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 claims 135-152 (Group I) in the reply filed on 03/12/2026 is acknowledged.
Claims 153 and 154 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 03/12/2026.
Accordingly, claims 135-152 are pending and under consideration.
Priority
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. The earliest effective filing date to which the instant claim set is entitled is 12/22/2020.
Information Disclosure Statement
Receipt of information disclosure statements on 01/16/2024, 12/02/2024, 02/27/2025, 07/02/2025, 10/28/2025, and 12/23/2023 is acknowledged. The signed and initialed PTO-1449‘s have been mailed with this action.
Drawings
The drawings are objected to because:
With regard to Figures 6A and 6B, the text labeling the schematic illustrations depicted therein is of insufficient quality to be clearly legible. It would be remedial to increase the quality of this text such that it is clearly legible.
With regard to Figures 7A-7D, the keys labeling each graph are of insufficient quality to be clearly legible. Furthermore, the data labels do not facilitate clear interpretation of the data shown therein. It would be remedial to increase the quality of the keys as well as to ensure that the data labels facilitate clear interpretation of the data shown therein.
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Specification
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code (see paragraphs [0177], [0499], and [0502]). Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
The lengthy specification has not been checked to the extent necessary to determine the presence of all possible minor errors. Applicant’s cooperation is requested in correcting any errors of which applicant may become aware in the specification.
Claim Objections
Claims 135, 136, 144, and 147 are objected to because of the following informalities:
Claim 135 recites the acronym “DNMT” without first defining said acronym. While the term “DNMT” is known to correspond to the enzyme DNA methyltransferase (as disclosed at paragraph [0073] of the instant specification), it is nonetheless proper to define all acronyms at their first recitation. It would be remedial to define the acronym “DNMT” at instant claim 135, for example by reciting “DNA methyltransferase (DNMT).” This is merely an example set forth by the Examiner and is not intended to be limiting.
Instant claims 136 and 144 both recite a range of sequence identifiers, wherein the range of sequence of identifiers is preceded by “SEQ ID NO:”. However, given that multiple sequence identifiers are recited in said range, it is grammatically proper to precede the claimed range with “SEQ ID NOs:” (bolded and underlined emphasis added). It would be remedial to amend the instant claims to comport with standard grammatical conventions, as set forth above.
Furthermore, while both instant claims 136 and 144 recite a range of sequence identifiers, the recitation of claim 136 includes a colon following the phrase “selected from the group consisting of” that is not included at claim 144. For purposes of internal consistency, it would be remedial to amend the instant claims such that the colon following the phrase “selected from the group consisting of” is used consistently throughout the instant claim set.
Finally, instant claim 147 recites “the DNA binding domain comprises CRISPR-Cas protein bound to the guide polynucleotide,” which does not comport with standard grammatical and/or linguistic conventions, as there is no article preceding the claimed “CRISPR-Cas protein.” It would be remedial to amend the instant claim such that it comports with standard grammatical and/or linguistic conventions by reciting an article such as ”a” preceding the claimed “CRISPR-Cas protein.”
Appropriate correction is required.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 135-152 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 135 (from which all other claims directly or indirectly depend) is drawn to an epigenetic editor fusion protein comprising a first DNMT domain, a DNA binding domain, and a repressor domain, wherein the repressor domain is selected from a defined group of repressor domains and fragments thereof. The rejected claims thus comprise a set of epigenetic editors that themselves comprise any of the defined repressor domains, as well as any fragment thereof. Per paragraph [0071] of the instant specification, “repressor domain[s]” typically refer to a part of a transcription repression protein which provides for the transcriptional repressive effect on a target gene. Additionally, dependent claim 138 recites that the claimed repressor domain must function to specifically bind to an epigenetic effector protein in a cell comprising a target gene and direct the epigenetic editor to the target gene to effect an epigenetic modification. While dependent claim 139 further limits the claimed repressor domain to a smaller group of species, this claim also recites that fragments thereof may function as the claimed repressor domain. Thus, the instantly claimed repressor domain is broadly and functionally claimed such that the claims are drawn to a genus of epigenetic editor fusion proteins that are in part solely defined by the ability function to repress transcription by binding to an epigenetic effector protein and facilitating site-specific targeting.
With regard to the claimed “fragments thereof” of the instantly claimed repressor domains, the instant specification defines the term “fragment” to refer to a portion of a protein that has less than the full length of the protein and optionally maintains the function of the protein at paragraph [0060]. This definition necessarily encompasses fragments that do not maintain the function of the protein and would therefore not meet the structural/functional requirements of the claim. To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of a complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, and any combination thereof. The specification describes testing of candidate repression domains at paragraph [0504], disclosing fusion of candidate repression domains (identified and extracted from the full protein sequence) to a DNA-binding domain such as Cas9. However, no description is provided of fragments of repressor domains that meet the definition of paragraph [0060] and satisfy the structural/functional requirements of the instant claim set.
Further, with regard to the site-specific targeting facilitated by the instantly claimed repressor domain at claim 138, to provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of a complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, and any combination thereof. The specification describes fusion of repressor domains to zinc finger and Cas9-based DNA binding domains for site-specific targeting (Examples 1 and 2; paragraph [0504]). No description is provided of any repressor domain capable of both binding to an epigenetic effector protein and facilitating site-specific targeting.
Even if one accepts that the examples described in the specification meet the claim limitations of the rejected claims with regard to structure and function, the examples are only representative of site-specific targeting facilitated by zinc finger and Cas9-based DNA binding domains fused to unspecified repressor domains. The results are not necessarily predictive of the function of any of the claimed repressor domains or fragments thereof, which are not known to facilitate site-specific targeting and are not required to maintain repressor function per paragraph [0060] of the instant specification. Thus, it is impossible for one to extrapolate from the few examples described herein those repressor domains that would necessarily meet the structural/functional characteristics of the rejected claim.
The prior art does not appear to offset the deficiencies of the instant specification in that it does not describe a set of repressor domains or fragments thereof capable of functioning as instantly claimed. Additionally, regarding the recited site-specific targeting, the prior art teaches that repressor domains such as KRAB domains (i.e. derived from ZIM3 as reported in Alerasool et al., 2020; cited in the IDS filed 01/16/2024) are purely repressive domains (reviewed in Ecco et al., 2017; cited in the IDS filed 01/16/2024; see Figure 1). When combined with zinc finger proteins (ZFP), KRAB-ZFPs display sequence specificity, which is conferred by the ZFPs and not the KRAB domains, as instantly claimed (reviewed in Ecco et al., 2017; cited in the IDS filed 01/16/2024; see Figure 1). This is supported by the state of the art of CRISPR interference, which facilitates site-specific transcriptional and epigenetic regulation by fusing deactivated variants of Cas9 to a transcriptional repressor domain, such as a KRAB domain (reviewed in Barrangou and Doudna, 2016; see page 934, column 1, paragraph 2 and Figure 5). Crucially, this sequence specificity is conferred by the deactivated Cas9 variant and not the KRAB domain, which is purely a transcriptional repressor (reviewed in Barrangou and Doudna, 2016; see Figure 5 and Box 1). Absent any evidence to the contrary, neither the prior art nor the instant specification discloses a repressor domain or fragment thereof that would necessarily meet the structural/functional characteristics of the rejected claim.
Therefore, the skilled artisan would have reasonably concluded applicants were not in possession of the claimed invention for claims 135-152.
