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 .
Applicant’s response filed 10/31/2025 has been received and considered entered. This is a response to amendments and arguments filed 10/31/2025.
Election/Restrictions
Claims 38-39, 41-42, 48-49, 54-55, 58-62, 65, 67 stand withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions (claims 38-39 and 41-42 are drawn to unelected invention of Group II; claim 48 is drawn to unelected invention of Group III; claim 49 is drawn to unelected Group IV; claims 54-55 are drawn to unelected invention of Group V; claim 58 is drawn to unelected invention of Group VI; claims 59-62, 65, and 67 are drawn to unelected invention of Group VII), there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 06/03/2025.
Claims Status
Claims 3-7, 10-16, 18-20, 23, 29, 31, 34, 36, 38- 43, 46-49, 52, 54-70 is/are cancelled. Claims 1-2, 8-9, 17, 21-22, 24-28, 30, 32-33, 35, 37, 44-45, 50-51, 53 is/are currently pending with claims 38-39, 41-42, 48-49, 54-55, 58-62, 65, 67 withdrawn. Claims 1-2, 8-9, 17, 21-22, 24-28, 30, 32-33, 35, 37, 44-45, 50-51, 53 is/are under examination.
Information Disclosure Statement
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.
The information disclosure statement filed 12/09/2021 fails to comply with 37 CFR 1.98(a)(2), which requires a legible copy of each cited foreign patent document; each non-patent literature publication or that portion which caused it to be listed; and all other information or that portion which caused it to be listed. It has been placed in the application file, but the information referred to therein has not been considered. Copies of FOR12 and 17 and NPL 21, 23, and 25-27 were not provided. Furthermore, the examiner notes that the following are duplicate listings in this IDS: FOR1 and FOR19; FOR 16 and FOR21; FOR5 and FOR22; FOR7 and FOR11; NPL23 and NPL26.
Claim Objections
Claims 9 and 50 are objected to because of the following informalities:
Claim 9 recites: “one expression vector, comprising two genes encoding recombinases specific to the paired recombinase recognition sites are under tissue-specific promoters” (lines 2-3). While it is clear from context that it is the two genes that are under the control of tissue-specific promoters, the clause should be amended for grammatical and clarity reasons. The examiner suggests the following amendment: “one expression vector, comprising two genes encoding recombinases specific to the paired recombinase sites and which genes are under the control of tissue-specific promoters”.
Claim 9 recites: “two expression vectors, the first expression vector comprising one gene encoding a first recombinase that is specific to one of the paired recombinase recognition sites, and the second expression vector comprising one gene encoding a second recombinase that is specific to the other of the paired recombinase recognition sites are under tissue-specific promoters” (lines 4-7). While it is clear from context that it is the genes encoding recombinases which are under the control of tissue-specific promoters, the clause should be amended for grammatical and clarity reasons. The examiner suggests the following amendment: “two expression vectors, the first expression vector comprising one gene encoding a first recombinase that is specific to one of the paired recombinase recognition sites, and the second expression vector comprising one gene encoding a second recombinase that is specific to the other of the paired recombinase recognition sites, wherein the gene of the first expression vector and the gene of the second expression vector are each under the control of a tissue-specific promoter”.
Regarding claim 50, the preamble “A isolated mammalian cell” should be amended to “An isolated mammalian cell”.
Appropriate correction is required.
Claim Rejections - 35 USC § 112
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.
Claim 45 is 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 rejection is maintained.
To satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V, v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116. Possession may be shown in a variety of ways including description of an actual reduction to practice, or by showing that the invention was "ready for patenting" such as by the disclosure of drawings or structural chemical formulas that show that the invention was complete, or by describing distinguishing identifying characteristics sufficient to show that the applicant was in possession of the claimed invention. See, e.g., Pfaff v. Wells Eiees., Inc., 525 U.S. 55, 68, 119 S.Ct. 304, 312, 48 USPQ2d 1641,1647 (1998); Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406; Amgen, Inc. v. Chugai Pharm., 927 F. 2d 1200, 1206, 18 USPQ2d 1016, 1021 (Fed. Cir. 1991) (one must define a compound by "whatever characteristics sufficiently distinguish it”).
Claim 45 recites the limitation that the non-human animal model “comprises a gain of function mutation (GOF), an loss of function mutation (LOF), or both”; however, claim 45 does not recite any specific gene or gene family which comprises a GOF or LOF mutation. As such, the broadest reasonable interpretation of this limitation is that any gene comprised in the non-human animal model comprises a GOF or LOF mutation. This creates an enormous genus of mutations that is not adequately described.
Both the claims and specification disclose tumor suppressor genes comprising LOF mutations (e.g., claim 44), proto-oncogenes comprising GOF mutations (e.g., claim 44), and, more broadly, transgenes (comprised in the promoter-less donor vector) comprising GOF or LOF mutations (e.g., paragraph [0008]). However, the disclosure does not describe GOF or LOF mutations comprised in the non-human animal model which are not also comprised in the transgene comprised in the non-human animal model. The specification also does not disclose a representative number of species of GOF or LOF mutations comprised in any gene in a non-human animal model, nor does the specification describe any function or further defining or identifiable characteristic of GOF or LOF mutations comprised in a non-human animal model which would sufficiently further describe or limit the genus of species created by claim 45.
