DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
This Office Action is in response to the paper filed 28 May 2026. Claims 1, 4, 6, 7, and 19 have been amended. Claims 8-18 remain withdrawn. Claims 1-7, 19, and 20 are currently pending and under examination.
This application claims benefit of priority to U.S. Provisional Application No. 63/488475, filed March 3, 2023.
Withdrawal of Objections:
The objection to claim 1, is withdrawn.
Maintenance/Modification of Rejections Necessitated by Amendment:
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1-7, 19, and 20 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
With regard to claim 1, this claim as amended recites:
A three to four week accelerated Alzheimer's Disease (AD) model system comprising a cell type having one or more AD associated phenotypes wherein said cell type is derived from cultured neuronal progenitor cells, or
induced pluripotent stem cells (iPSCs) expressing a familial Alzheimer's (FAD) gene mutation, and wherein said cell type has been (i) engineered to express progerin and (ii) subjected to cell culture conditions leading to neuronal differentiation and wherein said cultured cells develop into the cell type having the one or more AD associated phenotypes.
The claim as amended is still indefinite, because it is unclear whether the cell type in the AD model system (final cell) is intended to express progerin in addition to having one or more AD associated phenotypes, or instead, if only the iPSCs (precursor cells) are engineered to express progerin. Additionally, it is unclear if (i) and (ii) are both intended to refer to the final cells in the AD model, to the precursor iPSCs/progenitors, or to both (e.g. (i) refers to the final cells, and (ii) refers to the precursor cells). Further, it is unclear if just the iPSCs are intended to express a FAD gene mutation, or if either of the neuronal progenitor cells and the iPSCs are intended to express a FAD gene mutation. For the purposes of examination, this claim is interpreted to require the cell type in the final cell system to have an AD associated phenotype, and not required to express progerin.
The noted limitations, which are also present in independent claim 19 are likewise rejected and interpreted as set forth above.
Claims 2-7 and 20 are included in this rejection, as these claims depend from above rejected claims and fail to remedy the noted deficiencies.
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claims 2, 3, and 5 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claims 2 and 3 recite that that the one or more AD associated phenotypes are observed in less than 6 weeks (claim 2), or in 3-4 weeks (claim 3). However, claim 1 as amended, from which these claims depend, now recites that the system is a “three to four week accelerated Alzheimer’s Disease (AD) model system.” As such, claim 3 fails to further limit claim 1, and claim 2 fails to further limit claim 1 in that it includes times between four and six weeks, and less than three weeks.
Claim 5 recites that the neuronal progenitor cells or iPSCs further express a familial AD gene mutation. However, claim 1 as amended, from which this claim depends, now indicates that at least the iPSCs further express a familial AD gene mutation. As such, claim 5 fails to further limit the subject matter of claim 1.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 102/103
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.
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.
Claims 1-7, 19, and 20 are rejected under 35 U.S.C. 102(a)(1) as anticipated by or, in the alternative, under 35 U.S.C. 103 as obvious over Studer et al. (US 2018/0230424; Published 2018).
Regarding claims 1-7, Studer et al. teach an accelerated disease model system for the study of late-onset diseases including Alzheimer’s disease (AD), the model system including age-appropriate old/mature cells (Abs.; Para. 64). The model system comprising induced pluripotent stem cells (iPSCs) or neuronal progenitor cells engineered to express progerin, and cultured under conditions to provide neuronal differentiation including to a cell type that has one or more AD associated phenotypes, including pathological aggregation of tau protein, which is Tau phosphorylation (Abs.; Para. 30, 86, 172).
Claims 1-7 are directed to the accelerated Alzheimer’s Disease model system, which is produced by the claimed process. "[E]ven though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. The patentability of a product does not depend on its method of production. If the product in the product-by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process." In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985).
Here, Studer et al. similarly teach an Alzheimer’s Disease model system that includes cells differentiated to develop an AD-associated phenotype, including pathological aggregation of tau protein, which is Tau phosphorylation (Abs.; Para. 30, 53, 64, 86, 172). The model system is used for the same purpose as claimed: for the study of late-onset diseases, including Alzheimer’s Disease. Functionally, the Alzheimer’s Disease model system of Studer et al. is the same as the claimed system. Therefore, the model system of Studer et al. is the same as, or would have rendered obvious, the model system produced by the claimed process.
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"The Patent Office bears a lesser burden of proof in making out a case of prima facie obviousness for product-by-process claims because of their peculiar nature" than when a product is claimed in the conventional fashion. In re Fessmann, 489 F.2d 742, 744, 180 USPQ 324, 326 (CCPA 1974). Once the examiner provides a rationale tending to show that the claimed product appears to be the same or similar to that of the prior art, although produced by a different process, the burden shifts to applicant to come forward with evidence establishing an unobvious difference between the claimed product and the prior art product. In re Marosi, 710 F.2d 798, 802, 218 USPQ 289, 292 (Fed. Cir. 1983).
