DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Preliminary Remark
Claims 9-12, 24-28, and 30-33 are canceled.
Election/Restrictions
Applicant’s election of Group II in the reply filed on April 9, 2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Claims 1-8, 12, 23, and 29 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on April 9, 2026.
Information Disclosure Statement
The IDS received on May 1, 2024 is proper and is being considered by the Examiner.
Drawings
The replacement drawings received on April 20, 2024 are acceptable.
Specification
Specific deficiency – Nucleotide and/or amino acid sequences appearing in the drawings are not identified by sequence identifiers in accordance with 37 CFR 1.821(d). Sequence identifiers for nucleotide and/or amino acid sequences must appear either in the drawings or in the Brief Description of the Drawings (see Figure 2A, where nucleotide sequence is disclosed without its SEQ ID Number nor described in the Brief Description of Drawings section).
Required response – Applicant must provide:
Replacement and annotated drawings in accordance with 37 CFR 1.121(d) inserting the required sequence identifiers;
AND/OR
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required sequence identifiers into the Brief Description of the Drawings, consisting of:
A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
A copy of the amended specification without markings (clean version); and
A statement that the substitute specification contains no new matter.
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 13-22 are rejected under 35 U.S.C. 101 because the claimed invention is directed to the judicial exception of a naturally existing phenomenon without significantly more. The claims recite a naturally existing correlation that exist between the methylation pattern of a promoter of a DNA and cancer. This judicial exception is not integrated into a practical application because the means of ascertaining the naturally existing correlation from a sample is not meaningfully applied so as to limit this judicial exception, due to the utilization of highly general claim language and steps that have been well-known, routine, and conventionally adopted.
The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exception based on the analysis under the current Patent Eligibility Guidelines (herein, “PEG”) as discussed below.
Step 1 Inquiry under PEG
Step 1 inquiry under Patent Eligibility Guidelines (herein, “PEG”) determines whether or not the claimed invention is drawn to one of the recognized statutory classes of invention. Claims 13-21 satisfy the present inquiry as being drawn to a method.
Step 2A Inquiry under PEG
A recently revised PEG now performs step 2A inquiry under a 2-prong analysis, and the subject claims analyzed accordingly as follows:
Prong 1:
Prong-1 inquiry under step 2A determines whether the claim(s) recites an abstract idea, a law of nature, or a natural phenomenon. As stated above, claims 13-17 are directed to a method of assessing a risk of cancer based on the judicial exception that exists between the methylation pattern of a promoter of a DNA sequence (in CpGs); and claims 18-22 are directed to a method of assessing the likelihood of mortality tied to same methylation pattern.
Prong 2:
Prong-2 inquiry under step 2A determines whether or not the claims recite additional elements that integrate the judicial exception into a practical application in a manner that imposes a meaningful limit on the judicial exception.
The independent claims 13 and 18 recite the additional element of treating a sample of the subject with an agent that differentially affects the methylated vs. non-methylated cytosine, and comparison of the methylation pattern observed in the subject’s sample to a reference methylation pattern observed from a non-cancerous subject.
However, the treatment of the sample with said agent is recited in a highly general nature and does not provide a meaningful limit to the judicial exception other than an extra-solution activity so as to obtain the naturally existing correlation.
As well, claims 13 and 18 also recite the additional step of “comparing” the subject’s sample to a reference data (i.e., methylation pattern), but such comparison step is deemed that which is for the purpose of revealing the naturally existing correlation and therefore is not deemed significantly more than the judicial exception.
Claims 15 and 20 recite that the agent through which the methylated and unmethylated cytosine are distinguished is bisulfite of a methylation-specific enzyme; and claims 16, 17, 21, and 22 recite that the determination of the methylation pattern involves amplification means, such as PCR.
However, these are steps which are not deemed significant for the same reasons discussed above in that the steps are deemed that which are employed to reveal the naturally existing correlation, wherein the steps are conventional in the art.
