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 .
Claims status
Claim 1 is amended.
Claims 2-5,7, and 9-19 are withdrawn
Claims 1,8, and 23-24 are pending and under examination.
Edited rejection necessitated by claims amendment
Claim Rejections - 35 USC § 103
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 text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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 1, 8, and 23-24 are rejected under 35 U.S.C. 103 as being unpatentable over Goldman et al ( WO 2019/246262 A2) in view of Matsuda et al ( The Journal of Neuroscience, 2008), and Matsuda et al (The Journal of Biological Chemistry, 2005).
Regarding claims 1,8, and 23-24, Goldman et al teach methods of treating or inhibiting onset of Huntington disease (See abstract). In one aspect of the disclosure, Goldman et al disclose that the treatment methods also include administering to the selected subject a preparation of human glial progenitor cells (hGPCs), this reads on claims 1 and 8.( See paragraph [0108]). Goldman et al teach that the hGPCs may be derived from human induced pluripotent stem cells (iPSCs), embryonic stem cells, or fetal tissue, this reads on claim 23-24. In one of the embodiment Goldman et al state that “ The glial progenitor cells of the administered preparation can optionally be genetically modified to express other proteins of interest. For example, the glial progenitor cells of the preparations can be optionally modified to overexpress an endogenous biological molecule, targeting moiety, and/or marker”. ( See paragraph [0121]). Goldman et al also teach the transplantation and engraftment of a genetically modified mutant Huntingtin (mHTT)-expressing hGPCs (mHTT hGPCs) that also overexpress SOX10 and MYRF into the brains of neonatal shiverer mice. Goldman et al demonstrate that shiverer mice receiving mHTT hGPCs overexpressing both genes generated a significant number of oligodendrocytes in the host’s engrafted white matter relative to the control, suggesting that the genetically modified cells maintain their ability to migrate and engraft.(See [0173], and Fig. 10).
Goldman et al do not teach a genetically modified human glial progenitor cells that overexpress ITM2B.
Matsuda et al. (2008) teach the generation of a knockout BRI2 (i.e. ITM2B) mouse model to validate the role of BRI2 in APP processing and Aβ degradation. Matsuda et al teach that crossing BRl2 knockout mice (Bri2 -/+ and Bri2 -/-) with a mouse model of Alzheimer’s disease (AD) increased Aβ accumulation compared to the aged-matched control carrying the wildtype Bri+/+ . (See Fig.3). This suggests that BRl2 is involved in Aβ degradation, and may contribute to neurodegenerative diseases associated with Aβ accumulation, such as Alzheimer and frontotemporal dementia (FTD).
Matsuda et al (2005) demonstrate that different cellular model of Alzheimer’s (i.e. N2a, Hela, and Hek293 cells expressing AβPP gene) can be genetically modified to overexpress ITM2B. Matsuda et al (2005) et al further demonstrate that expressing ITM2B in different cell types maintain its physiological function to reduce Aβ amyloid production. Specifically, Matsuda et al generate HeLa, HEK293, and N2a cells that overexpress FLAG-tagged BRI2, together with AβPP-Gal4, a luciferase reporter under the control of a Gal4 promoter and β-galactosidase. According to Matsuda, AβPP-Gal4 is a fusion of the yeast transcription factor Gal4 and the cytoplasmic domain of AβPP, thereby γ-Cleavage of AβPP-Gal4 will release the AβPP intracellular domain (i.e. AID-Gal4) from the membrane to the nucleus with consequent activation of luciferase transcription. Matsuda et al demonstrate that overexpression of BRI2 reduces luciferase activity, suggesting a significant reduction in Aβ accumulation in all three cell lines. (See abstract, and page 28915, right column, last paragraph, and Figure.3a).
