DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
Applicant's election with traverse of Group I, claims 1-4, 6, 8, 20-23, 34 and 35 in the reply filed on 11/10/2025 is acknowledged. The traversal is on the ground(s) that Groups I-IV are closely related and searching these groups do not substantially increase the search burden. This is not found persuasive because the withdrawn groups require materially distinct and separate protocols that are not required by the claimed non-human animal and a burdensome search is required since, for example, determining toxicity of an anti-GLP1R antibody in the elected non-human animal would require a distinct search separate from the claimed invention.
The requirement is still deemed proper and is therefore made FINAL.
Claims 11, 14, 15, 17-19, 38 and 52 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 11/10/2025.
Claim Objections
Claim 6 is objected to because of the following informalities: claim 6 should be amended to recite “non-human animal” to be consistent with claim 1. Appropriate correction is required.
Claim 8 is objected to because of the following informalities: claim 6 should be amended to recite “non-human animal” to be consistent with claim 1. Appropriate correction is required.
Claim 23 is objected to because of the following informalities: claim 6 should be amended to recite “non-human animal” to be consistent with claim 1. Appropriate correction is required.
Claim 34 is objected to because of the following informalities: claim 6 should be amended to recite “non-human animal” to be consistent with claim 1. Appropriate correction is required.
Claim Rejections - 35 USC § 112
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 1-4, 6, 8, 20-23, 34 and 35 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for:
a transgenic mouse whose genome comprises at the endogenous glucagon-like peptide-1 receptor (GLP1R) locus a nucleotide sequence encoding human GLP1R, wherein said mouse expresses human GLP1R; and
a method of making a transgenic mouse comprising the steps of:
introducing into mouse embryonic stem (mES) cells a targeting vector comprising the nucleotide sequence encoding human GLP1R, wherein the targeting vector inserts the human nucleotide sequence encoding GLP1R into Exon 1 of the endogenous GLP1R locus,
inserting the mES cells obtained in step (i) into a blastocyst,
implanting the blastocyst obtained in step (ii) into a surrogate female mouse,
obtaining a chimeric mouse,
breeding the chimeric mouse of step (iv) with a wild-type mouse to obtain a transgenic mouse which expresses human GLP1R, wherein said transgenic mouse expresses human GLP1R,
does not reasonably provide enablement for a non-human animal of any species other than a mouse and a non-human animal which expresses no phenotype. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims.
While determining whether a specification is enabling, one considers whether the claimed invention provides sufficient guidance to make and use the claimed invention, if not, whether an artisan would have required undue experimentation to make and use the claimed invention and whether working examples have been provided. When determining whether a specification meets the enablement requirements, some of the factors that need to be analyzed are: the breadth of the claims, the nature of the invention, the state of the prior art, the level of one of ordinary skill, the level of predictability in the art, the amount of direction provided by the inventor, the existence of working examples, and whether the quantity of any necessary experimentation to make or use the invention based on the content of the disclosure is ''undue'' (In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)). Furthermore, USPTO does not have laboratory facilities to test if an invention will function as claimed when working examples are not disclosed in the specification, therefore, enablement issues are raised and discussed based on the state of knowledge pertinent to an art at the time of the invention, therefore skepticism raised in the enablement rejections are those raised in the art by artisans of expertise.
The breadth of claimed invention encompasses any non-human animal including any rodent, insects such as spiders, aquatic animals such as starfish and flatworms such as C. elegans and whose genome will comprise at least one chromosome comprising a sequence encoding a human or chimeric GLP1R.
Given the breadth encompassed by the claims, the skilled artisan would find that even species of rodents such as rats are unpredictable to be modified to be transgenic as embraced by the claims. As detailed below, the art teaches there is significant unpredictability even for the creation of transgenic mice and rats as well as predicted phenotypes in mice.
One of skill in the art would not know how to use a non-human animal as encompassed by the claims without a phenotype since it would be indistinguishable from a normal (non-transgenic) animal (i.e. wild-type mouse). It is only when the transgenic non-human animal (i.e. mouse), with respect to the claimed invention, expresses a human GLP1R that a skilled artisan would find an enabled use for the claimed invention.
Working Examples
The specification teaches the creation of transgenic mice that express human GLP1R and mouse GLP1R (heterozygous) and transgenic mice that only express human GLP1R (homozygous), see Example 1, pgs. 42-49 of the specification. However, a review of the instant specification and the examples, the specification teaches that only via insertion of a targeting construct into mouse ES was Applicant able to create the claimed transgenic mouse.
