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 .
Application Status
Applicant’s response filed July 9, 2026, including remarks and amendments to the claims, is acknowledged. Claims 36-38 were amended. Claims 36-65 are pending and under examination hereinafter.
Priority
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of 35 U.S.C. 112(a) or the first paragraph of pre-AIA 35 U.S.C. 112, except for the best mode requirement. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, Application No. 62/359,534, fails to provide adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. Specifically, Application No. 62/359,534 fails to disclose amino acid substitutions at residues 131, 175, 210, 216, 217, or 219 as recited in instant independent claims 36, and 42-43. The first disclosure of the amino acid substitutions at the aforementioned residues is in Application No. 62/486,779, filed April 18, 2017 (see at least pg. 16, lines 6-14). Accordingly, the effective filing date of all claims under examination is April 18, 2017.
Withdrawn Rejections
Applicant’s response has been considered. The amendments to the claims are sufficient to overcome the § 102 rejection of claim 38 over Sternson, and the nonstatutory double patenting rejection of claim 38 over U.S. Patent No. 8,435,762. These rejections are withdrawn, accordingly. Applicant’s amendments to cancel all previously pending claims in co-pending Application No. 19/530,123 are sufficient to overcome the nonstatutory double patenting rejections raised over co-pending Application No. 19/530,123 as presented in the previous action. These rejections are also withdrawn, accordingly.
Applicant’s remarks and amendments to the claims have been considered, but are not persuasive to place the claims in condition for allowance for the reasons that follow. Any objection or rejection not reiterated herein has been overcome by amendment.
Claim Objections
Claim 38 is objected to because of the following informalities:
Claim 38 recites “wherein the α7-nAChR LBD comprises an L131G amino acid substitution, a Q139L amino acid substitution, and/or a Y217F amino acid substitution.” Given the limitations of claims 36-37, it is reasonably clear that the α7-nAChR LBD must comprise the Q139L amino acid substitution (because the α7-nAChR LBD of claim 37 must further comprise either a Q139L or Q139G amino acid substitution), and an L131G and/or Y217F amino acid substitution, rather than comprising any one or more of the recited substitutions as the “and/or” phrasing implies. The claim should be amended to recite the following, accordingly: “wherein the α7-nAChR LBD comprises the Q139L amino acid substitution, and an L131G amino acid substitution
Appropriate correction is required.
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.
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.
Claims 36-41, 56, and 63 are 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. The rejections that follow are new and necessitated by Applicant’s amendments to the claims.
Claim 36 recites “wherein the amino acid substitution at residue 141 is L141F or L141P.” The claim does not previously recite an amino acid substitution at residue 141. This phrase lacks sufficient antecedent basis in the claim.
Claims 37-41, 56, and 63 are rejected for depending from claim 36 and failing to remedy the indefiniteness. Claim 36 is interpreted hereinafter as encompassing an α7-nAChR LBD comprising an amino acid modification comprising 1-6 amino acid substitution at one or more amino acid residues selected from the group consisting of 27, 41, 115, 131, 141, 175, 210, 216, 217, and 219, and wherein the amino acid substitution at residue 141 is L141F or L141P.
Claim Rejections - 35 USC § 102 – Sternson
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 36-37, 40-41, 56, and 63 are rejected under 35 U.S.C. 102(a)(1) and 35 U.S.C. 102(a)(2) as being anticipated by Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). The rejections that follow are maintained and modified, as necessitated by Applicant’s amendments to the claims.
Hereinafter, the phrases “as numbered in SEQ ID NO: X” are interpreted as requiring that the α7-nAChR LBD or GlyR IPD comprise the specific substitutions with reference to the positions in the recited SEQ ID NO(s). These phrases are not interpreted as requiring that the α7-nAChR LBD or GlyR IPD comprise the nucleotide sequences of the recited SEQ ID NOs.
Regarding claims 36, and 40-41, Sternson teaches a modified ligand gated ion channel (LGIC) comprising at least one modified LGIC subunit (“the chimeric receptor comprises a ligand binding domain from an α7 nicotinic acetylcholine receptor fused to a transmembrane domain from a ligand-gated ion channel protein, wherein the ligand binding domain comprises at least one mutation that confers selective binding to a compound”, [0007]; claims 16-18, pg. 45). Sternson teaches nucleic acids encoding the modified LGIC comprising at least one modified LGIC subunit (“The present invention also encompasses nucleic acids encoding the mutant chimeric receptors of the invention”, [0038]; claims 1-2, and 6-7, pg. 45).
Sternson teaches the modified LGIC subunit comprises a) a modified human alpha7 nicotinic acetylcholine receptor (α7-nAChR) ligand binding domain (LBD), and b) a human glycine receptor (GlyR) ion pore domain (IPD) (“the chimeric receptor comprises a ligand binding domain from an α7 nicotinic acetylcholine receptor fused to a transmembrane domain from a glycine receptor”, [0013]; [0030]; [0033]; “the first and second proteins may be from the same species (i.e., both human proteins)”, [0031]). Sternson teaches the sequence of such a modified LGIC subunit (i.e., SEQ ID NO: 6), which as shown in the alignment of record in Appendix I (pgs. 1-2) has an α7-nAChR LBD 100% identical to the human α7 nAChR LBD set forth in instant SEQ ID NO: 2. Thus, Sternson’s α7-nAChR LBD comprises at least 97 percent identity to a sequence set forth in residues 23-229 of SEQ ID NO: 2.
