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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 12/18/2025 has been entered.
Claim Status
In the submission, claims 49-52 have been cancelled. Claims 1, 11 and 21 have been amended. Claims 21, 23-26 and 28 remain withdrawn as being directed to un-elected invention. Accordingly, claims 1-2, 4-7, 10-11 and 20 are pending and under current examination.
Priority
The instant application is a national stage entry of PCT application PCT/US2020/029804, filed 04/24/2020. Acknowledgement is made of the applicant's claim for benefit to prior-filed U.S. provisional patent applications 62/839,336, which is filed 04/26/2019.
Status of Prior Rejection/Response to Arguments
The rejection to claims 51-52 under 35 U.S.C. §112(b) is withdrawn:
The cancellation of claims 51-52 render the rejection thereto moot. The rejection is withdrawn.
The rejection to claims 11 and 20 under 35 U.S.C. §102(a)(1)and 102(a)(2) over Lundberg et al. is maintained:
Applicant amends claim 11, asserts the incorporation of the limitations of previous claim 52, which limits the sequence encoding the first guide RNA is SEQ ID NO:4, and the sequence encoding the second guide RNA is SEQ ID NO:5, is sufficient to overcome the rejection (Remarks, p5).
Applicant’s argument is not found persuasive. Specifically, instant claim 11 is directed to a composition comprising a vector comprising a first guide RNA and a second guide RNA. Lundberg et al. teach a vector comprising one or more gRNA or one or more sgRNA (see parag 0006 and parag 00026). Lundberg et al. also teach promoters for guide RNAs (see parag 000208). Moreover, Lundberg et al. teach the sequence of gRNAs, wherein SEQ ID NO: 54611 is 100% identical to SEQ ID NO: 4 in instant claim, SEQ ID NO: 54498 is 100% identical to SEQ ID NO: 5 in instant claim (sequence alignment can be found on office action mailed 09/22/2025). Therefore Lundberg et al. anticipate instant claims. The rejection is maintained and modified necessitated by Applicant’s amendment.
The rejection to claims 1-2, 4-6, 10-11, 20 and 49-52 under 35 U.S.C. §103 over Lundberg et al. and Chamberlain et al. is maintained:
The rejection to claims 1-2, 4-7, 10-11, 20 and 49-52 under 35 U.S.C. §103 over Lundberg et al., Chamberlain et al. and Gray et al. is maintained:
The cancellation of claims 49-52 renders the rejection thereto moot. The rejection to claims 49-52 is withdrawn.
Regarding claims 1-2, 4-7, 10-11 and 20, Applicant’s amendment to claims 1 and 11 limits the sequence encoding the first guide RNA is SEQ ID NO:4, and the sequence encoding the second guide RNA is SEQ ID NO:5. Applicant asserts that neither Lundberg alone nor in combination with Chamberlain teaches or suggests selecting the specific gRNA sequences in combination as disclosed in the instant claims (Remarks, p7). Specifically, Lundberg only provides a long list of potential gRNAs, and screens them individually (Remarks, p6). Lundberg provides a laundry list of possible gRNAs to test. Lundberg did not test or demonstrate that using the specific combination of gRNAs claimed in the instant invention would provide a benefit over any of the other sequences disclosed in Lundberg. Lundberg does not provide any motivation or suggestion to select the sequences used in the instant claims (Remarks, p6). Furthermore, Applicant discloses an example to demonstrate that different combinations of gRNAs to knockdown specifically ATXN2 isoform variant 1 are not predictable, only certain pairs are effective at knocking down all isoforms while most specifically targets ATXN2 isoform variant 1 (Remarks, p8).
