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 .
Response to Amendment
Receipt of Arguments/Remarks filed on 06/24/2026 is acknowledged. Claims 16-26,29,30 and 33 were amended. Claims 16-33 are pending and under examination.
Priority
This application is a 371 of PCT/US2022/029213, filed 05/13/2022 which claims benefit of 63/188,573, filed 05/14/2021 as reflected by the most recent filing receipt.
Withdrawn Objections and Rejections
Applicant’s arguments and amendments, see page 7, filed 06/24/2026, with respect to the objections to claims 16-20,22-25,29 and 30 have been fully considered and are persuasive due to the amendments to the claims correcting the objected to wording. The objections have been withdrawn.
Applicant’s arguments and amendments, see page 7, filed 06/24/2026, with respect to the objections to FIG. 1 and 26 as not being clear and legible have been fully considered and are persuasive due to providing clear, legible versions of FIG. 1 and 26. The objection has been withdrawn.
Applicant’s arguments and amendments, see page 9, filed 06/24/2026, with respect to the 35 U.S.C. 112(b) rejection of claims 16-33 have been fully considered and are persuasive due to the amendments to the claims correcting the issues of antecedent basis and issues of indefiniteness. The 35 U.S.C. 112(b) rejection of claims 16-33 has been withdrawn.
Applicant’s arguments and amendments, see page 7, filed 06/24/2026, with respect to the rejection(s) of claim(s)16-33 under 35 U.S.C. 101 under Statutory Double Patenting have been fully considered and are persuasive due to the amendment to claim 16 to recite the isolated nucleic acid molecule encoding a variant of sirtuin 6 (SIRT6) having at least 95% identity with SEQ ID NO: 1, and therefore no longer recites the exact same invention as copending Application No. 19/553,770. Therefore, the 35 U.S.C. 101 Statutory Double Patenting rejection has been withdrawn. However, upon further consideration, a new ground(s) of rejection is made in view of the amendment to claim 16 to recite at least 95% identity to SEQ ID NO: 1 and therefore the claims are rejected under Nonstatutory Double Patenting. See the rejection below.
Maintained Rejections- Modified based on Amendment
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.
Claims 16-25 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a product of nature without significantly more.
Regarding Step 1 of the Eligibility Analysis for 35 USC 101, claims 16-20 recite an isolated nucleic acid molecule and claims 21-25 recite an isolated polypeptide encoded by the nucleic acid molecule, and are therefore directed to a product, which is one of the statutory categories of invention.
Regarding Step 2A Prong One of the Eligibility Analysis, claims 16-25 recite at least one judicial exception that is a product of nature, which is an isolated nucleic acid molecule encoding a variant of SIRT6 having at least 95% identity with SEQ ID NO: 1, the variant having at least one mutations selected from the group consisting of a substitution N308K and a substitution A313S with respect to SEQ ID NO: 1, and claims 17-20 recite specific nucleic acid sequences of the variants (SEQ ID NOs: 6,7,8). Claim 21 recites an isolated polypeptide encoded by the nucleic acid molecule according to claim 16, with claims 21-25 reciting specific amino acid sequences of SEQ ID NOs: 2,3,4). Based on the broadest reasonable interpretation, the recited isolated nucleic acid molecule and isolated polypeptide encoded by the nucleic acid molecule reads on a product of nature as the instant specification discloses the inventors performed targeted sequencing of 301 genes involved in genome maintenance (GM), in 496 Ashkenazi Jewish (AJ) centenarians, and sequencing was performed to identify rare variants in these genes in DNA from peripheral blood of Ashkenazi Jewish centenarians and AJ individuals between 60 and 70 (paragraphs 0075-0076, 0220). The specification discloses among the ten GM genes containing nominally significant missense genetic variants enriched in the centenarian genome, was SIRT6 (paragraphs 0075-0076), and the SIRT6 allele found enriched in centenarians containing two missense mutations within the highly flexible C-terminus, converting a polar asparagine 308 to a charged lysine (N308K) and a hydrophobic alanine 313 to a polar serine (A313S), and that genotyping in centenarian carriers confirmed that these two SIRT6 variants occurred as linked double variants which were named centSIRT6 (paragraph 0222). The allele was vary rare in the whole exome sequence data of 50,726 adult participants of predominantly European ancestry in the Geisinger Health system (paragraph 0222). Therefore, the recited isolated nucleic acid molecules and isolated polypeptide thereof, are products of nature as they are SIRT6 variants that were naturally found in the genome of Ashkenazi Jewish (AJ) centenarians. Claims 16-25 do not have markedly different characteristics from the SIRT6 variants found in nature in the genome of Ashkenazi Jewish (AJ) centenarians, as there are no modifications recited in the molecule.
Next then, Step 2A Prong Two is analyzed to determine if the claim recites additional elements that integrate the judicial exception into a practical application. Regarding claims 16-25, no additional elements are recited. Therefore the claims do not recite additional elements that integrate the judicial into a practical application.
Next, Step 2B of the Eligibility Analysis on whether a claim amounts to significantly more than the judicial exception is evaluated. Claims 16-25 do not include any additional elements in addition to the isolated nucleic acid molecule or the isolated polypeptide. The claims do not add significantly more because of generally linking the use of the judicial exception to a particular technological environment or field of use. See MPEP 2106.05(h).
Therefore, it is concluded that claims 16-25 fail all of the steps of the test for subject matter eligibility under 35 USC 101.
Response to Arguments
Applicant's arguments filed 06/24/2026 have been fully considered but they are not persuasive.
