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 .
Applicant’s response filed 12/04/2025 has been received and considered entered. This is a response to amendments and arguments filed 12/04/2025.
Election/Restrictions
Claims 129, 131-133, and 147-148 stand withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention (claims 147-148) or nonelected species (claims 131-133, nonelected species of Group B), there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 07/08/2025.
Claims Status
Claims 1-125, 128-133, 145, 147-148 is/are cancelled. Claims 149-150 are newly added. Claims 126-127, 134-144, 146, 149-150 is/are currently pending with claims 129, 131-133, and 147-148 are withdrawn. Claims 126-127, 134-144, 146, 149-150 is/are under examination.
Information Disclosure Statement
The information disclosure statement filed 08/17/2025 fails to comply with 37 CFR 1.98(a)(2), which requires a legible copy of each cited foreign patent document; each non-patent literature publication or that portion which caused it to be listed; and all other information or that portion which caused it to be listed. It has been placed in the application file, but the information referred to therein has not been considered. References not considered for failure to provide a legible copy have been struck through on the annotated IDS forms. Piageri et al. (citation 004) has not been provided.
The information disclosure statement filed 08/17/2025 fails to comply with 37 CFR 1.98(a)(1), which requires the following: (1) a list of all patents, publications, applications, or other information submitted for consideration by the Office; (2) U.S. patents and U.S. patent application publications listed in a section separately from citations of other documents; (3) the application number of the application in which the information disclosure statement is being submitted on each page of the list; (4) a column that provides a blank space next to each document to be considered, for the examiner’s initials; and (5) a heading that clearly indicates that the list is an information disclosure statement. A copy of Przychodzen (2013) has been provided with this IDS but was not listed in the IDS.
Claim Objections
Claim 138 is objected to because of the following informalities: “method of claim 134126” should read “method of claim 126” or “method of claim 134”. Appropriate correction is required.
Claim Rejections - 35 USC § 112
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.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
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 of carrying out his invention.
Enablement:
Claims 126-127, 134-144, 146, 149-150 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for methods of modulating alternative splicing of SYNGAP1 intron 10-alternative exon 11 in vitro comprising administering ASOs comprising at most one mismatch to, and comprising at least 8 consecutive nucleotides 100% complementary to, a sequence of at least 12 nucleotides of SYNGAP1 intron 10-alternative exon 11, does not reasonably provide enablement for methods of treating a disease in vivo with the described compositions. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. This rejection is modified in response to amendments and maintained.
The factors to be considered in determining whether a disclosure would require undue experimentation include:
A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In re Wands, 8 USPQ2d, 1400 (CAFC 1988) and MPEP 2164.01.
The breadth of the claims:
With respect to claim breadth, the standard under 35 U.S.C. §112, first paragraph, entails the determination of what the claims recite and what the claims mean as a whole. As such, the broadest reasonable interpretation of the claimed methods of claims 126-130 and 134-144 is that they encompass methods of using an antisense oligomer to modulate a SYNGAP1 NSAE broadly, encompassing methods of treating a disease; the broadest reasonable interpretation of the claimed method of 146 is that it encompasses methods of using an ASO to modulate a SYNGAP1 NSAE in a method of treating any disease. A skilled artisan would not know how to use the method with a reasonable expectation of success based solely on what is disclosed in the specification.
