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 .
This office action is in response to the paper filed on 1/20/2026. Claims 1-54 were previously presented. No new claims are added.
Election/Restriction
Applicant’s election of the inventions of Group I (Claims 1-25, 32, and 51-54), without traverse, in the reply filed on 1/20/2026, is acknowledged.
Applicant elects the invention of Group I (Claims 1-25, 32, and 51-54) and the following species: SEQ ID NO: 2.
Claims 26-31 and 33-50 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to nonelected inventions, there being no allowable generic or linking claim.
Applicant is reminded that upon the cancelation of claims to a non-elected invention, the inventorship must be corrected in compliance with 37 CFR 1.48(a) if one or more of the currently named inventors is no longer an inventor of at least one claim remaining in the application. A request to correct inventorship under 37 CFR 1.48(a) must be accompanied by an application data sheet in accordance with 37 CFR 1.76 that identifies each inventor by his or her legal name and by the processing fee required under 37 CFR 1.17(i).
Application Status
This action is written in response to applicant’s correspondence received on 1/20/2026. Claims 1-25, 32, and 51-54 are currently under examination on the merits.
Priority
The application claims priority to provisional application 63/317,154 filed on 3/7/2022.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(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 12, 14, 15, 16, 17, 19, 20, 21, 22, 23 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Chamberlain et al. (WO 2020/061528, Published 3/26/2020), herein referred to as ‘Chamberlain’.
Regarding claim 12, Chamberlain teaches a polynucleotide wherein the first nucleotide sequence encodes a shRNA (see paragraph 0025). Chamberlain discloses that the first nucleotide sequence may be SEQ ID NO: 2, or a modified version of SEQ ID NO: 2 wherein the bold nucleotides in SEQ ID NO: 2 is replaced by any of SEQ ID NOs: 9-508 and the italicized nucleotides in SEQ ID NO: 2 is replaced by nucleotides complementary to those in SEQ ID NOs: 9-508 (see paragraph 0027). SEQ ID NO: 503 of Chamberlain and SEQ ID NO: 7 of the instant application has 100% identity.
Regarding claim 14, Chamberlain teaches a novel treatment approach for Angelman Syndrome through gene therapy by inhibiting the silencing of paternal UBE3A and enabling the expression of paternal UBE3A from its native regulatory elements (see paragraph 0006).
Regarding claim 15, Chamberlain discloses where Fig. 4 shows shRNAs knockdown of UBE3A-ATS and activate paternal UBE3A.
Regarding claim 16, Chamberlain teaches where the invention provides an expression vector comprising the polynucleotide and a promoter (see paragraph 0008).
Regarding claim 17, Chamberlain teaches where the selection of promoters can readily be accomplished. Suitable promoters can include animal transcriptional control regions, which exhibit tissue specificity and have been utilized in transgenic animals (see paragraph 0072). Chamberlain discloses the myelin basic protein gene control region which is active in oligodendrocyte cells in the brain (see paragraph 0072).
Regarding claim 19, Chamberlain teaches an example of a suitable promoter is an RNA polymerase II or III promoter, such as the U6 promoter (see paragraph 0072).
Regarding claim 20, Chamberlain teaches where a viral vector can be used in the invention (see paragraph 0071), and wherein the viral vector can be a lentiviral vector or an adeno-associated viral (AAV) vector (see paragraph 0059).
Regarding claim 21, Chamberlain teaches where AAVs may be readily selected from among any AAV serotype, including, without limitation, AAVs 1-10 (see paragraph
Regarding claim 22, Chamberlain discloses where the expression vector of claim 14 (an expression vector comprising the polynucleotide of claim 1 and a promoter), wherein the polynucleotide is a DNA polynucleotide (see claim 16 of Chamberlain).
Regarding claim 23, Chamberlain teaches where the viral particles comprising the desired coding sequences for the shRNA can be formulated for administration to a patient or human in need by any means suitable for administration. Such formulation involves the use of a pharmaceutically and/or physiologically acceptable vehicle or carrier, particularly one suitable for administration to the brain (see paragraph 0089).
