DETAILED ACTION
Applicant’s amendment submitted 3/30/2026 is acknowledged. Claims 16 and 24 are currently amended. Claims 1-15, 17-23, and 25-32 are canceled. Claims 33-37 are newly added. Claims 16, 24, and 33-37 are pending and the subject of this office 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
The instant application is a U.S. National Phase of PCT/EP2021/058296, filed on 3/30/2021, and claims foreign priority to EP20166826.6, filed on 3/30/2020.
Response to Amendment
Applicant’s amendment to the specification to incorporate by reference the sequence listing and to identify embedded sequences by their sequence identifier has overcome the objections previously set forth 10/1/2025.
Applicant’s amendment to claims 16 and 24 overcome the objections and 112(b) rejections previously set forth 10/1/2025. Accordingly, the 112(b) rejections of claim 16 are withdrawn.
Applicant’s cancelation of claims 17-23 and 25-32 renders moot the objections, 112(b), 101, and 102 rejections of each claim.
Drawings
The drawings are objected to because Figures 3A and 5A appear to be missing a color intensity scale to accompany the heat maps depicted. An ordinarily skilled artisan cannot determine the expression levels due to the lack of a color intensity scale for these figures. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Claim Objections
Claims 16 and 33 are objected to because of the following informalities:
The genes recited in claims 16 and 33 should be italicized.
Claim 33 redundantly recites “the further steps of” in line 2.
Appropriate correction is required.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Modified Rejection as Necessitated by Amendment: Claims 16, 24, and 33-37 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a natural phenomenon without significantly more.
The claims recite a method of treating preeclampsia and/or unstable moderate early-onset preeclampsia in a subject having a baby. The method seeks to determine the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof in a biological sample from the subject and to deliver the subject’s baby based on the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof measured. The step of determining the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof in a biological sample seeks to correlate the natural phenomenon of the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof measured to the condition status of preeclampsia and/or unstable moderate early-onset preeclampsia in order to determine whether the subject’s baby should be delivered, which is directed to natural processes in the human body. This judicial exception is not integrated into a practical application because the additional steps recited are directed to insignificant extra-solution data gathering activity, abstract mental process, and well-understood, routine, and conventional practices in the relevant field. The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the additional claims are directed to insignificant extra-solution data gathering activity, abstract mental steps, or the natural phenomenon without significantly more.
Regarding claim 16, the step of “determining the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof in a biological sample from the subject;” is insignificant extra-solution data gathering activity. The step of “comparing the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof in the biological sample from the subject with the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof in a normal sample;” is an abstract process that can be practically performed in the human mind. The step of “delivering the baby when the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof in the biological sample is greater than the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof in the normal sample; thereby treating the preeclampsia and/or unstable moderate early-onset preeclampsia” embraces a natural process of labor in a woman and comprises an abstract process that can be practically performed in the human mind. Furthermore, US2010/0016173 to Nagalla discloses evidence that fibronectin (FN1) serum levels are associated with preeclampsia in pregnant female mammals when the levels are significantly different relative to the level in a normal maternal serum (see paragraphs [0012], [0023], [0123], [0129], Tables 2, 3a-b, 5a-b, 6a-b, 7, and Claims 1 and 30). Nagalla further discloses evidence that “the only treatment for preeclampsia is delivery [of the baby]” (see paragraph [0011]). US2019/0187145 to Hickock teaches biomarker proteins and peptides in biological samples taken from pregnant females that are useful for determining the probability of preeclampsia and teaches human C5 peptides as a biomarker for preeclampsia (see Abstract, paragraphs [0007]-[0009], [0013], [0020], [0041], [0060], and Tables 1, 8-10, 13-14, and 18). Therefore, the steps of determining quantitative levels of the biomarkers FN1 and C5 in a pregnant female mammalian, comparing the same to the levels of FN1 and C5 in a normal control, and treating the pregnant female mammalian by delivering the baby based on determining that she has preeclampsia is well-understood, routine, and conventional in the relevant field.
