Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 01/12/2026 has been acknowledged.
Applicant's amendment and response filed on 11/21/2025 has been received and entered into the case.
Amendments
In the reply filed 11/21/2025, Applicant has amended claim 25.
Claim Status
Claims 25, 30-31 and 87-93, 95-96 and 101-108 are pending.
Claims 90, 95-96, 101 and 105-106 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to non-elected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 08/21/2023 and during a telephonic interview on 10/20/2023.
Claims 25, 30-31, 87-89, 91-93, 102-104 and 107-108 are considered on the merits.
New 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 25, 30-31, 87-89, 91-93, 102-104 and 107-108 are rejected under 35 U.S.C. 101 because the claimed invention is not directed to patent eligible subject matter. Based upon an analysis with respect to the claim as a whole, the claims listed above do not recite something significantly different than a judicial exception. Judicial exceptions include abstract ideas, laws of nature/natural principles, natural phenomena, and natural products. As described in MPEP § 2106, in addition to the terms laws of nature, physical phenomena, and abstract ideas, judicial exceptions have been described using various other terms, including natural phenomena, products of nature, natural products, naturally occurring things, scientific principles, systems that depend on human intelligence alone, disembodied concepts, mental processes and disembodied mathematical algorithms and formulas, for example. The exceptions reflect the judicial view that these fundamental tools of scientific and technological work are not patentable.
The claimed invention is not patent eligible since each claim, as a whole, does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the claims relate to a decision tree required by the claimed invention both before and after administering a cardiomyopathy therapy that involve steps that may be performed mentally and that do not add significantly more to the claimed invention.
Specifically, the amended independent claim 25 recites a step of “detecting in a subject a population of activated cardiac fibroblasts having a genetic signature comprising increased expression, relative to a normal subject or a population of normal subjects, of FAM155A, TSHZ2, COL22A1, POSTN and THBS4”, and claims 102-103 recite administering an agent capable of modulating the genetic signature, the modulating comprising increasing or decreasing the expression of one or more gene products of the genetic signature. It is noted that the step of detecting a population of activated cardiac fibroblasts having the genetic signature implicitly comprises a step of comparing the expression of gene products in the sample relative to a normal control, and a step of determining the presence of a population of activated cardiac fibroblasts having the genetic signature comprising increased expression of the gene products, as well as a step of comparing the expression after administration relative to that before administration of the agent. These steps of comparing and determining may be performed mentally.
This conclusion was reached by following the procedure set forth in an official guidance memorandum issued on March 4, 2014 by Andrew Hirshfeld, Deputy Commissioner for Patent Examination Policy, entitled “Guidance For Determining Subject Matter Eligibility Of Claims Reciting Or Involving Laws of Nature, Natural Phenomena, & Natural Products” (hereinafter “guidance”; available at http://www.uspto.gov/patents/law/exam/myriad-mayo_guidance.pdf).
To expound upon the above, the decision in Alice Corp. v. CLS Bank made clear that it applies the framework set forth in Mayo Collaborative Services v. Prometheus Laboratories, Inc., 566 U.S. (2012) (Mayo) to analyze all claims directed to laws of nature, natural phenomena and abstract ideas for subject matter eligibility under 35 USC 101 (also see reasoning set forth below regarding natural principals). The instructions in Alice indicate the following:
1) The same analysis should be used for all types of judicial exceptions, whereas prior USPTO guidance applied a different analysis to abstract ideas (Bilski guidance in MPEP at 2106 (II)(B)) than to claims with laws of nature (Mayo guidance in MPEP 2106.01).
2) The same analysis should be used for all categories of claims (e.g., product and process claims) where prior guidance applied a different analysis to process claims (Bilski guidance).
The basic inquiries remain the same, however, as explained in MPEP 2106(I). With regard to that, and analyzing the instant claims herein, the first question to ask is do the claims fall into one of the four categories of invention (i.e., step 1)? The answer here is “yes”. The claims are drawn to a process.
