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 .
Priority
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or
under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. This application is a 371 of PCT/US2020/019147 filed 02/21/2020 and claims benefit of 62/809,920 filed 02/25/2019. Based on the filing receipt, the effective filing date of this application is February 25, 2019 which is the filing date of Application 62/809,920 from which the benefit of priority is claimed.
Information Disclosure Statements
The information disclosure statements (IDS) submitted 11/15/2021 and 12/27/2022 have been considered by the examiner.
Status of Claims
Claims 2, 14-15, 18-19, 22-23, and 28-30 have been canceled by the Applicant. Group I, comprising claims 1 and 3-13, has been elected.
Claims 16, 17, 20, 21, and 24-27 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected Group II, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 02/04/2025.
Claims 1 and 3-13 are under examination.
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.
Claim 3 is newly 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. The rejection is necessitated by amendments filed 08/22/2025.
Claim 3 recites, “The cell of claim 1, wherein the at least 1000 times more OATP2A1 mRNA compared to the control cell is measured by real-time polymerase chain reaction (PCR) using the 2-ΔΔCt method”. It is unclear what is meant by “measured by real-time polymerase chain reaction (PCR) using the 2-ΔΔCt method”. The 2-ΔΔCt method is an analysis method, not a measurement method, therefore, the metes and bounds of the claim cannot be ascertained. For the purposes of compact prosecution, the claim will be interpreted as limited to cell mRNA expression measured by real-time polymerase chain reaction.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1 and 3-6 stand rejected under 35 U.S.C. 102(a)(1) as being clearly anticipated by Mandery, et al. ("Influence of Cyclooxygenase Inhibitors on the Function of the Prostaglandin Transporter Organic Anion-Transporting Polypeptide 2A1 Expressed in Human Gastroduodenal Mucosa", published 2010-02, cited in PTO-892 dated 04/24/2025). The rejections have been modified, necessitated by amendments filed 08/22/2025.
The rejection has been modified to address amended claim limitations filed 08/22/2025.
In regards to claim 1, Mandery teaches a cell overexpressing a human organic anion transporting polypeptide 2A1 (OATP2A1), wherein the cell expresses at least 1000 times more OATP2A1 mRNA compared to a control cell (see, e.g., p. 349, under “Fig. 3.”, panel “A”; and p. 347, col. 2, under “Characterization of HEK293-OATP2A1 Cell Line Stably Expressing OATP2A1.”: “we established a cell line stably expressing OATP2A1”). Panel “A” of “Fig. 3.” from Mandery discloses the OATP2A1 mRNA expression of a HEK293-OATP2A1 cell line is approximately 100 arbitrary units and the HEK293 cells transfected with the empty vector is approximately 0 arbitrary units. The examiner understands the disclosure of 100 arbitrary units of OATP2A1 mRNA from the OATP2A1-expressing cells compared to 0 arbitrary units from the control cells would be interpreted to be equivalent to at least 1000 times more OATP2A1 mRNA expression. The cell as claimed does not read on a naturally occurring cell because naturally occurring cells do not reach a level of OATP2A1 mRNA expression that is 1000 times more than the OATP2A1 mRNA expression of control cells. See, e.g., “Figure 1”, panel “A” from the journal article “Interplay between the Nuclear Receptor Pregnane X Receptor and the Uptake Transporter Organic Anion Transporter Polypeptide 1A2 Selectively Enhances Estrogen Effects in Breast Cancer” by Schwabedissen, et al. Also, see “Fig. 1”, panel “b” of the journal article “Organic Anion Transporting Polypeptides Expressed in Pancreatic Cancer May Serve As Potential Diagnostic Markers and Therapeutic Targets for Early Stage Adenocarcinomas” by Hays, et al. Both of these references have cells with OATP2A1 mRNA expression less than 1000 times more than the OATP2A1 mRNA expression of control cells
In regards to claim 3, Mandery teaches a cell overexpressing a human organic anion transporting polypeptide 2A1 (OATP2A1), wherein the cell expresses at least 1000 times more OATP2A1 mRNA compared to a control cell as measured by real-time polymerase chain reaction (see, e.g., cell expression of OATP2A1 - p. 349, under “Fig. 3.”, panel “A” ; and p. 347, col. 2, under “Characterization of HEK293-OATP2A1 Cell Line Stably Expressing OATP2A1.”: “we established a cell line stably expressing OATP2A1”; measured by real-time polymerase chain reaction – p. 346, under “Real-Time PCR.”). Panel “A” of “Fig. 3.” from Mandery discloses the OATP2A1 mRNA expression of a HEK293-OATP2A1 cell line is approximately 100 arbitrary units and the HEK293 cells transfected with the empty vector is approximately 0 arbitrary units. The examiner understands the disclosure of 100 arbitrary units of OATP2A1 mRNA from the OATP2A1 expressing cells compared to 0 arbitrary units from the control cells is interpreted to be equivalent to at least 1000 times more OATP2A1 mRNA expression.
