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 .
Status of Claims
The amended claims filed 11/24/2025 are acknowledged and entered.
Claims 1, 2, 4-7, 9-17, 29, 36, 39, 41, 43, 46, and 48 have been amended
Claims 3, 8, 18-28, 30-35, 40, 42, and 47 are cancelled
Claims 36-39, 41, 43-46, and 48 are withdrawn.
Claims 1, 2, 4-7, 9-17, and 29 are pending and examined on their merits.
Response to Amendment
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office Action.
Claim Rejections - 35 USC § 112 withdrawn
1. The rejections for claim 4 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as ), second paragraph, as being indefinite is withdrawn in view Applicant’s amendment of claim 4.
2. The rejection of claim 4 under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends (claim 3) is withdrawn in view of Applicant’s cancellation of claim 3 and the amended claim 4 depends from claim 1.
Claim Rejections - 35 USC § 103 withdrawn
3. The rejections of claims 1-7 and 29 and 25 under 35 U.S.C. 103 as being unpatentable over Cullen (US 2019/0100761 A1, Cullen, published on April 4, 2019), in view of Barrett (WO 2017/180587 A2 Barrett, prior filing date: April 1, 2017-04-11), Qin (PLoS ONE May 2010 | Volume 5 | Issue 5, 1-4) and Daniels (Clinical Immunology (2006) 121, 144-158) are withdrawn in view of Applicant’s amendments to claim 1, and 4-7.
4. The rejection of claims 1, 8-17 under 35 U.S.C. 103 as being unpatentable over Cullen, Barrett and Daniels in view of Zhang (Biomarker Research (2017) 5:22. 1-6) and Liu (Sci Rep 7, 2193 (2017) pages 1-9) are withdrawn in view of Applicant’s amendments to claim 9-17 and cancellation of claim 8.
New Rejections Based on Amendments
Claim Rejections - 35 USC § 102
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 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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1-2 and 9 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Fritsch (US2018/0153975/A1).
Fritsch teaches chimeric antigen receptors (CARs) that are used in order to generate immune-responsive cells, such as T cells, specific for selected targets [0718]. T cells expressing a desired CAR and these CART cells have specific cytotoxic activity against antigen-bearing tumors [0720]. Fritsch also teaches the IREB2 gene [0151] and Table 8 also teaches IREB2 and provides a sequence for IREB2 (instant claims 1 and 2). First-generation CARs typically consist of a single-chain variable fragment of an antibody specific for an antigen, a transmembrane domain, to the transmembrane and intracellular signaling domains. Second-generation CARs incorporate the intracellular domains of one or more costimulatory molecules and Third-generation CARs include a combination of costimulatory endodomains (instant claim 9).
Therefore, the reference teachings anticipate the claimed invention.
Claim Rejections - 35 USC § 103
Claims 1, 2, 4-7, 9-17, and 29 are rejected under 35 U.S.C. 103 as being unpatentable over Cullen, Barrett and Zhang, in view of Qin, Liu and Daniels,
Cullen teaches that recombinant DNA technology involves the cloning of a gene encoding a desired polypeptide into a suitable expression vector. The expression vector encoding the desired polypeptide is then transfected into a host cell, which is cultured to produce the RNA encoding the polypeptide. The RNA is translated to produce the polypeptide [0005] (instant claim 1). Cullen also teaches “suitable cells": such as eukaryotic cells (including animal cells and human cells) ……. including a T cell such as a CD4 T cell [0058] (which can infiltrate various tissues), (instant claim 3-4) and that promoters useful in the practice of the invention include, but are not limited to, constitutive promoters [0052] (instant claims 5-6).
Cullen does not teach that the desired polypeptide is IRP-2 as set forth in SEQ ID NO: 2, or that the constitutive promoter is EF-1alpha and does not teach pharmaceutical compositions. Cullen does not teach the T cell further comprising a Chimeric antigen receptors (CAR) or the CAR transcriptionally linked to IRP-2 by a sequenced encoding a self-cleaving peptide.
Barrett teaches a pharmaceutical composition comprising suitable carriers and excipients (page 2788, [0336]) (instant claim 29). Barrett also teaches the IRP-2 protein encoded by the gene IREB2 which is 100% identical to SEQ ID NO: 2 (instant claim 2). See sequence alignment below:
Title: US-17-635-534-2
Sequence: 1 MDAPKAGYAFEYLIETLNDS..........VEITLYKHGGLLNFVARKFS 963
US-16-092-829B-42035
Sequence 42035, US/16092829B
Publication No. US20190192691A1
GENERAL INFORMATION
APPLICANT: BARRETT, PETER
APPLICANT: GLADSTONE, MICHAEL N.
