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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 11/14/2025 has been entered.
Claims Status
Claims 1, 3, and 5 are amended.
Claims 1, 3, 5, 10 and 15-20 are under examination.
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 1-3, and 10 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.
Regarding claims 1-3, the terms “mitotic fraction” of the isolated GPCs being “ larger” than that of resident progenitor cells” are relative terms which render the claims indefinite. Under the broadest reasonable interpretation, the subject matter of claims 1-3 includes glial progenitor cells (GPCs) that have been isolated directly from a subject’s brain, whether the subject is a fetal or adult, as well as human glial progenitor cells that have been differentiated in vitro from pluripotent or multipotent stem cells. When the cells are isolated from a subject the terms “ mitotic fraction ” being “larger” becomes relative because "mitotic fraction" and "larger" are numerical values (numerator/denominator), they are each dependent upon the relative size (denominator) of the respective first and second cell populations that are being compared from which "fraction" and/or "larger" (numerator) is/are to be determined. For example, how many cells in vivo are to be measured from which to ascertain the overall "mitotic fraction" and/or the relative number being larger, smaller, or essentially the same? It is not clear how the fraction is calculated, is it dependent on the total number of oligodendrocytes in the brain (e.g. larger denominator) or the total number of oligodendrocytes in a damaged region of the brain (e.g. smaller denominator), while one may detect mitotic cells in some portion of the brain (numerator 1), or multiple, dispersed regions of the brain (numerator 2), the "mitotic fraction" changes depending upon the denominator, and one with ordinary skill in the art would not reasonably know how the mitotic fraction/cell division of the isolated glial progenitor cells are determined to be “larger” than the glial progenitor cells in the subject, rendering the claim indefinite. The term “mitotic fraction” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one with ordinary skill would not be reasonably appraised of the scope of the invention.
Regarding claim 10, the term “Young” in claim 10 is a relative term which renders the claim indefinite. Under the broadest reasonable interpretation, and as discussed above the subject matter of claim 1 includes human glial progenitor cells that have been isolated directly from a subject’s brain ,whether the subject is a fetal or adult, as well as human glial progenitor cells that have been differentiated in vitro from pluripotent or multipotent stem cells. When the cells are isolated from a subject the term “ Younger” becomes relative to both the age of the donor and the host subject, and one with ordinary skill in the art would not reasonably know how the age of the glial progenitor cells are determined to be “ Younger” than the glial progenitor cells in the subject, rendering the claim indefinite. The term “Young” is not defined by the claim, the specification provides multiple definitions of what constitutes and does not constitute young, and hence Applicants do not provide specific definition. (See the paragraph below copied from page 54 lines 22-33 of instant application). Therefore, one of ordinary skill in the art would not be reasonably apprised of the scope of the invention.
As per Applicants specification on page 54 lines 22-33, Applicants state “ in one embodiment the term "young" glial or glial progenitor cells refers to cells that are induced to start differentiation into glial progenitor cell in an in vitro setting (about 105 days from cell isolation from fetal donor tissue). In another embodiments, the term "young glial cells" refers to differentiated glial progenitor cells that are ready for transplantation into an
animal (about 160 days from cell isolation from fetal donor tissue). In some embodiments,
the term "young glial cells" refers to glial progenitor cells or their progeny that are within 1-
20 weeks of transplantation. The term "older glial cells" is used in relative to the term "young
glial cells". Compared with older glial cells, young glial cells may have one or more of the
following characteristics: (i) growing or proliferating or dividing faster, (ii) having lower
levels than old of senescence-associated transcripts encoding CDKNlA (p21Cipl) and
CDKN2/p16(INK4) and pl4(ARF), and (iii) longer telomeres or higher telomerase activity or
both.
For examination purposes, the term “younger” is interpreted to encompass the cells that may have one or more of the following characteristics: (i) growing or proliferating or dividing faster, (ii) having lower levels than old of senescence-associated transcripts encoding CDKNlA (p21Cipl) and CDKN2/p16(INK4) and pl4(ARF), and (iii) longer telomeres or higher telomerase activity or both.
Claim interpretation.
Claim 10 recites a functional limitation for which the specification provided multiple definitions, therefore no specific definition was provided for the office to distinguish the isolated glial progenitor cells of the instant disclosure from prior art. For examination purposes, the term “younger” is interpreted to encompass the cells that would be growing or proliferating or dividing at a faster rate than the resident glial progenitor cells in the subject.
