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 .
Claim Status
Claims 1, 30, 45, 50, 57-58, 60, 62, 145, 148, 235, 259, 264-265, 268, 271, and 276-281 are under consideration in this office action.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on January 16, 2026 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the IDS is being considered by the examiner.
Withdrawn Rejections
The rejections of claim 45 under 35 U.S.C. 112(d) as being of improper dependent form and under 35 U.S.C. 112(a) as failing to comply with the written description requirement is withdrawn in view of applicant’s amendment to remove the percent identity language from claim 45.
Maintained Rejections
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1, 30, 45, 50, 57-58, 60, 62, 145, 259, 264-265, 268, 271, and 276-281 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2016/090312, published June 9, 2016 (“Jens”; IDS from 12/17/21, Foreign Patent Documents 194) in view of CN108239144, published July 3, 2018 (“Zhang”; IDS from 12/17/21, Foreign Patent Document 114).
The claims are directed to a chimeric antigen receptor (CAR) comprising an extracellular antigen-binding domain that binds human GPRC5D, a spacer comprising of SEQ ID NO: 17, a transmembrane domain, and an intracellular signaling region comprising CD3-zeta.
Jens teaches a CAR comprising an extracellular antigen-binding domain that recognizes GPRC5D, a transmembrane domain, and an intracellular domain (pg 2, ln 31-33 to pg 3, ln 1-3), as in claim 1. The antigen binding domain that recognizes GPRC5D is comprised of a heavy chain variable region (HCVR) of amino acid sequence SEQ ID NO: 65 and a light chain variable region (LCVR) of amino acid sequence SEQ ID NO: 66 (pg 6, ln 32-34 to pg 7, ln 1), which are identical to the HCVR of SEQ ID NO: 27 and LCVR of SEQ ID NO: 66, as in claims 1 and 60. The extracellular antigen-binding domain is a single-chain variable fragment (scFv), as in claim 30. Jens teaches a pharmaceutical composition comprising immunosuppressive cells expressing GPRC5D-specific CAR (pg 37-38), as instant claim 145.
The transmembrane domain of Jens comprises a CD4, CD28, or CD8 (pg 154, ln 16-22), as in claims 57, 60, 62, and 264-265. The CD28 polypeptide can have an amino acid sequence of SEQ ID NO: 270 or a fragment thereof, comprised of up to three conservative amino acid substitutions (pg 154, ln 23-34 to pg 155, ln 1-17), as in the transmembrane domain of SEQ ID NO: 18 of instant claims 276-277.
The intracellular domain of the CAR comprises a CD3 zeta polypeptide (pg 156, ln 26-30), as in claims 1, 60, and 62. The CD3 zeta polypeptide can have an amino acid sequence of SEQ ID NO: 272 or a fragment thereof, comprised of up to three conservative amino acid substitutions (pg 156, ln30-36), as in the intracellular domain of SEQ ID NO: 20 of instant claims 276-277.
The intracellular domain of the CAR of Jens may also be comprised of a 4-IBB polypeptide (pg 157, ln 23-25), as in claims 50 and 268. The 4-1BB polypeptide can have an amino acid sequence of SEQ ID NO: 274 or a fragment thereof (pg 158, ln 19-30), as in the intracellular domain of SEQ ID NO: 19 of instant claims 276-277.
The scFv of instant claim 45 and 278-279 of SEQ ID NO: 8 is identical to SEQ ID NO: 166 of Jens, which is directed to an scFv extracellular antigen-binding domain that recognizes GPRC5D (pg 116, ln 1-5).
Although Jens teaches that the CAR can be comprised of a spacer region that links the extracellular antigen-binding domain to the transmembrane domain and that the spacer region can be the hinge region from IgG1 or the CH2CH3 region of immunoglobulin and portions of CD3 (pg 156, ln 19-24), Jens does not teach a spacer comprising the amino sequence of SEQ ID NO: 17, as required by claims 1, 60, and 62 or a spacer encoded by the nucleotide sequence SEQ NO: 74, as required by claim 259.