The next question relates to whether the claimed invention is directed to a law of nature, a natural phenomenon, or an abstract idea (i.e. step 2A prong one)? The invention as presently claimed is directed to a judicial exception, since, as stated supra, the claimed invention requires the act of comparing the expression of gene products between samples and determining the presence of a population of activated cardiac fibroblasts having increased expression of the gene products. Each of these steps can be performed mentally, and are thus considered abstract ideas. Furthermore, the steps of comparing and determining to identify a correlation between the presence of activated cardiac fibroblasts and cardiomyopathy are considered being directed to a law of nature. The answer to step 2A prong one is thus “yes”.
Proceeding to step 2A prone two of the analysis becomes important to determine whether the claims recite additional elements that integrate the judicial exception into a practical application. Although the claims recite an additional element of administering a cardiomyopathy therapy to the subject based on the steps directed to judicial exceptions, the steps directed to judicial exceptions, i.e., comparing and determining the presence of a population of activated cardiac fibroblasts in a subject, are merely directed to the diagnosis of cardiomyopathy in the subject, but do not provide improvement to a method of cardiomyopathy therapy in any aspect, e.g., providing new therapeutic targets or having improved efficacy. Furthermore, the administering step is cited at a high level that comprises “exercise, surgery, use of a medical device, and/or pharmacological intervention”, but does not require application of such a therapy in a specific way. The answer to step 2A prong two is thus “no”.
Turning to step 2B, the claims as a whole do not amount to significantly more than the abstract ideas or identifying a law of nature since they do not comprise an improvement to an technology or field, or a computer, or effect a transformation of a particular article to a different state or thing or add significantly specific limitations to the abstract ideas or a law of nature other than what is well understood, routine and conventional in the field. It is well established that the mere physical or tangible nature of additional elements such as the obtaining or detecting step does not automatically confer eligibility on a claim directed to an abstract idea (see, e.g., Alice Corp. v. CLS Bank Int’l, 134 S.Ct. 2347, 2358-59 (2014)). The claimed invention is thus drawn to abstract ideas (that cannot confer patent eligibility as discussed above), and a step of administering a cardiomyopathy therapy to the subject after detecting a population of activated cardiac fibroblasts having the genetic signatures.
Here however, the step of administering a cardiomyopathy therapy, cannot be relied upon to confer eligibility. This is because that this element does not add significantly specific limitations to the judicial exceptions other than what is well understood, routine and conventional in the field. This is particularly true as the “administering a cardiomyopathy therapy to the subject” step is recited at a high level, e.g., comprising “exercise, surgery, use of a medical device, and/or pharmacological intervention”, thus encompassing all the therapies that are well understood, routine and conventional in the field. Accordingly, the claims encompass methods that do not apply the abstract idea or a law of nature in a meaningful or specific way so as to render the claims practically applied. The answer to question 2B above is thus “no”.
In light of the above considerations and cited guidance, the claims are thus drawn to patent ineligible subject matter and are rejected therefore.
Withdrawn Claim Rejections - 35 USC § 103
The prior rejection of claims 25, 30-31, 87-89, 91-93, 102-104 and 107-108 under 35 U.S.C. 103 set forth in the prior Office action mailed on 08/21/2025 has been withdrawn in light of Applicant’s amendment to claim 25 to recite new limitation of detecting in a subject a population of activated cardiac fibroblasts having a genetic signature comprising increased expression, relative to a normal subject or a population of normal subjects, of FAM155A, TSHZ2, COL22A1, POSTN and THBS4.
New Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 25, 30-31, 87-89, 91-93, 102-104 and 107-108 are rejected under 35 U.S.C. 103 as being unpatentable over Jin et al., (Circulation. 2001;103:736-742. Prior art of record) in view of Daseke et al (Matrix Biology. 2020; 91-92: 109-116. Prior art of record) and Pfeffer et al., (Am J Physiol. 1991; 260(5 Pt 2):H1406-14. Prior art of record).