Sternson teaches that the α7 nAChR LBD comprises an amino acid substitution at amino acid residue 141 (“there is at least one mutation in the ligand binding domain of the α7 nAChR that confers selective binding to a compound (e.g., selectivity-inducing mutation). The mutation can include a point mutation in the amino acid residue in position 77, 79, 139, or 141 in the amino acid sequence listed in SEQ ID NO: 1, SEQ ID NO: 6, or SEQ ID NO: 10”, [0034]). Sternson teaches the amino acid substitution at position 141 may be “L141F” or “L141P” (“Non-limiting examples of the point mutations include… L141F, L141P,” [0034]).
Regarding claim 37, Sternson teaches the α7 nAChR LBD further comprises an amino acid substitution at position 139, wherein the substitution is “Q139L” or “Q139G”(“Other suitable amino acid point mutations that also confer selectivity are shown in FIG. 3 and include Q79C, Q79D, Q79E, Q79H, Q79L, Q79P, Q79R, Q79S, Q79T, Q79W, Q139A, Q139C, Q139D, Q139F, Q139G, Q139H, Q1391, Q139K, Q139L”, [0034]; “Suitable point mutations that reduce binding to acetylcholine include… Q139G… These mutations can be combined with any of the selectivity-inducing mutations as described herein, such as Q79G and L141F,” [0035]).
Regarding claims 56 and 63, Sternson teaches a viral vector comprising the nucleic acid encoding the modified LGIC, wherein the viral vector is an adeno-associated viral vector (“the nucleic acid encoding the chimeric receptor is contained within a plasmid or viral vector.”, [0038]; “Viral vectors, and especially retroviral vectors, have become the most widely used method for inserting genes into mammalian, e.g., human cells. Other viral vectors can be derived from lentivirus, poxviruses, herpes simplex virus I, adenoviruses and adeno-associated viruses, vaccinia virus, and the like”, [0048]).
Response to Remarks – 35 USC § 102
Applicant’s remarks regarding the § 102 rejections raised in the prior action have been reviewed. Applicant submits that the amendments to claim 36 to “delete the recitation of amino acid substitutions at positions 77, 79, 139, or 141” are sufficient to distinguish the instant claims from Sternson. Examiner respectfully disagrees, because the teachings of Sternson meet the scope of claim 36 as interpreted herein for the reasons described above. Under the interpretation applied herein based on the indefiniteness described above, the claims encompass an α7 nAChR LBD comprising an amino acid substitution at position 141 (“wherein the amino acid substitution at residue 141 is L141F or L141P”), as well as an amino acid substitution at position 139 (see claim 37). The rejections are maintained and modified, accordingly.
Notice to Joint Inventors
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.
Claim Rejections - 35 USC § 103 – Sternson in view of Lynagh
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 39 is rejected under 35 U.S.C. 103 as being unpatentable over Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record) as applied to claims 36-37, 40-41, 56, and 63, in further view of Lynagh (Lynagh and Lynch, 2010, The Journal of Biological Chemistry, Vol. 285, No. 20, pg. 14890-14897; of record). The rejection that follows is maintained and modified, as necessitated by Applicant’s amendments to the claims.
Based on the specification, the “A298G amino acid substitution as numbered in [the α7-GlyR chimeric receptor of] SEQ ID NO: 7” is equivalent to the “A288G” amino acid substitution in a full length glycine receptor channel (“T258S and A288G, GlyR numbering; equivalent to T268S and A298G for α7-GlyR numbering”, pg. 41, lines 16-20).
The teachings of Sternson are described above and applied as to claims 36-37, 40-41, 56, and 63 hereinafter. In addition, Sternson teaches that the modified LGICs are used to modulate the electrical activity of specific neuronal populations ([0028]-[0029]). Sternson teaches that mutations in the α7 nAChR LBD confer pharmacological specificity to ligands that bind uniquely to the mutant receptor ([0029]), which allows the skilled artisan to manipulate neuronal activity in a targeted manner, and avoid perturbing electrical activity in “undesired cell populations” ([0029]-[0030]). Sternson also teaches that the modified LGICs may have “mutations in the transmembrane domain… which affect conductance and desensitization properties” ([0037]).
Sternson does not teach that the GlyR IPD is a modified GlyR IPD comprising an A298G amino acid substitution as numbered in SEQ ID NO: 7, which is interpreted as being equivalent to A288G in full length glycine receptor channels.
Lynagh teaches that “[t]he ability to silence the electrical activity of defined neuronal populations in vivo is dramatically advancing our understanding of brain function… [and] may eventually be clinically useful for treating a variety of neuropathological disorders caused by excessive neuronal activity” (Abstract, pg. 14890). Lynagh teaches that glycine receptor chloride channels (GlyRs) “may hold promise as silencing receptors” because they are directly activated by ivermectin, “a safe, well tolerated drug that reaches the brain following systemic administration,” they should have improved expression in individual neurons and a large single channel conductance, and are endogenous to humans, thereby alleviating antigenicity concerns associated with clinical use (Abstract; pg. 14891, left col.). Lynagh teaches a modified human GlyR IPD comprising an A288G mutation which “result[s] in a dramatic increase in sensitivity to both glycine and ivermectin” relative to a wildtype human GlyR IPD (pg. 14894; Fig. 3C-D; Table 1). Lynagh also teaches that the modified human GlyR IPD comprising the A288G mutation is agonized by ivermectin analogues which may be preferable to ivermectin given their “side effect profiles, pharmacokinetics, ability to cross the blood-brain barrier, and silencing receptor potency” (Fig. 5-B; Table 2; pg. 14896, left col.).
