DETAILED ACTION
Election/Restrictions
Applicant’s election without traverse of Group I, claims 1-4, 6-20 and 33, drawn to a method of treating or preventing a disease or condition of gastrointestinal tissue in a subject and the following species: SNP5 (claim 16) and antibody A100 (claim 20), and a method of treating or preventing a disease or condition of gastrointestinal tissue in a subject (claim 1 and independent claim 33, in the reply filed on 02/27/2026 is acknowledged.
Claim 5 and 34 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected Groups II-III, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 02/27/2026.
Claims Status
Claims 1-4, 6-20 and 33 are pending.
Claims 5 and 34 are withdrawn.
Claims 1-4, 6-20 and 33 are currently under examination.
Priority
This application is a 371 of PCT/US2021/035543 06/02/2021 which claims benefit of U.S. Provisional Application No. 63/034,278 filed 06/03/2020. The priority date of claim set filed on 02/27/2026, is determined to be 06/03/2020.
Drawings
The drawings are objected to because Fig. 28B on Pg. 41 should be corrected to Fig. 29B, since there is already a Fig. 28B on Pg. 40. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. 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. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. 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.
Specification
The abstract of the disclosure is objected to because the abstract is not on a separate sheet. A corrected abstract of the disclosure is required and must be presented on a separate sheet, apart from any other text. See MPEP § 608.01(b).
Claim Objections
Claim 17 is objected to because of the following informalities: Claim 17 recites the limitation “provided the presence of the genotype is detected in (b)” (ln 3). Claim 1 which claim 17 depends on does not comprise a step (b). Appropriate correction is required.
Claim 19 is objected to because of the following informalities: Claim 19 recites the limitation “provided the presence of the genotype is detected in (b)” (ln 3). Claim 1 which claim 19 depends on does not comprise a step (b). Appropriate correction is required.
Claim Rejections - 35 USC § 112 (Improper Markush)
Claims 16 and 20 are rejected on the basis that it contains an improper Markush grouping of alternatives. See In re Harnisch, 631 F.2d 716, 721-22 (CCPA 1980) and Ex parte Hozumi, 3 USPQ2d 1059, 1060 (Bd. Pat. App. & Int. 1984).
A Markush grouping is proper if the alternatives defined by the Markush group (i.e., alternatives from which a selection is to be made in the context of a combination or process, or alternative chemical compounds as a whole) share a “single structural similarity” and a common use. A Markush grouping meets these requirements in two situations. First, a Markush grouping is proper if the alternatives are all members of the same recognized physical or chemical class or the same art-recognized class, and are disclosed in the specification or known in the art to be functionally equivalent and have a common use. Second, where a Markush grouping describes alternative chemical compounds, whether by words or chemical formulas, and the alternatives do not belong to a recognized class as set forth above, the members of the Markush grouping may be considered to share a “single structural similarity” and common use where the alternatives share both a substantial structural feature and a common use that flows from the substantial structural feature. See MPEP § 2117.
A Markush claim contains an “improper Markush grouping” if:
(1) the species of the Markush group do not share a “single structural similarity,” or (2) the species do not share a common use. Members of a Markush group share a “single structural similarity” when they belong to the same recognized physical or chemical class or to the same art-recognized class. Members of a Markush group share a common use when they are disclosed in the specification or known in the art to be functionally equivalent. See MPEP § 2117.
The Markush grouping of SNPs listed in Claim 16 is improper because the alternatives defined by the Markush grouping do not share both a single structural similarity and a common use for the following reasons: The recited alternative species in the groups set forth here do not share a single structural similarity, as each different SNP that could be detected is itself located in a separate region of the genome and has its own structure. The SNPs recited in the instant claims, do not share a single structural similarity since each consists of a different nucleotide sequences with different expression patterns and functions. The only structural similarity present is that all detected positions are part of nucleic acid molecules. The fact that the SNPs comprise nucleotides per se does not support a conclusion that they have a common single structural similarity because the structure of comprising a nucleotide alone is not essential to the common activity of being correlated with a disease or condition of gastrointestinal tissue. Accordingly, while the different SNPs are asserted to have the property of having a single nucleotide polymorphism, they do not share a single structural similarity.