Applicant argues on page 8 that the claimed molecules are not products of nature and are directed to isolated nucleic acid molecules and polypeptides encoding or comprising specific SIRT6 variants (N308K, A313S and N308K/A313S) with at least 75% identity to SEQ ID NO: 1, and the claimed molecules are not naturally occurring in isolated form, nor are they found in nature with the specific sequence modifications and percentage identity recited in the claims. Applicant argues the specification indicates the claimed nucleic acids and polypeptides are engineered and isolated (paragraphs 0031,0012,0014,0097,0104) and are not simply naturally occurring genomic DNA or proteins, and the term “isolated” is defined as being removed from its natural biological context (paragraph 0031). Applicant argues the claims further require at least one mutation (N308K and/or A313S) and a minimum of 75% sequence identity which encompasses a range of engineered variants not found in nature in the context of an isolated molecule (paragraphs 0012,0079,0080,0082,0097,0099).
This is not found persuasive. Claims 16-25 have been amended to recite at least 95% identity, and do not recite that the nucleic acid molecule or polypeptide is engineered or recombinant. While the claims recite the nucleic acid molecule and the polypeptide are isolated, this recitation does not cause it to no longer be a product of nature. As stated in the rejection, the instant specification discloses the inventors performed targeted sequencing of 301 genes involved in genome maintenance (GM), in 496 Ashkenazi Jewish (AJ) centenarians, and sequencing was performed to identify rare variants in these genes in DNA from peripheral blood of Ashkenazi Jewish centenarians and AJ individuals between 60 and 70 (paragraphs 0075-0076, 0220). Among the ten GM genes containing nominally significant missense genetic variants enriched in the centenarian genome, was SIRT6 (paragraphs 0075-0076), and the SIRT6 allele found enriched in centenarians containing two missense mutations within the highly flexible C-terminus, converting a polar asparagine 308 to a charged lysine (N308K) and a hydrophobic alanine 313 to a polar serine (A313S), and that genotyping in centenarian carriers confirmed that these two SIRT6 variants occurred as linked double variants which were named centSIRT6 (paragraph 0222). The allele was very rare in the whole exome sequence data of 50,726 adult participants of predominantly European ancestry in the Geisinger Health system (paragraph 0222). The instant specification states that the variant SIRT6 nucleic acid molecules and polypeptides were identified and occur as variants in the AJ centenarians. Therefore, all of the evidence shows that these variants that Applicant is claiming occur naturally in the AJ centenarians, rather than some modification to the genome that the inventors did to create the variant. Isolating the product of nature does not cause it to no longer be a product of nature. See Appendix 1 to the October 2019 Update: Subject Matter Eligibility Life Sciences and Data Processing Examples, Example 44: Denveric Acid. In this example, Applicant discovered a protein in the bark of the Rocky Mountain cassia tree that it calls “denveric acid” and claim 1 recites “A dosage unit comprising denveric acid in a container”. Claim 1 was determined to be ineligible in all of the steps. While the claim in this example does not specifically recite “isolated denveric acid”, it is claimed in a container and therefore would be isolated, and was still determined to be a nature-based product limitation.
Applicant argues that the claimed SIRT6 variants exhibit markedly different functional and structural characteristics compared to naturally occurring SIRT6, and the specification demonstrates that the centenarian SIRT6 allele (centSIRT6, N308K/A313S) and single mutants have altered enzymatic activities, altered protein conformation, enhanced biological functions including improved DNA repair, increased resistance to DNA damage, enhanced LINE1 suppression, increased anti-tumor activity (paragraph 0077-0078,0229-0234). These functional differences are supported by experimental data including in vitro and cell-based assays, showing the claimed products are not mere products of nature but possess new and advantageous properties (paragraphs 0223-0234,0257-0265). Applicants assert that a product with “markedly different characteristics” from any found in nature is not a judicial exception.
This is not found persuasive. The markedly different characteristics analysis is performed by comparing the nature-based product limitation in the claim to its naturally occurring counterpart to determine if it has markedly different characteristics from the counterpart. MPEP 2106.04(c)(II). The counterpart is not wild-type SIRT6, but rather the closest natural counterpart is the naturally occurring nucleic acid molecule encoding a variant of SIRT6 having at least one N308K and/or A313S mutation and polypeptide thereof which was identified as occurring in the AJ centenarians as disclosed in paragraph 0222. When the claimed isolated nucleic acid molecule and isolated polypeptide is compared to this counterpart, there is no difference in structure, function or other characteristics. No difference between the variant that is disclosed as being identified and occurring in the AJ centenarians is recited in the product of the instant claims.
Applicants argue the specification also provides practical applications of the claimed molecules and recite methods of treatment of age-related diseases by administering the claimed molecules to an individual in need thereof, and the specification provides detailed guidance on pharmaceutical compositions, routes of administration, dosage and co-administration with other drugs, demonstrating the claims are integrated into a practical application and are not merely abstract ides or products of nature.
This is not found persuasive, because claims 16-25 are what are rejected under 35 U.S.C. 101, and not claims 26-33 which recite the method of using the nature based product. Claims 16-25 do not include any additional elements in the claims or practical applications recited. Regarding Applicant’s arguments that the specification provides guidance on pharmaceutical compositions, routes of administration, dosage and co-administration with other drugs, what is disclosed in the specification is not brought into the claims reciting the judicial exception, but rather the content of the claims is what is analyzed to determine if any additional elements or practical applications are recited. Again, see Appendix 1 to the October 2019 Update: Subject Matter Eligibility Life Sciences and Data Processing Examples, Example 44: Denveric Acid, where even a claim reciting “A dosage unit comprising denveric acid in a container” failed Step 2A Prong 2 as the “container” recited was generic and did not meaningfully limit the claim and failed Step 2B as while the claim recited an additional element of a generic container, it is at best the equivalent of merely adding the words “apply it” to the judicial exception and is not eligible. Claims 16-25 simply do not recite any additional elements and do not recite any practical applications.
For these reasons, the 35 U.S.C. 101 rejection is maintained.