According to the MPEP § 2163, "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 (see i)(A) above), reduction to drawings (see i)(B) above), 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 i)(C) above). See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406. A "representative number of species" means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus. See AbbVie Deutsch land GmbH & Co., KG v. Janssen Biotech, Inc., 759 F.3d 1285, 1300, 111 USPQ2d 1780, 1790 (Fed. Cir. 2014) (Claims directed to a functionally defined genus of antibodies were not supported by a disclosure that "only describe[d] one type of structurally similar antibodies" that "are not representative of the full variety or scope of the genus.")."
In conclusion, claim 45 creates an enormous genus of non-human animal models comprising any GOF or LOF gene mutation in any gene. As discussed above, the disclosure does not disclose a representative number of species of this genus, nor does the specification disclose additional further descriptions which narrow or sufficiently describe the recited genus. As such, claim 45 does not provide sufficient written description.
Response to Arguments
Applicant's arguments filed 10/31/2025 have been fully considered but they are not persuasive. Applicant has argued that one of ordinary skill in the art would recognize that applicants were in possession of animal models “used to recapitulate a disease condition that can be caused by a GOF or LOF” (page 12). However, claim 45 does not require that the animal model by a disease model. The requirements of claim 45 can be fulfilled by a non-human animal model comprising the claimed system and comprising any GOF or LOF, regardless of the correlation of said GOF or LOF with any disease, or the correlation of the transgene or nucleic acid encoding an RNA of the system with any disease. Furthermore, as noted in the rejection above and newly emphasized, the disclosure only describes non-human animal models wherein the GOF or LOF is comprised in the transgene of the claimed system. An artisan would not be able to determine based on the present disclosure that the applicants were in possession of the full breadth of the claimed genus of non-human animal models comprising any GOF or LOF gene mutation in any gene, including a gene that is not comprised in the claimed donor vector. As such, the written description rejection of claim 45 is maintained.
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.
Claim(s) 1-2, 17, 21, 24-28, 30, 32, 35, 37, 44-45, 50 is/are rejected under 35 U.S.C. 103 as being unpatentable over Breunig (WO2017131926A1) in view of Gierut (2014). This is a new grounds of rejection necessitated by amendment.
Regarding claim 1, Breunig teaches a system comprising:
A promoter-less donor vector comprising:
A polyadenylation signal or transcription stop element upstream from a transgene;
The transgene;
Paired recombinase recognition sites;
And one expression vector comprising two genes encoding recombinases specific to the paired recombinase recognition sites, or
Two expression vectors, the first expression vector comprising one gene encoding a first recombinase that is specific to one of the paired recombinase recognition sites, and the second expression vector comprising one gene encoding a second recombinase that is specific to the other of the paired recombinase recognition sites (claim 1).
Regarding claim 2, Breunig teaches that the promoter-less donor vector may further comprise an ORF beginning with a splice acceptor (paragraph [0047]). Breunig also teaches that the promoter-less donor vector comprises a fluorescent reporter (paragraphs [0047]-[0048]). Breunig teaches that the promoter-less donor vector further comprises a polyadenylation signal downstream from the transgene (claim 3). Breunig teaches that the promoter-less donor vector further comprises a post-transcriptional regulatory element (claim 2). Breunig teaches that the promoter-less donor vector comprises at least four polyadenylation signals upstream from the transgene (Fig. 2H). Breunig teaches that the promoter-less donor vector is a viral vector (paragraph [0044]-[0045]), a bacterial artificial chromosome (BAC) (paragraph [0048]), or a plasmid (paragraphs [0029]-[0030], [0048]).
Regarding claim 10, Breunig teaches that the paired recombinase sites are loxP and flippase recognition target (FRT), and the recombinases are cre and flp (claim 5). Breunig also teaches that the paired recognition sites can be Vlox, Slox, or attb, and the recombinases can be VCre, SCre, or phiC31, respectively (paragraph [0062]).
Regarding claim 17, Breunig teaches that the transgene comprises disease-associated mutations (claim 9), the transgene comprises a gain-of function mutation or a loss-of-function mutation (paragraph [0064]), the transgene encodes a factor that increases the proliferation of a neuronal cell (paragraph [0038]), or the transgene encodes a factor which promotes differentiation of a neuronal cell (paragraph [0021]; Fig. 16).
Regarding claim 21, Breunig teaches that the transgene encodes a growth factor (paragraph [0106]).
Regarding claim 24, Breunig teaches that the promoter-less donor vector comprises a PGK polyadenylation signal (pA), a trimerized SV40pA, the transgene, loxP and FRT, a rabbit beta-globin pA, and a woodchuck hepatitis virus post-transcriptional regulatory element (WPRE) (claim 4).
Regarding claim 25, Breunig teaches a promoter-less donor vector comprising: a polyadenylation signal or transcription stop element upstream from a transgene; the transgene; and paired recombinase recognition sites (claims 1, 10).
