinal diseases and as Isacoff teaches that optogenetic approaches are needed for treating inherited retinal diseases. One would have a reasonable expectation of success in making the substitution as Khabou 2018 demonstrates that the pR1.7 promoter improved cone-specific targeting compared to another red cone opsin promoter when applied to a similar AAV-delivered gene therapy.
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, 6, 10, and 15 of this application are patentably indistinct from claims 17-18 of Application No. 19/121,671. Pursuant to 37 CFR 1.78(f), when two or more applications filed by the same applicant or assignee contain patentably indistinct claims, elimination of such claims from all but one application may be required in the absence of good and sufficient reason for their retention during pendency in more than one application. Applicant is required to either cancel the patentably indistinct claims from all but one application or maintain a clear line of demarcation between the applications. See MPEP § 822.
Claims 1, 6, 10, and 15 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 17-18 of copending Application No. 19/121,671 (reference application, hereafter '671). This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Although the claims at issue are not identical, they are not patentably distinct from each other because claims 17-18 of '671 encompass a pharmaceutical composition comprising viral vectors comprising SEQ ID NO: 40, a nucleic acid encoding G-protein-gated inwardly rectifying potassium channel 4 (GIRK4) with the point mutation S143T (GIRK4 S143T).
Regarding claim 1 of the immediate application, claims 17-18 of '671 encompass a viral vector comprising GIRK4 S143T (SEQ ID NO: 40 in '671).
Regarding claim 1 of the immediate application, claims 17-18 of '671 encompass SEQ ID NO: 40 of '671, which is identical to SEQ ID NO: 3 of the immediate application (see alignment below).
Regarding claims 10 and 15 of the immediate application, claims 17-18 of '671 encompass a viral vector. The specification does not provide a definition by which the inventor or joint inventor regards as a pharmaceutically acceptable carrier. Therefore, any substance used as an inactive ingredient in a pharmaceutical composition is considered to be a pharmaceutically acceptable carrier, including a viral vector.
Therefore, claims 17-18 anticipate the subject matter of claims 1, 6, 10, and 15 of the immediate application.
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Claims 1-16 of this application is patentably indistinct from claims 1-16 of Application No. 18/563,959. Pursuant to 37 CFR 1.78(f), when two or more applications filed by the same applicant or assignee contain patentably indistinct claims, elimination of such claims from all but one application may be required in the absence of good and sufficient reason for their retention during pendency in more than one application. Applicant is required to either cancel the patentably indistinct claims from all but one application or maintain a clear line of demarcation between the applications. See MPEP § 822.
Claims 1-5 and 7-16 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 8, 12-14, and 16 of copending Application No. 18/563,959 (reference application, hereafter '959) in view of Vivaudou (M. Vivaudou, et al. J Biol Chem, 1997). This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 8, 12-14, and 16 of '959 encompass a vector comprising a nucleic acid encoding G-protein-gated inwardly rectifying potassium channel 1 (GIRK1) with the point mutation F137S (GIRK1 F137S). Claims 8, 12-14, and 16 of '959 encompass all of the elements of claims 1-5 and 7-16 of the immediate application except that claims 1-5 and 7-16 of the immediate application are drawn to a nucleotide sequence encoding G-protein-gated inwardly rectifying potassium channel 4 (GIRK4) with the point mutation S143T (GIRK4 S143T) rather than GIRK1 F137S.
Claims 8, 12-14, and 16 of '959 recite all of the elements of claims 1-5, 7, and 9-12 of the immediate application except that claims 1-5, 7, and 9-12 of immediate application are drawn to a nucleotide sequence encoding GIRK4 S143T rather than GIRK1 F137S.
Regarding claim 1 of the immediate application, claim 12 of '959 further recites a vector comprising a nucleotide sequence encoding GIRK1 F137S.
Regarding claim 2 of the immediate application, claim 12 of '959 further recites that the vector is a virus selected from an AAV, an adenovirus, a lentivirus, and an SV40 virus.
