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 .
Election/Restrictions
Applicant’s election without traverse of group I comprising claims 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 with species election of amino acid position 2019, Formula I at position X2, and unmodified sugars at positions X1 and X3 in the reply filed on November 24, 2025 is acknowledged.
Status of Claims
Claims 1, 3, 10-11, 14-17, 19-20, 28, 103, 107, 129, 138, 145, and 147 are currently pending in the instant application. Claims 103, 107, and 147 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Accordingly, claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are under examination on the merits in the instant application.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on November 8, 2023 has been considered by the examiner. Note that NPL Citation No. C62 is considered only insofar as its English language title and abstract at page 486.
Specification
The disclosure is objected to because of the following informalities:
The non-black, light colored font for text in column 4 of Table 5 in the substitute specification makes reading difficult. Note that the disclosure of the specification must be clearly legible and “the USPTO strongly recommends use of a black colored font for text on a white background.” See MPEP §608.01. Appropriate correction is required.
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.
Claims 1, 3, 10-11, and 14-17 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Klein et al. (WO 2016/097212 A1, applicant’s citation).
Klein discloses a method of editing/correcting the G2019S mutation in the LRRK2 transcript caused by “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) for the treatment of Parkinson’s disease, wherein the method comprises contacting a human cell in vivo with a therapeutic antisense oligonucleotide targeting the LRRK2 G2019S mutation, thereby resulting in the alteration of the “A” base to “I” base, consequently providing a normal allele comprising “G” base encoding glycine (G) instead of the mutated serine (S) in the cell thus treating the genetic disease where the alteration of the adenosine base in the target LRRK2 sequence “will bring about a (potentially) beneficial change”, wherein the antisense oligonucleotide is linked to “the recruiting portion” that “recruits ADAR activity, to edit an A to I conversion in the target RNA”. See pages17-21, 24-27, 38-40; claim 28.
Klein teaches that human ADARs including “hADAR1 and hADAR2” are expressed in humans and that the “cells are treated ex vivo and are then introduced into a living organism” for providing treatment. See pages 16-19.
Accordingly, claims 1, 3, 10-11, and 14-17 are described by Klein et al.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Turunen et al. (US 2019/0218552 A1) as evidenced by Jaenisch et al. (US 2012/0192301 A1).
It is noted that the “alternative nucleotide” claimed in claims 19 and dependent claims thereof is described to read on alternative sugars such as LNA and UNA as well as alternative nucleobases such as 5-methylcytosine. See pages 24-25 and 107-108.
Turunen discloses a method of editing LRRK2 mutation, “G6055A mutation”, in a cell of a subject for treating a genetic disease such as Parkinson’s disease via “the specific deamination of a target adenosine present in the target RNA sequence to an inosine”, wherein the method comprises administering to the cell comprising endogenous ADAR enzyme an antisense oligonucleotide comprising a central triplet comprising a second base (“C”) that is opposite of the target adenosine, wherein the central triplet does not have a 2’-O-methyl modification but rather at least one nucleotide “comprises a sugar modification and/or a base modification” such as unlocked nucleic acid (UNA) or locked nucleic acid (LNA) or 5-methylcytosine, wherein the oligonucleotide comprises at least 4 consecutive phosphorothioate linkages in the 5’ and 3’ termini and the remaining nucleotides are 2’-O-methyl modified. See paragraphs 0011-0014, 0038-0040, 0082, 0096-0101; claims 1-19; Figures 1-2.
Turunen teaches that cells can be contacted with the antisense oligonucleotide ex vivo and “are then introduced into a living organism” for treatment. See paragraph 0075.
Turunen teaches that use of an antisense oligonucleotide that further comprises an ADAR recruitment portion that “acts in recruiting a natural ADAR enzyme present in the cell” is known in the art. See paragraph 0008.
Turunen does not expressly disclose the nexus between the LRRK2 “G6055A mutation” and “Parkinson’s disease”, a genetic disease that is taught to be treated. However, it was an art-recognized, scientific fact that the “G6055A mutation” that is taught to be edited in Turunen is a mutant SNP (“rs34637584”) in the LRKK2 gene, wherein the SNP results in the G2019S LRRK2 mutant allele, which causes Parkinson’s disease (PD) as evidenced by the teachings of Jaenisch. See paragraph 0008 disclosing that “the LRRK2 mutation G2019S has been suggested to play an important role in PD”, wherein the “SNP responsible for this missense mutation in patients is annotated as rs34637584 in the human genome, and is a G to A substitution at the genomic level (6055G>A).”
