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
1. The Amendment filed April 10, 2026 response to the Office Action of December 10, 2025 is acknowledged and has been entered. Claims 1, 11-14, 16, and 18 were amended. Claims 2, 3, 15, 17, and 19-21 were canceled. New claims 22-26 were herein added.
2. Claims 1, 11-14, 16, 18, and 22-26 are currently being examined.
Priority
3. Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of the first paragraph of 35 U.S.C. 112. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of all of the prior-filed applications fail to provide adequate support or enablement in the manner provided by the first paragraph of 35 U.S.C. 112 for one or more claims of this application. Examiner has established a priority date of November 06, 2020 for the claims 1, 11-14, 16, 18, and 22-26 because the claims as currently amended recite: a method of enhancing expansion of natural killer (NK) cells in a subject, the method comprising: administering to the subject a first population of T cells comprising a first chimeric antigen receptor (CAR) binding a GUCY2C and a second population of T cells comprising a second CAR binding CD19, wherein the first CAR comprises SEQ ID NO: 11 allowing the first and second populations of T cells to expand in peripheral blood of the subject, wherein expansion of NK cells in the subject is enhanced as compared to a subject administered the first population of T cells without the second population of T cells. A review of the parent applications does not reveal support for the claimed method. Applicant is invited to submit evidence pointing to the serial number, page and line where support can be found establishing an earlier priority date.
New Grounds of Rejection
Claim Rejections - 35 USC § 102
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.
4. Claim(s) 1, 11-14, 16, 18, 23, 24 and 26 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by US 2019/0314411 A1 (Xiao et al. Oct. 17, 2019, of record), “Xiao”.
Xiao teaches the present disclosure relates to compositions and methods for enhancing T cell response and/or CAR cell expansion and/or maintenance in vivo and/or in vitro. For example, a method of enhancing T cell-based therapy comprises administering genetically modified T cells comprising a first chimeric antigen receptor (CAR) and a second CAR, wherein a binding domain of the first CAR binds a first antigen, and a binding domain of the second CAR binds a second antigen. The first antigen is different from the second antigen. In embodiments, the first CAR binds a surface molecule or antigen of a white blood cell. See abstract.
Xiao teaches a method of enhancing expansion of cells in a subject or treating the subject having cancer, the method comprising: administering an effective amount of a composition to the subject having a form of cancer expressing a tumor antigen, the composition comprising a first population of cells comprising a first CAR binding a first antigen, and a second population of cells comprising a second CAR binding a second antigen, wherein the second antigen is a tumor antigen and is different from the first antigen. See claim 1.
Xiao teaches the cells are CAR T cells. See ¶¶ 0006-0010.
Xiao teaches administration of the CAR cells by intravenous and infusion techniques. See ¶¶ 0107, 0194 and 0196. This would allow administered CAR T cells in the to expand in the peripheral blood.
Xiao teaches the present disclosure describes methods of expanding and/or maintaining cells expressing an antigen binding domain in vivo. The method includes administering an effective amount of a mixed population of modified cells or a composition including a mixed population of modified cells described herein to a subject. These methods described herein are useful for expanding T cells, NK cells, macrophages and/or dendritic cells. See ¶¶ 0157.
Xiao teaches a method of enhancing expansion of cells in a subject, the method comprising: administering an effective amount of the first population of cells of one of claims 341-345; and administering an effective amount of the second population of cells.
352. The composition or the method of one of claims 341-351, wherein the first or second antigen is or comprises a surface molecule of a white blood cell (WBC), a tumor antigen, or a solid tumor antigen.
353. The composition or the method of one of claims 341-352, wherein the cells are modified T cells, modified NK cells, or modified dendritic cells.
354. The composition or the method of claim 352, wherein the WBC is a granulocyte, a monocyte, or lymphocyte.
355. The composition or the method of claim 354, wherein the WBC is a B cell.
358. The composition or the method of claim 354, wherein the cell surface molecule of the WBC is CD19.
359. The composition or the method of claim 354, wherein the tumor antigen is a solid tumor antigen.
360. The composition or the method of claim 354, wherein the solid tumor antigen is GUCY2C, ACPP, or PAP. See paragraphs [0128] and [0233-0235] and claims 1-10 .
