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 .
Application Status
This action is written in response to applicant’s correspondence received on 3/26/2026. Claims 1-28 and 30 are pending. Claims 1-2 and 12 have been amended. Claim 29 has been cancelled. Claims 12-20, 23, 26-28, and 30 were withdrawn.
Upon further consideration of the claims and subject matter, claims 12-20, and 23, 26-28, and 30 have been rejoined. Claims 1-28 and 30 are currently under examination.
Any rejection of record in the previous office actions not addressed herein is withdrawn. New grounds of rejection are presented herein that were not necessitated by applicant’s amendment of the claims since the office action mailed 12/29/2025. Therefore, this action is not final.
102 Rejection – Withdrawn
The Applicant has amended claim 1 to remove SEQ ID NO: 5262. A prior art search and ABSS/NCBI BLAST database search was performed on the remaining sequences in claim 1. The sequences recited in claim 1, namely, 4628, 4693, 4741, 4752, 4753, and 5873 were found to be free of the prior art. The former prior art rejection(s) have therefore been withdrawn.
Double Patenting Rejection – Withdrawn
The Applicant has amended claim 1 to remove recitation of SEQ ID NO: 5262, and has therefore obviated the double patenting rejection with regards to 18,965,675.
The Applicant has submitted a terminal disclaimer for copending application 17,761,292. The double patenting rejection with respect to ‘292 is therefore withdrawn.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claims 13-14 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Regarding claims 13-14, these claims recite that the truncations are between 20 and 350 amino acids in length. Claims 13-14 depend from claim 12. Claim 12 recites a Type VI Cas protein with 98% sequence identity to one of SEQ ID NOs 4628, 4693, 4741, 4752, 4753, and 5873. The recited sequences range in length from 790-805 amino acids. Thus, given that the longest sequence is 805 amino acids, a sequence with 98% sequence identity would accommodate (0.02) x (805) = 16.1, or 16 variations (i.e., a given sequence can have a maximum of 16 mutations, deletions, etc., according to the claim language). Accordingly, recitation of truncations ranging from 20-350 amino acids as recited in claims 13-14 do not include the limitations of claim 12, which includes a maximum variation from the recited sequences of 16 amino acids.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 112 – New Matter Rejection
Claims 12-20, 23, 26-28, and 30 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. This is a new matter rejection.
Regarding claim 12, claim 12 recites a Type VI Cas protein with 98% sequence identity to one of SEQ ID NOs 4628, 4693, 4741, 4752, 4753, and 5873. The recited sequences range in length from 790-805 amino acids. Thus, given that the longest sequence is 805 amino acids, a sequence with 98% sequence identity would accommodate (0.02) x (805) = 16.1, or 16 variations in the amino acid sequence (i.e., a given sequence can have a maximum of 16 mutations, deletions, etc., according to the claim language).
With regards to the specification, the Applicant offers a discussion of embodiments of Cas proteins with truncations (paragraphs 338-341). The specification recites embodiments of truncations ranging from truncations of 20 amino acids to 400 amino acids (paragraphs 339). Thus, the specification does not appear to contemplate truncations of the N- and C- termini where the truncations include 16 amino acids or fewer, as presently recited in the claims.
Claims 13-20, 23, 26-28, and 30 depend from claim 12 and do not resolve this new matter issue and are therefore also rejected.
Claim Rejections - 35 USC § 112 – New Rejection
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.
Claims 5, 12-20, 23-28 and 30 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.
Regarding claim 5, claim 5 recites that the Cas protein is associated with one or more “functional domains.” Thus, claim 5 is broadly drawn to a genus of “functional domains” where furthermore such functional domains can comprise any number of combinations or embodiments (“one or more” functional domains). This claim language is problematic because it is known in the art that protein functional domains can comprise diverse and unpredictable functions, where the complexity and unpredictability of the recited functional domains is compounded by the fact that the claim language includes embodiments where functional domains are combined (“one or more”). The specification does not demonstrate possession of the genus “functional domains” as presently recited.