Claims 135-144 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 135 (from which claims 136-144 directly or indirectly depend) is drawn to an epigenetic editor fusion protein comprising a first DNMT domain, a DNA binding domain, and a repressor domain, wherein the repressor domain is selected from a defined group of repressor domains. The rejected claims thus comprise a set of epigenetic editors that themselves comprise any DNA binding domain. Dependent claims 136-144 do not further limit the claimed DNA binding domain and therefore inherit the rejection of independent claim 135. While the first DNMT domain is also broadly and functionally claimed, the instant specification discloses a number of DNMT species fused to DNA binding domains (SEQ ID NOs: 1092-1133) and is considered to provide adequate support for the claim language. Thus, the claims are drawn to a genus of epigenetic editor fusion proteins that are in part solely defined by the ability function to bind DNA.
To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of a complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, and any combination thereof. The specification describes zinc finger and Cas9-based DNA binding domains (Examples 1 and 2; SEQ ID NOs: 1092-1133). No description is provided of any other DNA binding domains.
Even if one accepts that the examples described in the specification meet the claim limitations of the rejected claims with regard to structure and function, the examples are only representative of zinc finger and Cas9-based DNA binding domains. The results are not necessarily predictive of any other DNA binding domain. Thus, it is impossible for one to extrapolate from the two examples of DNA binding domains described herein those DNA binding domains that would necessarily meet the structural/functional characteristics of the rejected claims.
The prior art does not appear to offset the deficiencies of the instant specification in that it does not describe a set of DNA binding domains capable of functioning with the instantly claimed system for epigenetic editing. As set forth at paragraph [0074] of the instant specification, the term “DNA binding domain” is a term known in the art and typically refers to a part of a protein which binds to DNA in a nucleus. However, while embodiments are envisioned in which the DNA-binding domain is selected from a CRISPR Cas protein, a TAL protein, a zinc finger protein, a transcription repression protein, and a transcription activation protein (paragraph [0074]), the examples provided in the instant specification address only DNA-binding domains derived from a CRISPR Cas protein and a zinc finger protein (Examples 1 and 2; SEQ ID NOs: 1092-1133). As reviewed in Alberts et al., 2000 (hereinafter Alberts), DNA binding domains may include a number of different species, such as helix-turn-helix motifs, homeodomains, zinc finger motifs, β sheets, leucine zipper motifs, and helix-loop-helix motifs (reviewed in Alberts). However, while these species have been well-characterized, the manner in which they bind to target DNA cannot be de novo predicted with a simple amino acid-target base pair recognition code (page 10: section “It Is Not Yet Possible to Accurately Predict the DNA Sequences Recognized by All Gene Regulatory Proteins). While Alberts discloses design of proteins that bind specific DNA sequences (page 10: section “It Is Not Yet Possible to Accurately Predict the DNA Sequences Recognized by All Gene Regulatory Proteins) and that such binding can be experimentally detected (page 12: section “The DNA Sequence Recognized by a Gene Regulatory Protein Can Be Determined”), the instant claim set does not require such design and/or validation, encompassing any DNA binding domain, which may bind to any target or any number of targets in an unpredictable fashion. The instant specification is silent as to any considerations regarding addressing the unpredictable nature of how any DNA binding domain may bind to any target or any number of targets.
Therefore, the skilled artisan would have reasonably concluded applicants were not in possession of the claimed invention for claims 135-144.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 136 and 152 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 136 recites the limitation "at least one of the repressor domains" (bolded and underlined emphasis added) in lines 1-2. There is insufficient antecedent basis for this limitation in the claim. Claim 136 depends from independent claim 135, which recites “a fusion protein…compris[ing]: (a) a first DNMT domain; (b) a DNA binding domain; and (c) a repressor domain...” (bolded emphasis added). Thus, the independent claim recites only a single repressor domain, while the dependent claim encompasses multiple repressor domains. In order to clearly establish the metes and bounds of protection sought by the instant claim set, it would be remedial to clearly recite whether a single repressor domain is being claimed or multiple repressor domains are being claimed. For purposes of examination, the Examiner has interpreted the instant claim set to require a single repressor domain, as recited at independent claim 135.
Claim 152 recites the limitation “the fusion protein domain [of the epigenetic editor of claim 135] comprises…” (bolded emphasis added) in lines 1-2. There is insufficient antecedent basis for this limitation in the claim. Claim 152 depends from independent claim 135, which recites “a fusion protein or a nucleic acid encoding the fusion protein thereof,” wherein the fusion protein is comprised of several defined domains. Thus, claim 135 recites a fusion protein in its entirety rather than a single domain thereof. For purposes of examination, the Examiner has interpreted instant claim 152 to recite “the epigenetic editor of claim 135, wherein the fusion protein comprises from N-terminus to C-terminus…”.
Further, claim 152 recites the limitation "DNMT3A-DNMT3L-dSpCas9-the repressor domain" (bolded emphasis added) in lines 2-3. There is insufficient antecedent basis for this limitation in the claim. Claim 152 depends from independent claim 135, which recites “a fusion protein…compris[ing]: (a) a first DNMT domain; (b) a DNA binding domain; and (c) a repressor domain...” (bolded emphasis added). Claim 135 does not recite DNMT3A, DNMT3L, or dSpCas9, although it does recite a generic first DNMT domain and a DNA binding domain. It would be remedial to amend the instant claim language and/or claim dependency such that there is proper antecedent basis for every claim term.
Claim Rejections - 35 USC § 103
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 135-137, 139-144 and 146-152 are rejected under 35 U.S.C. 103 as being unpatentable over US 2019/0024090 A1 (hereinafter Cathomen; as cited in the IDS filed 02/27/2025) in view of Alerasool et al., 2020 (hereinafter Alerasool; as cited in the IDS filed 01/16/2024), UniProt Entry Q96PE6 (as cited in the IDS filed 12/23/2025), UniProt Entry Q9UJW3 (aligned sequence released 02/15/2017), and UniProt Entry A0A386IRG9_STAAU (aligned sequence released 12/05/2018), as evidenced by Barrangou and Doudna, 2016 (hereinafter Barrangou).
With regard to claim 135, which recites “an epigenetic editor comprising a fusion protein or a nucleic acid encoding the fusion protein thereof, wherein the fusion protein comprises:
a first DNMT domain;
a DNA binding domain; and
a repressor domain, wherein the repressor domain is selected from the group consisting of: ZIM3…and fragments thereof,”
Cathomen discloses a construct for editing epigenetic marks of genes governing the expression thereof, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous) (paragraphs [0012]-[0018]). Thus, Cathomen discloses an epigenetic editor comprising a fusion protein, said fusion protein comprising a first DNMT domain, a DNA binding domain, and a repressor domain, as instantly claimed. Regarding the instantly claimed repressor domain, per paragraph [0009], the KRAB zinc finger proteins taught therein include an effector motif called KRAB, wherein KRAB serves to recruit histone deacetylase complexes, thereby repressing gene expression. Per paragraphs [0071] and [0072] of the instant specification, KRAB is a known transcription repressor domain. Thus, it is considered that the KRAB zinc finger protein disclosed in Cathomen generally reads on the instantly claimed repressor domain. However, Cahtomen is silent as to a repressor domain, wherein the repressor domain is ZIM3, as instantly claimed.
