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 .
Priority
Applicant’s claim to priority from International Application No. PCT/US2022/021263 filed 03/22/2022 and from Provisional Applications Nos. 63/304,170 filed 01/28/2022 and 63/164,396 filed 03/22/2021 is hereby acknowledged.
Election/Restrictions
Applicant’s election without traverse of invention Group I (claims 1-2, 4-6, 8, 13-14, 19, 22 and 24, drawn to a method for increasing the endogenous expression of a Low-Density Lipoprotein Receptor (LDLR) gene in a cell) in the reply filed on 03/10/2026 is acknowledged.
Claims 28-29, 32, and 34-39 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.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 03/10/2026.
Applicant is reminded that upon the cancelation of claims to a non-elected invention, the inventorship must be corrected in compliance with 37 CFR 1.48(a) if one or more of the currently named inventors is no longer an inventor of at least one claim remaining in the application. A request to correct inventorship under 37 CFR 1.48(a) must be accompanied by an application data sheet in accordance with 37 CFR 1.76 that identifies each inventor by his or her legal name and by the processing fee required under 37 CFR 1.17(i).
Application Status
The instant Application is a National Entry phase of Application No. PCT/US2022/021263 filed 03/22/2022 under 35 U.S.C. §371.
Preliminary amendments of claims filed 03/10/2026 are hereby acknowledged.
Claims 1-27, 30-31, and 33 are cancelled. Claims 28-29, 32 and 34-39 are withdrawn. Claims 40-49 are newly added. Therefore, claims 28-29, 32, 34-39 and 40-49 are pending; however, only claims 40-49 are considered and under examination in this Office Action.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 09/21/2023 is hereby acknowledged. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
However, the listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Drawings
The Drawings filed 09/21/2023 are acceptable.
Specification
The use of the terms “Dylight” (page 6, line 31; page 7, line 6; page 8, lines 10 and 20), “ Sonitron 2000” (page 33, line 30), “PiggyBac” (page 34, line 4), “EnGeneIC delivery vehicles (EDVs)” (page 34, [0162]), which are trade names or marks used in commerce, has been noted in this application. The terms should be accompanied by the generic terminology; furthermore the terms should be capitalized wherever they appear or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
Claim Rejections - 35 USC § 112
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 41-49 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.
Claims 41-43 and 47-48 recite the limitation " The method of claim 1" in preamble. There is insufficient antecedent basis for this limitation in the claim. Claim 1 is cancelled.
Claims 44-45 recite the limitation " The method of claim 4" in preamble. There is insufficient antecedent basis for this limitation in the claim. Claim 4 is cancelled.
Claim 46 recites the limitation " The method of claim 6" in preamble. There is insufficient antecedent basis for this limitation in the claim. Claim 6 is cancelled.
Claim 49 recites the limitation " The method of claim 9" in preamble. There is insufficient antecedent basis for this limitation in the claim. Claim 9 is cancelled.
Regarding claim 49, it further recites “wherein the one or more deletions
delete substantially all of the 3’ UTR of the LDLR gene”.
A definition of the term “substantially” in the Specification is as follows: “Unless otherwise stated, adjectives such as "substantially" and "about" modifying a condition or relationship characteristic of a feature or features of an embodiment of the invention, are understood to mean that the condition or characteristic is defined to within tolerances that are acceptable for operation of the embodiment for an application for which it is intended.” (See [0037]).
The terms “the condition or characteristic is defined to within tolerances that are acceptable for operation of the embodiment” are unclear. Therefore, the language of claim 49 is unclear, and does not permit one of ordinary skills in the art to assess clearly the metes and bounds, and the scope of the invention.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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 40-41, 43-44 and 47-49 are rejected under 35 U.S.C. §103 as being unpatentable over Zhao (Zhao, H. et al. “In vivo AAV-CRISPR/Cas9-mediated gene editing ameliorates atherosclerosis in Familial Hypercholesterolemia”. Circulation, Vol. 141 (2020), pp: 67-79), in view of Björnsson (Björnsson, E. et al.“ Lifelong reduction in LDL (Low-Density Lipoprotein) Cholesterol due to a gain-of-function mutation in LDLR”. Circulation: Genomic and Precision Medicine, Vol. 14, No. 1 (Dec., 14 2020), DOI: 10.1161/CIRCGEN.120.003029), Jiang (Jiang, H. et al. “microRNA-185 modulates low density lipoprotein receptor expression as a key posttranscriptional regulator”. Atherosclerosis, Vol. 243 (2015), pp: 523-532) and Brandl (Brandl, C. et al. “Creation of targeted genomic deletions using TALEN or CRISPR/Cas nuclease pairs in one-cell mouse embryos”. FEBS Open Bio, Vol. 5 (2015), pp: 26-35).