Regarding the specification, the specification does not offer a clear definition for “functional domain,” thus the plain meaning of the term in this context is taken to mean a protein domain with any given function. Thus, recitation of ‘functional domain” broadly includes any protein domain with a function. With regards to reduction to practice, the specification offers Examples 1-4. Examples 1-2 relate to detection methods using systems described in the specification, where Example 2 describes the characterization of novel Cas enzymes. Example 3 characterizes exemplary small Cas proteins. In Example 3, the Applicants fused the novel Cas enzymes with deaminases functional domains and demonstrated that such fusions were capable of site-specific base conversions (paragraphs 1162-1163). Example 4 is directed to identical subject matter as Example 3. Thus, the Applicant has fused deaminase domains with the recited Cas proteins and demonstrated functionality of such fusions.
Regarding the state of the art, it is known that functional domains of proteins are complex and unpredictable. For example, Goodacre (Goodacre NF et al. mBio. 2013 Dec 31;5(1):e00744-13) is a research article which focuses on protein domains of unknown function within bacteria (Title, Abstract, and throughout). Goodacre teaches that:
“More than 20% of all protein domains are currently annotated as “domains of unknown function” (DUFs). About 2,700 DUFs are found in bacteria compared with just over 1,500 in eukaryotes. Over 800 DUFs are shared between bacteria and eukaryotes, and about 300 of these are also present in archaea. A total of 2,786 bacterial Pfam domains even occur in animals, including 320 DUFs,” (Abstract).
Thus, Goodacre teaches that the genus of protein “functional domains” is known to be uncharacterized and by extension unpredictable because it is known in the art that large portions of protein domains are not functionally characterized across multiple organisms (Goodacre, above). Furthermore, the issue of uncertainty and complexity are compounded by the fact that, given that thousands of protein functional domains are undefined, their functionality with a “Type VI Cas protein,” and/or how such unknown protein domains may influence or interfere with such a Cas protein is similarly unpredictable. In addition, such unpredictability is compounded by the fact that claim 5 recites that “one or more” functional domains may be present which includes combinations of undefined protein domains.
The Applicant has not shown possession of the genus “functional domain” because it is known as taught by Goodacre that such a genus is uncharacterized, where furthermore the Applicant’s specification has not demonstrated possession of this genus.
Regarding claims 12, claim 12 recites that the Cas protein “comprises an N-terminal truncation, a C-terminal truncation, or both.” Thus, claim 12 is broadly drawn to a protein with recited functionality of being a Cas protein, where furthermore the Cas protein is recited with structural modifications including N- and/or C-terminal truncations. This claim language is problematic because the Applicant has not characterized truncated Cas proteins commensurate in scope with what is being claimed.
Regarding the guidance provided in the specification, the Applicant recites that N- and C-terminal truncations can comprise between 20-400 amino acid truncations from either the N or C-termini (paragraph 339). Regarding the recited sequences in claim 12 (SEQ ID NOs 4628, 4693, 4741, 4752, 4753, and 5873), these sequences are roughly 800 amino acids in length. Thus, the Applicant is broadly claiming in claims 12 and 13 embodiments of the recited sequences which are truncated by, for instance, 350 amino acids at the N and C-termini. A truncation of 350 amino acids at both of the termini would therefore yield a Cas protein that is approximately 100 amino acids in length, where such a sequence is recited with the functional limitations of being a “Cas” protein. The Applicant has not reduced to practice in the Examples embodiments with such extreme truncations, nor given clear indication that such truncations would yield functional Cas proteins.
Regarding the state of the art, it is known that Cas proteins require functional domains, and furthermore that Cas proteins are not known to be as short as presently claimed. For instance, Savage (Savage DF. Biochemistry. 2019 Feb 26;58(8):1024-1025) is a research article which focuses on small Cas variants (Title, Abstract, and throughout). Savage teaches that “recently discovered CasX variant, but are notable for their extremely small size, being roughly ~400–700, rather than the typical 1000+ amino acids of Class 2 variants,” (page 1, second paragraph). Savage therefore teaches that “extremely” small Cas variants range in size from 400-700; thus, lower limits of functional Cas proteins are larger than the presently recited truncated Cas variants. Given that the Applicant has not characterized truncated variants in the size ranges presently encompassed and recited in the claims, and further that the smallest Cas proteins known are between 400-700 residues in length, a greater burden exists on the Applicant to demonstrate that the claimed genus of truncated Cas variants would retain the structure-function relationship presently recited in the claims (i.e., claim 12 recites that the sequences are Cas proteins which imparts functionality on them which is structurally coupled to truncated versions of these sequences).