This deficiency is cured by Alerasool, which discloses CRISPR interference constructs comprising fusion of inactive Cas9 (dCas9) to the ZIM3 KRAB domain, which is an exceptionally potent repressor (abstract; page 1093, column 2, paragraph 2; Figures 1 and 2). Therefore, while Cathomen does not disclose that the KRAB fusion taught therein specifically comprises the ZIM3 KRAB domain, Alerasool discloses that the ZIM3 KRAB domain is a potent repressor compatible with targeted gene silencing by fusing it to dCas9 (i.e. a DNA binding domain). Therefore, it is considered that Cathomen and Alerasool collectively disclose the invention of instant claim 135, as set forth in greater detail below.
With regard to claim 136, which recites “at least one of the repressor domains [of the epigenetic editor of claim 135] is selected from the group consisting of: SEQ ID NO[s]s: 67-595,” as set forth above, Cathomen discloses fusion of KRAB to a DNA binding domain and two DNMT domains for targeted silencing of genes via epigenetic modification, while Alerasool discloses fusion specifically of the ZIM3 KRAB domain to dCas9 to facilitate potent repression of gene expression. However, neither Cathomen nor Alerasool discloses the sequence of the ZIM3 repressor domain corresponding to SEQ ID NO: 67. This deficiency is cured by UniProt Entry Q96PE6. As shown in the alignment of Appendix I, UniProt Entry Q96PE6 (corresponding to human ZIM3) comprises 100% identity to instant SEQ ID NO: 67. Thus, it is considered that UniProt Entry Q96PE6 discloses each and every additional limitation of instant claim 136.
With regard to claim 137, which recites “the DNA binding domain [of the epigenetic editor of claim 135] binds to a target sequence in a target chromosome comprising a target gene,” as set forth above, Cathomen discloses a fusion construct for epigenetic editing. Furthermore, as shown in Figures 1B and 2A of Cathomen, the DEM (designer epigenome modifier per paragraph [0013], the DNA binding portion of the DEM directs the DEM to a specific target site in the promoter or any other regulatory element of the target gene, leading to the methylation of the neighboring CpG di-residues and the deacetylation of neighboring histone tails, thereby silencing the target gene of interest (paragraphs [0061] and [0063]). This targeted binding reads on each and every additional limitation of instant claim 137. Thus, it is considered that Cathomen discloses each and every additional limitation of instant claim 137.
With regard to claim 139, which recites “the repressor domain [of the epigenetic editor of claim 135] is selected from the group consisting of: ZIM3…and fragments thereof,” as set forth above, Alerasool discloses CRISPR interference constructs comprising fusion of inactive Cas9 (dCas9) to the ZIM3 KRAB domain, which is an exceptionally potent repressor (abstract; page 1093, column 2, paragraph 2; Figures 1 and 2). Thus, it is considered that Alerasool discloses each and every additional limitation of instant claim 139.
With regard to claim 140, which recites “the fusion protein [of the epigenetic editor of claim 135] further comprises a second DNMT domain,” as set forth above, Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous) (paragraphs [0012]-[0018]). Thus, it is considered that Cathomen discloses each and every additional limitation of instant claim 140.
With regard to claim 141, which recites “the first DNMT domain [of the epigenetic editor of claim 135] is selected from the group consisting of a DNMT3A domain, a DNMT3B domain, a DNMT3C domain, and a DNMT3L domain,” as set forth above, Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous) (paragraphs [0012]-[0018]). Thus, it is considered that Cathomen discloses each and every additional limitation of instant claim 141.
With regard to claim 142, which recites “the first DNMT domain [of the epigenetic editor of claim 135] is a human DNMT3A domain or a human DMNT3L domain,” as set forth above, Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous) (paragraphs [0012]-[0018]). Thus, it is considered that Cathomen discloses each and every additional limitation of instant claim 142.
With regard to claim 143, which recites “the first DNMT domain [of the epigenetic editor of claim 140] is a DNMT3A domain and the second DNMT domain is a DNMT3L domain, or a catalytic portion thereof,” as set forth above, Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous) (paragraphs [0012]-[0018]). Thus, it is considered that Cathomen discloses each and every additional limitation of instant claim 143.
With regard to instant claim 144, which recites “the first DNMT domain and the second DNMT domain [of the epigenetic editor of claim 140] are selected from the group consisting of SEQ ID NO[s]: 32-66,” as set forth above, Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous) (paragraphs [0012]-[0018]). Additionally, Cathomen further discloses that the murine DNMT3L of the fusion protein taught therein may alternatively be human DNMT3L at paragraph [0051]. Cathomen further discloses that SEQ ID NO: 3 taught therein corresponds to human DNMT3A. As shown in the alignment of Appendix II, SEQ ID NO: 3 of Cathomen comprises 100% identity to instant SEQ ID NO: 34. However, while Cathomen discloses that the murine DNMT3L may alternatively be human DNMT3L, Cathomen is silent as to the specific sequence of human DNMT3L. This deficiency is cured by UniProt Entry Q9UJW3, which discloses the human DNMT3L sequence. As shown in the alignment of Appendix III, UniProt Entry Q9UJW3comprises 100% identity to instant SEQ ID NO: 38. Thus, it is considered that Cathomen and UniProt Entry Q9UJW3 collectively disclose each and every additional limitation of instant claim 144.
With regard to claim 146, which recites “the DNA binding domain [of the epigenetic editor of claim 135] comprises a nucleic acid guided DNA binding domain bound to a guide polynucleotide,” the construct of Cathomen is disclosed to comprise a TALE-derived DNA binding domain (paragraph [0044]) rather than the instantly claimed nucleic acid guided DNA binding domain bound to a guide polynucleotide. However, as set forth above, Alerasool discloses CRISPR interference constructs comprising fusion of inactive Cas9 (dCas9) to the ZIM3 KRAB domain, which is an exceptionally potent repressor (abstract; page 1093, column 2, paragraph 2; Figures 1 and 2). Alerasool further discloses that the CRISPR interference (CRISPRi) achieved therein using the fusion protein set forth above is particularly sensitive to guide RNA (gRNA) selection (page 1093, column 1, paragraphs 1-2). As depicted in Figure 1a of Alerasool, different gRNAs target the dCas9 to different loci. Furthermore, these gRNAs are indispensable to functioning of the system, as target genes are fully expressed in the absence of the gRNAs, as shown in Figure 2a. While Alerasool does not specify that the gRNA is bound to the dCas9 taught therein, it is known to those of ordinary skill in the art that gRNAs function by binding to their target sequences as well as to the Cas9 protein to assemble a functional editing complex (see Box 1 of Barrangou). Thus, it is considered that Alerasool (as evidenced by Barrangou) discloses each and every additional limitation of instant claim 146.
With regard to claim 147, which recites “the DNA binding domain [of the epigenetic editor of claim 146] comprises [a] CRISPR-Cas protein bound to the guide polynucleotide,” as set forth above, Alerasool discloses CRISPRi achieved via fusion of ZIM3 to dCas9 (a CRISPR-Cas protein), which is guided to a target locus by the associated gRNA (Figure 1a). Furthermore, it is known to those of ordinary skill in the art that gRNAs function by binding to their target sequences as well as to the Cas9 protein to assemble a functional editing complex (see Box 1 of Barrangou). Thus, it is considered that Alerasool (as evidenced by Barrangou) discloses each and every additional limitation of instant claim 147.
With regard to claim 148, which recites “the guide polynucleotide [of the epigenetic editor of claim 146] hybridizes with a target sequence,” as set forth above, Alerasool discloses CRISPRi achieved via fusion of ZIM3 to dCas9 (a CRISPR-Cas protein), which is guided to a target locus by the associated gRNA (Figure 1a). Furthermore, it is known to those of ordinary skill in the art that gRNAs function by binding to their target sequences as well as to the Cas9 protein to assemble a functional editing complex (see Box 1 of Barrangou). Thus, it is considered that Alerasool (as evidenced by Barrangou) discloses each and every additional limitation of instant claim 148.