As stated in MPEP 2106.05(d)(II):
“The courts have recognized that the following laboratory techniques as well-understood, routine, conventional activity in the life science arts when they are claimed in a merely generic manner (e.g., at a high level of generality) or as insignificant extra-solution activity”
The same section discusses that “Determining the level of a biomarker in blood by any means (Mayo, 566, U.S. at 79, 101 USPQ2d at 1968; Cleveland Foundation v. True Health Diagnostics, LLC, 859 F.3d 1352, 1362, 123 USPQ2d 1081, 1088 (Fed. Cir. 2017)” and “Using polymerase chain reaction to amplify and detect DNA, Genetic Techs v. Merial LLC, 818 F.3d 1369, 1376, 118 USPQ2d 1541, 1546 (Fed. Cir. 2016); Ariosa Diagnostics, Inc. v. Sequenom, Inc., 788 F.3d 1371, 1377, 115 USPQ2d 1152, 1157 (Fed. Cir. 2015).
Therefore, the additionally recited elements of the claims do not add more to the recited judicial exception.
As explained by the Supreme Court, in order to transform a judicial exception into a patent-eligible application, the additional element or combination of elements must do ‘more than simply stat[e] the [judicial exception] while adding the words ‘apply it’”. Alice Corp. v. CLS Bank, 573 U.S. __, 134 S. Ct. 2347, 2357, 110 USPQ2d 1976, 1982-83 (2014) (quoting Mayo Collaborative Servs. V. Prometheus Labs., Inc., 566 U.S. 66, 72, 101 USPQ2d 1961, 1965). Thus, for example, claims that amount to nothing more than an instruction to apply the abstract idea using a generic computer do not render an abstract idea eligible. Alice Corp., 134 S. Ct. at 2358, 110 USPQ2d at 1983. See also 134 S. Ct. at 2389, 110 USPQ2d at 1984 (warning against a § 101 analysis that turns on “the draftsman’s art”) (MPEP 2106.05(f))
Step 2B Inquiry under PEG
Step 2B inquiry of the PEG determines whether or not additional elements are provided and whether such elements amount to significantly more than the judicial exception in the claims.
As stated above, the additional elements recited are well-known means of distinguishing between cytosines that are differentially methylated with amplification means that are also conventionally utilized in the field of molecular diagnostics, and therefore, fail to further add more than the judicial exception.
Therefore, these elements are not deemed significantly more than inclusion of that are commonly used, routine and conventional.
Therefore, the present claims lack patent eligibility.
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 13-22 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 13 and 18 makes reference to steps “(1) to (3).” There is an insufficient antecedent basis for these steps. For the purpose of prosecution, the steps have been construed to mean steps (a) to (c) being repeated with a normal/healthy sample.
Claims 14-17 and 19-22 are indefinite by way of their dependency on claims 13 and 18, respectively.
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 13-17 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for the method of assessing risk of cancer, or assessing likelihood of mortality from cancer in patients (as presently claimed), wherein said cancer is colorectal, gastric and nasopharyngeal cancer, does not reasonably provide enablement for any and all types of cancers. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims.
Factors to be considered in determining whether a disclosure would require undue experimentation are summarized in In Re Wands (858 F.2d 731, 8 USPQ2d 1400 (Fed. Cir. 1988)). They include (A) the quantity of experimentation necessary, (B) the amount of direction or guidance presented, (C) the presence or absence of working examples, (D) the nature of the invention, (E) the state of the prior art, (F) the relative skill of those in the art, (G) the predictability or unpredictability of the art, and (H) the breadth of the claims.
Nature of the Invention and Breadth of Claims:
The nature of the invention relates to a gene silencing based on methylation, and its correlation to tumorigenesis. The breadth of claims covers the increased methylation pattern in a sample of a subject found in CpGs of SEQ ID Number 3 (or its fragment), also KIA0495 promoter and its correlation to any cancer.
State of the Prior art & Unpredictability of the Art:
Wong et al. (Molecular Cancer, 2015, vol. 14, pages 1-5) demonstrates the state of prior art, wherein the artisans evidences the practice of studying gene-silencing effects from hypermethylation of genes and correlation to tumorigenesis.
