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
Claims 1-18 are pending and under exam. Claims 19-20 are withdrawn.
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 06/08/2026 has been entered.
WITHDRAWN REJECTIONS
Claim Rejections - 35 USC § 103
Claims 1-2, 5-6 and 9 were rejected under 35 U.S.C. 103 as being unpatentable over Liu et al (cited in IDS of 12/27/2021, hereinafter "Liu") in view of Marcinkiewicz (Nat Biotechnol, 2017, hereinafter "Marcinkiewicz", See PTO-892), Sadelain (Cancer Discov. 2013 Apr, hereinafter "Sadelain", See PTO-892) and Wang et al (Clin Cancer Res. 2017 May 1, hereinafter "Wang", See PTO-892).
Claims 3-4, 7-8 and 14-18 were rejected under 35 U.S.C. 103 as being unpatentable over Liu et al (cited in IDS of 12/27/2021, hereinafter "Liu") in view of Marcinkiewicz (Nat Biotechnol, 2017, hereinafter "Marcinkiewicz", See PTO-892 of 5/6/2025), Sadelain (Cancer Discov. 2013 Apr, hereinafter "Sadelain", See PTO-892 of 5/6/2025); Wang et al (Clin Cancer Res. 2017 May 1, hereinafter "Wang", See PTO-892 of 5/6/2025) and Eyquem (cited in IDS of 12/27/2021, hereinafter "Eyquem").
Claim 10 was rejected under 35 U.S.C. 103 as being unpatentable over Liu et al (cited in IDS of 12/27/2021, hereinafter "Liu") in view of Marcinkiewicz (Nat Biotechnol, 2017, hereinafter "Marcinkiewicz", See PTO-892 of 5/6/2025), Sadelain (Cancer Discov. 2013 Apr, hereinafter "Sadelain", See PTO-892 of 5/6/2025) and Wang et al (Clin Cancer Res. 2017 May 1, hereinafter "Wang", See PTO-892 of 5/6/2025) and McDonagh et al (US8067546B2; Published 2011-11-29; See IDS filed 12/27/2021; hereinafter "McDonagh).
The rejections are withdrawn following Applicant arguments. New rejections are set forth below.
NEW REJECTIONS
Claim Rejections - 35 USC § 103
Claims 1-2, 5-6 and 9 remain rejected under 35 U.S.C. 103 as being unpatentable over Liu et al (cited in IDS of 12/27/2021, hereinafter "Liu") in view of Marcinkiewicz (Nat Biotechnol, 2017, hereinafter "Marcinkiewicz", See PTO-892 of 5/6/2025), Milone (Mol Ther. 2009 Aug, hereinafter "Milone", See PTO-892) and Duchateau et al (US10836998B2; first published as WO2015121454A1 on Aug 20, 2015; hereinafter "Duchateau;" See PTO-892).
Regarding claim 1: Liu Taught that “αβ T-cell receptor (TCR) on allogeneic CAR-T cells needs to be eliminated to avoid graft-versus-host-disease (GVHD), and human leukocyte antigens class I (HLA-Is) on CAR-T cells need to be removed to minimize their immunogenicity.” Liu taught to disrupt TRAC and B2M genes in CAR-T cells as a solution. (See Liu at p. 154, col. 1, 1st para). Liu also found that tumor size in a lymphoma mouse model was substantially smaller in all of the mice treated with standard CAR-T cells and TRAC and B2M disrupted CAR-T cells, whereas progressive tumor growth was observed in the control group treated with unmodified T cells or PBS. (See Liu, p. 157, col. 1, para 3). Liu taught that
T
R
A
C
-
B
2
M
-
CAR-T cells are “promising reagents for cancer therapy.” (See Liu p. 157, para 1). Liu did not teach CD70 CAR inserted in Trac locus as required by instant claims.