The Markush grouping of antibodies listed in Table 1 recited in Claim 20 is improper because the alternatives defined by the Markush grouping do not share both a single structural similarity and a common use for the following reasons: The recited alternative species in the groups set forth here do not share a single structural similarity, as each different antibody has separate heavy chain (HC) variable and light chain (LC) variable regions and has its own structure. The antibodies referenced in the Table 1 of the instant claims, do not share a single structural similarity since each consists of a different protein sequences with different binding efficiencies and functions. The only structural similarity present is that all of the proteins are part of antibody molecules. The fact that the antibodies comprise HC and LC domains per se does not support a conclusion that they have a common single structural similarity because the structure of comprising a antibody alone is not essential to the common activity of being correlated with TLA and DR3. Accordingly, while the different antibodies are asserted to have the property of binding TL1A or DR3, they do not share a single structural similarity.
To overcome these rejections, Applicant may set forth each alternative (or grouping of patentably indistinct alternatives) within an improper Markush grouping in a series of independent or dependent claims and/or present convincing arguments that the group members recited in the alternative within a single claim in fact share a single structural similarity as well as a common use.
Claim X is indefinite over the limitation
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1-4 and 6-20 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being incomplete for omitting essential structural cooperative relationships of elements, such omission amounting to a gap between the necessary structural connections. See MPEP § 2172.01. The omitted structural cooperative relationships are: lndel1 to a specific Indel1 and SNP1 to a specific SNP1, as they do not have an accepted meaning in the art and would be different for any specific genotype as would be indicated. SNP1 is referenced as SNP rs2149092 in para. 54 of the instant specification. In the same paragraph, lndel1 is defined as rs16900967. Claims 2-4 and 6-20 depend on claim 1.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1-4, 6-12 and 17-20 are rejected under 35 U.S.C. 103 as being unpatentable over Gonsky et al. (“Gonsky”; Patent App. Pub. WO 2017161342 A1, Sept. 21, 2017).
Gonsky discloses “The present invention describes methods of diagnosing inflammatory bowel disease, including but not limited to Crohn's Disease (CD), Ulcerative Colitis (UC), and/or Medically Refractive Ulcerative Colitis (MR-UC), using RNASET2, TL1A and/or IFN-ϒ. The invention further provides a process for patient identification and/or stratification..” (Abstract).
Regarding claim 1, Gonsky comprising a method wherein “Described herein are methods of diagnosing inflammatory bowel disease using RNASET2, TL1 A and/or IFN-γ as a biomarker of disease severity in a patient population and selecting the patient population for anti-TLlA therapy. Further described are methods of treating these patient populations” (Para. 64). Gonsky teaches a method comprising “the association of RNASET2 disease risk variant SNPs with disease recurrence in 38 patients who were not receiving postoperative prophylaxis” (Para.46). Gonsky teaches a method comprising “The inventors demonstrate a functional association of RNASET2 disease risk SNPs with decreased expression and hyper-methylation in T cells isolated from CD patients, as well as an association with clinical parameters suggestive of complicated/resistant disease behavior and rapid recurrence of disease...The data distinguish RNASET2 as a potential therapeutic biomarker and identify unique pathways for additional therapeutic modulation within a defined IBD population” (Para.69). Gonsky teaches a method comprising “The data presented above demonstrate significant overlap between more than a hundred CD RNASET2 risk variants, many in linkage disequilibrium” (Para. 176). Gonsky also teaches “ A method of diagnosing inflammatory bowel disease (IBD) in a subject, comprising: obtaining a sample from the subject; subjecting the sample to an assay adapted to determine the presence or absence of one or more risk variants at the RNASET2 gene; and diagnosing IBD in the subject based on the presence of one or more risk variants at the RNASET2 gene” (Claim 1). Thus, Gonsky suggests a method of treating or preventing a disease or condition of gastrointestinal tissue in a subject comprising administering a therapeutic agent to the subject, provided the subject is identified as having a high likelihood of recurrence of the disease or condition following surgical treatment of the disease or disorder based at least partially on a presence of a genotype being detected in a sample obtained from the subject, wherein the genotype comprises an indel at Indel 1, a single nucleotide polymorphism (SNP) at SNP 1, or a SNP in linkage disequilibrium (LD) therewith, or a combination thereof.
