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 .
Application Status
Claims 1-20 are pending and examined on the merits herein.
Grounds of Rejection Withdrawn
Previous objections to the specification are withdrawn in view of amendment.
Previous rejection of claims 1-19 under 35 U.S.C. 101 are withdrawn in view of claim amendments.
Claim Objections
Claim 7, 19, and 20 are objected to because of the following informalities:
The claims recite the abbreviated term iCol I without writing out the entire meaning first. Please correct to clarify as intact type I collagen (iCol I);
Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
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 1-20 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.
Claim 1 is drawn to a method of treating a subject suffering from cancer with a higher level of cCol I in a tumor as compared to a subject without cancer or a cancer with a lower level of cCol I and having a longer expected overall survival
This renders the claim indefinite as it is unclear how a sample of tumor could be derived from a patient not suffering from a cancer; further it is not clearly defined what the threshold is for the lower level of cCol I is or how the longer expected overall survival is to be determined.
The instant specification discloses that the method comprises isolating a tumor sample by tumor resection, liquid biopsy or needle biopsy (para 0082), but does not clarify where the control sample is derived from.
The instant specification discloses that a higher level of cCol I as compared to the cCol I level a subject not suffering from the cancer indicates that the subject is less likely to experience longer survival and a lower level of cCol I as compared to the cCol I level in a subject not suffering from the cancer indicates that the subject is less likely to experience shorter survival (para 0073). Fig 5b also disclosed a correlation between cCol I expression and overall survival as determined by IH of resected patient PDAC samples
This indicates that the lower cCol I level is relative to a patient without cancer, but as the sample is derived from a tumor it is unclear how this comparison would be established; or how a patient with lower cCol I could have a more favorable outcome versus a patient not suffering from a cancer. Further as the claim recites measuring cCol I; determining it’s relative expression to a control AND an expected longer overall survival it would be circular to have that longer overall survival determined by the measurement of cCol I.
Claim 2 is further drawn to a tumor with higher DDR1 level and or NRF2 as compared to a subject not suffering from cancer or having a cancer with a lower level of DDR1 or NRF2 and/ or a more favorable outcome.
This renders the claim indefinite as it is unclear how a sample of tumor could be derived from a patient not suffering from a cancer; further it is not clearly defined what the lower level of DDR1/NRF2 is in comparison to or the more favorable outcome.
The instant specification discloses that the method further comprises isolating a tumor sample by tumor resection, liquid biopsy or needle biopsy (para 0082), but does not clarify where the control sample is derived from.
The instant specification discloses that the lower DDR1/NRF2 level in cancer patients in comparison to a patient not suffering from a cancer are more likely to experience longer survival (para 0074).
This indicates that the lower DDR1/NRF2 level is relative to a patient without cancer, but as the sample is derived from a tumor it is unclear how this comparison would be established; or how a patient with lower DDR1/NRF2 could have a more favorable outcome versus a patient not suffering from a cancer.
Claims 3-11 depend from claim 1 or 2 without correcting the issue(s) identified above and are therefore included in this rejection.
Claim 12 is drawn to a method for determining if a subject suffering from a cancer selected from a desmoplastic cancer, a fibrolytic cancer or pancreatic ductal adenocarcinoma (PDAC) is more or less likely to experience a longer survival comprising detecting the level of cleaved type I collagen (cCol I), in a tumor sample isolated from the subject, wherein a lower level of cCol I in the tumor sample as compared to a reference sample isolated from a subject not suffering from the cancer or a subject having the cancer but having a higher level of cCol I indicates that the subject is more likely to experience longer survival, and wherein a higher level of cCol I in the tumor sample as compared to a reference sample isolated from a subject not suffering from the cancer or having a lower level of cCol indicates that the subject is more likely to experience shorter survival, and following a determination that the subject is less likely to experience survival, administering to the subject having a higher level of cCol I, an effective amount of a therapy that inhibits DDR1- stimulated NF-xB or mitochondrial biogenesis.
