Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
Applicant’s election without traverse of Group II (Claims 15, 19, and 32-33; drawn to a human G-CSF knock-in rodent further deficient in Fcer1g and Fcgr2b) in the reply filed on September 24, 2024, is acknowledged.
Claims 1, 5, 20-21, 24, 28, and 30-31 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention (Groups II and III), there being no allowable generic or linking claim.
DETAILED ACTION
The amended claims filed on June 11, 2026, have been acknowledged. Claims 2-4, 6-14, 16-18, 22-23, and 29 were cancelled. Claim 19 was amended. In light of the Applicant’s elected invention, claims 1, 5, 20-21, 24-28, and 30-31 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Claims 15, 19, and 32-33 are pending and examined on the merits.
Applicant’s response has been considered. Rejections and/or objections not reiterated from the previous office action mailed January 28, 2026, are hereby withdrawn. The following rejections and/or objections are either newly applied or are reiterated and are the only rejections and/or objections presently applied to the instant application.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Priority
Acknowledgment is made of Applicant’s claim for foreign priority under 35 U.S.C. 119(a)-(d).The applicant claims foreign priority from JP2019-062919 filed on March 28, 2019. Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55, received September 27, 2021. Receipt is acknowledged of a certified English translation of said foreign patent application on February 3, 2025. Applicant has not complied with one or more conditions for receiving priority to an earlier filing date under 35 U.S.C. 119(a)-119(d) for the reasons as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original foreign application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of 35 U.S.C. 112(a) or the first paragraph of pre-AIA 35 U.S.C. 112, except for the best mode requirement. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, Application No. JP2019-062919 filed on March 28, 2019, fail to provide adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. This provisional application does not provide information related to an immunodeficient rodent with knock-in of human G-CSF at a G-CSF receptor locus and wherein the rodent is further deficient in Fcer1g and Fcgr2b. However, Application No. PCT/JP2020/013635, filed on March 26, 2020, did provide the above information. Therefore, claims 15, 19, and 32-33 receive domestic benefit from Application No. PCT/JP2020/013635, filed on March 26, 2020.
Withdrawn Claim Rejections - 35 USC § 112
The prior rejection of Claim 19 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 is withdrawn in light of Applicant’s amendment to claim 19 to recite the immunodeficient rodent instead of the humanized rodent.
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.
Claims 15, 19, and 32-33 are rejected under 35 U.S.C. 103 as being unpatentable over Ito et al. (Poster PS2-1-2. October 2018; referenced in IDS), Li et al. (Mol Cancer Ther; 18: 780-787. 2019, previous art of record), Ito et al. (Experimental Hematology 40: 953–963. 2012), Smith et al. (PNAS 109: 6181-6186. 2012), Inoue (J Immunol 179: 764–774 2007), and Bruhns et al. (Immunological Reviews 268: 25–51. 2015). This rejection is repeated with regards to the previous rejection in the Non-final Office action mailed on January 28, 2026. Applicant’s traversal is addressed below.
Regarding claim 15, Ito 2018 teaches that they generated humanized G-CSF knock-in mouse wherein the knock-in occurs at the G-CSFR locus and teaches that G-CSFR expression is abolished in granulocytes while human G-CSF is highly expressed (Section 3). Ito 2018 teaches that humanized mice, in which the human hematopoietic system is reconstituted in immunodeficient mice, are a useful animal model for studying human hematology and immunology. Furthermore, Ito 2018 teaches that although human T or B lymphocytes significantly differentiate in human HSC-transferred humanized mice, myeloid lineage cells, especially granulocytes, do not fully develop in them. In this study, they generated a novel NOG mouse strain, human G-CSF knock.in mouse, to induce mature human neutrophils in their circulation. During weeks 4-12 of transplantation, human neutrophils and monocytes were significantly differentiated and detected in the peripheral blood of hG-CSF Kl mice compared to conventional NOG mice (abstract and Sections 3-4). Ito 2018 teaches that they transplanted 104-105 human HSPCs into their G-CSF knock-in mouse after irradiating the mouse and generated circulating neutrophils (Section 4).
Ito 2018 does not teach wherein the G-CSF gene knock-in mouse is also deficient in Fcer1g and Fcgr2b.