Furthermore, Gonsky teaches the limitations of dependent claims 2-4, 6-7, 10, and 17-20 which depend on claim 1. Claims 8-9 depend on claim 7, which depends on claim 1. Claims 11-12 depend on claim 10, which depends on claim 1.
Regarding claim 2, Gonsky teaches a method wherein “TL1A, is associated with IBD and are key mediators of mucosal inflammation. In IBD patients, elevated TL1A levels correlate with disease severity and genotype. TL1A mediates marked enhancement of IFN-γ production. TLIA response biomarkers were identified by RNAseq and verified by qPCR in T cells isolated from IBD patients (20 Crohn's [CD], 20 ulcerative colitis [UC]) compared to normal (NL).” (Para.139). Thus, Gonsky suggests a method wherein the high likelihood is relative to a likelihood of an individual that does not have the genotype to experience recurrence of the disease or condition following surgical treatment.
Regarding claims 3 and 4, Gonsky teaches a method wherein “the inventor believes that RNASET2 serves as a therapeutic biomarker associated with severe disease pathobiology and allows for the identification of a patient population most likely to benefit from therapy targeted to the TLlA-driven inflammatory pathway” (Para. 68). Gonsky also teaches a method wherein “the subjects diagnosed with MR-UC are treated with non-conventional treatments, such as, but not limited to treatments that mimics, modulates and/or targets RNASET2, TL1A and/or IFN-γ. In various embodiments, treatments that mimics, modulates and/or targets RNASET2, TL1A and/or IFN-γ can comprise antibodies and or silencing oligonucleotides.” (Para. 84). Thus, Gonsky suggests a method wherein the therapeutic agent is a modulator of Ribonuclease T2 (RNASET2) activity or expression; and wherein the therapeutic agent is a modulator of Tumor necrosis factor ligand-related molecule 1 A (TL1A) activity or expression.
Regarding claim 6, Gonsky teaches a method wherein “TL1A, is a key mediator of mucosal inflammation. TL1A expression is up-regulated in inflamed regions of the intestine in both CD and UC. In IBD patients, elevated TL1A levels correlate with T FSF15 genotype and disease severity. CD patients with elevated serum/tissue levels of TL1A have increased risk of developing fibrosis/stricturing disease behavior.” (Para. 5). Gonsky also teaches a method wherein “TL1A expression is enhanced in inflammatory bowel disease and higher TL1A levels are associated with disease severity” (Para. 66). Thus, Gonsky suggests a method wherein the disease or condition is mediated by TL1A.
Regarding claims 7-9, Gonsky teaches a method wherein “Inflammatory bowel disease (IBD) has two common forms, Crohn's disease (CD) and ulcerative colitis (UC), which are chronic, relapsing inflammatory disorders of the gastrointestinal tract” (Para. 4) and “inflammatory bowel disease” (Para. 64). Thus, Gonsky suggests a method wherein the disease or condition is an inflammatory disease or condition; wherein the inflammatory disease or condition is an inflammatory bowel disease; and wherein the inflammatory bowel disease is Crohn's disease, perianal Crohn's disease, ulcerative colitis, intestinal fibrosis, or intestinal fibrostenosis, or a combination thereof.