Claim Rejections - 35 USC § 112
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.
Written Description Rejection
Claims 26-33 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.
Claim 26-28 and 33 encompass treating and/or reducing the likelihood of occurrence of a large genus of age-related diseases in an individual in need thereof comprising administering to the individual a therapeutically efficient amount of the isolated nucleic acid molecule according to claim 16 or an isolated polypeptide encoding by the nucleic acid molecule. The isolated nucleic acid molecule of claim 16 requires 95% identity with SEQ ID NO: 1, and has at least one mutation selected from the group consisting of a substitution N308K and a substitution A313S with respect to SEQ ID NO: 1. Therefore, the nucleic acid or polypeptide administered only requires one of these substitutions and requires 95% identity to SEQ ID NO: 1, which is a large genus of nucleic acid/polypeptide molecules that may be administered. SEQ ID NO: 1 is 355 amino acids in length. 95% identity thereto allows for up to an 18 amino acid difference and the specification does not describe what other amino acids or parts of the sequence can be modified and still perform the recited function.
Claim 29 recites specific species of age-related diseases including progeria, Werner syndrome, neurodegenerative disease, Alzheimer’s disease, cancer, cardiovascular disease, obesity, type 2 diabetes, hypercholesterolemia, hypertension, ocular disorders, cataracts, glaucoma, osteoporosis, blood clotting disorders, arthritis, hearing loss and stroke, which still encompasses many different types of diseases affecting different parts of the body that are being prevented or treated with the recited isolated nucleic acid molecule or polypeptide thereof. Claims 30-32 further limit the diseases, with claim 32 limiting to cancer, however this encompasses preventing and/or treating any type of cancer including solid tissue cancers as well as blood cancers, affecting different parts of the body.
Regarding the state of the art, the prior art does not teach the instantly claimed SIRT6 variant and therefore the state of the art is silent with regards to treating and/or reducing the likelihood of occurrence of age-related diseases in an individual by administering the recited SIRT6 variant.
Li et al. (Front Cell Dev Biol. 2021 Mar 29;9:641315) teach SIRT6 is widely expressed in all mammalian organs and regulates multiple senescence associated biological processes, including oxidative stress, glucose and fat homeostasis, inflammatory responses, autophagy, genome integrity, and telomeres homeostasis, and therefore SIRT6 is involved in many kinds of aging related diseases such as neurodegenerative disease, cancer, CVDs (page 2, left column). Li et al. teach in Alzheimer’s disease patients, SIRT6 plays AD-protective function via maintaining genomic stability and preventing DNA damage in the brain, and shows a close relationship between the aberration of SIRT6 with human neurodegenerative diseases (page 2, right column).
Li et al. teach with regards to cancer, SIRT6 was considered as a double-edged sword due to its dual role of both tumor suppression and promotion depending on the type of tumors, as it protects against tumor growth though the function of controlling DNA damage repair, genomic stability, cellular metabolic homeostasis, and apoptosis, while it is also associated with the poor clinical outcomes by its enzyme activity regulating cancer pathways in cancers such as hepatocellular and colon cancers (page 2, right column).
Li et al. teach in the cardiovascular system, SIRT6 plays a protective function by improving vascular endothelial dysfunction to some extent, delaying the formation of atherosclerotic plaques and inhibiting cardiac hypertrophy and heart failure, and that some studies have shown that SIRT6 is a principal regulator of glucose metabolism homeostasis (page 2, right column). Li et al. teach the regulation of SIRT6 activity might influence various human diseases and prolong life. Nonetheless, the molecular mechanism of regulating the activity and function of SIRT6 in the process of anti-aging as well as prevention and treatment of CVDs warrants deeper understanding (Conclusion, page 11).
Regarding the unpredictability of extrapolating in vitro results to in vivo, Liu et al. (Frontiers in Pharmacology, January 2020, Vol. 10, Article 1489) teach In vivo and in vitro experimental systems are two essential ways to discover functional performance during drug-discovery, vital processes occurring in living organisms and toxicological research (Intro, page 1). Liu et al. teach that the goal of using in vitro data to substitute for in vivo data is greatly impeded by the inconsistency between in vivo and in vitro data and many researchers are challenged by the fact that in vitro data demonstrate poor correlations with in vivo data and have questioned the validity of IVIVE models (page 2, right column).
Liu et al. teach according to current investigations, in addition to the response signals from drug effects, many variables need to be considered inner-environmental factors that impact genetic variations in in vivo assays, such as cell types, culture conditions, time course of exposure, and measured end points, and differences are found when demonstrating the immune response components (effectors) of in vivo and in vitro hepatocytes (page 2, right column). It has been indicated that the inner environment of a living subject has different patterns of physiological function and mechanism, and with the comprehensive effects and variables that are determined by the complicated inner-environment of in vivo data, an inconsistent gap has emerged between in vivo data and in vitro data, and this inconsistency is further reflected at the level of gene expression (page 2, right column). Liu et al. teach the differences in the response components of a living system are reflected differently between gene expression profiles from in vivo and in vitro data (page 3, left column).
The specification discloses the variant amino acid sequences and nucleic acid sequences as SEQ ID NO: 2 as the SIRT6 N308K variant amino acid sequence, SEQ ID NO: 3, as the SIRT6 A313S variant amino acid sequence, SEQ ID NO: 4 as the SIRT6 N308K A313 variant (centSIRT6), amino acid sequence, SEQ ID NO: 6 as the SIRT6 N308K variant nucleic acid sequence, SEQ ID NO: 7 as the SIRT6 A313S variant nucleic acid sequence, and SEQ ID NO: 8 as the SIRT6 N308K A313S variant (centSIRT6) nucleic acid sequence (pages 65-68). Therefore, the above sequences show the complete structure of the amino acid and nucleic acid sequences of the SIRT6 variants. Claim 16 however encompasses a genus of isolated nucleic acid molecules having many possible sequences as the claim only requires at least 95% identity with SEQ ID NO: 1 and having one or both of the recited mutations. In addition, the specification does not provide written description that these disclosed SIRT6 variant sequences carry out the function of treating and/or reducing the likelihood of occurrence of a genus of age-related diseases in an individual.