Xiao teaches 341. A composition comprising a first population of cells comprising a first CAR binding a first antigen and a second population of cells comprising a second CAR binding a second antigen, wherein the second antigen is a tumor antigen and the first antigen and second antigen are different antigens. See paragraph [0228] and claim 1.
Xiao teaches wherein the CAR comprises an antigen binding domain, a transmembrane domain, a co-stimulatory domain, and a CD3 zeta domain, wherein the co-stimulatory domain comprises the intracellular domain of CD27, CD28, 4-1BB, OX40, CD30, CD40, PD-1, ICOS, lymphocyte function-associated antigen-1 (LFA-1), CD2, CD7, LIGHT, NKG2C, B7-H3, a ligand that specifically binds with CD83, or a combination thereof.. See paragraphs [0235-0237] and claims 12 and 13.
Xiao teaches wherein an antigen binding domain of the first CAR comprises the SEQ ID NO: 5. See claim 15.
Xiao teaches wherein the second population of cells comprises a lentiviral vector encoding the second CAR and a dominant negative form of PD-1. See claim 16.
Xiao teaches wherein the first population of cells comprises a lentiviral vector encoding the first CAR and a therapeutic agent. See claim 17.
Xiao teaches wherein the therapeutic agent comprises a cytokine. See claim 18.
Xiao teaches wherein the cytokine is at least one of IL6, IL12, TNF-α, or IFN-γ. See claims 19 and 20. See also paragraph [0238].
Xiao teaches SEQ ID NO: 11 which comprises the currently claimed SEQ ID NO: 11 as a scFv to GUCY2C. See Table 4 and Appendix of the Office Action of 01/24/2025.
Xiao teaches SEQ ID NO: 5 which comprises the currently claimed SEQ ID NO: 5 as a scFv to CD19. See Table 4 and Appendix of the Office Action of 01/24/2025.
Xiao teaches the co-stimulatory domain SEQ ID NO: 3, which comprises the claimed SEQ ID NO: 3. See Table 4-p. 37 and Appendix.
Xiao teaches treating colorectal cancer with the cells of the invention. See ¶¶ 0208 and ¶0227-243.
Although Xiao does not explicitly teach that expansion of NK cells in the subject is enhanced as compared to a subject administered the first population of T cells without the second population of T cells, given that Xiao teaches administering a GUCY2C CAR T cell population, comprising SEQ ID NO: 11, and administering a CD19 CAR T cell population comprising SEQ ID NO: 5, which are the same as claimed, the method would enhance the expansion of NK cells in the subject as claimed.
It is noted that Applicant had previously overcome the rejection of the claims under 102(a)(1) as being anticipated by US 2019/0314411 A1 (Xiao et al. Oct. 17, 2019), in the response filed October 09, 2025 relying on the prior art exception defined under 35 U.S.C. § 102(b)(1)(A). However, the claims as amended now have a priority date November 06, 2020, as set forth above. Thus, the Xiao disclosure is greater than 1 year from the priority date and so the prior art exception under 35 U.S.C. § 102(b)(1)(A) does not apply to the amended claims.
New Grounds of 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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
5. Claim(s) 22 is rejected under 35 U.S.C. 103 as being unpatentable over US 2019/0314411 A1 (Xiao et al. Oct. 17, 2019, of record), “Xiao” as applied to claims 1, 11-14, 16, 18, 23, 24 and 26 above, and further in view of 2018/0334490 A1 (Brogdon et al. Nov. 22, 2018, of record), “Brogdon”.
Xiao teaches as set forth above, but does not teach a CD3 zeta signaling domain encoded by SEQ ID NO: 19.