In regards to claim 4, Mandery teaches the cell is transfected with an OATP2A1 nucleic acid (see, e.g., p. 346, under “Cell Culture and Generation of a HEK293 Cell Line Stably Expressing OATP2A1.”, para. 2).
In regards to claim 5, Mandery teaches the cell is stably transfected with the OATP2A1 nucleic acid (see, e.g., transfected with the OATP2A1 nucleic acid - p. 346, under “Cell Culture and Generation of a HEK293 Cell Line Stably Expressing OATP2A1.”, para. 2; stably expressing – p. 350, col. 2, para. 2: “We generated a HEK293 cell line stably expressing OATP2A1, which showed a significantly higher transport of PGE2 compared with that in control cells.”).
In regards to claim 6, Mandery teaches the cell is a human embryonic kidney 293 (HEK293) cell (see, e.g., p. 350, col. 2, para. 2: “We generated a HEK293 cell line stably expressing OATP2A1, which showed a significantly higher transport of PGE2 compared with that in control cells.”).
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.
Claim 7 stands rejected under 35 U.S.C. 103 as being unpatentable over Mandery (cited above), as applied to claims 1 and 3-6 above, and further in view of Thomas, et al. ("HEK293 cell line: A vehicle for the expression of recombinant proteins", published 2005, cited in PTO-892 dated 04/24/2025).
With respect to claim 7, Mandery teaches cultured cells expressing OATP2A1. Specifically, Mandery teaches cells were routinely subcultured by trypsinization using trypsin (0.05%)-EDTA (0.02%) solution (see p. 346, first column, under “Cell Culture and Generation of a HEK293 Cell Line Stably Expressing OATP2A1”.)
However, Mandery does not explicitly teach that the cells can be cultured for at least 20 passages without a significant reduction in OATP2A1 expression, as in claim 7.
However, Thomas discloses that stock HEK cells “are generally reliable in terms of their native phenotype, transfection efficiency and electrophysiological stability for 20–30 passages before a new stock needs to be thawed and regenerated”, as in claim 7 (see, e.g., p. 190, col. 2, under “2. Methods for preparation and maintenance of HEK cells”, para. 1). The examiner understands transfection efficiency to be a measure of expression of the transfected nucleic acid, in this case the nucleic acid for OATP2A1.
Mandery and Thomas are analogous to the field of the claimed invention because they are both in the field of cell transfection. One of ordinary skill in the art before the effective filing date of the application would have found it obvious to apply the knowledge that HEK cells have transfection efficiency for 20-30 passages, as disclosed by Thomas, to the cells of Mandery. That knowledge would have allowed the artisan to avoid the unnecessary effort and cost of prematurely thawing and regenerating new stock cells.
Claim 8 stands rejected under 35 U.S.C. 103 as being unpatentable over Mandery (cited above), as applied to claims 1 and 3-6 above, and further in view of Kamo, et al. (“Impact of FDA-Approved Drugs on the Prostaglandin Transporter OATP2A1/SLCO2A1”, published 2017-09, cited in PTO-892 dated 04/24/2025).
Mandery teaches as set forth above. Mandery further teaches transport assays to evaluate the cells (see p. 346, column 2, under “Transport Assays”) but fails to teach the use of 6-carboxyfluorescein (6-CF), as in claim 8.
However, Kamo rectifies this deficiency in a journal article on the impact of drugs on OATP2A1-mediated activity (see, e.g., p. 2483, under “ABSTRACT”). Kamo teaches the uptake of 6-CF by OATP2A1-expressing HEK293 cells, as in claim 8 (see, e.g., p. 2483, under “ABSTRACT”).
Mandery and Kamo are analogous to the field of the claimed invention because they are both in the field of cellular transport. One of ordinary skill in the art before the effective filing date of the application would have found it obvious to use the 6-CF taught by Kamo in the cells of Mandery because 6-CF is a well-known fluorescent substrate for OATP2A1 uptake by HEK293 cells expressing OATP2A1 (see, e.g., Kamo, p. 2484, col. 1, para. 2). The incorporation by the artisan would have allowed the artisan to “understand interaction of drugs with the prostaglandin transporter OATP2A1/SLCO2A1 that regulates disposition of prostaglandins” (see, e.g., Kamo, p. 2483, under “ABSTRACT”). The artisan would have had a reasonable expectation of success based on the cumulative disclosures of these prior art references.
