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 .
DETAILED ACTION
Claim status
Claims 1-10 are pending
Claims 1-10 are under examination
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 9/14/2023 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
However, Applicant is reminded that the listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Priority
The instant application was filed 9/14/2023 and is a continuation of application 16/346,003 filed 4/29/2019, which is now US Patent 11,800,859, and is a national stage entry of PCT/US2017/058952 filed 10/30/2017 and claims priority to provisional application 62/414,863, filed 10/31/2016.
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) 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 nonprovisional application or provisional 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 the first paragraph of 35 U.S.C. 112. 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. 16/346,003, fails to provide adequate support or enablement in the manner provided by the first paragraph of 35 U.S.C. 112 for one or more claims of this application. Review of the application No. 16/346,003 did not reveal support for a “kit” comprising the knock-in rat, a compound, and a means for detecting phenotypic misexpression. Thus, Claims 8-10 are being given the filing date of 9/14/2023.
Applicant states that this application is a continuation of the prior-filed application. A continuation or divisional application cannot include new matter. Applicant is required to delete the benefit claim or change the relationship (continuation application) to continuation-in-part because this application contains the aforementioned matter not disclosed in the prior-filed application. See MPEP § 211.
Sequence Compliance
Objection to Drawings
Figure 1 (nucleic acid sequences) of the Specification do not conform to sequence rules, requiring the use of “SEQ ID NO:” (37 CFR 1.821-1.825).
Where the description or claims of a patent application discuss a sequence that is set forth in the “Sequence Listing” in accordance with paragraph (c) of this section, reference must be made to the sequence by use of the sequence identifier, preceded by “SEQ ID NO:” in the text of the description or claims, even if the sequence is also embedded in the text of the description or claims of the patent application. 37 CFR 1.821 (d). Specifically, the cited section indicates that nucleotide and/or amino acid sequences are an unbranched sequence of 4 or more amino acids or an unbranched sequence of 10 or more nucleotides. Branched sequences are specifically excluded from this definition. Sequences with fewer than four specifically defined nucleotides or amino acids are specifically excluded from this section.
Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Objection to Specification
The applicant is reminded that the specification must be amended in order to comply with regulations cited above. All references to sequences in claims and specification should be referred to as “SEQ ID NO:1”, for example. To avoid all doubts of the examiner and to ensure correct interpretation of the claims and specification, the identification of sequences with proper sequence identifiers is required. Currently, Applicant specification uses the phrase “SEQ ID” (e.g., Table 1, see also text on pgs 16, 21, etc.), which should be changed to “SEQ ID NO:”.
Claim Objections
Claims 1-8 are objected to because of the following informalities: instant claims uses the terms “non-human” and “nonhuman”, which are used interchangeably between and within claims. Applicant should select a single term and use it consistently among claims.
Furthermore, the term “non-human” (or “nonhuman”) as a prefix in the phrase “non-human knock-in rat” is redundant and overly verbose. The simple phrase “knock-in rat” is more than adequate to describe applicant’s invention.
Claims 4 and 5 are objected to because they do not conform to sequence rules, requiring the use of “SEQ ID NO:” (37 CFR 1.821-1.825).
Furthermore, Claims 4 and 5 recite the phrases “ wherein p.Arg364Trp mutation” and “wherein p.His361Tyr mutation”, respectively, which are not only grammatically incorrect for lacking a proper preposition phrase, but also use alternative terms for the Arg364Trp and His361Tyr mutations. Applicant should select a single term for the mutations and use it consistently among claims.
Claim 8 is objected to because of the following informalities: there is more than one (1) period: one after “a”, “b”, “c” and another after “rat”. The claim should be amended to include only one period. MPEP 608.01(m) states, “Each claim begins with a capital letter and ends with a period. Periods may not be used elsewhere in the claims except for abbreviations.”
Appropriate corrections are required.
Claim Interpretation
The following is a quotation of 35 U.S.C. 112(f):
(f) ELEMENT IN CLAIM FOR A COMBINATION.—An element in a claim for a combination may be expressed as a means or step for performing a specified function without the recital of structure, material, or acts in support thereof, and such claim shall be construed to cover the corresponding structure, material, or acts described in the specification and equivalents thereof.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), sixth paragraph:
An element in a claim for a combination may be expressed as a means or step for performing a specified function without the recital of structure, material, or acts in support thereof, and such claim shall be construed to cover the corresponding structure, material, or acts described in the specification and equivalents thereof.
The claims in this application are given their broadest reasonable interpretation using the plain meaning of the claim language in light of the specification as it would be understood by one of ordinary skill in the art. The broadest reasonable interpretation of a claim element (also commonly referred to as a claim limitation) is limited by the description in the specification when 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, is invoked.
As explained in MPEP § 2181, subsection I, claim limitations that meet the following three-prong test will be interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph:
(A) the claim limitation uses the term "means" or "step" or a term used as a substitute for "means" that is a generic placeholder (also called a nonce term or a non-structural term having no specific structural meaning) for performing the claimed function;
(B) the term "means" or "step" or the generic placeholder is modified by functional language, typically, but not always linked by the transition word "for" (e.g., "means for") or another linking word or phrase, such as "configured to" or "so that"; and
(C) the term "means" or "step" or the generic placeholder is not modified by sufficient structure, material, or acts for performing the claimed function.