Claims 13-20, 26-28 and 30 depend from claim 12 and do not resolve this 112(a) issue and are therefore also rejected.
Claim Rejections - 35 USC § 112 – Maintained/Updated to Include Rejoined Claims Not Previously Examined
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 24-28 and 30 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.
MPEP 2163.II.A.3.(a).i) states, “Whether the specification shows that applicant was in possession of the claimed invention is not a single, simple determination, but rather is a factual determination reached by considering a number of factors. Factors to be considered in determining whether there is sufficient evidence of possession include the level of skill and knowledge in the art, partial structure, physical and/or chemical properties, functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and the method of making the claimed invention”.
For claims drawn to a genus, MPEP § 2163 states the written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus. See Regents of the University of California v. Eli Lilly & Co, 119 F.3d at 1568, 43 USPQ2d at 1406.
Regarding claim 24, claim 24 recites a method of treating a disease associated with RNA splicing, transport, localization, translation, and/or turnover, comprising administering a composition of claim 1, where the composition modulates splicing, transport, localization, translation, and/or turnover associated with the disease. Claim 24 therefore recites the claim limitation of claim 1, where claim 1 recites a composition comprising a Cas protein which forms a complex with a gRNA which directs the complex to a target sequence. Claim 24 therefore broadly recites “target sequences,” where furthermore the claim recites that a disease is treated by the administering of the composition of claim 1, which requires a “target” to be bound by the complex of claim 1. Claim 24 therefore broadly recites the genus of “target sequence” which can be targeted to affect a change/treatment in a disease associated with, for instance, DNA splicing. As discussed further below, the Applicant was not in possession of the broad genus of such targets as those recited with the specific function of treating a disease associated with RNA splicing because, as it was known in the art at the time of filing, RNA splicing variants and targets associated with diseases were known to be an unpredictable genus.
Furthermore, claim 26 encompasses the same genus as claim 24, where claim 26 depends from claim 12 which recites a Cas protein which requires a “target” where claim 26 is recited to treat a disease. Claim 26 therefore recites the genus of “target sequences” (per claim 12) which could functionally be targeted to treat a disease, which would reasonably include diseases associated with RNA splicing as presently recited in claim 24. Thus, the present rejection focuses on diseases associated with RNA splicing, as such subject matter is encompassed by both of the method claims of claims 24 and 26, and their dependent claims.
With regards to the specification, the Applicant has not shown possession of the claimed subject matter. The Applicant has classified and characterized a few Cas enzymes and reduced their functionality to practice. For instance, the Applicant recites Example 4 and demonstrated that the smaller Cas proteins identified can act as RNA base editors (paragraphs 1265-1274). The Applicant has reduced to practice such methods in HEK293 reporter constructs (paragraph 1269). The Applicant has not taught and reduced to practice specific targets using their methods for diseases such as cancer and AMD (as recited in claim 25). The Applicant recites RNA knockdown and editing assays (e.g., paragraphs 1299-1304). The Applicant also offers Table 10 which includes a list of diseases and genes associated with said diseases which could potentially be targeted by their systems (Table 10, paragraph 962).
However, with regards to the state-of-the-art, it is known that targets for diseases associated with RNA splicing are complex and unpredictable. For instance, Truty (Truty R et al. Am J Hum Genet. 2021 Apr 1;108(4):696-708) is a research article which focuses on RNA splicing variants and their association with disease (Title, Abstract, and throughout). Truty teaches that:
“The complexities of gene expression pose challenges for the clinical interpretation of splicing variants. To better understand splicing variants and their contribution to hereditary disease, we evaluated their prevalence, clinical classifications, and associations with diseases, inheritance, and functional characteristics in a 689,321-person clinical cohort and two large public datasets. In the clinical cohort, splicing variants represented 13% of all variants classified as pathogenic (P), likely pathogenic (LP), or variants of uncertain significance (VUSs). Most splicing variants were outside essential splice sites and were classified as VUSs,” (Abstract).