“we have studied and reported methylation of KIAA0495 in myeloma cell-lines, primary myeloma marrow samples at diagnosis, and at relapse/progression”
(page 2, 2nd col, bottom para to page 3, 1st col)
“[n]one of the 14 healthy controls showed KIAA0495 methylation … On the other hand, in myeloma cell lines, KMS-12-PE, LP-1, NCI-H929, OPM-2, and OCI-MY5 were partially methylated … for KIAA0495 … These data suggested that methylation of KIAA0495 was tumour-specific, consistent with other tumour suppressor protein-encoding genes and non-coding miRNAs in myeloma”
(page 3, 2nd col, bottom para to page 4, 1st col, 1st para).
However, not all methylation pattern is of predictive value in a clinical setting as the artisans conclude that while the methylation pattern observance was found in cell-lines, none were actually observed in clinical samples (i.e., primary tumor samples from patients) (Wang et al. below):
“To examine if methylation of KIAA0495 was also detected in primary samples, methylation of KIAA0495 was studied in 61 primary samples at diagnosis and 16 primary samples at relapse by MSP. However, none of these samples showed methylation of KIAA0495 … indicating methylation of KIAA0495 was rarely detected in primary myeloma samples. Hence, similar to the studies of miR-9-1, miR-9-3, and miR-124-1 … these data suggested that methylation of certain tumor suppressor encoding miRNAs or lncRNA was acquired in vitro during continuous culture of myeloma cells, hence not pathogenic. Therefore, methylation was not the mechanism leading to the progressive downregulation of KIAA0495 from normal plasma cell to MUGS to symptomatic myeloma, suggestive of other mechanisms, such as histone modification of miRNA-mediated regression, may come into play” (page 4, 2nd column)
Indeed, such unpredictable nature is also shared by Applicants’ own published paper (Li et al., Cell Death & Differentiation, February 23, 2023, vol. 30, pages 1166-1183), wherein some of the cancerous primary samples did not exhibit significant methylation of KIAA0495:
“we examined KIAA0495 methylation in a series of primary tumors. KIAA0495 methylation was frequently detected in primary tumors of colorectal (14/23, 61%), gastric (15/51, 30%) and nasopharyngeal (28/48, 58%) cancers, but less in esophageal (7/46, 15%) and breast (3/40, 7.5%) cancers (Fig. 3F, Suppl. Fig. S5B). In contrast, no normal nasopharyngeal (0/6), esophageal (0/7), and gastric (0/4) tissues showed KIAA0495 methylation (Fig. 3F, Table 1)” (page 1170, 1st column, bottom paragraph)
Absence of Working Examples:
The specification does not provide any additional data relating to the genus of cancer samples that show significant correlation between the methylation of KIAA0495 and caner risk or cancer outcome prognostics.
Skill Level, Quantification of Experimentation, & Conclusion:
While the skill level of the artisan may be high based on such unpredictable nature that exist in pathogenicity of cancer, which is multi-factorial, with explicit evidence showing the unpredictability relating to the methylation status of KIAA0495 and different types of cancers, one of skill in the art would not be capable of practicing the invention as claimed fully commensurate with the scope of the claims without undue experimentation.
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 13-17 are rejected under 35 U.S.C. 103 as being unpatentable over Li et al. (Cell Death & Differentiation, February 23, 2023, vol. 30, pages 1166-1183).
With regard to claims 13, 15, and 18, Li et al. teach a method that comprise the steps of:
treating DNA from a sample taken from a subject with an agent that differentially modifies methylated and unmethylated DNA (“validated the MSP results in several cell lines using high-resolution bisulfite genomic sequencing (BGS) analysis of 50 individual CpG sites within the KIAA0495 CGI”, page 1170, 1st column, 1st paragraph; also “we examined KIA0495 methylation in a series of primary tumors of colorectal … gastric … and nasopharyngeal …”, page 1170, 1st column, bottom paragraph);
determining the number of CpGs in a genomic sequence comprising at least 10 CpGs (see above 50 CpG sites);
comparing the number of methylated CpGs from (b) with the number of methylated CpGs n the genomic sequence from a non-cancer sample of the corresponding type and processed through steps (a) and (b) (“no normal nasopharyngeal … esophageal … and gastric … tissues showed KIAA0495 methylation …”, page 1170, 1st column bottom paragraph to 2nd column, 1st paragraph); and
determining that the sample contains more methylated CpGs in the genomic sequence determined in (b) compared to the number of methylated CpGs with the number of methylated CpGs in the genomic sequence from a non-cancer sample and processed through steps (1) to (3) (see above).