However, Li teaches that NSG and NOG mice undergo rapid clearance of therapeutic antibodies. Li teaches that macrophages that express FcγRs may be responsible for the antibody clearance (abstract, page 784, column 2, paragraphs 4-5, and Figure 4). Li teaches that before entering clinical trials, the efficacy and toxicity of antibody drugs are studied in various in vitro and in vivo models. Most oncology drugs are tested using xenografts, which are implanted in immuno-deficient mouse strains such as NSG mice. Compared with wild-type mice, these mice lack one or more types of immune cells, allowing the engraftment of foreign tumor cells. Among them, NSG mice are considered the most immune-compromised, because they lack mature T cells, B cells, and natural killer (NK) cells. They also have defective macrophages and dendritic cells due to impaired IL2R signaling (page 780, column 1, paragraph 2).
Although Li did not examine NOG mice for FcγR expression, Ito 2012 teaches that NOG mice lack T, B, and natural killer cells but still comprise macrophages with reduced function, similar to NSG mice (page 953, column 1, paragraph 1-column 2, paragraph 1). Therefore, as NOG and NSG mice similarly lack mature T cells, B cells, and natural killer (NK) cells and NOG mice have similar antibody clearance as NSG mice, it is reasonable to conclude that NOG mice also have macrophages that express FcγRs.
Furthermore, Li teaches that humanized mice derived from immunodeficient mice are adopted to study infectious disease, cancer, and graft versus host disease. Their study shows that the study of therapeutic antibodies may have been penalized due to macrophages that express FcγRs may be responsible for the antibody clearance. However, one can circumvent the caveat by using transgenic strains containing human FcRn or FcgR genes and serve as better animal models for preclinical evaluation of therapeutic antibodies (abstract and page 786, column 1, paragraph 2). Li cites to Smith for teaching one of the mouse transgenic strains containing human FcRn or FcgR genes.
Smith teaches that they developed a mouse model in which all murine FcγRs have been deleted and human FcγRs, encoded as transgenes, have been inserted into the mouse genome resulting in recapitulation of the unique profile of human FcγR expression. These human FcγRs are shown to function to mediate the immunomodulatory, inflammatory, and cytotoxic activities of human IgG antibodies and Fc engineered variants and provide a platform for the detailed mechanistic analysis of therapeutic and pathogenic IgG antibodies (abstract). Attempts to model huIgG interactions with human FcγR-expressing cells in vitro fail to mirror the diversity of cellular populations that may be required for an in vivo response. Therefore, new systems to study the in vivo function of the huFcγR system and the biological effects of engaging the activating and inhibitory huFcγRs by IgG are required. Furthermore, the increasing number of Ab-based therapeutics being developed for the treatment of neoplastic, infectious, and autoimmune diseases requires a system in which evaluation of the consequences of huFcγR interactions be addressed. The FcγR humanized mice recapitulate huFcγR expression patterns and expression levels and are functional in a variety of huIgG-mediated models of inflammation, cytotoxicity, and tumor clearance (page 6181, column 2, paragraph 1).
Smith does not identify whether their knockout mouse model lacks mFcεRI. However, Inoue teaches a FCRγ-/- mouse (abstract) which the instant specification identifies that the FCRγ-/- mice of Inoue are FcR KO mice deficient in Fcer1g and Fcgr2b (Example 2). Additionally, Bruhns teaches that FCRγ-/- mice have abrogated expression of mFcγRI, mFcγRIII, mFcγRIV, and mFcεRI (page 28, column 2, paragraph 3-page 29, column 1, paragraph 1). Inoue teaches that they mated their FCRγ-/- mice with immunodeficient NOD mice and were able to generate successfully progeny for experimentation (whole document).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have combined the G-CSF knock-in mouse of Ito 2018 with the FCRγ-/- mouse of Inoue to arrive at the instantly claimed invention. One of ordinary skill in the art would have a reason to combine with a reasonable expectation of success because Ito 2018, Li, and Smith each teach that humanized immunodeficient mice are commonly used to recapitulate human immune systems to assess human immunology in relation to infectious diseases in an animal model and Li and Smith teach examining the efficacy of antibodies for treating various disorders, such as cancer and infectious diseases in humanized mice.
Furthermore, Li provides evidence that NOG mice comprise macrophages that express FcγRs that may be responsible for rapid antibody clearance. However, Li specifically identifies that one can circumvent this issue by using transgenic strains containing human FcRn or FcgR genes and serve as better animal models for preclinical evaluation of therapeutic antibodies and cites to Smith for teaching one of the mouse transgenic strains containing knockout of all murine FcγRs and insertion of human FcγRs into the mouse genome resulting in recapitulation of the unique profile of human FcγR expression. Similarly, Inoue teaches a FCRγ-/- mouse that is deficient in Fcer1g and Fcgr2b and has already been previously used to generate immunodeficient mice lacking FCRγ expression.