Claim Rejections - 35 USC § 102
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1,3,5,10, and 15-20 are rejected under 35 U.S.C. 102 (a)(1) as being anticipated by Goldman et al ( WO 2019/246262 A2).
Regarding claims 1,3, and 5, 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) ( See paragraph [0108]). Goldman et al also teach wherein the subject is human. (See claim 44).
Goldman et al do not explicitly state that the isolated GPCs have a mitotic fraction that is larger than the resident glial progenitor cells in the subject. However, the source of the isolated 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 isolated GPCs (Wang et al., "Human iPSC-derived Oligodendrocyte Progenitor Cells can Myelinate and Rescue a Mouse Model of Congenital Hypomyelination," Cell Stem Cell 12:252-264 (2013). ( See paragraph [0136] and [0168] in Goldman et al, and example 1 on page 90-91 of instant application). Since the source of the isolated glial progenitor cells and/or the method of isolation appear to be identical between the prior art (i.e. Goldman et al) and instant application, then the cells of Goldman et al are presumed to inherently have a mitotic fraction that differs from the resident cells in the subject. The receiving subject determines whether the mitotic fraction of Goldman’s et al is larger, smaller, or the equal to that of the resident glia. It is noted that the animal model utilized by Goldman et al, for example the shiverer mice (shi/shi x Rag 2 -/-, see [0137]), differs from the animal model utilized by instant specification (i.e. Rag1 -/-, See page 91 line 30). Therefore, the relative mitotic fraction of Goldman et al’s cells, whether is smaller or larger, would be calculated relative to the resident GPCs in the Shiverer mouse model. Goldman et al do not explicitly state that the mitotic fraction of the isolated glial progenitor cells is larger than the resident glial progenitor cells in the shiverer mice. However, Applicant’s own previous publication (Windrem et al, Cell Stem Cell, 2008) also utilizes the same cell isolation method as of Goldman ( See [0168] lines 29-34 on page 85), and use the same animal model as of Goldman et al, clearly shows that the isolated GPCs as claimed has a larger mitotic fraction than the resident GPCs in the shiverer mice.
For example, Windrem et al teach engrafting hGPCs into the brain of immunodeficient shiverer mice. Windrem et al state that “The selective expansion of the human glial population in the shiverer mouse white matter appears to be at least in part a product of the more sustained proliferation of the transplanted human GPCs (Figures 6B and 6D), which as derived from the late second- trimester fetal SVZ, would be expected to have continued actively dividing for at least another 9–12 months, assuming cell-autonomous regulation of expansion potential. Accordingly, when we plotted the number of all-human cells in the recipient mouse brains, as a function of time, we found that the initial dose of 300,000 cells per recipient had expanded to an average of 12 million human donor glia by 12–14 months in the long-term survivors (Figure 6A). When the incidence of Ki67+ cells was assessed in three sample regions—the corpus callosum, fimbria, and cerebellar white matter—the fraction of mitotic human donor cells was found to be much higher than that of the local host cells, both perinatally and for many months thereafter; only at a year after engraftment was the Ki67+ fraction of human donor cells observed to fall below 2% (Figure 6B). Even then, the fraction of Ki67+ human glia remained higher than the corresponding proportion of Ki67+ mouse cells, in both the transplanted hosts and in the rag2 wild-type or shi/shi x rag2-/- mouse controls”. ( See Windrem et al section “ Long-Term Survival Was Associated with Humanization of the Recipient White Matter”)
Therefore, this functional limitation “ wherein the mitotic fraction of the isolated glial
progenitor cells is larger than the resident glial progenitor cells in the subject ” are considered to be prima facie present per natural law of cell biology in the teachings of Goldman et al and they reasonably fulfill the functional limitation that is being claimed. To the extent Applicants argue otherwise, see the above 112b rejection.
As per the MPEP "Products of identical chemical composition cannot have mutual exclusive properties." A compound and its properties are inseparable (In re Papesch, 315 F.2d 381, 137 USPQ 43 (CCPA 1963)). Any properties exhibited by or benefits from are not given any patentable weight over the prior art provided the composition is inherent. A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the disclosed properties are necessarily present. In re Spada, 911 F.2d 705,709, 15 USPQ 1655, 1658 (Fed. Cir. 1990). See MPEP §2112.01. The burden is shifted to the applicant to show that the prior art product does not inherently possess the same properties as the instantly claimed product.
