DETAILED ACTION
Claims 1-12 are pending.
Information Disclosure Statement
The information disclosure statement (IDS) filed on 05/03/2024 has been considered by the examiner.
Priority
Should applicant desire to obtain the benefit of foreign priority under 35 U.S.C. 119(a)-(d) prior to declaration of an interference, a certified English translation of the foreign application must be submitted in reply to this action. 37 CFR 41.154(b) and 41.202(e).
Failure to provide a certified translation may result in no benefit being accorded for the non-English application.
Claim Objections
1.Claims 2, 7, and 11 are objected to because of the following informalities: Claims 2, 7, and 11 recite the abbreviation and/or acronym of “SNM” which should be spelled out at their first usage followed by the abbreviation/acronym in parenthesis. Appropriate correction is required.
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.
2.Claims 1-8 are rejected under 35 U.S.C. 101 because the claimed method is directed to a judicial exception (i.e., a law of nature, a natural phenomenon, or an abstract idea) without significantly more. The judicial exception is not integrated into a practical application and the claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception.
Step 1
This part of the eligibility analysis evaluates whether the claim falls within any statutory
category per MPEP 2106.03
Regarding instant claims 1-8, Example 43 of “2019 PEG” is particularly enlightening because the fact pattern of claim 1 of example 43 is most similar to the instant application claims 1-8.
Regarding claim 1 of example 43 of the “2019 PEG” and per Step 1, the claim is
directed to a process, which is one of the statutory categories of invention as the claim recites
“A treatment method comprising: (a) calculating a ratio of C11 to C13 levels measured in a
blood sample from a patient diagnosed with Nephritic Autoimmune Syndrome Type 3 (NAS-3)
to identify the patient as having a non-responder phenotype; (b) administering a treatment to the
patient having a non-responder phenotype.” (Step 1: YES).
Similarly, instant claims 1-8 are directed to a statutory method that measures naturally occurring component proteins of survival motor neuron complex or an antigenic partial peptide thereof and correlating the levels or presence of the complex or peptide to the severity and prognosis of a patient with mixed connective tissue disease (step 1: YES).
Step 2A, Prong 1: Does the claim recite a judicial exception?
This part of the eligibility analysis evaluates whether the claim recites a judicial exception. As explained in MPEP 2106.04(II) and the October 2019 Update, a claim “recites” a
judicial exception when the judicial exception is “set forth” or “described” in the claim.
Regarding instant claims 1-8, Example 43 of the “2019 PEG” shows a similar fact
pattern.
Regarding claim 1 in Example 43 of the “2019 PEG” and per Step 2A, prong 1, the claim
recites the judicial exception of “calculating a ratio of C11 to C13 levels measured in a blood
sample from a patient diagnosed with Nephritic Autoimmune Syndrome Type 3 (NAS-3)
to identify the patient as having a non-responder phenotype,” and according to broadest
reasonable interpretation (BRI), an arithmetic calculation of a division is required to obtain the
ratio of C11 to C13 that can be used to identify whether the patient has the non-respondent
phenotype.
Specifically, limitation (a) in claim 1 of Example 43 of the “2019 PEG” recites “calculating
a ratio of C11 to C13 levels measured in a blood sample from a patient diagnosed with Nephritic
Autoimmune Syndrome Type 3 (NAS-3) to identify the patient as having a non-responder
phenotype,” which has a BRI that requires performing an arithmetic calculation (division) in
order to obtain the ratio of C11 to C13 levels, and then using this ratio to identify whether thepatient has the non-responder phenotype (i.e., the patient has a calculated ratio of 3:1 or
greater and thus is not responding, or will not respond, to glucocorticoids). This limitation
therefore recites a mathematical calculation. The grouping of “mathematical concepts” in the
2019 PEG includes “mathematical calculations” as an exemplar of an abstract idea. 2019 PEG
Section I, 84 Fed. Reg. at 52. Thus, limitation (a) falls into the “mathematical concept” grouping
of abstract ideas. In addition, this type of simple arithmetic calculation (division) can be
practically performed in the human mind, and is in fact performed in the human mind on a daily
basis, for instance by school-aged children studying mathematics. Note that even if most
humans would use a physical aid (e.g., pen and paper, a slide rule, or a calculator) to help them
complete the recited calculation, the use of such physical aid does not negate the mental nature
of this limitation. Thus, limitation (a) also falls into the “mental process” groupings of abstract
ideas.