It would have been obvious to the ordinary skilled artisan before the effective filing date of the claimed invention to have substituted a generic “mutation[] in the transmembrane domain… which affect[s] conductance and desensitization properties” in the human GlyR IPD of the modified LGIC subunit of Sternson, for an A288G mutation taught by Lynagh. It would have amounted to a simple substitution of a generic mutation affecting conductance and desensitization properties for a specific, known mutation for the same purpose, by known means to yield predictable results. Lynagh teaches that an A288G mutation in a human GlyR IPD “result[s] in a dramatic increase in sensitivity to both glycine and ivermectin,” and thus, the skilled artisan would have had a reasonable expectation that an A288G substitution would similarly affect the sensitivity of the human GlyR IPD in the modified LGIC subunit of Sternson above. Sternson teaches that the modified LGICs incorporate mutations that confer pharmacological specificity to ligands that bind uniquely to the mutant receptor. In view of Sternson and Lynagh, the skilled artisan would have recognized the utility of the A288G substitution in conferring dramatically increased sensitivity to ivermectin, and the skilled artisan would have been motivated to incorporate the A288G substitution in the human GlyR IPD of the modified LGIC subunit of Sternson.
Response to Remarks – 35 USC § 103
Applicant’s remarks regarding the § 103 rejections raised in the prior action have been reviewed. Applicant submits that the amendments to claim 36 are sufficient to distinguish the instant claims from Sternson, and therefore, from Sternson in view of Lynagh. As described above in the response to remarks over the § 102 rejections, Examiner respectfully disagrees, because the teachings of Sternson meet the scope of claim 36 as interpreted herein for the reasons described above. The rejections are maintained and modified, accordingly.
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.
U.S. Patent No. 8,435,762
Claims 36-37, 40-41, and 56 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-60 of U.S. Patent No. 8,435,762. Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
The patented methods of claims 1 and 45 recite genetic constructs (i.e., vectors) encoding a chimeric receptor, wherein the chimeric receptor comprises “(i) a transmembrane domain from a ligand-gated ion channel protein; and (ii) a ligand binding domain from an α7 nicotinic acetylcholine receptor, wherein the ligand binding domain from the α7 nicotinic acetylcholine receptor is fused to the transmembrane domain from the ligand-gated ion channel protein, and wherein the amino acid sequence of the ligand binding domain from an α7 nicotinic acetylcholine receptor comprises at least one selectivity-inducing mutation, the selectivity-inducing mutation being selected from an amino acid substitution at one or more positions 77, 79, 139, or 141 in the amino acid sequence of SEQ ID NO:1, SEQ ID NO: 6, or SEQ ID NO: 10,” or “(i) a transmembrane domain from a ligand-gated ion channel protein; and (ii) a ligand binding domain from an α7 nicotinic acetylcholine receptor, wherein the ligand binding domain from the α7 nicotinic acetylcholine receptor is fused to the transmembrane domain from the ligand-gated ion channel protein, and wherein the amino acid sequence of the ligand binding domain from an α7 nicotinic acetylcholine receptor comprises at least one selectivity-inducing mutation, the selectivity-inducing mutation being selected from an amino acid substitution at position 141 in the amino acid sequence of SEQ ID NO:1, SEQ ID NO: 6, or SEQ ID NO: 10.”
Patented claims 20 and 56 recite a chimeric receptor comprising “a transmembrane domain from a ligand-gated ion channel protein,” and “a ligand binding domain from an α7 nicotinic acetylcholine receptor, wherein the ligand binding domain from the α7 nicotinic acetylcholine receptor is fused to the transmembrane domain from the ligand-gated ion channel protein, and wherein the amino acid sequence of the ligand binding domain from an α7 nicotinic acetylcholine receptor comprises at least one selectivity-inducing mutation, the selectivity-inducing mutation being selected from an amino acid substitution at one or more positions 77, 79 139 or 141 in the amino acid sequence of SEQ ID NO:1, SEQ ID NO: 6, or SEQ ID NO: 10.”
SEQ ID NO: 6 recited in the patented claims comprises an α7-nAChR LBD 100% identical to the human α7 nAChR LBD set forth in instant SEQ ID NO: 2.
The aforementioned patented claims are generic with respect to the transmembrane domain from a ligand-gated ion channel protein, and do not specifically recite the amino acid substitutions at the residues.
However, the patented claims recite that the transmembrane domain is a glycine receptor (see, e.g., claims 2, 7, 21-22, 46, 51). The patented claims also recite specific amino acid substitutions at the recited residues, including, e.g., ‘Q139G,” “Q139L,” “L141P,” “L141F” (see, e.g., claims 9-11, 39-44, etc.).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the generic chimeric receptor of the patented claims with a glycine receptor transmembrane domain, and one of the specific amino acid substitutions at positions 139 and 141, so as to arrive at instant claims 36-37, 40-41, and 56. It would have amounted to modifying a generic chimeric receptor with a known transmembrane domain and amino acid substitutions compatible with the chimeric receptor, by known means to yield predictable results. The skilled artisan would have been motivated to modify the generic chimeric receptor with reasonable expectation of success because the patented claims teach the specific modifications to the generic chimeric receptor which would have enabled the skilled artisan to prepare the invention of instant claims 36-37, 40-41, and 56.