Claims 9-10 and 12 stand rejected under 35 U.S.C. 103 as being unpatentable over Mandery (cited above) and Kamo (cited above), as applied to claim 8 above, and further in view of Hanaoka (US 20180118943 A1, published 2018-05-03, cited in PTO-892 dated 04/24/2025).
With respect to claim 9, Mandery and Kamo teach a transport assay where cells are incubated with radiolabels (see, e.g., Mandery, p. 347, col. 1, para. 1) or fluorescent labels (see, e.g., Kamo, p. 2484, col. 1, para. 2).
However, Mandery and Kamo differ from the instant invention in failing to teach the use of 5, 6-Carboxy-seminaphthorhaodafluor (5, 6-Carboxy-SNARF) in their transport assays.
Hanaoka rectifies these teachings in a patent on pH-sensitive fluorescent probes for use in cells (see, e.g., under “ABSTRACT”). Hanaoka teaches two types of pH probes widely used in biochemical research: 5, 6-Carboxy-SNARF and carboxyfluoresceins (see, e.g., p. 1, para. [0008]-[0010]; and under “FIG. 1”).
Mandery, Kamo, and Hanaoka are analogous to the field of the claimed invention because they are all in the field of biochemical research. One of ordinary skill in the art before the effective filing date of the application would have found it obvious to simply substitute the probes in the assays/cells of Mandery and Kamo with the 5, 6-Carboxy-SNARF of Hanaoka. The substitution by the artisan would have been obvious because Hanaoka discloses that SNARF is “The most widely used pH probe” (see, e.g., p. 1, para. [0009]). Hanaoka further discloses that the use of SNARF allows the “pH measurement of the cytoplasm because it is mainly localized in the cytoplasm and has a pKa (=7.5) suited to the pH fluctuation zone of the cytoplasm” (see, e.g., p. 1, para. [0009]). The uptake of SNARF by OATP2A1 would lead to a change in fluorescence as the pH environment of the substrate changes as the substrate enters the cytoplasm of the cell. The artisan would have had a reasonable expectation of success based on the cumulative disclosures of these prior art references.
With respect to claim 10, Mandery and Kamo teach as set forth above. They also teach that OATP2A1 binds to the molecules that they transport (see, e.g., Kamo, p. 2487, para. 2: “the presence of different binding sites of 6-CF from PGE2”). Note that the use of SNARF is taught by Hanaoka as discussed above. Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the application to use the SNARF label as taught by Hanaoka in the transport assays taught by Mandery as modified by Kamo for the reasons articulated above. Additionally, a skilled artisan would have clearly observed that a OATP2A1-mediated transport or uptake assay necessarily requires the polypeptide to binds to the molecules that it transports.
With respect to claim 12, Kamo teaches the uptake of a fluorescent probe substrate by OATP2A1-expressing HEK293 cells that is greater than the uptake by control cells (see, e.g., Kamo, p. 2485, under “Figure 1.”). Also, Mandery discloses that the addition of certain molecules can increase the OATP2A1-mediated activity of OATP2A1-expressing cells when compared to control cells (see, e.g., p. 350, under “Fig. 4.”; and p. 351, para. 1: “indomethacin, ketoprofen, and naproxen stimulated OATP2A1-mediated PGE2 uptake in a concentration-dependent manner”).
But, they fail to teach OATP2A1-mediated uptake of a SNARF substrate that is at least 100 times greater than an OATP2A1-mediated uptake in a control cell. However, it would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the application to perform routine optimization of the components in the claimed invention to make and use the claimed invention. To reiterate, Mandery discloses the OATP2A1-mediated uptake is only 17.4 times greater than the OATP2A1-mediated uptake of the control cells. However, Mandery further discloses that OATP2A1-mediated uptake can be modulated by the addition of certain molecules. Therefore, it would have been obvious that the cells of Mandery could be optimized to induce OATP2A1-mediated uptake of a SNARF substrate that is at least 100 times greater than the OATP2A1-mediated uptake of control cells. As noted in In re Aller, 105 USPQ 233 at 235, more particularly, where the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation. Routine optimization is not considered inventive and no evidence has been presented that arriving at the claimed cells was anything other than routine, that the properties of the cells from the optimization has any unexpected properties, or that the results should be considered unexpected in any way as compared to the closest prior art. Optimization of parameters is a routine practice that would be obvious for the artisan to employ. See MPEP § 2144.05. The artisan would have had a reasonable expectation of success based on the cumulative disclosure of Mandery, Kamo, and Hanaoka.