Zhang teaches a CAR comprised of antigen-binding domain, hinge region, transmembrane region, and intracellular signal domain (pg 1, ln 25-31). In order to prolong the survival of CAR-T cells and/or improve the ability of CAR-T cells to infiltrate tumors, Zhang modified the amino acid sequence of the hinge region (pg 2, ln 48-51), as in instant claim 60. Zhang teaches a hinge/spacer region of SEQ ID NO: 2 that is capable of improving the ability of CAR-T cells to infiltrate tumors (pg 2, ln 53-55); SEQ ID NO: 2 is identical to the amino acid sequence of instant SEQ ID NO: 17, as in claims 1, 60 and 62. The nucleotide sequence set forth in SEQ ID NO: 74 of instant claim 259 encodes the amino acid sequence of instant SEQ ID NO: 17. Thus, Zhang teaches both the amino acid sequence and nucleotide sequence of the spacer.
Claims 58 and 280 are directed to a CAR comprising the amino acid sequence of SEQ ID NO: 290. SEQ ID NO: 290 is comprised of the scFv of SEQ ID NO: 8, the spacer of SEQ ID NO: 17, the transmembrane domain of SEQ ID NO: 18, the intracellular cellular signaling domain of SEQ ID NO: 19, and the cytoplasmic signaling domain of SEQ ID NO: 20. As Jens teaches a CAR comprised of the same amino acid sequences in the same order and Zhang teaches the spacer; the combined references teach the sequence of instant SEQ ID NO: 290. Claims 271 and 281 are directed to a chimeric antigen receptor encoded by the nucleotide sequence of SEQ ID NO 289. As instant SEQ ID NO: 289 encodes the amino acid sequence of SEQ ID NO: 290, the nucleotide sequence is obvious over the combined teachings of Jens in view of Zhang.
Given that Jens teaches a CAR comprising the claimed GPRC5D binding domain, a spacer, a transmembrane domain, and an intracellular domain and further given that Zhang teaches the claimed spacer, it would have been obvious to one of ordinary skill in the art to use the hinge of Zhang in the CAR of Jens. This is because there were a finite number of identified and predictable solutions for the spacer at the time the application was filed. For example, Zhang teaches that hinge regions of different lengths have different effects on the stability of CAR-T cells (pg 2). One would use the spacer of Zhang in the CAR of Jens and have a reasonable expectation of success, because of its demonstrated advantages in prolonging the memory of CAR T cells and their ability to infiltrate tumors (pg 1, ln 20-23). The additional steps of determining spacer length are via methods described in the art (see all of Zhang). See MPEP 2143.02.II: The court held the claimed method would have been obvious over the prior art relied upon because one reference contained a detailed enabling methodology, a suggestion to modify the prior art to produce the claimed invention, and evidence suggesting the modification would be successful.
Claims 1, 30, 45, 50, 57-58, 60, 62, 145, 148, 235, 259, 264-265, 268, 271, and 276-281 are rejected under 35 U.S.C. 103 as being unpatentable over Jens in view of Zhang as applied to claims 1, 30, 45, 50, 57-58, 60, 62, 145, 259, 264-265, 268, 271, and 276-281 above, and further in view of Ebert et al, published online March 2018 (PTO-892 from 10/23/24).
The teachings of Jens in view of Zhang are discussed above. They do not teach a combination of two different cells, as required by claims 148 and 235.
Ebert et al teaches that combining single-specificity CAR-T cells can be particularly useful for targeting two antigens, which are expressed on distinct cell types within cancers to enhance the anti-cancer effect, as in the combination of a plurality of first cells comprising a first CAR and a plurality of second cells comprising another CAR, as in claim 235. For example, CAR-T cells targeting FAP have been mixed with those targeting EphA2 to enable simultaneous attack of A549 lung cancer cells (EphA2+) and their supporting stroma (FAP+ cancer-associated fibroblasts), resulting in significantly enhanced anti-cancer efficacy compared with either CAR-T cell (pg 393; “Pooling CAR-T cells of single specificities”).