The specification discloses SIRT6 variants carrying one or two mutations associated with human exceptional longevity (SIRT6 N308K, centSIRT6) were overexpressed in a variety of cell lines and assessed how this affected their specific cellular functions (Example 2, page 62, paragraph 0257). Example 2 discloses a human Werner Syndrome model using immortalized fibroblasts, that SIRT6 WT/SIRT6 N308K/centSIRT6 did not affect cell viability, proliferation or telomere length, and centSIRT6 decreased telomerase activity (Paragraph 0258), and that Werner Syndrome immortalized fibroblasts are poorly characterized lines that might have carcinogenic properties, and in the event that this is the case, decreasing telomerase activity would be a beneficial effect (paragraph 0259).
Example 2 also discloses a human hepatocellular carcinoma model in HCC cells, in which SIRT6 WT/SIRT6 N308K/centSIRT6 overexpression was lethal with a larger effect observed for SIRT6 N308K/centSIRT6, and therefore mutated SIRT6 may be useful for treating cancer (paragraph 0260, FIG. 31A, 31B).
Example 2 discloses that SIRT6 plays a role in the increase of adipogenic differentiation (FIG 32) consistent with the role of this protein in energy homeostasis, and that the SIRT6 mutants (SIRT6 N308K and centSIRT6) retain this property, which is of interest for treatment of ageing and ageing-related diseases (paragraph 0262). The examples also disclose that centSIRT6 significantly decreased the mRNA expression of aSMA, a major fibrogenic marker (Fig 33E) which suggests a potential anti-fibrotic effect of centSIRT6 in preventing liver fibrosis and/or promoting its resolution (paragraphs 0264-0265).
Thus, the examples only test the SIRT6 variants (SIRT6 N308K, centSIRT6) in a few cell lines that act as models for a few age-related diseases, and there are no in vivo examples in any animal or human models showing any treatment and/or reducing the likelihood of occurrence of any age-related diseases in an individual in need thereof comprising administering to said individual of a therapeutically efficient amount of the isolated nucleic acid molecule according to claim 16 or an isolated polypeptide encoded by the nucleic acid molecule.
Therefore, the specification provides insufficient written description to support the genus encompassed by the claim. Note: MPEP 2163.
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, (Fed. Cir. 1991), makes clear that "applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the 'written description' inquiry, whatever is now claimed." (See page 1117.) The specification does not "clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed." (See Vas-Cath at page 1116.)
Univ. of Rochester v. G.D. Searle, 69 USPQ2d 1886, 1892 (CAFC 2004), further supports this by stating that:
The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement. A description of an anti-inflammatory steroid, i.e., a steroid (a generic structural term) described even in terms of its functioning of lessening inflammation of tissues fails to distinguish any steroid from others having the same activity or function. A description of what a material does, rather than of what it is, usually does not suffice…. The disclosure must allow one skilled in the art to visualize or recognize the identity of the subject matter purportedly described. (Emphasis added).
With the exception of the above specifically disclosed SIRT6 variants (SEQ ID NOs: 2,3,4,6,7,8) the skilled artisan cannot envision the detailed chemical structure of the encompassed variants, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method for isolating it. The chemical structure itself is required. See Fiers v. Revel, 25 USPQ2d 1601, 1606 (Fed. Circ. 1993) and Amgen Inc. V. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016, (Fed. Cir. 1991). In Fiddes v. Baird, 30 USPQ2d 1481, 1483, (Bd. Pat. App. & Int. 1993), claims directed to mammalian FGF's were found unpatentable due to lack of written description for the broad class. The specification provided only the bovine sequence. Finally, University of California v. Eli Lilly and Co., 43 USPQ2d 1398, 1404, 1405 (Fed. Cir. 1997) held that:
...To fulfill the written description requirement, a patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude that "the inventor invented the claimed invention." Lockwood v. American Airlines, Inc., 107 F.3d 1565, 1572, 41 USPQ2d 1961, 1966 (Fed. Cir. 1997); In re Gosteli, 872 F.2d 1008, 1012, 10 USPQ2d 1614, 1618 (Fed. Cir. 1989) (" [T]he description must clearly allow persons of ordinary skill in the art to recognize that [the inventor] invented what is claimed."). Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations, not that which makes it obvious," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention." Lockwood, 107 F.3d at 1572, 41 USPQ2d at 1966.
Furthermore, to the extent that a functional description can meet the requirement for an adequate written description, it can do so only in accordance with PTO guidelines stating that the requirement can be met by disclosing “sufficiently detailed, relevant identifying characteristics,” including “functional characteristics when coupled with a known or disclosed correlation between function and structure.” Univ. of Rochester v. G.D. Searle, 68 USPQ2d 1424, 1432 (DC WNY 2003).
The instant specification does not provide written description for any of the SIRT6 variants as carrying out the function of function of treating and/or reducing the likelihood of occurrence of a genus of age-related diseases in an individual in need thereof. The species specifically disclosed are not representative of the genus because the genus is highly variant. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 USC § 112 is severable from its enablement provision. (See page 1115.)
Response to Arguments
Applicant's arguments filed 06/24/2026 have been fully considered but they are not persuasive.