Accordingly, claims 1, 3, 10-11, 14-17, 19, 129, and 138 are described by Turunen et al. as evidenced by the scientific knowledge as evidenced by Jaenisch et al.
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.
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.
Claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are rejected under 35 U.S.C. 103 as being unpatentable over Turunen et al. (US 2019/0218552 A1) in view of Li et al. (Biochemistry, 2006, 45:4141-4152) and Jaenisch et al. (US 2012/0192301 A1).
Turunen discloses a method of editing LRRK2 mutation, “G6055A mutation”, in a cell of a subject for treating a genetic disease such as Parkinson’s disease via “the specific deamination of a target adenosine present in the target RNA sequence to an inosine”, wherein the method comprises administering to the cell comprising endogenous ADAR enzyme an antisense oligonucleotide comprising a central triplet comprising a second base (“C”) that is opposite of the target adenosine, wherein the oligonucleotide comprises at least 4 consecutive phosphorothioate linkages in the 5’ and 3’ termini and the remaining nucleotides are 2’-O-methyl modified. See paragraphs 0011-0014, 0038-0040, 0082, 0096-0101; claims 1-19; Figures 1-2.
Turunen teaches that cells can be contacted with the antisense oligonucleotide ex vivo and “are then introduced into a living organism” for treatment. See paragraph 0075.
Turunen teaches that use of an antisense oligonucleotide that further comprises an ADAR recruitment portion that “acts in recruiting a natural ADAR enzyme present in the cell” is known in the art. See paragraph 0008.
Turunen exemplifies an oligonucleotide (“ADAR60-7”) having the triplex (e.g., YXZ) that has ribosyl moiety modified with 2’-F, which is “small enough not to cause steric interference with ADAR2” and is useful to “protect the AON from nucleases”. See paragraph 0110. See also the modifications in “ADAR60-7” disclosed in Figure 2 as reproduced below, wherein “*” represents phosphorothioate linkages and “(ucg)” represents 2’-fluoro RNA modified nucleotides for the triplet comprising the “C” base that is opposite of the target “A” base.
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Turunen does not teach that the “C” base in the 2’-F modified RNA in the triplet “(ucg)” has the arabinose ring structure in Formula I, thereby forming 2’-fluoro-arabinonucleic acid (FANA).
Li teaches that 2’-fluoro-arabinonucleic acid (FANA) analogue “displays increased RNA affinity” compared to RNA or DNA such that “the observed trend for the stability of heteroduplexes between RNA and antisense oligonucleotides (AONs) is as follows: FANA > RNA > DNA > PS-DNA >> ANA”. See page 4141. See also the structure of FANA in Figure 1B as reproduced below.
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Jaenisch discloses that “the LRRK2 mutation G2019S has been suggested to play an important role in PD”, wherein the “SNP responsible for this missense mutation in patients is annotated as rs34637584 in the human genome, and is a G to A substitution at the genomic level (6055G>A).” See paragraph 0008.