Additionally, Ito 2018 teaches that although human T or B lymphocytes significantly differentiate in human HSC-transferred humanized mice, myeloid lineage cells, especially granulocytes, do not fully develop in them. In this study, they generated a novel NOG mouse strain, human G-CSF knock.in mouse, to induce mature human neutrophils in their circulation. During weeks 4-12 of transplantation, human neutrophils and monocytes were significantly differentiated and detected in the peripheral blood of hG-CSF Kl mice compared to conventional NOG mice.
Therefore, it would have been obvious that one of ordinary skill in the art could combine the mice of Ito 2018 with the FCRγ-/- mice of Inoue and transgenic expression of human FCRγ genes as Li has already discussed the need for combining immunodeficient mice with knockout of mouse FCRγ genes and knockin of human FCRγ genes to produce a better animal model for translation to humans and the combination of mutations produce a mouse model that more accurately recapitulates the human immune system when humanized through better differentiation of myeloid cells and recapitulation of huFcγR expression patterns and expression levels that are functional in a variety of huIgG-mediated models of inflammation, cytotoxicity, and tumor clearance. Furthermore, this allows for better assessment of the efficacy of human antibodies to treat cancer or infection in an in vivo model. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
Regarding claim 19, Ito 2018 teaches that their mouse would be useful to study innate host defense in human against bacterial infection (abstract). As such, Ito 2018 specifically contemplates that these mice could be infected with a bacterium to examine innate immunity.
Regarding claims 32-33, Ito 2018, as stated supra, teaches that they transplanted 104-105 human HSPCs into their G-CSF knock-in mouse after irradiating the mouse and generated circulating neutrophils (Section 4). As the human neutrophils are circulating in the irradiated G-CSF knockin mice, an immune response to the neutrophils was inactivated. Otherwise, there would be no neutrophils, as seen in the control NOG mice (Section 4).
Response to Arguments
Applicant's arguments filed June 11, 2026, are acknowledged.
Applicant argues the cited references are directed to different research objectives, and the Office Action does not establish a sufficient reason why a person of ordinary skill in the art would have combined them in the manner required to arrive at the presently claimed invention. Ito I is directed to improving differentiation and maintenance of human neutrophils in a humanized immunodeficient mouse by knocking in human G-CSF at the mouse G-CSF receptor locus. In contrast, Li and Smith are directed to therapeutic antibody studies, including antibody clearance and Fe receptor-mediated antibody functions. The Office Action therefore has not established a sufficient reason why a skilled artisan would have combined these antibody-focused references with Ito I's neutrophil-differentiation model (page 6, paragraph 2).
Applicant's arguments have been fully considered but they are not persuasive.
Ito 2018 teaches that humanized mice, in which the human hematopoietic system is reconstituted in immunodeficient mice, are a useful animal model for studying human hematology and immunology (abstract and Sections 3-4).
Li teaches that humanized mice derived from immunodeficient mice are adopted to study infectious disease, cancer, and graft versus host disease. Li teaches that before entering clinical trials, the efficacy and toxicity of antibody drugs are studied in various in vitro and in vivo models. Most oncology drugs are tested using xenografts, which are implanted in immuno-deficient mouse strains such as NSG mice. Compared with wild-type mice, these mice lack one or more types of immune cells, allowing the engraftment of foreign tumor cells. Among them, NSG mice are considered the most immune-compromised, because they lack mature T cells, B cells, and natural killer (NK) cells.
Li shows that the study of therapeutic antibodies may have been penalized due to macrophages that express FcγRs may be responsible for the antibody clearance. Li teaches that NSG and NOG mice undergo rapid clearance of therapeutic antibodies. However, one can circumvent the caveat by using transgenic strains containing human FcRn or FcgR genes and serve as better animal models for preclinical evaluation of therapeutic antibodies (abstract, page 780, column 1, paragraph 2, page 784, column 2, paragraphs 4-5, page 786, column 1, paragraph 2, and Figure 4).
Although Li did not examine NOG mice for FcγR expression, Ito 2012 teaches that NOG mice lack T, B, and natural killer cells but still comprise macrophages with reduced function, similar to NSG mice (page 953, column 1, paragraph 1-column 2, paragraph 1). Therefore, as NOG and NSG mice similarly lack mature T cells, B cells, and natural killer (NK) cells and NOG mice have similar antibody clearance as NSG mice, it is reasonable to conclude that NOG mice also have macrophages that express FcγRs.