Furthermore, there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the time of invention, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003).
Regarding claim 10, Goldman et al do not explicitly teach that the isolated GPCs are younger than the resident glial progenitor cells in the subject.
However, Applicant’s own post-filing art “US 2023/0159890 A1” and the previous publication by Windrem et al (Cell Stem Cell, 2008) are considered relevant arts for attesting that the instant functional limitation of the isolated glial progenitor cells being “Younger” than the resident glial progenitor in the subject is an inherent property of Goldman’s et al cells. This is evident from the statement disclosed in the US’890 reciting that “ In some embodiments, the term ''young glial progenitor cells" refers to stem cells that are induced to start differentiation into glial progenitor cell in an in vitro setting at differentiation stage 6 based on the protocol of Wang et al”. As previously discussed, Goldman et al also utilized the cells of Wang et al, therefore the cell source of Goldman et al is the same as the cell source of US ‘890. US ‘890 further state that “ Compared with old glial progenitor cells, young glial progenitor cells may have 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). See paragraph [0175]. Therefore, the cell of Goldman et al are presumed to be young as inferred from the specific definition provided by US ‘890.
Furthermore, and as discussed above, Windrem et al (Cell Stem Cell, 2008), which is also one of Applicant’s own previous publication who also utilize the same cell source and the same animal model of Goldman et al clearly shows that the isolated GPCs of Goldman et al are younger than the resident cells in the subject evident by the statement recited by Windrem et al that “ the fraction of mitotic human donor cells was found to be much higher than that of the local host cells, both perinatally and for many months thereafter; only at a year after engraftment was the Ki67+ fraction of human donor cells observed to fall below 2% (Figure 6B)”. (See Windrem et al section “ Long-Term Survival Was Associated with Humanization of the Recipient White Matter”). Because Goldman et al utilize the same cell source and the same animal model as Windrem et al, it is clear that the cells of Goldman et al reasonably fulfill the specific definition of young progenitor cells recited in US ‘890 (i.e. growing or proliferating or dividing faster). It is also evident that the isolated GPCs of Goldman et al are younger than the resident cells in the subject as Windrem et al have clearly demonstrated.
Therefore, the functional limitation “ wherein the isolated glial progenitor cells is younger than that of resident glial progenitor cells ” are considered to be prima facie present per natural law of cell biology in the teachings of Goldman et al and they reasonably fulfill the functional limitation that is being claimed. To the extent Applicants argue otherwise, see the above 112b rejection.
Regarding claims 15-17, Goldman et al further teach that the hGPCs may be derived from human induced pluripotent stem cells (iPSCs), embryonic stem cells, or fetal tissue. (See claims 45-47).
Regarding claim 18-20, The method of Goldman et al involves administering hGPCs via intracerebral delivery, intrathecal delivery, or via direct infusion into brain ventricles (i.e. intraventricular). (See claim 39). Goldman et al also teach that the prepared glial progenitor cells can be administered to the subject’s striatum, forebrain, and/or cerebellum. (See pargraph [0129]). Goldman et al further disclose that xenogeneic GPCs can be administered into the subject’s brain, because the CNS is an immunologically privileged site. (See paragraph [0134]).
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 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 1,3,5,10, and 18-20 are rejected under 35 U.S.C. 103 as being
unpatentable over Benraiss et al (Nature communication, 2016),
Regarding claims 1, 3, and 5, Benraiss et al disclose a cell-based method for ameliorating Huntington disease in a mouse model. The method of Benraiss involves engrafting astrocyte-biased GPCs derived from fetal human brain into the striata of newborn R6/2 (120 CAG) mice, which transgenically express a mutant exon 1 of the Huntington’s (HTT) gene and normally dies by 20 weeks of age (i.e. a mouse model of HD). Benraiss et al show that engrafting normal hGPCs can ameliorate disease phenotype in transgenic HD mice, as striatal
transplantation of normal glia rescues aspects of electrophysiological and behavioral
phenotype, restores interstitial potassium homeostasis, slows disease progression and
extends survival in R6/2 HD mice, this reads on claims 1,3, and 5. (See abstract, Fig.5A-C, and Fig.8). Benraiss et al state that “ Together, these observations implicate glial pathology in the pathogenesis and progression of HD, and strongly suggest that colonization of diseased striata with healthy glia may be a viable strategy for slowing disease progression in HD”. ( See Discussion, page 10, 1st column, 1st pargraph). Benraiss et al further state that “ our data lend strong support to the possibility of transplanting normal glial progenitor cells into the HD striatum, both as for the treatment of manifest HD, and as a means to delay disease appearance in premanifest cases”. ( See Discussion, page 10, 2nd column).