APPLICANT: KASSUM, TARIQ A.
APPLICANT: SURI, VIPIN
APPLICANT: LI, DAN JUN
APPLICANT: SUN, DEXUE
APPLICANT: DOLINSKI, BRIAN
TITLE OF INVENTION: REGULATED BIOCIRCUIT SYSTEMS
FILE REFERENCE: 2095.1300US371
CURRENT APPLICATION NUMBER: US/16/092,829B
CURRENT FILING DATE: 2018-10-11
PRIOR APPLICATION NUMBER: PCT/US2017/026950
PRIOR FILING DATE: 2017-04-11
PRIOR APPLICATION NUMBER: 62/320,864
PRIOR FILING DATE: 2016-04-11
PRIOR APPLICATION NUMBER: 62/466,596
PRIOR FILING DATE: 2017-03-03
NUMBER OF SEQ ID NOS: 213456
SEQ ID NO 42035
LENGTH: 963
TYPE: PRT
ORGANISM: Homo sapiens
FEATURE:
OTHER INFORMATION: Payload ID: 8547
FEATURE:
OTHER INFORMATION: Gene Symbol: IREB2
FEATURE:
OTHER INFORMATION: Gene Name:
iron-responsive element binding protein 2
FEATURE:
OTHER INFORMATION: ENSP ID: ENSP00000258886
Query Match 100.0%; Score 5004; Length 963;
Best Local Similarity 100.0%;
Matches 963; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 MDAPKAGYAFEYLIETLNDSSHKKFFDVSKLGTKYDVLPYSIRVLLEAAVRNCDGFLMKK 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MDAPKAGYAFEYLIETLNDSSHKKFFDVSKLGTKYDVLPYSIRVLLEAAVRNCDGFLMKK 60
Qy 61 EDVMNILDWKTKQSNVEVPFFPARVLLQDFTGIPAMVDFAAMREAVKTLGGDPEKVHPAC
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 EDVMNILDWKTKQSNVEVPFFPARVLLQDFTGIPAMVDFAAMREAVKTLGGDPEKVHPAC
Qy 121 PTDLTVDHSLQIDFSKCAIQNAPNPGGGDLQKAGKLSPLKVQPKKLPCRGQTTCRGSCDS
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 PTDLTVDHSLQIDFSKCAIQNAPNPGGGDLQKAGKLSPLKVQPKKLPCRGQTTCRGSCDS
Qy 181 GELGRNSGTFSSQIENTPILCPFHLQPVPEPETVLKNQEVEFGRNRERLQFFKWSSRVFK
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 GELGRNSGTFSSQIENTPILCPFHLQPVPEPETVLKNQEVEFGRNRERLQFFKWSSRVFK
Qy 241 NVAVIPPGTGMAHQINLEYLSRVVFEEKDLLFPDSVVGTDSHITMVNGLGILGWGVGGIE
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 NVAVIPPGTGMAHQINLEYLSRVVFEEKDLLFPDSVVGTDSHITMVNGLGILGWGVGGIE
Qy 301 TEAVMLGLPVSLTLPEVVGCELTGSSNPFVTSIDVVLGITKHLRQVGVAGKFVEFFGSGV
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 TEAVMLGLPVSLTLPEVVGCELTGSSNPFVTSIDVVLGITKHLRQVGVAGKFVEFFGSGV
Qy 361 SQLSIVDRTTIANMCPEYGAILSFFPVDNVTLKHLEHTGFSKAKLESMETYLKAVKLFRN
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 SQLSIVDRTTIANMCPEYGAILSFFPVDNVTLKHLEHTGFSKAKLESMETYLKAVKLFRN
Qy 421 DQNSSGEPEYSQVIQINLNSIVPSVSGPKRPQDRVAVTDMKSDFQACLNEKVGFKGFQIA
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 421 DQNSSGEPEYSQVIQINLNSIVPSVSGPKRPQDRVAVTDMKSDFQACLNEKVGFKGFQIA
Qy 481 AEKQKDIVSIHYEGSEYKLSHGSVVIAAVISCTNNCNPSVMLAAGLLAKKAVEAGLRVKP
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 481 AEKQKDIVSIHYEGSEYKLSHGSVVIAAVISCTNNCNPSVMLAAGLLAKKAVEAGLRVKP
Qy 541 YIRTSLSPGSGMVTHYLSSSGVLPYLSKLGFEIVGYGCSICVGNTAPLSDAVLNAVKQGD
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 541 YIRTSLSPGSGMVTHYLSSSGVLPYLSKLGFEIVGYGCSICVGNTAPLSDAVLNAVKQGD
Qy 601 LVTCGILSGNKNFEGRLCDCVRANYLASPPLVVAYAIA GTVNIDFQTEPLGTDPTGKNIY
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 601 LVTCGILSGNKNFEGRLCDCVRANYLASPPLVVAYAIA GTVNIDFQTEPLGTDPTGKNIY
Qy 661 LHDIWPSREEVHRVEEEHVILSMFKALKDKIEMGNKRWNSLEAPDSVLFPWDLKSTYIRC
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 661 LHDIWPSREEVHRVEEEHVILSMFKALKDKIEMGNKRWNSLEAPDSVLFPWDLKSTYIRC
Qy 721 PSFFDKLTKEPIALQAIENAHVLLYLGDSVTTDHISPAGSIARNSAAAKYLTNRGLTPRE
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 721 PSFFDKLTKEPIALQAIENAHVLLYLGDSVTTDHISPAGSIARNSAAAKYLTNRGLTPRE
Qy 781 FNSYGARRGNDAVMTRGTFANIKLFNKFIGKPAPKTIHFPSGQTLDVFEAAELYQKEGIP