With respect to claim 24, the peptide expression products of the genes FN1 and C5 relate to determining the quantitative level of the one or more biomarkers which is insignificant extra-solution data gathering activity that is known in the art. US2010/0016173 to Nagalla discloses evidence that fibronectin (FN1) serum levels are associated with preeclampsia in pregnant female mammals when the levels are significantly different relative to the level in a normal maternal serum (see paragraphs [0012], [0023], [0123], [0129], Tables 2, 3a-b, 5a-b, 6a-b, 7, and Claims 1 and 30). Nagalla discloses FN1 comprises a sequence identified by SEQ ID NO: 15 having 100% sequence identity to SEQ ID NOs: 1, 3-6, and 37 of the instant application (see Appendix A – p.1-6). Furthermore, US2019/0187145 to Hickock teaches biomarker proteins and peptides in biological samples taken from pregnant females that are useful for determining the probability of preeclampsia and teaches human C5 peptides as a biomarker for preeclampsia (see Abstract, paragraphs [0007]-[0009], [0013], [0020], [0041], [0060], and Tables 1, 8-10, 13-14, and 18). Hickock discloses C5 comprising SEQ ID NO: 246 having 100% sequence identity to SEQ ID NO: 10 of the instant application (see Appendix B – p.1-2). Thus, claim 24 is directed to well-understood, routine, and conventional matters in the relevant field.
With respect to claim 33, the step of “determining the quantitative level of one or more genes selected from the groups consisting of CPB2, ORM2, IGLC2, C9, ENDOD1, FGA, HBD, PSG1, STOM, EHD1, DNM1L, PRDX2, FBLN1, AMBP, C3, GUSB, CCT7, PSG2, CFB, HBB, SERPINA1, APOC3, FGG, IGHG2, COL4A2, APOE, PSG9, ALB, PRKAR2B, LBP, HPSE, PSG3, SHBG, SVEP1, UBE2L3, and SERPIND1 or an expression product of each thereof in the biological sample from the subject;” is insignificant extra-solution data gathering activity. The step of “comparing the quantitative level of one or more genes selected from the groups consisting of CPB2, ORM2, IGLC2, C9, ENDOD1, FGA, HBD, PSG1, STOM, EHD1, DNM1L, PRDX2, FBLN1, AMBP, C3, GUSB, CCT7, PSG2, CFB, HBB, SERPINA1, APOC3, FGG, IGHG2, COL4A2, APOE, PSG9, ALB, PRKAR2B, LBP, HPSE, PSG3, SHBG, SVEP1, UBE2L3, and SERPIND1 or an expression product of each thereof in the biological sample from the subject with the quantitative level of the one or more genes selected from the group consisting of CPB2, ORM2, IGLC2, C9, ENDOD1, FGA, HBD, PSG1, STOM, EHD1, DNM1L, PRDX2, FBLN1, AMBP, C3, GUSB, CCT7, PSG2, CFB, HBB, SERPINA1, APOC3, FGG, IGHG2, COL4A2, APOE, PSG9, ALB, PRKAR2B, LBP, HPSE, PSG3, SHBG, SVEP1, UBE2L3, and SERPIND1 or an expression product of each thereof in a normal sample;” is an abstract process that can be practically performed in the human mind. The step of delivering the baby when the quantitative level of the one or more genes selected from the group consisting of CPB2, ORM2, IGLC2, C9, ENDOD1, FGA, HBD, PSG1, STOM, EHD1, DNM1L, PRDX2, FBLN1, AMBP, C3, GUSB, CCT7, PSG2, CFB, HBB, SERPINA1, APOC3, FGG, IGHG2, COL4A2, APOE, PSG9, ALB, PRKAR2B, LBP, HPSE, PSG3, SHBG, SVEP1, UBE2L3, and SERPIND1 or an expression product of each thereof in the biological sample is greater than the quantitative level of the one or more genes selected from the group consisting of CPB2, ORM2, IGLC2, C9, ENDOD1, FGA, HBD, PSG1, STOM, EHD1, DNM1L, PRDX2, FBLN1, AMBP, C3, GUSB, CCT7, PSG2, CFB, HBB, SERPINA1, APOC3, FGG, IGHG2, COL4A2, APOE, PSG9, ALB, PRKAR2B, LBP, HPSE, PSG3, SHBG, SVEP1, UBE2L3, and SERPIND1 or an expression product of each thereof in the normal sample” embraces a natural process of labor in a woman and comprises an abstract process that can be practically performed in the human mind. Furthermore, US2010/0016173 to Nagalla discloses evidence that fibronectin (FN1), apolipoprotein C-III (APOC3), carboxypeptidase B2 (CPB2), fibrinogen alpha chain (FGA), lipopolysaccharide binding protein (LBP), and pregnancy-specific