With respect to claim 25, Jin teaches a method of identifying cardiac gene expression in a myocardial infarction (MI) model and a step of administering a cardiomyopathy therapy (title, abstract).
Regarding a step of detecting in a subject a population of activated cardiac fibroblasts having a genetic signature comprising increased expression, relative to normal subjects, of a list of gene products including thrombospondin-4 (THBS4), Jin first teaches detecting gene expression in a cardiac tissue by DNA microarray and real-time PCR (abstract, p. 737, left col, last three sections). Jin compares differentially expressed genes between the untreated MI group to a sham control (normal subjects) (e.g., abstract, see Table 2), and teaches the cardiac tissue from the MI group (i.e., with cardiomyopathy) comprises increased expression of thrombospondin-4 and collagen I (Col1a1) compared to control (e.g., abstract, p. 737, left col, last three sections and right col, last section “Effects of MI on Myocardial Gene Expression”, also see Table 2 and Fig 4).
However, Jin is silent on the presence of a population of activated cardiac fibroblasts having a genetic signature in the MI sample.
Daseke teaches cardiac fibroblast activation occurs after myocardial infarction (MI) (see abstract and Fig 1) and teaches activated cardiac fibroblasts are the major players in scar formation following MI (p. 113, “Conclusions” para 1). Daseke teaches collagen I alpha 1 (Col1a1, also taught by Jin) is increased in activated cardiac fibroblasts from day 1 after MI (and sustains to at least 28 days, see Fig 1, also see teaching of secretome analysis at day 7 in infarct cardiac fibroblast culture in p. 113, left col, para 1), thus teaches Col1a1 is a genetic signature for activated cardiac fibroblasts.
Therefore, it would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have appreciated that there would have been a population of activated cardiac fibroblasts, having a genetic signature comprising increased expression of thrombospondin-4 and collagen I (Col1a1), present in the cardiac samples from the MI group in Jin’s method as suggested by Daseke with a reasonable expectation of success, because Jin teaches increased expression of thrombospondin-4 and collagen I (Col1a1) in the cardiac samples provided from the MI group relative to the control (p. 737, last section) and because Daseke teaches cardiac fibroblasts are activated after MI (see abstract and Fig 1) and collagen I alpha 1 (Col1a1) is a genetic signature for activated cardiac fibroblasts after MI (with increased expression from day 1 to at least day 28, see e.g., Fig 1).
Regarding the genetic signature comprising increased expression of FAM155A, TSHZ2, COL22A1, POSTN and thrombospondin-4 (THBS4), as stated supra, the prior art Jin, in view of Daseke, makes it clear that Jin’s cardiomyopathy subjects would have had a population of activated cardiac fibroblasts having the genetic signature comprising increased expression of Col1a1, thrombospondin-4 (THBS4), and periostin (POSTN) (Jin, p. 737, last full para, see Table 2 and Fig 4 for increased Col1a1 and THBS4. Also see Daseke’s teaching of increased Col1a1 (Fig 1 and p. 113, left col, para 1) and periostin (POSTN) in activated cardiac fibroblasts (i.e., contractile fibroblasts, p. 112, right col, para 2)).
However, Jin and Daseke are silent on increased expression of FAM155A, TSHZ2 and COL22A1 in the activated cardiac fibroblasts as instantly claimed.
Nonetheless, Jin teaches increased expression of Col1a1 and thrombospondin-4 (THBS4) in cardiac samples collected 8 weeks after MI (Jin, p. 737, right col, last section “Effects of MI on Myocardial Gene Expression”), and teaches the MI model is produced by left coronary arterial ligation as described previously in Jin’s Reference #6 (Jin, p. 736, last para. It is noted that Jin’s reference #6 is Pfeffer cited herein).