This renders the claim indefinite as it is unclear how a tumor sample with lower cCol I compared to a reference sample from a subject not suffering from cancer can indicate longer survival. If the reference sample is from a subject not suffering from cancer how can this indicate longer survival for the subject with cancer?
The instant specification discloses that the lower cCol I level in cancer patients in comparison to a patient not suffering from a cancer are more likely to experience longer survival (para 0073).
This indicates that the lower cCol I level is relative to a patient without cancer, but it is unclear how a patient with lower cCol I could have longer survival versus a patient not suffering from a cancer.
Claims 13-20 depend from claim 12 without correcting the issue identified above and are therefore included in this rejection.
Response to Arguments
Applicant's arguments filed 06/02/2026 have been fully considered but they are not persuasive.
Applicant submits: One of ordinary skill in the art of cancer diagnostics and biomarker analysis would understand that the phrase "as compared to a sample isolated from a subject not suffering from the cancer" refers to a baseline or reference expression level that serves as a comparator. This is standard practice in the biomarker field, where expression levels are routinely compared to control values derived from non-diseased tissue (which may include normal pancreatic tissue, normal serum, or other appropriate control samples from subjects without cancer). The specification supports this interpretation at paragraph [0073], which discloses that "subjects with lower levels of cCol I are more likely to experience a longer survival and subjects with higher levels of cCol I are less likely to experience a longer survival." The specification at paragraph [0082] discloses that "the method further comprises isolating a tumor sample by tumor resection, liquid biopsy or needle biopsy," making clear that the sample is obtained from the patient being tested, while the comparison is to an established reference value from healthy patients or patients with longer expected overall survival.
Furthermore, the prior art itself demonstrates that such comparisons to subjects without cancer are standard in the art. The Office's own cited reference, Willumsen, expressly "confirmed that collagen turnover measured in serum by C1M, C3M and C4M is elevated in PDAC compared to healthy controls" (Office Action at page 12). If Willumsen could compare PDAC patient biomarker levels to healthy controls, then a person of ordinary skill in the art would readily understand the comparison claimed by Applicant. The comparison language simply denotes that the cCol I (or DDR1/NRF2) level in the patient's tumor sample is higher relative to what would be observed in a non-cancerous state or in cancer patients with more favorable outcomes - a concept well within the understanding of one skilled in the oncology and biomarker arts.
In response: While one of ordinary skill in the art is familiar with biomarker use and comparison to control samples it is unclear in the verbiage of the claim what the control sample is. The prior art cited uses serum samples which are easily obtainable from patients with and without a tumor, but a tumor sample is not easily obtainable from subjects with and without cancer. The specification very clearly delineates where and how the cancer specimen is obtained but the reference sample was not clearly specified and therefore open to interpretation. Further the language “having a longer expected overall survival” adds another indefinite issue as the specification is drawn to the level of cCol I for determining whether the patient is likely to experience a longer survival and therefore determining relative cCol I and whether a patient is expected to have longer survival based on the cCol I measurement is a circular determination and unclear how the expectation of longer survival is to be determined.
Examiner’s note: Having all claims with expression comparisons conform to the language of a “reference sample isolated from a subject not suffering from a cancer” as recited in claim 12; clearly delineating how longer expected survival is to be determined and how the ordinary artisan can determine where the threshold is between low and high cCol I would clarify the 112b issues identified above.
Claim Rejections - 35 USC § 103
New Rejection Necessitated by Amendment
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, 6-9, 11-15, and 17-20 are rejected under 35 U.S.C. 103 as being unpatentable over Willumsen (Sci Rep. 2019 Dec 24;9(1):19761; cited in OA 03/04/2026), Aguilera (Molecular Cancer Therapeutics, 2017, 16(11): 2473-85; IDS entered 02/08/2024), Ruiz-Castro (2016, CH 12, Discoidin Domain Receptors in Health and Disease. Springer, New York, NY; PTO-892) and Vijver (Front. Immunol, 2021, 12:733561; cited in OA 03/04/2026).