Applicant argues on page 10 of response a person skilled in the art would be able to recognize in Applicant’s disclosure a description of these limitations. Applicant states the scope was limited to 95% variability, and a 5% variability corresponds to very minor variations of the sequence, and a person of ordinary skill in the art appreciates that substitutions and minor variations that preserve overall sequence identity, particularly at high level of identity such as 95% do not alter the three-dimensional structure and biological function of the polypeptide encoded by such a sequence. Applicant argues the specification discloses explicit sequences for representative nucleic acid molecules (SEQ ID NOs: 6,7,8) and polypeptides (SEQ ID NOs: 2,3,4), and a threshold of 95% identity represents a narrow scope that covers only close analogs and is fully supported by the disclosure of SEQ ID NOs: 2-4 and 6-8 because of person of ordinary skill would immediately appreciate that it can be reasonably extrapolated from this disclosure that very closely related variants of the claimed nucleic acid and polypeptide enable the technical effect of treating an age-related disease. Applicant stresses that the mutations that are relevant to the technical effect (N308K and/or A313S) are always included in the scope of the claim, and the recited sequence variability will not affect the technical effect obtained with mutations N308K and/or A313S. In addition, Applicants have replaced the term “preventing” with “reducing the likelihood of occurrence of” the disease which does not involved 100% prevention of the disease.
This is not found persuasive. Regarding the arguments pertaining to 95% identity with SEQ ID NO: 1, SEQ ID NO: 1 is 355 amino acids in length. 95% identity thereto allows for up to an 18 amino acid difference and the specification does not describe what other amino acids or parts of the sequence can be modified and still perform the recited function. While Applicant states that the mutations that are relevant to the technical effect (N308K and/or A313S) are always included in the scope of the claim, and the recited sequence variability will not affect the technical effect obtained with mutations N308K and/or A313S, the specification fails to show a core structure of this genus that performs the recited functions. For example, SEQ ID NO: 2 is 99.7% identical to instant SEQ ID NO: 1, with the only difference being the N308K substitution, SEQ ID NO: 3 is 99.8% identical to instant SEQ ID NO: 1 with the only difference being the A313S substitution, and SEQ ID NO: 4 is 99.5% identical to instant SEQ ID NO: 1 with the other differences being the N308K and A313S substitutions.
The core issue however, is that the specification does not show a structure-function correlation. While these specific sequences show structures, the specification does not show them as carrying out the functions recited in the claims. The examples only test the SIRT6 variants (SIRT6 N308K, centSIRT6) in a few cell lines that act as models for a few age-related diseases, and there are no in vivo examples in any animal or human models showing any treatment and/or reducing the likelihood of occurrence of any age-related diseases in an individual in need thereof comprising administering to said individual of a therapeutically efficient amount of the isolated nucleic acid molecule according to claim 16 or an isolated polypeptide encoded by the nucleic acid molecule. Therefore, the specification does not show the function of treating and/or reducing the likelihood of occurrence of a genus of age-related diseases with the SIRT6 N308K and centSIRT6 variants.
Claim Rejections-Scope of Enablement
Claims 26-33 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for the in vitro overexpression of SIRT6 carrying one or two mutations (SIRT N308K and centSIRT6) in Werner Syndrome immortalized fibroblasts, in human hepatocellular carcinoma cells, adipocytes, and in hepatic stellate cells, does not reasonably provide enablement for an in vivo method for treatment and/or reducing the likelihood of occurrence of a genus of age-related diseases in any individual in need thereof, comprising the administration by any route of administration to said individual of a therapeutically efficient amount of the isolated molecule according to claim 16 or of an isolated polypeptide encoded by the nucleic acid molecule. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
As stated in MPEP §2164.01(a), “there are many factors to consider when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any experimentation is ‘undue’.” These factors include, but are not limited to:
1. The breadth of the claims;
2. The nature of the invention;
3. The state of the prior art;
4. The level of skill in the art;
5. The level of predictability in the art;
6. The amount of direction provided by the inventor;
7. The presence or absence of working examples;
8. The quantity of experimentation necessary needed to make or use the invention based on the disclosure.
See In re Wands USPQ 2d 1400 (CAFC 1988).
The Breadth of the Claims and The Nature of the Invention
Claim 26-28 and 33 encompass treating and/or reducing the likelihood of occurrence a large genus of age-related diseases in an individual in need thereof comprising administering to the individual a therapeutically efficient amount of the isolated nucleic acid molecule according to claim 16 or an isolated polypeptide encoding by the nucleic acid molecule. The isolated nucleic acid molecule of claim 16 requires 95% identity with SEQ ID NO: 1, and has at least one mutation selected from the group comprising or consisting of a substitution N308K and a substitution A313S with respect to SEQ ID NO: 1. Therefore, the nucleic acid administered only requires one of these substitutions and requires 95% identity to SEQ ID NO: 1, which is a large genus of nucleic acid molecules that may be administered.
Claim 29 recites specific species of age-related diseases including progeria, Werner syndrome, neurodegenerative disease, Alzheimer’s disease, cancer, cardiovascular disease, obesity, type 2 diabetes, hypercholesterolemia, hypertension, ocular disorders, cataracts, glaucoma, osteoporosis, blood clotting disorders, arthritis, hearing loss and stroke, which still encompasses many different types of diseases affecting different parts of the body that are being prevented or treated with the recited isolated nucleic acid molecule or polypeptide thereof. Claims 30-32 further limit the diseases, with claim 32 limiting to cancer, however this encompasses treating and/or reducing the likelihood of occurrence of any type of cancer including solid tissue cancers as well as blood cancers, affecting different parts of the body.
The State of the Prior Art
The prior art does not teach the instantly claimed SIRT6 variant and therefore the state of the art is silent with regards to preventing and/or treating age-related diseases in an individual by administering the recited SIRT6 variant.