Regarding claim 26, Breunig teaches that the promoter-less donor vector is a viral vector (paragraph [0044]-[0045]), a bacterial artificial chromosome (BAC) (paragraph [0048]), or a plasmid (paragraphs [0029]-[0030], [0048]).
Regarding claim 27, Breunig teaches that the promoter-less donor vector comprises at least four polyadenylation signals upstream from the transgene (Fig. 2H).
Regarding claim 28, Breunig teaches that the promoter-less donor vector further comprises a polyadenylation signal downstream from the transgene (claims 3, 12) and that the promoter-less donor vector further comprises a post-transcriptional regulatory element (claims 2, 11).
Regarding claim 30, Breunig teaches that the transgene is an oncogene or a proto-oncogene comprising a GOF mutation (paragraph [0065]), or encodes a factor that increases the proliferation of a neuronal cell (paragraph [0038]) or promotes differentiation of a neuronal cell (paragraph [0021]; Fig. 16).
Regarding claim 32, Breunig teaches that the transgene encodes a growth factor (paragraph [0106]).
Regarding claim 35, Breunig teaches that the promoter-less donor vector is introduced into a neuronal stem cell (paragraph [0029]). Breunig also teaches that one or more of the recombinase recognition sites can comprise a mutation (paragraph [0014], Fig. 9: “top sequence loxP” and “bottom sequence loxP” differ by eight nucleotides; this “inversion” of a portion of the loxP sequence constitutes a mutation).
Regarding claim 37, Breunig teaches that the promoter-less donor vector comprises a PGK polyadenylation signal (pA), a trimerized SV40pA, the transgene, loxP and FRT, a rabbit beta-globin pA, and a woodchuck hepatitis virus post-transcriptional regulatory element (WPRE) (claims 4, 13).
Regarding claim 44, Breunig teaches a non-human animal model comprising the system (claim 14). Breunig teaches that the transgene of this system is an oncogene or proto-oncogene comprising a GOF mutation (paragraph [0065]).
Regarding claim 45, Breunig teaches that the non-human animal model is “personalized” in order to model a human subject’s cancer, disease, or condition by designing the transgene such that it encodes a protein which causes or promotes the cancer, disease, or condition (paragraph [0039]).
Regarding claim 50, Breunig teaches an isolated mammalian cell comprising the system (claim 19; paragraph [0029]).
However, Breunig does not teach that the loxP and FRT recognition sites are variant loxP and FRT recognition sites, as required by claims 1 and 25.
Gierut teaches that variant loxP and FRT recognition sites were known in the art as alternatives to wild-type loxP and FRT recognition sites.
Regarding claims 1 and 25, Gierut teaches that variant loxP recognition sites lox2272, lox m2, lox66, and lox71 are recognized by wild-type Cre, and that variant flippase recognition sites F3 and F5 are recognized by wild-type flippase (FLP) (Table 1).
As Gierut teaches that variant loxP and FRT recombination sites were known in the art at the time of filing and were compatible with wild-type Cre and Flp, respectively, it would have been obvious to an artisan to substitute variant loxP and FRT recombination sites for wild-type loxP and FRT recombination sites as equivalent structures with equivalent function. Moreover, Gierut teaches that variant Cre and Flp target sites can be used in systems where multiple different recombination sites are desired, as variant Cre and Flp recombination sites exhibit no or low recombination with wild-type Cre and Flp recombination sites, respectively (pages 346-347). A particular example Gierut describes is the targeting of multiple different mutated genes by a recombinase system (pages 346-347). One stated purpose of the system of Breunig is the creation of disease models (claim 17) and of lineage-tracing populations of modified and unmodified cells and animals (paragraphs [0017], [0037]). Based on the teachings of Gierut, the system of Breunig could be enhanced to improve modeling of diseases associated with multiple different mutant alleles or studying the effects of different gene mutation combinations by adding to the system a second promoter-less donor vector comprising variant loxP and FRT recombination sites and a different transgene or nucleic acid encoding an RNA. For example, multiple insertion site/donor vector combinations depicted in Fig. 12 could be combined in one cell or animal, allowing for cell and animal models of multi-allele diseases and for control over the precise insertion site of each donor vector.
Claim(s) 1-2, 8-9 is/are rejected under 35 U.S.C. 103 as being unpatentable over Breunig (WO2017131926A1) and Gierut (2014), as applied to claims 1-2 above, and further in view of Jackson (2016). This rejection is amended to reflect that claims 1-2 are newly rejected over Breunig and Gierut, and is otherwise maintained.
The teachings of Breunig and Gierut can be combined to render obvious the required limitations of claims 1-2, as described above.
However, Breunig does not teach that the donor vector is an adeno-associated viral (AAV) vector, nor that tissue-specific promoters are used.
Jackson teaches the use of AAV vectors and tissue-specific promoters in methods of neuronal transduction.
Regarding claim 8, Jackson teaches tissue-specific promoters, such as the synapsin promoter (abstract; pages 1-2).
Regarding claim 9, Jackson teaches that AAV vectors, such as AAV9 and AAV-PHP.B, are used in methods of neuronal gene transduction, including for transfer of cre-lox systems, for tissue specificity (abstract; pages 1-2; page 5).