In addition, limitation (a) describes a naturally occurring relationship between the ratio
of C11 to C13 and the non-responder phenotype, and thus may also be considered to recite a
law of nature. Accordingly, limitation (a) recites a judicial exception (an abstract idea that falls
within the mathematical concept and mental process groupings in the “2019 PEG”, and a law of
nature), and the analysis must therefore proceed to Step 2A Prong Two.
Similarly, instant claims 1-8 recite a method that measures naturally occurring component proteins of survival motor neuron complex or an antigenic partial peptide thereof and correlating the levels or presence of the complex or peptide to the severity and prognosis of a patient with mixed connective tissue disease, and thus is considered a law of nature.
Accordingly, instant claims 1-8 recites a judicial exception (a law of nature) and the analysis must therefore proceed to Step 2A Prong Two.
Step 2A Prong 2: Does the claim recite additional elements that integrate the exception into a practical application?
Regarding instant claims 1-8, Example 43 of “2019 PEG” shows a similar fact pattern.
In claim 1 of example 43 of the “2019 PEG” and per Step 2A, prong 2, the claim as a
whole does not integrate the recited judicial exception into a practical application of the
exception. This evaluation is performed by (a) identifying whether there are any additional
elements recited in the claim beyond the judicial exception, and (b) evaluating those additional
elements individually and in combination to determine whether the claim as a whole integrates
the exception into a practical application. Besides the abstract idea, the claim 1 of example 43
of the “2019 PEG” recites the additional element of “(b) administering a treatment to the patient
having a non-responder phenotype”. Although this limitation indicates that a treatment is to be
administered, it does not provide any information as to how the patient is to be treated, or what
the treatment is, but instead covers any possible treatment that a doctor decides to administer
to the patient. In fact, this limitation is recited at such a high level of generality that it does not
even require a doctor to take the calculation step’s outcome (the patient’s phenotype) into
account when deciding which treatment to administer, making the limitation’s inclusion in this
claim at best nominal. Thus, limitation (b) of example 43 of the “2019 PEG” fails to
meaningfully limit the claim because it does not require any particular application of the recited
calculation, and is at best the equivalent of merely adding the words “apply it” to the judicial
exception. Accordingly, limitation (b) of example 43 of the “2019 PEG” does not integrate the
recited judicial exception into a practical application and the claim is therefore directed to the
judicial exception.
Similarly, instant claims 1-8 do not have additional elements that would integrate the
judicial exception cited above into a practical application. In comparison to claim 43, Example
43 did not pass step 2A prong 2 with step of general treatment. Instant claims 1-8 do not even recite a general treatment.
Therefore, instant claims 1-8 do not integrate the judicial exception into a practical application.
Step 2B: Does the claim recite significantly more?
Regarding instant claims 1-8, this part of the eligibility analysis evaluates whether the claim as a whole amounts to significantly more than the recited exception, i.e., whether any additional element, or combination of additional elements, adds an inventive concept to the
claim. MPEP 2106.05. As explained with respect to Step 2A Prong Two, the claim does not recite any active steps.
Instant claims 1-8 recite “1) a step of bringing a biological sample separated from a patient with mixed connective tissue disease into contact with a carrier in which an antigen containing one or more of component proteins of survival motor neuron complex or an antigenic partial peptide thereof is immobilized on a solid phase to form a complex of an autoantibody in the biological sample and the antigen immobilized on the solid phase, 2) a step of detecting the autoantibody in the complex of the autoantibody and the immobilized antigen, and 3) a step of associating the patient with a severe mixed connective tissue disease when the autoantibody is detected from the biological sample separated from the patient in step 2)”, which are just the steps for determining the natural correlation and is thus directed to a law of nature.
Instant claims 3 and 8 recites “wherein the detection of the autoantibody is performed by bringing an anti-human IgG antibody or a functional binding fragment thereof into contact with the complex of the autoantibody and the immobilized antigen”, which are just steps for determining the natural correlation, and is thus directed to a law of nature.
Accordingly, instant claims 1-8 are not eligible (Step 2B: NO).
Thus, instant claims 1-8 are rejected under 35 USC 101.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
3.Claim(s) 1-2, 5, and 9-11 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Satoh et al., Autoantibodies to survival of motor neuron complex in patients with polymyositis: immunoprecipitation of D, E, F, and G proteins without other components of small nuclear ribonucleoproteins. Arthritis Rheum. 2011 Jul;63(7):1972-8. doi: 10.1002/art.30349. PMID: 21425128; PMCID: PMC3123691 (IDS filed on 05/03/2024).