Claim 39 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-60 of U.S. Patent No. 8,435,762 in view of Lynagh (Lynagh and Lynch, 2010, The Journal of Biological Chemistry, Vol. 285, No. 20, pg. 14890-14897; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejection that follows is maintained and modified as necessitated by Applicant’s amendments to the claims.
Regarding instant claim 39, the patented claims do not recite that the human GlyR IPD comprises an A298G amino acid substitution as numbered in SEQ ID NO: 7, which is interpreted as being equivalent to A288G in full length glycine receptor channels.
The teachings of Lynagh are described above and applied hereinafter. The obviousness of substituting the GlyR IPD in the chimeric receptor rendered obvious above, for a human GlyR IPD comprising an A288G substitution is described in paragraph 20 above and applied here.
Claim 63 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-60 of U.S. Patent No. 8,435,762 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejection that follows is maintained and modified as necessitated by Applicant’s amendments to the claims.
Regarding instant claim 63, the patented claims do not recite that the genetic constructs (i.e., vectors) are adeno-associated viral vectors.
The teachings of Sternson are described above and applied hereinafter.
It would have been obvious to one of ordinary skill before the effective filing date of the claimed invention to have substituted the generic genetic construct of the patented claims for an adeno-associated viral vector in view of Sternson. It would have amounted to a simple substitution of a generic construct for delivering a nucleic acid to a cell, for a specific type of construct for the same purpose, by known means to yield predictable results. Because Sternson teaches that “[v]iral vectors, and especially retroviral vectors, have become the most widely used method for inserting genes into mammalian, e.g., human cells,” and Sternson teaches lentivirus, herpes simplex virus, and adeno-associated viruses vectors are suitable for such a method, the skilled artisan would have been motivated to substitute the generic genetic construct, with a specific, “widely used” genetic construct (i.e., a specific, known viral vector) with a reasonable expectation of success for use in the patented claims.
U.S. Patent No. 10,961,296
Claims 36-38, 40-53, and 56-65 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 of U.S. Patent No. 10,961,296 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained from the prior action.
The patented claims recite a “modified ligand gated ion channel (LGIC) comprising at least one modified LGIC subunit, said modified LGIC subunit comprising: a human alpha 7 nicotinic acetylcholine receptor (α7-nAChR) ligand binding domain (LBD) comprising a L131G amino acid substitution, a Q139L amino acid substitution, and/or a Y217F amino acid substitution, and an ion pore domain (IPD), wherein the IPD is an IPD from a receptor selected from the group consisting of a serotonin 3 receptor (5HT3) IPD, a glycine receptor (GlyR) IPD, a gamma-aminobutyric acid (GABA) receptor IPD, and an alpha 7 nicotinic acetylcholine receptor (α7-nAChR) IPD.”
The patented claims do not recite that the modified alpha 7 nicotinic acetylcholine receptor (α7-nAChR) ligand binding domain (LBD) comprises at least 97 percent sequence identity to instant SEQ ID NO: 2.
The teachings of Sternson are described above and applied hereinafter.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have substituted the generic modified LGIC comprising a modified LGIC subunit of the patented claims for the modified LGIC comprising a modified LGIC subunit disclosed by Sternson as SEQ ID NO: 6, which as shown in the alignment of record in Appendix I is 100% identical to instant SEQ ID NO: 2. It would have amounted to a simple substitution of a generic modified LGIC sequence, for a specific, known modified LGIC sequence, by known means to yield predictable results. The skilled artisan would have been motivated to substitute the generic modified LGIC with reasonable expectation of success because Sternson and the patented claims teach substantially identical modified LGICs, and the patented claims are silent as to the sequence of the modified LGIC in which to make the amino acid substitutions.
The patented claims also do not recite a viral vector comprising a nucleic acid encoding the modified LGIC comprising a modified LGIC subunit, wherein the viral vector is an adeno-associated viral vector.
The teachings of Sternson are described above and applied hereinafter.
It would have been obvious to one of ordinary skill before the effective filing date of the claimed invention to have prepared the modified LGIC comprising a modified LGIC subunit above, in an adeno-associated viral vector in view of Sternson. It would have amounted to preparing an obvious modified LGIC in a known vector suitable for delivering a modified LGIC to a cell, by known means to yield predictable results. Because Sternson teaches that “[v]iral vectors, and especially retroviral vectors, have become the most widely used method for inserting genes into mammalian, e.g., human cells,” and Sternson teaches lentivirus, herpes simplex virus, and adeno-associated viruses vectors are suitable for delivering modified LGIC substantially identical to the patented modified LGIC, the skilled artisan would have been motivated to prepare the modified LGIC in a specific, “widely used” genetic construct (i.e., a specific, known viral vector) with a reasonable expectation of success.
Accordingly, in view of Sternson, the patented claims render obvious instant claims 36-38, 40-53, and 56-63.
Regarding instant claims 64-65, the patented claims do not recite that the modified LGIC comprising a modified LGIC subunit is operably linked to a synapsin promoter.
However, Sternson teaches operably linking a modified LGIC comprising a modified LGIC subunit to a synapsin promoter ([0023]; [0038]; [0094]; [0114]). Sternson demonstrates that linking a modified LGIC to a synapsin promoter allows the skilled artisan to restrict expression to neuronal cell types, which would be desirable in the methods of treatment disclosed by Sternson ([0094]; [0114]).