Regarding claims 1, 3-4, 6, 8-9, 11-12, 17, and 19-20, Willumsen teaches that pancreatic ductal adenocarcinoma (PDAC) patients have poor prognosis and poor response to treatment being associated with a dense and active stroma and tumor fibrosis (desmoplasia) which is characterized by excessive degradation and formation of the extracellular matrix (ECM) generating collagen fragments that are released into circulation (abstract). Willumsen further teaches measurement of matrix metalloprotease (MMP)-degraded type I collagen (C1M) by ELISA in pre-treatment serum of stage III/ IV PDAC. The specification does not specifically define the structure of cCol I. However, the ordinary definition appears to indicate that it is a broad categorical term encompassing any cleaved collagen I fragment therefore C1M is considered a cCol I fragment. Willumsen further teaches that the measurement of C1M in pre-treatment compared treated with 5-fluorouracil based therapy and evaluation of correlation with overall survival (OS) (abstract) and confirmed that collagen turnover measured in serum by C1M, C3M and C4M is elevated in PDAC compared to healthy controls (discussion, para 2). Willumsen further teaches that higher levels of C1M were found in the PDAC patients versus the normal reference range (Fig 1) and that these levels were associated with significantly shorter OS and further that this marker could have a prognostic/ predictive potential for future treatment trials (abstract). Willumsen further teaches that one arm of the trial received octreotide (somatostatin, a somatotrophin-release inhibiting factor analogue) and continuous infusion of 5-fluorouracil (5-FU) and another arm received placebo and 5-FU (patients and study design). The instant specification discloses that aggressive treatments include multimodal therapies (para 0069).
Willumsen does not teach measurement in a tumor sample, or measurement of DDR1 or NRF2 or administration of a DDR1 inhibitor or inhibitor of mitochondrial biogenesis.
Regarding claims 1-3, 7-9, 11, 13-15, and 18, Aguilera teaches that the ECM is a principal component of PDAC and is rich in fibrillar collagens that facilitate tumor cell survival and chemoresistance and further that discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase that specifically binds fibrillar collagens and has been implicated in promoting cell proliferation, migration, adhesion, ECM remodeling, and response to growth factors (abstract). Aguilera further teaches that pharmacologic inhibition of DDR1 with an ATP-competitive orally available small-molecule kinase inhibitor (7rh) abrogated collagen-induced DDR1 signaling in pancreatic tumor cells and showed striking efficacy in combination with chemotherapy in orthotopic xenografts and autochthonous pancreatic tumors by reducing primary tumor burden and improving chemoresponse (abstract). Aguilera further teaches measurement of level of phosphor-DDR1 by immunohistochemistry in primary tumor samples as well as patient matched xenografts (Fig 1). Aguilera further demonstrates measurement of DDR1 and collagen signaling in a mouse model of PDAC tumors before and after treatment, that showed that combination treatment with a DDR1 inhibitor and chemotherapy provided improved overall survival as well as reduced phosphor-DDR1 levels and collagen signaling (Fig 6).
Ruiz-Castro teaches that collagen-activated DDR1 signals through NF-kB, PI3K/Akt and p38, JNK, and ERK1/2 MAPKs (Fig 12.2) and that DDRs have elevated expression in pancreatic cancer and inhibition of DDR1 with small interfering RNAs (siRNAs) has been shown to inhibit tumorigenicity and bone metastasis in lung cancer and to reduce cancer cell chemoresistance (page 219, para 3). Ruiz-Castro further teaches a potent and selective inhibitor of DDR1, compound 1 that was able to inhibit the downstream signaling of DDR1 in NCI-H23 non-small cell lung cancer (NSCLC) cells (page 230-231). Compound 1 (as seen in Fig 12.6) is 7rh, the same inhibitor used in Aguilera.