Use of the word "means" (or "step") in a claim with functional language creates a rebuttable presumption that the claim limitation is to be treated in accordance with 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph. The presumption that the claim limitation is interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, is rebutted when the claim limitation recites function without reciting sufficient structure, material or acts to entirely perform the recited function.
Absence of the word "means" (or "step") in a claim creates a rebuttable presumption that the claim limitation is not to be treated in accordance with 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph. The presumption that the claim limitation is not interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, is rebutted when the claim limitation recites function without reciting sufficient structure, material or acts to entirely perform the recited function.
Claim limitations in this application that use the word "means" (or "step") are being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, except as otherwise indicated in an Office action. Conversely, claim limitations in this application that do not use the word "means" (or "step") are not being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, except as otherwise indicated in an Office action.
Such claim limitations are in claims 8-10 directed to a “means for detecting phenotypic misexpression”.
Because this/these claim limitation(s) is/are being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, they are being interpreted to cover the corresponding structure described in the specification as performing the claimed function, and equivalents thereof.
If applicant does not intend to have this/these limitation(s) interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, applicant may: (1) amend the claim limitation(s) to avoid it/them being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph (e.g., by reciting sufficient structure to perform the claimed function); or (2) present a sufficient showing that the claim limitation(s) recite(s) sufficient structure to perform the claimed function so as to avoid it/them being interpreted under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph.
Claim Rejections - 35 USC § 112(b)
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 4-7, and 8-10 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 pre-AIA the applicant regards as the invention.
Claims 4 and 5 recite the phrases directed to the “mutation contains the knock-in SEQ ID…”, which is indefinite not only because SEQ ID NOs: 2 and 5 are directed to nucleic acid sequences, while R364W and H361Y are amino acid sequences, but also because the claims fail to make clear the scope of the SEQ ID NOs relative to the knock-in amino acid mutations. In light of the specification’s description of SEQ ID NOs: 2 and 5 as nucleic acid donors designed to introduce the R364W mutation by converting CGG to TGG (as per SEQ ID NO:2), and designed to introduce the H361Y mutation by converting CAC to TAT (as per SEQ ID NO:5), the Examiner has interpreted the claims as only requiring the relevant portions of these SEQ ID NOs necessary and sufficient to generate their respective mutations.
Claim 6 recites the limitation "the misexpression" in regard to Claim 1. There is insufficient antecedent basis for this limitation in the claim because Claim 1 is silent to a misexpression, thereby rendering Claim 6 indefinite.
Claim 7 recites the limitation that the method is for identifying “useful compounds”. A claim may be rendered indefinite by reference to subjective term (see MPEP 2173.05(b), IV). Specifically, the phrase “useful compounds” is a subjective phrase which renders the claim indefinite. In other words, a compound that is considered useful to one individual may not be considered useful to another. The phrase "useful compounds" is not defined by the claim, the specification does not define or recite the phrase “useful compounds”, nor does it provide a standard for some standard for measuring the scope of the “useful compounds”, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention.
Claims 8-10 recite the limitation that the kit comprises a means for detecting “phenotypic misexpression”. A claim may be rendered indefinite by reference to term of an object that is variable (see MPEP 2173.05(b), II). Specifically, the phrase “phenotypic misexpression” is a relative term which renders the claim indefinite. In other words, the misexpression of a phenotype is relative to the expression of another phenotype. The phrase “phenotypic misexpression" is not defined by the claim, the specification does not define or recite the phrase “phenotypic misexpression”, nor does it provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention.
Claims 8-10 limitations directed to “means for detecting phenotypic misexpression” invokes 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph. However, the written description fails to disclose the corresponding structure, material, or acts for performing the entire claimed function and to clearly link the structure, material, or acts to the function for detecting phenotypic misexpression. Although, dependent claims 9 and 10 recite the means for detecting phenotypic misexpression “is observed in electrophysiological features for Charcot-Marie-Tooth Disease 2A” and “results from reduced density myelinated axons and active axonal degeneration in distal nerves”, respectively, there is no recitation of a structure, material, or process that would provide the means for detecting phenotypic misexpression.
A claim may also be indefinite when the 3-prong analysis for determining whether the claim limitation should be interpreted under 35 U.S.C. 112(f) is inconclusive because of ambiguous words in the claim.
As stated above, the phrase “phenotypic misexpression” is not defined or recited by the specification, and is indefinite as being relative terminology. Although Applicant defines the term “phenotype” broadly ranging from “cellular, biochemical, histological, behavioral, or whole organismal properties” (p. 14, 2nd para.), it is unclear what are the means for detecting such a broad array of phenotypes that are “misexpressed” when no comparable standard is provided. Furthermore, dependent Claim 9 directed to the misexpression in “electrophysiological features” for CMT2A is not described by Applicant’s specification in any manner, and dependent Claim 10 directed to the misexpression “results from” reduced axons does not describe a structure, material, or process for performing the function.