Brogdon teaches the anti-cancer therapeutic agent includes an immune effector cell, e.g., a T cell or an NK cell, that expresses a CAR that targets (e.g., binds to) a tumor antigen, referred to herein as a “treatment CAR cell” (“CAR-Tx”). Without wishing to be bound by theory, treatment with a preconditioning agent, e.g., CAR-Pc, is believed to improve the distribution and/or efficacy of an anti-cancer therapy (e.g., a CAR-Tx) in a subject, e.g., by one or more of: increasing one or more of proliferation, tumor infiltration, and/or persistence of the CAR-Tx, e.g., as compared to administering the CAR-Tx alone; modulating the tumor microenvironment; decreasing the level of B cells, e.g., B cell antigen-expressing cells; decrease the level of regulatory B cells (e.g., B regs) and/or regulatory T cells (T regs), e.g., in the tumor microenvironment; increasing the level of Th1 or Th17 cells; increasing the tolerance for the CAR-Tx; preventing or reducing an adverse response to the CAR-Tx; decreasing the likelihood of the subject's immune response to the CAR-Tx; or increasing anti-tumor activity of the CAR-Tx. See ¶¶ 0005-0006.
Brogdon teaches the preconditioning agent includes an immune effector cell, e.g., a T cell or an NK cell, expressing a chimeric antigen receptor (CAR) molecule that targets B cells, e.g., binds to a B cell antigen. See ¶¶ 0005.
Brogdon teaches the preconditioning agent CAR (CAR-Pc) can bind CD19. See ¶¶ 0006-0012.
Brogdon teaches the CD19 CAR is a murine scFv domain that binds to human CD19, e.g., CTL019 (e.g., SEQ ID NO: 95). See ¶¶ 0021.
Brogdon teaches the intracellular signaling domain comprises a functional signaling domain of 4-1BB and/or a functional signaling domain of CD3 zeta. See ¶¶ 0039, 0092 and 0117.
Brogdon teaches that the CD3 zeta signaling domain comprises SEQ ID NO: 18 or SEQ ID NO: 20. See ¶¶ 0039, 0122 and 0193.
SEQ ID NO: 20 is encoded by the claimed SEQ ID NO: 19. See Appendix.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of Xiao and Brogdon and use the CD3 zeta signaling domain of SEQ ID NO: 20 of Brogdon in the CARs of Xiao because Brogdon teaches that SEQ ID NO: 20 is a CD3 zeta signaling domain effective for use in CARs, like a CD19 CAR. One would have been motivated to use the CD3 zeta signaling domain of SEQ ID NO: 20 of Brogdon in the CARs of Xiao to optimize the activity of the CARs of Xiao.
6. Claim(s) 25 is rejected under 35 U.S.C. 103 as being unpatentable over US 2019/0314411 A1 (Xiao et al. Oct. 17, 2019, of record), “Xiao” as applied to claims 1, 11-14, 16, 18, 23, 24 and 26 above, and further in view of US 2007/0172455 A1 (Revel et al. July 26, 2007), “Revel”.
Xiao teaches as set forth above, but does not teach the sequence of IL-6 used in the methods of the invention.
Revel teaches a chimeric sIL-6R/IL-6 protein that can be produced in human cells for proper glycosylation . See abstract and ¶¶ 0009 and0073.
Revel teaches chimeric sIL-6R/IL-6 protein is more effective at inhibiting the growth of tumor cells than IL-6 or sIL-6R alone. See ¶¶ 0014, 0073, 0074, Example 3 and Figs. 5 and 6.
Revel teaches chimeric sIL-6R/IL-6 protein sequence is SEQ ID NO: 8, which comprises the claimed SEQ ID NO: 35. See ¶¶ 0071, Fig. 11 and Appendix.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of Xiao and Revel and use the chimeric sIL-6R/IL-6 of Revel in the methods of cancer treatment of Xiao because Revel teaches that the chimeric sIL-6R/IL-6 protein is more effective at inhibiting the growth of tumor cells than IL-6 or sIL-6R alone. Given the advantages of the chimeric sIL-6R/IL-6 of Revel for treating cancer, one would have been motivated to use it in the methods of Xiao.