Vijver teaches that the ECM undergoes a dramatic transformation during tumor development due to tissue remodeling and that changes in collagen expression, density and stiffness correlate with worse prognosis of cancer patients (discussion, para 1). Vijver further teaches that ECM signatures, increased collagen expression, and increased expression of collagen-crosslinking enzymes are associated with poor prognosis of cancer patients (discussion, para 2) and further that collagen remodeling by matrix metalloproteinases (MMPs) generates specific collagen fragments, that can be detected in the circulation of cancer patients and correlate with poor disease outcome (abstract).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to measure DDR1 in tumor samples and selectively inhibit DDR1 in combination with standard treatment as taught by Aguilera and Ruiz-Castro in the measurement of cleaved collagen I in serum combined with aggressive treatment of PDAC as taught by Willumsen because of the correlation between increased collagen expression and signaling concomitant with increased cleaved collagen in the circulation and poor prognosis in cancer patients as taught by Vijver. The ordinary artisan would have been motivated to do so because Willumsen teaches that PDAC patients have poor prognosis and poor response to treatment and both Willumsen and Aguilera teach that PDAC has extensive ECM involvement through collagen and that DDR1 is downstream of collagen signaling. Willumsen teaches measurement of c Col I (or C1M) in the serum of patients with and without PDAC and Aguilera teaches elevated levels of DDR1 in numerous cancers and specifically detection of phosphor-DDR1 in PDAC tumor samples. As Vijver teaches that cancer increases both expression of collagen which in turn increases downstream signaling, as well as circulation of cleaved collagen fragments which both correlate with poor prognosis, Willumsen teaches that patients with an increased measurement of cCol I had improved OS with aggressive treatment, and Aguilera teaches that inhibition of DDR1 enhanced standard of care chemotherapy response and overall survival in a PDAC mouse model. The ordinary artisan would have a reasonable expectation of success to measure cCol I and/ or DDR1 in a sample from a PDAC patient and if elevated relative to a control to treat with a DDR1 inhibitor in combination with a standard of care chemotherapeutic or another aggressive treatment modality to improve overall survival of the patient(s).
Claims 5, 10, and 16 are rejected under 35 U.S.C. 103 as being unpatentable over Willumsen (Sci Rep. 2019 Dec 24;9(1):19761; cited in OA 03/04/2026), Aguilera (Molecular Cancer Therapeutics, 2017, 16(11): 2473-85; IDS entered 02/08/2024), Ruiz-Castro (2016, CH 12, Discoidin Domain Receptors in Health and Disease. Springer, New York, NY; PTO-892) and Vijver (Front. Immunol, 2021, 12:733561; cited in OA 03/04/2026) as applied to claims 1-4, 6-9, 11-15, and 17-20 above, and further in view of Sakaguchi (Pancreatology. 2019 Jul;19(5):672-680; cited in OA 03/04/2026).
The teachings of Willumsen, Aguilera, Ruiz-Castro, and Vijver regarding claims 1-4, 6-9, 11-15, and 17-20 are detailed above.
Willumsen, Aguilera, Ruiz-Castro and Vijver do not teach that the cancer has metastasized to the liver or that the method further comprises resection or radiation therapy.