Benraiss et al do not teach administering hGPCs into human subjects. However, because the therapeutic benefit of glial replacement in the animal model of HD, as demonstrated by Benraiss et al, raises the possibility that glial cell replacement may prove of therapeutic benefits in treating Huntington disease in a human subject, it would have been prima facie obvious to one with ordinary skill in the art, at the time the invention was filed, to envision administering hGPCs to a subject with Huntington disease for the purpose of treating HD. There would be a reasonable expectation of success in doing so because the teachings of Benraiss et al include motivation, suggestion, and teachings, as well as experimental basis for one skilled in the art to readily envision engrafting hGPCs to treat a subject with a Huntington disease, and with a higher expectation of success. See MPEP 2143 (I)(G).
Benraiss et al also do not explicitly state that the isolated GPCs have the functional properties of “a mitotic fraction that is larger than that of the resident glial progenitor cells in the human subject”. However, it is noted that the source of the isolated glial progenitor cells and/or the method of isolation, as well as the animal model of the working examples appear to be identical if not substantially the same as the GPCs and animal model utilized by Benraiss et al. For example, the working examples of instant application and the disclosure by Benraiss et al reference Wang et al as the source of the isolated GPCs (Wang et al., "Human iPSC-derived Oligodendrocyte Progenitor Cells can Myelinate and Rescue a Mouse Model of Congenital Hypomyelination," Cell Stem Cell 12:252-264 (2013). ( See “Production of GPCs from embryonic stem cells” on page 11 in Benraiss et al , and example 1, page 90-91, of instant application). It is clear that the source of the isolated glial progenitor cells of Benraiss et al appears to be identical if not substantially the same as the isolated GPCs of instant application. It is also noted that one of the animal model utilized by Benraiss et al, for example Rag 1 -/-, see section “ Animals” on page 11 in Benraiss et all), is the same animal model utilized by instant specification (i.e. Rag1 -/-, See page 91 line 30). Therefore, because the method of isolation/cell source as well as the animal system of Benraiss et al is identical if not substantially the same as the ones utilized in the working examples of instant specification, these functional limitation “ wherein the mitotic fraction of the isolated glial progenitor cells is larger than that of resident glial progenitor cells ” are considered to be prima facie present per natural law of cell biology in the teachings of Goldman et al and they reasonably fulfill the functional limitation that is being claimed. To the extent Applicants argue otherwise, see the above 112b rejection.
As per the MPEP "Products of identical chemical composition cannot have mutual exclusive properties." A compound and its properties are inseparable (In re Papesch, 315 F.2d 381, 137 USPQ 43 (CCPA 1963)). Any properties exhibited by or benefits from are not given any patentable weight over the prior art provided the composition is inherent. A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the disclosed properties are necessarily present. In re Spada, 911 F.2d 705,709, 15 USPQ 1655, 1658 (Fed. Cir. 1990). See MPEP §2112.01. The burden is shifted to the applicant to show that the prior art product does not inherently possess the same properties as the instantly claimed product.
Furthermore, there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the time of invention, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003).
Regarding claims 10, following the discussion of claims 1,3,and 5 above, because the isolated glial progenitor cells as well as the animal model of the working examples appear to be identical if not substantially the same as the GPCs and animal model utilized by Benraiss et al, the functional limitation “ wherein the isolated GPCs are “younger” than the resident glial progenitor cells in the subject” are considered to be prima facie present per the natural law of cell biology in the teachings of Benraiss et al and they reasonably fulfill the functional limitation that is being claimed. To the extent Applicants argue otherwise, see the above 112b rejections.