Pfeffer teaches the MI model has significant ventricular dilation (see Pfeffer, Figs 1-2, especially Fig 1B and 2B “moderate” since this is the infarct size used by Jin) from day 7 and later (note that Jin uses a time point of 8 weeks, i.e., day 56). Thus, Pfeffer teaches the cardiomyopathy model produced in Jin has dilated cardiomyopathy.
It is noted that Applicant has identified a population of activated cardiac fibroblasts from 2989 fibroblast nuclei from 12 patients with dilated cardiomyopathy (largely derived from a single DCM patient #P1304, see instant specification, Fig 4A, [0093]), and identified a genetic signature in these activated cardiac fibroblasts comprising upregulation of known markers periostin (POSTN), COL1A1, thrombospondin-4 (THBS4) and COL22A1, as well as previously unreported genes such as FAM155A and TSHZ2 (specification [0093]).
Accordingly, both prior art Jin (in view of Daseke and Pfeffer) and the present Application teach detecting a population of activated cardiac fibroblasts from subjects having dilated cardiomyopathy and both teach this population of activated cardiac fibroblasts has a genetic signature of increased expression of known markers of periostin, COL1A1 and thrombospondin-4. Thus, both prior art and the present Application detect the same type of cells (i.e., a population of activated cardiac fibroblasts) from the same type of subjects (i.e., having the same dilated cardiomyopathy). Therefore, one of ordinary skill in the art would have immediately expected that the same population of activated cardiac fibroblasts from the same dilated cardiomyopathy in the prior art would likely have had the same genetic signature comprising increased expression of FAM155A, TSHZ2, COL22A1, as well as POSTN and THBS4, as instantly claimed, with a reasonable expectation of success.
Additionally, MPEP 2145 (II) states that “mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention”, and “the fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious.” Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985)”. In instant case, the prior art Jin in view of Daseke and Pfeffer suggests a method comprising detecting in a subject with dilated cardiomyopathy a population of activated cardiac fibroblasts having a genetic signature comprising increased expression of COL1A1, POSTN and THBS4 and further administering a cardiomyopathy therapy to the subject. Thus, the fact that applicant has merely recognized other latent properties in the prior art (i.e., the activated cardiac fibroblasts having increased expression of FAM155A, TSHZ2 and COL22A1) does not render nonobvious an otherwise known invention.
Regarding a step of administering a cardiomyopathy therapy to the subject, Jin teaches a subject with cardiomyopathy (a rat MI model) is given a pharmacological intervention of a small molecule ACE inhibitor captopril (p. 736, last para).
With respect to claim 30 directed to the cardiomyopathy therapy comprising pharmacological intervention and claim 31 directed to the therapy comprising use of an ACE inhibitor, as stated supra, Jin teaches a pharmacological intervention is given by administering a small molecule ACE inhibitor captopril (p. 736, last para).
With respect to claim 87 directed to the subject being at risk of having cardiomyopathy, claim 88 directed to the subject having cardiac disease predisposing the subject to cardiomyopathy, and claim 89 directed to the cardiomyopathy being dilated cardiomyopathy, as stated supra, Jin teaches the MI model is produced by left coronary arterial ligation as described previously in Reference #6 (p. 736, last para. The reference #6 is Pfeffer et al.) and teaches the rat model has moderate-sized infarcts (p. 737, Results subsection 1). Pfeffer teaches the MI model has significant ventricular dilation (see Pfeffer, Figs 1-2, especially Fig 1B and 2B “moderate” since this is the infarct size used by Jin) from day 7 and later (note that Jin uses a time point of 8 weeks, i.e., day 56), thus teaches the cardiomyopathy model produced in Jin has dilated cardiomyopathy. Thus, Jin in view of Pfeffer teaches the subject is at risk of having cardiomyopathy (i.e., after MI) in claim 87, and has cardiac disease (i.e., MI) predisposing the subject to cardiomyopathy in claim 88, and the cardiomyopathy is dilated cardiomyopathy in claim 89.