For the purpose of examination, the Examiner interprets that the “base claim” for claims 41, 43-44, and 47-49 is claim 40.
Regarding claim 40, the claim recites “A method of increasing an amount of a Low-Density Lipoprotein Receptor (LDLR) expression in a cell, the method comprising: cleaving an LDLR gene at a first target sequence within the 3' untranslated region (3' UTR) using a first nuclease, and cleaving the LDLR gene at a second target sequence within the 3' UTR using a second nuclease, wherein the method results in one or more deletions within the 3' UTR of the LDLR gene.”
Zhao teaches gene editing in vivo using a AAV-CRISPR/Cas9 system for the correction of LDLR gene (see title and abstract on page 67). Zhao teaches that the gene editing was capable of effectively ameliorate atherosclerosis phenotypes in LDLR mutants (see “Conclusions” on page 67). Therefore, Zhao teaches the use of a CRISPR/Cas9 nuclease system for cleaving an LDLR gene at a target sequence, comprising a single guide RNA and a donor template for homologous recombination and repair (see Figures 1A and 3A). Zhao teaches that the expression of LDLR was partially recovered and detectable after the repair (see Figure 3F). Zhao teaches a net increase in LDLR expression in Group 3 and Group 4 in Figure 3F in terms of protein expression; Zhao teaches an increase in relative mRNA expression in LDLR mRNA in both groups as well (see Figure 3E, G and I).
Although, Zhao teaches the use of nuclease Cas9 to edit LDLR gene, Zhao does not teach a modification within the 3’ untranslated region (3’UTR) of LDLR gene. Zhao does not teach a first and a second target, nor a first and second nuclease, with a result of one or more deletions within the 3’UTR of the LDLR gene.
However, Björnsson teaches the discovery of a 2.5 kb deletion overlapping the 3’ untranslated region (3’UTR) of LDLR in heterozygous carriers in which levels of LDL cholesterol was 74% lower than in non-carriers (see page 2, Abstract). Björnsson teaches that the deletion results in an alternative mRNA isoform with a truncated 3’UTR and expression of said isoform in transformed lymphocytes leads to a 1.84-fold increase in expression of the deletion isoform compared to wild type and 1.79-fold increase of surface expression of the LDL receptor than in non-carriers. Björnsson teaches that this gain-of-function truncation mutation leads to a loss of target sites for microRNAs known to repress translation of LDLR (see page 2, Abstract, “Results” section).
Also, Jiang teaches that the posttranscriptional regulation of LDLR has been reported to be controlled by the 3’-untranslated region (3’UTR)-mediated modulation of mRNA stability, microRNAs being a class of posttranscriptional regulators mostly associated to the 3’UTR of mRNAs (see page 524, left column, lines 5-8 and 20-21). Jiang teaches that miR-185 is among these posttranscriptional regulators of LDLR mRNA (see title and abstract).
Jiang teaches that miR-185 is capable of regulating LDLR expression by direct binding to LDLR mRNA 3’UTR (see page 526, section 3.1). Jiang teaches that miR-185 binding sites are located within Alu-Rich elements (ARE1 and ARE2) (see page 526, right column, lines 9-10).
Jiang teaches the use of an antisense against miR-185 and teaches that this miR-185 inhibitor is capable of increasing the expression of LDLR (see Figure 4B). Jiang teaches that this miR-185 inhibitor not only increases hepatic LDLR expression, but also reduces atherosclerosis progression in vivo (see page 528, section 3.4), by promoting the clearance of plasma cholesterol (see page 530, left column, lines 8-11).
Brandl teaches that CRISPR/Cas and TALEN can be used as pairs of nucleases, i.e., using a first nuclease with a first sgRNA and a second nuclease with a second sgRNA targeting two sites, to create large deletions between the two sites in the genome (see title, Abstract, and section 2.2). Brandl teaches the use of CRISPR/Cas system as an alternative for deletion of 3.2, 10.4, 31.8 or 51.8 kb (see section 2.2, and Figure 3).
