Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Detailed Action
The Amendments and Remarks filed 2/25/26 in response to the Office Action of 11/25/25 are acknowledged and have been entered.
Claims 64-67 have been added by Applicant.
Claims 25-30, 32, 34-36, 42, and 48-67 are pending.
Claims 28-30 remain withdrawn.
Claims 25-27, 32, 34-36, 42, and 48-67 are currently under examination.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
The following Office Action contains NEW GROUNDS of rejections Necessitated by Amendments.
Rejections Maintained
Claim Rejections - 35 USC § 103
Claims 25, 32, 35, 42, 49, 58, are 63 remain rejected under 35 U.S.C. 103(a) as being unpatentable over Didonato et al (US 2021/0155713 A1; 5/27/21) in view of Xiao et al (WO 2018/191188 A1; 10/18/2018), Gu et al (PLOS One, 2015, 10(5): e0124135; 12 pages; “Gu1”) and Gu et al (PLOS One, 2014, 9(5): e97292; 10 pages; “Gu2”).
Didonato et al teaches anti-CD73 antibodies that inhibit CD73 ([0782], in particular). Didonato et al further teaches biparatopic antibodies are antigen-binding proteins comprising binding specificity to two distinct epitopes ([0439], in particular). Didonato et al further teaches said anti-CD73 antibodies in pharmaceutical compositions comprising a pharmaceutically acceptable carrier (see claim 52 and [1132] of Didonato et al, in particular). Didonato et al further teaches the CD73 antibodies that inhibit CD73 are administered in methods of treating cancer ([0356] and [0367], in particular). Didonato et al further teaches the antibodies as human or humanized ([0350], in particular) that have the benefit of minimizing immune responses to the antibodies ([0589], in particular). As defined by instant claim 42, cancer is a “CD73-mediated disease”.
Didonato et al does not specifically teach the anti-CD73 antibodies that inhibit CD73 are biparatopic antibodies. However, these deficiencies are made up in the teachings of Xiao et al, Gu1, and Gu2.
At [0005], Xiao et al teaches targeting two antigens or two epitopes on the same antigen with one biparatopic antibody has been shown to be superior to targeting with an individual antibody alone, or with a combination of two separate antibodies. An example for the former case is a biparatopic antibody is DVD-Ig of Gu1. An example of the later is a DVD-Ig molecule of Gu2 which both paratopes target the same antigen at two different non-overlapping epitopes (right column on page 1 of Gu2, in particular).
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a combined method of treating cancer comprising the method of Didonato et al wherein the administered composition comprising anti-CD73 antibodies that inhibit CD73 comprises human or humanized biparatopic anti-CD73 antibodies that inhibit CD73 and target two distinct, non-overlapping, epitopes on CD73 in a pharmaceutically acceptable carrier because Xiao et al teaches targeting two antigens or two epitopes on the same antibody with one biparatopic antibody has been shown to be superior to targeting with an individual antibody alone, or with a combination of two separate antibodies ([0005], in particular). This is an example of some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention. See MPEP 2143.
As recited by instant claim 32, one would predict said biparatopic anti-CD73 antibodies would have higher inhibitory activity on CD73 cared to one or both a first monospecific parental antibody comprsing binding specificity to the first CD73 epitope and a second monospecific parental antibody comprsing binding specificity to the second CD73 epitope because Xiao et al teaches targeting two antigens or two epitopes on the same antibody with one biparatopic antibody has been shown to be superior to targeting with an individual antibody alone, or with a combination of two separate antibodies ([0005], in particular).
As recited by instant claim 35, said biparatopic anti-CD73 antibodies are capable of crosslinking two or more CD73 dimer molecules because the biparatopic CD73 antibodies bind epitopes on CD73 ([0439], in particular).
Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Response to Arguments
In the Reply of 2/25/26, Applicant notes that Didonato focuses on ENTPD2 antibodies and discloses optional combinations with at least one additional therapeutic agent that is an A2AR antagonist. See, e.g., id. at Abstract ("Provided herein are antibodies or antigen-binding fragments thereof, e.g., monoclonal antibodies or antigen binding fragments thereof, that specifically bind to ENTPD2 (e.g., human ENTPD2 protein), and methods of using these antibodies or antigen-binding fragments."). Applicant further states that in some embodiments, the A2AR antagonist is a CD73 antibody. See, e.g., Didonato, paragraphs [0366-0367]. Applicant further states that, Didonato does not focus on CD73 antibodies, much less biparatopic CD73 antigen-binding proteins. Applicant further states that in addition to not teaching CD73 biparatopic antigen-binding proteins, Didonato does not teach CD73 biparatopic antigen-binding proteins with high CD73 inhibitory activity, such as recited in claims 64-67, or CD73 biparatopic antigen- binding proteins capable of crosslinking separate CD73 monomers, as recited in claim 34. Applicant further states none of the cited references specifically teach CD73 biparatopic antigen-binding proteins in any form, let alone CD73 biparatopic antigen-binding proteins with the claimed high CD73 inhibitory activity. Applicant submits that Xiao, Gu 1, and Gu 2 do not cure the deficiencies of Didonato. Applicant further states none of these references teach biparatopic CD73 antibodies. Applicant further states there is no mention of CD73 antibodies in Xiao, Gu 1, or Gu 2. Applicant further states Xiao focuses on antibodies that target human epidermal growth factor receptor 2. Gu 1 and Gu 2 focus on antibodies that target epidermal growth factor receptors and/or epidermal growth factor receptor tyrosine kinases. Applicant concludes based on the disclosures of Didonato, Xiao, Gu 1, and Gu 2, a person of ordinary skill in the art would not have arrived at the instant claims, directed to biparatopic CD73 antibodies, with a reasonable expectation of success. In view of the foregoing, Applicant respectfully requests reconsideration and withdrawal of this rejection.
The arguments found in the Reply of 2/25/26 have been carefully considered, but are not deemed persuasive. In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
In regards to the argument that based on the disclosures of Didonato, Xiao, Gu 1, and Gu 2, a person of ordinary skill in the art would not have arrived at the instant claims, directed to biparatopic CD73 antibodies, with a reasonable expectation of success, the examiner maintains one of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a combined method of treating cancer comprising the method of Didonato et al wherein the administered composition comprising anti-CD73 antibodies that inhibit CD73 comprises human or humanized biparatopic anti-CD73 antibodies that inhibit CD73 and target two distinct, non-overlapping, epitopes on CD73 in a pharmaceutically acceptable carrier because Xiao et al teaches targeting two antigens or two epitopes on the same antigen with one biparatopic antibody has been shown to be superior to targeting with an individual antibody alone, or with a combination of two separate antibodies ([0005], in particular). This is an example of some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention. See MPEP 2143. As recited by instant claim 32, one would predict said biparatopic anti-CD73 antibodies would have higher inhibitory activity on CD73 cared to one or both a first monospecific parental antibody comprsing binding specificity to the first CD73 epitope and a second monospecific parental antibody comprsing binding specificity to the second CD73 epitope because Xiao et al teaches targeting two antigens or two epitopes on the same antibody with one biparatopic antibody has been shown to be superior to targeting with an individual antibody alone, or with a combination of two separate antibodies ([0005], in particular). As recited by instant claim 35, said biparatopic anti-CD73 antibodies are capable of crosslinking two or more CD73 dimer molecules because the biparatopic CD73 antibodies bind epitopes on CD73 ([0439], in particular). Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Claim Rejections - 35 USC § 103
Claim(s) 25, 32, 35, 36, 42, and 48-63 remain rejected under 35 U.S.C. 103 as being unpatentable over Didonato et al (US 2021/0155713 A1; 5/27/21) in view of Xiao et al (WO 2018/191188 A1; 10/18/2018), Gu et al (PLOS One, 2015, 10(5): e0124135; 12 pages; “Gu1”) and Gu et al (PLOS One, 2014, 9(5): e97292; 10 pages; “Gu2”) as applied to claim 25, 32, 35, 42, 49, 58, are 63 above, and further in view of Gramer et al (mAbs, 2013, 5(6): 962-973; 6/13/23 IDS).
Didonato et al, Xiao et al, Gu1, and Gu2 are discussed above.
Didonato et al, Xiao et al, Gu1, and Gu2 do not specifically teach the biparatopic anti-CD73 antibodies are produced by Fab arm exchange, that the biparatopic anti-CD73 antibodies are chimeric antibodies comprising FC regions with F405L and K409R mutations, or nucleic acids encoding the biparatopic anti-CD73 antibodies. However, these deficiencies are made up in the teachings of Gramer et al.