Breunig teaches that genetically-engineered mouse models are useful for tissue-specific genetic studies (paragraph [0002]), but does not describe methods for promoting such tissue specificity. Furthermore, Breunig teaches the use of promoter-less donor vectors in neuronal stem cells and brain tissues (see, for example, Figs. 1-2), and teaches that cells comprising the promoter-less donor vectors can be administered locally or systemically (paragraph [0102]). Given that Breunig teaches that tissue specificity is desirable and optimal, it would have been obvious to a person of ordinary skill in the art at the time of filing that specific sequence or structural elements, or delivery mechanisms, must be added to the system taught by Breunig in order to ensure or promote tissue specificity. Jackson teaches that AAV vectors are widely used for gene transfer (including transfer of cre-lox systems, like that of Breunig; page 1), and that furthermore, specific AAV serotypes can be used to promote transduction of specific cell types and tissues (pages 1-2). Furthermore, Jackson teaches that it is commonly known that cell-type specific promoters are necessary for neuronal targeting, and promoters like the synapsin promoter are commonly used for neuronal targeting of transgene expression (page 2). Therefore, it would have been obvious to a person of ordinary skill in the art at the time of filing that the system of Breunig should be modified by placing the recombinase genes under the control of tissue-specific promoters and by utilizing an AAV vector as the donor vector, in order to restrict transduction and expression of the donor vector and donor sequence to the specific desired cell populations or tissues.
Claim(s) 17, 21, 22, 25, 30, 32-33, 50-51, 53 is/are rejected under 35 U.S.C. 103 as being unpatentable over Breunig (WO2017131926A1) and Gierut (2014) as applied to claim 1 above, and further in view of Akhtar (2018; cited and provided by applicant with IDS filed 12/09/2021, listed as NPL24). This rejection is amended to reflect that claim 1 is newly rejected over Breunig and Gierut, and is otherwise maintained.
The teachings of Breunig and Gierut are discussed above and can be combined to render obvious the limitations of claim 1.
Regarding claim 17, Breunig teaches that the transgene comprises disease-associated mutations (claim 9), the transgene comprises a gain-of function mutation or a loss-of-function mutation (paragraph [0064]), the transgene encodes a factor that increases the proliferation of a neuronal cell (paragraph [0038]), or the transgene encodes a factor which promotes differentiation of a neuronal cell (paragraph [0021]; Fig. 16).
Regarding claim 21, Breunig teaches that the transgene encodes a growth factor (paragraph [0106]).
Regarding claim 25, Breunig teaches a promoter-less donor vector comprising: a polyadenylation signal or transcription stop element upstream from a transgene; the transgene; and paired recombinase recognition sites (claims 1, 10).
Regarding claim 30, Breunig teaches that the transgene is an oncogene or a proto-oncogene comprising a GOF mutation (paragraph [0065]), or encodes a factor that increases the proliferation of a neuronal cell (paragraph [0038]) or promotes differentiation of a neuronal cell (paragraph [0021]; Fig. 16).
Regarding claim 32, Breunig teaches that the transgene encodes a growth factor (paragraph [0106]).
Regarding claim 50, Breunig teaches a mammalian cell comprising the system (claim 19; paragraph [0029]).
However, Breunig does not teach that the growth factor comprises GDNF, neurturin, GDF5, MANF, or CDNF (required by claims 22 and 33), or that the mammalian cell is an induced pluripotent stem cell (required by claims 51 and 53).
Akhtar teaches that GDNF can be expressed in iPSCs to treat a model of a neurodegenerative disease.
Regarding claims 22 and 33, Akhtar teaches that GDNF can be stably expressed from a donor vector (page 1; Fig. 1).
Regarding claims 51 and 53, Akhtar teaches that iPSCs can be transduced with a donor vector encoding a transgene (page 1; Fig. 1; Fig. 2).
Breunig teaches that the systems and promoter-less donor vectors can be used to treat neurodegenerative diseases—specifically, Breunig teaches that cells comprising the systems and promoter-less donor vectors can be transplanted into a subject in order to deliver growth factors to the subject, thereby treating a neurodegenerative disease (paragraph [0106]). However, Breunig does not teach any specific neurodegenerative disease (or model of a disease), specific types of cells for transplant, or specific growth factors. Akhtar teaches a method of expression GDNF in a mouse brain, which method comprises intracranial administration of iPSCs (Fig. 3A) genetically engineered to express GDNF from a donor vector (Fig. 1). Akhtar further teaches that administration or increased expression of GDNF has been shown to provide therapeutic benefits in Parkinson’s disease (Summary; page 1). It therefore would have been obvious to a person of ordinary skill in the art at the time of filing that in order to treat a specific neurodegenerative disease (or model thereof), the donor vector should be designed such that the transgene encodes a therapeutically-beneficial protein; in the case of Parkinson’s disease, the teachings of Akhtar render obvious that the transgene should encode GDNF. Furthermore, both Breunig and Akhtar teach methods of using transplantation of genetically modified stem cells to treat a disease in a subject; Akhtar specifically teaches that ex vivo iPSC transplantation increases the safety of gene therapy in the brain and provides beneficial effects by virtue of transplantation of healthy neural stem/progenitor cells (Akhtar page 1702). It would have been obvious to a person of ordinary skill in the art that, in order to treat the neurodegenerative disease Parkinson’s disease, the type of stem cell used in the methods of Breunig should be an iPSC, in order to provide the safety and other benefits taught by Akhtar as inherent to transplanted iPSCs.