In this regard, the issue of enablement is that only transgenic mice were enabled at the time of filing to make and use the invention as claimed and that even rats and pigs have issues of enablement regarding their creation from stem cells as well as predicted phenotypes when made.
Unpredictability of Transgenesis and Expected Phenotypes in Transgenic Mice
Regarding the unpredictability of transgenesis, the art teaches that even in mice, the strain of the mouse significantly impacts the phenotype observed when expressing an exogenous gene.
For example, Garcia-Arocena D. (2014, The Jackson Laboratory, Same Mutation, Different Phenotype?) teaches that the genetic background of a mouse significantly impacted the phenotype in transgenic mice overexpressing a mutant form of SOD1*G93A. Specifically, Garcia-Aroceno teaches “Classic mouse models of familial ALS are transgenic mice that overexpress a mutant form of human superoxide dismutase 1 (Tg(SOD1*G93A)1Gur; aka SOD1*G93A). Transgenic, hemizygote carriers manifest phenotypes that resemble ALS in humans: they become paralyzed in one or more limbs due to loss of motor neurons from the spinal cord. The genetic background of the original SOD1*G93A transgenic mice (002726) were on a non-uniform mixture of SJL/J and C57BL/6J. The transfer of this transgene on to different backgrounds has produced congenic strains with either early or late onset of symptoms:
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Garcia-Aroceno continues to teach that “Early onset strains include ALR/LtJ and SJL/J congenic mice, which first show symptoms starting at 116 and 119 days of age (±10 days), respectively. Late onset strains include C57BL/6J and DBA/2J that don’t develop overt ALS symptoms until 161 and 169 days of age (±10 days), respectively.
Similarly, hemizygous SOD1*G93A transgenic carriers on the mixed B6SJL background also have a decreased lifespan compared to hemizygotes on the congenic C57BL/6J background: 50% survive to 128.9 (± 9.1 days) versus 157.1 (± 9.3 days), respectively.”
Lastly, Garcia-Aroceno teaches that “Mice with the G93A-SOD1 transgene on the mixed B6SJL background show abnormalities that are not evident on the B6 background. Some of these phenotypes are anomalous mitochondria morphology and cellular physiology, slow postnatal weight gain and atypical capillary morphology.”
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Further expanding the teachings of Garcia-Aroceno are the teachings of Heimain-Patterson et al. (2011, Amyotrophic Lateral Schlerosis, Vol. 00, pgs. 1-8) who does a large analysis of twenty different mouse strains and their impact on the phenotypes observed when expressing the exogenous human SOD1 transgene (see Abstract). In Table I, Heimain-Patterson teaches the significant differences that the strain of the mouse has on survival (reproduced below).
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Heiman-Patterson concludes by teaching “Finally, and importantly, our data indicate that
genetic background has a large influence on lifespan in the SOD1 mutant mouse model of ALS, underscoring the need to interpret positive lifespan results with double-transgenic mortality studies carefully. Any future work must factor in these genetic variables” (pg. 6 col. 2 parag. 2 lines 1-7).
Thus, as demonstrated by the teachings of Heiman-Patterson, even within one species of murine animal such as the mouse, there is significant variability in a phenotype that can occur due to the genetic background of the animal. Given that the claimed invention encompasses any species of non-human animal (claim 1) and claim 1 recites no phenotypes at all, and these non-human animals will each have varying genetic backgrounds, the skilled artisan would find that predicting and expecting a specific phenotype or any phenotype at all due to introduction of human gene sequences as embraced by the claims is unpredictable.
Again, the art teaches that even among transgenic mice, considerable experimentation is required to ascertain the validity of the observed phenotypes i.e. the phenotypes observed are a direct result to the particular genes provided. Thus, based upon these teachings in the art above, the skilled artisan would find the animals as claimed unpredictable.
Unpredictability of Any Genetically Modified Non-Human Animal
The claim invention encompasses any species of animal to be made transgenic via modification of ES cells. In this regard, the art teaches that creating transgenic animals from any species of animal is unpredictable in a variety of animal (particularly non-human mammals) species, except for mice.
The issue of unpredictability regarding the claimed invention involves the unavailability of ES cells from non-mouse species of animal. As the art teaches below, there is significant unpredictability in isolating, characterizing and using ES cells isolated from non-mouse species, and that pluripotency has not been validated or verified in any species of animal other than the mouse.