Gramer et al teaches bispecific antibodies are chimerically produced by expressing nucleic acid vectors encoding the antibodies in host cells (left column on page 967, in particular) and wherein a Fab arm exchanged is performed by (a) mixing equimolar amounts of a first parental, monospecific antigen-binding Fab-arm comprising an IgG1 Fc region comprising F405L and a second parental, monospecific antigen-binding Fab-arm comprising an IgG1 Fc region comprising K409R to product a mixture (wherein the mutations drive efficient recombination); (b) placing the mixture under reducing conditions with a reducing agent MEA for 5 hours at room temperature of about 18-30° C; (c) placing the reduced mixture under oxidizing conditions, and (d) isolating the biparatopic antigen-binding protein wherein the biparatopic antigen-binding protein comprises one or more full-length antibody human or humanized heavy chains comprising an IgG1 Fc region (page 968 and Abstract, in particular).
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to generate the human and humanized biparatopic anti-CD73 antibodies of the combined method of Didonato et al, Xiao et al, Gu1, and Gu2 by expressing nucleic acid vectors encoding the antibodies in host cells (left column on page 967, in particular) and wherein a Fab arm exchanged is performed by (a) mixing equimolar amounts of a first parental, monospecific CD73-binding Fab arm comprising an IgG1 Fc region comprising F405L and a second parental, monospecific CD73-binding Fab arm comprising an IgG1 Fc region comprising K409R to product a mixture (wherein the mutations drive efficient recombination); (b) placing the mixture under reducing conditions with a reducing agent MEA for 5 hours at room temperature of about 18-30° C; (c) placing the reduced mixture under oxidizing conditions, and (d) isolating the biparatopic antigen-binding protein wherein the biparatopic antigen-binding protein comprises one or more full-length antibody human or humanized heavy chains comprising an IgG1 Fc region because biparatopic anti-CD73 antibodies of the combined method are bispecific antibodies and Gramer et al teaches bispecific antibodies are chimerically produced by expressing nucleic acid vectors encoding the antibodies in host cells (left column on page 967, in particular) and wherein a Fab arm exchanged is performed by (a) mixing equimolar amounts of a first parental, monospecific antigen-binding Fab-arm comprising an IgG1 Fc region comprising F405L and a second parental, monospecific antigen-binding Fab-arm comprising an IgG1 Fc region comprising K409R to product a mixture (wherein the mutations drive efficient recombination); (b) placing the mixture under reducing conditions with a reducing agent MEA for 5 hours at room temperature of about 18-30° C; (c) placing the reduced mixture under oxidizing conditions, and (d) isolating the biparatopic antigen-binding protein wherein the biparatopic antigen-binding protein comprises one or more full-length antibody human or humanized heavy chains comprising an IgG1 Fc region (page 968 and Abstract, in particular). Regarding instant claim 59, said biparatopic antigen-binding protein is a ”monoclonal” antibody. Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Response to Arguments
In the Reply of 2/25/26, Applicant repeats arguments addressed above.
New Rejections Necessitated by Amendments
Claim Rejections - 35 USC § 112
Claims 64-67 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention. In the instant case, the claims are inclusive of: (i) a genus of biparatopic antigen-binding proteins comprising binding specificity to a first CD73 epitope and a second CD73 epitope, comprising higher inhibitory activity of CD73 compared to one or both of a first monospecific parental antibody comprising binding specificity to the first CD73 epitope and a second monospecific parental antibody comprising binding specificity to the second CD73 epitope, wherein the biparatopic antigen-binding protein comprises 70-100% inhibition of CD73 activity; (ii) a genus of biparatopic antigen-binding proteins comprising binding specificity to a first CD73 epitope and a second CD73 epitope, comprising higher inhibitory activity of CD73 compared to one or both of a first monospecific parental antibody comprising binding specificity to the first CD73 epitope and a second monospecific parental antibody comprising binding specificity to the second CD73 epitope, wherein the biparatopic antigen-binding protein comprises 70-100% inhibition of CD73 activity, wherein the inhibition of CD73 activity is determined by measuring adenosine formation; (iii) a genus of biparatopic antigen-binding proteins comprising binding specificity to a first CD73 epitope and a second CD73 epitope, comprising higher inhibitory activity of CD73 compared to one or both of a first monospecific parental antibody comprising binding specificity to the first CD73 epitope and a second monospecific parental antibody comprising binding specificity to the second CD73 epitope, wherein the biparatopic antigen-binding protein comprises 70-100% inhibition of CD73 activity, wherein the inhibition of CD73 activity is determined by measuring adenosine formation quantitated by liquid chromatograph-mass spectrometry (LC/MS); and (iv) a genus of biparatopic antigen-binding proteins comprising binding specificity to a first CD73 epitope and a second CD73 epitope, comprising higher inhibitory activity of CD73 compared to one or both of a first monospecific parental antibody comprising binding specificity to the first CD73 epitope and a second monospecific parental antibody comprising binding specificity to the second CD73 epitope, wherein the biparatopic antigen-binding protein comprises 70-100% inhibition of CD73 activity, wherein the inhibition of CD73 activity is determined by measuring adenosine formation in COR-L23 lung carcinoma cells expressing human CD73. The written description in this case sets forth the biparatopic antibodies of claims 26, 27, and 34. The specification does not disclose, and the art does not teach, the genera as broadly encompassed in the claims.