Marcinkiewicz taught that the “CRISPR technology [can be used] to insert a B-cell-specific CAR into the TRAC locus, putting the CAR under the control of the endogenous TRAC promoter and simultaneously disrupting the endogenous TCR by knocking out one of its multiple subunits. This elegant move addressed two possible shortcomings of CAR-T cells—variable CAR expression levels and interference from TCR activity.” (See Marcinkiewicz col. 1, para 3). Marcinkiewicz further taught that whether the design can be “broadly applicable to other types of CARs and malignancies remains to be determined. It will be important to test the approach against solid tumors, which have proved difficult to target with CAR-T cells.” (See Marcinkiewicz col. 3, para 2). Further, Milone taught that expression of CAR transgenes in lentiviral T-cell engineering constructs depends on the internal promoter driving transcription, and the promoter identity directly affects both level and stability of CAR expression in primary human T-cells. Milone further compared multiple promoters and demonstrated that EF-1α provided superior and stabler CAR expression relative to other promoters including CMV promoter, which exhibited early but unstable expression. Based on these results, Milone selected EF-1α promoter for CAR expression in subsequent studies. (See Milone p. 1455, col. 1). As such, Milone taught the importance of the promoter identity and strength and stability for CAR expression.
As such, a person in reading Marcinkiewicz in view of Milone would have been motivated to use the trac locus for expression of a CAR and use an exogenous promoter as taught by Milone to optimize cytokine secretion by the CAR. It has been held that "a person with 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 the product not of innovation but of ordinary skill and common sense." See KSR International Co. v Teleflex, Inc. 82 USPQ2d 1385 at 1390. It is obvious to a person of ordinary skill in the art to try to use exogenous promoters for integration of a CAR into TRAC locus as taught by Marcinkiewicz in view of teachings of Milone. None of the cited references taught the use of CD70 CARs for cancer therapy.
Duchateau taught CAR constructs directed against CD70 expressing tumor cells. (See Dutchateau Abstract). Dutchateau taught that “CARs are synthetic receptors consisting of a targeting moiety that is associated with one or more signaling domains in a single fusion molecule. In general, the binding moiety of a CAR consists of an antigen-binding domain of a single-chain antibody (scFv), comprising the light and variable fragments of a monoclonal antibody joined by a flexible linker. Binding moieties based on receptor or ligand domains have also been used successfully. The signaling domains for first generation CARs are derived from the cytoplasmic region of the CD3zeta or the Fc receptor gamma chains. First generation CARs have been shown to successfully redirect T cell cytotoxicity, however, they failed to provide prolonged expansion and anti-tumor activity in vivo. Signaling domains from co-stimulatory molecules including CD28, OX-40 (CD134), and 4-1BB (CD137) have been added alone (second generation) or in combination (third generation) to enhance survival and increase proliferation of CAR modified T cells.” (See Dutchateau, col. 1 lines 45-col. 2, line 5). Dutchateau taught that CD70 is an attractive target for CAR therapy and disclosed CAR constructs comprising an anti-CD70 scFv together with conventional CAR signaling domains. (See SEQ ID NO: 93 of Dutchateau or Ab4, or Ab4 CAR).
Wang taught that a lot of tumors express CD70 including solid cancers such as clear cell renal cancer (RCC), glioblastoma, and hematological malignancies, and that it is a potential immunotherapeutic target. Wang taught that CD70 CARs in which different portions of CD27 were fused with various co-stimulatory signaling domains from 41BB and/or CD28, and CD3-zeta, in a murine model was effective in vitro and in vivo, respectively. (See Wang p. 2, para 2).
A person of ordinary skill in the art would have been motivated to utilize a known exogenous promoter operably linked to the CAR transgene integrated into TRAC locus of Marcinkiewicz in order to control and optimize the expression of the introduced CAR. Such modification would merely involve one known expression-control strategy from a finite number of options recognized to optimize transgenic protein (CD70) expression, with a reasonable expectation of successfully expressing the integrated CD70. The person would have recognized that the resulting product would have predictably combined the advantages taught by Liu (reduced GVHD immunogenicity), Marcinkiewicz (TRAC-targeted CAR integration), and Milone (controlled transgene expression through promoter selection).