Applicant’s argument is fully considered but found not persuasive. Specifically, Applicant is reminded that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In instant case, Lundberg et al. teach the dual DSB-induced deletion strategy can involve excising the entire abnormal repeat expansion or a portion thereof in the ATXN2 gene by inducing two or more double stranded breaks at both sides of the repeat region with one or more CRISPR endonucleases and two or more sgRNAs (parag 0075), this teaching suggests using two gRNAs (e.g., a first and second gRNA) for targeting and knocking out ATXN2 gene. Lundberg et al. also teach one or more gRNA or one or more sgRNA for editing a ATXN2 gene; wherein the one or more gRNAs or sgRNAs comprise a spacer sequence selected from the group consisting of nucleic acid sequences in SEQ ID NOs: 5305 - 108,217 of the Sequence Listing” (parag 0035), this teaching suggests the potential gRNAs for targeting to ATXN2 gene. Though Lundberg et al. provide a long list of potential gRNAs, all these gRNAs target to a single gene (ATXN2 gene), one of ordinary skill in the art, based on their knowledge, would not just randomly pick two gRNAs for the gene editing, instead they would utilize general knowledge about gRNA design (i.e., define the target region, use the tools / algorithms which are capable of predicting gRNAs’ deleting efficiency and off-target effects) to pre-screen the potential gRNAs, obtain a reasonable number of gRNA candidates to further combine and test gRNAs to optimize the gene knockout effect. Therefore one of ordinary skill in the art would have been inspired by Lundberg et al.’s teaching and combine with general knowledge to obtain the pair of gRNAs for knocking down/knocking out ATXN2 gene as recited in instant application. Moreover, generally it is common practice to design and utilize multiple gRNAs for the gene editing in the art, therefore is not considered novel for designing two gRNAs as a combination for target gene fragments.
Regarding Applicant’s argument that only certain pairs of gRNAs are effective for the gene knockdown/knockout therefore the result is unpredictable, Applicant is reminded that it is not required that the expectation of success be a certainty; only one that is reasonable to a person of ordinary skill. In re Longi, 759 F.2d 887, 897 (Fed. Cir. 1985) (“Only a reasonable expectation of success, not absolute predictability, is necessary fora conclusion of obviousness”). In instant case, Lundberg et al. teach dual DSB-induced deletion strategy can involve excising the entire abnormal repeat expansion or a portion thereof in the ATXN2 gene by inducing two or more double stranded breaks at both sides of the repeat region with one or more CRISPR endonucleases and two or more sgRNAs (parag 0075), also provide
the list of gRNA candidates, one of ordinary skill in the art, with the knowledge that different gRNAs target to different DNA fragment (i.e., different regulatory elements or protein-encoding sequence) will result in deletion of different portion of the gene and different level of protein expression, would have reasonable expectation of success for selecting certain pair of gRNAs which efficiently knockout/knockdown the protein. The rejection is maintained and modified as necessitated by the claim amendments.
Modified 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 11 and 20 stand rejected under 35 U.S.C. 102(a)(1)and 102(a)(2) as being anticipated by Lundberg et al. (WO 2018/154462 A2). The rejection is modified as necessitated by Applicant’s amendment.
Lundberg et al. provides materials and methods for treating a patient with one or more conditions or disorders associated with ATXN2 whether ex vivo or in vivo (Abstract).
Regarding claim 11, Lundberg et al. teach ex vivo and in vivo methods for creating permanent
changes to the genome by deleting and/or correcting the trinucleotide repeat expansion or replacing one or more nucleotide bases, or one or more exons and/or intrans within or near the Spinocerebellar Ataxia Type 2 Protein (ATXN2) gene, as well as components and compositions, and vectors for performing such methods (parag 0006). The methods comprise introducing one or more gRNA or one or more sgRNA (parag 00026). The one or more gRNA or one or more sgRNA can be encoded in an AAV vector particle (parag 0028). Lundberg et al. teach using two gRNAs or sgRNAs: for example, the dual DSB-induced deletion strategy can involve excising the entire abnormal repeat expansion or a portion thereof in the ATXN2 gene by inducing two or more double stranded breaks at both sides of the repeat region with one or more CRISPR endonucleases and two or more sgRNAs. Moreover, Lundberg et al. teach promoters for expressing small RNAs, including guide RNAs used in connection with Cas endonuclease, various promoters such as RNA polymerase III promoters, including for example U6 and H1, can be advantageous (parag 000208). This teaching reads on the promoters for the gRNAs. Lundberg et al. further teach one or more gRNA or one or more sgRNA for editing a ATXN2 gene; wherein the one or more gRNAs or sgRNAs comprise a spacer sequence selected from the group consisting of nucleic acid sequences in SEQ ID NOs: 5305 - 108,217 of the Sequence Listing (parag 00035), wherein the SEQ ID NO: 54611 is 100% identical to SEQ ID NO: 4 in instant claim, wherein the SEQ ID NO: 54498 is 100% identical to SEQ ID NO: 5 in instant claim. This teaching anticipates the composition as recited in instant claim.