With regard to claims 16, 17, 21, and 22 the artisans also employ PCR amplification reaction (see additional Data attached, “methylation-specific PCR (MSP) … were carried out”, page 2, 2nd paragraph).
The artisans do not explicitly teach that SEQ ID Number 3 or its fragment is analyzed (claims 14 and 19), nor the explicit step of taking a sample from a subject and rendering a determination that the subject has an increased risk for cancer (claim 13, in-part).
The artisans do not explicitly teach that the methylation relationship discovered should be employed in a method of determining a likelihood of mortality in patient by comparing the methylation status of a patient to that of another patient.
However, it would have been prima facie obvious to take the teachings of Li et al. and arrive at the invention as claimed for the following reasons.
With regard to application of the naturally existing correlation discovered by Li et al. and apply the discovery to assess a subject’s risk for cancer, doing so would have been obvious because discovery of a marker’s correlation to a disease is conventionally and routinely applied as a diagnostic tool in the molecular diagnostics discipline. As discussed by Li et al., the methylation pattern of the promoter region KIAA0495 behaves similarly as that which is known in the art as a tumor suppressor, wherein its inactivation via hypermethylation results in the decreased expression of the encoded product, increasing the risk of cancer:
“TSGs are involved in tumor initiation and progression and frequently inactivated by either genetic mutations and/or promoter methylation in various tumors” (page 1166, 1st column)
“we identified a 1p36.3 lncRNA KIAA0495 (previously also named as PDAM or TP73-AS1), as a methylated target in multiple tumors. KIAA0495 was frequently silenced by promoter CpG methylation in multiple tumors which could serve as a potential biomarker …” (page 1167, 1st column, 2nd paragraph)
“[w]e further found that decreased expression of KIAA0495 was associated with high-grade tumors in colorectal, breast, and bladder cancer patients … and poor survival of patients with colorectal, esophageal, lung, breast, bladder, and ovarian cancers … These results suggest that silencing of the 1p36.3 transcript KIAA0495, through epigenetic abnormalities, is common during tumorigenesis and associated with poor survival of cancer patients of multiple tissue origins” (page 1167, 2nd column)
“we examined KIAA0495 methylation in a series of primary tumors. KIAA0495 methylation was frequently detected in primary tumors of colorectal (14/23, 61%), gastric (15/51, 30%) and nasopharyngeal (28/48, 58%) cancers, but less in esophageal (7/46, 15%) and breast (3/40, 7.5%) cancers (Fig. 3F, Suppl. Fig. S5B). In contrast, no normal nasopharyngeal (0/6), esophageal (0/7), and gastric (0/4) tissues showed KIAA0495 methylation (Fig. 3F, Table 1)” (page 1170, 1st column, bottom paragraph)
Therefore, one of ordinary skill in the art would have been motivated to take the findings of Li et al. and utilize the methylation pattern correlation to diagnose cancer of a subject, wherein the increased methylation of KIAA0495 promoter in the subject, compared to a healthy individual, as indicia of an increased risk of cancer.
As to correlation of the amount of methylation of KIAA0495 promoter being a worse prognosticator of cancer in a subject by comparison to another cancer subject’s methylation pattern when said methylation is higher, such a conclusion would have been obvious application based on the understanding of epigenetic silencing of a gene that is involved in tumorigenesis, as greater methylation of the region of interest would have resulted in lesser expression of KIAA495 product that is involved in tumor suppression.
Indeed, Li et al. evidences such common conclusion in their statement:
“Clinically, through analyzing TCGA cancer dataset, higher KIAA0495 promoter methylation level is significantly associated with poor outcomes of patients with rectum, esophageal, and breast cancers (Fig. 3I). These findings demonstrate the translational value of tumor-specific KIAA0495 promoter methylation as a cancer biomarker, and also the important role of KIAA0495 inactivation during tumor pathogenesis.” (page 1170, 2nd column, 2nd paragraph)
Therefore, the application of the correlation that exist between the methylation pattern in the promoter of KIAA0495 and cancer for diagnosis and prognosis would have yielded no more than a predictable outcome.