Regarding claim 2: Sadelain taught a EF-1α promoter, a eukaryotic promoter.
Regarding claims 5 and 6: Liu taught disruption of TRAC and B2M using CRISPR/Cas9.
Regarding claim 9: As indicated Dutchateau taught a SEQ ID NO: 93 comprising:
a SEQ ID NO: 81, encoding a Ab4 which was indicated to be an anti-CD70 scFv,
a SEQ ID NO: 33, which was indicated to be a 4-1BB costimulatory domain,
a SEQ ID NO: 34, which was indicated to be a CD3 zeta activation domain.
It is submitted that Dutchateau taught a CD70 CAR with antiCD70 scFv, 4-1BB costimulatory domain and CD3 zeta activation domain.
Claims 3-4, 7-8 and 14-18 are rejected under 35 U.S.C. 103 as being unpatentable over Liu et al (cited in IDS of 12/27/2021, hereinafter "Liu") in view of Marcinkiewicz (Nat Biotechnol, 2017, hereinafter "Marcinkiewicz", See PTO-892 of 5/6/2025), Milone (Mol Ther. 2009 Aug, hereinafter "Milone", See PTO-892) Duchateau et al (US10836998B2; first published as WO2015121454A1 on Aug 20, 2015; hereinafter "Duchateau;" See PTO-892) and Eyquem (cited in IDS of 12/27/2021, hereinafter "Eyquem").
Regarding claims 3 and 4: The teachings of Liu in view of Marcinkiewicz, Milone and Duchateau are set forth above. Briefly, the prior art taught the benefits of a TRAC, B2M disrupted CAR-T-cell for cancer therapy. Additionally, Marcinkiewicz taught the use of TRAC locus for CAR integration but indicated that it remains to be probed for all CAR expression. Milone taught the importance of primer strength titration for eliciting appropriate cytokine release from a CAR and Wang taught the use of CD70 CAR for certain cancers. None of the references specifically taught the use of EF-1alpha promoter for CAR expression as required by the claim. Eyquem taught an EF-1alpha promoter for expressing a CAR inserted into a TRAC locus. Eyquem taught that the EF-1alpha promoter was able to elicit much higher CAR expression compared to endogenous TRAC promoter.
It would have been obvious for a person of ordinary skill in the art to use a stronger promoter for expression of a CAR.
Regarding claims 7-8: Eyquem taught the design of “[a] gRNA to target the first exon of the constant chain of the TCRα gene (TRAC). The sequence targeted is located upstream of the transmembrane domain of the TCRα. This domain is required for the TCRα and β assembly and addressing to the cell-surface. Both, non-homologous end joining (NHEJ) and integration of the CAR by HDR at this locus would then efficiently disrupt the TCR complex.” As such Eyquem taught integrating a CAR at the disrupted TRAC location as required by claims 7-8.
Regarding claim 14: Eyquem taught that a population of cells that have been modified by a CRISPR/Cas9 mediated CAR gene targeted into the TRAC locus. Eyquem observed over 70% TCR- human primary T cells (Page 10, Graph (d)), and over 90% CAR+ cells.
Regarding claim 15-18: Eyquem taught that the T cells used in their experiments were taken from healthy donors, see page 7, 1st full ¶. Mice were injected with NALM-6 cells (pre-B acute lymphoblastic leukemia), followed by CAR T cells injected four days later. (Liu et al. taught wherein the cells are allogeneic and wherein the patient has a B-cell malignancy, claims 17-18, page 154, 1st col).