Regarding claim 20, following the discussion above, Lundberg et al. teach ex vivo and in vivo methods for gene editing of Spinocerebellar Ataxia Type 2 Protein (ATXN2) gene, as well as components and compositions, and vectors for performing such methods (see parag 0006). The method can comprise introducing into the cell one or more DNA endonucleases to effect one or more SSBs or DSBs within or near the ATXN2 gene or ATXN2 regulatory elements (parag 0008). The one or more DNA endonuclease can be encoded in an AAV vector particle (parag 0028). The DNA endonuclease can be a Cas9 or Cpfl endonuclease(parag 00032). The methods can further comprise introducing one or more gRNA or one or more sgRNA (parag 00026). The one or more gRNA or one or more sgRNA can be encoded in an AAV vector particle (parag 0028). In some examples, vectors can be capable of directing the expression of nucleic acids to which they are operatively linked (parag 000203). The term "operably linked" means that the nucleotide sequence of interest is linked to regulatory sequence(s) in a manner that allows for expression of the nucleotide sequence. The term "regulatory sequence" is intended to include, for example, promoters, enhancers and other expression control elements (parag 000204). The teaching reads on the composition comprising a vector having a nuclease, two gRNAs, as well as (the first and second) promoters for the two gRNAs and (the third) promoter for said nuclease (e.g., Cas9), as recited in instant claim.
Modified 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 text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 1-2, 4-6, 10-11 and 20 stand rejected under 35 U.S.C. 103 as being unpatentable over Lundberg et al. (WO 2018/154462 A2) in view of Chamberlain et al. (US 2017/0362635 A1). The rejection is modified as necessitated by Applicant’s amendment.
Lundberg et al. provides materials and methods for treating a patient with one or more conditions or disorders associated with ATXN2 whether ex vivo or in vivo (Abstract).
Regarding claim 1, Lundberg et al. teach ex vivo and in vivo methods for creating permanent
changes to the genome by deleting and/or correcting the trinucleotide repeat expansion or replacing one or more nucleotide bases, or one or more exons and/or intrans within or near the Spinocerebellar Ataxia Type 2 Protein (ATXN2) gene, as well as components and compositions, and vectors for performing such methods (parag 0006). The method can comprise introducing into the cell one or more DNA endonucleases to effect one or more SSBs or DSBs within or near the ATXN2 gene or ATXN2 regulatory elements (parag 0008). The one or more DNA endonuclease can be encoded in an AAV vector particle (parag 0028).In some examples, vectors can be capable of directing the expression of nucleic acids to which they are operatively linked (parag 000203). The term "operably linked" means that the nucleotide sequence of interest is linked to regulatory sequence(s) in a manner that allows for expression of the nucleotide sequence. The term "regulatory sequence" is intended to include, for example, promoters, enhancers and other expression control elements (parag 000204). This teaching reads on a vector comprising Cas9 and the promoter drives the expression of the Cas9 in instant claim.
Lundberg et al. teach the methods can further comprise introducing one or more guide RNA (gRNA) or one or more single guide RNA (sgRNA) (parag 00026). The one or more gRNA or one or more sgRNA can be encoded in an AAV vector particle (parag 0028). For expressing small RNAs, including guide RNAs used in connection with Cas endonuclease, various promoters such as RNA polymerase III promoters, including for example U6 and H1, can be advantageous (parag 000208). This teaching indicates a vector comprising one or more gRNAs (e.g., two gRNAs), which can have promoter for expressing said gRNAs. Lundberg et al. teach one or more gRNA or one or more sgRNA for editing a ATXN2 gene; wherein the one or more gRNAs or sgRNAs comprise a spacer sequence selected from the group consisting of nucleic acid sequences in SEQ ID NOs: 5305 - 108,217 of the Sequence Listing (parag 00035), wherein the SEQ ID NO: 54611 is 100% identical to SEQ ID NO: 4 in instant claim, SEQ ID NO: 54498 is 100% identical to SEQ ID NO: 5 in instant claim.
Instant claim differs from Lundberg et al. is instant claim specifically limits that the composition has gRNAs and nuclease in the separate vectors. However, this modification is prima facie obvious in view of Chamberlain et al..
Chamberlain et al. teach pharmaceutical compositions including a muscle-specific nuclease cassette, one or more guide RNA cassettes, and a delivery system for delivery of the muscle-specific nuclease cassette and the one or more gRNA cassettes (Abstract).