Taken together, it would have been prima facie obvious to one with ordinary skill in the art at the time the invention was filed to combine the teachings of Goldman et al, and Matsuda, to engraft genetically modified hGPCs that overexpress ITM2B into a subject’s brain to replace diseased cells. Goldman et al teach a method of transplanting hGPCs into the brain of a subject suffering from or at risk of Huntingtin disease. Goldman et al also suggest that the hGPCs can be genetically modified to express other proteins of interest prior administration and still maintain the ability to proliferate and integrate in a subject’s brain. Matsuda et al. (2005 and 2008) teach overexpression of ITM2B in different cell types, and link BRI2 to amyloid degradation. Thus, one would have been motivated to genetically modify the cells of Goldman (i.e. hGPCs) to overexpress ITM2B and then to transplant them into the brain of a subject in need to replace diseased cells. There would be a reasonable expectation of success, when transplanting hGPCs overexpressing ITM2B, that the modified cells will continue to proliferate, integrate, and eventually differentiate into oligodendrocytes and astrocytes that also overexpress ITM2B in the subject’s brain, and potentially aiding in Aβ degradation. See MPEP 2143 (I)(G).
It is also noted that Goldman et al do not explicitly state that the modified glial progenitor cells have one or more of the following characteristic: (i) growing or proliferating or dividing faster, (ii) longer telomeres and/or higher telomerase activity, and (iii) having lower levels of senescence-associated transcripts encoding CDKNlA (p21Cipl) and CDKN2/pl6(INK4) and pl4(ARF). However, according to Applicant’s disclosure, the expression of ITM2B, one of the youth-related genes, when expressed in hGPCs provides the modified hGPCs cells with these characteristic, implying that these characteristics are inherent properties.( See [0183-0184] of instant application). As previously noted, the combined teachings of Goldman et al, Matsuda et al. (2008), and Matsuda et al (2005) render obvious the same cells of the instant claim. Therefore, these characteristics are considered to be inherent in the combined teachings of the recited prior arts.
In addition, it is noted that the source of the modified glial progenitor cells of the working examples appear to be identical if not substantially the same as the source of the cells utilized by Goldman et al. For example, the working examples of instant application and the disclosure of Goldman et al reference Wang et al as the source of the modified GPCs (Wang et al., "Human iPSC-derived Oligodendrocyte Progenitor Cells can Myelinate and Rescue a Mouse Model of Congenital Hypomyelination," Ce// Stem Cell 12:252-264 (2013). ( See paragraph [0136] and [0168] in Goldman et al, and [0183-0184] of instant application). Since the source of the modified glial progenitor cells appears to be identical between the prior art (i.e. Goldman et al) and instant application, then the cells of Goldman et al, when modified to overexpress ITM2B as suggested by Matsuda 2005 and 2008, will produce the same cells of instant claim. Therefore, these characteristics are considered to be inherent in the combined teachings of the recited prior arts.
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.
Claims 1,8, and 23-24 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 4-8, and 18 of U.S patent No.12303549 B2 in view of Goldman et al ( WO 2019/246262 A2), Matsuda et al ( The Journal of Neuroscience, 2008), and Matsuda et al (The Journal of Biological Chemistry, 2005).
Regarding claims 1, 8 and 23-24, the claims 4-8, and 18 of U.S patent No.12303549 teach a method of treating or inhibiting onset of Huntington disease by administering a preparation of genetically modified hGPCs to the forebrain or brain stem, wherein the cells have an increased expression of a gene that is involved in increasing myelination in a subject, such as SOX10 and MYRF.
U.S patent No.12303549 does not teach administering genetically modified glial progenitor cells with an increased expression of ITM2B.
The teachings of Goldman, Matsuda (2005), and Matsuda (2008) are set forth above.