With regard to claims 149 and 150, which respectively recite “the CRISPR-Cas protein [of the epigenetic editor of claim 147] comprises a nuclease inactive Cas9 (dCas9),” specifically “dSpCas9,” as set forth above, Alerasool discloses CRISPRi achieved via fusion of ZIM3 to dCas9, which is guided to a target locus by the associated gRNA (Figure 1a). Alerasool specifically discloses that the dCas9 utilized therein is derived from Streptococcus pyogenes dCas9 (page 1097, column 1, paragraph 4). Thus, it is considered that Alerasool discloses each and every additional limitation of instant claims 149 and 150.
With regard to claim 151, which recites “the dSpCas9 [of the epigenetic editor of claim 150] is defined as SEQ ID NO: 3,” as set forth above Alerasool specifically discloses that the dCas9 utilized therein is derived from Streptococcus pyogenes dCas9 (page 1097, column 1, paragraph 4). However, Alerasool does not disclose that the sequence of said dSpCas9 is defined as instant SEQ ID NO: 3. This deficiency is cured by UniProt Entry A0A386IRG9_STAAU, which discloses the sequence of dSpCas9. As shown in the alignment of Appendix IV, UniProt Entry A0A386IRG9_STAAU comprises 100% identity to instant SEQ ID NO: 3. Thus, it is considered that Alerasool and UniProt Entry A0A386IRG9_STAAU collectively disclose each and every additional limitation of instant claim 151.
With regard to claim 152, which recites “the fusion protein…[of the epigenetic editor of claim 135] comprises from N-terminus to C-terminus DNMT3A-DNMT3L-dSpCas9-the repressor domain,” as set forth above, Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous) (paragraphs [0012]-[0018]). The structure of the epigenetic modifier construct of Cathomen is disclosed at Figure 1A, comprising the repressor domain, the DNA binding domain, and the DNMT domains. While the DNA binding domain of Cathomen is a TALE-derived DNA binding domain (paragraph [0044]), Alerasool discloses the utility of dCas9 fusion proteins for targeted epigenetic modification (abstract; Figures 1 and 2). While the N and C termini are not specified, it is known to those of ordinary skill in the art that proteins are typically written from left-to-right from the N terminus to the C terminus. Therefore, while Cathomen and Alerasool collectively disclose all the components of the claimed fusion protein, the order is opposite of that which is instantly claimed. However, per MPEP § 2144.04(VI)(C), it is not inventive to rearrange parts of an invention when all parts of the invention have been disclosed in the prior art, as in the instant case. Accordingly, it is considered that Cathomen and Alerasool collectively disclose the claimed fusion protein and that it would require routine experimentation by someone of ordinary skill in the art to optimize the order of domains in the claimed fusion protein.
Given that Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous), and that Alerasool discloses that the ZIM3 KRAB domain facilitates potent repression via CRISPRi when fused to dSpCas9, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to utilize the ZIM3 KRAB domain disclosed in Alerasool as the KRAB repressor domain disclosed in Cathomen as part of a construct for epigenetic modification and further to substitute the TALE-derived DNA binding domain of Cathomen for dCas9 (as disclosed in Alerasool) to predictably facilitate user-specified sequence-specific targeting for epigenetic modification (as reviewed in Barrangou). One would have been motivated to make such a modification in order to receive the expected benefit of facilitating user-specified sequence-specific targeting for epigenetic modification.
Claim 145 is rejected under 35 U.S.C. 103 as being unpatentable over US 2019/0024090 A1 (hereinafter Cathomen; as cited in the IDS filed 02/27/2025) in view of Alerasool et al., 2020 (hereinafter Alerasool; as cited in the IDS filed 01/16/2024), UniProt Entry Q96PE6 (as cited in the IDS filed 12/23/2025), UniProt Entry Q9UJW3 (aligned sequence released 02/15/2017), and UniProt Entry A0A386IRG9_STAAU (aligned sequence released 12/05/2018), as evidenced by Barrangou and Doudna, 2016 (hereinafter Barrangou) as applied to claim 135 above, and further in view of US 2019/0032049 A1 (hereinafter Naldini; as cited in the IDS filed 01/16/2024), as evidenced by Eom et al., 2016 (hereinafter Eom).
The combined disclosures of Cathomen, Alerasool, UniProt Entry Q96PE6, UniProt Entry Q9UJW3, UniProt Entry A0A386IRG9_STAAU, and Barrangou are described above and applied as before. However, these disclosures do not teach the DNA binding domain comprising a zinc finger motif or a zinc finger array of instant claim 145.
With regard to claim 145, which recites “the DNA binding domain [of the epigenetic editor of claim 135] comprises a zinc finger motif or a zinc finger array,” as set forth above, Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous) (paragraphs [0012]-[0018]). However, the DNA binding domain of Cathomen is a TALE-derived DNA binding domain (paragraph [0044]), which does not comprise a zinc finger motif or a zinc finger array. This deficiency is cured by Naldini.
Naldini discloses artificial transcription repressors that establish robust and permanent states of epigenetic repression, said artificial transcription repressors comprising a DNA-binding domain operably linked to a KRAB domain, a DNMT3A domain, and/or a DNMT3L domain (paragraphs [0014], [0016], and [0024]-[0029]). As depicted in Figure 1 of Naldini, this system facilitates epigenetic silencing of a targeted gene of interest. Naldini discloses that the DNA binding domain taught therein may be a zinc finger domain (paragraphs [0037] and [0253]). As is known to those of ordinary skill in the art, zinc finger domains comprise zinc finger motifs (reviewed in Eom: see especially page 2023, column 2, paragraph 2). Thus, Naldini discloses that zinc finger domains (comprising zinc finger motifs) are capable of functioning as a DNA binding domain that targets a locus of interest for epigenetic modification thereof, as instantly claimed.
Given that Cathomen discloses a construct for epigenetic modification of genes, said construct comprising a Krϋppel-associated box (KRAB) zinc finger protein (or homologous), a DNA region capable of binding to the target gene (or homologous), and two DNA methyltransferases (DNMT) (human DNMT3A or homologous and murine Dnmt3L or homologous), and that Naldini discloses that zinc finger domains are capable of functioning as a DNA binding domain that targets a locus of interest for epigenetic modification thereof, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to utilize the zinc finger domains disclosed in Naldini as the DNA binding domain for use in the construct for epigenetic modification disclosed in Cathomen to predictably facilitate user-specified sequence-specific targeting for epigenetic modification. One would have been motivated to make such a modification in order to receive the expected benefit of facilitating user-specified sequence-specific targeting for epigenetic modification.
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 135-137, 139-144, and 146-151 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-11, 15-19 of U.S. Patent No. 12,390,538 B2. Although the claims at issue are not identical, they are not patentably distinct from each other.
MPEP 804(II)(B)(1) states:
The specification can be used as a dictionary to learn the meaning of a term in the patent claim. Toro Co. v. White Consol. Indus., Inc., 199 F.3d 1295, 1299, 53 USPQ2d 1065, 1067 (Fed. Cir. 1999)… Further, those portions of the specification which provide support for the patent claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the patent. In re Vogel, 422 F.2d 438, 441-42, 164 USPQ 619, 622 (CCPA 1970).