Regarding claim 1, Chamberlain et al. teach strategies for creating a dystrophin mRNA carrying an ORF by removing the mdx4 cv TAA premature stop codon (see figure 1). Panel A depicts strategy 1 (Δ5253), which utilizes both dual- and single-AAV vector approaches to target intrans 51 and 53 to direct excision of exons 52 and 53 (panel B). Panel C depicts strategy 2 (53*), which utilizes a dual-vector approach to target exon 53 on either side of the stop codon, relying on homology directed repair (HDR) utilizing a WT DNA template, or non-homologous end joining (NHEJ) to generate either full-length WT dystrophin (panel D) or a partial in-frame deletion of exon 53 (parag 0006). For the dual-AAV vectors, the nuclease (spCas9) and gRNA are in separate vectors.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Lundberg et al.’s AAV vector(s) comprising nuclease and gRNAs for gene editing of ATXN2 gene, and produce a dual-vector with gRNA and nuclease in the separate vectors as taught by Chamberlain et al.. The skilled artisan would have been motivated to make a dual-vector for the gene editing since Chamberlain et al. teach that a dual-vector approach may currently offer more flexibility in terms of allowing for variations in the ratio between administered nuclease versus targeting components, which may prove important for efficiency (parag 0050). There would be a reasonable expectation of success of having a dual-vector with gRNAs and nuclease in the separate vectors since Chamberlain et al. teach the strategy of the dual-vector system (see figure 1).
Regarding claim 2, Chamberlain et al. teach using two vectors can allow one to vary the ratios of the components. A constant total vector dose can be used, but 5 ratios may be tested, Cas9: sgRNA vector at 1:9; 2.5:7.5, 5:5, 7.5:2.5, and 9:1. If the ratio of Cas9 to sgRNA proves important, the idea of testing regulatory cassettes with stronger/weaker activity to enable adjusting the ratios within a single vector can be revisited (parag 0084).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Lundberg et al.’s AAV vector(s) comprising nuclease and gRNAs for gene editing of ATXN2 gene, and produce a dual-vector with gRNA and nuclease in the separate vectors, further make the amount of the first vector to the second vector at different ratios (e.g., 1:9; 2.5:7.5; 5:5), as taught by Chamberlain et al.. The skilled artisan would have been motivated to make a dual-vector have a ratio of the first vector to the second vector at different ratios (e.g., 1:9; 2.5:7.5; 5:5) to test the efficiency, since Chamberlain et al. teach a dual-vector approach may currently offer more flexibility in terms of allowing for variations in the ratio between administered nuclease versus targeting components, which may prove important for efficiency (parag 0050). There would be a reasonable expectation of success of having a dual-vector have a ratio of the first vector to the second vector at different ratios (e.g., 1:9; 2.5:7.5; 5:5), since Chamberlain et al. teach testing the ratio of Cas9: sgRNA vector at 1:9; 2.5:7.5, 5:5, 7.5:2.5, and 9:1, and an artisan knows how to test and optimize the ratio to obtain the best efficiency.
Regarding claim 4, Lundberg et al. teach the one or more DNA endonuclease can be encoded in an AAV vector particle, the one or more gRNA or one or more sgRNA can be encoded in an AAV vector particle (parag 0028). Lundberg et al. also teach AAV vector serotypes be matched to target cell types (parag 000351). AAV vector serotypes refers to the type of capsid protein which is considered as a sequence isolated or derived from an AAV.
Regarding claims 5 and 6, Lundberg et al. teach guide RNAs used in connection with Cas endonuclease, various promoters such as RNA polymerase III promoters, including for example U6 and HI (parag 000208). This teaching indicates the promoter for gRNA (e.g., herein the first and second promoter for first and second gRNA) comprises U6.
Regarding claim 10, Lundberg et al. teach pharmaceutically acceptable carriers used for their method (see p72, part III).
Regarding claim 11, following the discussion above, Lundberg et al. teach ex vivo and in vivo methods for creating permanent changes to the genome by deleting and/or correcting the trinucleotide repeat expansion or replacing one or more nucleotide bases, or one or more exons and/or intrans within or near the Spinocerebellar Ataxia Type 2 Protein (ATXN2) gene, as well as components and compositions, and vectors for performing such methods (parag 0006). The methods comprise introducing one or more gRNA or one or more sgRNA (parag 00026). The one or more gRNA or one or more sgRNA can be encoded in an AAV vector particle (parag 0028). Lundberg et al. teach using two gRNAs or sgRNAs: for example, the dual DSB-induced deletion strategy can involve excising the entire abnormal repeat expansion or a portion thereof in the ATXN2 gene by inducing two or more double stranded breaks at both sides of the repeat region with one or more CRISPR endonucleases and two or more sgRNAs. Moreover, Lundberg et al. teach promoters for expressing small RNAs, including guide RNAs used in connection with Cas endonuclease, various promoters such as RNA polymerase III promoters, including for example U6 and H1, can be advantageous (parag 000208). This teaching reads on the promoters for the gRNAs. Lundberg et al. further teach one or more gRNA or one or more sgRNA for editing a ATXN2 gene; wherein the one or more gRNAs or sgRNAs comprise a spacer sequence selected from the group consisting of nucleic acid sequences in SEQ ID NOs: 5305 - 108,217 of the Sequence Listing (parag 00035), wherein the SEQ ID NO: 54611 is 100% identical to SEQ ID NO: 4 in instant claim, wherein the SEQ ID NO: 54498 is 100% identical to SEQ ID NO: 5 in instant claim.