With respect to claim 91 directed to the genetic signature further comprising increased expression of additional gene product, claims 92-93 directed to additional gene product being COL1A1, and claim 104 directed to the genetic signature further comprising increased expression of COL1A1, as stated supra, Jin teaches expression of Collagen I (Accession number Z78279, which is rat Col1a1) is increased (see Table 2 and Fig 4). Regarding the increased Col1a1 being a genetic signature for activated cardiac fibroblasts, as stated supra, Daseke teaches collagen I alpha 1 (Col1a1) is increased in activated cardiac fibroblasts from day 1 after MI (and sustains to at least 28 days, see Fig 1, also see teaching of secretome analysis at day 7 in infarct cardiac fibroblast culture in p. 113, left col, para 1), thus teaches Col1a1 is a genetic signature for activated cardiac fibroblasts.
With respect to claim 102 directed to the therapy comprising a therapeutically effective amount of an agent capable of modulating the genetic signature and claim 103 directed to the modulating the genetic signature comprising decreasing the expression of a gene product of the genetic signature, as stated supra, Jin teaches the treatment comprises an ACE inhibitor captopril and teaches treatment decreases the expression of thrombospondin-4 (p. 741, right col, 1st full para, see Table 2), thus teaches the treatment comprises a therapeutically effective amount of an agent (i.e., captopril) that is capable of decreasing the expression of thrombospondin-4.
With respect to claim 107 directed to the agent being a small molecule and claim 108 directed to the agent being a small molecule ACE inhibitor, as stated supra, Jin teaches the therapeutic agent is a small molecule ACE inhibitor captopril (p. 736, last para).
Hence, the claimed invention as a whole was prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention in the absence of evidence to the contrary.
Response to Traversal:
Applicant’s arguments filed on 11/21/2025 are acknowledged.
Applicant argues that Examiner has not provided any rationale or evidence to support that the activated cardiac fibroblast populations disclosed in Jin and Daseke necessarily have the genetic signature recited in claim 25. In the present Application, a cluster of activated cardiac fibroblasts having the genetic signature recited in claim 25 has been found in 2989 DCM patients (that in fact being 2989 cell nuclei from 12 patients with dilated cardiomyopathy and largely derived from a single DCM patient #P1304, see Fig 4A. Added and emphasized by examiner). This population of activated cardiac fibroblasts is highly specific for identifying individuals with cardiomyopathy, and in particular, the upregulation of FAM155A and TSHZ2 is not known to be associated with cardiomyopathy prior to the filing of the present Application (Remarks, p. 8).
Applicant’s arguments have been fully considered but become moot.
In response to Applicant’s arguments, as a first matter, the prior rejection under 35 U.S.C. 103 set forth in the prior Office action mailed on 08/21/2025 has been withdrawn in light of Applicant’s amendment to claim 25 to recite new limitation of detecting in a subject a population of activated cardiac fibroblasts having a genetic signature comprising increased expression, relative to a normal subject or a population of normal subjects, of FAM155A, TSHZ2, COL22A1, POSTN and THBS4. As necessitated by amendment, new grounds of rejection under 101 and 103 have been made as discussed above.
Specifically, regarding the 101 rejection, the claimed invention requires the act of comparing the expression of gene products between samples and determining the presence of a population of activated cardiac fibroblasts having increased expression of the gene products. Each of these steps can be performed mentally, and are thus considered abstract ideas. Furthermore, the steps of comparing and determining to identify a correlation between the presence of a population of activated cardiac fibroblasts and cardiomyopathy are considered being directed to a law of nature (as supported by Applicant’s argument above that “This population of activated cardiac fibroblasts is highly specific for identifying individuals with cardiomyopathy”).
In regard to the new ground of 103 rejection regarding the upregulation of FAM155A and TSHZ2 in the activated cardiac fibroblasts, it is first noted that the new ground of rejection no longer relies on the rationale that the activated cardiac fibroblasts disclosed in Jin and Daseke necessarily have a genetic signature that includes upregulated expression of FAM155A, TSHZ2, and COL22A1, thus Applicant’s arguments regarding the inherency (Remarks, p. 8-9) become moot.