Response to Arguments
Applicant’s arguments filed 10/31/2025 with respect to rejections under 35 USC 103 of claim(s) 1-2, 17, 21, 24-28, 30, 32, 35, 37, 44-45, 50 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. These claims were previously rejected under 35 USC 102(a)(1) over Breunig. This rejection was withdrawn due to amendments made to claims 1 and 25 which were not taught by Breunig. These claims have been newly rejected under 35 USC 103 over Breunig in view of Gierut, rendering obvious the amended claims. As the applicant traversed the rejections of claims 8-9, 17, 21-22, 25, 30, 32-33, 50-51, and 53 under 35 USC 103 solely on the basis that the previously-presented rejection of claims 1-2 and 25 over Breunig under 35 USC 102(a)(1) was overcome by the claim amendments, and these claim amendments have been addressed by the new grounds of rejection above over Breunig and Gierut, the rejections of claims 8-9, 17, 21-22, 25, 30, 32-33, 50-51, and 53 under 35 USC 103 are maintained.
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.
US 11466290 B2:
Claims 1-2, 17, 24-25, 27-28, 37 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 of U.S. Patent No. 11466290 B2 in view of Gierut (2014). This is a new grounds of rejection necessitated by amendment.
The issued claims recite systems comprising promoter-less donor vectors, wherein the only limitation of instant claims 1-2, 17, 24-25, 27-28, and 37 that ~290 does not recite is that the loxP and FRT recognition sites are variant loxP and FRT recognition sites.
Gierut teaches that variant loxP and FRT recognition sites were known in the art as alternatives to wild-type loxP and FRT recognition sites.
Regarding claims 1 and 25, Gierut teaches that variant loxP recognition sites lox2272, lox m2, lox66, and lox71 are recognized by wild-type Cre, and that variant flippase recognition sites F3 and F5 are recognized by wild-type flippase (FLP) (Table 1).
As Gierut teaches that variant loxP and FRT recombination sites were known in the art at the time of filing and were compatible with wild-type Cre and Flp, respectively, it would have been obvious to an artisan to substitute variant loxP and FRT recombination sites for the wild-type loxP and FRT recombination sites of the issued claims as equivalent structures with equivalent function.
Claim(s) 21, 26, 30, 32, 35, 44-45, 50 is/are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 9 U.S. Patent No. 11466290 B2 and Gierut (2014), as applied to claims 1, 17, 25 above, and further in view of Breunig (WO2017131926A1). This rejection is amended to reflect that claims 1, 17, and 25 are newly rejected over ~290 in view of Gierut.
The limitations recited by the claims of ~290 are discussed above and render obvious the limitations of instant claims 1, 17, and 25. However, the claims of ~290 do not recite the limitations that the transgene encodes a growth factor (required by claims 21, 30, 32), one or both paired recombinase recognition sites comprise a mutation (required by claim 35), a non-human animal model comprising the system (required by claims 44-45), or a cell comprising the system (required by claim 50).
Breunig teaches a promoter-less donor vector and a system comprising the promoter-less donor vector comprising all the limitations recited in the claims of ~290 and the instant claims (see claims 1-13; Fig. 2H).
Regarding claim 21, Breunig teaches that the transgene encodes a growth factor (paragraph [0106]).
Regarding claim 26, Breunig teaches that the promoter-less donor vector is a viral vector (paragraph [0044]-[0045]), a bacterial artificial chromosome (BAC) (paragraph [0048]), or a plasmid (paragraphs [0029]-[0030], [0048]).
Regarding claim 30, Breunig teaches that the transgene is an oncogene or a proto-oncogene comprising a GOF mutation (paragraph [0065]), or encodes a factor that increases the proliferation of a neuronal cell (paragraph [0038]) or promotes differentiation of a neuronal cell (paragraph [0021]; Fig. 16).
Regarding claim 32, Breunig teaches that the transgene encodes a growth factor (paragraph [0106]).
Regarding claim 35, Breunig teaches that the promoter-less donor vector is introduced into a neuronal stem cell (paragraph [0029]). Breunig also teaches that one or more of the recombinase recognition sites can comprise a mutation (paragraph [0014], Fig. 9: “top sequence loxP” and “bottom sequence loxP” differ by eight nucleotides; this “inversion” of a portion of the loxP sequence constitutes a mutation).
Regarding claim 44, Breunig teaches a non-human animal model comprising the system (claim 14). Breunig teaches that the transgene of this system is an oncogene or proto-oncogene comprising a GOF mutation (paragraph [0065]).
Regarding claim 45, Breunig teaches that the non-human animal model is “personalized” in order to model a human subject’s cancer, disease, or condition by designing the transgene such that it encodes a protein which causes or promotes the cancer, disease, or condition (paragraph [0039]).
Regarding claim 50, Breunig teaches a mammalian cell comprising the system (claim 19; paragraph [0029]).