Regarding claim 10, Gonsky teaches a method wherein “surgical intervention for disease management” (Para.15; Para. 71). Thus, Gonsky suggests a method wherein at least a portion of the gastrointestinal tissue was removed to treat the disease or condition.
Regarding claims 11 and 12, Gonsky teaches a method wherein “the small intestine sample comprises the duodenum, jejunum, and/or the ileum” (Para. 106). Thus, Gonsky suggests a method wherein the gastrointestinal tissue is the small intestine; and wherein the small intestine is the ileum.
Regarding claim 17-20, Gonsky teaches a method wherein “treated with non-conventional treatments, such as, but not limited to treatments that mimics, modulates and/or targets RNASET2, TL1A and/or IFN-γ. In various embodiments, treatments that mimics, modulates and/or targets RNASET2, TL1A and/or IFN-γ can comprise antibodies and or silencing oligonucleotides.” (Para. 84). Gonsky teaches a method wherein “inventors believe that RNASET2 serves as a novel potential disease severity biomarker to identify a subset of CD patients most likely to benefit from anti-TL1 A therapy” (Para. 104). Thus, Gonsky suggests a method further comprising administering to the subject a therapeutically effective amount of a modulator of RNASET2 activity or expression; wherein the modulator of RNASET2 activity or expression is an agonist of RNASET2 activity or expression; further comprising administering to the subject a therapeutically effective amount of a modulator of TL1A activity or expression; and wherein the modulator of TL1A comprises an anti-TL1A.
Therefore, the invention as recited in claims 1-4, 6-12 and 17-20 are prima facie obvious over the prior art Gonsky et al. One of ordinary skill in the art would have had a reasonable expectation of success given the lack of novelty. It would have been obvious to provide a method of treating or preventing a disease or condition of gastrointestinal tissue in a subject comprising administering a therapeutic agent to the subject according to the limitations of the instant application claims 1-4, 6-12 and 17-20 based on Gonsky et al (Patent App. Pub. No. WO 2017161342 A1, Sept. 21, 2017).
Claim 13 is rejected under 35 U.S.C. 103 as being unpatentable over Gonsky et al. (“Gonsky”; Patent App. Pub. WO 2017161342 A1, Sept. 21, 2017) as applied to claim 1 above, and further in view of Gonsky et al. (“Gonsky 2019”; Patent App. Pub. EP3430172A1, Jan. 23, 2019).
The teachings of Gonsky are documented above in the rejection of claims 1-4, 6-12 and 17-20 under 35 U.S.C. 103. Claim 13 depends on claim 1. Gonsky does not explicitly teach the limitations of claim 13.
Gonsky 2019 discloses “The present invention describes methods of diagnosing inflammatory bowel disease, including but not limited to Crohn's Disease (CD), Ulcerative Colitis (UC), and/or Medically Refractive Ulcerative Colitis (MR-UC), using RNASET2, TL1A and/or IFN-γ. The invention further provides a process for patient identification and/or stratification.” (Abstract).
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Regarding claim 13, Gonsky 2019 teaches a sequence that aligns with SEQ ID 400 with 100% identity and 100 coverage. (Sequence listing; See alignment from search result below). Thus, Gonsky 2019 suggests a method wherein the genotype comprising the indel at Indel 1 is CCAGGGCTGGGTGAGGG (SEQ ID NO:400).