Therefore, it would have been prima facie obvious to one with ordinary skill in the art at the time the invention was filed to combine the teachings of U.S patent No.12303549 ,Goldman et al, and Matsuda to engraft genetically modified hGPCs that overexpress ITM2B into a subject’s brain to replace diseased cells. U.S patent No.12303549 teach a method of treating or inhibiting onset of Huntington disease by administering a preparation of genetically modified hGPCs to the forebrain or brain stem of a subject in need. Goldman et al teach a method of transplanting hGPCs into the brain of a subject suffering from or at risk of Huntingtin disease. Goldman et al also suggest that the hGPCs can be genetically modified to express other proteins of interest prior administration. Matsuda et al. (2005 and 2008) teach overexpression of ITM2B in different cell types, and link ITM2B to amyloid degradation. Thus, one would have been motivated to combine the teachings of U.S patent No. 12303549, Goldman, and Matsuda to transplant genetically modified hGPCs overexpressing ITM2B into a subject’s brain to replace damaged cells. There would be a reasonable expectation of success in doing so because the cited prior art provides motivation, suggestions, and teachings, as well as experimental basis for one skilled in the art to readily envision overexpressing ITM2B in the hGPCs and using the genetically modified hGPCs to treat a brain disorder, with a higher expectation of success. See MPEP 2143 (I)(G).
It is also noted that U.S patent No.12303549 do not explicitly state that the modified glial progenitor cells have one or more of the following characteristic: (i) growing or proliferating or dividing faster, (ii) longer telomeres and/or higher telomerase activity, and (iii) having lower levels of senescence-associated transcripts encoding CDKNlA (p21Cipl) and CDKN2/pl6(INK4) and pl4(ARF). However, according to Applicant’s disclosure, the expression of ITM2B, one of the youth-related genes, when expressed in hGPCs provides the modified hGPCs cells with these characteristic, implying that these characteristics are inherent properties.( See [0183-0184] of instant application). The combined teachings of U.S patent No.12303549, Goldman et al, Matsuda et al. (2008), and Matsuda et al (2005) render obvious the same cells of the instant claim. Therefore, these characteristics are considered to be inherent in the combined teachings of the recited prior arts.
Claims 1, and 23-24 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, and 5-8 of (U.S patent No.11690876 B2). in view of Goldman et al ( WO 2019/246262 A2), Matsuda et al ( The Journal of Neuroscience, 2008), and Matsuda et al (The Journal of Biological Chemistry, 2005).
Regarding claims 1, and 23-24, The claims 1-3, and 7-8 of U.S patent No.11690876 teach a method of treating neuropsychiatric disorders by administering a preparation of hGPCs at an effective dosage to a human subject. U.S patent No. 11690876 teaches that the hGPCs are derived from fetal tissue, embryonic stem cells, or induced pluripotent stem cells. Furthermore, under the broadest reasonable interpretation, the subject matter of claim1 of U.S patent No.11690876 encompasses any preparation of hGPCs, including genetically modified ones.
U.S patent No. 11690876 does not teach administering genetically modified glial progenitor cells with an increased expression of ITM2B.
The teachings of Goldman, Matsuda (2005), and Matsuda (2008 are set forth above.
Therefore, it would have been prima facie obvious to one with ordinary skill in the art at the time the invention was filed to combine the teachings of U.S patent No.11690876 ,Goldman et al, and Matsuda to engraft genetically modified hGPCs that overexpress ITM2B into a subject’s brain to replace diseased cells. U.S patent No.11690876 teaches administering a preparation of hGPCs at an effective dosage to treat a neuropsychiatric disorder in a human subject. Goldman et al teach a method of transplanting hGPCs into the brain of a subject suffering from or at risk of Huntingtin disease. Goldman et al also suggest that the hGPCs can be genetically modified to express other proteins of interest prior administration. Matsuda et al. (2005 and 2008) teach overexpression of ITM2B in different cell types and link ITM2B to amyloid degradation. Thus, one would have been motivated to combine the teachings of U.S patent No.11690876, Goldman, and Matsuda to transplant genetically modified hGPCs overexpressing ITM2B into a subject’s brain to replace damaged cells. There would be a reasonable expectation of success in doing so because the cited prior art provides motivation, suggestions, and teachings, as well as experimental basis for one skilled in the art to readily envision overexpressing ITM2B in the hGPCs and using the genetically modified hGPCs to treat a brain disorder, with a higher expectation of success. See MPEP 2143 (I)(G).