It would have been obvious to one of ordinary skill before the effective filing date of the claimed invention to have operably linked a patented modified LGIC comprising a modified LGIC subunit in the vector rendered obvious above to a synapsin promoter in view of Sternson. It would have amounted to linking a known modified LGIC or LGIC subunit within a known vector to a known element used to control expression of modified LGIC. The skilled artisan would have been motivated to operably link the modified LGIC or LGIC subunit to a synapsin promoter in the vector, with a reasonable expectation of success, because Sternson and the patented claims teach substantially identical modified LGIC and LGIC subunits, and Sternson demonstrates that the skilled artisan can use vectors in which modified LGIC or LGIC subunits are operably linked to synapsin promoter to restrict expression to neuronal cell types, e.g., for use in methods of treatment.
Claims 39, and 54-55 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 of U.S. Patent No. 10,961,296 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record), and in further view of Lynagh (Lynagh and Lynch, 2010, The Journal of Biological Chemistry, Vol. 285, No. 20, pg. 14890-14897; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained from the prior action.
Regarding instant claims 39, and 54-55, the patented claims do not recite that the human GlyR IPD comprises an A298G amino acid substitution as numbered in SEQ ID NO: 7, which is interpreted as being equivalent to A288G in full length glycine receptor channels.
The teachings of Lynagh are described above and applied hereinafter. The obviousness of substituting the GlyR IPD in the chimeric receptor above, for a human GlyR IPD comprising an A288G substitution is described in paragraph 20 above and applied here.
U.S. Patent No. 10,981,962
Claims 36-65 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 10,981,962 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Patented claims 1, 18, and 20 recite a modified LGIC comprising a modified LGIC subunit which meets each limitation of instant claims 36-37, and 42-43. Patented claim 7 recites a modified LGIC comprising a modified LGIC subunit which meets each limitation of instant claims 39, and 54-55. Patented claims 14-16 recite a modified LGIC comprising a modified LGIC subunit which meets the limitations of instant claims 40-41. Patented claims 4, 19, and 21 recite a modified LGIC comprising a modified LGIC subunit which meets each limitation of instant claims 38, 44-53.
The patented claims do not recite a viral vector comprising a nucleic acid encoding the modified LGIC, wherein the viral vector is an adeno-associated viral vector.
The teachings of Sternson are described above and applied hereinafter. The obviousness of preparing a patented modified LGIC or LGIC subunit in an adeno-associated viral vector in view of Sternson is described above in paragraph 33 and applied hereinafter.
Accordingly, in view of Sternson, the patented claims render obvious instant claims 36-63.
Regarding instant claims 64-65, the patented claims do not recite that the modified LGIC or LGIC subunit is operably linked to a synapsin promoter.
The teachings of Sternson regarding the synapsin promoter are described in paragraph 35 above and applied hereinafter. The obviousness of operably linking a patented modified LGIC or LGIC subunit in the vector rendered obvious above to a synapsin promoter in view of Sternson is also described in paragraph 35 and applied hereinafter.
U.S. Patent No. 11,084,853
Claims 36-65 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-17 of U.S. Patent No. 11,084,853 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
The instant application claims priority to Application No. 15/644,295, now U.S. Patent No. 11,084,853 (the reference patented herein). The restriction requirement maintained throughout prosecution of Application No. 15/644,295 was between methods and proteins. The instant claims, which are directed to nucleic acids, are not consonant with the restriction requirement maintained in Application No. 15/644,295, and therefore, U.S. Patent No. 11,084,853 may be applied for the purposes of non-statutory double patenting.
Patented claims 1 and 16 recite a modified LGIC comprising a modified LGIC subunit which meets each limitation of instant claims 36 and 40. Patented claim 2 recites a modified LGIC comprising a modified LGIC subunit which meets each limitation of instant claims 37-38, and 42-53. Patented claim 8 recites a modified LGIC comprising a modified LGIC subunit which meets each limitation of instant claims 39, and 54-55. Patented claims 13 and 17 recite a modified LGIC comprising a modified LGIC subunit which meets each limitation of instant claim 41.
The patented claims do not recite a viral vector comprising a nucleic acid encoding the modified LGIC, wherein the viral vector is an adeno-associated viral vector.
The teachings of Sternson are described above and applied hereinafter. The obviousness of preparing a patented modified LGIC or LGIC subunit in an adeno-associated viral vector in view of Sternson is described above in paragraph 33 and applied hereinafter.
Accordingly, in view of Sternson, the patented claims render obvious instant claims 36-63.
Regarding instant claims 64-65, the patented claims do not recite that the modified LGIC or LGIC subunit is operably linked to a synapsin promoter.
The teachings of Sternson regarding the synapsin promoter are described in paragraph 35 above and applied hereinafter. The obviousness of operably linking a patented modified LGIC or LGIC subunit in the vector rendered obvious above to a synapsin promoter in view of Sternson is also described in paragraph 35 and applied hereinafter.
U.S. Patent No. 11,124,554
Claims 36-38, 40-53, and 56-65 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 6 of U.S. Patent No. 11,124,554 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Patented claim 6 recites a modified LGIC comprising a modified LGIC subunit comprising the amino acid substitutions as recited in instant claim 36.