Gonsky and Gonsky 2019 are both considered to be analogous to the claimed invention because they are in the same field of processes involving the analysis of nucleic acids for diseases caused by alterations of genetic material. Therefore, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method comprising administering a therapeutic agent to the subject, provided the subject is identified as having a high likelihood of recurrence of the disease or condition following surgical treatment of the disease or disorder based at least partially on a presence of a genotype being detected in a sample obtained from the subject, wherein the genotype comprises an indel at Indel 1, a single nucleotide polymorphism (SNP) at SNP 1, or a SNP in linkage disequilibrium (LD) therewith, or a combination thereof as taught by Gonsky to incorporate the genotype comprising SEQ ID NO:400 as taught by Gonsky 2019 and provide a method for a method of treating a disease or condition of gastrointestinal tissue in a subject, wherein the genotype comprises the indel that is SEQ ID 400. These claim elements were known in the art and one of skill in the art could have combined these elements by known methods with no change in their respective functions, and the combination would have yielded the predictable outcome according to the limitations of claims 13. Doing so would allow for the association of the indel of SEQ ID: 400 as a disease biomarker to provide identification of subjects not responsive to current treatment strategies who may benefit from alternate therapeutic approaches.
Claim 14 is rejected under 35 U.S.C. 103 as being unpatentable over Gonsky et al. (“Gonsky”; Patent App. Pub. WO 2017161342 A1, Sept. 21, 2017) as applied to claim 1 above, and further in view of Targan et al. (“Targan”; Patent App. Pub. US 20150376707 A1, Dec. 31, 2015).
The teachings of Gonsky are documented above in the rejection of claims 1-4, 6-12 and 17-20 under 35 U.S.C. 103. Claim 14 depends on claim 1. Gonsky does not explicitly teach the limitations of claim 14.
Targan discloses “The present invention also provides various methods, kits and compositions for diagnosing, prognosing, and treating various conditions including but not limited to inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease. Also, the present invention provides various methods, kits and compositions for determining susceptibility to or a low probability of various conditions including but not limited to inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease. These methods, kits and compositions may involve detecting risk/protective variants or haplotypes, serological markers, increased or decreased gene methylation, and increased or decreased cytokine secretion.” (Abstract).
Regarding claim 14, Targan teaches a method wherein “the one or more risk genetic variants include SNP rs1861494 with a “T” allele.” (Para.154). Thus, Targan suggests a method wherein the genotype comprising the SNP at SNP1 is a "T".
Gonsky and Targan are both considered to be analogous to the claimed invention because they are in the same field of processes involving the analysis of nucleic acids afor diseases caused by alterations of genetic material. Therefore, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method comprising administering a therapeutic agent to the subject, provided the subject is identified as having a high likelihood of recurrence of the disease or condition following surgical treatment of the disease or disorder based at least partially on a presence of a genotype being detected in a sample obtained from the subject, wherein the genotype comprises an indel at Indel 1, a single nucleotide polymorphism (SNP) at SNP 1, or a SNP in linkage disequilibrium (LD) therewith, or a combination thereof as taught by Gonsky to incorporate the method wherein the genotype comprising the SNP at SNP1 is a "T" as taught by Targan and provide a method of treating a disease or condition of gastrointestinal tissue in a subject, wherein genotype comprising the SNP at SNP1 is a "T". These claim elements were known in the art and one of skill in the art could have combined these elements by known methods with no change in their respective functions, and the combination would have yielded the predictable outcome according to the limitations of claim 14. Doing so would allow for the association of methylation levels with a SNP that is a "T as a disease biomarker to provide identification of subjects not responsive to current treatment strategies who may benefit from alternate therapeutic approaches.
Claims 15 and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Gonsky et al. (“Gonsky”; Patent App. Pub. WO 2017161342 A1, Sept. 21, 2017) as applied to claim 1 above, and further in view of McGovern et al. (“McGovern”; Patent App. Pub. US 20180305459 A1, Oct. 25, 2018).
The teachings of Gonsky are documented above in the rejection of claims 1-4, 6-12 and 17-20 under 35 U.S.C. 103. Claims 15 and 20 depend on claim 1. Gonsky does not explicitly teach the limitations of claims 15 and 20.
McGovern discloses “The aspects disclosed herein describe methods of identifying a subject that is non-responsive to anti-TNF therapy. The aspects disclosed herein further provide for a method of selecting a therapy for a subject with Inflammatory Bowel Disease (IBD), and treating the subject with the therapy.” (Abstract).