It is also noted that U.S patent No.11690876 do not explicitly state that the modified glial progenitor cells have one or more of the following characteristic: (i) growing or proliferating or dividing faster, (ii) longer telomeres and/or higher telomerase activity, and (iii) having lower levels of senescence-associated transcripts encoding CDKNlA (p21Cipl) and CDKN2/pl6(INK4) and pl4(ARF). However, according to Applicant’s disclosure, the expression of ITM2B, one of the youth-related genes, when expressed in hGPCs provides the modified hGPCs cells with these characteristic, implying that these characteristics are inherent properties.( See [0183-0184] of instant application). The combined teachings of U.S patent No.11690876, Goldman et al, Matsuda et al. (2008), and Matsuda et al (2005) render obvious the same cells of the instant claim. Therefore, these characteristics are considered to be inherent in the combined teachings of the recited prior arts.
Claims 1, and 23-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 28,29,31-33 of the copending application No 17430768, in view of Goldman et al ( WO 2019/246262 A2), Matsuda et al ( The Journal of Neuroscience, 2008), and Matsuda et al (The Journal of Biological Chemistry, 2005).
Regarding claims 1, and 23-24, The copending claims 28,29,31-33 of application No. 17430768 teach a method of administering a preparation of hGPCs into the brain or brain stem of a subject. U.S No. 17430768 teaches that the hGPCs are derived from fetal tissue, embryonic stem cells, or induced pluripotent stem cells. Furthermore, under the broadest reasonable interpretation, the subject matter of claim 28 encompasses any preparation of hGPCs, including genetically modified ones.
U.S No. 17430768 does not teach administering genetically modified glial progenitor cells with an increased expression of ITM2B.
The teachings of Goldman, Matsuda (2005), and Matsuda (2008) are set forth above.
Therefore, it would have been prima facie obvious to one with ordinary skill in the art at the time the invention was filed to combine the teachings of U.S No. 17430768 ,Goldman et al, and Matsuda to engraft genetically modified hGPCs that overexpress ITM2B into a subject’s brain to replace diseased cells. U.S No. 17430768 teach administering a preparation of hGPCs into the brain or brain stem of a subject . Goldman et al teach a method of transplanting hGPCs into the brain of a subject suffering from or at risk of Huntingtin disease. Goldman et al also suggest that the hGPCs can be genetically modified to express other proteins of interest prior administration. Matsuda et al. (2005 and 2008) teach overexpression of ITM2B in different cell types, and link ITM2B to amyloid degradation. Thus, one would have been motivated to combine the teachings of U.S No. 17430768, Goldman, and Matsuda to transplant genetically modified hGPCs overexpressing ITM2B into a subject’s brain to replace damaged cells. There would be a reasonable expectation of success in doing so because the cited prior art provides motivation, suggestions, and teachings, as well as experimental basis for one skilled in the art to readily envision overexpressing ITM2B in the hGPCs and using the genetically modified hGPCs to treat a brain disorder, with a higher expectation of success. See MPEP 2143 (I)(G).
It is also noted that U.S No. 17430768 do not explicitly state that the modified glial progenitor cells have one or more of the following characteristic: (i) growing or proliferating or dividing faster, (ii) longer telomeres and/or higher telomerase activity, and (iii) having lower levels of senescence-associated transcripts encoding CDKNlA (p21Cipl) and CDKN2/pl6(INK4) and pl4(ARF). However, according to Applicant’s disclosure, the expression of ITM2B, one of the youth-related genes, when expressed in hGPCs provides the modified hGPCs cells with these characteristic, implying that these characteristics are inherent properties.( See [0183-0184] of instant application). The combined teachings of U.S No. 17430768, Goldman et al, Matsuda et al. (2008), and Matsuda et al (2005) render obvious the same cells of the instant claim. Therefore, these characteristics are considered to be inherent in the combined teachings of the recited prior arts.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not been patented.