Furthermore, as stated supra, Pfeffer teaches the cardiomyopathy model produced in Jin has dilated cardiomyopathy. It is noted that Applicant has identified a population of activated cardiac fibroblasts from 12 patients with dilated cardiomyopathy (largely derived from a single DCM patient #P1304, see instant specification, Fig 4A, [0093]), and identified a genetic signature in these activated cardiac fibroblasts comprising upregulation of known markers periostin (POSTN), COL1A1, thrombospondin-4 (THBS4) and COL22A1, as well as previously unreported genes such as FAM155A and TSHZ2 (specification [0093]).
Accordingly, both prior art and the present Application detect the same type of cells (i.e., a population of activated cardiac fibroblasts) from the same type of subjects (i.e., having the same dilated cardiomyopathy). Therefore, one of ordinary skill in the art would have immediately expected that the same population of activated cardiac fibroblasts from the same dilated cardiomyopathy in the prior art would likely have had the same genetic signature comprising increased expression of FAM155A, TSHZ2, COL22A1, as well as POSTN and THBS4, as instantly claimed, with a reasonable expectation of success.
Additionally, MPEP 2145 (II) states that “mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention”, and “the fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious.” Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985)”. In instant case, the prior art Jin in view of Daseke and Pfeffer suggests a method comprising detecting in a subject with dilated cardiomyopathy a population of activated cardiac fibroblasts having a genetic signature comprising increased expression of COL1A1, POSTN and THBS4 and further administering a cardiomyopathy therapy to the subject. Thus, the fact that applicant has merely recognized other latent properties in the prior art (i.e., the activated cardiac fibroblasts having increased expression of FAM155A, TSHZ2 and COL22A1) does not render nonobvious an otherwise known invention as suggested by Jin in view of Daseke and Pfeffer.
Applicant further argues that the activated cardiac fibroblasts may have more than a single genetic signature because Daseke shows 13 different genes that may or may not be upregulated in different populations of activated cardiac fibroblasts depending on the timing point at which gene expression was assessed (Remarks, p. 8).
Applicant’s arguments have been fully considered but they are not persuasive.
As stated supra, Jin teaches increased expression of thrombospondin-4 and collagen I (Col1a1) in the cardiac samples provided from the MI group (8 weeks after MI) relative to the control (p. 737, last section, see Table 2 and Fig 4), and Daseke teaches cardiac fibroblasts are activated after MI (see abstract and Fig 1) and collagen I alpha 1 (Col1a1) is a genetic signature for activated cardiac fibroblasts after MI (with sustained increased expression from day 1 to at least day 28, see e.g., Fig 1) and periostin (POSTN) expression is increased in activated cardiac fibroblasts (i.e., contractile fibroblasts in the infarct region of MI to maintain structural integrity during the process of scar formation, p. 112, right col, para 2).
Accordingly, one of ordinary skill in the art would have appreciated that Jin’s cardiac samples from MI group would have comprised a population of activated cardiac fibroblasts, and the increased expression of thrombospondin-4 and Col1a1 in the MI samples would have been due to the sustained increased expression of the genes from the activated cardiac fibroblasts present in the samples as suggested by Daseke. Applicant’s argument that Daseke shows 13 different genes that may not be upregulated depending on the timing points (it is noted that none of these genes is recited by Jin or instant claim 25 except Col1a1), does not negate the teaching of Daseke that Col1a1 is a genetic signature for a population of activated cardiac fibroblasts after MI that has sustained increased expression of Col1a1 from day 1 to at least day 28 (see e.g., Fig 1).
Conclusion
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Jianjian Zhu whose telephone number is (571)272-0956. The examiner can normally be reached M - F 8:30AM - 4PM (EST).
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James Douglas (Doug) Schultz can be reached on (571) 272-0763. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/JIANJIAN ZHU/Examiner, Art Unit 1631
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