Regarding claim 15, McGovern teaches a method wherein “two copies of the genetic risk variant confers a homozygous risk genotype.” (Para. 16). Thus, McGovern suggests a method wherein the genotype is homozygous.
Does not explicitly teach the species elected for claim 20 antibody A100.
Regarding claim 20, McGovern teaches a method wherein “the anti-TL1A antibody is A100” (Para. 65) and SEQ ID No: 215 and 216, which correspond to SEQ ID No:.9 and 10, respectively. (Sequence listing; See alignments from sequence search results below.).
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Thus, McGovern suggests a method wherein the modulator of TL1A comprises an anti-TL1A antibody, wherein the anti-TL1A antibody is A100.
Gonsky and McGovern are both considered to be analogous to the claimed invention because they are in the same field of processes involving the analysis of nucleic acids for diseases caused by alterations of genetic material. Therefore, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method comprising administering a therapeutic agent to the subject, provided the subject is identified as having a high likelihood of recurrence of the disease or condition following surgical treatment of the disease or disorder based at least partially on a presence of a genotype being detected in a sample obtained from the subject, wherein the genotype comprises an indel at Indel 1, a single nucleotide polymorphism (SNP) at SNP 1, or a SNP in linkage disequilibrium (LD) therewith, or a combination thereof as taught by Gonsky to incorporate the method wherein the genotype is homozygous and wherein the modulator of TL1A is an anti-TL1A antibody, A100 which comprises the seq ID no. 215 and 216 as taught by McGovern and provide a method of treating a disease or condition of gastrointestinal tissue in a subject, wherein the genotype is homozygous and the modulator of TL1A is A100. These claim elements were known in the art and one of skill in the art could have combined these elements by known methods with no change in their respective functions, and the combination would have yielded the predictable outcome according to the limitations of claims 15 and 20. Doing so would allow for two copies of the genetic risk variant to confer a homozygous risk genotype as a disease biomarker to aide in determining treatment strategies.
Claim 16 is rejected under 35 U.S.C. 103 as being unpatentable over Gonsky et al. (“Gonsky”; Patent App. Pub. WO 2017161342 A1, Sept. 21, 2017) as applied to claim 1 above, and further in view of Elding, H; (2015) Dissecting the genetics of Inflammatory Bowel Disease. Doctoral thesis, UCL (University College London).
The teachings of Gonsky are documented above in the rejection of claims 1-4, 6-12 and 17-20 under 35 U.S.C. 103 Claim 16 depends on claim 1. Gonsky does not explicitly teach the limitations of claim 16.
Elding discloses “Inflammatory Bowel Disease (IBD) can be classified into two main subtypes: Crohn’s Disease (CD) and Ulcerative Colitis (UC). The aim of this study is to identify the genetic contribution to the susceptibility to IBD. In the first part of the study, I focused on Crohn’s Disease, the subtype that shows the greatest heritability. Using both pooled and sub-phenotype data, followed by replication, the results reveal substantial genetic heterogeneity and the total number of confirmed CD susceptibility loci was increased from 71 published by others to 200. This was achieved by analyzing the data using a multimarker approach and high-resolution genetic maps in Linkage Disequilibrium Units. In the second part of the study, I focused on Ulcerative Colitis. The results show that although UC has a lower reported heritability, many loci were also found for Ulcerative Colitis. Some of these overlap with those found for Crohn’s Disease.” (Abstract).