The following rejections are in view of the decision of the Court of Appeals for the Federal Circuit in Pfizer Inc, v Teva pharmaceuticals USA Inc., 86 USPQ2d 1001, at page 1008 (March 2008), which indicates that there is no patentable distinction between claims to a product and a method of using that product disclosed in the specification of the application and that the preclusion of such a double patenting rejection under 35 USC 121 does not apply where the present application is other than a divisional application of the patent application containing such patentably indistinct claims.
Patent ‘538 recites a method, said method comprising administering an epigenetic editing system to a subject, said editing system comprising a fusion protein comprising a dCas9 protein domain from Streptococcus pyogenes and an associated guide RNA targeting a specified genomic locus, a DNMT3A domain, a DNMT3L domain, and a human ZIM3 KRAB domain (recited at claims 1-3, 5, 10, and 15). This epigenetic editor fusion protein reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 137, 139, 140-143, and 146-150, which comprises a DNA binding domain comprising a CRISPR Cas protein (such as dSpCas9) guided by a guide polynucleotide that hybridizes with a target sequence, a ZIM3 repressor domain, and human DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of patent ‘538 are not patentably distinct.
Regarding the sequence of the instantly claimed ZIM3 repressor domain, instant SEQ ID NO: 67 (as recited at instant claim 136) is identical to SEQ ID NO: 495 of patent ‘538 (as recited at claims 9 and 11 of patent ‘538), as shown in the alignment of Appendix V. Thus, the instantly claimed ZIM3 repressor and that of patent ‘538 are not patentably distinct.
Regarding the sequence of the instantly claimed dSpCas9, instant SEQ ID NO: 3 (as recited at instant claim 151) is identical to SEQ ID NO: 12 of patent ‘538 (as recited at claims 4 and 6 of patent ‘538), as shown in the alignment of Appendix VI. Thus, the instantly claimed dSpCas9 and that of patent ‘538 are not patentably distinct.
Regarding the sequence of the instantly claimed DNMT3A domain, instant SEQ ID NO: 34 (as recited at instant claim 144) is identical to SEQ ID NO: 1029 of patent ‘538 (recited at claims 7 and 8 of patent ‘538), as shown in the alignment of Appendix VII. Thus, the instantly claimed DNMT3A domain and that of patent ‘538 are not patentably distinct.
Regarding the sequence of the instantly claimed DNMT3L domain, instant SEQ ID NO: 38 (as recited at instant claim 144) is identical to SEQ ID NO: 1033 of patent ‘538 (recited at claims 16 and 17 of patent ‘538), as shown in the alignment of Appendix VIII. Thus, the instantly claimed DNMT3L domain and that of patent ‘538 are not patentably distinct.
Regarding claims 18 and 19 of patent ‘538, both claims recite “the dCas9 protein domain comprises a sequence [or a sequence with at least 99% sequence identity thereto] of SEQ ID NO: 12, the DNMT3A domain comprises a sequence of SEQ ID NO: 1029, and the human KRAB domain comprises a sequence of SEQ ID NO: 495,” as set forth above, these sequences are all recited in the instant application. Thus, the instantly claimed epigenetic editor and that of patent ‘538 are not patentably distinct.
Claims 135, 137, 139, 140, 141, 143, 146, 147, 148, 149, 150, and 152 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, 4, 5, 10, 12, and 13 of U.S. Patent No. 12,558,437 B2. Although the claims at issue are not identical, they are not patentably distinct from each other.
MPEP 804(II)(B)(1) states:
The specification can be used as a dictionary to learn the meaning of a term in the patent claim. Toro Co. v. White Consol. Indus., Inc., 199 F.3d 1295, 1299, 53 USPQ2d 1065, 1067 (Fed. Cir. 1999)… Further, those portions of the specification which provide support for the patent claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the patent. In re Vogel, 422 F.2d 438, 441-42, 164 USPQ 619, 622 (CCPA 1970).
The following rejections are in view of the decision of the Court of Appeals for the Federal Circuit in Pfizer Inc, v Teva pharmaceuticals USA Inc., 86 USPQ2d 1001, at page 1008 (March 2008), which indicates that there is no patentable distinction between claims to a product and a method of using that product disclosed in the specification of the application and that the preclusion of such a double patenting rejection under 35 USC 121 does not apply where the present application is other than a divisional application of the patent application containing such patentably indistinct claims.
Patent ‘437 recites a method, said method comprising administering an epigenetic editing system, said editing system comprising a fusion protein (or a nucleic acid encoding the same) comprising a first dCas9 protein domain derived from Streptococcus pyogenes and an associated guide RNA targeting a specified genomic locus, a first and second DNMT domain corresponding to DNMT3A and DNTM3L domains, and a ZIM3 KRAB epigenetic repression domain (recited at claims 1, 3, 4, 5, 10, 12, and 13). This epigenetic editor fusion protein reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 137, 139, 140, 141, 143, 146, 147, 148, 149, and 150, which comprises a DNA binding domain comprising a CRISPR Cas protein (such as dSpCas9) guided by a guide polynucleotide that hybridizes with a target sequence, a ZIM3 repressor domain, and human DNMT3A and DNMT3L domains. The instantly claimed order of said domains is recited at instant claim 152, and this order is identical to that recited at claim 10 of patent ‘437. Thus, the instantly claimed epigenetic editor and that of patent ‘437 are not patentably distinct.
Claims 135, 137, and 139-152 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 4, 6, 9, 10, 14, 17-23, 25, 38, and 40 of copending Application No. 18/861,783 (reference application; not yet published). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘783 is drawn to a system for repressing transcription of a human PCSK9 gene in a human cell, said system comprising one or more fusion proteins collectively comprising a DNMT3A domain, a DNMT3L domain, a DNA-binding domain derived from dead CRISPR Cas such as dCas9, and a ZIM3 transcriptional repressor that binds to a target sequence (as recited at copending claims 1, 2, 4, 14, 18-23, 25, 38, and 40). This epigenetic editor fusion protein reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 137, 139, 140-143, 146-150, and 152, which comprises a DNA binding domain comprising a CRISPR Cas protein (such as dSpCas9) guided by a guide polynucleotide that hybridizes with a target sequence, a ZIM3 repressor domain, and human DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘783 are not patentably distinct.
Regarding the sequence of the dCas9 species of the instant and copending applications, instant claim 151 defines the dSpCas9 claimed therein as SEQ ID NO: 3, which is identical to the copending dCas9 sequence of SEQ ID NO: 12 as recited at copending claim 6, as shown in the alignment of Appendix IX.
Regarding the sequence of the DNMT3A domains of the instant and copending applications, instant claim 144 defines the DNMT3A and DNMT3L domains claimed therein as corresponding to SEQ ID NOs: 34 and 38 (as elected by Applicant), respectively. These sequences are identical to the DNMT3A domain sequence recited at copending claim 9 (SEQ ID NO: 574) and the DNMT3L domain sequence recited at copending claim 10 (SEQ ID NO: 579), as shown in the alignment of Appendices X and XI.
Furthermore, instant claim 145 recites “the DNA binding domain comprises a zinc finger motif or a zinc finger array,” which is not patentably distinct from the recitation of copending claim 4, which also recites that the DNA binding domain claimed therein comprises a zinc finger protein domain.