Regarding claim 54, Chamberlain teaches a polynucleotide sequence where the first nucleotide sequence may be SEQ ID NO: 2. The first nucleotide sequence may also be a modified SEQ ID NO: 2 having the bold matches in SEQ ID NO: 2 replaced by any of SEQ ID NOs: 9-508 (see paragraph 0027). SEQ ID NO: 503 of Chamberlain and SEQ ID NO: 7 of the instant application have 100% identity. Furthermore, SEQ ID NO: 2 of Chamberlain discloses a stem-loop structure of SEQ ID NO: 2 consisting of 6 nucleotides ‘CTCGAG’ (see paragraph 0035). This stem-loop structure that is 6 nucleotides long has 100% identity with SEQ ID NO: 490 of the instant application.
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.
Claims 1, 2, 3, 4, 6, 7, 8, 9, 13, 32, and 53 are rejected under 35 U.S.C. 103 as being unpatentable over Chamberlain et al. (WO 2020/061528 A1, Published 3/26/2020) in view of Bofill-De Ros et al. (Guidelines for the optimal design of miRNA-based shRNAs, Methods 103, Pg. 157-166, 2016), as disclosed in the IDS.
Regarding claim 1, Chamberlain teaches the stem-loop sequence of SEQ ID NO: 2, ‘CTCGAG’, with 100% identity (see SEQ ID NO: 2 of Chamberlain).
Regarding claim 2, 3, 4, 6, 7, 8, 9, 13, 32, and 53, Chamberlain teaches some of the embodiments of these claims as described above, that being a polynucleotide sequence, an expression vector selected from AAV 1-10, and a pharmaceutical composition with a pharmaceutically acceptable carrier. Chamberlain further teaches a polynucleotide encoding a shRNA which targets the UBE3A-ATS, wherein the shRNA is capable of inhibiting the silencing of paternal UBE3A (see paragraph 0006). Chamberlain further teaches wherein the loop structure of SEQ ID NO: 2, ‘CTCGAG’, has 100% identity with SEQ ID NO: 490.
Chamberlain does not teach SEQ ID NO: 2 of the instant application, recited in claims 1 and 13.
Bofill-De Ros discloses a review article teaching a general methodology for designing shRNA against a target of interest (see abstract and introduction). Bofill teaches that shRNA comprise a perfect paired stem of at least 21 nucleotides in length and a loop of 6 nucleotides, wherein one of the 21 nucleotide stem strands is complementary to the target site (i.e. 21 nucleotides corresponding to the target site, followed by a 6 nucleotide loop sequences, followed by a 21 nucleotide sequence that is reverse complementary to the first 21 nucleotide sequence) (see section 3 - Processing/Maturation, section 7 – Instructions for shRNA design and cloning, and Fig. 2). Bofill further teaches that “selecting the target sequence … appears to be straightforward, as RNAi is famous for its ability to target ‘any’ sequence (see section 5 – Selection of target sequence).
It would have been obvious to one of ordinary skill in the art, at the time of the invention, to prepare an shRNA against human UBE3A-ATS capable of increasing the expression of paternal UBE3A as taught by Chamberlain, wherein the shRNA comprises SEQ ID NO: 2 of the instant application. It would have been obvious to combine prior art elements according to known methods to yield predictable results. SEQ ID NO: 2 of the instant application shares the same loop sequence (SEQ ID NO: 490 of the instant application) with 100% identity to the loop region of SEQ ID NO: 2 of Chamberlain with the difference being the 21 nucleotide target sequence and complimentary sequence. Bofill teaches that target selection is typically permissive, therefore, one would expect to reach the 21 nucleotide targeting sequence of the instant SEQ ID NO: 2 through routine experimentation. Furthermore, selecting the instant SEQ ID NO: 2 as the target sequence for the shRNA would have led to predictable results with a reasonable expectation of success because Chamberlin teaches a large number of shRNA target sequences could be used for successfully modifying the expression of paternal UBE3A.
In view of the foregoing, claims 1, 2, 3, 4, 6, 7, 8, 9, 13, 32, and 53 are rejected under 35 U.S.C. 103 as being prima facie obvious before the effective filing date.