Sakaguchi teaches that in a comprehensive literature review on metastatic PDAC patients who underwent resection for synchronous liver metastasis after chemotherapy had favorable overall survival (abstract). Sakaguchi further teaches that the incidence of PDAC is equal to its mortality, virtually 100% of diagnosed patients will die from the disease irrespectively from the therapeutic approach and the majority of patients have synchronous metastatic disease on an initial presentation (background). Sakaguchi further teaches that aggressive chemotherapy can convert unresectable disease to resectable disease (page 673, col 1, para 1). Sakaguchi further teaches that favorable prognoses can be expected for highly selected patients under certain circumstances: (i) conversion surgery, which can be defined as additional surgical resection after favorable response to anti-cancer treatments in patients with initially unresectable PDAC and (ii) resection with only a few metastases (so-called oligometastases, which can be defined as distant metastases to a single or limited number of organs and a number of metastases consistent with a high potential for a complete operative resection (page 673, col 1, para 1). Table 1 summarizes the studies used for resection of liver metastasis. Sakaguchi further teaches that there are substantial survival benefits of conversion surgery for patients with synchronous mPDAC of the liver and peritoneum who responded favorably to initial chemotherapy for a certain period of time (conclusion).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to add resection to the method of treatment when the PDAC metastasizes to the liver as taught by Sakaguchi to the method of treatment comprising measuring cCol I/ DDR1 in tumor samples and selectively inhibiting DDR1 or other aggressive anti-cancer therapy in PDAC patients as taught by Willumsen, Aguilera, Ruiz-Castro, and Vijver. The ordinary artisan would have been motivated to do so because Sakaguchi teaches that there are substantial survival benefits of conversion surgery for patients with synchronous mPDAC of the liver who responded favorably to initial chemotherapy for a certain period of time. Therefore, the ordinary artisan has a reasonable expectation of success to add resection to the treatment for patients with synchronous liver metastasis of PDAC with the measurement of c Col I/ DDR1 and aggressive anti-tumor therapy.
Response to Arguments
Applicant's arguments filed 06/02/2026 have been fully considered but they are not persuasive.
Applicant submits: Accordingly, claim 1 specifically requires "administering an effective amount of a therapy that inhibits DDR1-stimulated NF-kB or mitochondrial biogenesis." Neither Willumsen, Aguilera, nor Vijver, alone or in combination, teaches or suggests this specific therapeutic target. Aguilera teaches pharmacologic inhibition of DDR1 kinase activity with 7rh, an ATP-competitive small-molecule DDR1 kinase inhibitor.
Aguilera teaches inhibition of DDR1 kinase activity itself (i.e., blocking DDR1 autophosphorylation), but does not teach inhibiting the downstream NF-kB signaling pathway that is stimulated by DDR1, nor does it teach inhibiting mitochondrial biogenesis. The claimed therapy targets a specific downstream consequence of DDR1 activation - the NF-kB-p62-NRF2 cascade that drives macropinocytosis and mitochondrial biogenesis - which is a mechanistic insight disclosed for the first time in Applicant's specification (paragraphs [0091] and [0101]).
In response: As Aguilera teaches a specific DDR1 inhibitor and the claim is drawn to DDR1-stimulated NF-kB inhibition the ordinary artisan would understand that any drug that interferes with the DDRNF-kB pathway would anticipate the claim. In other words, the claim does not recite a specific target; rather anything that interferes with the DDR-stimulated NF-kB. Inhibition would naturally flow from upstream signal inhibition in the cellular signaling cascade. Therefore, a specific inhibitor of DDR1 as taught by Aguilera, would inhibit downstream signaling including NF-kB and mitochondrial biogenesis; meeting the limitation of the claim.
Further in the updated 103 rejection above Ruiz-Castro teaches a specific DDR1 inhibitor that also inhibits downstream DDR1 signaling.
Applicant submits: Moreover, the cited combination fails to teach or suggest measuring cCol I in a tumor sample.
Willumsen measures C1M (a collagen degradation fragment) in serum. There is a fundamental distinction between measuring a circulating collagen degradation fragment in serum (Willumsen) and detecting cCol I (cleaved type I collagen, specifically the 3/4 fragment) in tumor tissue by immunohistochemistry as taught by Applicant's specification. The C1M fragment measured by Willumsen via ELISA in serum is a neo-epitope generated by MMP cleavage that reflects systemic collagen turnover, not the specific state of the collagen in the tumor microenvironment. In contrast, Applicant's claims are directed to detecting cCol I (the 3/4 Col I fragment) within the tumor itself, which reflects the local stromal state of the tumor and its mechanistic impact on DDR1 signaling, macropinocytosis, and mitochondrial biogenesis.