Therefore, the claims are indefinite and are rejected under 35 U.S.C. 112(b) or pre-AIA 35 U.S.C. 112, second paragraph.
Applicant may:
(a) Amend the claim so that the claim limitation will no longer be interpreted as a limitation under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph;
(b) Amend the written description of the specification such that it expressly recites what structure, material, or acts perform the entire claimed function, without introducing any new matter (35 U.S.C. 132(a)); or
(c) Amend the written description of the specification such that it clearly links the structure, material, or acts disclosed therein to the function recited in the claim, without introducing any new matter (35 U.S.C. 132(a)).
If applicant is of the opinion that “misexpression” is an unambiguous word, and that the written description of the specification already implicitly or inherently discloses the corresponding structure, material, or acts and clearly links them to the function so that one of ordinary skill in the art would recognize what structure, material, or acts perform the claimed function, applicant should clarify the record by either:
(a) Amending the written description of the specification such that it expressly recites the corresponding structure, material, or acts for performing the claimed function and clearly links or associates the structure, material, or acts to the claimed function, without introducing any new matter (35 U.S.C. 132(a)); or
(b) Stating on the record what the corresponding structure, material, or acts, which are implicitly or inherently set forth in the written description of the specification, perform the claimed function. For more information, see 37 CFR 1.75(d) and MPEP §§ 608.01(o) and 2181.
Claim Rejections - 35 USC § 112(a)
(Written Description)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 8-10 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
Independent claim 8 encompasses a kit comprising a “means for detecting phenotypic misexpression”.
Dependent claims 9 and 10 recite the means for detecting phenotypic misexpression “is observed in electrophysiological features for Charcot-Marie-Tooth Disease 2A” and “results from reduced density myelinated axons and active axonal degeneration in distal nerves”, respectively.
Under the written description guidelines (see MPEP 2163) the Examiner is directed to determine whether one skilled in the art would recognize that the Applicant was in possession of the claimed invention as a whole at the time of filing. The following considerations are critical to this determination.
To satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116. An original claim may lack written description support when (1) the claim defines the invention in functional language specifying a desired result but the disclosure fails to sufficiently identify how the function is performed or the result is achieved or (2) a broad genus claim is presented but the disclosure only describes a narrow species with no evidence that the genus is contemplated. See Ariad Pharms., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1349-50 (Fed. Cir. 2010) (en banc). The written description requirement is not necessarily met when the claim language appears in ipsis verbis in the specification. "Even if a claim is supported by the specification, the language of the specification, to the extent possible, must describe the claimed invention so that one skilled in the art can recognize what is claimed. The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement." Enzo Biochem, Inc. v. Gen-Probe, Inc., 323 F.3d 956, 968, 63 USPQ2d 1609, 1616 (Fed. Cir. 2002).
Accordingly, to satisfy the written description requirement, the specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. Vas-Cath, Inc. v. Mahurkar, 935 F.2d 1555, 1562-63, 19 USPQ2d 1111 (Fed. Cir. 1991). See also MPEP 2163.
ACTUAL REDUCTION TO PRACTICE
In regard to claims 8-10 encompassing a kit comprising a “means for detecting phenotypic misexpression”, the specification provides no description for such a kit, and no description of a structure that performs detection of phenotypic misexpression.
Accordingly, Applicant did not demonstrate a reduction to practice a kit that comprises a means for detecting phenotypic misexpression. Furthermore, Applicant has not adequately set forth in terms of distinguishing identifying characteristics as evidenced by other descriptions of the invention that are sufficiently detailed to show that Applicant was in possession of the claimed kit that would predictably function to detect phenotypic misexpression in a knock-in rat.
DISCLOSURE OF STRUCTURE AND SUFFICIENT RELEVANT IDENTIFYING CHARACTERISTICS
As stated above, the phrase “phenotypic misexpression” is not defined or recited by the specification, and is indefinite as being relative terminology. Although Applicant defines the term “phenotype” broadly ranging from “cellular, biochemical, histological, behavioral, or whole organismal properties” (p. 14, 2nd para.), Applicant’s specification does not describe a relationship between the structure of the claimed genus of kit components and the ability to predictably detect phenotypic misexpression in a knock-in rat. Furthermore, dependent Claim 9 directed to the misexpression in “electrophysiological features” for CMT2A is not described by Applicant’s specification in any manner whatsoever, and dependent Claim 10 directed to the misexpression “results from” reduced axons does not describe any structure, material, or process for performing the function.
STATE OF THE ART & QUANTITY OF EXPERIMENTATION
Although the making of kits were known comprising genetically modified animals, one of skill in the art would neither expect nor predict the appropriate function of a means for detecting phenotypic misexpression in a knock-in rat based on the written description of instant application.