Finally, copending claim 17 recites that the transcriptional repressor domain may be derived from species such as TOX3, which is also recited at instant claim 139. Accordingly, these recitations are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 137, 139-143, and 145-149 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 3, 17, 20, and 21 of copending Application No. 18/877,796 (reference application; corresponds to US 2025/0387518 A1). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘796 is drawn to a system for repressing transcription of a human B2M gene in a human cell, said system comprising one or more fusion proteins that collectively comprise a human DNMT3A and/or a DNMT3L domain and a transcriptional repressor domain linked to a DNA-binding domain (i.e. dCas or a ZFP domain) that binds to a targeted genomic locus, wherein said transcriptional repressor domain is derived from a ZIM3 KRAB domain or a TOX3 transcriptional repressor domain (as recited at copending claims 1, 2, 17, 20, and 21). Copending application ‘796 further recites that when the DNA-binding domain claimed therein comprises a dCas9 domain, the system further comprises one or more guide RNAs to direct the fusion protein to the targeted genomic locus (copending claim 3).
This epigenetic editor fusion protein reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 137, 139-143, 145-149, which comprises a DNA binding domain comprising a CRISPR Cas protein (such as dSpCas9) guided by a guide polynucleotide that hybridizes with a target sequence in the genome or alternatively a zinc finger motif/array, a ZIM3 or TOX3 repressor domain, and human DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘783 are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 137, 139-143, 145-151 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-5, 13, 16, 17-22, 24, 26, 31, 33, 34, 36, 37, and 39 of copending Application No. 18/877,818 (reference application; corresponds to US 2025/0387514 A1). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘818 is drawn to a system for repressing transcription of a human TRAC gene in a human cell, said system comprising a human DNMT3A and/or a DNMT3L domain and a transcriptional repressor domain linked to a DNA-binding domain (i.e. dSpCas9 or a ZFP domain) that binds to a targeted genomic locus, wherein said transcriptional repressor domain is derived from a ZIM3, ZN627, or ZFP28 KRAB domain or a TOX3 transcriptional repressor domain (as recited at copending claims 1-3, 13, 16, 17-22, 24, 26, 31, 33, 34, 36, 37, and 39). Copending application ‘818 further recites that when the DNA-binding domain claimed therein comprises a dCas9 domain, the system further comprises one or more guide RNAs to direct the fusion protein to the targeted genomic locus (copending claim 4).
This epigenetic editor fusion protein reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 137, 139-143, 145-150, which comprises a DNA binding domain comprising a CRISPR Cas protein (such as dSpCas9) guided by a guide polynucleotide that hybridizes with a target sequence in the genome or alternatively a zinc finger motif/array, a ZIM3, ZN627, ZFP28, or TOX3 repressor domain, and human DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘818 are not patentably distinct.
Furthermore, copending claim 5 recites that the dCas9 claimed therein has a sequence with at least 90% identity to SEQ ID NOs: 12 or 13. As shown in the alignment of Appendix XII, instant SEQ ID NO: 3 (recited at instant claim 151) is identical to copending SEQ ID NO: 12.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 136, 139-141, 143, 144, and 146-150 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 41, 46-51, 58, and 60 of copending Application No. 18/981,846 (reference application; corresponds to US 2025/0197818 A1; as cited in the IDS filed 07/02/2025). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘846 is drawn to an epigenetic editing system, said system comprising a DNA-binding domain (i.e. dCas9 guided by a guide RNA), a DNMT3L domain, a DNMT3A domain, and a transcriptional repressor domain such as a ZIM3, ZFP28, or ZN627 KRAB domain (as recited at copending claims 41, 46-51, 58, and 60).
This epigenetic editor fusion protein reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 139-141, 143, 144, and 146-150, which comprises a DNA binding domain comprising a CRISPR Cas protein (such as dCas9) guided by a guide polynucleotide that hybridizes with a target sequence in the genome, a ZIM3, ZN627, or ZFP28 repressor domain, and DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘846 are not patentably distinct.
Furthermore, copending claim 50 recites that the ZIM3 claimed therein has a sequence with at least 90% identity to SEQ ID NO: 60. As shown in the alignment of Appendix XIII, instant SEQ ID NO: 67 (recited at instant claim 136) is identical to copending SEQ ID NO: 60.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 139, and 140-143 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 148, 157, 158, 160, 161, 163, and 165 of copending Application No. 18/989,126 (reference application; corresponds to US 2025/0320478 A1). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘126 is drawn to an epigenetic editing system, said system comprising a fusion protein comprising a transcriptional repressor domain (i.e. a ZIM3 KRAB domain), a DNA-binding domain, and a first and second DNMT domain (i.e. human DNMT3A and DNMT3L) (as recited at copending claims 148, 157, 158, 160, 161, 163, and 165).
This epigenetic editor fusion protein reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 139, and 140-143, which comprises a DNA binding domain, a ZIM3 repressor domain, and human DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘126 are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135-137, 139-146, and 146-149 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 7, 8, 13, 14, 19, and 20 of copending Application No. 19/060,404 (reference application; corresponds to US 2025/0236847 A1). Although the claims at issue are not identical, they are not patentably distinct from each other.
MPEP 804(II)(B)(1) states:
The specification can be used as a dictionary to learn the meaning of a term in the patent claim. Toro Co. v. White Consol. Indus., Inc., 199 F.3d 1295, 1299, 53 USPQ2d 1065, 1067 (Fed. Cir. 1999)… Further, those portions of the specification which provide support for the patent claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the patent. In re Vogel, 422 F.2d 438, 441-42, 164 USPQ 619, 622 (CCPA 1970).
The following rejections are in view of the decision of the Court of Appeals for the Federal Circuit in Pfizer Inc, v Teva pharmaceuticals USA Inc., 86 USPQ2d 1001, at page 1008 (March 2008), which indicates that there is no patentable distinction between claims to a product and a method of using that product disclosed in the specification of the application and that the preclusion of such a double patenting rejection under 35 USC 121 does not apply where the present application is other than a divisional application of the patent application containing such patentably indistinct claims.
Copending application ‘404 is drawn to a method for repressing expression of an HBV genome, said method comprising contacting the HBV genome with an epigenetic editing system, said system comprising a fusion protein or a nucleic acid encoding the same, wherein the fusion protein comprises a catalytically inactive Cas9 DNA binding domain guided by a guide RNA to a target region of the HBV genome, a ZIM3 KRAB repression domain, and a DNMT3L and DNMT3L domain (as recited at copending claims 1, 2, 7, 8, 13, 14, 19, and 20).
This epigenetic editing system reads on the epigenetic editor comprising a fusion protein (or a nucleic acid encoding the same) recited at instant claims 135, 137, 139-143, and 146-149, which comprises a DNA binding domain, a ZIM3 repressor domain, and human DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘404 are not patentably distinct.
Furthermore, copending claims 2, 8, 14, and 20 recite that the ZIM3 claimed therein has a sequence with at least 90% identity to SEQ ID NO: 495. As shown in the alignment of Appendix XIV, instant SEQ ID NO: 67 (recited at instant claim 136) is identical to copending SEQ ID NO: 495.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135-137, 139-144, and 146-151 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-11 and 13-19 of copending Application No. 19/224,549 (reference application; corresponds to US 2025/0288691 A1). Although the claims at issue are not identical, they are not patentably distinct from each other.
MPEP 804(II)(B)(1) states:
The specification can be used as a dictionary to learn the meaning of a term in the patent claim. Toro Co. v. White Consol. Indus., Inc., 199 F.3d 1295, 1299, 53 USPQ2d 1065, 1067 (Fed. Cir. 1999)… Further, those portions of the specification which provide support for the patent claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the patent. In re Vogel, 422 F.2d 438, 441-42, 164 USPQ 619, 622 (CCPA 1970).