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 781 FNSYGARRGNDAVMTRGTFANIKLFNKFIGKPAPKTIHFPSGQTLDVFEAAELYQKEGIP
Qy 841 LIILAGKKYGSGNSRDWAAKGPYLLGVKAVLAESYEKIHKDHLIGIGIAPLQFLPGENAD
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 841 LIILAGKKYGSGNSRDWAAKGPYLLGVKAVLAESYEKIHKDHLIGIGIAPLQFLPGENAD
Qy 901 SLGLSGRETFSLTFPEELSPGITLNIQTSTGKVFSVIASFEDDVEITLYKHGGLLNFVAR
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 901 SLGLSGRETFSLTFPEELSPGITLNIQTSTGKVFSVIASFEDDVEITLYKHGGLLNFVAR
Qy 961 KFS 963
|||
Db 961 KFS 963
Barrett does not teach the T cell further comprising a Chimeric antigen receptors (CAR) or the CAR transcriptionally linked to IRP-2 by a sequence encoding a self-cleaving peptide. Barrett does not teach the constitutive promoter being EF-1alpha
Zhang teaches that CARs are engineered receptors that can graft an arbitrary specificity onto an immune effector cell (T cell) (instant claim 1). CARs include three parts: (1) an extracellular (instant claim 13) antigen recognition domain of the single-chain Fragment variant (scFv) (instant claim 11) derived from an antibody (instant claim 10), (2) a transmembrane domain and (3) an intracellular T cell activation domain of CD3ζ. (instant claim 9) (page 1, Background section). The third-generation CARs are made by combining multiple signaling domains to augment potency with stronger cytokine production and killing ability (page 3, Third generation section) (instant claim 9). CAR-T cell therapy is designed to redirect a patient’s or donor’s T cells to specifically target (a tumor antigen) and destroy tumor cells (page 1, Background section) (instant claims 12 and 13).
Zhang does not teach the CAR transcriptionally linked to IRP-2 by a sequence encoding a self-cleaving peptide. It does not teach the constitutive promoter being EF-1alpha.
Liu teaches a systematic comparison of 2A peptides for cloning multi-genes in a polycistronic vector (title, entire article). The construction of a multi-gene co-expression vector with 2A sequences and a schematic representation of the mechanism of “self-cleaving” 2A peptides is taught in Figure 1(A). Basically, Gene 1 and Gene 2 are linked by the 2A sequence in one construct (instant claims 14-16). Figure 2 teaches bi-cistronic 2A constructs including M-T2A-GFP construct where the two genes (M and GFP) are separated by the T2A sequence (instant claim 17).
Liu does not teach the constitutive promoter being EF-1alpha.
Qin teaches that the human elongation factor 1 alpha promoter (EF1A) is a constitutive promoter (abstract) (instant claim 7) and is consistently strong in most cell types (page 1, Results and discussion section).
Daniels teaches that IRP-2 regulates the expression of CD71 (TfR, Transferrin receptor) (page 145, last paragraph). CD71 is ubiquitously expressed at low levels on normal cells and is expressed at greater levels on cells with a high proliferation rate (page 146 first column, second paragraph). In addition, CD71 plays an immunoregulatory role in T cell activation and can provide the second stimulus required for the activation of T cells (page 149, first column, second paragraph) (instant claim 4). Antibodies against CD71 leads to the downregulation of CD71 on the surface of the cells and inhibits the proliferation of mitogen activated T cells (page 152, second column, first paragraph).