For example, Okamoto teaches a measuring kit comprising a nonhuman animal comprising genetically modified cells, a compound potentially useful for treatment of the cells, and a means for detecting phenotypic expression of the cells by using transcriptional activity as a measure of cell quantity [0020-0080, 0086, 0202-0203, 0309-0310].
However, the specification has not disclosed such genus of kits comprising a means for detecting phenotypic misexpression, and has not set forth in terms of distinguishing identifying characteristics as evidenced by other descriptions of the invention that are sufficiently detailed to show that Applicant was in possession of the claimed genus of kits capable of performing the claimed function.
CONCLUSION
Therefore, the Examiner concludes that there is insufficient written description of the instantly claimed genus of kits comprising a means for detecting phenotypic misexpression. Specifically, there is limited description of the structure-function relationship between the claimed genus of means for detecting phenotypic misexpression and their ability to predictably perform the claimed function, and the Examiner further concludes a skilled artisan would find the specification inadequately describes the claimed genus of kits.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claim 7 is rejected under 35 U.S.C. 101 because the claimed invention is directed to a judicial exception (i.e., a law of nature, a natural phenomenon, or an abstract idea) without significantly more. Claim 7 is directed to a screening method for identifying a useful compound based on a mental process (i.e., observing a phenotypic change). The claim does not include additional elements or steps that are sufficient to amount to significantly more than the judicial exception because they are not substantially more.
Briefly summarized here, the subject eligibility guidance cites a two part test: is the claimed invention directed to a statutory class of invention (Step 1), if so then is the claimed invention as a whole directed to a law of nature, natural phenomena, or an abstract idea (i.e. set forth or described in the claim) (Step 2A, prong one), if so then is the claimed invention recite additional elements that integrate the judicial exception into a practical application (Step 2A, prong two), if not then does the claim as a whole amount to significantly more than the judicial exception (Step 2B).
In regard to Step 1, Claim 7 is drawn to a process, a screening method for identifying useful compounds.
In regard to Step 2A prong one, this part of the eligibility analysis evaluates whether the claim recites a judicial exception. Claim 7 recites that “wherein a change in phenotype for Charcot-Marie-Tooth disease 2A is observed”. Under its broadest reasonable interpretation consistent with the specification, the plain and ordinary meaning of this limitation requires observing a knock-in rat. As this step simply requires observation, the limitation falls into the “mental process” grouping of abstract ideas because the evaluation can be practically performed in the human mind. Thus, the claim is directed to the judicial exception of a mental process-type abstract idea (Step 2A, Prong One: YES).
In regard to Step 2A, prong two: this part of the eligibility analysis evaluates whether the claim as a whole integrates the recited judicial exception into a practical application of the exception. In the present situation, although the claims recite this method comprises a knock-in rat as an attempt to generally link the judicial exception to a field of use, but this attempt amounts to a generic instruction for applying the mental process (i.e., observing a knock-in rat). Thus, even when considering the elements in combination, the claim as a whole does not meaningfully integrate the recited exception into a practical application (Step 2A, prong two: No).
In regard to Step 2B, the claim does not include additional elements that are sufficient to amount to significantly more than the judicial exception.
As stated supra, additional elements such as observing a knock-in rat is at most a generic instruction to apply the abstract idea. Consequently, for the reasons discussed above, the additional elements individually or in combination with the judicial exception do not provide an inventive concept; so, the claim as a whole does not amount to significantly more than a generic instruction to “apply” the judicial exception. (Step 2B: NO).
For the reasons set forth above, the claim is not considered to recite something significantly different than a judicial exception and thereby are not directed to patent eligible subject matter.
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 of this title, 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 set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied 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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim 1-7 are rejected under 35 U.S.C. 103 as being unpatentable over Cartoni et al., 2010 (Journal of Neurology, Vol. 133, p. 1460-1469, see IDS filed 9/14/2023) in view of Feely et al., 2011 (Neurology, 76: 1690-1696, see IDS filed 9/14/2023), Inglese et al. (US 2014/0080787, filed 9/13/2013, published 3/20/2014) and Ostertag et al. (US 8,558,055, filed 7/23/2010, patented 10/15/2013)
Cartoni discloses Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal form of peripheral neuropathy caused by mutations in the human Mitofusion 2 (MFN2) gene. Cartoni generated a transgenic mouse expressing mutation R94Q and shows mice expressing mitofusin 2R94Q developed locomotor impairments and gait defects thus mimicking the Charcot-Marie-Tooth disease type 2A neuropathy (e.g. Abstract).
However, in regard to claim 1, Cartoni does not specifically teach R364W mutation or H361Y mutation of MFN2 gene for CMT2A.