Truty further teaches that natural variations of splicing confound the clinical relevance of splice variants (Abstract).
Truty teaches that:
“Variants that may alter RNA splicing can be computationally predicted, and these predictions can be confirmed by RNA analysis. However, assessing the clinical consequences of abnormal splicing can be challenging because of an incomplete understanding of alternative splicing and normal RNA expression profiles across tissues. Some studies have revealed previously unrecognized variety in RNA transcript isoforms associated with well-studied genes, including BRCA1 and BRCA2, showing that our understanding of naturally occurring alternative splicing of disease gene transcripts is still evolving. Recent studies have also illuminated how differential expression of transcript isoforms can influence whether certain sequence variants are tolerated. As a result of this underappreciated complexity, variants that allow biologically viable alternative
splicing may be incorrectly classified as disease causing. Therefore, investigating both the spectrum of variants predicted or assumed to cause abnormal splicing
across a broad variety of genes and their contribution to naturally existing genomic variation is essential to understanding their overall involvement in hereditary disease,” (Introduction, first paragraph).
Thus, Truty teaches that there is known unpredictability when attempting to define RNA splicing associated with diseases, where large cohort models and direct RNA analysis is required in order to help clinical interpretation (Abstract, and Introduction).
Truty further teaches that:
“Several computational tools are used to predict the potential splicing effects of variants encountered during clinical genetic testing for hereditary disease. However, these tools often do not have a high positive predictive
value when used individually, particularly for variants outside the essential splice site(s) (ESS). Therefore, their predictions are often not considered usable evidence for variant interpretation unless there is consensus among them,” (Introduction, first paragraph).
Truty therefore teaches that prediction methods for the effects of RNA splice variants and their clinical roles are unpredictable, where Truty further teaches that previously identified variants with unknown significance can be classified as pathogenic splice variants or benign based upon further analysis (Introduction, first paragraph, final sentence).
Truty further teaches that:
“Furthermore, the challenge of interpreting splicing variants is not limited to hereditary cancer and has been noted in other disease areas, such as inherited retinal diseases. To avoid negative outcomes, it is essential to consider a variety of types of evidence for variant interpretation and to use appropriate control samples during RNA analysis. Compounding the challenge of accurately interpreting the effects of a splicing variant is the conundrum of defining which one or a subset of transcript isoforms may be affected. This has implications for identifying molecular etiologies of disease through genetic testing because clinical laboratories may sometimes choose a single reference transcript when reporting observed variants. In some cases, the chosen reference transcript may not be fully relevant to the disease in question (and the prediction of splicing effects can be dependent on the transcript chosen), leading to missed diagnoses. It is expected that clinical interpretation of variants identified during genetic testing for inherited disease will eventually consider the individual expression patterns of specific transcripts for each disease gene and how those patterns may affect the manifestation of disease. Various studies have shed light on the complexity of gene expression through discovery of novel exons, complex interactions between splicing variants and tissue-specific effects, the effect of cellular context on splicing in the absence of variants that affect splicing (e.g., in the progeria-related LMNA gene [MIM:150330]), and quantitative effects of transcript isoforms on clinical phenotypes,” (page 704, left column, paragraphs 1-2).
Truty therefore teaches that RNA splice variants and their exact roles in diseases – including cancer and retinal diseases such as those recited in instant claims 25 and 30 – are complex and undefined. Given that such uncertainty and complexity exists concerning the classification and roles of specific RNA splice variants in disease, the effects of targeting such an RNA in the context of a given disease are also unpredictable. The Applicant was therefore not in possession of the genus “target sequence” as recited in claim 1 and by extension claims 24-28 and 30 as such a genus is unpredictable and uncharacterized. Furthermore, the teachings of Truty generally teach that the genus of target in the context of what such a target would be in order to act as a treatment in the context of disease is largely undefined (see specific passages quoted above, and throughout Truty). In short, the genus of “target” in the context of DNA-splicing associated disease is known to be uncharacterized; the Applicant has not characterized this genus or defined and recited specific targets commensurate in scope with what is claimed.