It would be obvious to one of ordinary skill in the art to combine the teachings of Cullen, Barrett and Zhang to generate a T cell comprising (1) IRP2 (as taught by Cullen and Barrett) and (2) a CAR. The CAR would comprise an antigen biding domain (an antibody or a scFv fragment binding a tumor antigen on the cell surface), a transmembrane domain and one or more signaling domains as taught by Zhang.
It would further be obvious to combine the teachings of Cullen, Barrett and Zhang with Liu and Qin. This T cell can be generated by using a bicistronic construct as taught by Liu where the IRP-2 gene is linked to the CAR polynucleotide by a self-cleaving peptide, such as 2A or T2A, and link the IRP-2 polynucleotide sequence of Barrett to a constitutive promoter such as EF-1alpha so the gene would be always turned on and thus overexpressing the protein (as taught by Qin). Thus, it would be obvious to combine all the above references to arrive at the claimed invention.
The artisan would be motivated to generate the T cell as described above: a CAR T cell that (over)express (1) a synthetic IRP-2 and/or (2) a tumor antigen biding domain on the cell surface for the following reasons. IRP-2 is involved in cellular iron homeostasis and the regulation of CD71 gene expression. When IRP-2 is overexpressed, there would be an upregulation of CD71 leading to the proliferation of the activated T cell as taught by Daniels. That is, IRP-2 overexpression would lead to the proliferation of the CAR T cell when stimulated with an tumor antigen eliciting stronger cytokine production and killing ability. There would be a reasonable expectation of success because the recombinant DNA technology taught by Cullen and the structure of a CAR (Zhang) are well known in the art and it is routinely practiced in many molecular biology laboratories in the world. In addition, there would be a reasonable expectation of success because CAR-T cell therapy is designed to redirect a patient’s or donor’s T cells to specifically target and destroy tumor cells.
From the combined teachings of the references, it is apparent that one of ordinary skill in the art would have had a reasonable expectation of success in producing the claimed invention. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
Relevant arguments that apply to new claims
Applicant argues as set forth above. Thus, for the reasons set forth above and the reasons of record, the rejection is maintained.
Applicant’s arguments are as follow:
- (a) Rejection of Claims 1-7 and 29 Under 35 U.S.C 4 103. Applicant notes that claim 8 is not rejected in view of the Cullen, Barrett, Qin and Daniels. Claim 1 is amended herein to incorporate the subject matter of unrejected claim 8.
- (b) A Person of Ordinary Skill in the Art Would not have Arrived at the Claimed T cell in
view of the Cited References. The Office has not established a prima facie case of obviousness with respect to claims 1 and 9-17 because the Office has not articulated a rational underpinning for why a person of ordinary skill in the art, reviewing the cited references, would have sought to express IRP2 in a CAR T cell to arrive at the claimed T cell. Although the Office has cited Daniels as support that IRP2 regulates the expression of CD71 (transferrin receptor, TfR), neither Daniels nor the other references disclose or remotely suggest expressing IRP2 in a recombinant host cell, much less, expressing IRP2 in a CAR T cell. The only reference that mentions CAR T cells is Zhang, which is a review article. The Office has not identified any such reason that would have prompted a person of ordinary skill in the art to express IRP2 in a CAR T cell, as claimed.
- (c) The Claimed CAR T Cells Possess Unexpectedly Superior Properties. The claimed CAR T cells show unexpectedly superior proliferation in a manner dependent on T cell activation, as described in Example 10 of the specification. This T cell activation-dependent proliferation of the claimed CAR T cells indicates that the claimed CAR T cells will persist longer in vivo. Notably, not all patients respond to CAR T cell therapies (using CAR T cells that do not express IRP2) because of poor persistence of the CAR T cells in vivo. The claimed CAR T cells, due to their improved proliferation detailed below, have greater therapeutic potential compared to control CAR T cells that do not express IRP2.
When the claimed CAR T cells are activated by the presence of a tumor antigen (human prostate-specific membrane antigen, hPSMA), the expression of IRP2 promotes CAR T cell proliferation (FIG. 8K, lower panel). A higher percentage of CAR T cells expressing IRP2 (dark gray bars) undergo one or two cell divisions, as compared to CAR T cells that do not express IRP2 (or T cells. when the claimed CAR T cells are not activated, the expressed IRP2 protein does not lead to spontaneous proliferation.