Feely discloses CMT2A is caused by mutations in MFN2, a nuclear encoded gene essential for mitochondria fusion and tethering the endoplasmic reticulum to mitochondria (e.g. Abstract). Table 1 shows MFN2 mutations and phenotypes in human patients and the mutation includes R364W and H361Y. Three of the mutations within the GTPase domain, 2 mutations in the R3 region (H361Y, R364W), and one mutation in the C-terminus coiled-coil domain have previously been reported to cause CMT2A (e.g. p. 1692, right column).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate a transgenic mouse whose genome comprises R364W mutation or H361Y mutation in MFN2 gene because Cartoni discloses Charcot-Marie-Tooth disease type 2A is an autosomal dominant axonal form of peripheral neuropathy caused by mutations in the mitofusion 2 gene and Cartoni generated a transgenic mouse expressing mitofusin 2R94Q that developed locomotor impairments and gait defects thus mimicking the Charcot-Marie-Tooth disease type 2A neuropathy, and Feely teaches MFN2 mutations and phenotypes in human patients and mutations in the R3 region (H361Y, R364W) of the MFN2 gene can cause CMT2A in human. Both Cartoni and Feely teach MFN2 gene mutations are correlated to CMT2A disease and Feely teaches mutations in the R3 region (H361Y, R364W) of the MFN2 gene can cause CMT2A in human. Since Cartoni teaches generation of transgenic mouse model mimicking the Charcot-Marie-Tooth disease type 2A neuropathy, it would be obvious for one of ordinary skill in the art to generate a transgenic mouse harboring the R364W or H361Y mutation so as to produce a transgenic mouse model for the human CMT2A disease with reasonable expectation of success.
However, in regard to claim 1, Cartoni does not specifically teach producing a genetically modified rat model for the human CMT2A wherein the R364W or H361Y mutations are knocked-in the mitofusin2 gene of the rat.
Inglese et al. teaches a transgenic rat model for the human CMT1A, and methods of using the transgenic rat to test compounds useful for treating Charcot-Marie-Tooth disease type 1A neuropathy [0009, 0036, 0047, 0049], see Examples 3 and 4).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate a transgenic mouse whose genome comprises R364W mutation or H361Y mutation in the MFN2 gene as suggested by Cartoni et al., and to substitute the mouse for a rat as taught by Inglese with reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Ostertag because rats are larger than mice, thereby providing a means by which investigators can perform clinically relevant instrumentation studies or imaging studies, which are impossible in mouse models (col 2, 1st para.). Furthermore, Ostertag teaches knocking-in of exogenous DNA for insertional mutagenesis in the rat (col 6, 4th para., col 13, last four para.), which would allow the mutants to be expressed under the control of the rat mitofusin2 gene’s endogenous promoter.
Finally, in regard to claim 1, as per the wherein clause directed to the knock-in rat exhibiting peripheral motor nerve cell axons and Schwann cells having a spatially, and age-dependent progressive degeneration, Freely teaches that at least for the R364W mutation, “younger patients had normal or only mildly abnormal proprioception loss, whereas older patients had much more pronounced proprioception deficiencies” (p. 1695, last para.). Furthermore, Freely teaches that both the R364W and H361Y patients presented with a “severe” Charcot-Maire-Tooth Neuropathology score, with “moderate” motor dysfunction (p. 1692, Table 1). Thus, the clinical characterization of these mutations in human suggest an age-dependent progressive degeneration of neurons, and since proprioception and motor function rely on both sensory and motor neurons in the peripheral nervous system that are associated with Schwann cells, it would have been reasonable to expect that the mutations lead to age-dependent progressive degeneration of motor nerve cell axons and their associated Schwann cells in the spatially distinct peripheral nervous system.
In regard to claims 2, 3 and 6, as stated supra, Freely teaches a severe CMT phenotype with the R364W and H361Y mutations, and also teaches the presence of optic nerve atrophy with these mutations (p. 1692, Results, last para.), which is considered a distal myelinated axon. Furthermore, in regard to claim 3, as stated supra, Freely teaches sensory defects in proprioception, which would have implicated the fasciculus gracilis nerve tract in dorsal column of the spinal cord.
In regard to claims 4 and 5, as stated supra, only the relevant portions of SEQ ID NOs: 2 and 3 comprising the codon changes for said amino acid mutations are being considered, therefore one of ordinary skill in the art would have immediately envisioned these codon sequences due the limited number of nucleotide changes that would yield Tryptophan (only one codon is available “TGG”) and to a Tyrosine (only two codon combination are available “TAT” or “TAC”).
In regard to claim 7, although Cartoni teaches the genetically modified nonhuman animal model of CMT2A should make possible the evaluation of future therapeutic approaches (Discussion, last para.), and they disclose multiple methods for observing changes in a CMT2A phenotype (e.g., behavioral tests, anatomy and histology, and neurophysiology, see Materials and methods), they are silent to a screening method for identifying useful compounds, wherein a change in a phenotype for CMT2A is observed.
Nevertheless, Inglese et al. (2014) teaches that similar rat models of CTM1A were used to screen for useful compounds, wherein a change in a phenotype for CMT1A was observed [0034-0036, 0047-0050].
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate a knock-in rat whose genome comprises R364W mutation or H361Y mutation in its mitofusin 2 gene, and to screen for useful compounds wherein a change in a phenotype is observed as taught by Inglese with reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so because to screen for useful compounds would have been an obvious use for future therapeutic approaches as suggested by Cartoni.