The amount of direction provided by the inventor and the level of predictability in the art:
The specification teaches NSAE-modulating ASOs which target intron 10 or alternative exon 11 of the SYNGAP1 pre-mRNA (see Table 1) and methods of using these ASOs to modulate alternative splicing of SYNGAP1 and thus modulate protein expression in HEK293 cells and mouse embryonic fibroblasts (see Figs. 11-12). Regarding the method of treating diseases of claim 146, the art at the time of filing teaches that antisense oligonucleotides cannot be assumed to retain efficacy and safety observed in in vitro preclinical studies when translated to in vivo studies, particularly in human subjects (see Frazier, 2014). Claims 149 and 150 further limit the claimed disease or condition to autosomal dominant mental retardation, epileptic encephalopathy, and autism. However, while SYNGAP1 mutations were known in the art to be associated with (or in some cases, causative of) certain forms of autosomal dominant mental retardation 5, autism, and epileptic encephalopathy, at the time of filing, no genetic therapies had been tested in humans or animal models, and gene therapies (including splice modulation) were not considered promising future or near-future therapeutic options (see Vlaskamp, 2019: the only treatments discussed in Vlaskamp are antiepileptics such as valproate, levetiracetam, and steroids, page e103). Thus the art at the time of filing did not teach or suggest splice-modifying therapies, such as claimed in the instant claims, or any other gene therapy for treatment of diseases known to be caused by SYNGAP1 mutations. The specification as filed does not provide guidance that overcomes this unpredictability within the art.
The existence of working examples:
What is enabled by the working examples is narrow in comparison to the breadth of the claims: The specification discloses methods of modulating protein expression by modulating alternative splicing of intron 10-alternative exon 11 of SYNGAP1 in vitro (Figs. 11-12; paragraphs [0867]-[0870]), while providing merely prophetic examples of in vivo methods (paragraphs [0871]-[0872]).
The quantity of experimentation needed to make or use the invention:
The standard of an enabling disclosure is not the ability to make and test if the invention works but one of the ability to make and use with a reasonable expectation of success. A patent is granted for a completed invention, not the general suggestion of an idea (MPEP 2164.03 and Chiron Corp. v. Genentech Inc., 363 F.3d 1247, 1254, 70 USPQ2d 1321, 1325-26 (Fed. Cir. 2004). The instant specification is not enabling because one cannot follow the guidance presented therein, or within the art at the time of filing, and practice the claimed method without first making a substantial inventive contribution. Given that the nature of the invention of claims 126-130, 134-144, and 146 encompasses methods of treating any disease using an NSAE-modulating ASO, a person having ordinary skill in the art would have to perform multiple further experiments, in human clinical trials, in animal models representative of treatment of a representative number of diseases, and in vitro (regarding claims 126-130 and 134-146), in order to demonstrate the invention could be used with a reasonable expectation of success. The amount of experimentation required for enabling guidance, commensurate in scope with what is claimed, goes beyond what is considered ‘routine' within the art, and constitutes undue further experimentation in order to use the method with a reasonable expectation of successfully treating any CNS disorder or neurodegenerative disease. Therefore, Claims 126-130, 134-144, 146, 149-150 are rejected under 35 U.S.C. 112, first paragraph, for failing to meet the enablement requirement.
Response to Arguments
Applicant's arguments filed 12/04/2025 have been fully considered but they are not persuasive.
Applicant argues that SYNGAP1 protein deficiency is well-known to be associated with diseases, including autosomal dominant mental retardation, epileptic encephalopathy, and autism, and that “a skilled artisan would understand that the claimed method could be used to treat a disease or condition associated with a functional-SYNGAP1 protein deficiency” (pages 10-11). While functional SYNGAP1 protein deficiency was known to be associated with or causative of some cases of autosomal dominant mental retardation, epileptic encephalopathy, and autism, the art at the time of filing did not teach or suggest that these diseases associated with or caused by a functional SYNGAP1 protein deficiency could be or should be treated by modifying SYNGAP1 splicing or otherwise targeting the SYNGAP1 gene or mRNA. Vlaskamp is referenced in the rejection above as evidence of such. Further discussion of treatment of disorders associated with functional SYNGAP1 protein deficiency can be found in: Holder (2019), which, similar to Vlaskamp, indicates anti-seizure medications as standard treatment, in addition to behavioral or pharmaceutical therapies standard for autism spectrum disorder, gastrostomy feeding, and genetic counseling. Based on the state of the art, an artisan would not be able to reasonably assume that any composition targeting the SYNGAP1 gene or mRNA (including but not limited to compositions altering the splicing of the SYNGAP1 mRNA) could treat a disorder associated with or caused by a functional SYNGAP1 protein deficiency, as no such composition had been tried in human patients or in representative animal models, or was understood by artisans to be a promising future treatment.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claim(s) 126-127, 134-137, 140-144 is/are rejected under 35 U.S.C. 103 as being unpatentable over Du (2007; provided with IDS filed by Applicant 03/14/2022), as evidenced by Coutinho (2005; provided with IDS filed by Applicant 03/14/2022), Khorkova (2017; provided with IDS filed by Applicant 04/17/2024), and Kralovicova (2016; provided with IDS filed by Applicant 03/14/2022), in view of Prchalova (2017; provided by Applicant with IDS filed 04/17/2024) and Chen (1998). Limitations from previously presented claims 141-142 have been incorporated by amendment into independent claim 126, necessitating an amendment of the previously presented rejection under 35 USC 103 of claims 126, 134, and 138-139 to incorporate these limitations. Teachings of Du, Coutinho, Khorkova, and Kralovicova applied to claims 127, 134-137, and 140 in the previously presented rejection under 35 USC 102 have been incorporated in response to the amendment of claim 126.