With regard to the region of methylation being SEQ ID number 3 or its fragment, absent evidenced to the contrary, the Office contends that the region disclosed by Li et al. is the same region as the authors of the publication are found as inventors of the instant application.
In KSR, the Supreme Court particularly emphasized “the need for caution in granting a patent based on the combination of elements found in the prior art,” Id. at 415, 82 USPQ2d at 1395, and discussed circumstances in which a patent might be determined to be obvious. Importantly, the Supreme Court reaffirmed principles based on its precedent that “[t]he combination of familiar elements according to known methods is likely to be obvious when it does no more than yield predictable results.” Id. at 415-16, 82 USPQ2d at 1395. The Supreme Court stated that there are “[t]hree cases decided after Graham [that] illustrate this doctrine.” Id. at 416, 82 USPQ2d at 1395. (1) “In United States v. Adams, . . . [t]he Court recognized that when a patent claims a structure already known in the prior art that is altered by the mere substitution of one element for another known in the field, the combination must do more than yield a predictable result.”
For these reasons, the invention as claimed is deemed prima facie obvious over Li et al.
Claims 13-17 are rejected under 35 U.S.C. 103 as being unpatentable over Pang et al. (Brain Pathology, 2010, vol. 20, pages 1021-1032).
With regard to claims 13, 15, and 18, Pang et al. teach a method that comprise the steps of:
treating DNA from a sample taken from a subject with an agent that differentially modifies methylated and unmethylated DNA (“[o]ne microgram of genomic DNA from each sample was treated with sodium bisulfite using Methyllam™ One-step DNA modification kit”, page 1022, 2nd column, Bisulfite sequencing);
determining the number of CpGs in a genomic sequence comprising at least 10 CpGs (“[w]e questioned if promoter hypermethylation played a role in PDAM1 downregulation. A stretch of 30 CpG dinucleotides located in the putative promoter region was interrogated for aberrant methylation by bisulfite sequencing”, page 1026, 2nd column);
comparing the number of methylated CpGs from (b) with the number of methylated CpGs n the genomic sequence from a non-cancer sample of the corresponding type and processed through steps (a) and (b) (“[a] total of 56 OT [Oligodendroglial Tumor] and four normal brain samples were assessed … results revealed rare hypermethylation at CpG island in 1 normal brain tissues but hypermethylation in 36 of 56 (64.3%) Ots examined … Promoter hypermethylation of PDAM was detected in 30 of 37 (81.1%) OTs with reduced PDAM expression, and the two parameters were significantly associated”, page 1026 and 1027, 1st column, 1st para); and
determining that the sample contains more methylated CpGs in the genomic sequence determined in (b) compared to the number of methylated CpGs with the number of methylated CpGs in the genomic sequence from a non-cancer sample and processed through steps (1) to (3) (“findings strongly indicates that genomic loss and epigenetic modifications are major mechanism contributing to PDAM inactivation”, page 1030, 1st column, bottom paragraph, also “our study reveals for the first time that aberrant PDAM expression is frequent in OTs, suggesting that PDAM deregulation may be involved in OT development”, page 1031, 1st column).
With regard to claims 16, 17, 21, and 22 the artisans also employ PCR amplification reaction (see page 1022, 2nd column, Bisulfite sequencing section).
The artisans do not explicitly teach that SEQ ID Number 3 or its fragment is analyzed (claims 14 and 19), nor the explicit step of taking a sample from a subject and rendering a determination that the subject has an increased risk for cancer (claim 13, in-part).
The artisans do not explicitly teach that the methylation relationship discovered should be employed in a method of determining a likelihood of mortality in patient by comparing the methylation status of a patient to that of another patient.
However, it would have been prima facie obvious to take the teachings of Pang et al. and arrive at the invention as claimed for the following reasons.