The claimed CAR T cells exhibit improved proliferation in the presence of target cells (e.g., a target cell expressing a tumor antigen or a viral antigen), thereby promoting better therapeutic outcomes, while not undergoing spontaneous proliferation in the absence of target cells, thereby avoiding safety concerns.
Applicant’s arguments have been considered but are not persuasive. In response to Applicant’s arguments:
- Regarding item (a), Claim 8 was rejected along claims 1, 9-17 5 under 35 U.S.C. 103 as being unpatentable over Cullen, Barrett and Daniels in view of Zhang and Liu. Nevertheless, New Claim Rejections under 35 USC § 103 have been presented. Please see discussion above.
- Regarding item (b), The previous First Office Action on the Merits mailed on 7/22/2015 discussed the following “One of ordinary skill would have been motivated to do so (combined the cited references) because IRP-2 overexpression would lead to the proliferation of the CAR T cell when stimulated with an tumor antigen eliciting stronger cytokine production and killing ability. There would be a reasonable expectation of success because CAR-T cell therapy is designed to redirect a patient’s or donor’s T cells to specifically target and destroy tumor cells. Applicant has failed to provide a reason as to why the provided motivation to combine the references has not established a prima facie case of obviousness. Also please see New Claim Rejections under 35 USC § 103 discussion above for more details.
In addition, 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). Applicant has not sufficiently described why there is no prima facie case for obviousness. See discussion above for more details regarding the teachings of Cullen, Barrett , Zhang, Liu, Qin and Daniels. relevant to the rejection under 35 U.S.C. 103 and the motivation to combine these references.
- Regarding item (c), Applicant's arguments above are based on a comparison between the claimed invention (CAR T expressing IRP2) and a negative control (CAR T cells that do not express IRP2, or T cells). In addition, when the claimed CAR T cells are not activated, the expressed IRP2 protein does not lead to spontaneous proliferation. This result is expected because there is no activation and therefore, there would be no proliferation since proliferation is dependent on activation. Greater proliferation is expected when T cells are activated.
Moreover, applicant argues that the claimed CAR T cells expressing IRP2 show unexpectedly superior proliferation in a manner dependent on T cell activation. However, Daniels teaches that when IRP-2 is overexpressed, there would be an upregulation of CD71 leading to the proliferation of the activated T cells (see discussion above). Therefore, the role of IRP2 leading to cell proliferation is known in the art and comparing the results to a negative control is not evidence of unexpected results when proliferation is expected.
Furthermore, a showing of unexpected results must be based on evidence, not argument or speculation. In re Mayne, 104 F.3d 1339, 1343-44, 41 USPQ2d 1451, 1455-56 (Fed. Cir. 1997) (conclusory statements that claimed compound possesses unusually low immune response or unexpected biological activity that is unsupported by comparative data held insufficient to overcome prima facie case of obviousness). MPEP § 2145. A greater than expected result is an evidentiary factor pertinent to the legal conclusion of obviousness ... of the claims at issue.” In re Corkill, 711 F.2d 1496, 226 USPQ 1005 (Fed. Cir. 1985). MPEP 716.02 (a). The evidence relied * > upon < should establish “that the differences in results are in fact unexpected and unobvious and of both statistical and practical significance.” Ex parte Gelles, 22 USPQ2d 1318, 1319 (Bd. Pat. App. & Inter. 1992). MPEP 716.02 (b). Applicant must further show that the results were greater than those which would have been expected from the prior art to an unobvious extent, and that the results are of a significant, practical advantage. Ex parte The NutraSweet Co., 19 USPQ2d 1586 (Bd. Pat. App. & Inter. 1991). MPEP 716.02 (b). See also In re Nolan, 553 F.2d 1261, 1267, 193 USPQ 641, 645 (CCPA 1977) and In re Eli Lilly, 902 F.2d 943, 14 USPQ2d 1741 (Fed. Cir. 1990) as discussed in MPEP § 716.02(c). Applicant has failed to provide evidence of unexpected results as the data is only compared to the negative control. Evidence of results already described in the art is not evidence of unexpected results (greater than expected results).
Applicant argues as set forth above. Thus, for the reasons set forth above and the reasons of record, the rejection is maintained.
Conclusion
No claims are 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to IMMA BARRERA whose telephone number is (571) 272-0674. The examiner can normally be reached Monday - Friday 9 to 5.
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/IMMA BARRERA/
Examiner, Art Unit 1671
/RACHEL B GILL/Primary Examiner, Art Unit 1671
Prosecution Insights