Regarding claim 16, Elding teaches a method wherein “SNP1” and “SNP5” (Pg. 40. Figure 5) Furthermore, Elding teaches a method wherein “linkage studies still successfully identified linkage peaks for UC, notably on chromosomes 1, 4, 6, 12, 22 and X, some of which were shared with CD” (Pg. 23) and “6q27 … FGFR1OP/RNASET2” (Pg. 97 Table 8). Thus, Elding suggests a method wherein the genotype comprises a second SNP comprising SNP5, SNP6, SNP7, SNP8, SNP9, SNP10, SNP11, SNP12, SNP13,SNP14, SNP15, SNP16, SNP17, SNP18, SNP19, SNP20, SNP21, SNP22, SNP23, SNP24, SNP25, SNP26, SNP27, SNP28, SNP29, SNP30, SNP31, SNP32, SNP33,SNP34, SNP35, SNP36, or a SNP in LD therewith, or any combination thereof.
Gonsky and Elding are both considered to be analogous to the claimed invention because they are in the same field of processes involving the analysis of nucleic acids for diseases caused by alterations of genetic material. Therefore, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method comprising administering a therapeutic agent to the subject, provided the subject is identified as having a high likelihood of recurrence of the disease or condition following surgical treatment of the disease or disorder based at least partially on a presence of a genotype being detected in a sample obtained from the subject, wherein the genotype comprises an indel at Indel 1, a single nucleotide polymorphism (SNP) at SNP 1, or a SNP in linkage disequilibrium (LD) therewith, or a combination thereof as taught by Gonsky to incorporate the method wherein the genotype comprises a second SNP comprising SNP5 as taught by Elding and provide a method for a method of treating a disease or condition of gastrointestinal tissue in a subject, wherein the genotype comprises a second SNP comprising SNP5. These claim elements were known in the art and one of skill in the art could have combined these elements by known methods with no change in their respective functions, and the combination would have yielded the predictable outcome according to the limitations of claim 16. Doing so would allow for the identification of linkage peaks for the inflammatory bowel disease on chromosomes.
Claim 33 is rejected under 35 U.S.C. 103 as being unpatentable over Gonsky et al. (“Gonsky”; Patent App. Pub. WO 2017161342 A1, Sept. 21, 2017).
Gonsky discloses “The present invention describes methods of diagnosing inflammatory bowel disease, including but not limited to Crohn's Disease (CD), Ulcerative Colitis (UC), and/or Medically Refractive Ulcerative Colitis (MR-UC), using RNASET2, TL1A and/or IFN-ϒ. The invention further provides a process for patient identification and/or stratification..” (Abstract).
Regarding claim 33, Gonsky comprising a method wherein “Described herein are methods of diagnosing inflammatory bowel disease using RNASET2, TL1 A and/or IFN-γ as a biomarker of disease severity in a patient population and selecting the patient population for anti-TLlA therapy. Further described are methods of treating these patient populations” (Para. 64). Gonsky teaches a method comprising “The inventors demonstrate a functional association of RNASET2 disease risk SNPs with decreased expression and hyper-methylation in T cells isolated from CD patients, as well as an association with clinical parameters suggestive of complicated/resistant disease behavior and rapid recurrence of disease...The data distinguish RNASET2 as a potential therapeutic biomarker and identify unique pathways for additional therapeutic modulation within a defined IBD population” (Para.69). Gonsky teaches a method comprising “The data presented above demonstrate significant overlap between more than a hundred CD RNASET2 risk variants, many in linkage disequilibrium” (Para. 176). Gonsky also teaches “ A method of diagnosing inflammatory bowel disease (IBD) in a subject, comprising:
obtaining a sample from the subject; subjecting the sample to an assay adapted to determine the presence or absence of one or more risk variants at the RNASET2 gene; and diagnosing IBD in the subject based on the presence of one or more risk variants at the RNASET2 gene” (Claim 1). Thus, Gonsky suggests a method of treating or preventing a disease or condition of gastrointestinal tissue in a subject comprising administering a therapeutic agent to the subject, provided the subject is identified as having a high likelihood of recurrence of the disease or condition following surgical treatment of the disease or disorder based at least partially on a presence of a genotype being detected in a sample obtained from the subject, wherein the genotype comprises an indel at Indel 1, a single nucleotide polymorphism (SNP) at SNP 1, or a SNP in linkage disequilibrium (LD) therewith, or a combination thereof.