Satoh teaches a method for evaluating severity of a patient with mixed connective tissue disease, which comprises
1) a step of bringing a biological sample separated from a patient with mixed connective tissue disease into contact with a carrier in which an antigen containing SMN, Gemin 3, Gemin 4 and/or Gemin 5 (see page 1973 under “Immunoprecipitation” and “Affinity purify ation of SMN complex and Western blotting” and “Analysis of immunofluorescent antinuclear antibodies”, see figure 1 showing the measurement of SMN, Gemin 3, and Gemin 4) (instant claims 2 and 11) is immobilized on a solid phase to form a complex of an autoantibody in the biological sample and the antigen immobilized on the solid phase (see page 1974 under “immunofluorescence staining of anti-SMN-positive sera, see figures 1- 2),
2) a step of detecting the autoantibody in the complex of the autoantibody and the immobilized antigen (see figure 1, see page 1974 under “Identification of RNA components of immuno-precipitated autoantigens” and “immunofluorescence staining of anti-SMN-positive sera”), and
3) a step of associating the patient with a severe mixed connective tissue disease when the autoantibody is detected from the biological sample separated from the patient in step 2) (see abstract “Methods. Autoantibodies in sera from 1,966 American patients (including 434 with systemic lupus erythematosus, 121 with scleroderma, 86 with polymyositis/ dermatomyositis [PM/DM]) and 248 Italian patients with autoimmune diseases were screened by immunoprecipitation of 35S-methionine–labeled cell extracts. Sera with which D, E, F, and G proteins of snRNP was immunoprecipitated, but without the other snRNP proteins, were further examined by analysis of RNA components by immunoprecipitation (silver staining), Western blotting using survival of motor neuron (SMN) complex, and immunofluorescence.”, see page 1977 “In summary, we have identified SMN complex as a new multiprotein complex autoantigen in Cajal bodies and in the cytoplasm of patients with PM”) (instant claims 1 and 9-10). Satoh teaches treating the patient who is positive for autoantibodies against SMN with a glucocorticoid (see page 1975 under “Clinical manifestations of patients with anti-SMN complex antibodies”, see table 1 where PSL stands for prednisolone which is a known glucocorticoid. Table 1 shows the patients receiving 60-80 mg/day for prednisolone) (instant claim 9).
Satoh teaches the severe mixed connective tissue disease is accompanied by all of the idiopathic inflammatory myopathy-like clinical symptoms ((the instant specification teaches on page 15 that idiopathic inflammatory myopathy-like symptoms are muscle weakness, high levels of serum creatine kinase (CK), and myogenic abnormalities on electromyogram and systemic sclerosis like clinical symptoms being skin hardening, interstitial lung disease, high level of KL-6, or the like), see abstract teaching polymyositis and systemic sclerosis, see table 1 teaching the clinical disease features of symmetric muscle weakness, muscle biopsy findings, elevated muscle enzymes, EMG findings, dermatologic findings, interstitial lung disease, esophageal hypermotility, Raynaud’s phenomenon, Sclerodactyly, pitting scars, arthritis, and CPK levels) (instant claim 5).
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
4.Claims 3-4 and 12 are rejected under 35 U.S.C. 103 as being unpatentable over Satoh as applied to claims 1-2, 5, and 9-11 above, in view of Takeshita et al., Antigen-driven autoantibody production in lungs of interstitial lung disease with autoimmune disease. J Autoimmun. 2021;121:102661. doi:10.1016/j.jaut.2021.10266.
The teachings of Satoh as it pertains to claims 1-2, 5, and 9-11 are discussed in the 35 USC 102 rejection above.
Satoh does not each the use of anti-human IgG. Satoh does not explicitly teach the mixed connective tissue disease is being complicated by interstitial lung disease.
Takeshita teaches wherein the detection of the autoantibody is performed by bringing an anti-human IgG antibody or a functional binding fragment thereof into contact with the complex of the autoantibody and the immobilized antigen (see page 3 under “ELISA”) (instant claims 3 and 12). Takeshita teaches the mixed connective tissue disease is complicated by interstitial lung disease (see abstract) (instant claim 4).