Regarding claim 126, Du teaches a method of modulating protein expression in a cell, comprising contacting the cell with an antisense morpholino oligonucleotide (AMO) (see Figs. 1-3; pages 6007-6019). This AMO modulates a nonsense-mediated RNA decay-associated alternative exon: the retained intronic sequence of ATM seen in AT203LA cells, described by Du on page 6008, comprises the nonsense-mediated decay-associated alternative exon, NSE, and retained intronic sequence upstream of canonical exon 29, further described by Coutinho and Kralovicova, and thus, the AMOs taught by Du, by modulating alternative splicing of this intronic sequence, in fact modulate splicing of an NSAE (see Coutinho Figs. 1, 3-4; Kralovicova abstract, pages 392-395). The NSAE-modulating AMO of Du interacts with a target motif within a pre-processed mRNA transcript to modulate splicing at an alternative 3’ splice site (claim 126) of the pre-processed mRNA transcript, thereby promoting inclusion of a canonical exon and exclusion of an alternative exon from the pre-processed mRNA transcript, wherein the target motif is located in an intronic region between two canonical exons, and wherein the alternative exon comprises a canonical exon and at least a portion of an intron immediately upstream of the canonical exon (Fig. 1C; Fig. 2C; pages 6008-6009). While Du does not disclose that one alternate splice form of AT203LA ATM gene comprises an alternative exon 29 which comprises canonical exon 29 and an intronic sequence immediately upstream of canonical exon 29, Coutinho teaches that this splice form is naturally occurring in AT203LA cells, as a minor isoform (Fig. 4). Therefore, by correcting splicing of ATM pre-mRNA, Du teaches methods which inherently promote the exclusion of this minor ATM alternative exon 29 (alternative exon comprising canonical exon 29 and an intronic sequence immediately upstream of canonical exon 29) and promote the inclusion of canonical exon 29. Du teaches that the alternative 3’ splice site flanks the alternative exon, is upstream of a 3’ splice site flanking the canonical exon, and is within the intron immediately preceding the canonical exon (see Fig. 1). Du teaches that the NSAE-modulating agent is an antisense oligomer (Fig. 1; abstract).
Regarding claim 127, Du teaches that the processed mRNA transcript encodes a target protein (ATM) and the AMO increases expression of the target protein in the cell (pages 6008-6009).
Regarding claim 134, Du teaches that the method comprises contacting the ASO with the cell (Figs. 1-3; pages 6007-6019).
Regarding claim 135, Du teaches that the antisense oligomer is 100% complementary to a sequence in the target motif (page 6008).
Regarding claims 136-137, Du teaches that the antisense oligomers are antisense morpholino oligomers (abstract; page 6007), wherein “morpholinos” by definition comprise backbones “composed of methylenemorpholine rings and phosphorodiamidate linkages” (Khorkova, Fig. 2).
Regarding claim 140, Du teaches that the antisense oligomers are 25 nucleotides long (page 6007).