Therefore, the invention as recited in claim 33 is prima facie obvious over the prior art Gonsky et al. One of ordinary skill in the art would have had a reasonable expectation of success given the lack of novelty. It would have been obvious to provide a method of treating or preventing a disease or condition of gastrointestinal tissue in a subject comprising administering a therapeutic agent to the subject according to the limitations of the instant application claim 33 based on Gonsky et al (Patent App. Pub. No. WO 2017161342 A1, Sept. 21, 2017).
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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Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. US 11186872 B2 in view of Gonsky et al. (“Gonsky”; Patent App. Pub. WO 2017161342 A1, Sept. 21, 2017. Although the claims at issue are not identical, they are not patentably distinct from each other because the instantly claimed invention is made obvious over the claims of U.S. Patent No. US 11186872 B2 in view of Gonsky.
The claims of U.S. Patent No. US 11186872 B2 are drawn to:
“1. A method of treating Inflammatory Bowel Disease (IBD) in a subject, the method comprising administering a therapeutically effective amount of a therapeutic agent to the subject, provided a single nucleotide polymorphism (SNP) at rs2149092 comprising a “T” at a nucleoposition 501 within SEQ ID NO: 2 is detected in a sample obtained from the subject.”
The teachings of Gonsky are documented above in the rejection of claims 1-4, 6-12 and 17-20 under 35 U.S.C. 103.
Therefore, the invention as recited in claims 1 is prima facie obvious over the U.S. Patent No. US 11186872 B2 in view of Gonsky. One of ordinary skill in the art would have had a reasonable expectation of success given the given the claims of U.S. Patent No. US 11186872 B2 and the teachings of Gonsky It would have been obvious to use a method for a method of treating or preventing a disease or condition of gastrointestinal tissue in a subject comprising administering a therapeutic agent to the subject according to the limitations recited in claim 1 of the instant application based on claim 1 of U.S. Patent No. US 11186872 B2 in view of Gonsky.
This is a nonstatutory double patenting rejection.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. US 12540358 B2 in view of Gonsky et al. (“Gonsky”; Patent App. Pub. WO 2017161342 A1, Sept. 21, 2017. Although the claims at issue are not identical, they are not patentably distinct from each other because the instantly claimed invention is made obvious over the claims of U.S. Patent No. US 12540358 B2 in view of Gonsky.
The claims of U.S. Patent No. US 12540358 B2 are drawn to:
“1. A method of treating or preventing an inflammatory bowel disease (IBD) in a subject, the method comprising administering a therapeutic agent comprising an anti-Tumor Necrosis Factor Ligand 1 (TL1A) antibody comprising a means for binding TL1A or an anti-Death Receptor 3 (DR3) antibody comprising a means for binding DR3 to the subject, provided a genotype comprising an indel at rs16900967 is detected in a sample obtained from the subject.”
The teachings of Gonsky are documented above in the rejection of claims 1-4, 6-12 and 17-20 under 35 U.S.C. 103.
Therefore, the invention as recited in claims 1 is prima facie obvious over the U.S. Patent No. US 12540358 B2 in view of Gonsky. One of ordinary skill in the art would have had a reasonable expectation of success given the given the claims of U.S. Patent No. US 12540358 B2 and the teachings of Gonsky. It would have been obvious to use a method for a method of treating or preventing a disease or condition of gastrointestinal tissue in a subject comprising administering a therapeutic agent to the subject according to the limitations recited in claim 1 of the instant application based on claim 1 of U.S. Patent No. US 12540358 B2 in view of Gonsky.
This is a nonstatutory double patenting rejection.
Conclusion
No claims are in condition for allowance.
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/KENDRA R VANN-OJUEKAIYE/Examiner, Art Unit 1682
/WU CHENG W SHEN/Supervisory Patent Examiner, Art Unit 1682