Claims 1,8, and 23-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1,3, 5, 10,15, 16, 17, and 19 ,of the copending application No 18047758, in view of Goldman et al ( WO 2019/246262 A2), Matsuda et al ( The Journal of Neuroscience, 2008), and Matsuda et al (The Journal of Biological Chemistry, 2005).
Regarding claims 1,8 and 23-24, The copending claims 1,3, 5, 10,15, 16, 17, and 19 of application No. 18047758 teach a method of treating conditions mediated by age-related loss in oligodendrocyte, astrocyte, and white matter by administering a preparation of hGPCs into the brain of a subject in need for treatment. U.S No. 18047758 teaches that the hGPCs are derived from fetal tissue, embryonic stem cells, or induced pluripotent stem cells. Furthermore, under the broadest reasonable interpretation, the subject matter of claims 1,3,5 encompasses any preparation of hGPCs, including genetically modified ones.
U.S No. 18047758 does not teach administering genetically modified glial progenitor cells with an increased expression of ITM2B.
The teachings of Goldman, Matsuda (2005), Matsuda and (2008) are set forth above.
Therefore, it would have been prima facie obvious to one with ordinary skill in the art at the time the invention was filed to combine the teachings of U.S No. 18047758 ,Goldman et al, and Matsuda to engraft genetically modified hGPCs that overexpress ITM2B into a subject’s brain to replace diseased cells. U.S No. 18047758 teaches a method of treating conditions mediated by age-related loss in oligodendrocyte, astrocyte, and white matter by administering a preparation of hGPCs into the brain of a subject in need for treatment. Goldman et al teach a method of transplanting hGPCs into the brain of a subject suffering from or at risk of Huntingtin disease. Goldman et al also suggest that the hGPCs can be genetically modified to express other proteins of interest prior administration. Matsuda et al. (2005 and 2008) teach overexpression of ITM2B in different cell types, and link BRI2 to amyloid degradation. Thus, one would have been motivated to combine the teachings of U.S No. 18047758, Goldman, and Matsuda to transplant genetically modified hGPCs overexpressing ITM2B into a subject’s brain to replace damaged cells. There would be a reasonable expectation of success in doing so because the cited prior art provides motivation, suggestions, and teachings, as well as experimental basis for one skilled in the art to readily envision overexpressing ITM2B in the hGPCs and using the genetically modified hGPCs to treat a brain disorder, with a higher expectation of success. See MPEP 2143 (I)(G).
It is also noted that U.S No. 18047758 do not explicitly state that the modified glial progenitor cells have one or more of the following characteristic: (i) growing or proliferating or dividing faster, (ii) longer telomeres and/or higher telomerase activity, and (iii) having lower levels of senescence-associated transcripts encoding CDKNlA (p21Cipl) and CDKN2/pl6(INK4) and pl4(ARF). However, according to Applicant’s disclosure, the expression of ITM2B, one of the youth-related genes, when expressed in hGPCs provides the modified hGPCs cells with these characteristic, implying that these characteristics are inherent properties.( See [0183-0184] of instant application). The combined teachings of U.S No. 18047758, Goldman et al, Matsuda et al. (2008), and Matsuda et al (2005) render obvious the same cells of the instant claim. Therefore, these characteristics are considered to be inherent in the combined teachings of the recited prior arts.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not been patented.
Response to Arguments
Applicant's arguments filed 01/28/2026 have been fully considered but they are not persuasive.
Applicants argue that Goldman et al. is entirely silent with respect to genetically modified glial progenitor cells being younger than the unmodified glial progenitor cells.