Regarding claims 3, 7, and 12 of the immediate application, claim 12 of '959 further recites a recombinant AAV9 virus wherein the VP1 capsid protein comprising an insertion peptide comprising the sequence LGETTRP (SEQ ID NO: 7 of '959) localized between amino acids 588 and 589 of wild-type AAV9 VP1 capsid protein. SEQ ID NO: 7 of '959 is identical SEQ ID NO: 7 of the immediate application recited in claims 3, 7, and 12.
Regarding claims 4, 5, and 7 of the immediate application, claim 12 of '959 further recites that the nucleotide sequence encoding GIRK1 F137S is under control of the cone-specific promoter pR1.7.
Regarding claims 9 and 12 of the immediate application, claim 12 of '959 further recites a nucleotide encompassing a mammalian cone opsin under control of a pR1.7 promoter.
Regarding claims 10-12 of the immediate application, claim 12 of '959 further recites a pharmaceutically acceptable carrier comprising the vector comprising the nucleotide sequence encoding a mammalian cone opsin and the nucleotide sequence encoding GIRK1 F137S.
Claim 8 of '959 further recites that the AAV insertion peptide comprises AALGETTRPA (SEQ ID NO: 10 of '959), LALGETTRPA (SEQ ID NO: 11 of '959), or GLGETTRPA (SEQ ID NO: 12 of '959). All of the elements of claim 8 of the immediate application except that claim 8 of immediate application is drawn to a nucleic acid encoding GIRK4 S143T rather than GIRK1 F137S. SEQ ID NO: 10 of '959 is identical to SEQ ID NO: 10 of the immediate application recited in claim 8. SEQ ID NO: 11 of '959 is identical to SEQ ID NO: 11 of the immediate application recited in claim 8. SEQ ID NO: 12 of '959 is identical to SEQ ID NO: 12 of the immediate application recited in claim 8.
Claim 13 of '959 further recites a pharmaceutically acceptable carrier chosen from solid-lipid nanoparticles, chitosan nanoparticles, liposomes, lipoplexes, and cationic polymers. All of the elements of claim 13 of the immediate application except that claim 13 of immediate application is drawn to a nucleotide sequence encoding GIRK4 S143T rather than GIRK1 F137S.
Claim 14 of '959 further recites a pharmaceutically acceptable carrier comprising the vector comprising a nucleotide sequence encoding a short wavelength cone opsin. All of the elements of claim 14 of the immediate application except that claim 14 of immediate application is drawn to a nucleotide sequence encoding GIRK4 S143T rather than GIRK1 F137S.
Claim 16 of '959 further recites a pharmaceutical composition comprising a nucleotide sequence encoding a mammalian cone opsin and a diluent or excipient. All of the elements of claims 15-16 of the immediate application except that claims 15-16 of immediate application are drawn to a nucleotide sequence encoding GIRK4 S143T rather than GIRK1 F137S.
However, Vivaudou teaches a plasmid vector comprising G-protein-gated inwardly rectifying potassium channel 4 (GIRK4) with the point mutation S143T (GIRK4 S143T) (Abstract and Experimental Procedures p. 31554). Vivaudou further teaches that wild-type GIRK1 and GIRK4 are homologous proteins that complex to form heteromeric potassium channels (Introduction p. 31553). Vivaudou further teaches that F137S mutation in GIRK1 and S143T mutation in GIRK4 allows for the mutant GIRK proteins to form homomeric potassium channels, each with activity comparable to wild-type heteromeric channels (Conclusions p. 31559).
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to substitute GIRK1 F137S in '959 for GIRK4 S143T as taught by Vivaudou to arrive at the claimed invention. One would be motivated to make such a substitution as Vivaudou teaches that GIRK1 F137S and GIRK4 S143T are functional equivalents. One would have a reasonable expectation of success in making the substitution as Vivaudou teaches that GIRK1 and GIRK4 are homologous proteins and that GIRK1 F137S and GIRK4 S143T both form homomeric potassium channels that are functionally equivalent to each other and to wild-type heteromeric potassium channels.
Conclusion
No claim is allowed.
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/Eric B Wright/Examiner, Art Unit 1632
/PETER PARAS JR/Supervisory Patent Examiner, Art Unit 1632
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