It would have been obvious to one of ordinary skill in the art before the effective filing date to modify the method of Turunen for editing the LRRK2 “G6055A mutation” known to cause the LRRK2 G2019S mutant allele responsible for Parkinson’s disease by replacing the non-2’-O-methyl (e.g., 2’-F) modified RNAs in the triplet comprising a cytosine base at position 2 of the triplet with FANA in all three positions of the triplet or only at position 2 of the triplet. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success in order to enhance the stability and binding affinity of the “G6055A mutation”-editing antisense oligonucleotide, thereby providing more effective editing of the mutation-causing base in LRRK2, thereby correcting the LRRK2 G2019S mutant allele in a patient having Parkinson’s disease (PD) for treating the PD patient in view of the art-recognized knowledge pertaining to the genetic link between the LRRK2 G6055A mutation and PD as evidenced by Jaenisch, because use of a target base-editing antisense oligonucleotide comprising non-2’-O-methyl modified nucleotides in the triplet comprising a base to be edited at position 2 was an art-recognized methodology as evidenced by Turunen, who taught that 2’-F ribosyl moiety for the triplet is useful to “protect the AON from nucleases”, wherein the fluoro moiety at position 2 (2’-F) of the ribose sugar ring was known to not interfere with the ADAR-mediated base editing because it is “small enough not to cause steric interference with ADAR2”, and because the 2’-fluoro-arabinonucleic acid (FANA) analogue modification was known to have a higher stability and binding affinity compared to RNA as taught by Li. As such, in view of the benefits associated with FANA analogues as taught by Li, one of ordinary skill in the art would have reasonably incorporated one, two, or three FANA analogues into the non-2’-O-methyl modified (e.g., 2’-F) triple RNA sequence for correcting the LRRK2 G2019S mutant allele, wherein one of ordinary skill in the art would have pursued the finite number (seven) of readily identifiable positions (e.g., position 1 alone; position 2 alone; position 3 alone; positions 1-2; positions 1 and 3; positions 2-3; all positions 1-3) for FANA modification in the triplet, thereby arriving at the instantly claimed subject matter with a reasonable expectation of success.
In view of the foregoing, claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 taken as a whole would have been prima facie obvious before the effective filing date.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of U.S. Patent No. 11,453,878 B2 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘878 patent claims drawn to a method of treating a disorder in a subject in need thereof comprising administering an oligonucleotide that provides deamination of an adenosine in a target mRNA, wherein the oligonucleotide further comprises ADAR recruiting domains and comprises at least 20% 2’-O-methyl modified nucleotides and four terminal phosphorothioate linkages. It is noted that the “disorder” being treated in the ‘878 patent claims is defined to encompass “Parkinson’s disease”. See E152 in the ‘878 patent specification. It would have been obvious to design the oligonucleotide of the ‘878 patent claims to target the “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation of the LRRK2 gene for treatment of PD as taught by Klein, thereby treating the “disorder” encompassed by the ‘878 patent claims.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 17 of U.S. Patent No. 11,479,575 B2 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘575 patent claim drawn to a method of deaminating an adenosine in an mRNA in a cell comprising contacting the cell with an oligonucleotide having the structure satisfying the instantly claimed oligonucleotide. It would have been obvious to design the oligonucleotide of the ‘575 patent claim to target the “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 23-24 and 26 of U.S. Patent No. 12,031,131 B2 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘131 patent claims drawn to a method of treating a disorder in a subject in need thereof comprising administering an oligonucleotide that provides deamination of an adenosine in a target mRNA, wherein the oligonucleotide further comprises ADAR recruiting domains and comprises at least 20% 2’-O-methyl modified nucleotides and four terminal phosphorothioate linkages. It is noted that the “disorder” being treated in the ‘131 patent claims is defined to encompass “Parkinson’s disease”. See E152 in the ‘131 patent specification. It would have been obvious to design the oligonucleotide of the ‘131 patent claims to target the “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation of the LRRK2 gene for treatment of PD as taught by Klein, thereby treating the “disorder” encompassed by the ‘131 patent claims.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 17 of U.S. Patent No. 12,152,050 B2 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘050 patent claim drawn to a method of deaminating an adenosine in an mRNA in a cell comprising contacting the cell with an oligonucleotide having the structure satisfying the instantly claimed oligonucleotide. It would have been obvious to design the oligonucleotide of the ‘050 patent claim to target the “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein.
Claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 18-19 and 21 of U.S. Patent No. 12,173,285 B2 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over and overlap in scope with the ‘285 patent claim drawn to a method of treating a disorder comprising administering an oligonucleotide structure comprising “Formula I”, which is identical to “Formula I” claimed in the instant case, thereby satisfying the instantly claimed oligonucleotide, wherein the “disorder” being treated in the ‘285 patent claims is defined to encompass “Parkinson’s disease”. See E176 in the ‘285 patent specification. It would have been obvious to design the oligonucleotide of the ‘285 patent claim to target the “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein, thereby treating the “disorder” encompassed by the ‘285 patent claims.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 19-20 of U.S. Patent No. 12,448,620 B2 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘620 patent claims drawn to a method of treating a disorder in a subject in need thereof comprising administering an oligonucleotide that provides deamination of an adenosine in a target mRNA, wherein the oligonucleotide further comprises ADAR recruiting domains and comprises at least 20% 2’-O-methyl modified nucleotides and four terminal phosphorothioate linkages. It is noted that the “disorder” being treated in the ‘620 patent claims is defined to encompass “Parkinson’s disease”. See E152 in the ‘620 patent specification. It would have been obvious to design the oligonucleotide of the ‘620 patent claim to target the “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein, thereby treating the “disorder” encompassed by the ‘620 patent claims.
Claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 52 and 61 of copending Application No. 18/290,062 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation), Turunen et al. (US 2019/0218552 A1), and Li et al. (Biochemistry, 2006, 45:4141-4152).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘062 claims drawn to a method of editing LRRK2 for treating a disease comprising using an oligonucleotide targeting LRRK2 that is capable of providing ADAR-mediated adenosine to inosine alteration in the target mRNA, wherein the oligonucleotide forms a double-stranded structure by further comprising an ADAR recruiting sequence. It would have been obvious to design the oligonucleotide of the ‘062 claims to target the “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation was an art-recognized mutation in the LRRK2 target mRNA claimed in the ‘062 claims as taught by Klein. Furthermore, it would have been obvious to make and use the instantly claimed oligonucleotide in view of the combined teachings of Turunen and Li as explained in the §103 rejection above, which is fully incorporated by reference herein.
Claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 41 and 50 of copending Application No. 18/570,918 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation), Turunen et al. (US 2019/0218552 A1), and Li et al. (Biochemistry, 2006, 45:4141-4152).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘918 claims drawn to a method of editing an SNP in a target sequence for treating a disease comprising using an oligonucleotide targeting the SNP and further comprises an ADAR recruiting sequence. It would have been obvious to design the oligonucleotide of the ‘918 claims to target the SNP “rs34637584” associated with “the G to A mutation in exon 41 at position G6055” of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation (SNP “rs34637584”) of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein, thereby treating the “disease” encompassed by the ‘918 claims. Furthermore, it would have been obvious to incorporate at least one FANA modification into X1, X2, and X3 of the oligonucleotide used in the ‘918 claims in view of the combined teachings of Turunen and Li as explained in the §103 rejection above, which is fully incorporated by reference herein.
Claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 46 and 55 of copending Application No. 18/570,938 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation), Turunen et al. (US 2019/0218552 A1), and Li et al. (Biochemistry, 2006, 45:4141-4152).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘938 claims drawn to a method of editing an SNP in a target sequence for treating a disease comprising using an oligonucleotide targeting the SNP and further comprises an ADAR recruiting sequence. It would have been obvious to design the oligonucleotide of the ‘938 claims to target the SNP “rs34637584” associated with “the G to A mutation in exon 41 at position G6055” of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation (SNP “rs34637584”) of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein, thereby treating the “disease” encompassed by the ‘938 claims. Furthermore, it would have been obvious to incorporate at least one FANA modification into X1, X2, and X3 of the oligonucleotide used in the ‘938 claims in view of the combined teachings of Turunen and Li as explained in the §103 rejection above, which is fully incorporated by reference herein.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 74-75 of copending Application No. 18/927,268 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘268 claims drawn to a method of treating a disorder by deaminating an adenosine in a target mRNA comprising using an oligonucleotide that is capable of effecting ADAR-mediated adenosine to inosine alteration in the target mRNA. It is noted that the disorder encompassed by and claimed in the ‘268 claims is defined to read on Parkinson’s disease as evidenced by page 18 of the ‘268 specification. It would have been obvious to design the oligonucleotide of the ‘268 claims to target the SNP “rs34637584” associated with “the G to A mutation in exon 41 at position G6055” of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation (SNP “rs34637584”) of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein, thereby treating the “disorder” encompassed by the ‘268 claims.
Claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 24-25 and 27 of copending Application No. 18/941,793 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘793 claims drawn to a method of treating a disorder by deaminating an adenosine in a target mRNA comprising using an oligonucleotide that is capable of effecting ADAR-mediated adenosine to inosine alteration in the target mRNA, wherein the oligonucleotide of the ‘793 claims comprises “Formula I”, which is identical to “Formula I” claimed in the instant case, thereby satisfying the instantly claimed oligonucleotide. It is noted that the disorder encompassed by and claimed in the ‘793 claims is defined to read on Parkinson’s disease as evidenced by page 19 of the ‘793 specification. It would have been obvious to target the art-recognized PD-causing genetic mutation (SNP) in LRRK2 in view of the teachings of Klein, who taught making and using a base-editing oligonucleotide targeting the G6055A mutation (SNP “rs34637584”) of the LRRK2 gene for editing the G2019S mutation for PD treatment.
Claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 29-30 of copending Application No. 19/189,150 in view of in view of Klein et al. (WO 2016/097212 A1, applicant’s citation), Turunen et al. (US 2019/0218552 A1), and Li et al. (Biochemistry, 2006, 45:4141-4152).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘150 claims drawn to a method of editing a target mRNA comprising using an oligonucleotide that is capable of effecting ADAR-mediated adenosine to inosine alteration in the target mRNA. It would have been obvious to design the oligonucleotide of the ‘150 claims to target the SNP “rs34637584” associated with “the G to A mutation in exon 41 at position G6055” of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation (SNP “rs34637584”) of the LRRK2 gene for editing the pathogenic mutant base responsible for PD as taught by Klein. Furthermore, it would have been obvious to incorporate the FANA modification into X2 of the oligonucleotide used in the ‘150 claims in view of the combined teachings of Turunen and Li as explained in the §103 rejection above, which is fully incorporated by reference herein.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 80-81 of copending Application No. 19/296,642 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘642 claims drawn to a method of treating a disorder by deaminating an adenosine in a target mRNA comprising using an oligonucleotide that is capable of effecting ADAR-mediated adenosine to inosine alteration in the target mRNA. It is noted that the disorder encompassed by and claimed in the ‘642 claims is defined to read on Parkinson’s disease as evidenced by page 17 of the ‘642 specification. It would have been obvious to design the oligonucleotide of the ‘642 claims to target the SNP “rs34637584” associated with “the G to A mutation in exon 41 at position G6055” of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation (SNP “rs34637584”) of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein, thereby treating the “disorder” encompassed by the ‘642 claims.
Claims 1, 3, 10-11, 14-17, 19-20, 28, 129, 138, and 145 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 5-11, 15-27, and 30-41 of copending Application No. 19/479,642 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation), Turunen et al. (US 2019/0218552 A1), and Li et al. (Biochemistry, 2006, 45:4141-4152).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘642 claims drawn to a method of treating a genetic disorder via adenosine deaminase including ADAR1 and ADAR2 comprising using an antisense RNA oligonucleotide that is complementary to a target RNA. It would have been obvious to design the oligonucleotide of the ‘642 claims to target the SNP “rs34637584” associated with “the G to A mutation in exon 41 at position G6055” of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation (SNP “rs34637584”) of the LRRK2 gene for editing the pathogenic mutant base responsible for PD as taught by Klein. Furthermore, it would have been obvious to make and use the instantly claimed oligonucleotide comprising the FANA modification at X2 in view of the combined teachings of Turunen and Li as explained in the §103 rejection above, which is fully incorporated by reference herein.
Claims 1, 3, 10-11, 14-17, 19, 129, and 138 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 33 of copending Application No. 19/493,944 in view of Klein et al. (WO 2016/097212 A1, applicant’s citation).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘944 claim drawn to a method of editing a target adenosine in a target RNA comprising using an oligonucleotide that is capable of effecting ADAR-mediated adenosine to inosine alteration in the target RNA. It would have been obvious to design the oligonucleotide used in the ‘944 claim to target the “the G to A mutation in exon 41 at position G6055” (identified as “rs34637584”) of the LRRK2 gene, resulting in the G2019S mutation causing Parkinson’s disease (PD) because it was an art-recognized goal to make and use a base-editing oligonucleotide targeting the G6055A mutation of the LRRK2 gene for editing the pathogenic mutant base for treatment of PD as taught by Klein.
Conclusion
No claim is allowed.
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/DANA H SHIN/Primary Examiner, Art Unit 1635