Regarding SIRT6, Li et al. (Front Cell Dev Biol. 2021 Mar 29;9:641315) teach SIRT6 is widely expressed in all mammalian organs and regulates multiple senescence associated biological processes, including oxidative stress, glucose and fat homeostasis, inflammatory responses, autophagy, genome integrity, and telomeres homeostasis, and therefore SIRT6 is involved in many kinds of aging related diseases such as neurodegenerative disease, cancer, CVDs (page 2, left column). Li et al. teach in Alzheimer’s disease patients, SIRT6 plays AD-protective function via maintaining genomic stability and preventing DNA damage in the brain, and shows a close relationship between the aberration of SIRT6 with human neurodegenerative diseases (page 2, right column).
Li et al. teach with regards to cancer, SIRT6 was considered as a double-edged sword due to its dual role of both tumor suppression and promotion depending on the type of tumors, as it protects against tumor growth though the function of controlling DNA damage repair, genomic stability, cellular metabolic homeostasis, and apoptosis, while it is also associated with the poor clinical outcomes by its enzyme activity regulating cancer pathways in cancers such as hepatocellular and colon cancers (page 2, right column).
Li et al. teach in the cardiovascular system, SIRT6 plays a protective function by improving vascular endothelial dysfunction to some extent, delaying the formation of atherosclerotic plaques and inhibiting cardiac hypertrophy and heart failure, and that some studies have shown that SIRT6 is a principal regulator of glucose metabolism homeostasis (page 2, right column). Li et al. teach the regulation of SIRT6 activity might influence various human diseases and prolong life. Nonetheless, the molecular mechanism of regulating the activity and function of SIRT6 in the process of anti-aging as well as prevention and treatment of CVDs warrants deeper understanding (Conclusion, page 11).
Regarding the unpredictability of extrapolating in vitro results to in vivo, Liu et al. (Frontiers in Pharmacology, January 2020, Vol. 10, Article 1489) teach In vivo and in vitro experimental systems are two essential ways to discover functional performance during drug-discovery, vital processes occurring in living organisms and toxicological research (Intro, page 1). Liu et al. teach that the goal of using in vitro data to substitute for in vivo data is greatly impeded by the inconsistency between in vivo and in vitro data and many researchers are challenged by the fact that in vitro data demonstrate poor correlations with in vivo data and have questioned the validity of IVIVE models (page 2, right column).
Liu et al. teach according to current investigations, in addition to the response signals from drug effects, many variables need to be considered inner-environmental factors that impact genetic variations in in vivo assays, such as cell types, culture conditions, time course of exposure, and measured end points, and differences are found when demonstrating the immune response components (effectors) of in vivo and in vitro hepatocytes (page 2, right column). It has been indicated that the inner environment of a living subject has different patterns of physiological function and mechanism, and with the comprehensive effects and variables that are determined by the complicated inner-environment of in vivo data, an inconsistent gap has emerged between in vivo data and in vitro data, and this inconsistency is further reflected at the level of gene expression (page 2, right column). Liu et al. teach the differences in the response components of a living system are reflected differently between gene expression profiles from in vivo and in vitro data (page 3, left column).
Therefore, the state of the art shows while SIRT6 is involved in many kinds of aging related diseases, its role in cancer is unpredictable, and in addition, the state of the art teaches the unpredictability of extrapolating results of in vitro studies to in vivo.
The Level of Predictability in the Art
The instant claimed invention is highly unpredictable due to the claims encompassing treating and/or reducing the likelihood of occurrence of a genus of age-related diseases by a genus of routes of administration of a therapeutically efficient amount of the isolated nucleic acid molecule according to claim 16 or of an isolated polypeptide encoded by the nucleic acid molecule. The isolated nucleic acid molecule according to claim 16 requires 95% identity to instant SEQ ID NO: 1 and having at least one mutation (N308K and/or A313S) and therefore is a genus of SIRT6 nucleic acid sequences and polypeptide sequences.
It would be unpredictable that any age-related disease could be treated because the genus of age-related diseases encompassed by the instant claims is vast. Each disease affects different organs and tissues of the body. Even neurodegenerative disease encompasses many different types of neurodegenerative diseases which are not predictable in treating, and regarding cancer, the genus of cancer includes both solid tissue and blood cancers affecting different parts of the body, and it is not predictable to be able to treat any type of cancer with the same therapeutic. Li et al., cited above, taught the unpredictability of SIRT6 with regards to cancer due to its dual role of both tumor suppression and promotion depending on the type of tumors, as it protects against tumor growth though the function of controlling DNA damage repair, genomic stability, cellular metabolic homeostasis, and apoptosis, while it is also associated with the poor clinical outcomes by its enzyme activity regulating cancer pathways in cancers such as hepatocellular and colon cancers.
Liu et al., cited above, taught the inconsistency between in vivo and in vitro data and many researchers are challenged by the fact that in vitro data demonstrate poor correlations with in vivo data.
In addition, the instant claims do not recite any particular route of administration. Certain diseases will require a particular route of administration depending on the affected tissues and organs of that disease. For example, neurodegenerative diseases and Alzheimer’s disease will need a route of administration that will deliver the nucleic acid to the central nervous system in order for there to be a therapeutic effect. Certain types of cancers may require particular routes of administration for the nucleic acid molecule to get to the affected tissue or organ.
The Amount of Direction Provided by the Inventor and
The Presence or Absence of Working Examples
Regarding claims 26-33, the specification does not enable any person skilled in the art to which it pertains to make and/or use the invention commensurate in scope with the claims.
The specification discloses the variant amino acid sequences and nucleic acid sequences as SEQ ID NO: 2 as the SIRT6 N308K variant amino acid sequence, SEQ ID NO: 3, as the SIRT6 A313S variant amino acid sequence, SEQ ID NO: 4 as the SIRT6 N308K A313 variant (centSIRT6), amino acid sequence, SEQ ID NO: 6 as the SIRT6 N308K variant nucleic acid sequence, SEQ ID NO: 7 as the SIRT6 A313S variant nucleic acid sequence, and SEQ ID NO: 8 as the SIRT6 N308K A313S variant (centSIRT6) nucleic acid sequence (pages 65-68).