Regarding ES cells, the art teaches that while mouse ES cells have been established, no validated porcine ES cells are available (Brevini et al., 2010, Theriogenology, Vol. 74, pgs. 544-550, see Abstract). Brevini continues to teach that conflicting data regarding the expression of pluripotency markers in porcine ESCs further complicates the understanding and establishment of a porcine ESC cell line (pg. 548 col. 2 parag. 4). Brevini concludes by teaching that “Many factors, some of which are briefly discussed in the present manuscript, make the establishment of ESC lines in the pig, and in animal species other than mouse and human, a very slow process.” (pg. 548 col. 2 parag. 5 lines 1-4). Brevini continues to teach that “Compared with the large number of studies exploring the appropriate culture conditions for mouse and human ESCs, there is a minimal amount of data available for domestic species ESC. That limited information is mainly based on mouse ESC culture systems. As a result, such conditions did not appear to be effective for maintaining stable undifferentiated ESC lines in domestic animals. We are convinced that a major goal at present is to develop better culture formulations in order to obtain homogenous pluripotent outgrowths from pig embryos and identify the best in vitro environment that would facilitate derivation of stable pESC culture” (pg. 546 col. 1 parag. 2 bridge col. 2 parag. 1). Brevini continues that “Conflicting data regarding the expression of other pluripotency markers (SSEA1, SSEA4, Alkaline Phosphatase, Sox2, Rex1) further complicates our understanding of pESC. Although these factors are considered characteristic of ESC in other species, they cannot be regarded as definitive markers in the pig [1,50,59].” (pg. 548 col. 2 parag. 4). Thus, Brevini teaches that both the culture conditions and markers used to identify porcine pluripotent stem cells is unpredictable at the time of filing.
Regarding equine ES cells, Paris et al. (2010, Theriogenology, Vol. 74, pgs. 516-524) teach that a golden rule in the characterization of ESCs is that their behavior should recapitulate what occurs naturally in vivo and that markers for pluripotency in ESCs should only be expressed in cells destined to form the embryonic ICM (pg. 519 col. 2 parag. 2 lines 1-5). Paris continues to teach that SSEA1, SSEA3, and SSEA4 are all cell surface antigens associated with pluripotent stem cells, but their precise functions in the maintenance of pluripotency is not known, thus, none of these markers can be used in isolation as a cross-species definitive indicator of pluripotency because there are considerable between-species differences in their expression in both ESCs and embryos (pg. 519 col. 2 parag. 2 lines 5-10). Paris concludes by teachings that while several lines of stem cells have been isolated from the horse, the absence of any data verifying in vivo pluripotency of the cells means that the cells cannot yet be definitively classified as ESCs (pg. 519 col. 1 parag. 2 lines 7-10).
The art continues to teach that the validation and establishment of bovine ES cells remains unpredictable. For example, Munoz et al. (2008, Theriogenology, Vol. 69, pgs. 1159-1164) teach that there are significant differences in the distribution of genes involved in the self-renewal among bovine, mouse and human embryos, particularly those genes involved in pluripotency, such as NANOG and OCT-4 (pg. 1160 col. 1 parag. 1 lines 2-8). Munoz continues to teach that while several bovine-ES cell like lines have been established, their pluripotency needs to be confirmed and that further research is necessary to identify reliable pluripotency markers for bovine ESCs (pg. 1163 col. 1 parag. 1 last 9 lines bridge parag. 2).
Regarding feline pluripotent stem cells, the art teaches that while cat ES cells have been identified, they were not truly pluripotent. For example, Gomez et al. (2010, Theriogenology, Vol. 74, pgs. 498-515) teaches “In the present study, cat primary colonies and cESL cell lines 1) were generated with in vitro derived blastocysts, 2) were characterized by their cell morphology and expression of pluripotent markers, and 3) spontaneously differentiated into fibroblasts, cardiomyocytes and embryoid bodies. Nonetheless, the cells lost their self-renewal capacity and did not exhibit true pluripotency. Obtaining cells that do not exhibit all of the characteristics necessary to be categorized as ESCs, but, are nevertheless able to maintain some pluripotent characteristics that allow their use as donor nuclei for nuclear transfer may improve the efficiency of interspecies-nuclear transfer for preserving endangered cats.” (pg. 513, col. 2 parag. 2 lines 1-13).
The art continues to teach that validating pluripotency in stem cells is challenging. For example Buta et al. (2013, Stem Cell Res., Vol. 11, pgs. 552-562) teach that “Attributes such as the pluripotentcy and differentiation potential are based on experimental criteria and need to be thoroughly addressed via functional and molecular assays. Therefore, approaches to increase the stringency of results should be applied. From the standpoint of developmental biology many researchers regard in vitro differentiation e.g. in embryoid bodies (EBs) as the least stringent functional test of pluripotency of cultured stem cells. The generation of teratoma is perceived as being the next level of stringency. While these two approaches are suitable for stem cells of animal and human origin, they are limited since they do not test the ability of the cells to undergo normal development.” (pg. 556 col. 2 last parag.).