It would have been obvious to one of ordinary skill in the art at the time of the instant application to combine the teachings of measuring SMN, Gemin 3, and Gemin 4 in order to evaluate a patient with a mixed connective tissue disease taught by Satoh, with the teachings of using an anti-human IgG antibody and the connection of interstitial lung disease and a mixed connective tissue disease taught by Takeshita. Takeshita provides motivation by teaching that IgG has more somatic hypermutations than IgM and that silent and nonsilent mutations were significantly more frequent in IgG autoantibodies (see page 9 under “3.4. Characteristics of the sequences of autoantibodies”). Takeshita teaches that IgG autoantibodies are found in the lungs and were produced in an antigen-driven manner (see page 9). Takeshita provides motivation by teaching connective tissue disease with interstitial lung disease is caused by an autoimmune reaction in the lungs (see page 2, see page 7). The artisan would have reasonable expectation of success based on the cumulative disclosures of these prior art references.
5.Claims 1-2 and 4-7 are rejected under 35 U.S.C. 103 as being unpatentable over El Kamouni et al. Anti-SMN autoantibodies in mixed connective tissue disease are associated with a severe systemic sclerosis phenotype. RMD Open. 2023;9:e003431 https://doi.org/10.1136/rmdopen-2023-003431, in view of Clark et al., ELISA techniques, Methods in Enzymology, Academic Press, Volume 118, 1986, Pages 742-766, ISSN 0076-6879, ISBN 9780121820183, https://doi.org/10.1016/0076-6879(86)18114-6 (1986).
Kamouni teaches a method for evaluating prognosis and severity of a patient with mixed connective tissue disease, which comprises measuring SMN (see abstract, see page 1 “autoantibodies (aAbs) to the SMN complex as novel biomarkers in patients with systemic sclerosis (SSc) and myositis”) (instant claims 2 and 7) in a biological sample from a patient with mixed connective tissue disease (see page 2 “The aim of this study was therefore to evaluate the prevalence of anti-SMN aAbs in MCTD patients, and to compare phenotypic features in patients with and without anti-SMN aAbs”, see page 2 under “Anti-SMN aAbs in MCTD are associated with a severe systemic sclerosis phenotype”, see abstract) (instant claims 1 and 6). Kamouni teaches an autoantibody complex (see abstract, see page 1) and detecting the autoantibody in a complex of autoantibody and an antigen (see page 2 under “Serology”), and associating the levels of SMN with patient prognosis (see page 3 “aAbs encountered in patients with autoimmune diseases are useful biomarkers to help or predict diagnosis, clinical phenotype, prognosis and treatment decision-making”, see page 5 “Since myocarditis and lower GI involvement increase morbidity and mortality in SSc patients17–19, anti-SMN aAbs may therefore identify a subset of MCTD patients with a poorer prognosis with important implications for clinical management and therapeutic strategies”) (instant claims 1 and 6). Kamouni teaches the mixed connective tissue disease is complicated by pulmonary arterial hypertension and/or interstitial lung disease (see table 1 teaching patients with pulmonary arterial hypertension and/or interstitial lung disease) (instant claim 4). Kamouni teaches the mixed connective tissue disease is accompanied by all the idiopathic inflammatory myopathy-like clinical symptoms ((the instant specification teaches on page 15 that idiopathic inflammatory myopathy-like symptoms are muscle weakness, high levels of serum creatine kinase (CK), and myogenic abnormalities on electromyogram), See page 2 under “Study variables”, see table 1)) (instant claim 5).
Kamouni does not explicitly teach bringing the biological sample from a patient with mixed connective tissue disease into contact with a carrier in which an antigen containing SMN is immobilized on a solid phase to form a complex immobilized on the solid phase.
Clark teaches enzyme linked immunosorbent assay (ELISA) methods that consists of an antigen that is immobilized on a solid phase and an antibody (see page 744 “ELISA procedures used in plant virology are either "direct," in which antigen immobilized on a solid phase is detected directly with labeled specific antibody”, see page 758 under “protocol N. Rapid ELISA Using Direct Absorption of Antigen to the Solid Phased (Antigen Coating)”) (instant claims 1 and 6).
It would have been obvious to one of ordinary skill in the art at the time of the instant application to combine the methods of SMN detection in patients with mixed connective tissue diseases of Kamouni with the ELISA methods taught by Clark. One of ordinary skill in the art would have been motivated to use the ELISA assay to detect the biomarkers taught by Kamouni as it is a common technique in the art. Clark provides motivation for using an ELISA assay by teaching that the advantages of an ELISA include high sensitivity, speed, scale, versatility, specificity, low cost, long shelf life of reagents, and simplicity of basic equipment (see page 743). Clark further provides motivation by teaching that these advantages have encouraged widespread acceptance and use of ELISA methodology (see page 743). The artisan would have reasonable expectation of success based on the cumulative disclosures of these prior art references.