A description of a genus may be achieved by means of a recitation of a representative number of species falling within the scope of the genus or by describing structural features common to that genus that “constitute a substantial portion of the genus.” See University of California v. Eli Lilly and Co., 119 F.3d 1559, 1568, 43 USPQ2d 1398, 1406 (Fed. Cir. 1997): “A description of a genus of cDNAs may be achieved by means of a recitation of a representative number of cDNA, defined by nucleotide sequence, falling within the scope of the genus or of a recitation of structural features common to the members of the genus, which features constitute a substantial portion of the genus.”
The inventions at issue in Lilly were DNA constructs per se, the holdings of that case is also applicable to claims such as those at issue here. Further, disclosure that does not adequately describe a product itself logically cannot adequately describe a method of using that product. See Ariad, 598 F.3d at 1354-55 (“Regardless whether the asserted claims recite a compound, Ariad still must describe some way of performing the claimed methods... the specification must demonstrate that Ariad possessed the claimed methods by sufficiently disclosing molecules capable of reducing NF-kB activity so as to ‘satisfy the inventor’s obligation to disclose the technologic knowledge upon which the patent is based, and to demonstrate that the patentee was in possession of the invention that is claimed.’”) (internal citation omitted); see also Univ. of Rochester v. G.D. Searle& Co., Inc., 358 F.3d916,918 (Fed.Cir.2004) (applying the same analysis to assess written description for claims to a “method for selectively inhibiting” a particular enzyme by administering a functionally defined compound, i.e., a “non-steroidal compound that selectively inhibits activity” of the gene product for that enzyme).
In regards to claims to a product defined by function, without a correlation between structure and function, the claim does little more than define the claimed invention by function. That is not sufficient to satisfy the written description requirement. See Eli Lilly, 119 at1568 USPQ2d at 1406 (“definition by function…does not suffice to define the genus because it is only an indication of what the gene does, rather than what it is”).
The instant specification fails to provide sufficient descriptive information, such as definitive structural features that are common to the genera. That is, the specification provides neither a representative number of biparatopic antibodies that encompass the genera nor does it provide a description of structural features that are common to the genera so that one of skill in the art can ‘visualize or recognize’ the members of the genera. “[A] sufficient description of a genus . . . requires the disclosure of either a representative number of species falling within the scope of the genus or structural features common to the members of the genus so that one of skill in the art can ‘visualize or recognize’ the members of the genus.” Ariad, 598 F.3d at 1350 (quoting Eli Lilly, 119 F.3d at 1568-69). A “representative number of species” means that those species that are adequately described are representative of the entire genus. AbbVie Deutschland GMBH v. Janssen Biotech, 111 USPQ2d 1780, 1790 (Fed. Cir. 2014) (“The ’128 and ’485 patents, however, only describe species of structurally similar antibodies that were derived from Joe-9. Although the number of the described species appears high quantitatively, the described species are all of the similar type and do not qualitatively represent other types of antibodies encompassed by the genus.”). Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus to provide a "representative number” of species. Further, in view of Amgen v. Sanofi, 872 F.3d 1367 (Fed. Cir. 2017) and the Office’s February 2018 memo clarifying written description guidance for claims drawn to antibodies, the 2008 Written Description Training Materials are outdated and should not be relied upon as reflecting the current state of law regarding 35 U.S.C. 112. Further, a “newly characterized antigen” test flouts basic legal principles of the written description requirement (Amgen v. Sanofi, 872 F.3d 1367 (Fed. Cir. 2017)). Adequate written description of a newly characterized antigen alone is not considered adequate written description of a claimed antibody to that newly characterized antigen. Where an antibody binds to an antigen tells one nothing about the structure of any other antibody. Also, see the Board’s decision in Appeal 2017-010877 (claims to “A monoclonal antibody that binds a conformational epitope formed by amino acids 42-66 of SEQ ID NO:1”).