beta-1-glycoprotein 1 (PSG1) serum levels are associated with preeclampsia in pregnant female mammals when the levels are significantly different relative to the level in a normal maternal serum (see paragraphs [0012], [0023], [0123], [0129], Tables 2, 3a-b, 5a-b, 6a-b, 7, and Claims 1 and 30). Nagalla further discloses evidence that “the only treatment for preeclampsia is delivery [of the baby]” (see paragraph [0011]). US2019/0187145 to Hickock teaches biomarker proteins and peptides in biological samples taken from pregnant females that are useful for determining the probability of preeclampsia and teaches human APOC3, C3, C5, C9, PSG1, PSG2, PSG3, PSG9, FBLN1, AMBP, APOE, LBP, and SHBG peptides as a biomarker for preeclampsia (see Abstract, paragraphs [0007]-[0009], [0013], [0020], [0041], [0060], and Tables 1, 8-10, 13-14, and 18). Therefore, the steps of determining quantitative levels of one or more genes selected from the group consisting of CPB2, ORM2, IGLC2, C9, ENDOD1, FGA, HBD, PSG1, STOM, EHD1, DNM1L, PRDX2, FBLN1, AMBP, C3, GUSB, CCT7, PSG2, CFB, HBB, SERPINA1, APOC3, FGG, IGHG2, COL4A2, APOE, PSG9, ALB, PRKAR2B, LBP, HPSE, PSG3, SHBG, SVEP1, UBE2L3, and SERPIND1 or an expression product of each thereof in the biological sample in a pregnant female mammalian, comparing the same to the levels one or more genes selected from the group consisting of CPB2, ORM2, IGLC2, C9, ENDOD1, FGA, HBD, PSG1, STOM, EHD1, DNM1L, PRDX2, FBLN1, AMBP, C3, GUSB, CCT7, PSG2, CFB, HBB, SERPINA1, APOC3, FGG, IGHG2, COL4A2, APOE, PSG9, ALB, PRKAR2B, LBP, HPSE, PSG3, SHBG, SVEP1, UBE2L3, and SERPIND1 or an expression product of each thereof in the biological sample in a normal control, and treating the pregnant female mammalian by delivering the baby based on determining that she has preeclampsia is well-understood, routine, and conventional in the relevant field.
With respect to claim 34, the peptide expression products of the genes FN1 and C5 relate to determining the quantitative level of the one or more biomarkers which is insignificant extra-solution data gathering activity that is known in the art. US2010/0016173 to Nagalla discloses evidence that fibronectin (FN1) serum levels are associated with preeclampsia in pregnant female mammals when the levels are significantly different relative to the level in a normal maternal serum (see paragraphs [0012], [0023], [0123], [0129], Tables 2, 3a-b, 5a-b, 6a-b, 7, and Claims 1 and 30). Nagalla discloses FN1 comprises a sequence identified by SEQ ID NO: 15 having 100% sequence identity to SEQ ID NOs: 1, 3-6, and 37 of the instant application (see Appendix A – p.1-6). Furthermore, US2019/0187145 to Hickock teaches biomarker proteins and peptides in biological samples taken from pregnant females that are useful for determining the probability of preeclampsia and teaches human C5 peptides as a biomarker for preeclampsia (see Abstract, paragraphs [0007]-[0009], [0013], [0020], [0041], [0060], and Tables 1, 8-10, 13-14, and 18). Hickock discloses C5 comprising SEQ ID NO: 473 having 100% sequence identity to SEQ ID NO: 38 of the instant application (see Appendix B – p.3-4). Thus, claim 34 is directed to well-understood, routine, and conventional matters in the relevant field and seeks to correlate levels of biomarkers to a state of preeclampsia, which is a natural process.
Claim 35 recites “wherein the normal sample is a biological sample from a subject not suffering from preeclampsia,” which is directed to well-understood, routine and conventional matters in the relevant field. Claim 36 recites “wherein the normal sample is a biological sample from a healthy pregnant subject,” which is directed to well-understood, routine, and conventional matters in the relevant field. Nagalla teaches comparing the levels of preeclampsia biomarkers to normal maternal serum levels (see paragraphs [0012], [0021]-[0023], [0033]-[0035], [0040]-[0042], and [0046]-[0047]).