Given that Jens in view Zhang teaches a CAR comprising the claimed GPRC5D binding domain, a spacer comprising an IgG4/2 chimeric hinge or modified IgG4 hinge, and IgG2/4 chimeric CH2 region, and IgG4 CH3 region, a transmembrane domain, and an intracellular domain and further given that Ebert et al teaches the combination of two cell populations for the treatment of cancer, it would have been obvious to combine cells expressing the CAR and another antigen target, because, as Ebert et al teach, pooling CAR-T cells of multiple specificities may overcome the problems of tumor antigen heterogeneity and antigen escape, as well as on-target, off-tumor toxicity (pg 393, paragraph). Performing such a modification is within the ability of the ordinary artisan and requires only routine experimentation.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 30, 45, 50, 57-58, 60, 62, 145, 148, 235, 259, 264-265, 268, 271, and 276-281 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3, 5, 8-13, and 17-49 of U.S. Patent No. 10,633,426 in view of CN108239144 (“Zhang”; IDS from 12/17/21, Foreign Patent Document 114) and Ebert et al (PTO-892 from 10/23/24).
Patent ‘426 teaches a CAR comprising an extracellular antigen-binding domain that binds to GPRC5D, a transmembrane domain, and an intracellular signaling domain. ‘426 teaches an antigen binding domain that recognizes GPRC5D that is comprised of a heavy chain variable region (HCVR) of amino acid sequence of SEQ ID NO: 65 and a light chain variable region (LCVR) of amino acid sequence of SEQ ID NO: 66. The HCVR and LCVR pair of ‘426 is identical to the HCVR of SEQ ID NO: 27 and LCVR of SEQ ID NO: 66, as in claims 1, 60, 62, 260, 267. The extracellular antigen-binding domain is a single-chain variable fragment (scFv), as in claim 30.
In claim 17 of ‘426, the transmembrane domain comprises a CD4, CD28, or CD8 , as in claims 30, 57, 60, 62, and 264-265.
The intracellular domain of the CAR comprises a CD3 zeta polypeptide (‘426 claim 17), as in instant claims 60 and 62. The intracellular domain of the CAR may also be comprised of a 4-IBB polypeptide (‘426 claim 23), as in instant claims 50 and 268.
‘426 does not teach a spacer nor does it teach a spacer comprising a SEQ ID NO: 17, as required by claims 1, 60, and 62 or a spacer comprising the amino sequence encoded by the nucleotide sequence SEQ NO: 74, as required by claim 259.
Zhang teaches a CAR comprised of antigen-binding domain, hinge region, transmembrane region, and intracellular signal domain (pg 1, ln 25-31). In order to prolong the survival of CAR-T cells and/or improve the ability of CAR-T cells to infiltrate tumors, Zhang modified the amino acid sequence of the hinge region (pg 2, ln 48-51), as in instant claim 60. Zhang teaches a hinge region of SEQ ID NO: 2 that is capable of improving the ability of CAR-T cells to infiltrate tumors (pg 2, ln 53-55); SEQ ID NO: 2 is identical to the amino acid sequence of instant SEQ ID NO: 17, as in claims 1, 60 and 62. The nucleotide sequence set forth in SEQ ID NO: 74 of instant claim 259 encodes the amino acid sequence of instant SEQ ID NO: 17. Thus, Zhang teaches both the amino acid sequence and nucleotide sequence of the spacer.
Claim 58 and 280 are directed to a CAR comprising the amino acid sequence of SEQ ID NO: 290. SEQ ID NO: 290 is comprised of the scFv of SEQ ID NO: 8, the spacer of SEQ ID NO: 17, the transmembrane domain of SEQ ID NO: 18, the intracellular cellular signaling domain of SEQ ID NO: 19, and the cytoplasmic signaling domain of SEQ ID NO: 20. As ‘426 teaches a CAR comprised of the same amino acid sequences in the same order and Zhang teaches the spacer; the combined references teach the sequence of instant SEQ ID NO: 290. Claims 271 and 281 are directed to a chimeric antigen receptor encoded by the nucleotide sequence of SEQ ID NO 289. As instant SEQ ID NO: 289 encodes the amino acid sequence of SEQ ID NO: 290, the nucleotide sequence is obvious over the combined teachings of ‘426 in view of Zhang.
Given that ‘426 teaches a CAR comprising the claimed GPRC5D binding domain, a spacer, a transmembrane domain, and an intracellular domain and further given that Zhang teaches the claimed spacer, it would have been obvious to one of ordinary skill in the art to use the hinge of Zhang in the CAR of ‘426. This is because there were a finite number of identified and predictable solutions for the spacer at the time the application was filed. For example, Zhang teaches that hinge regions of different lengths have different effects on the stability of CAR-T cells (pg 2). One would use the spacer of Zhang in the CAR of ‘426 and have a reasonable expectation of success, because of its demonstrated advantages in prolonging the memory of CAR T cells and their ability to infiltrate tumors (pg 1, ln 20-23).