Smith teaches that they developed a mouse model in which all murine FcγRs have been deleted and human FcγRs, encoded as transgenes, have been inserted into the mouse genome resulting in recapitulation of the unique profile of human FcγR expression. These human FcγRs are shown to function to mediate the immunomodulatory, inflammatory, and cytotoxic activities of human IgG antibodies and Fc engineered variants and provide a platform for the detailed mechanistic analysis of therapeutic and pathogenic IgG antibodies (abstract). Attempts to model huIgG interactions with human FcγR-expressing cells in vitro fail to mirror the diversity of cellular populations that may be required for an in vivo response. Therefore, new systems to study the in vivo function of the huFcγR system and the biological effects of engaging the activating and inhibitory huFcγRs by IgG are required. Furthermore, the increasing number of Ab-based therapeutics being developed for the treatment of neoplastic, infectious, and autoimmune diseases requires a system in which evaluation of the consequences of huFcγR interactions be addressed (page 6181, column 2, paragraph 1).
Inoue teaches that they mated their FCRγ-/- mice with immunodeficient NOD mice and were able to generate successfully progeny for experimentation (whole document).
Ito 2018, Li, and Smith each teach that humanized immunodeficient mice are commonly used to recapitulate human immune systems to assess human immunology in relation to infectious diseases in an animal model and Li and Smith teach examining the efficacy of antibodies for treating various disorders, such as cancer and infectious diseases in humanized mice.
Therefore, it would have been obvious that one of ordinary skill in the art could combine the mice of Ito 2018 with the FCRγ-/- mice of Inoue and transgenic expression of human FCRγ genes as Li has already discussed the need for combining immunodeficient mice with knockout of mouse FCRγ genes and knockin of human FCRγ genes to produce a better animal model for translation to humans and the combination of mutations produce a mouse model that more accurately recapitulates the human immune system when humanized through better differentiation of myeloid cells and recapitulation of huFcγR expression patterns and expression levels that are functional in a variety of huIgG-mediated models of inflammation, cytotoxicity, and tumor clearance. Furthermore, this allows for better assessment of the efficacy of human antibodies to treat cancer or infection in an in vivo model. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
As can be seen above, one of ordinary skill in the art would identify the mouse of Ito 2018 as being more representative of the human immune system as it generates neutrophils while other models don’t. Therefore, it represents a better animal model of the human immune system for testing different treatments, such as antibody treatments, and their effects on the human immune system. Similarly, Li specifically identifies that transgenic strains containing human FcRn or FcgR genes serve as better animal models for preclinical evaluation of therapeutic antibodies. Therefore, it would have been well understood that combining the animal models of Ito 2018 and Inoue through mating would generate an improved animal model of the human immune system and would achieve better translatable data than ones that are currently being used. As such, there is a clear nexus between the work of Ito 2018, Li, Smith, and Inoue as they are all interested in generating a better animal model of the human immune system.
The Applicant further argues that the Examiner's rationale also depends on antibody-related mechanisms that would not have provided a basis for a skilled artisan to expect the claimed result. As noted previously and as reflected in the present specification, the claimed rodents are immunodeficient rodents. In particular, NOG mice lack functional B cells and do not produce antibodies in the manner assumed by the Office Action. NOG mice and related immunodeficient mice do not provide the conventional setting in which antibody production and antibody-mediated clearance would be expected to occur. Thus, even if Li suggests that Fcy receptor-expressing macrophages may be involved in rapid clearance of administered therapeutic antibodies, that teaching is not relevant to the present claims, which are not directed to administration of therapeutic antibodies. Li concerns exogenously administered antibodies, whereas the present claims concern an immunodeficient rodent in which human neutrophils are obtained by transplantation of human hematopoietic stem cells. The cited art does not teach or suggest that deleting Fcerlg and Fcgr2b in this specific hG-CSF knock-in immunodeficient background would increase human neutrophils.
Accordingly, a person of ordinary skill in the art would not have had a reasonable expectation that Fc receptor deficiency would increase human neutrophils in the presently claimed rodent. The present invention is based on the discovery that further deletion of Fcerlg and Fcgr2b in the hG-CSF knock-in background leads to substantially increased human neutrophils after transplantation of human hematopoietic stem cells. As shown in Example 2 and Figure 19 of the present application, the ratio of human neutrophils in human leukocytes is about 2-5% in hG-CSF KI mice, whereas the ratio is 15-20% in hG-CSF Kl, FcR KO mice. The cited prior art does not teach or suggest this result, nor does it provide a reason to expect it (page 6, paragraph 3-page 7, paragraph 2).