The following rejections are in view of the decision of the Court of Appeals for the Federal Circuit in Pfizer Inc, v Teva pharmaceuticals USA Inc., 86 USPQ2d 1001, at page 1008 (March 2008), which indicates that there is no patentable distinction between claims to a product and a method of using that product disclosed in the specification of the application and that the preclusion of such a double patenting rejection under 35 USC 121 does not apply where the present application is other than a divisional application of the patent application containing such patentably indistinct claims.
Copending application ‘549 is drawn to a method, said method comprising administering an epigenetic editing system to a subject, said system comprising a fusion protein comprising a dCas9 protein domain (defined by SEQ ID NO: 12 and derived from Streptococcus pyogenes) guided by a guide RNA to a target sequence, a DNMT3A domain (defined by SEQ ID NO: 1029), a human DNMT3L domain (defined by SEQ ID NO: 1033), and a ZIM3 KRAB domain (defined by SEQ ID NO: 495) (as recited at copending claims 1-11 and 13-19).
This epigenetic editing system reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 137, 139-143, and 146-150, which comprises a DNA binding domain, a ZIM3 repressor domain, and human DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘549 are not patentably distinct.
Furthermore, copending claims 136, 144, and 151 recite that the ZIM3, DNMT3A and DNMT3L, and dSpCas9 claimed therein are defined by SEQ ID NOs: 67, 34, 38, and 3, respectively. As shown in the alignments of Appendices XV-XVIII, these sequences are identical to those recited in the copending application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 137, 139-144, 146-150, and 152 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6-14, 16, and 21-29 of copending Application No. 19/390,246 (reference application; not yet published). Although the claims at issue are not identical, they are not patentably distinct from each other.
MPEP 804(II)(B)(1) states:
The specification can be used as a dictionary to learn the meaning of a term in the patent claim. Toro Co. v. White Consol. Indus., Inc., 199 F.3d 1295, 1299, 53 USPQ2d 1065, 1067 (Fed. Cir. 1999)… Further, those portions of the specification which provide support for the patent claims may also be examined and considered when addressing the issue of whether a claim in the application defines an obvious variation of an invention claimed in the patent. In re Vogel, 422 F.2d 438, 441-42, 164 USPQ 619, 622 (CCPA 1970).
The following rejections are in view of the decision of the Court of Appeals for the Federal Circuit in Pfizer Inc, v Teva pharmaceuticals USA Inc., 86 USPQ2d 1001, at page 1008 (March 2008), which indicates that there is no patentable distinction between claims to a product and a method of using that product disclosed in the specification of the application and that the preclusion of such a double patenting rejection under 35 USC 121 does not apply where the present application is other than a divisional application of the patent application containing such patentably indistinct claims.
Copending application ‘246 recites a method of administering an epigenetic editing system comprising a fusion protein with a configuration of DNMT3A-DNMT3L-dCas9-ZIM3 KRAB, wherein the dCas9 is from Streptococcus pyogenes and guided to a target sequence by an associated guide RNA, and DNMT3A and DNTM3L are defined by SEQ ID NOs: 1029 and 1033 (as recited at copending claims 1, 6-14, 16, and 21-29).
This epigenetic editing system reads on the epigenetic editor comprising a fusion protein recited at instant claims 135, 137, 139-144, 146-150, and 152 which comprises a DNA binding domain, a ZIM3 repressor domain, and human DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘246 are not patentably distinct.
With regard to the copending and instantly claimed sequences, copending claim 144 recites that DNMT3A and DNMT3L are defined by SEQ ID NOs: 34 and 38, which are identical to copending SEQ ID NOs: 1029 and 1033, as shown in the alignments of Appendices XIX and XX.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 139-141, 143, and 145 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 7, 10, 11, and 39 of copending Application No. 19/476,668 (reference application; not yet published). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘668 recites a fusion protein (and a nucleic acid encoding the same) comprising one or more DNMT domains (such as DNMT3A and/or DNMT3L), two or more DNA-binding zinc finger domains, and one or more transcriptional repressor domains (such as ZIM3 or TOX3) (as recited at copending claims 1, 7, 10, 11, and 39.
This fusion protein reads on the epigenetic editor comprising a fusion protein (and a nucleic acid encoding the same) recited at instant claims 135, 139-141, 143, and 145, which comprises a zinc finger DNA binding domain, a ZIM3 or TOX3 repressor domain, and DNMT3A and DNMT3L domains. Thus, the instantly claimed epigenetic editor and that of copending application ‘668 are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 137, and 139-152 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4-6, 9, 10, 14, 17-23, 32, 34, 35, 37, 38, and 40 of copending Application No. 19/480,313 (reference application; not yet published). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘313 is drawn to a system for repressing transcription of a human PCSK9 gene, said system comprising one or more fusion proteins (or nucleic acids encoding the same) that collectively comprise a human DNMT3A and/or a DNMT3L domain and a transcriptional repressor domain (such as ZIM3, ZFP28, ZN627, or TOX3) linked to a DNA binding domain (such as a dCas9 or zinc finger domain) that binds to a target region in the human PCSK9 gene (as recited at copending claims 1, 4, 14, 17-23, 32, 34, 35, 37, 38, and 40).
This fusion protein reads on the epigenetic editor comprising a fusion protein (and a nucleic acid encoding the same) recited at instant claims 135, 137, 139-143, 145-150, and 152, which comprises a DNA binding domain comprising a zinc finger domain or a dCas9 domain, DNMT3A and DNMT3L domains that may be from humans, and a transcriptional repressor domain such as ZIM3, ZFP28, ZN627, or TOX3. Per instant claim 152, these domains are ordered from the N to C terminus as DNMT3A-DNMT3L-dSpCas9-the repressor domain, which is identical to the order recited at copending claims 32, 35, and 38.
With regard to the copending and instantly claimed sequences, the DNA binding domain of the copending application is recited to comprise a dCas9 domain corresponding to copending SEQ ID NO: 12 (as recited at copending claims 4-6), which is identical to instant SEQ ID NO: 3 (derived from dSpCas9; as recited at instant claim 151), as shown in the alignment of Appendix XXI.
Additionally, the DNMT3A and DNMT3L sequences of the copending application are recited to comprise SEQ ID NOs: 575 and 579 (as recited at copending claims 9 and 10), which are identical to instant SEQ ID NOs: 34 and 38 (as recited at instant claim 144), respectively, as shown in the alignments of Appendices XXII and XXIII.
Thus, the instantly claimed epigenetic editor and that of copending application ‘313 are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 137, and 139-152 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-19, 21, 22, 26, 29-35, 44, 46, 47, 49, 50, 52, 74-80, 82, 83, 87, 90-96, 105, 107, 108, 110, 111, 113, and 115 of copending Application No. 19/483,765 (reference application; not yet published). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘765 is drawn to systems for repressing transcription of target genes such as CD3D, said systems comprising one or more fusion proteins (or nucleic acids encoding the same) that collectively comprise a human DNMT3A and/or a DNMT3L domain and a transcriptional repressor domain (such as ZIM3, ZFP28, ZN627, or TOX3) linked to a DNA binding domain (such as a dCas9 or zinc finger domain) that binds to a target region in the targeted human gene (as recited at copending claims 1-18, 26, 29-35, 44, 46, 47, 49, 50, 52, 74-79, 87, 90-96, 105, 107, 108, 110, 111, 113, and 115).