Regarding claims 142-144, Du teaches AMOs which are 100% complementary to a target sequence, wherein the target sequence comprises an alternative splice site, and wherein hybridization of the AMOs to the target sequence block splicing at the alternative splice site (Fig. 1).
However, Du does not teach that the target protein is SYNGAP1, and that the target motif is comprised in SEQ ID NO:166.
Prchalova teaches an NSAE in the SYNGAP1 gene.
Regarding claims 126 and 141-144, Prchalova teaches that the human SYNGAP1 gene comprises an alternative 3’ splice site upstream of canonical exon 11 of SYNGAP1, wherein splicing at this alternative 3’ splice site results in the inclusion of an alternative exon 11, which is an NSAE and comprises canonical exon 11 and an intronic sequence immediately upstream of canonical exon 11 (Fig. 2C: inclusion of alternative exon 11 introduces an early stop codon). premrna_ENST00000293748.9 (i.e. SEQ ID NO:15836) is the known human SYNGAP1 sequence (see alignment below) (required by claim 141).
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Moreover, SEQ ID NO:166 is the known canonical intronic sequence of intron 10 of hSYNGAP1 (see alignments below) (required by claim 142).
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Furthermore, instant SEQ ID NO:156 is 100% complementary to an 18-nucleotide segment of canonical intron 10 of hSYNGAP1 which comprises the alternative 3’ splice site taught by Prchalova (Fig. 2C shows the position of the alternative 3’ splice site within canonical intron 10; see alignment below between SEQ ID NO:156 and SEQ ID NO:166, showing that SEQ ID NO:156 is 100% complementary to the 18 nucleotides immediately upstream of alternative exon 11, 176 nucleotides upstream of canonical exon 11 and 1633 nucleotides downstream of the 3’ end of canonical exon 10) (required by claims 143-144).
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Du teaches methods of correcting splicing of an alternatively-spliced mutant gene by designing and administering to cells AMOs 100% complementary to a sequence comprising the alternative splice site whose aberrant splicing results in inclusion of an alternative exon and nonsense-mediated decay of the processed mRNA. While Du does not teach that the target gene is hSYNGAP1, given that Du does teach that this AMO design is effective in correcting splicing at multiple different alternative splicing sites, it would have been obvious to a person of ordinary skill in the art at the time of filing that the methods of Du could be modified to correct splicing in other genes which contain 3’ alternative splice sites within intronic sequences, by modifying the nucleotide sequences of the AMOs of Du to instead be 100% complementary to a sequence comprising the 3’ alternative splice site whose repression is desired. A 25-mer AMO of Du, so modified to target the 3’ alternative splice site of hSYNGAP1 taught by Prchalova, would comprise the sequence of SEQ ID NO:166. The truncated protein resulting from the alternative splicing of hSYNGAP1 taught by Prchalova would lack the 1,379 C-terminal amino acids of SYNGAP1. Chen teaches that the C-terminus of SYNGAP1 comprises domains essential for the proper localization and function of SYNGAP1 in neurons, such as the Pro-rich and QTRV domains, and that the C-terminal 1379 amino acids of SYNGAP1 comprise a portion of the central Ras-GTPase domain (Chen Fig. 3; pages 896-897). Given the teachings of Chen, it would be obvious to a person of ordinary skill in the art at the time of filing that repression of alternative splicing of intron 10 of hSYNGAP1, through designing AMOs of Du to be 100% complementary to the 3’ alternative splice site within intron 10, would promote expression of a target protein (full-length SYNGAP1), providing enhanced binding affinities to neuronal proteins and ensuring the inclusion of the full sequence of the Ras-GTPase catalytic domain of SYNGAP1. Such modulation of alternative splicing of hSYNGAP1 would be beneficial for in vitro studies of protein-protein interactions of SYNGAP1 and neuronal proteins, and for in vitro studies of SYNGAP1 catalytic activity.