Claim 37 recites “wherein the step of delivering the baby comprises conducting a pre-term delivery of the baby,” is directed a natural process of delivery of a baby without significantly more.
Therefore, the claimed invention is directed to the natural phenomenon of correlating a quantitative level of the FN1 gene and the C5 gene with the condition status of preeclampsia in a pregnant subject, which is a natural process. The additional elements recited in claim 16 do not amount to more than the judicial exception because the additional elements are directed to well-understood, routine, and conventional practices in the relevant field. The dependent claims do not recite anything that amounts to more than the exception because the additional claims are directed to the natural phenomenon, abstract ideas, or insignificant extra-solution data gathering activity.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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.
New Rejection Necessitate by Amendment: Claims 16, 24, and 33-37 are rejected under 35 U.S.C. 103 as being unpatentable over Nagalla et al. (US2010/0016173; of record) in view of Hickock et al. (US2019/0187145).
Regarding claims 16 and 33, Nagalla teaches methods for diagnosing preeclampsia in a pregnant female mammalian subject, including humans and subjects in early gestation, by testing in a maternal serum sample obtained from said subject the level of two or more proteins including fibronectin (FN1), apolipoprotein C-III (APOC3), carboxypeptidase B2 (CPB2), fibrinogen alpha chain (FGA), lipopolysaccharide binding protein (LBP), and pregnancy-specific beta-1-glycoprotein 1 (PSG1), reading on limitations of claims 16 and 33, serum levels are associated with preeclampsia in pregnant female mammals when the levels are significantly different relative to the level in a normal maternal serum (see paragraphs [0012], [0023], [0123], [0129], Tables 2, 3a-b, 5a-b, 6a-b, 7, and Claims 1 and 30). Nagalla further teaches “the only treatment for preeclampsia is delivery [of the baby]” (see paragraph [0011]). Therefore, determining quantitative levels of the biomarkers FN1, APOC3, CPB2, FGA, LBP, and PSG1 in a pregnant female mammalian and treating the pregnant female mammalian by delivering the baby based on determining that she has preeclampsia is anticipated by Nagalla.
Nagalla does not teach determining the quantitative level of the gene C5 or an expression product thereof.
Hickock teaches biomarker proteins and peptides in biological samples taken from pregnant females that are useful for determining the probability of preeclampsia and teaches human APOC3, C3, C5, C9, PSG1, PSG2, PSG3, PSG9, FBLN1, AMBP, APOE, LBP, and SHBG peptides as a biomarker for preeclampsia (see Abstract, paragraphs [0007]-[0009], [0013], [0020], [0041], [0060], and Tables 1, 8-10, 13-14, and 18).
Therefore, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have further quantified the levels of C3, C5, C9, PSG2, PSG9, FBLN1, AMBP, APOE, and SHBG as biomarkers for preeclampsia, as taught by Hickock, in the maternal serum sample tested for preeclampsia by detecting levels of FN1, APOC3, CPB2, FGA, LBP, and PSG1, as taught by Nagalla, to arrive at the claimed invention. One of ordinary skill in the art would have been incorporating a known biomarkers useful for detecting and predicting preeclampsia, yielding predictable results. There would have been a reasonable expectation of success because of each of Nagalla and Hickock teach their methods are for testing for preeclampsia in samples taken from pregnant females.
Regarding claim 24, Nagalla teaches FN1 comprises a sequence identified by SEQ ID NO: 15 having 100% sequence identity to SEQ ID NOs: 1, 3-6, and 37 of the instant application (see Appendix A – p.1-6; of record). Hickock discloses C5 comprising SEQ ID NO: 246 having 100% sequence identity to SEQ ID NO: 10 of the instant application (see Appendix B – p.1-2).
Regarding claim 34, Nagalla teaches FN1 comprises a sequence identified by SEQ ID NO: 15 having 100% sequence identity to SEQ ID NOs: 1, 3-6, and 37 of the instant application (see Appendix A – p.1-6; of record). Hickock discloses C5 comprising SEQ ID NO: 473 having 100% sequence identity to SEQ ID NO: 38 of the instant application (see Appendix B – p.3-4).