Claims 10-11, and 24-25 are rejected under 35 U.S.C. 103 as being unpatentable over Chamberlain et al. (WO 2020/061528 A1, Published 3/26/2020) in view of Bofill-De Ros et al. (Guidelines for the optimal design of miRNA-based shRNAs, Methods 103, Pg. 157-166, 2016), Bi et al. (US 20210163555 A1, published 6/3/2021), and Borel et al. (Recombinant AAV as a Platform for Translating the Therapeutic Potential of RNA Interference, ASGCT Molecular Therapy, Volume 22, Issue 4, Pg. 692-701, 2014).
A polynucleotide sequence comprising SEQ ID NO: 2 of the instant application, as well as other embodiments including an expression vector and a pharmaceutical composition is taught by Chamberlain and Bofill as described above.
Both Chamberlain and Bofill does not teach where a pharmaceutical composition, wherein the polynucleotide sequence is contained within an expression vector, and wherein the expression vector is an AAV vector or a lentivirus vector (Chamberlain only teaches a pharmaceutical composition comprising of a polynucleotide and viral particles).
Bi teaches inhibitory RNAs that reduce the expression of P18, and viral vectors encoding such inhibitory RNAs (see paragraph 0008). Bi further teaches the invention relates to pharmaceutical compositions containing the inhibitory RNAs and viral vectors encoding the inhibitory RNAs (see paragraph 0008). Bi also disclose that UBE3A plays an important role in brain development and normal function, as UBE3A deficiency results in Angelman syndrome (AS). UBE3A expression and abnormal mTORC1 activation has been implicated in AS, therefore Bi aims to investigate the potential regulation of P18 levels by UBE3A (see paragraph 0006 and background section).
Borel teaches that the main limitations of RNAi therapeutics today are efficient delivery to organs other than the liver, longevity, and the associated innate immune response with each dose (see section ‘Limitations of Oligonucleotide-Mediated RNAi). Borel teaches vector-derived RNAi where a vector is used to express RNA transcripts (e.g. short-hairpin RNAs) could yield benefits such as lifelong persistence of the RNAi and the ability to achieve systemic delivery or tissue specificity (see conclusion).
It would have been obvious to one of ordinary skill in the art, at the time of the invention, to prepare a pharmaceutical composition comprising SEQ ID NO:2 of the instant application that further comprises the polynucleotide sequence and an expression vector. One would have been motivated to do so in order to generate a shRNA that can target UBE3A-ATS and modify parental UBE3A expression and wherein the challenges of administering shRNA are overcome as described in Borel. This routine experimentation would have yielded predictable results as Bi teaches administration of inhibitory RNAs with viral vectors and a pharmaceutical composition allows for the modification of P18 expression, a gene associated with UBE3A and the mTORC1 signaling pathway.
In view of the foregoing, claims 10-11, and 24-25 are rejected under 35 U.S.C. 103 as being prima facie obvious before the effective filing date.
Claims 5 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Chamberlain et al. (WO 2020/061528 A1, Published 3/26/2020) in view of Bofill-De Ros et al. (Guidelines for the optimal design of miRNA-based shRNAs, Methods 103, Pg. 157-166, 2016) and Nielsen et al. (Neuron-specific RNA interference using lentiviral vectors, The Journal of Gene Medicine, Volume 11, Issue 7, Pg. 559-569, 2009).
Regarding claims 5 and 18, Chamberlain and Bofill teach some embodiments of the claims as described above.
Chamberlain and Bofill do not teach wherein the expression vector has a neuron specific promoter that is neuron-specific enolase (NSE), synapsin I (Syn), or Ca2+/CaM-activated protein kinase II alpha (CaMKIIalpha).
Nielsen teaches neuron-specific RNA interference using lentiviral vectors where pol II promoters have been used to construct vectors for RNA interference. Nielsen teaches that, traditionally, viral vectors have been ubiquitously-expressing polymerase III promoters such as H1 and U6 to drive the expression of shRNAs because of a strict requirement of precise transcriptional initiation and termination to ensure that the transcript obtained is efficiently processed into functional RNAi molecules (see introduction). Because a precisely defined transcriptional start site is not known for the majority of Pol II promoters, the usefulness of these promoters in such shRNA-designs may be limited. However, recently, shRNAs have been embedded into a micro RNA context, thereby resembling the structure of naturally-occurring miRNA transcripts and, in this way, the endogenous miRNA processing machinery is used to obtain mature RNAi molecules, enabling the use of pol II promoters, including cell-specific promoters (see introduction).