Claim(s) 126, 134, 138-139 is/are rejected under 35 U.S.C. 103 as being unpatentable over Du (2007; provided with IDS filed by Applicant 03/14/2022), as evidenced by Coutinho (2005; provided with IDS filed by Applicant 03/14/2022), Khorkova (2017; provided with IDS filed by Applicant 04/17/2024), and Kralovicova (2016; provided with IDS filed by Applicant 03/14/2022), in view of Prchalova (2017; provided by Applicant with IDS filed 04/17/2024) and Chen (1998), as applied to claim 126 above, and further in view of Khorkova (2017; provided with IDS filed by Applicant 04/17/2024).
The teachings of Du, Coutinho, Kralovicova, Prchalova, and Chen can be combined to render obvious the limitations of claim 126.
However, Du does not teach that antisense morpholino oligonucleotides (AMOs) comprise at least one modified sugar moiety.
Khorkova teaches that 2’-O sugar modifications are beneficial for ASOs.
Regarding claims 138-139, Khorkova teaches that ASOs comprising 2’-O-methyl, 2’-Fluoro, or 2’-O-methoxyethyl sugar modifications exhibit “improved RNA/DNA binding affinity, and bioavailability, and decreased immunostimulatory effects and toxicity” (page 250; Fig. 2).
Given the benefits of 2’-O sugar modifications in ASOs, as taught by Khorkova, it would have been obvious for a person of ordinary skill in the art at the time of filing to modify the AMOs taught by Du with 2’-O sugar modifications—including 2’-O-methyl, 2’-O-Fluoro, or 2’-O-methoxyethyl—in order to improve binding affinity and decrease toxicity of the AMOs in the in vitro methods of Du.
Response to Arguments
Applicant's arguments filed 12/04/2025 have been fully considered but they are not persuasive.
Applicant argues that an artisan would have no motivation to modify the ASO of Du to be 100% complementary to a sequence comprised in instant SEQ ID NO:166 because instant SEQ ID NO:166 does not comprise the cryptid donor site found in the affected patients, but not healthy controls, of Prchalova, and that targeting an ASO to a sequence in instant SEQ ID NO:166 would not correct the alternative splicing of exon 10 found in affected patients but not healthy controls; instant SEQ ID NO:166 instead comprises the alternative 3’ splice acceptor site which drives inclusion of alternative exon 11 in both healthy subjects and patients in Prchalova, wherein Prchalova teaches that “[t]he inclusion of [alternative exon 11] results in premature termination, and the biological meaning of this alternative splicing event is unclear” (page 6 of Prchalova; Applicant’s arguments pages 13-15). Applicant indicates thus that the teaching of Prchalova that the function of the alternative splicing of exon 11 is unknown would provide no motivation to an artisan to target an ASO, such as a modified version of the ASO of Du, to the alternative 3’ splice acceptor site. However, the methods of Prchalova consist of karyotyping and microarray analysis, searches of public databases and literature, and RT-PCR with SYNGAP1 cDNA primers (page 4). The methods of Prchalova could not reasonably be assumed to be capable of identifying novel functions of splice variants. The teaching of Prchalova that this alternative splice variant exists in nature, in both healthy and diseased subjects, and its function is unknown would be a motivation for an artisan to identify a biological function or meaning of the alternative splicing event. The antisense oligonucleotide design of Du, modified to be 100% complementary to a sequence comprising the SYNGAP1 alternative 3’ splice acceptor site, would be obvious to use in a method of modulating the alternative splicing of exon 11 in order to determine whether any biological function or meaning of this alternative splicing exists.
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.
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18299956:
Claims 126-128,130 and 134-146 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 2-24 of copending Application No. 18299956 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the copending application claims a method of treating a disease by means of a method of modulating expression of a target protein, wherein the methods require administration of a composition whose claimed limitations are broader than those of the instant claims, but wherein the instant claimed compositions are considered specific species of the broader copending claims.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. This rejection is maintained.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/AFRICA M MCLEOD/ Examiner, Art Unit 1635
/KIMBERLY CHONG/Primary Examiner, Art Unit 1636