The patented claim does not recite that the modified alpha 7 nicotinic acetylcholine receptor (α7-nAChR) ligand binding domain (LBD) comprises at least 97 percent sequence identity to instant SEQ ID NO: 2.
The teachings of Sternson are described above and applied hereinafter. The obviousness of substituting the generic modified LGIC or LGIC subunit of the patented claims for the modified LGIC or LGIC subunit disclosed by Sternson as SEQ ID NO: 6, which as shown in the alignment of record is 100% identical to instant SEQ ID NO: 2, is described in paragraph 32 above and applied hereinafter.
The patented claim does not recite the specific combination of amino acid substitutions recited in instant claims 37-38, and 42-53, however, the patented claims recite each of the specific amino acid substitutions in the instant claims, i.e., “L131G,” “Q139L,” and “Y217F” as recited in claims 37-38, and 42-53.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have prepared a modified LGIC or LGIC subunit comprising the specific combination of amino acids recited in the instant claims. It would have amounted to preparing a patented modified LGIC or LGIC subunit, using known amino acid substitutions, by known means to yield predictable results. The skilled artisan would have been motivated to prepare a modified LGIC or LGIC subunit comprising the amino acid substitutions recited in the instant claims because the patented claims recite that any one or more of the amino acid substitutions are usable in the modified LGIC or LGIC subunit.
The patented claims do not recite a viral vector comprising a nucleic acid encoding the modified LGIC, wherein the viral vector is an adeno-associated viral vector.
The teachings of Sternson are described above and applied hereinafter. The obviousness of preparing a patented modified LGIC or LGIC subunit in an adeno-associated viral vector in view of Sternson is described above in paragraph 33 and applied hereinafter.
Accordingly, the patented claims in view of Sternson render obvious instant claims 36-38, 40-53, and 56-63.
Regarding instant claims 64-65, the patented claims do not recite that the modified LGIC or LGIC subunit is operably linked to a synapsin promoter.
The teachings of Sternson regarding the synapsin promoter are described in paragraph 35 above and applied hereinafter. The obviousness of operably linking a patented modified LGIC or LGIC subunit in the vector rendered obvious above to a synapsin promoter in view of Sternson is also described in paragraph 35 and applied hereinafter.
Claims 39, and 54-55 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 6 of U.S. Patent No. 11,124,554 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record), and in further view of Lynagh (Lynagh and Lynch, 2010, The Journal of Biological Chemistry, Vol. 285, No. 20, pg. 14890-14897; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Regarding instant claims 39, and 54-55, the patented claim does not recite that the human GlyR IPD comprises an A298G amino acid substitution as numbered in SEQ ID NO: 7, which is interpreted as being equivalent to A288G in full length glycine receptor channels.
The teachings of Lynagh are described above and applied hereinafter. The obviousness of substituting the GlyR IPD in the patented claims, for a human GlyR IPD comprising an A288G substitution is described in paragraph 20 above and applied here.
U.S. Patent No. 12,247,064
Claims 36-38, 40-53, and 56-65 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of U.S. Patent No. 12,247,064 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
The patented method claims recite a nucleic acid sequence encoding a modified LGIC subunit which can assemble into a modified LGIC. With the exception of the level of sequence identity required to one of SEQ ID NOs: 1, 2, or 11, the patented claims meets the limitations of instant claims 36-38, and 40-53.
The teachings of Sternson are described above and applied hereinafter. The obviousness of substituting the generic modified LGIC or LGIC subunit of the patented claims for the modified LGIC or LGIC subunit disclosed by Sternson as SEQ ID NO: 6, which as shown in the alignment of record is 100% identical to instant SEQ ID NO: 2, is described in paragraph 32 above and applied hereinafter.
Accordingly, the patented claims in view of Sternson render obvious instant claims 36-38, and 40-53.
Patented claims 4-6 meet the limitations of instant claims 56-63. Patented claim 9 meets the limitations of instant claims 64-65. Thus, in view of Sternson, instant claims 56-65 are also obvious over the patented claims.
Claims 39, and 54-55 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of U.S. Patent No. 12,247,064 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record), and in further view of Lynagh (Lynagh and Lynch, 2010, The Journal of Biological Chemistry, Vol. 285, No. 20, pg. 14890-14897; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Regarding instant claims 39, and 54-55, the patented claims do not recite that the human GlyR IPD comprises an A298G amino acid substitution as numbered in SEQ ID NO: 7, which is interpreted as being equivalent to A288G in full length glycine receptor channels.
The teachings of Lynagh are described above and applied hereinafter. The obviousness of substituting the GlyR IPD in the patented claims, for a human GlyR IPD comprising an A288G substitution is described in paragraph 20 above and applied here.
U.S. Patent No. 12,570,706
Claims 36-38, and 39-63 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 12,570,706. Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections of claims 36-37, and 39-63 are maintained and modified from the prior action, and the rejection of claim 38 is new, as necessitated by Applicant’s amendments to the claims.
Patented claims 1, 10, 14, and 18 recite a nucleic acid encoding a modified LGIC comprising a modified LGIC subunit which meets the limitations of instant claims 36-38, and 40-53. Patented claim 6 recites a nucleic acid encoding a modified LGIC comprising a modified LGIC subunit which meets the limitations of instant claims 39, and 54-55. Patented claims 7-9, 11-13, 15-17, and 19-20 meet the limitations of instant claims 56-63.
Accordingly, the patented claims anticipate the limitations of instant claims 36-38, and 39-63.