Further, regarding rat ES cells, the art teaches that they remain unpredictable for their use in the creation of transgenic rats. For example, Tong et al. (2010, Nature, Vol. 467(7312), pgs. 211-213) teaches:
“Failure of mouse ES cells to contribute to the germline is often caused by chromosomal abnormalities in ES cells18. This is also likely to be true for rat ES cells. We examined the karyotype of DAc8-p53-#1 rat ES cells and found that over 65 percent of the cells were polyploid (Supplementary Fig. 5a). This is likely the reason for its low germline transmission efficiency. From mouse ES cell studies, it has been suggested that chromosomal abnormalities are associated with a selective growth advantage, and that the use of small, slower growing clones rather than large, rapidly growing clones for blastocyst injection will significantly improve the germline transmission rate18. We investigated whether germline competency of DAc8-p53-#1 rat ES cells could be improved through subcloning. DAc8-p53-#1 rat ES cells were plated at a clonal density as has been reported for mouse ES cells19, 20. Around 10% of the cells formed round and compact colonies (Supplementary Fig. 5b). These colonies were picked and expanded to establish subclones. We karyotyped 20 DAc8-p53-#1 rat ES cell subclones and identified 2 subclones with euploid chromosome numbers (Supplementary Fig. 5c). The subclones grew as round and compact colonies (Supplementary Fig. 5d). The subclones were microinjected into a total of 39 F344 rat blastocysts. 2 male chimeras were produced and 1 was a germline chimera (Fig. 3a). This germline chimera generated 76 offspring among which were 6 germline pups. 3 of the germline pups, 1 male and 2 female, were GFP positive, indicating the inheritance of the p53tm1(EGFP-pac) allele (Fig. 3b). Genotyping and Southern blot analysis further confirmed that these 3 pups were p53 heterozygote animals carrying one wild-type and one targeted p53 alleles (Fig. 3c, d).” (pg. 3 parag. 2).
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Similarly, Hong et al. (2012, Stem Cells and Development, Vol. 21(9), pgs. 1571-1586) teaches that there is unpredictability even among ES cells from different strains of rat (see Abstract). Specifically, Hong teaches that while ES cells from either F344 or dark agouti rats could contribute to generate a chimera, only ES cells from dark agouti (DA) were determined to be germline competent (see Abstract and pg. 1584 col. 2 parag. 2).
Further Hong teaches that "In other laboratories, F344 ESCs have not produced chimeric rats after an injection into DA or SD blastocysts [3,4]. Here, for the first time, F344 ESCs that were injected into SD blastocysts produced chimeric rats. In other laboratories, F344 blastocysts were more efficient host blastocysts to produce germline transmission of ESCs when injected with DA ESCs [3,4], and F344 blastocysts produce the first ESC gene targeted knockout rats after an injection with DA ESCs [5]. In contrast, here we found that SD blastocysts were more
efficient to produce germline transmission of ESCs. We speculate that the DA and F344 blastocyst is not a compatible blastocyst for Tg or non-Tg F344 ESCs. The production of
gene targeting might be more efficient using F344 ESCs, as a BAC library is available for F344 to enable a recombineering approach.” (pg. 1583 col. 1 parag. 3).
Thus, while one laboratory was able to successfully use ES cells from F344 rats, other labs have not had the same success and thus their remains a general unpredictability of use rat ES cells to contribute to the germline for the creation of a transgenic rat. Accordingly, establishing and culturing ES cells from other species of animals having properties that are analogous to the mouse ES cells used in the methods of the claimed invention is highly unpredictable.
Conclusion
The art clearly teaches that phenotypes even in transgenic mice are unpredictable. Since the claims recite no phenotype for the claimed non-human animal (claim 1) and that the art teaches that the creation of non-mouse transgenic animals is unpredictable, the skilled artisan would find the claimed invention as unpredictable for its entire breadth and thus limiting the claimed invention to the scope set forth above is proper.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claim(s) 1-3, 6, 8, 20 and 22 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Gaitanaris et al. (WO 2004/040000 A2).
Regarding claims 1, 3, 6, 20 and 22, Gaitanaris et al. teach a method of making a transgenic mouse whose genome comprises a human gene encoding GLP1R (SEQ ID NO: 459) which is 91.8% identical to instantly recited SEQ ID NO: 2 (see Abstract, pg. 318 lines 14-21, claim 452 and Fig. 1). Specifically, Gaitanaris teaches that their “invention features a transgenic mouse expressing a transgene encoding a human GPCR polypeptide listed in Table 1” (pg. 125 lines 25-26).