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Examiner’s Comment
Applicant is reminded that affidavits or declarations, such as those submitted under 37 CFR 1.130, 1.131 and 1.132, filed during the prosecution of a prior application do not automatically become a part of continuing application. Where it is desired to rely on an earlier-filed affidavit or declaration, the Applicant should make the remarks of record in the examined application and include a copy of the original affidavit or declaration filed in the prior application (see MPEP 201.06, IX).
Claims 8-10 are rejected under 35 U.S.C. 103 as being unpatentable over Cartoni et al., 2010 (Journal of Neurology, Vol. 133, p. 1460-1469, see IDS filed 9/14/2023) in view of Feely et al., 2011 (Neurology, 76: 1690-1696, see IDS filed 9/14/2023), Inglese et al. (US 2014/0080787, filed 9/13/2013, published 3/20/2014), Ostertag et al. (US 8,558,055, filed 7/23/2010, patented 10/15/2013), and Okamoto et al., (2008/0077999, filed 4/28/2014, published 11/06/2014)
Cartoni discloses Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal form of peripheral neuropathy caused by mutations in the human Mitofusion 2 (MFN2) gene. Cartoni generated a transgenic mouse expressing mutation R94Q and shows mice expressing mitofusin 2R94Q developed locomotor impairments and gait defects thus mimicking the Charcot-Marie-Tooth disease type 2A neuropathy (e.g. Abstract).
However, in regard to claim 8, Cartoni does not specifically teach R364W mutation or H361Y mutation of MFN2 gene for CMT2A.
Feely discloses CMT2A is caused by mutations in MFN2, a nuclear encoded gene essential for mitochondria fusion and tethering the endoplasmic reticulum to mitochondria (e.g. Abstract). Table 1 shows MFN2 mutations and phenotypes in human patients and the mutation includes R364W and H361Y. Three of the mutations within the GTPase domain, 2 mutations in the R3 region (H361Y, R364W), and one mutation in the C-terminus coiled-coil domain have previously been reported to cause CMT2A (e.g. p. 1692, right column).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate a transgenic mouse whose genome comprises R364W mutation or H361Y mutation in MFN2 gene because Cartoni discloses Charcot-Marie-Tooth disease type 2A is an autosomal dominant axonal form of peripheral neuropathy caused by mutations in the mitofusion 2 gene and Cartoni generated a transgenic mouse expressing mitofusin 2R94Q that developed locomotor impairments and gait defects thus mimicking the Charcot-Marie-Tooth disease type 2A neuropathy, and Feely teaches MFN2 mutations and phenotypes in human patients and mutations in the R3 region (H361Y, R364W) of the MFN2 gene can cause CMT2A in human. Both Cartoni and Feely teach MFN2 gene mutations are correlated to CMT2A disease and Feely teaches mutations in the R3 region (H361Y, R364W) of the MFN2 gene can cause CMT2A in human. Since Cartoni teaches generation of transgenic mouse model mimicking the Charcot-Marie-Tooth disease type 2A neuropathy, it would be obvious for one of ordinary skill in the art to generate a transgenic mouse harboring the R364W or H361Y mutation so as to produce a transgenic mouse model for the human CMT2A disease with reasonable expectation of success.
However, in regard to claim 8, Cartoni does not specifically teach producing a genetically modified rat model for the human CMT2A wherein the R364W or H361Y mutations are knocked-in the mitofusin2 gene of the rat.
Inglese et al. teaches a transgenic rat model for the human CMT1A, and methods of using the transgenic rat to test compounds useful for treating Charcot-Marie-Tooth disease type 1A neuropathy [0009, 0036, 0047, 0049], see Examples 3 and 4).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate a transgenic mouse whose genome comprises R364W mutation or H361Y mutation in the MFN2 gene as suggested by Cartoni et al., and to substitute the mouse for a rat as taught by Inglese with reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Ostertag because rats are larger than mice, thereby providing a means by which investigators can perform clinically relevant instrumentation studies or imaging studies, which are impossible in mouse models (col 2, 1st para.). Furthermore, Ostertag teaches knocking-in of exogenous DNA for insertional mutagenesis in the rat (col 6, 4th para., col 13, last four para.), which would allow the mutants to be expressed under the control of the rat mitofusin2 gene’s endogenous promoter.
Finally, in regard to claim 8, as per the wherein clause directed to the knock-in rat exhibiting peripheral motor nerve cell axons and Schwann cells having a spatially, and age-dependent progressive degeneration, Freely teaches that at least for the R364W mutation, “younger patients had normal or only mildly abnormal proprioception loss, whereas older patients had much more pronounced proprioception deficiencies” (p. 1695, last para.). Furthermore, Freely teaches that both the R364W and H361Y patients presented with a “severe” Charcot-Maire-Tooth Neuropathology score, with “moderate” motor dysfunction (p. 1692, Table 1). Thus, the clinical characterization of these mutations in human suggest an age-dependent progressive degeneration of neurons, and since proprioception and motor function rely on both sensory and motor neurons in the peripheral nervous system that are associated with Schwann cells, it would have been reasonable to expect that the mutations lead to age-dependent progressive degeneration of motor nerve cell axons and their associated Schwann cells in the spatially distinct peripheral nervous system.