Claims 64-65 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 12,570,706 in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Regarding instant claims 64-65, the patented claims do not recite that the modified LGIC or LGIC subunit is operably linked to a synapsin promoter.
The teachings of Sternson regarding the synapsin promoter are described in paragraph 35 above and applied hereinafter. The obviousness of operably linking a patented modified LGIC or LGIC subunit in the vector rendered obvious above to a synapsin promoter in view of Sternson is also described in paragraph 35 and applied hereinafter.
Application No. 18/834,135
Claims 36-38, 40-53, and 56-65 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 13 of co-pending Application No. 18/834,135 (reference application) in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. The rejections of claims 36-37, 40-53, and 56-65 are maintained and modified from the prior action, and the rejection of claim 38 is new, as necessitated by Applicant’s amendments to the claims.
Claim 13 recites a modified LGIC comprising a modified LGIC subunit, which, with the exception of the level of sequence identity required to one of SEQ ID NOs: 1, 2, or 11, and the specific ion pore domain (i.e., GlyR IPD), meets the limitations of instant claims 36-38, and 40-53.
The teachings of Sternson are described above and applied hereinafter. The obviousness of substituting the generic modified LGIC or LGIC subunit of the co-pending claim for the modified LGIC or LGIC subunit disclosed by Sternson as SEQ ID NO: 6 which comprises a GlyR IPD, and which as shown in the alignment of record is 100% identical to instant SEQ ID NO: 2, is described in paragraph 32 above and applied hereinafter.
The co-pending claims do not recite a viral vector comprising a nucleic acid encoding the modified LGIC or LGIC subunit, wherein the viral vector is an adeno-associated viral vector.
The teachings of Sternson are described above and applied hereinafter. The obviousness of preparing the co-pending modified LGIC or LGIC subunit in an adeno-associated viral vector in view of Sternson is described above in paragraph 33 and applied hereinafter.
Accordingly, the co-pending claim in view of Sternson renders obvious instant claims 36-38, 40-53, and 56-63.
Regarding instant claims 64-65, the co-pending claims do not recite that the modified LGIC or LGIC subunit is operably linked to a synapsin promoter.
The teachings of Sternson regarding the synapsin promoter are described in paragraph 35 above and applied hereinafter. The obviousness of operably linking a co-pending modified LGIC or LGIC subunit in the vector rendered obvious above to a synapsin promoter in view of Sternson is also described in paragraph 35 and applied hereinafter.
Claims 39, and 54-55 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 13 of co-pending Application No. 18/834,135 (reference application) in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record), and in further view of Lynagh (Lynagh and Lynch, 2010, The Journal of Biological Chemistry, Vol. 285, No. 20, pg. 14890-14897; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Regarding instant claims 39, and 54-55, the co-pending claims do not recite that the human GlyR IPD comprises an A298G amino acid substitution as numbered in SEQ ID NO: 7, which is interpreted as being equivalent to A288G in full length glycine receptor channels.
The teachings of Lynagh are described above and applied hereinafter. The obviousness of substituting the GlyR IPD in the co-pending claims, for a human GlyR IPD comprising an A288G substitution is described in paragraph 20 above and applied here.
Application No. 19/061,239
Claim 36-38, 40-53, and 56-65 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 25 of co-pending Application No. 19/061,239 (reference application) in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Co-pending claim 25 recites an adeno-associated viral vector which, with the exception of the level of sequence identity required to one of SEQ ID NOs: 1, 2, or 11, and the specific ion pore domain (i.e., GlyR IPD), meets the limitations of instant claims 36-38, 40-53, and 56-65.
The teachings of Sternson are described above and applied hereinafter. The obviousness of substituting the generic modified LGIC or LGIC subunit of the co-pending claim for the modified LGIC or LGIC subunit disclosed by Sternson as SEQ ID NO: 6 which comprises a GlyR IPD, and which as shown in the alignment of record is 100% identical to instant SEQ ID NO: 2, is described in paragraph 32 above and applied hereinafter.
Accordingly, the co-pending claim in view of Sternson renders obvious instant claims 36-38, 40-53, and 56-65.
Claims 39, and 54-55 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 25 of co-pending Application No. 19/061,239 (reference application) in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record), and in further view of Lynagh (Lynagh and Lynch, 2010, The Journal of Biological Chemistry, Vol. 285, No. 20, pg. 14890-14897; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Regarding instant claims 39, and 54-55, the co-pending claims do not recite that the human GlyR IPD comprises an A298G amino acid substitution as numbered in SEQ ID NO: 7, which is interpreted as being equivalent to A288G in full length glycine receptor channels.
The teachings of Lynagh are described above and applied hereinafter. The obviousness of substituting the GlyR IPD in the co-pending claims, for a human GlyR IPD comprising an A288G substitution is described in paragraph 20 above and applied here.
Application No. 19/530,123
Claim 36-38, 40-53, and 56-65 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 36-65 of co-pending Application No. 19/530,123 (reference application) in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. The rejections that follow are new and necessitated by Applicant’s amendments to the co-pending claims (i.e., cancellation of all previously pending claims).
The co-pending claims recite a modified LGIC component (i.e., an α7-nAChR LBD) and a modified LGIC or modified LGIC subunit comprising the α7-nAChR LBD, which, with the exception of the specific ion pore domain (i.e., GlyR IPD), meets the limitations of instant claims 36-38, 40-53, and 56-65.