Nielsen further teaches that with the use of a smiRNA vector with the neuron-specific enolase (NSE) promoter. Nielsen was able to express the smiRNA cassette in neurons only, and hence neuron-specific knockdown should be possible (see section ‘Neuron-specific knockdown’). When tested, Nielsen shows that the NSE promoter shown high neuronal specificity and is useful in reducing the off-target effects of AAV-mediated shRNA vectors, such as toxicity and cell death (see conclusion).
It would have been obvious to one of ordinary skill in the art, at the time of the invention, to combine the expression vector comprising a polynucleotide in a pharmaceutical composition with a neuron-specific promoter. One would expect a reasonable expectation of success as Nielsen shows that they developed a lentiviral vector with a NSE promoter that exhibits a knockdown of neuronal gene expression, but remain fully normal in adjacent glial cells (see conclusion). One would be motivated to do so in order to safely administer the polynucleotide, encoding an shRNA, to target cells while minimizing off target effects such as cell death and toxicity.
In view of the foregoing, claims 5 and 18 are rejected under 35 U.S.C. 103 as being prima facie obvious before the effective filing date.
Claims 51 and 52 are rejected under 35 U.S.C. 103 as being unpatentable over Chamberlain et al. (WO 2020/061528 A1, Published 3/26/2020) in view of Bofill-De Ros et al. (Guidelines for the optimal design of miRNA-based shRNAs, Methods 103, Pg. 157-166, 2016) and Bi et al. (US 20210163555 A1, published 6/3/2021) and Ge et al. (Minimal-length short hairpin RNAs: The relationship of structure and RNAi activity, RNA Society, Volume 16, Pg. 106-117, 2010).
Regarding claims 51 and 52, Chamberlain and Bofill, combined, teach the shRNA encoded by SEQ ID NO: 2 as described above.
Chamberlain and Bofill do not teach an shRNA encoded by a portion of SEQ ID NO: 2, wherein the portion of SEQ ID NO: 2 defined by bold nucleotides is shortened by one, two, three, or four nucleotides of either end of the first segment, and wherein the second segment defined by italicized nucleotides is shortened by one, two, or three nucleotides at either end of the italicized nucleotide.
Ge teaches where shRNAs typically consist of a stem of 19-29 base pairs and a loop of at least 4 nucleotides, however, shRNAs with 19-bp or shorter stems (sshRNAs) possess some unique structure-activity features that depend on whether the antisense strand is positioned 5’ or 3’ to the loop. Ge teaches where a series of active L sshRNAs have been identified with a stem length of 19 bp or less and a minimal loop (see discussion section). Ge further discloses where the finding that highly potent shRNAs can be designed with short stems and very small or no added loops suggest considerable flexibility on the part of the RNAi machinery, and is encouraging for the development of shRNA therapeutics where high potency is critical and small size is important to keep the cost of manufacture manageable (see discussion section).
It would have been obvious to one of ordinary skill in the art, at the time of the invention, to combine the teachings of Chamberlain and Bofill with the teachings of Ge to arrive at an shRNA encoded by a portion of SEQ ID NO: 2. Chamberlain and Bofill teach how one would arrive at SEQ ID NO: 2 through routine experimentation of shRNA design as described previously. Ge teaches how shRNA stem length can be shortened sub 19 nucleotides, which would account for SEQ ID NO: 2 being shortened by 1-4 nucleotides at either end of the bold first segment and italicized second segment. One would expect a reasonable expectation of success as Ge identifies shortened shRNAs can still maintain high potency. One would be motivated to do so as Ge teaches that highly potent and flexible, shortened shRNAs are encouraging for shRNA therapeutics where the small size is important to keep the cost of manufacture manageable. Regarding claim 52, the SEQ ID NOs claimed are modified versions of SEQ ID NO: 2 that have been shortened, which would have been discovered through the routine experimentation of shortening the stem sequence as described in Ge.
In view of the foregoing, claims 51 and 52 are rejected under 35 U.S.C. 103 as being prima facie obvious before the effective filing date.