In Response: The C1M fragment released into the serum is reflective of collagen turnover from the cancer as seen from the results presented by Willumsen, although the ordinary artisan would also understand that it will also include total collagen turnover which is why comparison to a control sample is needed. Vivjer further teaches that MMP1 and MMP9 cleave collagen 1 to generate 2 fragments: a ¾ length fragment and a ¼ length fragment, and that the MMP generated ¾ fragment is defined as C1M (page 10, col 1, para 3), which is the same fragment measured in Willumsen and cited in the instant specification.
The instant specification discloses that three Col I-cleaving MMPs were highly expressed in the human PDAC samples, that specific MMP inhibitors are additional candidates for aggressive or precision therapy (para 0070) and that the main target of MMPs in desmoplastic tumors is Col I (para 0094). This indicates the same mechanism of collagen fragment generation as the prior art and therefore this is not staining for a novel epitope of cleaved collagen but a known product of collagen degradation.
Applicant submits: Moreover, the Office's rationale for combining Willumsen, Aguilera, and Vijver relies on the general correlation between increased collagen expression and poor prognosis. However, this rationale does not provide an articulated reasoning with a rational underpinning for arriving at the specific claimed invention - a method of treating a patient having elevated cCol I in a tumor with a therapy that inhibits DDR1-stimulated NF-kB or mitochondrial biogenesis. The references individually address different aspects: Willumsen addresses serum biomarkers for prognosis, Aguilera addresses DDR1 kinase inhibition, and Vijver addresses the general correlation between collagen and poor outcomes. The specific combination of detecting cCol I in tumor tissue and then administering a therapy directed at inhibiting DDR1-stimulated NF-kB or mitochondrial biogenesis is not suggested by any individual reference or their combination.
In Response: The rational underpinning for combining these arts is the overlapping understanding of extracellular matrix remodeling in cancer, specifically PDAC, and how the collagen I/ DDR1 signaling pathway is involved in this process. Further prior art teaches not only the involvement of the signaling pathway but also that inhibition of that pathway is a valid therapeutic approach for various diseases including cancer which is thoroughly covered in Ruiz-Castro. One of ordinary skill in the art would recognize that inhibition of an upstream signal in a cascade by necessity also inhibits the downstream signal.
Applicant submits: Furthermore, the Office's proposed combination relies on impermissible hindsight reconstruction using Applicant's own disclosure as a roadmap. It is only with the benefit of Applicant's discovery of the cCol I-DDR1-NF-kB-NRF2-mitochondrial biogenesis pathway that a person of ordinary skill would connect serum collagen fragment measurement (Willumsen), DDR1 kinase inhibition (Aguilera), and general collagen-prognosis correlations (Vijver) into the specific method claimed. Prior to Applicant's work, the mechanistic link between the stromal collagen state (cCol I versus iCol I) and DDR1-NF-kB-NRF2 signaling was unknown (specification at paragraph [0092]: "How the stromal state affects clinical outcome is unknown"). A person of ordinary skill would not have had reason to specifically inhibit DDR1-stimulated NF-kB or mitochondrial biogenesis in patients with elevated cCol I because this mechanism was not recognized in the art.
In Response: In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Further the DDR1 signaling pathways were known in the prior art as seen in Ruiz-Castro. Including that DDR1 is activated by collagen I and that the activation is inhibited by collagen and DDR1 degradation by MMPs; and further that inhibition of DDR1 which would inhibit the downstream signals is a useful therapeutic pathway for fibrotic disease and cancers.
In response to applicant's argument that applicant recognized the mechanistic link between inhibition of mitochondrial biogenesis/ inhibition of DDR1 stimulated NF-kB in patients with elevated cCol I, the fact that the inventor 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. See Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985).
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to AMBER K FAUST whose telephone number is (703)756-1661. The examiner can normally be reached Monday - Thursday 9:00am-6:00pm EST.
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/AMBER K FAUST/ Examiner, Art Unit 1643
/GARY B NICKOL/ Primary Examiner, Art Unit 1643
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