Studer et al. teach or render obvious the Alzheimer’s Disease model as claimed, including the components as claimed. As the model cannot be separated from its properties, use of the model as claimed/rendered obvious would necessarily provide for an accelerated AD model, including observation of the AD associated phenotype(s) in 3-4 weeks, or in less than 6 weeks.
With regard to claims 19 and 20 Studer et al. teach that cell cultures derived from a patient with a late-onset disease, including AD, are utilized to construct the model system (Para. 53), wherein cells collected from a patient are necessarily collected in a container. It is further taught that Progerin and other reagents are provided to accelerate cell maturation/aging (Abs.; Para. 56). The disclosure of Studer et al. is instructions for the use of the taught components. As discussed previously, Studer et al. teach or render obvious an accelerated Alzheimer’s Disease model system that includes cells differentiated to a cell type that has an AD-associated phenotype, including pathological aggregation of tau protein, which is Tau phosphorylation (see rejection of claim 1 above). As such, Studer et al. teach or render obvious a kit that is capable of being used for diagnosing or prognosing AD in a subject, identifying a subject at risk of development of AD, or prescribing a therapeutic regimen or predicting benefit from therapy in a subject having AD.
Response to Arguments
With regard to the previous indefiniteness rejection, Applicant urges that the claims as amended overcome this rejection.
Applicant’s arguments have been fully considered, but have not been found persuasive for the reasons set forth in the modified 112(b) rejection above.
With regard to the 102/103 rejection over Studer et al., Applicant urges that the claims as amended are directed to a 3-4 week accelerated AD model system, where prior art systems require a substantially longer maturation period. Additionally, Studer is directed toward modeling Parkinsons disease and does not recognize, suggest, or motivate the use of progerin expression in combination with FAD mutations for generating accelerated AD-specific pathological phenotypes.
Applicant’s arguments have been fully considered, but have not been found persuasive.
It is noted that Applicant’s arguments are directed to a method of making an accelerated AD model system, and not to a per se accelerated AD model system as currently claimed. "[E]ven though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. The patentability of a product does not depend on its method of production. If the product in the product-by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process." In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985). Here, Studer et al. similarly teach an Alzheimer’s Disease model system that includes cells differentiated to develop an AD-associated phenotype, including pathological aggregation of tau protein, which is Tau phosphorylation (Abs.; Para. 30, 53, 64, 86, 172). The model system is used for the same purpose as claimed: for the study of late-onset diseases, including Alzheimer’s Disease. Functionally, the accelerated Alzheimer’s Disease model system of Studer et al. is the same as the claimed system. Therefore, the model system of Studer et al. is the same as, or would have rendered obvious, the model system produced by the claimed process.
With regard to Applicant’s argument that Studer is directed toward modeling Parkinsons disease and not an AD model as claimed; Studer et al. specifically teach:
Late-onset disorders and/or diseases can occur in a variety of physiological systems. For example, neurodegenerative disorders such as Parkinson's disease (PD) or Alzheimer’s disease (AD) are becoming a growing burden to society (emphasis added) (Para. 5).
Conventional reprogramming of somatic cells to induced pluripotent stem cells (iPSCs) resets their phenotype back to an embryonic age, and thus presents a significant hurdle for modeling late-onset disorders…. This strategy can be applied to cell cultures derived from a patient with a late-onset disease and/or disorder including… a neurodegenerative disease, such as Alzheimer's disease (AD)…to derive age-appropriate cell cultures that more accurately represent patient age and thus the disease state (emphasis added) (Para. 53).
As used herein, the term “late-onset disease” refers to a disease or medical condition of a patient manifesting as a clinical condition in middle age and old age patients . Such that a late-onset disease may include but not limited to degenerative, such as neurodegenerative diseases, such as Parkinson's disease (PD), amyotrophic lateral sclerosis, Alzheimer ' s… (emphasis added) (Para. 64).
In some embodiments, aged iPSC-derived cell types obtained as described herein may find use in disease modeling and for identifying therapeutically relevant cell stages during development, such as identifying progerin aged cellular stages for use in testing new drug compounds for use as therapeutics and for actual use in treatment of patients. Thus in some embodiments, primary somatic cell donors for iPSC-derived cell types have a disease or a disease phenotype induced in iPSC-derived cell/tissue culture including but are not limited to actual or model neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease… (emphasis added) (Para. 172).
Nonlimiting examples of specific iPSC-derived cell types and associated disease(s) which can be used in conjunction with progerin-like protein compositions and aging induction methods of the present disclosure include… iPSC derived cortical neurons for Alzheimer's… (emphasis added) (Para. 173).
Given these teachings, it is clear that Studer teaches and/or renders obvious Alzheimer’s disease modeling.
Conclusion
No claims are allowable.
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 JENNIFER M.H. TICHY whose telephone number is (571)272-3274. The examiner can normally be reached Monday-Thursday, 9:00am-7:00pm ET.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Sharmila G. Landau can be reached at (571)272-0614. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/JENNIFER M.H. TICHY/Primary Examiner, Art Unit 1653
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