‘426 in view of Zhang does not teach a combination of two different cells, as required by claims 148 and 235.
Ebert et al teaches that combining single-specificity CAR-T cells can be particularly useful for targeting two antigens, which are expressed on distinct cell types within cancers to enhance the anti-cancer effect, as in the combination of a plurality of first cells comprising a first CAR and a plurality of second cells comprising another CAR. For example, CAR-T cells targeting FAP have been mixed with those targeting EphA2 to enable simultaneous attack of A549 lung cancer cells (EphA2+) and their supporting stroma (FAP+ cancer-associated fibroblasts), resulting in significantly enhanced anti-cancer efficacy compared with either CAR-T cell (pg 393; “Pooling CAR-T cells of single specificities).
Given that ‘426 in view of Zhang teaches a CAR comprising the claimed GPRC5D binding domain, a spacer, a transmembrane domain, and an intracellular domain and further given that Ebert et al teaches the combination of two cell populations for the treatment of cancer, it would have been obvious to combine cells expressing the CAR and another antigen target, because, as Ebert et al teach, pooling CAR-T cells of multiple specificities may overcome the problems of tumor antigen heterogeneity and antigen escape, as well as on-target, off-tumor toxicity (pg 393, paragraph). Performing such a modification is within the ability of the ordinary artisan and requires only routine experimentation.
Therefore, given that the claims of patent ‘426 in view of Zhang and Ebert et al are directed to the same antigen binding domain, spacer, transmembrane domain, and intracellular domain and other variants, the claims are not patentable over each other.
Response to Arguments
Applicant's arguments filed January 16, 2026 have been fully considered but they are not persuasive.
Applicant asserts that a prima facie case of obviousness has not been established because the rejection does not identify substantial evidence that a person of ordinary skill in the art would have had a reasonable expectation of success when transplanting Zhang’s spacer into Jen’s anti-GPRC5D CAR (remarks, pg 9). Because Zhang teaches the spacer in an anti-PSCA CAR and that the hinge regions of different lengths have different effects on stability and function, it was not reasonably predictable which spacer hinge would work in Jen’s CAR directed to GPRC5D (remarks, pg 10). Additional discussion by applicant related to unpredictability in the art based on the teachings of Watanabe et al and Kunkele (remarks, pg 11-12) is acknowledged. However, these arguments are not persuasive. Jens teaches a GPRC5D binding CAR comprised of spacer, a transmembrane domain, and an intracellular signaling region of CD3-zeta. Zhang teaches the claimed spacer and other spacers of different lengths. Moreover, Zhang recognizes the obstacles to be overcome in the development of CARs and suggests a finite number of ways to overcome these obstacles; these being short spacer (hinge only), medium spacer (hinge-CH3), and long spacer (hinge-CH2-CH3) spacers. Furthermore, Zhang teaches methods for assessing the ability of CAR-T cells expressing CARs with different spacer lengths to infiltrate tumors (pg 5-6). Thus, the claims are obvious because one of ordinary skill in the art would have been able to test the known spacers in known methods for assessing the function of CARs of different spacer lengths. One would have a reasonable expectation of success in the identification of the optimal spacer in the CAR of Jens.
Arguments related to a lack of absolute predictability of how each spacer will perform for each CAR are not persuasive. The motivation to use the spacer of Zhang need not be supported by a finding that the prior art suggested that the combination claimed by the applicant was the preferred or most desirable combination over the other alternatives. It would have been obvious to one of ordinary skill in the art at the time the application was filed to use the spacer of Zhang in the GPRC5D-targeted CAR of Jens because Zhang has identified the advantages of such a spacer. Not only does Zhang teach the spacer claimed but also teaches the other spacers (i.e. hinge only and hinge-CH3) that were investigated by applicant (see specification filed 4/29/2021; pg 285). An "obvious to try" rationale may support a conclusion that a claim would have been obvious where one skilled in the art is choosing from a finite number of identified, predictable solutions, with a reasonable expectation of success. " [A] person of ordinary skill has good reason to pursue the known options within his or her technical grasp. If this leads to the anticipated success, it is likely that product [was] not of innovation but of ordinary skill and common sense. In that instance the fact that a combination was obvious to try might show that it was obvious under 35 U.S.C. 103." KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 421, 82 USPQ2d 1385, 1397 (2007). The teachings of Zhang demonstrate that the ordinary artisan was aware of the criteria to determine optimization of a CAR comprised of a spacer; further, it was known that these criteria had been met for several other CARs. Thus, it would be conventional and within the skill of one in the art to identify the optimum spacer length for the CAR of Jens.