Therefore, it would have been obvious to one with ordinary skills in the art, before the effective filing date of the claimed invention, to have modified the target site in the CRISPR/Cas system as taught by Zhao, and targeted the 3’UTR region of LDLR mRNA. One with ordinary skills in the art motivated in treating hypercholesterolemia, in absence of a clearly established polymorphism found responsible for the loss of LDLR expression, and motivated in translating the teachings of Björnsson, Jiang and Brandl into a path to a medicament usable in a wider and genetically heterogenous population, could have targeted the 2.5 kb overlapping the 3’UTR of LDLR mRNA taught by Björnsson, and used two CRISPR/Cas9 systems targeting two sites with specific sgRNAs at each site as taught by Brandl, to reproduce the mutant and phenotype taught by Björnsson, and reduce circulating LDL cholesterol levels in affected subjects. One with ordinary skills in the art could have performed this modification with a reasonable expectation of success, since Zhao and Brandl teach using CRISPR/Cas systems, and Brandl teaches success for deleting longer sequence than 2.5 kb, and arrived at the claimed invention.
Regarding claim 41, the combination of references Zhao, Björnsson, Jiang and Brandl renders the elements of claim 41 obvious, since the CRISPR/Cas system nucleases and sgRNAs are capable of cleaving, and deleting large fragments of genomic DNA. The obviousness of the combination of references is discussed above.
Regarding claims 43 and 44, Jiang teaches that the LDLR’s 3’UTR contains miR-185 site that can be inhibited leading to an increase in LDLR expression (see title and abstract). The combination of references Zhao, Björnsson, Jiang and Brandl renders the elements of claims 43 and 44 obvious, i.e., the deletion of one or more miRNA binding sites from the 3’UTR of the LDLR gene. The obviousness of the combination of references is discussed above.
Regarding claim 47, Jiang teaches that miR-185 binding sites are located within an AU-rich (AUR) region of the 3’UTR of LDLR. Therefore, the combination of references Zhao, Björnsson, Jiang and Brandl renders the elements of claim 47 obvious, i.e., the deletion of one AU-Rich region from the 3’UTR of the LDLR gene. The obviousness of the combination of references is discussed above.
Regarding claim 48, Björnsson teaches that deletion of 2.5 kb results in an increase of 1.84 fold of LDLR expression and a decrease of 74% of LDL in blood of carriers of this mutation (see title and abstract). Therefore, deleting more than 1,000 base pairs from the targeted sequence is rendered obvious by the combination of references Zhao, Björnsson, Jiang and Brandl. The obviousness of the combination of references is discussed above.
Regarding claim 49, Björnsson teaches that deletion of 2,485 bp overlapping the poly-A tail end and part of the 3’UTR (see page 5, lines 4-7). Jiang teaches that the Human LDLR mRNA contains a 2.5 Kb—long 3’ UTR in which four AU-rich elements are identified as crucial cis-regulatory elements for the rapid decay of LDLR mRNA (see page 524, lines 5-11). Jiang also teaches that deleting multiple regions of the 3’UTR and different AUR is enough to increase the expression of a recombinant construct more than 2-fold (see Figure 3D and 3E).
It would have been therefore obvious to one with ordinary skills in the art, before the effective filing date of the claimed invention, to have deleted the whole 3’UTR region, i.e., 2.5 Kb, of the LDLR gene as taught by the Jiang and Björnsson, and modified the CRISPR/Cas system using two sgRNAs that allow for deletion for the 3’UTR region of LDLR, as taught by Zhao modified by Brandl. One with ordinary skills in the art, motivated to increase the expression of LDLR gene by at least 1.84-fold and obtain a reduction in blood LDL cholesterol by 74% in patients presenting with hypercholesterolemia, could have performed this modification with a reasonable expectation of success and arrived at the claimed invention.