Claims 11 and 13 stand rejected under 35 U.S.C. 103 as being unpatentable over Mandery (cited above), as applied to claims 1 and 3-6 above.
With respect to claim 11, Mandery discloses that the cells have OATP2A1-mediated activity 17.4 times the OATP2A1-mediated activity of control cells (see, e.g., p.349, under “Fig. 3.”, under panel “D”). Mandery also discloses that the addition of certain molecules can increase the OATP2A1-mediated activity of OATP2A1-expressing cells when compared to control cells (see, e.g., p. 350, under “Fig. 4.”; and p. 351, para. 1: “indomethacin, ketoprofen, and naproxen stimulated OATP2A1-mediated PGE2 uptake in a concentration-dependent manner”).
With respect to claim 13, Mandery discloses the OATP2A1-mediated activity or uptake is measured at pH 7.3 (see, e.g., p. 346, under “Transport Assays.”, para. 1).
But, Mandery does not disclose the OATP2A1-mediated activity is at least 20 times greater than the OATP2A1-mediated uptake of the control cells, as in claim 11.
However, it would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to perform routine optimization of the components in the claimed invention to make and use the claimed invention. To reiterate, Mandery discloses the OATP2A1-mediated uptake is only 17.4 times greater than the OATP2A1-mediated uptake of the control cells. However, Mandery further discloses that OATP2A1-mediated uptake can be modulated by the addition of certain molecules. Therefore, it would have been obvious that the cells of Mandery could be optimized to induce OATP2A1-activity that is at least 20 times greater than the OATP2A1-mediated activity of control cells. As noted in In re Aller, 105 USPQ 233 at 235, more particularly, where the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation. Routine optimization is not considered inventive and no evidence has been presented that arriving at the claimed cells was anything other than routine, that the properties of the cells from the optimization has any unexpected properties, or that the results should be considered unexpected in any way as compared to the closest prior art. Optimization of parameters is a routine practice that would be obvious for the artisan to employ. See MPEP § 2144.05. The artisan would have had a reasonable expectation of success based on the cumulative disclosure of Mandery.
Response to Arguments
Applicant’s arguments submitted on 22 August 2025 have been considered but are not
persuasive and/or moot due to reasons of record made below.
Claim Rejections – 35 U.S.C. 102
The applicant argues that the Office does not provide evidence that 100 arbitrary units compared to 0 arbitrary units is equivalent to at least 1000 times more OATP2A1 mRNA expression. In fact, the evidence is panel “A” of “Fig. 3.” from Mandery, which discloses the OATP2A1 mRNA expression of a HEK293-OATP2A1 cell line is approximately 100 arbitrary units and the HEK293 cells transfected with the empty vector is approximately 0 arbitrary units. The limit of 100 divided by a number approaching zero, goes to infinity, which is equivalent to at least 1000 times more.
Claim Rejections – 35 U.S.C. 103
Claim 7
The applicant argues that dependent claim 7 is not obvious over Mandery in view of Thomas because Mandery does not anticipate independent claim 1. However, the anticipation of claim 1 by Mandery is discussed above, therefore, the rejection of claim 7 by Mandery in view of Thomas is maintained.
Claim 8
The applicant argues that dependent claim 8 is not obvious over Mandery in view of Kamo because Mandery does not anticipate independent claim 1. However, the anticipation of claim 1 by Mandery is discussed above, therefore, the rejection of claim 8 by Mandery in view of Kamo is maintained.
Claims 11 and 13
The applicant argues that dependent claims 11 and 13 are not obvious over Mandery because Mandery does not anticipate independent claim 1. However, the anticipation of claim 1 by Mandery is discussed above, therefore, the rejections of claims 11 and 13 by Mandery are maintained.
Claims 9, 10, and 12
The applicant argues that Kamo and Hanaoka collectively do not cure the deficiency of Mandery with respect to claim 1. However, the anticipation of claim 1 by Mandery is discussed above.
The applicant continues by arguing that the combination of Mandery, Kamo, and Hanaoka do not teach or suggest a 5, 6-Carboxy-SNARF bound to the OATP2A1, as recited by claim 10. The applicant states that Kamo’s disclosure that there may be “different binding sites of 6-CF from PGE2” on OATP2A1 is not a disclosure that would be understood by an artisan of ordinary skill in the art that another substrate 5, 6-Carboxy-SNARF, would also be bound to the OATP2A1, as recited by claim 10. However, the applicant does not discuss the given disclosure of Hanaoka which identifies both 5, 6-Carboxy-SNARF and carboxyfluoresceins as widely used pH probes in biochemical research (see, e.g., Hanaoka, para. [0008]). The office stated that the simple substitution of widely used pH probes was obvious in view of the given disclosures. Further, the office recited Hanaoka’s disclosure that SNARF is the most widely used pH probe and the use of SNARF allows pH measurement of the cytoplasm (see, e.g., para. [0009]).