Claim 10 is rejected under 35 U.S.C. 103 as being unpatentable over Liu et al (cited in IDS of 12/27/2021, hereinafter "Liu") in view of Marcinkiewicz (Nat Biotechnol, 2017, hereinafter "Marcinkiewicz", See PTO-892 of 5/6/2025), Milone (Mol Ther. 2009 Aug, hereinafter "Milone", See PTO-892) and Duchateau et al (US10836998B2; first published as WO2015121454A1 on Aug 20, 2015; hereinafter "Duchateau;" See PTO-892) and McDonagh et al (US8067546B2; Published 2011-11-29; See IDS filed 12/27/2021; hereinafter "McDonagh).
Regarding claim 10: The teachings of Liu in view of Marcinkiewicz, Milone and Duchateau are set forth above. None of the cited prior art taught the use of a CAR comprising an anti-CD70 antigen binding fragment comprising the recited sequences.
McDonagh taught an anti-CD70 antigen binding fragment comprising SEQ ID NO: 14 and SEQ ID NO: 24 which are 100% identical to claimed SEQ ID NO: 1592 and SEQ ID NO: 1593 (See Alignment below). McDonagh showed that the treatment of multiple myeloma mice with the CD70 antibody comprising recited sequence prolonged survival of the mice. (See McDonagh, FIGs 7A-C). As such it would have been obvious for a person of ordinary skill in the art to use a CAR comprising the claimed heavy and light chain variable regions comprising the recites sequence.
Query 1 QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY 60
QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY
Sbjct 1 QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY 60
Query 61 ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSS 118
ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSS
Sbjct 61 ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSS 118
SEQ ID NO: 1592 is 100% identical to SEQ ID NO: 14 of McDonagh
Query 1 DIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLES 60
DIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLES
Sbjct 1 DIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLES 60
Query 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGTKVEIK 111
GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGTKVEIK
Sbjct 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGTKVEIK 111
SEQ ID NO: 1593 is 100% identical to SEQ ID NO: 24 of McDonagh
Response to Arguments: Applicants argued that the cited references do not teach or suggest all the elements of the claimed invention as “the cited paragraphs from Sadelain refer to expression of exogenous cytokines, and not to expression of a CAR. Applicants argued that the Office has not identified any teaching, in any of the cited references, that would have led a skilled artisan to operably link an exogenous
promoter to a CD70-binding CAR inserted in the TRAC locus in view of the teachings of Marcinkiewicz, which characterizes placement of the CAR under the endogenous TRAC promoter as an "elegant move" that "addressed two possible shortcomings of CAR-T cells-variable CAR expression levels and interference from TCR activity".
Applicants further pointed out that Wand did not disclose an anti-CD70 scFv with regards to claim 9.
Applicant’s arguments have been fully considered but are not persuasive.
As an initial matter the rejection has been revised to rely upon Milone rather than Sadelain for the teaching of an exogenous promoter operably linked to a CAR transgene. Milone expressly taught that promoter selection is an important determinant of CAR expression in engineered T-cells and demonstrated that different promoters produce distinct and predictable expression profiles. Milone as such taught that promoter identity is a known result-effective variable routinely optimized by a person of ordinary skill in the art to obtain desired CAR expression characteristics. Applicant’s arguments against Marcinkiewicz teaching away from use of an exogenous promoter is likewise unpersuasive. A reference teaches away when it criticizes, discredits or otherwise discourages the path taken by the Applicant. Marcinkiewicz did not criticize, discredit or discourage the use of exogenous promoters , rather disclosed one embodiment in which CAR expression is driven from the TRAC locus following targeted integration. The fact that Marcinkiewicz identified advantages associated with endogenous promoter-driven transgene expression does not amount to a teaching away from alternative promoter strategies, particularly where the prior art recognized promoter choice as a result-effective variable. Furthermore, Applicant’s characterization of the rejection as requiring substitution of a required feature of Marcinkiewicz is not consistent with the actual grounds of the rejection. The rejection relies on Marcinkiewicz for the teaching of targeted integration of a CAR construct into the TRAC locus and relies upon Milone for the well—known practice of selecting promoters to achieve desired CAR expression characteristics. As such it is maintained that the claimed method would have been obvious to a person of ordinary skill in the art at the time of invention.