6. Claims 3 and 8-12 are rejected under 35 U.S.C. 103 as being unpatentable over Clark and Kamouni as applied to claims 1-2 and 4-7 above, in view of Takeshita et al., Antigen-driven autoantibody production in lungs of interstitial lung disease with autoimmune disease. J Autoimmun. 2021;121:102661. doi:10.1016/j.jaut.2021.10266.
The teachings of Clark and Kamouni as it pertains to claims 1-2 and 4-7 are discussed in the 35 USC 103 rejection above.
Kamouni teaches detecting an SMN autoantibody in a biological sample separated from a patient with MCTD (see abstract, see page 1 “autoantibodies (aAbs) to the SMN complex as novel biomarkers in patients with systemic sclerosis (SSc) and myositis”, see page 2 “The aim of this study was therefore to evaluate the prevalence of anti-SMN aAbs in MCTD patients, and to compare phenotypic features in patients with and without anti-SMN aAbs”, see page 2 under “Anti-SMN aAbs in MCTD are associated with a severe systemic sclerosis phenotype”) (instant claims 9 and 11). Kamouni teaches detecting the autoantibody in a complex of autoantibody and an antigen (see page 2 under “Serology”), and associating the levels of SMN with patient prognosis (see page 3 “aAbs encountered in patients with autoimmune diseases are useful biomarkers to help or predict diagnosis, clinical phenotype, prognosis and treatment decision-making”, see page 5 “Since myocarditis and lower GI involvement increase morbidity and mortality in SSc patients17–19, anti-SMN aAbs may therefore identify a subset of MCTD patients with a poorer prognosis with important implications for clinical management and therapeutic strategies”) (instant claim 10).
Kamouni does not teach treating the patient who is positive for autoantigens with a glucocorticoid. Kamouni does not explicitly teach bringing the biological sample from a patient with mixed connective tissue disease into contact with a carrier in which an antigen containing SMN is immobilized on a solid phase to form a complex immobilized on the solid phase. Kamouni does not teach the use of anti-human IgG.
Clark teaches enzyme linked immunosorbent assay (ELISA) methods that consists of an antigen that is immobilized on a solid phase and an antibody (see page 744 “ELISA procedures used in plant virology are either "direct," in which antigen immobilized on a solid phase is detected directly with labeled specific antibody”, see page 758 under “protocol N. Rapid ELISA Using Direct Absorption of Antigen to the Solid Phased (Antigen Coating)”) (instant claim 10).
Clark does not teach the use of anti-human IgG, nor treating the patient who is positive for autoantigens with a glucocorticoid.
Takeshita teaches wherein the detection of the autoantibody is performed by bringing an anti-human IgG antibody or a functional binding fragment thereof into contact with the complex of the autoantibody and the immobilized antigen (see page 3 under “ELISA”) (instant claims 3, 8, and 12). Takeshita teaches treating patients who is positive for the SMN autoantibodies with a glucocorticoid (see table 1 where PSL is prednisolone, which is a known glucocorticoid) (instant claim 9).
It would have been obvious to one of ordinary skill in the art at the time of the instant application to combine the methods of SMN detection in patients with mixed connective tissue diseases of Kamouni with the ELISA methods taught by Clark, with the methods of using anti-human IgG antibodies to contact the complex autoantibody and the immobilized antigen taught by Takeshita. Clark provides motivation for using an ELISA assay by teaching that the advantages of an ELISA include high sensitivity, speed, scale, versatility, specificity, low cost, long shelf life of reagents, and simplicity of basic equipment (see page 743). Clark further provides motivation by teaching that these advantages have encouraged widespread acceptance and use of ELISA methodology (see page 743). Takeshita provides motivation by teaching that there is a connection between anti-human IgG, mixed connective tissue disease, and interstitial lung disease by teaching that IgG autoantibodies are found in the lungs (see page 9). Takeshita provides further motivation by teaching that connective tissue disease with interstitial lung disease is caused by an autoimmune reaction in the lungs (see page 2, see page 7). The artisan would have reasonable expectation of success based on the cumulative disclosures of these prior art references.
Conclusion
No claim is allowed.
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/MCKENZIE A DUNN/Examiner, Art Unit 1678
/GREGORY S EMCH/Supervisory Patent Examiner, Art Unit 1678
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