Examiner’s Response to Traversal: Applicant’s arguments have been carefully considered but are not found persuasive. This is because Applicants have removed the recitation that "the genetically modified glial progenitor cells are younger than the glial progenitor cells in the subject" . In other words, the instant claim no longer requires the genetically modified cells to be younger than the unmodified glial progenitor, which makes this argument moot.
Furthermore, Applicants argue that Goldman et al. focuses on the treatment of Huntington' s disease and in contrast, Matsuda I (i.e. 2005) and II (i.e. 2008) pertains to reducing Aβ in connection with treating Alzheimer's disease. Thus, one of skill in the art would not have had a motivation or a reasonable expectation of success to arrive at the method of amended claim 1 in view of Goldman et al. and/or Matsuda I (i.e. 2005) and II (2008).
Examiner’s Response to Traversal: Applicant’s arguments have been carefully considered but are not found persuasive. This is because, as previously discussed, the test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981).The office 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, the instant claims are directed to a method of replacing glial cells in a subject with modified hGPCs that overexpress ITM2B, with the expectation that the genetically modified cells would still be able to integrate and proliferate in the subject’s brain. The cited primary reference by Goldman et al teach a method of transplanting hGPCs into the brain of a subject suffering from or at risk of Huntingtin disease. Goldman et al also suggest that the hGPCs can be genetically modified to express other proteins of interest prior to administration, and that such cells will still have the ability to proliferate and integrate in the subject’s brain. The office agrees with Applicants that Goldman et al fail to directly teach or suggest overexpression of ITMP2B in hGPCs. However, Matsuda et al. (2005 and 2008) were cited to cure the deficiency by showing that ITM2B can be stably expressed in different cellular models of Alzheimer (i.e. N2a,Hela, and Hek293 that express AβPP), and that its overexpression aids in reducing Aβ amyloid production. Therefore, a person of ordinary skill in the art who had reviewed Goldman et al could have come across Matsuda et al 2005 and 2008 and quickly recognized the strong possibility of genetically modifying the cells of Goldman (i.e. hGPCs) to overexpress ITM2B and then transplanting such cells in the brain of a subject with neurodegenerative disease such as Alzheimer’s, Huntington’s, or FTD, and with a high expectation of success. There would be a reasonable expectation of success ,when transplanting hGPCs overexpressing ITM2B , that the modified cells still be able to proliferate, integrate, and eventually differentiate into oligodendrocytes and astrocytes that also overexpress ITM2B in the subject’s brain, and potentially aiding in Aβ amyloid degradation.
Applicants also argue that neither Matsuda 2005 or Matsuda 2005 teach genetically modified glial progenitor cells having "one or more of the following characteristics: (i) growing or
proliferating or dividing faster, (ii) longer telomeres and/or higher telomerase activity, and (iii)
having lower levels than old of senescence-associated transcripts encoding CDKNlA (p21Cipl)
and CDKN2/pl6(INK4) and pl4(ARF)" as recited in amended claim 1.
Examiner’s Response to Traversal: Applicant’s arguments have been carefully considered but are not found persuasive. This is because, according to Applicants remarks, when ITM2B, one of the youth-related genes, is expressed in hGPCs provides the modified hGPCs cells with these characteristics, implying that these characteristics are inherent properties.( See Remarks -1st paragraph on page 9). While neither Matsuda 2005 nor Matsuda 2008 teach glial cells having the recited characteristics independently ; however, as previously noted, the combined teachings of Goldman et al, Matsuda et al. (2008), and Matsuda et al (2005) render obvious the same cells of the instant claim. Therefore, these characteristics are considered to be inherent in the combined teachings of the recited prior arts.
Conclusion
No claim is allowed.
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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to FATIMAH KHALAF MATALKAH whose telephone number is (703)756-5652. The examiner can normally be reached Monday-Friday,7:30 am-4:30 pm EST.
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/FATIMAH KHALAF MATALKAH/Examiner, Art Unit 1638
/Tracy Vivlemore/Supervisory Primary Examiner, Art Unit 1638