Claim 42 is rejected under 35 U.S.C. §103 as being unpatentable over Zhao (Zhao, H. et al. “In vivo AAV-CRISPR/Cas9-mediated gene editing ameliorates atherosclerosis in Familial Hypercholesterolemia”. Circulation, Vol. 141 (2020), pp: 67-79), in view of Björnsson (Björnsson, E. et al.“ Lifelong reduction in LDL (Low-Density Lipoprotein) Cholesterol due to a gain-of-function mutation in LDLR”. Circulation: Genomic and Precision Medicine, Vol. 14, No. 1 (Dec., 14 2020), DOI: 10.1161/CIRCGEN.120.003029), Jiang (Jiang, H. et al. “microRNA-185 modulates low density lipoprotein receptor expression as a key posttranscriptional regulator”. Atherosclerosis, Vol. 243 (2015), pp: 523-532) and Brandl (Brandl, C. et al. “Creation of targeted genomic deletions using TALEN or CRISPR/Cas nuclease pairs in one-cell mouse embryos”. FEBS Open Bio, Vol. 5 (2015), pp: 26-35), as applied to claim 40 above, and in further view of Pak (Pak, Y.K. et al. “Activation of LDL receptor gene expression in HepG2 cells by hepatocyte growth factor”. Journal of Lipid Research, Vol. 37 (1996), pp: 985-998).
For the purpose of examination, Examiner interprets that the “base claim” for claim 42 is claim 40.
The rejection of claim 40 is described above.
Regarding claim 42, Björnsson teaches that the deletion mutation overlapping 2.5 kb of 3’UTR of LDLR gene leads to a decrease of LDL cholesterol level of 74% in subjects compared to non-carriers (see page 2, Abstract). Björnsson teaches that the deletion results in an alternative mRNA isoform with a truncated 3’UTR and expression of said isoform in transformed lymphocytes leads to a 1.84-fold increase in expression of the deletion isoform compared to wild type and 1.79-fold increase of surface expression of the LDL receptor than in non-carriers (see page 2, Abstract).
Jiang teaches that the Human LDLR mRNA contains a 2.5 Kb—long 3’ UTR in which four AU-rich elements are identified as crucial cis-regulatory elements for the rapid decay of LDLR mRNA (see page 524, lines 5-11). Jiang also teaches that deleting multiple regions of the 3’UTR and different AUR is enough to increase the expression of a recombinant construct more than 2-fold (see Figure 3D and 3E).
However, manipulating the 3’UTR, deleting different AU-rich regions, Jiang was not able to show an increase of more than 1.8-2% in LDLR expression (see Figure 3B and 3C).
Zhao teaches that “Although the current AAV-CRISPR/Cas9-mediated Ldlr gene-editing system was not effective enough to completely rescue the atherosclerosis- or hypercholesterolemia-related phenotypes, the partial amelioration by gene therapy could be combined with conventional interventions such as medication for LDL cholesterol reduction and diet modification to provide better therapeutic effects for individuals” (see page 76, right column, lines 4-11).
Therefore, the combination of Zhao, Björnsson, Jiang and Brandl fails to teach an increase at least 2-fold in LDLR gene expression. However, Zhao suggests a combination of therapeutic approaches.
Examiner also interprets the claim stating “a method of increasing an amount of Low-Density Lipoprotein Receptor (LDLR) expression in a cell, the method comprising:”
Examiner interprets that the method can comprise a combination of approaches as suggested by Zhao.
Pak teaches that the LDLR gene expression can be activated by hepatocyte growth factor (HGF) (see title). Pak teaches that a sterol-mediated induction of the LDLR promoter is mediated by a ten nucleotide element called SRE-1 (see page 985, right column, last line). Pak teaches that increasing concentrations of HGF result in hepatocytes’ uptake of LDL (see Figure 1) and increase in LDLR expression (see Figure 4). In Figure 4, the expression in mRNA is increased from about 0.075 to 0.25 relative units. This represents an increase of 3.3-fold. Pak also shows that the increase in mRNA levels of LDLR is due to an increase of amount of mRNA, and not to an increase in mRNA stability (see Figure 5, and page 993, left column, lines 1-4). In Figure 5, panel A, comparing lanes 1 and 5, Pak teaches that the increase in mRNA level was 3.7-fold.