Rejections Maintained/Modified
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.
7. Claims 1, 11-14, 16, 18, 23, 24 and 26 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 4-13, 15, 19, 20, 23, 24, and 27 of U.S. Patent No. 10,869,888 B2 (Xiao et al. Dec. 22, 2020, IDS)
The ‘888 claims teach:
1. A method of enhancing expansion of cells in a subject, the method comprising: administering an effective amount of a composition to the subject having a form of cancer expressing a tumor antigen, wherein the composition comprises a first population of cells comprising a first chimeric antigen receptor (CAR) binding a first antigen, and a second population of cells comprising a second CAR binding a second antigen, the first and second population of cells comprising T cells, the first and second CAR comprising an antigen binding domain, a transmembrane domain, a costimulatory domain, and a CD3 zeta domain, and the first antigen comprising CD19 or BCMA and the second antigen comprising a solid tumor antigen; and allowing the first and second population of cells to expand, wherein expansion of the second population of cells in the subject is enhanced as compared to a subject administered a composition comprising the second population of cells without the first population of cells.
2. The method of claim 1, wherein the solid tumor antigen is tMUC 1, PRLR, CLCA1, MUC12, GUCY2C, GPR35, CR1L, MUC 17, TMPRSS11B, MUC21, TMPRSS11E, CD207, SLC30A8, CFC1, SLC12A3, SSTR1, GPR27, FZD10, TSHR, SIGLEC15, SLC6A3, KISS1R, QRFPR, GPR119, CLDN6, UPK2, ADAM12, SLC45A3, ACPP, MUC21, MUC16, MS4A12, ALPP, CEA, EphA2, FAP, GPC3, IL13-Rα2, Mesothelin, PSMA, ROR1, VEGFR-II, GD2, FR-α, ErbB2, EpCAM, EGFRvIII, B7-H3, or EGFR.
4. The method of claim 1, wherein the co-stimulatory domain comprises the intracellular domain of CD27, CD28, 4-1BB, OX40, CD30, CD40, PD-1, ICOS, lymphocyte function-associated antigen-1 (LFA-1), CD2, CD7, LIGHT, NKG2C, B7-H3, a ligand that binds CD83, or a combination thereof.
5. The method of claim 1, wherein the first CAR comprises a scFv binding CD19, an intracellular domain of 4-1BB or CD28, and a CD3 zeta domain, and the second CAR comprises a scFv binding tMUC1, an intracellular domain of 4-1BB or CD28, and a CD3 zeta domain.
6. The method of claim 1, wherein the antigen binding domain of the first CAR comprises amino acid sequence SEQ ID NO: 5 or 6 and the antigen binding domain of the second CAR comprises amino acid sequence SEQ ID NO: 8, 11, 70, or 439.
7. The method of claim 1, wherein the second population of cells comprises a lentiviral vector encoding the second CAR and a dominant negative form of PD-1.
8. The method of claim 1, wherein the first population of cells comprises a lentiviral vector encoding the first CAR and a therapeutic agent.
9. The method of claim 8, wherein the therapeutic agent comprises a cytokine.
10. The method of claim 9, wherein the cytokine is IL6 and/or IFN-γ.
11. The method of claim 9, wherein the cytokine is at least one of IL6, IL12, TNF-α, or IFN-γ.
12. The method of claim 1, wherein the method further comprises treating the subject having solid tumor cancer.
13. The method of claim 12, wherein the solid tumor cancer is cholangiocarcinoma, pancreatic cancer, breast cancer, colorectal cancer, thyroid cancer, or prostate cancer.
15. The method of claim 1, wherein the solid tumor antigen is GUCY2C.
19. The method of claim 1, wherein the first CAR comprises amino acid sequence SEQ ID NO: 5.
20. The method of claim 1, wherein the first CAR comprises amino acid sequence encoded by nucleic acid sequence SEQ ID NO: 28 (CD19 CAR, See Table 4).