The instant specification discloses that SIRT6 wild type or SIRT6 carrying one or two mutations associated with human exceptional longevity (SIRT6 N308K, centSIRT6) were overexpressed in a variety of cell lines and assessed how this affected their specific cellular functions (Example 2, page 62, paragraph 0257).
Example 2 discloses a human Werner Syndrome model using immortalized fibroblasts, that SIRT6 WT/SIRT6 N308K/centSIRT6 did not affect cell viability, proliferation or telomere length, and centSIRT6 decreased telomerase activity (Paragraph 0258), and that Werner Syndrome immortalized fibroblasts are poorly characterized lines that might have carcinogenic properties, and in the event that this is the case, decreasing telomerase activity would be a beneficial effect (paragraph 0259).
Example 2 also discloses a human hepatocellular carcinoma model in HCC cells, in which SIRT6 WT/SIRT6 N308K/centSIRT6 overexpression was lethal with a larger effect observed for SIRT6 N308K/centSIRT6, and therefore mutated SIRT6 may be useful for treating cancer (paragraph 0260, FIG. 31A, 31B).
Example 2 discloses that SIRT6 plays a role in the increase of adipogenic differentiation (FIG 32) consistent with the role of this protein in energy homeostasis, and that the SIRT6 mutants (SIRT6 N308K and centSIRT6) retain this property, which is of interest for treatment of ageing and ageing-related diseases (paragraph 0262). The examples also disclose that centSIRT6 significantly decreased the mRNA expression of aSMA, a major fibrogenic marker (Fig 33E) which suggests a potential anti-fibrotic effect of centSIRT6 in preventing liver fibrosis and/or promoting its resolution (paragraphs 0264-0265).
Thus, the examples only test the SIRT6 variants (SIRT6 N308K and centSIRT6) in a few cell lines that act as models for a few age-related diseases, and there are no in vivo examples in any animal or human models showing any treatment and/or reducing the likelihood of any age-related diseases in an individual in need thereof comprising administering to said individual of a therapeutically efficient amount of the isolated nucleic acid molecule according to claim 16 or an isolated polypeptide encoded by the nucleic acid molecule.
The Quantity of Experimentation Necessary
Regarding claims 26-33, in light of the unpredictability surrounding the breadth of the claimed method, one wishing to practice the presently claimed invention would be unable to do so without engaging in undue experimentation. As the instant specification only discloses overexpressing the SIRT6 mutants, SIRT6 N308K and centSIRT6, in a few in vitro cell line models of a few age-related diseases and assessing the cellular functions thereof, and the state of the art is silent in regards to the recited isolated nucleic acid molecule encoding the recited SIRT6 variant and the functions thereof, much more experimentation would be needed to determine if administering the recited isolated nucleic acid molecule of claim 16 or an isolated polypeptide encoded by the nucleic acid molecule would be capable of being administered by any route of administration to any individual in need thereof and result in treating and/or reducing the likelihood of occurrence of a genus of age-related diseases without undue experimentation.
Conclusion of 35 U.S.C. 112(a) (Enablement) Analysis
After applying the Wands factors and analysis to claims 26-33, in view of the applicant’s entire disclosure, it is concluded that the specification is not enabled for the full scope as discussed above. Therefore, claims 26-33 are rejected under 35 U.S.C. §112(a) for failing to disclose sufficient information to enable a person of skill in the art to use the invention commensurate in scope with these claims.
Response to Arguments
Applicant's arguments filed 06/24/2026 have been fully considered but they are not persuasive.
Applicant argues on page 11 that the specification describes in detail the structure, preparation and the use of the claimed nucleic acid molecules and polypeptides, as well as their application in the prevention and/or treatment of age-related diseases. The specification provides explicit sequences for representative nucleic acid molecules (SEQ ID NOs: 6,7,8) and polypeptides (SEQ ID NOs: 2,3,4) and describes how to generate additional variants with at least 75% identity and the specified mutations (paragraphs 0012-0014,0088-0091,0097-0103,0270-0277). Methods for constructing, expressing and purifying are described in paragraphs 0180-0217) and pharmaceutical compositions, vectors, formulations, and routes of administration suitable for delivering the molecule to individuals are described (paragraphs 0016-0025, 0130-0168). Applicant argues one of ordinary skill in the art given this disclosure would be able to make and use the claimed molecules and compositions without undue experimentation.
This is not found persuasive. While the Examiner agrees the specification provides nucleic acid molecules of SEQ ID NOs: 6,7 and 8 and polypeptides of SEQ ID NOs: 2,3 and 4, the Examiner does not see in the paragraphs pointed out above by Applicant where the specification describes how to generate additional variants that fall within the scope claimed. The specification also does not show how to use the full scope of the recited nucleic acid molecules and polypeptides thereof to treat the genus of diseases encompassed by the claims as stated in the rejection and an additional response is provided below.
Applicant argues on page 11, the specification provides detailed experimental evidence supporting the use of the claimed molecules for prevention and/or treatment of age-related diseases in paragraphs 0223-0234,0257-0265), i.e. highly relevant mechanisms for the treatment of age-related diseases. The specification provides in vitro and cell based data showing beneficial effects relevant to prevention and/or treatment of progeria, Werner Syndrome, Neurodegenerative diseases, Alzheimer’s disease, and cancer (paragraphs 0223-0234,0257-0265), as well as dosage ranges, routes of administration, co-administration with other drugs (paragraphs 0130-0168) providing practical guidance for therapeutic use. Applicant argues on page 12 that enablement does not require working examples for every disease or embodiment but sufficient guidance so that a skilled artisan can practice the full scope of the claims without undue experimentation, and argues the specification provides examples in various age-related disease models which can be reasonable extrapolated to the treatment of age-related diseases overall. Applicant argues the claims are not unduly broad relative to the disclosure and the specification provides representative examples and describes the common structural and functional features of the claimed genes (paragraphs 0012,0080,0082,0097,0099,0223-0234). The specification provides step-by-step protocols for generating the claimed molecules, expressing them in cells and testing their biological activity (paragraphs 0180-0217).