Therefore, it would have been obvious to one with ordinary skills in the art, before the effective filing date of the claimed invention, to have deleted the whole 3’UTR region, i.e., 2.5 Kb, of the LDLR gene, using a CRISPR/Cas9 system as taught by the combination of Zhao, Björnsson, Jiang and Brandl, and add a medication to supplement the gene therapy, as suggested by Zhao. One with ordinary skills in the art, could have combined the gene therapy with another molecule such as a recombinant HGF, or a vector carrying the recombinant HGF gene, with a reasonable expectation of success. One with ordinary skills in the art, motivated in increasing the expression of LDLR gene by more of 2-fold and obtaining a complete rescue of the phenotype in patients presenting with hypercholesterolemia, could have performed this modification with a reasonable expectation of success and arrived at the claimed invention.
Claims 45 and 46 are rejected under 35 U.S.C. §103 as being unpatentable over Zhao (Zhao, H. et al. “In vivo AAV-CRISPR/Cas9-mediated gene editing ameliorates atherosclerosis in Familial Hypercholesterolemia”. Circulation, Vol. 141 (2020), pp: 67-79), in view of Björnsson (Björnsson, E. et al.“ Lifelong reduction in LDL (Low-Density Lipoprotein) Cholesterol due to a gain-of-function mutation in LDLR”. Circulation: Genomic and Precision Medicine, Vol. 14, No. 1 (Dec., 14 2020), DOI: 10.1161/CIRCGEN.120.003029), Jiang (Jiang, H. et al. “microRNA-185 modulates low density lipoprotein receptor expression as a key posttranscriptional regulator”. Atherosclerosis, Vol. 243 (2015), pp: 523-532) and Brandl (Brandl, C. et al. “Creation of targeted genomic deletions using TALEN or CRISPR/Cas nuclease pairs in one-cell mouse embryos”. FEBS Open Bio, Vol. 5 (2015), pp: 26-35), as applied to claim 40 above, and in further view of Goedeke (Goedeke, L. et al. "MicroRNA-148a regulates LDL receptor and ABCA1 expression to control circulating lipoprotein levels." Nature Medicine, Vol. 21, No. 11 (2015), pp: 1280-1289, and online Methods) .
For the purpose of examination, Examiner interpreted that the “base claims” for claims 45 and 46 are claims 40 and 43.
The rejections of claims 40 and 43 are described above.
Regarding claims 45 and 46, Björnsson teaches that the deletion mutation
overlapping 2.5 kb of 3’UTR of LDLR gene leads to a decrease of LDL cholesterol level of 74% in subjects compared to non-carriers (see page 2, Abstract).
Jiang teaches that the Human LDLR mRNA contains a 2.5 Kb—long 3’ UTR in which four AU-rich elements are identified as crucial cis-regulatory elements for the rapid decay of LDLR mRNA (see page 524, lines 5-11). Jiang teaches deletion of at least 3 AU-Rich regions in LDLR gene (see Figure 3D).
The combination of references, Zhao, Björnsson, Jiang and Brandl, does not teach miR148 binding sites.
However, Goedeke teaches miR148 regulates LDLR gene expression and activity (see title, and page 1281, right column, second paragraph). Goedeke teaches that there are two predicted miR148 binding sites in 3’UTR of LDLR gene, at position 872-878 and 1971-1978 (see Figure 2B). Goedeke teaches that transfecting the cells with an inhibitor of miR148 results in an increase of LDLR mRNA level (see Figure 2E and 2F).
Therefore, it would be obvious to one with ordinary skills in the art, before the effective filing date of the claimed invention, to have deleted the whole 3’UTR region, i.e., 2.5 Kb, of the LDLR gene, using a CRISPR/Cas9 system as taught by the combination of Zhao, Björnsson, Jiang and Brandl, and consequently have deleted two binding sites for miR-148 as taught by Goedeke. One with ordinary skills in the art, could have combined the gene therapy as taught by the combination of Zhao, Björnsson, Jiang and Brandl, and would have obtained an LDLR gene truncated from 3’UTR that is also resistant to miR148-induced repression with a reasonable expectation of success. One with ordinary skills in the art, motivated to increase the expression of LDLR gene and obtain a rescue of the phenotype in patients presenting with hypercholesterolemia, could have performed this modification with a reasonable expectation of success and arrived at the claimed invention.
Conclusion
No claim is allowed.
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/A.D./Examiner, Art Unit 1636
/NANCY J LEITH/Primary Examiner, Art Unit 1636
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