Applicant argues that CAR activity cannot be predicted based on antigen binding domain or spacer length, thereby demonstrating unpredictability in the art, and that evidence of unexpectedly advantageous results support a finding of nonobviousness of the product itself (remarks, pg 14). The claimed CAR with spacer of SEQ ID NO: 17 exhibits low tonic signaling, high antigen-dependent activity, and superior in vivo survival, which is an unexpectedly favorable therapeutic profile (remarks, pg 16). Applicant discusses how evidentiary references Watanabe et al (“Fine-tuning the CAR spacer improves T-cell potency”, Oncoimmunology, 2016; PTO-892 from 10/16/2025) and Kunkele et al (“Functional Tuning of CARs Reveals Signaling Threshold above which CD8+ CTL Antitumor Potency Is Attenuated due to Cell Fas-FasL-Dependent ACICD”, Cancer Immunol Res, 2015; PTO-892 from 10/16/2025) support the unpredictability in the art. However, these references, like Zhang, provide a methodology for determining which spacer works optimally for a given CAR. Watanabe et al teaches how molecular refinements to the CAR spacer can impact multiple biological processes, including tonic signaling (see abstract), and that these changes can profoundly influence in vivo CAR T-cell potency (pg 1, column 1). Kunkele et al teaches that the extracellular spacer has a significant contribution on CAR T-cell performance and that CAR spacers need to adjust the biophysical synapse distance between a T cell and a tumor cell to one that is compatible for T-cell activation (pg 368, column 2). As such, the instant CAR construct was optimized via methods known in the art. If the inventive concept is determined by the application of a well-known problem-solving strategy, which is the work of a skilled artisan, the invention is obvious over the prior art teaching and is not patentable. What is claimed is merely the optimization of variables (e.g., spacer length) within the claims that flow from the “normal desire of scientists or artisans to improve upon what is already generally known.” In re Peterson, 315 F.3d 1325, 1330 (Fed.Cir.2003).
Further regarding the claim of unexpected results, case law holds that although the record may establish evidence of secondary consideration which are indicia of nonobviousness, the record may also establish such a strong case of obviousness that the objective evidence of nonobviousness is not sufficient to outweigh the evidence of obviousness. Newell Cos. V. Kenney Mfg. Co., 864 F.2d 757, 769, 9 USPQ2d 1417, 1427 (Fed. Cir. 1988), cert. denied, 493 U.S. 814 (1989). Given the combined teachings of Jens and Zhang, the claimed product would have been readily conceived by an ordinary artisan. One looking to achieve decreased tonic signaling and improved ability would have tried the spacer of Zhang, because it was well known in the art that spacer length is an important factor determining CAR functionality and efficacy (see Watanabe et al and Kunkele et al). In Kunkele et al, three spacer lengths were investigated: short spacer (hinge only), medium spacer (hinge-CH3), and long spacer (hinge-CH2-CH3) (pg 369, column 1). It is the Office’s position that the “long spacer” within the spacer genus can be at once envisaged because the species within this genus (e.g. short, medium, and long spacer) are sufficiently limited and well delineated in the prior art; see MPEP 2131.02(III).
Regarding the double patenting rejection, applicant argues that the claims are not obvious over U.S. Patent No. 10,633,426 in view of Zhang and Ebert, for reasons as applied to arguments related to the rejection under 35 U.S.C. 103. For reasons discussed above, the double patenting rejection is maintained.
Conclusion
No claim is allowed.
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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Jennifer Benavides
Examiner
Art Unit 1675
/JENNIFER A BENAVIDES/Examiner, Art Unit 1675
/AURORA M FONTAINHAS/Primary Examiner, Art Unit 1675