The teachings of Sternson are described above and applied hereinafter. Sternson teaches a modified LGIC or LGIC subunit corresponding to SEQ ID NO: 6 which comprises a α7-nAChR LBD and a GlyR IPD, and which as shown in the alignment of record is 100% identical to instant SEQ ID NO: 2.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have prepared a modified LGIC or LGIC subunit with a co-pending α7-nAChR LBD which meets the limitations of the instant claims and the GlyR IPD disclosed by Sternson, or to have substituted the IPD of a modified LGIC or LGIC subunit of the co-pending claims with the GlyR IPD disclosed by Sternson. It would have amounted to preparing a modified LGIC or LGIC subunit by known means to yield predictable results, or substituting two suitable IPD of a modified LGIC or LGIC subunit by known means to yield predictable results. The skilled artisan would have been motivated, and with a reasonable expectation of success, because Sternson and the co-pending claims teach substantially identical modified LGICs or LGIC subunits comprising α7-nAChR LBDs, and as indicated in both Sternson and the co-pending claims, various IPDs are compatible with the α7-nAChR LBD in modified LGIC or LGIC subunits, including GlyR IPD.
Accordingly, the co-pending claim in view of Sternson renders obvious instant claims 36-38, 40-53, and 56-63.
Claims 39, and 54-55 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 36-65 of co-pending Application No. 19/061,239 (reference application) in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record), and in further view of Lynagh (Lynagh and Lynch, 2010, The Journal of Biological Chemistry, Vol. 285, No. 20, pg. 14890-14897; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. The rejections that follow are new and necessitated by Applicant’s amendments to the co-pending claims (i.e., cancellation of all previously pending claims).
Regarding instant claims 39, and 54-55, the co-pending claims do not recite a human GlyR IPD comprising an A298G amino acid substitution as numbered in SEQ ID NO: 7, which is interpreted as being equivalent to A288G in full length glycine receptor channels.
The teachings of Lynagh are described above and applied hereinafter. The obviousness of substituting the GlyR IPD rendered obvious above, for a human GlyR IPD comprising an A288G substitution is described in paragraph 20 above and applied here.
Application No. 19/530,459
Claim 36-65 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 5-9, and 14 of co-pending Application No. 19/530,459 (reference application) in view of Sternson (Sternson et al., 27 May 2010, US 2010/0130420 A1; of record). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons that follow. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. The rejections that follow are maintained and modified as necessitated by Applicant’s amendments to the claims.
Co-pending claims 5-9 recite a modified LGIC comprising a modified LGIC subunit, which, with the exception of the level of sequence identity required to one of SEQ ID NOs: 1, 2, or 11, and the specific ion pore domain (i.e., GlyR IPD), meets the limitations of instant claims 36-38, and 40-53.
The teachings of Sternson are described above and applied hereinafter. The obviousness of substituting the generic modified LGIC or LGIC subunit of the co-pending claim for the modified LGIC or LGIC subunit disclosed by Sternson as SEQ ID NO: 6 which comprises a GlyR IPD, and which as shown in the alignment of record is 100% identical to instant SEQ ID NO: 2, is described in paragraph 32 above and applied hereinafter.
The co-pending claims do not recite a viral vector comprising a nucleic acid encoding the modified LGIC, wherein the viral vector is an adeno-associated viral vector.
The teachings of Sternson are described above and applied hereinafter. The obviousness of preparing the co-pending modified LGIC or LGIC subunit in an adeno-associated viral vector in view of Sternson is described above in paragraph 33 and applied hereinafter.
Accordingly, the co-pending claim in view of Sternson renders obvious instant claims 36-38, 40-53, and 56-63.
Co-pending claim 14 meets the limitations of instant claims 39, and 54-55.
Regarding instant claims 64-65, the co-pending claims do not recite that the modified LGIC or LGIC subunit is operably linked to a synapsin promoter.
The teachings of Sternson regarding the synapsin promoter are described in paragraph 35 above and applied hereinafter. The obviousness of operably linking a co-pending modified LGIC or LGIC subunit in the vector rendered obvious above to a synapsin promoter in view of Sternson is also described in paragraph 35 and applied hereinafter.
Response to Remarks – Double Patenting
Applicant’s remarks regarding the nonstatutory double patenting rejections raised in the prior action have been reviewed. With respect to the rejections raised over U.S. Patent No. 8,435,762, Applicant submits that the amendments to claim 36 distinguish the instant claims from the claims of U.S. Patent No. 8,435,762, and the ‘762 patent in view of Lynagh or Sternson. Examiner respectfully disagrees, because, as described above the claims of the ‘762 patent still meet the scope of claims 36-37, 40-41, and 56 as interpreted herein. The rejections over the ‘762 patent are maintained and modified, accordingly.
With respect to the remaining nonstatutory double patenting rejections raised in the previous action, Applicant has requested that the rejections be held in abeyance until allowable subject matter is identified in the present and/or co-pending application. Applicant’s request to hold the nonstatutory double patenting rejections in abeyance is denied. Applicant’s remarks do not address the propriety of the remaining nonstatutory double patenting rejections, allowable subject matter has not been identified, and no terminal disclaimers have been filed. The rejections will remain in place until they are overcome by amendment, terminal disclaimer, or otherwise.
Conclusion
No claims are allowed.
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/JENNA L PERSONS/Examiner, Art Unit 1637
/Soren Harward/Primary Examiner, TC 1600
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