The functional requirements of the claimed antibodies is the sort of wish list of properties which fails to satisfy the written description requirement because “antibodies with those properties have not been adequately described.” Centocor, 636 F.3d at 1352. The “claims merely recite a description of the problem to be solved while claiming all solutions to it and . . . cover any compound later actually invented and determined to fall within the claim’s functional boundaries— leaving it to the pharmaceutical industry to complete an unfinished invention.”Ariad Pharmaceuticals, Inc. v. EliLilly and Co.,598 F.3d 1336, 1353 (Fed. Cir. 2010).
Since the disclosure fails to describe common attributes or characteristics that adequately identify members of the genera, and because the genera are highly variant, the disclosure is insufficient to describe the genera. Thus, one of skill in the art would reasonably conclude that the disclosure fails to provide a representative number of species to describe the genera as broadly claimed.
Vas-Cath Inc. v. Mahurkar, 19USPQ2d 1111, clearly states “applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description’ inquiry, whatever is now claimed.” (See page 1117.) The specification does not “clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed.” (See Vas-Cath at page 1116). As discussed above, even though Applicant may propose methods of screening for possible members of the genera, the skilled artisan cannot envision the detailed chemical structure of the encompassed genera, and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolation. The compound itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. See Ariad, 94 USPQ2d at 1161; Centocor at 1876 (“The fact that a fully-human antibody could be made does not suffice to show that the inventors of the '775 patent possessed such an antibody.”)
One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483. In Fiddes, claims directed to mammalian FGF’s were found to be unpatentable due to lack of written description for that broad class. The specification provided only the bovine sequence. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. §112 is severable from its enablement provision (see page 1115).
Claim Rejections - 35 USC § 103
Claim(s) 64-67 is/are rejected under 35 U.S.C. 103 as being unpatentable over Didonato et al (US 2021/0155713 A1; 5/27/21) in view of Xiao et al (WO 2018/191188 A1; 10/18/2018), Gu et al (PLOS One, 2015, 10(5): e0124135; 12 pages; “Gu1”) and Gu et al (PLOS One, 2014, 9(5): e97292; 10 pages; “Gu2”) as applied to claims 25, 32, 35, 42, 49, 58, are 63 above, and further in view of McManus et al (SLAS Discovery, 2018, 23(3): 264-273; 6/13/23 IDS).
Teachings of Didonato et al, Xiao et al, Gu1, and Gu2 are discussed above. Didonato et al teaches the anti-CD73 inhibitor of the combined method of treating cancer as targeting production of adenosine by CD73 to reduce immunosuppressive effects of adenosine ([0782], in particular), that blockade of adenosine signaling induces anti-tumor responses ([1150], in particular), and that there is enhanced anti-tumor efficacy when blocking multiple nodes in the adenosine pathway ([1279], in particular).
Cited references do not specifically teach the biparatopic anti-CD73 antibodies of the combined method comprise “70-100% inhibition of CD73 activity” or that inhibition of CD73 activity is determined by measuring adenosine formation, quantifying adenosine formation by liquid chromatography-mass spectrometry (LC/MS), or that inhibition of CD73 activity is determined in COR-L23 lung carcinoma cells expressing human CD73. However, these deficiencies are made up in the teachings of Didonato et al, Xiao et al, Gu1, and Gu2 in combination with McManus et al.
McManus et al teaches methods of determining inhibition of adenosine formation by CD73 inhibitors, including quantifying adenosine formation by liquid chromatography-mass spectrometry (paragraph spanning columns of page 267, in particular) and that inhibition of CD73 activity is determined in human COR-L23 lung carcinoma cells expressing human CD73 (Figure 6, in particular).
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform the combined method of Didonato et al, Xiao et al, Gu1, and Gu2 of treating cancer wherein production of adenosine by CD73 is completely blocked (resulting in “70-100% inhibition of CD73 activity”) by the biparatopic anti-CD73 antibodies of the combined method because the combined method is to treat cancer, Didonato et al teaches the anti-CD73 inhibitor of the combined method of treating cancer as targeting production of adenosine by CD73 to reduce immunosuppressive effects of adenosine ([0782], in particular), that blockade of adenosine signaling induces anti-tumor responses ([1150], in particular), and that there is enhanced anti-tumor efficacy when blocking multiple nodes in the adenosine pathway ([1279], in particular). Further, McManus et al teaches methods of determining inhibition of adenosine formation by CD73 inhibitors, including quantifying adenosine formation by liquid chromatography-mass spectrometry (paragraph spanning columns of page 267, in particular) and that inhibition of CD73 activity is determined in human COR-L23 lung carcinoma cells expressing human CD73 (Figure 6, in particular). Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Allowable Subject Matter
Claims 26, 27, and 34 are objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
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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