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Regarding claim 2, Gaitanaris teaches that the human sequence encoding GLP1R is operably linked to an endogenous GLP1R locus (pg. 133 lines 10-16 and pg. 318 lines 14-21).
Regarding claim 8, Gaitanaris teaches that one or more cells will express the human GLP1R (see Abstract and claim 440).
Thus Gaitanaris clearly anticipates the invention of claims 1-3, 6, 8, 20 and 22.
Claim(s) 1, 4, 20, 21 and 23 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Jun et al. (2014, PLOS ONE, Vol. 9(4), pgs. 1-12).
Regarding claims 1 and 20, Jun et al. teach a method of making a humanized transgenic mouse expressing human GLP1-R (see Abstract).
Regarding claim 4, Jun teaches that the human GLP1-R is operably linked to the endogenous 5’UTR (pg. 2, col. 1 parag. 3).
Regarding claim 21, Jun teaches inserting Exons 1-13 of the human GLP1-R gene (Fig. 1A, reproduced below).
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Regarding claim 23, Jun teaches that the human GLP1R sequence is inserted within exon 1 of the mouse GLP1R locus (Fig. 1, figure legend).
Thus Jun clearly teaches the invention of claims 1, 4, 20, 21 and 23.
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.
Claim(s) 1, 34 and 35 is/are rejected under 35 U.S.C. 103 as being unpatentable over Jun et al. (2014, PLOS ONE, Vol. 9(4), pgs. 1-12) in view of Viuff et al. (2016, J. Controlled Release, Vol. 223, pgs. 22-30) and evidenced by the teachings of White et al. (1986, Nucleic Acid Research, Vol. 14(12), pgs. 4719-4730).
Regarding claim 1, Jun et al. teach a humanized transgenic mouse whose genome comprises a nucleic acid encoding human GLP1-R (see Abstract and Fig. 1).
Jun continues to teach that GLP-1 potentiates several therapeutic effects which are mediated by its receptor GLP1-R (pg. 1 cols. 1 and 2).
Jun concludes by teaching “Although much is now known about the role of GLP-1 in
controlling glucose metabolism, improving our understanding of the molecular mechanisms that regulate GLP-1R function in β cells and other tissues may enable development of improved GLP-1R-based therapies. An emerging area in GPCR biology is identifying partner or accessory proteins and understanding how GPCR interacting proteins help control signaling.” (pg. 11 col. 1 parag. 2 lines 1-7).
Jun does not teach:
a transgenic mouse further comprising a sequence encoding an additional human protein.
Regarding using an additional protein, Viuff et al. teach the benefits of generating
a double transgenic humanized mouse for studying the interaction between a ligand (albumin) and its receptor (neonatal Fc) (see Abstract and Introduction).Viuff continues to teach that “This work introduces a novel double transgenic humanized FcRn/ albumin mouse that maintains an autologous receptor/ligand interactionrequired for studying HSA-based drugs. The model was used successfully to discriminate PK profiles from albumins with different FcRn affinities in the presence of an endogenous pool of HSA. The model better mimics the human physiological conditions and, thus, has potential wide applications in the development of albumin-linked drugs or conventional drugs whose action is influenced by reversible binding to endogenous HSA.” (pg. 29 col. 1 parag. 3 bridge col. 2 lines 1-3).
Further, at the time of filing the nucleic acid sequence encoding human GLP1 was
known at the time of filing as evidenced by the teachings of White et al.
Thus at the time of filing the ordinary artisan would have found it prima facie obvious to modify the teachings of Jun regarding a humanized transgenic mouse whose genome comprises a nucleic acid encoding human GLP1-R with the teachings of Viuff regarding creating double transgenic mice that express a ligand and the corresponding receptor to arrive at the claimed invention.
One of ordinary skill in the art would have been motivated to make such a modification since Viuff teaches the advantages of generating double transgenic mice that express a ligand its receptor for the study of drug function and Jun teaching that GLP1-R is the receptor for GLP1.
There would have been a reasonable expectation of success that the humanized transgenic mouse, expressing human GLP1-R could further comprise and express human GLP1 since the nucleotide sequence encoding human GLP1 was known at the time of filing and Viuff teaching the successful creation of double transgenic mice.
Thus the cited art provides the requisite teachings and motivations to make and use the invention as claimed.
Conclusion
No claims are allowed.
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/DAVID A MONTANARI/Examiner, Art Unit 1632