As discussed above, the promoter-less donor vector and system comprising the promoter-less donor vector of ~290 comprises or renders obvious, when combined with Gierut, all the same structural and sequence elements recited in the instant application. As such, Breunig teaches applications of the promoter-less donor vector system claimed by ~290 (administration to mammalian cells) and further modifications not recited by the claims of ~290 (mutations of the recombinase recognition sites, the identity of the transgene, the type of vector used). Therefore, it would be obvious to a person of ordinary skill in the art that the promoter-less donor vector of ~290, being a narrow subset of the promoter-less donor vectors taught by Breunig, could be modified and applied as in Breunig in order to induce expression of the transgene of the donor vector in a cell.
Claim(s) 8-9 is/are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 9 U.S. Patent No. 11466290 B2 and Gierut (2014), as applied to claims 1-2 above, and further in view of Jackson (2016). This rejection is amended to reflect that claims 1-2 are newly rejected over ~290 in view of Gierut.
The claim limitations of ~290 claims 1 and 9 are discussed above and render obvious claims 1-2. However, the claims of ~290 do not recite the limitations that the donor vector be an AAV vector, and that the genes encoding recombinases bey under the control of tissue-specific promoters.
Jackson teaches the use of AAV vectors and tissue-specific promoters in methods of neuronal transduction.
Regarding claim 8, Jackson teaches tissue-specific promoters, such as the synapsin promoter (abstract; pages 1-2).
Regarding claim 9, Jackson teaches that AAV vectors, such as AAV9 and AAV-PHP.B, are used in methods of neuronal gene transduction, including for transfer of cre-lox systems, for tissue specificity (abstract; pages 1-2; page 5).
Jackson teaches that AAV vectors are widely used for gene transfer (including transfer of cre-lox systems, like that claimed in ~290; page 1), and that furthermore, specific AAV serotypes can be used to promote transduction of specific cell types and tissues (pages 1-2). Furthermore, Jackson teaches that it is commonly known that cell-type specific promoters are necessary for neuronal targeting, and promoters like the synapsin promoter are commonly used for neuronal targeting of transgene expression (page 2). It would have been obvious to a person of ordinary skill in the art at the time of filing that the system claimed in ~290 should be modified by placing the recombinase genes under the control of tissue-specific promoters and by utilizing an AAV vector as the donor vector, if the compositions claimed by ~290 are administered to cells for purposes of genetic engineering, in order to restrict transduction and expression of the donor vector and donor sequence to the specific desired cell populations or tissues.
Claim(s) 22, 33, 51, 53 is/are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 9 U.S. Patent No. 11466290 B2, Breunig (WO2017131926A1), and Gierut (2014), as applied to claims 1, 17, 25 above, and further in view of Akhtar (2018). This rejection is amended to reflect that claims 1 is newly rejected over ~290 in view of Gierut.
The teachings of Breunig and the claim limitations of ~290 are discussed above and can be combined to render obvious claims 1, 17, 21, 25, 30, 32, and 50. However, Breunig does not teach that the growth factor comprises GDNF, neurturin, GDF5, MANF, or CDNF (required by claims 22 and 33), or that the mammalian cell is an induced pluripotent stem cell (required by claims 51 and 53).
Akhtar teaches that GDNF can be expressed in iPSCs to treat a model of a neurodegenerative disease.
Regarding claims 22 and 33, Akhtar teaches that GDNF can be stably expressed from a donor vector (page 1; Fig. 1).
Regarding claims 51 and 53, Akhtar teaches that iPSCs can be transduced with a donor vector encoding a transgene (page 1; Fig. 1; Fig. 2).
Breunig teaches that the systems and promoter-less donor vectors of Breunig and ~290 can be used to treat neurodegenerative diseases—specifically, Breunig teaches that cells comprising the systems and promoter-less donor vectors can be transplanted into a subject in order to deliver growth factors to the subject, thereby treating a neurodegenerative disease (paragraph [0106]). However, Breunig does not teach any specific neurodegenerative disease (or model of a disease), specific types of cells for transplant, or specific growth factors. Akhtar teaches a method of expression GDNF in a mouse brain, which method comprises intracranial administration of iPSCs (Fig. 3A) genetically engineered to express GDNF from a donor vector (Fig. 1). Akhtar further teaches that administration or increased expression of GDNF has been shown to provide therapeutic benefits in Parkinson’s disease (Summary; page 1). It therefore would have been obvious to a person of ordinary skill in the art at the time of filing that in order to treat a specific neurodegenerative disease (or model thereof), the donor vector rendered obvious by Breunig, Gierut, and ~290 should be designed such that the transgene encodes a therapeutically-beneficial protein; in the case of Parkinson’s disease, the teachings of Akhtar render obvious that the transgene should encode GDNF. Furthermore, both Breunig and Akhtar teach methods of using transplantation of genetically modified stem cells to treat a disease in a subject; Akhtar specifically teaches that ex vivo iPSC transplantation increases the safety of gene therapy in the brain and provides beneficial effects by virtue of transplantation of healthy neural stem/progenitor cells (Akhtar page 1702). It would have been obvious to a person of ordinary skill in the art that, in order to treat the neurodegenerative disease Parkinson’s disease, the type of stem cell used in the methods of Breunig should be an iPSC, in order to provide the safety and other benefits taught by Akhtar as inherent to transplanted iPSCs.