Regarding claims 35-36, Nagalla teaches comparing the levels of preeclampsia biomarkers to normal maternal serum levels (see paragraphs [0012], [0021]-[0023], [0033]-[0035], [0040]-[0042], and [0046]-[0047]).
Regarding claim 37, Nagalla teaches “the only treatment for preeclampsia is delivery [of the baby]” and further teaches that preeclampsia usually manifests in the 20th week of gestation (see paragraphs [0006] and [0010]-[0011]). Thus, it is understood that a diagnosis of preeclampsia is treated by pre-term delivery of the baby.
Thus, claims 16, 24, and 33-37 are prima facie obvious over Nagalla in view of Hickock.
Response to Arguments
Applicant's arguments filed 3/30/2026 have been fully considered but they are not persuasive.
In Applicant’s Remarks, see p.9, 2nd paragraph,-p.10, 1st paragraph, Applicant argues Figures 3A and 5A were not objected to during the processing of the PCT application and thus comply with PCT Rule 11. Applicant further argues the purpose of the figures are to provide an illustration of the methodology employed and would be understood by one of ordinary skill in the art. This is not found persuasive. Without a color intensity scale, the expressions of the peptides presented in the Figures cannot be properly determined. Accordingly, Figures 3A and 5A are not in compliance since the expression levels are unknown.
In Applicant’s Remarks, see p.11, 1st paragraph-3rd paragraph, Applicant argues the claims do not refer to the natural delivery of a baby but to delivery of a baby assisted by/induced by and/or scheduled by medical personnel or others assisting at the birth based on the diagnostic method of the claim. Applicant further argues the scheduling/timing of the delivery is not natural and the pre-term delivery of a baby in a patient suffering from preeclampsia cannot be considered a natural process in the human body. Applicant argues the delivery of the baby at a time determined by the diagnostic method claimed integrates a natural relationship into a practical application, since it is performed at a time dictated by the diagnostic method employed. This is not found to be persuasive. The claimed invention does not require any unnatural induction that results in the delivery of the baby. Nevertheless, since the state of the art recognizes that delivery of the baby is the only treatment of preeclampsia, it is a standard practice that is well-understood, routine, and conventional in the relevant field (see Nagalla – paragraphs [0010]-[0011]). Furthermore, scheduling and timing are not required limitations of the claims and would in any case be considered abstract ideas that can be practically performed in the human mind. Thus, the claims are directed to correlating a quantitative level of the genes FN1 and C5 in a biological sample from a pregnant subject to a state of preeclampsia in the subject without significantly more. Accordingly, the 35 U.S.C. 101 rejection is maintained.
In Applicant’s Remarks, see p.11, 4th paragraph,-p.13, 3rd paragraph, Applicant argues that Nagalla does not teach delivering the baby when the quantitative level of the FN1 gene and the C5 gene or an expression product of each thereof is greater than in the normal sample. Applicant argues the instantly claimed invention provides an improved method of treating preeclampsia and/or unstable moderate early-onset preeclampsia in a subject having a baby and is non-obvious. This is not found persuasive. While Nagalla does not teach measuring the quantitative levels of the gene C5 or an expression product thereof, the prior art of Hickock obviates this claimed feature. Hickock teaches biomarker proteins and peptides in biological samples taken from pregnant females that are useful for determining the probability of preeclampsia and teaches human APOC3, C3, C5, C9, PSG1, PSG2, PSG3, PSG9, FBLN1, AMBP, APOE, LBP, and SHBG peptides as a biomarker for preeclampsia (see Abstract, paragraphs [0007]-[0009], [0013], [0020], [0041], [0060], and Tables 1, 8-10, 13-14, and 18). Thus, it would have been obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to have further measured the levels of C3, C5, C9, PSG2, PSG9, FBLN1, AMBP, APOE as they relate to preeclampsia, yielding predictable results. Therefore, the claimed invention is prima facie obvious over Nagalla in view of Hickock as set forth above in the new rejection necessitated by amendment.
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.
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/J.P.S./Examiner, Art Unit 1651
/MELENIE L GORDON/Supervisory Patent Examiner, Art Unit 1651
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