Regarding claim 20, following the discussion above, Lundberg et al. teach ex vivo and in vivo methods for gene editing of Spinocerebellar Ataxia Type 2 Protein (ATXN2) gene, as well as components and compositions, and vectors for performing such methods (see parag 0006). The method can comprise introducing into the cell one or more DNA endonucleases to effect one or more SSBs or DSBs within or near the ATXN2 gene or ATXN2 regulatory elements (parag 0008). The one or more DNA endonuclease can be encoded in an AAV vector particle (parag 0028). The DNA endonuclease can be a Cas9 or Cpfl endonuclease(parag 00032). The methods can further comprise introducing one or more gRNA or one or more sgRNA (parag 00026). The one or more gRNA or one or more sgRNA can be encoded in an AAV vector particle (parag 0028). In some examples, vectors can be capable of directing the expression of nucleic acids to which they are operatively linked (parag 000203). The term "operably linked" means that the nucleotide sequence of interest is linked to regulatory sequence(s) in a manner that allows for expression of the nucleotide sequence. The term "regulatory sequence" is intended to include, for example, promoters, enhancers and other expression control elements (parag 000204). The teaching reads on the composition comprising a vector having a nuclease, two gRNAs, as well as (the first and second) promoters for the two gRNAs and (the third) promoter for said nuclease (e.g., Cas9), as recited in instant claim.
Claims 1-2, 4-7, 10-11 and 20 stand rejected under 35 U.S.C. 103 as being unpatentable over Lundberg et al. (WO 2018/154462 A2) in view of Chamberlain et al. (US 2017/0362635 Al), further in view of Gray et al. (Human Gene Therapy, 2011).
The teaching of Lundberg et al. in view of Chamberlain et al. is set forth above.
Regarding claim 7, Lundberg et al. in view of Chamberlain et al. do not teach the second promoter comprises or consists of a Mecp2 promoter or a Synl promoter. However, it is prima facie obvious in view of Gray et al..
Gray et al. teach two novel promoters are now available to drive long-term neural expression: a novel version of the CBA promoter, called CBh, which provides long-term transgene expression in all cell types seen with the CBA or CMV promoter, at levels matching or exceeding each; and a truncated 229-bp promoter fragment from the murine methyl-CpG-binding protein-2 (MeCP2) gene that can drive
neuronal expression (see p1144, left column).
Regarding claim 7, Gray et al. teach MeCP2 promoter has low and mostly neuronal expression within the CNS (Abstract).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Lundberg et al.’s AAV vector for gene editing of ATXN2, and use a promoter of MeCP2 to drive the nuclease expression as taught by Gray et al.. The only difference between instant claim and Lundberg et al.’s AAV vector is instant claim use MeCP2 promoter to drive the nuclease expression while Lundberg et al. used U6 or HI (see parag 000208) promoter. Given that ATXN2 gene mutations cause Spinocerebellar ataxia type 2 (SCA2), which is a neurological disease, one of ordinary skill in the art would have substitute Lundberg et al.’s U6 promoter which is expressing in all cell types, and use a neuron-specific promoter to increase the neuronal expression specificity. This simple substitution of one known element (MeCP2 promoter) for another known element (U6 promoter) is likely to be obvious when predictable results are achieved. See KSR International Co. v. Teleflex Inc., 550 U.S. 398, 415-421, USPQ2d 1385, 1395 — 97 (2007) (see MPEP § 2143, B.).
Conclusion
No claims are allowed.
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/Q.G./Examiner, Art Unit 1633
/FEREYDOUN G SAJJADI/Supervisory Patent Examiner, Art Unit 1699