Response to Arguments
The Applicant’s arguments filed 3/26/2026 have been considered but are not persuasive. The Applicant argues that the specification discloses specific sequences for targeting a disease such as AMD, including VEGF, VEGF-R1, RTP801. The Applicant argues that they have disclosed/recited general RNA splicing targets to include targeting of splice junction and exonic splicing enhancers, and splicing defects associated with diseases cystic fibrosis. Thus, the Applicant has identified a few examples of specific targets.
This argument is not persuasive because as discussed above, Truty teaches that the identification of RNA targets and RNA splicing variant targets is an unpredictable and uncharacterized genus. Thus, the genus of “target sequence” was not shown to be in possession by the Applicant by offering only a limited number of examples (see the 112(a) rejection, above, for a further discussion of Truty and the uncharacterized genus of target sequences which could be associated with RNA splicing and disease). As the Applicant states, they have offered only specific examples (e.g., VEGF). However, the Applicant’s limited number of specific examples is not adequate to demonstrate possession of the larger genus owing to the known predictability of the genus as taught by Truty.
The Applicant argues that a practitioner at the time of filing would know/understand what RNA splicing deficiencies would be relevant for a given disease context, and that gRNAs would be easy to design for a given disease. This argument is not persuasive because it is an argument of counsel not supported by evidence. MPEP 716.01(c) makes clear that arguments of counsel cannot take the place of evidence in the record. While a gRNA could be synthesized, the ultimate issue relates to what the gRNA will target to treat a given disease. Given that Truty teaches the unpredictability of RNA splice variants in diseases, the genus of target sequence for a specific disease does not appear to be readily available knowledge for a practitioner, as the Applicant has argued.
The Applicant argues that Truty’s teaching of the complexity of RNA splice variants and targets has not bearing over the present application, arguing that the present specification offers specific examples of mRNA targets such as VEGF for AMD and splice junctions and ESEs for DMD. This argument is not persuasive because the present claims are drawn to a broad genus and not the specific targets recited in the specification. Truty’s teachings are relevant because they speak to the complexity of RNA targets in the context of disease (see 112(a) rejection, above). Given that the Applicant has not recited specific targets in the claims, offers only a few targets in the specification, and has not reduced to practice the treatment of disease, the evidence in the art teaches unpredictability and demonstrates the lack of possession of the presently recited subject matter of claims 24-28 and 30.
Allowable Subject Matter
Claim 1 and its dependent claims are drawn to Cas nucleases with 98% sequence identity to SEQ ID NOs 4628, 4693, 4741, 4752, 4753, and 5873. Both ABSS and NCBI BLAST (Patent and Cluster Databases) were searched. The search returned no prior art results for the recited sequences in the claims, nor a reasonable suggestion to arrive at such sequences, where the limitations of the claims require heterologous guide sequences which can form with the recited Cas proteins. Thus, claim 1 and its dependent claims are free of the art.
Furthermore, claim 1 recites a composition comprising Cas proteins and heterologous guide RNAs. Recitation of heterologous guide RNAs as a required limitation of the composition renders the claim subject matter eligible, as such a composition with heterologous guide RNAs would not be a naturally occurring product of nature. Claim 1 is therefore subject matter eligible.
Furthermore, the Applicant’s have identified six Cas13 enzymes, reduced to practice targeting of mammalian genes using two of the newly identified family of Cas13 enzymes, have performed HEPN domain mutational analysis to render catalytically dead/inactive forms of the Cas13 proteins, and fused the dCas13 proteins to active deaminases to direct A-to-I editing in mammalian targets (see Example 3). The Applicants have furthermore made mutational predictions and reduced to practice E620G and Q696L variants, where the mutants reduced off-target effects as predicted. Thus, the applicant was reasonably in possession of the claimed invention, where furthermore a practitioner is enabled without undue experimentation to make and use the invention of claims 1-4,6-11 and 21-22.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to DOUGLAS CHARLES RYAN whose telephone number is (571)272-8406. The examiner can normally be reached M-F 8AM - 5PM.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Ram Shukla can be reached at (571)-272-0735. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/D.C.R./Examiner, Art Unit 1635
/RAM R SHUKLA/Supervisory Patent Examiner, Art Unit 1635
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