As per the MPEP "Products of identical chemical composition cannot have mutual exclusive properties." A compound and its properties are inseparable (In re Papesch, 315 F.2d 381, 137 USPQ 43 (CCPA 1963)). Any properties exhibited by or benefits from are not given any patentable weight over the prior art provided the composition is inherent. A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the disclosed properties are necessarily present. In re Spada, 911 F.2d 705,709, 15 USPQ 1655, 1658 (Fed. Cir. 1990). See MPEP §2112.01. The burden is shifted to the applicant to show that the prior art product does not inherently possess the same properties as the instantly claimed product.
Regarding claim 18-20, The method of Benraiss et al involves an intracallosal injection of xenogeneic human GPCs into the recipient brain’s striatum. (See the Results, section “Colonization by normal glia slowed disease course in HD mice”, 2nd column, 1st paragraph, lines 7- 13, page 4).
Response to Arguments
Applicant's arguments filed 11/14/2025 have been fully considered but they are not persuasive.
Applicant argues that Benraiss et al. describes a cell-based method for ameliorating Huntington disease in a mouse model. However, it would not have been obvious to specifically administer young human glial progenitor cells (hGPCs) to a human subject in view of the animal data presented in Benraiss et al.
Examiner’s Response to Traversal: Applicant's arguments have been fully considered but they are not persuasive. This is because the method of treatment recited in independent claims 1,3,and 5 is recited at a high level of generality. As such, the claims have no therapeutic required results, so anything however minimal it might be, is minimally sufficient to fulfill the limitation of the claims. As discussed above, Benraiss et al show that engrafting normal hGPCs can ameliorate disease phenotype in transgenic HD mice, as striatal transplantation of normal glia rescues aspects of electrophysiological and behavioral phenotype, restores interstitial potassium homeostasis, slows disease progression and extends survival in R6/2 HD mice. Clearly, the teachings of Benraiss et al provide one with ordinary skill in the art with the experimental basis to envision administering a population of isolated glial progenitor cells to a subject in need and with a reasonable expectation of success. Furthermore, it is noted that the working examples of Applicants disclosure is also directed to animal mouse model. Thus, for these reasons, the argument is not found persuasive.
Applicants further argue that Benraiss et al did not consider the glial cell age as an important variable in competitive behavior, or even that glial cells can or do compete in adult brain tissue.
Examiner’s Response to Traversal: Applicant's arguments have been fully considered but they are not persuasive. This is because the claims did not require these limitations. In response to applicant's argument that the references fail to show certain features of the invention, it is noted that the features upon which applicant relies (i.e., age as an important variable in competitive behavior, or even that glial cells can or do compete in adult brain tissue) are not recited in the rejected claim(s). 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).
Applicants further argue unexpected results by stating that “It is surprising that aged resident glia confronted by their younger counterparts are actively eliminated via apoptosis triggered by their encounter with the younger hGPCs, whose greater relative fitness permitted their repopulation of the chimeric host striatum”.
Examiner’s Response to Traversal: Applicant's arguments have been fully considered but they are not persuasive. This is because Applicants do not provide any comparison between the claimed invention and the closest prior art to rebut a prima facie case of obviousness.
This is because per the MPEP “ Evidence of unexpected properties may be in the form of a direct or indirect comparison of the claimed invention with the closest prior art which is commensurate in scope with the claims. See In re Boesch, 617 F.2d 272, 205 USPQ 215 (CCPA 1980) and MPEP § 716.02(d) - § 716.02(e). An affidavit or declaration under 37 CFR 1.132 must compare the claimed subject matter with the closest prior art to be effective to rebut a prima facie case of obviousness. In re Burckel, 592 F.2d 1175, 201 USPQ 67 (CCPA 1979). “A comparison of the claimed invention with the disclosure of each cited reference to determine the number of claim limitations in common with each reference, bearing in mind the relative importance of particular limitations, will usually yield the closest single prior art reference.” In re Merchant, 575 F.2d 865, 868, 197 USPQ 785, 787 (CCPA 1978) (emphasis in original). Where the comparison is not identical with the reference disclosure, deviations therefrom should be explained, In re Finley, 174 F.2d 130, 81 USPQ 383 (CCPA 1949), and if not explained should be noted and evaluated, and if significant, explanation should be required. In re Armstrong, 280 F.2d 132, 126 USPQ 281 (CCPA 1960) (deviations from example were inconsequential). See also MPEP 716.02e.
Conclusion
No claim is allowed.
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