Applicant's arguments have been fully considered but they are not persuasive.
First, regarding Applicant’s argument that their immunodeficient mice do not produce antibodies and would not provide the conventional setting in which antibody production and antibody-mediated clearance would be expected to occur, the rejection as, as recited above, does not assume that the combined immunodeficient mouse of the combined teachings of Ito 2018, Li, Ito 2012, Smith, Inoue, and Bruhns would produce antibodies on its own. However, immunodeficient mice are routinely used to assess the efficacy of therapeutic antibodies in humanized mouse models of the human immune system. As stated above, Li teaches that humanized mice derived from immunodeficient mice are adopted to study infectious disease, cancer, and graft versus host disease. Li teaches that before entering clinical trials, the efficacy and toxicity of antibody drugs are studied in various in vitro and in vivo models. Most oncology drugs are tested using xenografts, which are implanted in immuno-deficient mouse strains such as NSG mice. Therefore, it was well understood in the art that immunodeficient mice can be humanized and administered therapeutic antibodies to assess treatment efficacy for translational potential.
Second, regarding Applicant’s argument that the present claims are not directed to administration of therapeutic antibodies, this limitation is not a part of the claims. Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993). The court explained that “reading a claim in light of the specification, to thereby interpret limitations explicitly recited in the claim, is a quite different thing from ‘reading limitations of the specification into a claim,’ to thereby narrow the scope of the claim by implicitly adding disclosed limitations which have no express basis in the claim.” The court found that applicant was advocating the latter, i.e., the impermissible importation of subject matter from the specification into the claim.). See also In re Morris, 127 F.3d 1048, 1054-55, 44 USPQ2d 1023, 1027-28 (Fed. Cir. 1997) (The court held that the PTO is not required, in the course of prosecution, to interpret claims in applications in the same manner as a court would interpret claims in an infringement suit. Rather, the “PTO applies to verbiage of the proposed claims the broadest reasonable meaning of the words in their ordinary usage as they would be understood by one of ordinary skill in the art, taking into account whatever enlightenment by way of definitions or otherwise that may be afforded by the written description contained in applicant’s specification.”). See MPEP 2111.
It was well understood in the art that immunodeficient mice can be humanized and administered therapeutic antibodies to assess treatment efficacy for translational potential. Therefore, it would have been obvious to combine the mice of Ito 2018 and Inoue to generate an improved animal model for testing therapeutic antibodies for clinical relevancy as the mouse of Ito 2018 shows improved recapitulation of human immune cells and the mouse of Inoue would circumvent macrophage based rapid clearance of therapeutic antibodies, as identified by Li. Furthermore, Inoue teaches that they mated their FCRγ-/- mice with immunodeficient NOD mice and were able to generate successfully progeny for experimentation (whole document). Therefore, it would be reasonable to expect that the FCRγ-/- mice could be mated with other immunodeficient mice and successfully produce progeny.
Regarding Applicant’s argument that the present claims concern an immunodeficient rodent in which human neutrophils are obtained by transplantation of human hematopoietic stem cells, in response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In this case, although the prior art did not identify increasing neutrophil counts as a motivation, this represents one potential motivation.
As stated supra, there was a clear motivation within the art to combine the mice of Ito 2018 and Inoue to produce an improved mouse model for translational studies on the efficacy of different therapeutic antibodies. It was well understood in the art that immunodeficient mice can be humanized and administered therapeutic antibodies to assess treatment efficacy for translational potential. Therefore, it would have been obvious to combine the mice of Ito 2018 and Inoue to generate an improved animal model for testing therapeutic antibodies for clinical relevancy as the mouse of Ito 2018 shows improved recapitulation of human immune cells and the mouse of Inoue would circumvent macrophage based rapid clearance of therapeutic antibodies, as identified by Li. Furthermore, Inoue teaches that they mated their FCRγ-/- mice with immunodeficient NOD mice and were able to generate successfully progeny for experimentation (whole document). Therefore, it would be reasonable to expect that the FCRγ-/- mice could be mated with other immunodeficient mice and successfully produce progeny.
Conclusion
THIS ACTION IS MADE FINAL. 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KEENAN A BATES whose telephone number is (571)270-0727. The examiner can normally be reached M-F 7:30-5:00.
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/KEENAN A BATES/Examiner, Art Unit 1631
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