This fusion protein reads on the epigenetic editor comprising a fusion protein (and a nucleic acid encoding the same) recited at instant claims 135, 137, 139-143, 145-150, and 152, which comprises a DNA binding domain comprising a zinc finger domain or a dCas9 domain, DNMT3A and DNMT3L domains that may be from humans, and a transcriptional repressor domain such as ZIM3, ZFP28, ZN627, or TOX3. Per instant claim 152, these domains are ordered from the N to C terminus as DNMT3A-DNMT3L-dSpCas9-the repressor domain, which is identical to the order recited at copending claims 44, 47, 50, 105, 108, and 111.
With regard to the copending and instantly claimed sequences, the DNA binding domain of the copending application is recited to comprise a dCas9 domain corresponding to copending SEQ ID NO: 12 (as recited at copending claims 19 and 80), which is identical to instant SEQ ID NO: 3 (derived from dSpCas9; as recited at instant claim 151), as shown in the alignment of Appendix XXIV.
Additionally, the DNMT3A and DNMT3L sequences of the copending application are recited to comprise SEQ ID NOs: 575 and 579 (as recited at copending claims 21, 22, 82, and 83), which are identical to instant SEQ ID NOs: 34 and 38 (as recited at instant claim 144), respectively, as shown in the alignments of Appendices XXV and XXVI.
Thus, the instantly claimed epigenetic editor and that of copending application ‘765 are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 137, 139-143, and 145-152 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8, 14, 17-23, 32, 34, 35, 37, 38, 40, and 62 of copending Application No. 19/502,682 (reference application; not yet published). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘682 is drawn to systems for repressing transcription of target genes such as RFXAP, said systems comprising one or more fusion proteins (or nucleic acids encoding the same) that collectively comprise a human DNMT3A and/or a DNMT3L domain and a transcriptional repressor domain (such as ZIM3, ZFP28, ZN627, or TOX3) linked to a DNA binding domain (such as a dCas9 or zinc finger domain) that binds to a target region in the targeted human gene (as recited at copending claims 1-6, 8, 14, 17, 18, 22, 23, 34, 37, 40, and 62).
This fusion protein reads on the epigenetic editor comprising a fusion protein (and a nucleic acid encoding the same) recited at instant claims 135, 137, 139-143, 145-150, and 152, which comprises a DNA binding domain comprising a zinc finger domain or a dCas9 domain, DNMT3A and DNMT3L domains that may be from humans, and a transcriptional repressor domain such as ZIM3, ZFP28, ZN627, or TOX3. Per instant claim 152, these domains are ordered from the N to C terminus as DNMT3A-DNMT3L-dSpCas9-the repressor domain, which is identical to the order recited at copending claims 32, 35, and 38.
With regard to the copending and instantly claimed sequences, the DNA binding domain of the copending application is recited to comprise a dCas9 domain corresponding to copending SEQ ID NO: 12 (as recited at copending claim7), which is identical to instant SEQ ID NO: 3 (derived from dSpCas9; as recited at instant claim 151), as shown in the alignment of Appendix XXVII.
Thus, the instantly claimed epigenetic editor and that of copending application ‘682 are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 137, and 139-152 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10, 14, 17-23, 32, 34, 35, 37, 38, and 40 of copending Application No. 19/515,156 (reference application; not yet published). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘156 is drawn to systems for repressing transcription of target genes such as TGFBR2, said systems comprising one or more fusion proteins (or nucleic acids encoding the same) that collectively comprise a human DNMT3A and/or a DNMT3L domain and a transcriptional repressor domain (such as ZIM3, ZFP28, ZN627, or TOX3) linked to a DNA binding domain (such as a dCas9 or zinc finger domain) that binds to a target region in the targeted human gene (as recited at copending claims 1-6, 8, 14, 17-23, 32, 34, 35, 37, 38, and 40).
This fusion protein reads on the epigenetic editor comprising a fusion protein (and a nucleic acid encoding the same) recited at instant claims 135, 137, 139-143, 145-150, and 152, which comprises a DNA binding domain comprising a zinc finger domain or a dCas9 domain, DNMT3A and DNMT3L domains that may be from humans, and a transcriptional repressor domain such as ZIM3, ZFP28, ZN627, or TOX3. Per instant claim 152, these domains are ordered from the N to C terminus as DNMT3A-DNMT3L-dSpCas9-the repressor domain, which is identical to the order recited at copending claims 32, 35, and 38.
With regard to the copending and instantly claimed sequences, the DNA binding domain of the copending application is recited to comprise a dCas9 domain corresponding to copending SEQ ID NO: 12 (as recited at copending claim 7), which is identical to instant SEQ ID NO: 3 (derived from dSpCas9; as recited at instant claim 151), as shown in the alignment of Appendix XXVIII.
Additionally, the DNMT3A and DNMT3L sequences of the copending application are recited to comprise SEQ ID NOs: 575 and 579 (as recited at copending claims 9 and 10), which are identical to instant SEQ ID NOs: 34 and 38 (as recited at instant claim 144), respectively, as shown in the alignments of Appendices XXIX and XXX.
Thus, the instantly claimed epigenetic editor and that of copending application ‘156 are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 135, 137, and 139-152 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10, 14, 17-23, 32, 34, 35, 37, 38, and 40 of copending Application No. 19/515,205 (reference application; not yet published). Although the claims at issue are not identical, they are not patentably distinct from each other.
Copending application ‘205 is drawn to systems for repressing transcription of target genes such as ADORA2A, said systems comprising one or more fusion proteins (or nucleic acids encoding the same) that collectively comprise a human DNMT3A and/or a DNMT3L domain and a transcriptional repressor domain (such as ZIM3, ZFP28, ZN627, or TOX3) linked to a DNA binding domain (such as a dCas9 or zinc finger domain) that binds to a target region in the targeted human gene (as recited at copending claims 1-6, 8, 14, 17-23, 32, 34, 35, 37, 38, and 40).
This fusion protein reads on the epigenetic editor comprising a fusion protein (and a nucleic acid encoding the same) recited at instant claims 135, 137, 139-143, 145-150, and 152, which comprises a DNA binding domain comprising a zinc finger domain or a dCas9 domain, DNMT3A and DNMT3L domains that may be from humans, and a transcriptional repressor domain such as ZIM3, ZFP28, ZN627, or TOX3. Per instant claim 152, these domains are ordered from the N to C terminus as DNMT3A-DNMT3L-dSpCas9-the repressor domain, which is identical to the order recited at copending claims 32, 35, and 38.
With regard to the copending and instantly claimed sequences, the DNA binding domain of the copending application is recited to comprise a dCas9 domain corresponding to copending SEQ ID NO: 12 (as recited at copending claim 7), which is identical to instant SEQ ID NO: 3 (derived from dSpCas9; as recited at instant claim 151), as shown in the alignment of Appendix XXXI.
Additionally, the DNMT3A and DNMT3L sequences of the copending application are recited to comprise SEQ ID NOs: 575 and 579 (as recited at copending claims 9 and 10), which are identical to instant SEQ ID NOs: 34 and 38 (as recited at instant claim 144), respectively, as shown in the alignments of Appendices XXXII and XXXIII.
Thus, the instantly claimed epigenetic editor and that of copending application ‘205 are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
No claims are allowed.
Claims 135, 136, 144, and 147 are objected to.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Sarah E Allen whose telephone number is (571)272-0408. The examiner can normally be reached M-Th 8-5, F 8-12.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jennifer Dunston can be reached at 571-272-2916. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/SARAH E ALLEN/ Examiner, Art Unit 1637
/J. E. ANGELL/ Primary Examiner, Art Unit 1637
Prosecution Insights