17930558:
Claims 1-2, 17, 24-25, 27-28, 37, 44, 50 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16, 19-20 of copending Application No. 17930558 in view of Gierut (2014). This is a new grounds of rejection necessitated by amendment.
This is a provisional nonstatutory double patenting rejection.
The issued claims recite systems comprising promoter-less donor vectors, wherein the only limitation of instant claims 1-2, 17, 24-25, 27-28, 37, 44, 50 that the copending claims does not recite is that the loxP and FRT recognition sites are variant loxP and FRT recognition sites.
Gierut teaches that variant loxP and FRT recognition sites were known in the art as alternatives to wild-type loxP and FRT recognition sites.
Regarding claims 1 and 25, Gierut teaches that variant loxP recognition sites lox2272, lox m2, lox66, and lox71 are recognized by wild-type Cre, and that variant flippase recognition sites F3 and F5 are recognized by wild-type flippase (FLP) (Table 1).
As Gierut teaches that variant loxP and FRT recombination sites were known in the art at the time of filing and were compatible with wild-type Cre and Flp, respectively, it would have been obvious to an artisan to substitute variant loxP and FRT recombination sites for the wild-type loxP and FRT recombination sites of the copending claims as equivalent structures with equivalent function.
Claim(s) 21, 26, 30, 32, 35, 44-45 is/are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6-10, 14-16 of copending Application No. 17930558 (reference application) and Gierut (2014), as applied to claims 1, 17, 25, 44 above, and further in view of Breunig (WO2017131926A1). This rejection is amended to reflect that claims 1, 17, 25, and 44 are newly rejected over the copending claims in view of Gierut.
The limitations recited by the copending claims are discussed above and render obvious the limitations of instant claims 1, 17, 25, 44. However, the copending claims do not recite the limitations that the transgene encodes a growth factor (required by claims 21, 30, 32), one or both paired recombinase recognition sites comprise a mutation (required by claim 35), or that the non-human animal model is a personalized non-human animal model (required by claim 45).
Breunig teaches a promoter-less donor vector and a system comprising the promoter-less donor vector comprising all the limitations recited in the copending claims and the instant claims (see claims 1-13; Fig. 2H).
Regarding claim 21, Breunig teaches that the transgene encodes a growth factor (paragraph [0106]).
Regarding claim 26, Breunig teaches that the promoter-less donor vector is a viral vector (paragraph [0044]-[0045]), a bacterial artificial chromosome (BAC) (paragraph [0048]), or a plasmid (paragraphs [0029]-[0030], [0048]).
Regarding claim 30, Breunig teaches that the transgene is an oncogene or a proto-oncogene comprising a GOF mutation (paragraph [0065]), or encodes a factor that increases the proliferation of a neuronal cell (paragraph [0038]) or promotes differentiation of a neuronal cell (paragraph [0021]; Fig. 16).
Regarding claim 32, Breunig teaches that the transgene encodes a growth factor (paragraph [0106]).
Regarding claim 35, Breunig teaches that the promoter-less donor vector is introduced into a neuronal stem cell (paragraph [0029]). Breunig also teaches that one or more of the recombinase recognition sites can comprise a mutation (paragraph [0014], Fig. 9: “top sequence loxP” and “bottom sequence loxP” differ by eight nucleotides; this “inversion” of a portion of the loxP sequence constitutes a mutation).
Regarding claim 44, Breunig teaches a non-human animal model comprising the system (claim 14). Breunig teaches that the transgene of this system is an oncogene or proto-oncogene comprising a GOF mutation (paragraph [0065]).
Regarding claim 45, Breunig teaches that the non-human animal model is “personalized” in order to model a human subject’s cancer, disease, or condition by designing the transgene such that it encodes a protein which causes or promotes the cancer, disease, or condition (paragraph [0039]).
As discussed above, the promoter-less donor vector and system comprising the promoter-less donor vector of Breunig comprises all the same structural and sequence elements recited in the copending claims, and when combined with Gierut, in the instant application. As such, Breunig teaches applications of the promoter-less donor vector system claimed by the copending application (administration to mammalian cells) and further modifications not recited by the copending claims (mutations of the recombinase recognition sites, the identity of the transgene, the type of vector used). Therefore, it would be obvious to a person of ordinary skill in the art that the promoter-less donor vector of the copending application, being a narrow subset of the promoter-less donor vectors taught by Breunig, could be modified and applied as in Breunig in order to induce expression of the transgene of the donor vector in a cell.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim(s) 8-9 is/are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 of copending Application No. 17930558 (reference application) and Gierut (2014), as applied to claims 1-2 above, and further in view of Jackson (2016). This rejection is amended to reflect that claims 1-2 are newly rejected over the copending claims in view of Gierut.
The claim limitations of copending application claims 1 and 9 are discussed above and render obvious claims 1-2. However, the copending claims do not recite the limitations that the donor vector be an AAV vector, and that the genes encoding recombinases bey under the control of tissue-specific promoters.