This is not found persuasive. The Examiner is not arguing that a working example is required for every disease or embodiment. However, as stated in the rejection, the examples only test the SIRT6 variants (SIRT6 N308K and centSIRT6) which are only 2 of the possible sequences encompassed by the claims in a few cell lines that act as models for a few age-related diseases. There are no in vivo examples in any animal or human models showing any treatment and/or reducing the likelihood of any age-related diseases in an individual in need thereof. The rejection provided references (Li et al. and Liu et al.) showing the state of the art and unpredictability of the instant claims. Li et al. taught while SIRT6 is involved in many kinds of aging related diseases, its role in cancer is unpredictable (SIRT6 has a dual role of both tumor suppression and promotion depending on the type of tumors). Instant Example 2 discloses a human hepatocellular carcinoma model in HCC cells, in which SIRT6 WT/SIRT6 N308K/centSIRT6 overexpression was lethal with a larger effect observed for SIRT6 N308K/centSIRT6, and therefore mutated SIRT6 may be useful for treating cancer (paragraph 0260, FIG. 31A, 31B). Liu et al. taught the unpredictability of extrapolating results of in vitro studies to in vivo. As the instant examples only provide in vitro testing in a few cell lines and ageing related diseases, there remains a high level of unpredictability and undue experimentation. No response regarding these references and unpredictability taught by them was provided by Applicant. MPEP 2164.03 states “In applications directed to inventions in arts where the results are unpredictable, the disclosure of a single species usually does not provide an adequate basis to support generic claims. In re Soll, 97 F.2d 623, 624, 38 USPQ 189, 191 (CCPA 1938). In cases involving unpredictable factors, such as most chemical reactions and physiological activity, more may be required. In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970) (contrasting mechanical and electrical elements with chemical reactions and physiological activity). See also In re Wright, 999 F.2d 1557, 1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993); In re Vaeck, 947 F.2d 488, 496, 20 USPQ2d 1438, 1445 (Fed. Cir. 1991). This is because in art areas having a high degree of uncertainty (i.e. the unpredictable arts) it is not reasonably predictable from the disclosure of one species, what other species will work”.
For these reasons, the rejection is maintained.
New Rejection-Necessitated by Amendment
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
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Claims 16-33 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of copending Application No. 19/553,770 (reference application).
Although the claims at issue are not identical, they are not patentably distinct from each other because instant claim 16 recites an isolated nucleic acid molecule encoding a variant of sirtuin 6 (SIRT6) having at least 95% identity with sequence SEQ ID NO: 1, the variant having at least one mutation selected in the group comprising or consisting of a substitution N308K and a substitution A313S with respect to sequence SEQ ID NO: 1, with claims 17-20 reciting specific nucleic acid sequences of SEQ ID NOs: 6,7 and 8 and claims 21-25 reciting an isolated polypeptide encoded by the nucleic acid molecule and reciting amino acid sequences of SEQ ID NOs: 2,3 and 4.
Claim 1 of ‘770 recites an isolated nucleic acid molecule encoding a variant of sirtuin 6 (SIRT6) having at least 75% identity with sequence SEQ ID NO: 1, the variant having at least one mutation selected in the group comprising or consisting of a substitution N308K and a substitution A313S with respect to sequence SEQ ID NO: 1. Claims 2-5 of ‘770 recite the same nucleic acid sequences (SEQ ID NOs: 6,7,8) as instant claims 17-20 and claims 6-10 of ‘770 recite an isolated polypeptide encoded by the nucleic acid molecule and recite the amino acid sequences of SEQ ID NOs 2,3 and 4, as instant claims 21-25.
Instant claim 26 recites “A method for the treatment and/or reducing the likelihood of occurrence of an age-related disease in an individual in need thereof, comprising the administration to said individual of a therapeutically efficient amount of the isolated nucleic acid molecule according to claim 16 or of an isolated polypeptide encoded by the nucleic acid molecule”, and claim 11 of ‘770 recites a method for the prevention and/or treatment of an age-related disease in an individual in need thereof, comprising the administration to said individual of a therapeutically efficient amount of the isolated nucleic acid molecule according to claim 1 or of an isolated polypeptide encoded by the nucleic acid molecule Instant claims 27-33 are identical to claims 12-18 of ‘770 regarding the individual being treating and the age-related diseases.
Therefore, the instant claims reciting the isolated nucleic acid molecule having at least 95% identity with SEQ ID NO: 1 or isolated polypeptide encoded by the nucleic acid molecule overlap in scope with the claims of ‘770 reciting the isolated nucleic acid molecule having at least 75% identity with SEQ ID NO: 1 or isolated polypeptide encoded by the nucleic acid molecule and would be an obvious variant thereof, and instant claims 17-20 and 22-25 recite the same sequences and therefore the same limitations as claims 2-5 and 7-10 of ‘770.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Claims 16-33 are rejected.
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 STEPHANIE L SULLIVAN whose telephone number is (703)756-4671. The examiner can normally be reached Monday-Friday, 7:30-3:30 EST.
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/STEPHANIE L SULLIVAN/Examiner, Art Unit 1635
/ABIGAIL VANHORN/Primary Examiner, Art Unit 1636
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