Non-Statutory 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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Claims 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 13, 14, 15, 16, 17, 19, 20, 21, 22, 23, 24, 25, and 32 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 5, 6, 7, 8, 13, 24, and 25 of U.S. Patent No. US 12221609B2 in view of Bofill et al. (Guidelines for the optimal design of miRNA-based shRNAs, Methods 103, Pg. 157-166, 2016).
Although the claims at issue are not identical, they are not patentably distinct from each other because both claim a polynucleotide comprising a nucleotide sequence encoding a short hairpin RNA (shRNA), wherein the shRNA is capable of inhibiting the silencing of paternal UBE3A gene.
Bofill-De Ros discloses a review article teaching a general methodology for designing shRNA against a target of interest (see abstract and introduction). Bofill teaches that shRNA comprise a perfect paired stem of at least 21 nucleotides in length and a loop of 6 nucleotides, wherein one of the 21 nucleotide stem strands is complementary to the target site (i.e. 21 nucleotides corresponding to the target site, followed by a 6 nucleotide loop sequences, followed by a 21 nucleotide sequence that is reverse complementary to the first 21 nucleotide sequence) (see section 3 - Processing/Maturation, section 7 – Instructions for shRNA design and cloning, and Fig. 2). Bofill further teaches that “selecting the target sequence … appears to be straightforward, as RNAi is famous for its ability to target ‘any’ sequence (see section 5 – Selection of target sequence).
It is disclosed in the specification of the issued patent that the shRNA used may ameliorate the effects/target UBE3A-ATS. Both SEQ ID NO: 2 of the issued patent and the instant application targets a portion of the human UBE3A-ATS genomic sequence. Therefore, it would have been obvious, before the effective filing date of the invention, for one to obtain SEQ ID NO: 2 of the instant application through routine experimentation of finding shRNA target sequences in the issued patent, as taught by Bofill.
Furthermore, though the issued patent does not claim a neuron specific promoter in the expression vector, it does claim where the polynucleotide of claim 1 and a promoter are combined to form an expression vector, wherein the promoter is a U6 promoter.
Nielsen teaches neuron-specific RNA interference using lentiviral vectors where pol II promoters have been used to construct vectors for RNA interference. Nielsen teaches that, traditionally, viral vectors have been ubiquitously-expressing polymerase III promoters such as H1 and U6 to drive the expression of shRNAs because of a strict requirement of precise transcriptional initiation and termination to ensure that the transcript obtained is efficiently processed into functional RNAi molecules (see introduction). Because a precisely defined transcriptional start site is not known for the majority of Pol II promoters, the usefulness of these promoters in such shRNA-designs may be limited. However, recently, shRNAs have been embedded into a micro RNA context, thereby resembling the structure of naturally-occurring miRNA transcripts and, in this way, the endogenous miRNA processing machinery is used to obtain mature RNAi molecules, enabling the use of pol II promoters, including cell-specific promoters (see introduction).
Nielsen further teaches that with the use of a smiRNA vector with the neuron-specific enolase (NSE) promoter. Nielsen was able to express the smiRNA cassette in neurons only, and hence neuron-specific knockdown should be possible (see section ‘Neuron-specific knockdown’). When tested, Nielsen shows that the NSE promoter shown high neuronal specificity and is useful in reducing the off-target effects of AAV-mediated shRNA vectors, such as toxicity and cell death (see conclusion).
It would have been obvious, before the effective filing date of the instant application, to modify the expression vector that comprise a polynucleotide targeting UBE3A-ATS, as recited in the issued patent, with a neuron specific promoter, specifically neuron-specific enolase (NSE), to arrive at the claimed invention of the instant application. One would expect a reasonable expectation of success as Nielsen shows that they developed a lentiviral vector with a NSE promoter exhibits a knockdown of neuronal gene expression, but remain fully normal in adjacent glial cells (see conclusion). One would be motivated to do so in order to safely administer the polynucleotide, encoding an shRNA, to target cells while minimizing off target effects such as cell death and toxicity.
Conclusion
No claims are allowed.
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/D.T.Y./Examiner, Art Unit 1635
/RAM R SHUKLA/Supervisory Patent Examiner, Art Unit 1635