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 indicated in the table below are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over pending claims of copending Application Nos. 17/776,871, 17/776,846 and 17/776,860 indicated below (reference applications). This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Although the claims at issue are not identical, they are not patentably distinct from each other.
Reference Application/Patent
Claim # of reference application/patent
Instant claim #
17/776,871
1
1, 18
34
9
35
10
36
11
37
12
17/776,846
1
1, 18
45
9
46
10
47
11
48
12
17/776,860
1
1, 18
34
9
35
10
36
11
37
12
Re. Reference application 17/776,860 and 17/776,846
Claim 1 of the reference applications require treatment of a cancer (as required by instant claim 1), specifically RCC (17/776,860 as required by claim 18) or hematological malignancy (17/776,846 as required by instant claim 18). The pending claim falls within the scope of pending claims 1 and 18, and represents a species of the broader claim 1 of the reference application. Issued claim 1 is therefore considered to anticipate the scope of instant claim.
Further as explained below, SEQ ID Nos: 49, 50, 48 and 46 are 100% identical to instant SEQ ID Nos: 1592, 1593, 1500 and 1276 respectively.
Query 1 QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY 60
QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY
Sbjct 1 QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY 60
Query 61 ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSS 118
ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSS
Sbjct 61 ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSS 118
SEQ ID NO: 1592 is 100% identical to SEQ ID NO: 49 of 17/776,871; 17/776,860 and 17/776,846
Query 1 DIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLES 60
DIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLES
Sbjct 1 DIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLES 60
Query 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGTKVEIK 111
GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGTKVEIK
Sbjct 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGTKVEIK 111
SEQ ID NO: 1593 is 100% identical to SEQ ID NO: 50 of 17/776,871; 17/776,860 and 17/776,846
Query 1 QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY 60
QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY
Sbjct 1 QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQAPGQGLKWMGWINTYTGEPTY 60
Query 61 ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSSGG 120
ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSSGG
Sbjct 61 ADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARDYGDYGMDYWGQGTTVTVSSGG 120
Query 121 GGSGGGGSGGGGSGDIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQ 180
GGSGGGGSGGGGSGDIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQ
Sbjct 121 GGSGGGGSGGGGSGDIVMTQSPDSLAVSLGERATINCRASKSVSTSGYSFMHWYQQKPGQ 180
Query 181 PPKLLIYLASNLESGVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGT 240
PPKLLIYLASNLESGVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGT
Sbjct 181 PPKLLIYLASNLESGVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQHSREVPWTFGQGT 240
Query 241 KVEIK 245
KVEIK
Sbjct 241 KVEIK 245
SEQ ID NO: 1500 is 100% identical to SEQ ID NO: 48 of 17/776,871; 17/776,860 and 17/776,846
Query 1 MALPVTALLLPLALLLHAARPQVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQ 60
MALPVTALLLPLALLLHAARPQVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQ
Sbjct 1 MALPVTALLLPLALLLHAARPQVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGMNWVRQ 60
Query 61 APGQGLKWMGWINTYTGEPTYADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARD 120
APGQGLKWMGWINTYTGEPTYADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARD
Sbjct 61 APGQGLKWMGWINTYTGEPTYADAFKGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARD 120
Query 121 YGDYGMDYWGQGTTVTVSSGGGGSGGGGSGGGGSGDIVMTQSPDSLAVSLGERATINCRA 180
YGDYGMDYWGQGTTVTVSSGGGGSGGGGSGGGGSGDIVMTQSPDSLAVSLGERATINCRA
Sbjct 121 YGDYGMDYWGQGTTVTVSSGGGGSGGGGSGGGGSGDIVMTQSPDSLAVSLGERATINCRA 180
Query 181 SKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLESGVPDRFSGSGSGTDFTLTISSLQAE 240
SKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLESGVPDRFSGSGSGTDFTLTISSLQAE
Sbjct 181 SKSVSTSGYSFMHWYQQKPGQPPKLLIYLASNLESGVPDRFSGSGSGTDFTLTISSLQAE 240
Query 241 DVAVYYCQHSREVPWTFGQGTKVEIKSAAAFVPVFLPAKPTTTPAPRPPTPAPTIASQPL 300
DVAVYYCQHSREVPWTFGQGTKVEIKSAAAFVPVFLPAKPTTTPAPRPPTPAPTIASQPL
Sbjct 241 DVAVYYCQHSREVPWTFGQGTKVEIKSAAAFVPVFLPAKPTTTPAPRPPTPAPTIASQPL 300
Query 301 SLRPEACRPAAGGAVHTRGLDFACDIYIWAPLAGTCGVLLLSLVITLYCNHRNRKRGRKK 360
SLRPEACRPAAGGAVHTRGLDFACDIYIWAPLAGTCGVLLLSLVITLYCNHRNRKRGRKK
Sbjct 301 SLRPEACRPAAGGAVHTRGLDFACDIYIWAPLAGTCGVLLLSLVITLYCNHRNRKRGRKK 360
Query 361 LLYIFKQPFMRPVQTTQEEDGCSCRFPEEEEGGCELRVKFSRSADAPAYQQGQNQLYNEL 420
LLYIFKQPFMRPVQTTQEEDGCSCRFPEEEEGGCELRVKFSRSADAPAYQQGQNQLYNEL
Sbjct 361 LLYIFKQPFMRPVQTTQEEDGCSCRFPEEEEGGCELRVKFSRSADAPAYQQGQNQLYNEL 420
Query 421 NLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGERRRGK 480
NLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGERRRGK
Sbjct 421 NLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNELQKDKMAEAYSEIGMKGERRRGK 480
Query 481 GHDGLYQGLSTATKDTYDALHMQALPPR 508
GHDGLYQGLSTATKDTYDALHMQALPPR
Sbjct 481 GHDGLYQGLSTATKDTYDALHMQALPPR 508
SEQ ID NO: 1276 is 100% identical to SEQ ID NO: 46 of 17/776,871; 17/776,860 and 17/776,846
Re. Reference application 17/776,871
Claim 1 of the reference application requires treatment of a cancer (as required by instant claim 1 and 18), specifically a CD70+ solid tumor (as required by claim 17) using a T-cell comprising a CAR binding CD70, a disrupted TRAC gene disrupted B2M wherein the CAR is inserted into the disrupted TRAC gene. The pending claim falls within the scope of pending claims 1 and 17-18, and represents a species of the broader claim 1 of the reference application. Issued claim 1 is therefore considered to anticipate the scope of instant claim.
Response to Arguments: Applicants argued that the present application has an effective filing date which is earlier than the effective filing date of U.S. Application Nos: 17/776,871, 17/776,846 and 17/776,860, for the 18/289,028. Consequently, pursuant to M.P.E.P. § 1490(VI)(D) this rejection should be withdrawn.
It is submitted that according to MPEP 804(I)(B)(1)(b)(i) and MPEP 1490(VI)(D)(2)(a), a provisional nonstatutory double patenting rejection is only withdrawn when it is the only rejection remaining in an application having the earliest effective U.S. filing date (taking into account any benefit under 35 U.S.C. 120, 121, 365(c), or 386(c) ) with respect to the conflicting claims); at which point the "provisional" nonstatutory double patenting rejection in the other (later filed) application(s) will be converted into a nonstatutory double patenting rejection when the application with the earliest U.S. effective filing date issues as a patent.
Conclusion
Claims 11 - 13 are found free of art.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JAGAMYA VIJAYARAGHAVAN whose telephone number is (703)756-5934. The examiner can normally be reached 9:00a-5:00p.
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/JAGAMYA NMN VIJAYARAGHAVAN/Examiner, Art Unit 1633
/EVELYN Y PYLA/Primary Examiner, Art Unit 1633
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