With regard to application of the naturally existing correlation discovered by Pang et al. and apply the discovery to assess a subject’s risk for cancer, doing so would have been obvious because discovery of a marker’s correlation to a disease is conventionally and routinely applied as a diagnostic tool in the molecular diagnostics discipline. As discussed by Pang et al., the methylation pattern of the promoter region PDAM (or KIAA0495), wherein hypermethylation is found on OT (see above).
Therefore, one of ordinary skill in the art would have been motivated to take the findings of Pang et al. and utilize the methylation pattern correlation to diagnose cancer of a subject, wherein the increased methylation of PDAM (or KIAA0495) promoter in the subject, compared to a healthy individual, as indicia of an increased risk of cancer.
As to correlation of the amount of methylation of PDAM promoter being a worse prognosticator of cancer in a subject by comparison to another cancer subject’s methylation pattern when said methylation is higher, such a conclusion would have been obvious application based on the understanding of epigenetic silencing of a gene that is involved in tumorigenesis, as greater methylation of the region of interest would have resulted in lesser expression of KIAA495 product that is involved in tumor suppression.
Indeed, Pang et al. evidences such common conclusion in their statement:
“Epigenetic regulation plays an important role in silencing transcription of cancer-related genes. We and others have demonstrated that promoter hypermethylation of many tumor suppressor genes and DNA repair genes is frequent in OTs … we have demonstrated that promoter hypermethylation is one of the key mechanisms for silencing PDAM, implicating specific inactivation of PDAM during OT formation”, page 1030, 2nd column, 2nd full paragraph)
Therefore, the application of the correlation that exist between the methylation pattern in the promoter of KIAA0495 and cancer for diagnosis and prognosis would have yielded no more than a predictable outcome.
With regard to the region of methylation being SEQ ID number 3 or its fragment, absent evidenced to the contrary, the Office contends that the region disclosed by Li et al. is the same region as the authors of the publication are found as inventors of the instant application.
In KSR, the Supreme Court particularly emphasized “the need for caution in granting a patent based on the combination of elements found in the prior art,” Id. at 415, 82 USPQ2d at 1395, and discussed circumstances in which a patent might be determined to be obvious. Importantly, the Supreme Court reaffirmed principles based on its precedent that “[t]he combination of familiar elements according to known methods is likely to be obvious when it does no more than yield predictable results.” Id. at 415-16, 82 USPQ2d at 1395. The Supreme Court stated that there are “[t]hree cases decided after Graham [that] illustrate this doctrine.” Id. at 416, 82 USPQ2d at 1395. (1) “In United States v. Adams, . . . [t]he Court recognized that when a patent claims a structure already known in the prior art that is altered by the mere substitution of one element for another known in the field, the combination must do more than yield a predictable result.”
For these reasons, the invention as claimed is deemed prima facie obvious over Pang et al.
Conclusion
No claims are allowable.
Inquiries
Any inquiry concerning this communication or earlier communications from the Examiner should be directed to Young J. Kim whose telephone number is (571) 272-0785. The Examiner can best be reached from 7:30 a.m. to 4:00 p.m (M-F). The Examiner can also be reached via e-mail to Young.Kim@uspto.gov. However, the office cannot guarantee security through the e-mail system nor should official papers be transmitted through this route.
If attempts to reach the Examiner by telephone are unsuccessful, the Examiner's supervisor, Gary Benzion, can be reached at (571) 272-0782.
Papers related to this application may be submitted to Art Unit 1681 by facsimile transmission. The faxing of such papers must conform with the notice published in the Official Gazette, 1156 OG 61 (November 16, 1993) and 1157 OG 94 (December 28, 1993) (see 37 CFR 1.6(d)). NOTE: If applicant does submit a paper by FAX, the original copy should be retained by applicant or applicant’s representative. NO DUPLICATE COPIES SHOULD BE SUBMITTED, so as to avoid the processing of duplicate papers in the Office. All official documents must be sent to the Official Tech Center Fax number: (571) 273-8300. Any inquiry of a general nature or relating to the status of this application should be directed to the Group receptionist whose telephone number is (571) 272-1600.
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/YOUNG J KIM/Primary Examiner
Art Unit 1637 June 3, 2026
/YJK/
1 KIAA0495 is also known as PDAM or TP73-AS1, see specification [0028].
Prosecution Insights