Jackson teaches the use of AAV vectors and tissue-specific promoters in methods of neuronal transduction.
Regarding claim 8, Jackson teaches tissue-specific promoters, such as the synapsin promoter (abstract; pages 1-2).
Regarding claim 9, Jackson teaches that AAV vectors, such as AAV9 and AAV-PHP.B, are used in methods of neuronal gene transduction, including for transfer of cre-lox systems, for tissue specificity (abstract; pages 1-2; page 5).
Jackson teaches that AAV vectors are widely used for gene transfer (including transfer of cre-lox systems, like that claimed in ~290; page 1), and that furthermore, specific AAV serotypes can be used to promote transduction of specific cell types and tissues (pages 1-2). Furthermore, Jackson teaches that it is commonly known that cell-type specific promoters are necessary for neuronal targeting, and promoters like the synapsin promoter are commonly used for neuronal targeting of transgene expression (page 2). It would have been obvious to a person of ordinary skill in the art at the time of filing that the system claimed in the copending application should be modified by placing the recombinase genes under the control of tissue-specific promoters and by utilizing an AAV vector as the donor vector, if the compositions claimed by the copending application are administered to cells for purposes of genetic engineering (as in copending claims 17-20), in order to restrict transduction and expression of the donor vector and donor sequence to the specific desired cell populations or tissues.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim(s) 22, 33, 51, 53 is/are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6-10, 14-20 of copending Application No. 17930558 (reference application), Gierut (2014), and Breunig (WO2017131926A1), as applied to claims 1, 17, 21, 25, 30, 32, 44, 50 above, and further in view of Akhtar (2018). This rejection is amended to reflect that claims 1, 17, 21, 25, 30, 32, 44, and 50 are newly rejected over the copending claims in view of Gierut.
The teachings of Breunig and the claim limitations of the copending application are discussed above and can be combined to render obvious claims 1, 17, 21, 25, 30, 32, and 50. However, Breunig does not teach that the growth factor comprises GDNF, neurturin, GDF5, MANF, or CDNF (required by claims 22 and 33), or that the mammalian cell is an induced pluripotent stem cell (required by claims 51 and 53).
Akhtar teaches that GDNF can be expressed in iPSCs to treat a model of a neurodegenerative disease.
Regarding claims 22 and 33, Akhtar teaches that GDNF can be stably expressed from a donor vector (page 1; Fig. 1).
Regarding claims 51 and 53, Akhtar teaches that iPSCs can be transduced with a donor vector encoding a transgene (page 1; Fig. 1; Fig. 2).
Breunig teaches that the systems and promoter-less donor vectors of Breunig and the copending application can be used to treat neurodegenerative diseases—specifically, Breunig teaches that cells comprising the systems and promoter-less donor vectors can be transplanted into a subject in order to deliver growth factors to the subject, thereby treating a neurodegenerative disease (paragraph [0106]). However, Breunig does not teach any specific neurodegenerative disease (or model of a disease), specific types of cells for transplant, or specific growth factors. Akhtar teaches a method of expression GDNF in a mouse brain, which method comprises intracranial administration of iPSCs (Fig. 3A) genetically engineered to express GDNF from a donor vector (Fig. 1). Akhtar further teaches that administration or increased expression of GDNF has been shown to provide therapeutic benefits in Parkinson’s disease (Summary; page 1). It therefore would have been obvious to a person of ordinary skill in the art at the time of filing that in order to treat a specific neurodegenerative disease (or model thereof), the donor vector of Breunig and the copending application should be designed such that the transgene encodes a therapeutically-beneficial protein; in the case of Parkinson’s disease, the teachings of Akhtar render obvious that the transgene should encode GDNF. Furthermore, Breunig, the copending claims (claims 19-20), and Akhtar teach methods of using transplantation of genetically modified stem cells to treat a disease in a subject; Akhtar specifically teaches that ex vivo iPSC transplantation increases the safety of gene therapy in the brain and provides beneficial effects by virtue of transplantation of healthy neural stem/progenitor cells (Akhtar page 1702). It would have been obvious to a person of ordinary skill in the art that, in order to treat the neurodegenerative disease Parkinson’s disease, the type of stem cell used in the methods of Breunig should be an iPSC, in order to provide the safety and other benefits taught by Akhtar as inherent to transplanted iPSCs.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Arguments
Applicant’s arguments filed 10/31/2025 with respect to nonstatutory rejections and provisional rejections of claim(s) 1-2, 17, 21, 24-28, 30, 32, 35, 37, 44-45, 50 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. The amendments to claims 1 and 25 requiring specific variants of loxP and FLT recognition sites overcome the previously-presented nonstatutory double patenting rejections. However, the teachings of Gierut render obvious that variant loxP and FLT recognition sites are obvious variants of wild-type loxP and FLT recognition sites, as described above. As this limitation was the sole basis for the applicant’s traverse of the previously-presented nonstatutory double patenting rejections, the new grounds of rejection, and the maintained rejections of dependent claims, are considered to not rely on any teaching or matter specifically challenged in the applicant’s arguments.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/AFRICA M MCLEOD/ Examiner, Art Unit 1635
/KIMBERLY CHONG/ Primary Examiner, Art Unit 1636