However, in regard to claims 8-10, although Cartoni teaches the genetically modified nonhuman animal model of CMT2A should make possible the evaluation of future therapeutic approaches (Discussion, last para.), and they disclose multiple methods for observing changes in a CMT2A phenotype (e.g., behavioral tests, anatomy and histology, and neurophysiology, see Materials and methods), they are silent to useful compounds useful for treating CMT2A.
Nevertheless, Inglese et al. (2014) teaches that similar rat models of CMT1A were used to screen for useful compounds for the treatment of CMT1A [0034-0036, 0047-0050].
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate a knock-in rat whose genome comprises R364W mutation or H361Y mutation in its mitofusin 2 gene, and to supply useful compounds for treating CMT as taught by Inglese with reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so because the inclusion of useful compounds would have been an obvious use for future therapeutic approaches as suggested by Cartoni.
However, in regard to claims 8-10, Cartoni does not specifically teach a kit comprising the genetically modified rat, a compound potentially useful for treatment, and a means for detecting behavioral/histological/electrophysiological phenotypic expression.
Okamoto teaches a measuring kit comprising a nonhuman animal comprising genetically modified cells, a compound potentially useful for treatment of the cells, and a means for detecting phenotypic expression of the cells [0020-0080, 0086, 0202-0203, 0309-0310].
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate a transgenic rat whose genome comprises R364W mutation or H361Y mutation in its mitofusin 2 gene, and a screening method for identifying useful compounds for treating CMT2A, as well as means for determining behavioral/histological/electrophysiological phenotypic expression as suggested by Cartoni et al., and to combine said agents into a kit as taught by Okamoto with reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Okamoto because the kit’s industrial applicability to allow the simple and accurate screening of compounds in a nonhuman animal model [0477].
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Examiner’s Comment
In light of Applicant’s loss of priority for Claims 8-10 as stated above, the following rejections are made over Applicant’s WIPO publication which is available as prior art:
Claims 8 and 10 are rejected under 35 U.S.C. 103 as being unpatentable over Scheideler et al. (WO 2018/081675, filed 10/30/2017, published 5/03/2018), in view of Okamoto et al., (US 2008/0077999, filed 4/28/2014, published 11/06/2014)
In regard to claims 8 and 10, Scheideler teaches a) a knock-in rat comprising R364W mutation or H361Y mutation in its mitofusin 2 gene that exhibits peripheral motor nerve cell axons and Schwann cells having a spatially, and age-dependent progressive degeneration, and b) a compound potentially useful for treating or alleviating the symptoms of CMT2A (see Claims 1-12, 14 and 15 of Scheideler).
However, in regard to claim 8, Scheideler is silent to a kit comprising the genetically modified rat, a compound potentially useful for treatment, and a means for detecting phenotypic expression.
Okamoto teaches a measuring kit comprising a nonhuman animal comprising genetically modified cells, a compound potentially useful for treatment of the cells, and a means for detecting phenotypic expression of cells by using transcriptional activity as a measure of cell quantity [0020-0080, 0086, 0202-0203, 0309-0310].
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate a knock-in rat whose genome comprises R364W mutation or H361Y mutation in its mitofusin 2 gene, and a screening method for identifying useful compounds for treating CMT2A, as taught by Scheideler et al., and to combine said agents into a kit with a means for quantifying cell number as taught by Okamoto with reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Okamoto because the kit’s industrial applicability to allow the simple and accurate screening of compounds in a nonhuman animal model [0477].
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Scheideler et al. (WO 2018/081675, filed 10/30/2017, published 5/03/2018), in view of Okamoto et al., (US 2008/0077999, filed 4/28/2014, published 11/06/2014), as applied to claim 8, in further view of Cartoni et al., 2010 (Journal of Neurology, Vol. 133, p. 1460-1469, see IDS filed 9/14/2023)
As stated supra, Scheideler in view of Okamoto suggest a kit comprising a knock-in rat, a compound, and means for determining phenotypic expression of a change in the quantity of cells.
In regard to claim 9, although Scheideler generically discloses the use electrophysiological analysis for human patients, they do not teach a means for electrophysiological analysis for CMT2A knock-in rat.
Nevertheless, Cartoni teaches a nonhuman animal model of CMT2A and discloses agents for the electrophysiological analysis of these animals (p. 1462, Compound action potential recording).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to generate the kit as suggested by Scheideler and Okamoto and to combine a means for measuring the electrophysiological features as taught by Cartoni with reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Cartoni because these compound action potential recordings are proportional to the number of activated fibers and to the square of their diameters, thereby providing a functional measure of the nerves (p. 1468, Discussion, 2nd para.).
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
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 obviousness-type 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); and 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 a nonstatutory double patenting ground provided the conflicting application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement.
Effective January 1, 1994, a registered attorney or agent of record may sign a terminal disclaimer. A terminal disclaimer signed by the assignee must fully comply with 37 CFR 3.73(b).