Secondly, the applicant argues that one of ordinary skill in the art would have no reason to optimize the OATP2A1 uptake rates outside of the ranges suggested by prior art conditions. However, Mandery, Kamo, and Hanaoka together teach the increased OATP2A1-mediated uptake of a SNARF substrate. Mandery discloses that the addition of certain molecules can increase OATP2A1-mediated uptake (see, e.g., p. 350, under “Fig. 4.”). Therefore, it would be obvious to the artisan of ordinary skill that OATP2A1-mediated uptake can be optimized to meet the limitations of claim 12. Optimization of parameters is a routine practice that would be obvious for the artisan to employ. See MPEP 2144.05.
Unexpected Features
The applicant states that the claimed cells have unique features such as enhanced uptake of 6-CF and 5, 6-carboxy-SNARF, a signal to background ration ranged from 36 to 48 and fell within the pH range from 6.5 to 8, uptake of 5, 6-Carboxy-SNARF by OATP2A1 overexpressing cells reaching saturation with KM of 29±9 µM, and a linear rate of uptake of 5, 6-Carboxy-SNARF with substantial signal to background ratio even after 15-20 minutes. However, the applicant fails to state why these “unique” features are unexpected. Without evidence that these features are unexpected, the office views these features as the result of routine optimization. See Peterson, 315 F.3d at 1330, 65 USPQ2d at 1382 (“The normal desire of scientists or artisans to improve upon what is already generally known provides the motivation to determine where in a disclosed set of percentage ranges is the optimum combination of percentages.”); In reHoeschele, 406 F.2d 1403, 160 USPQ 809 (CCPA 1969).
The applicant continues by explaining that the methodology for measuring OATP2A1 transporter activity is possible with the cells overexpressing OATP2A1 mRNA by over 1000-fold. However, as discussed above, Mandery anticipates cells overexpressing OATP2A1 mRNA by over 1000-fold. Furthermore, the “substantial” signal to background ratio is irrelevant to the novelty of the claims because the ratio is not incorporated into the claims and the applicant has provided no evidence that the signal to background ratio is unexpected.
In addition, the applicant continues by saying the claimed cells can be used in assays for testing different drugs at physiological conditions, at longer assay windows, and with greater resolution of signal over background readings, than those of the cited references. However, as discussed above, Mandery discloses measuring OATP2A1-mediated activity or uptake at physiological conditions, mainly physiological pH. The longer assay windows and greater resolution of signal over background readings are irrelevant to the novelty of the claims because the assay windows and signal to background ratios are not incorporated into the claims.
The applicant continues by citing that Mandery and Kamo do not have the same assay time, uptake kinetics, or signal to background ratio as the claimed invention. However, these features are not limitations in the present claims and are, therefore, irrelevant to the novelty of the claims.
The applicant states that the artisan of ordinary skill would have no reason to modify the respective OATP2A1 mRNA-overexpressing cells of Mandery and Kamo because they each report on successfully detecting the effect of therapeutic drugs on the function of OATP2A1 with the respective cells. However, the desire of scientists or artisans to improve upon what is generally known is identified as a normal desire. See Peterson, 315 F.3d at 1330, 65 USPQ2d at 1382 (“The normal desire of scientists or artisans to improve upon what is already generally known provides the motivation to determine where in a disclosed set of percentage ranges is the optimum combination of percentages.”); In reHoeschele, 406 F.2d 1403, 160 USPQ 809 (CCPA 1969). For all these reasons, the above rejections are maintained.
Conclusion
No claims are allowed.
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure. Schwabedissen, et al. ("Interplay between the Nuclear Receptor Pregnane X Receptor and the Uptake Transporter Organic Anion Transporter Polypeptide 1A2 Selectively Enhances Estrogen Effects in Breast Cancer", published 2008-11-14) and Hays, et al. ("Organic Anion Transporting Polypeptides Expressed in Pancreatic Cancer May Serve As Potential Diagnostic Markers and Therapeutic Targets for Early Stage Adenocarcinomas", published 2013-01-11).
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 MICHAEL C SVEIVEN whose telephone number is (703)756-4653. The examiner can normally be reached Monday to Friday - 8AM to 5PM PST.
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/MICHAEL CAMERON SVEIVEN/ Examiner, Art Unit 1678
/GREGORY S EMCH/ Supervisory Patent Examiner, Art Unit 1678