Claims 1-6 are rejected on the grounds of nonstatutory double patenting over claims 1-5 of U.S. Patent No.11,800,859 (Scheideler et al., Patented 10/31/2023).
The subject matter claimed in the instant application is disclosed in the referenced patent as follows: the method for determining whether a compound is potentially useful for treating CMT2A disease using a R364W or H361Y knock-in rat of cited patent makes obvious the R364W or H361Y knock-in rat of instant application . It is clear that elements of the cited patent claims are to be found in instant claim. The difference between the cited patent claims and the instant claims lies in the fact that the cited patent claims are the intended use of instantly claimed knock-in rat. Furthermore, as per instant claims 4 and 5, as stated supra, only the relevant portions of SEQ ID NOs: 2 and 3 comprising the codon changes for said amino acid mutations are being considered, therefore one of ordinary skill in the art would have immediately envisioned these codon sequences due the limited number of nucleotide changes that would yield Tryptophan (only one codon is available “TGG”) and to a Tyrosine (only two codon combination are available “TAT” or “TAC”).
Since the instant application claims are obvious over cited patent claims, said claims are not patentably distinct.
Claim 7 is rejected on the grounds of nonstatutory double patenting over claims 1-5 of U.S. Patent No.11,800,859 (Scheideler et al., Patented 10/31/2023).
The subject matter claimed in the instant application is fully disclosed in the referenced patent as follows: the method for determining whether a compound is potentially useful for treating CMT2A disease of cited patent anticipates the screening method of instant application. It is clear that all the elements of the cited patent claims are to be found in instant claim. The difference between the cited patent claims and the instant claim lies in the fact that the cited patent claims are much more specific with respect to the method steps. Thus the invention of said claims of the cited patent are in effect “species” of the “generic” invention of the instant claim. It has been held that the generic invention is “anticipated” by the “species”. See In re Goodman, 29 USPQ2d 2010 (Fed. Cir. 1993).
Since the instant application claim is anticipated by cited patent claims, said claims are not patentably distinct.
Claims 8 and 10 are rejected on the grounds of nonstatutory double patenting over claims 1-5 of U.S. Patent No.11,800,859 (Scheideler et al., Patented 10/31/2023) in view of Okamoto et al., (US 2008/0077999, filed 4/28/2014, published 11/06/2014).
The subject matter claimed in the instant application is disclosed in the referenced patent as follows: the method for determining whether a compound is potentially useful for treating CMT2A disease using a R364W or H361Y knock-in rat of cited patent makes obvious the kit comprising the R364W or H361Y knock-in rat, compounds, and means for detecting a phenotype of instant application. It is clear that elements of the cited patent claims are to be found in instant claim. The difference between the cited patent claims and the instant claims lies in the fact that the instant application claims the elements as a kit, and a means for detecting phenotypic expression.
Okamoto teaches a measuring kit comprising a nonhuman animal comprising genetically modified cells, a compound potentially useful for treatment of the cells, and a means for detecting phenotypic expression by using transcriptional activity as a measure of cell quantity [0020-0080, 0086, 0202-0203, 0309-0310].
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have patented a transgenic rat whose genome comprises R364W mutation or H361Y mutation in its mitofusin 2 gene, and a screening method for identifying useful compounds for treating CMT2A as claimed by Scheideler et al., and to combine said agents into a kit with a means for detecting cell quantity as taught by Okamoto with reasonable expectation of success. The ordinary skilled artisan would have been motivated to claim so as taught by Okamoto because the kit’s industrial applicability to allow the simple and accurate screening of compounds in a nonhuman animal model [0477].
Since the instant application claims are obvious over cited patent claims in view of Okamoto, said claims are not patentably distinct.
Claim 9 is rejected on the grounds of nonstatutory double patenting over claims 1-5 of U.S. Patent No.11,800,859 (Scheideler et al., Patented 10/31/2023) in view of Okamoto et al., (US 2008/0077999, filed 4/28/2014, published 11/06/2014), as applied to claim 8, in further view of Cartoni et al., 2010 (Journal of Neurology, Vol. 133, p. 1460-1469, see IDS filed 9/14/2023).
As stated supra, the subject matter claimed in the instant application is made obvious by the referenced patent in view of Okamoto.
However, in regard to claim 9, cited patent does not claim a means for electrophysiological analysis for CMT2A knock-in rat.
Nevertheless, Cartoni teaches a nonhuman animal model of CMT2A and discloses agents for the electrophysiological analysis of these animals (p. 1462, Compound action potential recording).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have claimed the kit as suggested by Scheideler and Okamoto and to combine a means for measuring the electrophysiological features as taught by Cartoni with reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Cartoni because these compound action potential recordings are proportional to the number of activated fibers and to the square of their diameters, thereby providing a functional measure of the nerves (p. 1468, Discussion, 2nd para.).
Since the instant application claim is obvious over cited patent claims in further view of Conti, said claims are not patentably distinct.
Conclusion
No claims are allowed.
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