23. The method of claim 1, wherein the second CAR comprises amino acid sequence SEQ ID NO: 11.
24. The method of claim 1, wherein the antigen binding domain of the first CAR comprises amino acid sequence SEQ ID NO: 5, and the solid tumor antigen comprises GUCY2C.
27. The method of claim 1, wherein the antigen binding domain of the first CAR comprises amino acid sequence SEQ ID NO: 5, and the antigen binding domain of the second CAR comprises amino acid sequence SEQ ID NO: 11.
SEQ ID NOs: 5 and 11 of the ‘888 claims are the same as the claimed SEQ ID NOs: 5 and 11. See Appendix of the Office Action of 01/24/2025.
SEQ ID NO: 28 encodes the co-stimulatory domain of SEQ ID NO: 3. See Appendix.
Although the ‘888 claims do not explicitly teach that expansion of NK cells in the subject is enhanced as compared to a subject administered the first population of T cells without the second population of T cells, given that the ‘888 claims teach administering a GUCY2C CAR T cell population, comprising SEQ ID NO: 11, and administering a CD19 CAR T cell population comprising SEQ ID NO: 5, which are the same as claimed, the method would enhance the expansion of NK cells in the subject as claimed.
Response to Arguments
8. Applicant argues that the Office has expressly acknowledged that the claims of the '888 Patent do not teach NK cells. Applicants respectfully submit that Spanholtz does not teach a method of expanding NK cells. Thus, the claims of the '888 patent in view of Spanholtz cannot render claims 1-3 and 11-21 of the instant application obvious. Accordingly, Applicants respectfully request withdrawal of the instant ODP rejection and reconsideration of the pending claims.
Applicant's arguments have been considered, but have not been found persuasive because the current rejection no longer relies on Spanholtz. Given that the ‘888 claims teach administering a GUCY2C CAR T cell population, comprising SEQ ID NO: 11, and administering a CD19 CAR T cell population comprising SEQ ID NO: 5, which are the same as claimed, the method would enhance the expansion of NK cells in the subject. Thus, the rejection is maintained.
9. Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 4-13, 15, 19, 20, 23, 24, and 27 of U.S. Patent No. 10,869,888 B2 (Xiao et al. Dec. 22, 2020, of record), as applied to claims 1, 11-14, 16, 18, 23, 24 and 26 above, in further view of 2018/0334490 A1 (Brogdon et al. Nov. 22, 2018, of record), “Brogdon”.
The ‘888 claims teach as set forth above, but does not teach a CD3 zeta signaling domain encoded by SEQ ID NO: 19.
Brogdon teaches as set forth above.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of the ‘888 claims and Brogdon and use the CD3 zeta signaling domain of SEQ ID NO: 20 of Brogdon in the CARs of the ‘888 claims because Brogdon teaches that SEQ ID NO: 20 is a CD3 zeta signaling domain effective for use in CARs, like a CD19 CAR. One would have been motivated to use the CD3 zeta signaling domain of SEQ ID NO: 20 of Brogdon in the CARs of the ‘888 claims to optimize the activity of the CARs of Xiao.
10. Claim 25 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 4-13, 15, 19, 20, 23, 24, and 27 of U.S. Patent No. 10,869,888 B2 (Xiao et al. Dec. 22, 2020, of record), as applied to claims 1, 11-14, 16, 18, 23, 24 and 26 above, in further view of US 2007/0172455 A1 (Revel et al. July 26, 2007), “Revel”.
The ‘888 claims teach as set forth above, but does not teach the sequence of IL-6 used in the methods of the invention.
Revel as set forth above.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of the ‘888 claims and Revel and use the chimeric sIL-6R/IL-6 of Revel in the methods of cancer treatment of the ‘888 claims because Revel teaches that the chimeric sIL-6R/IL-6 protein is more effective at inhibiting the growth of tumor cells than IL-6 or sIL-6R alone. Given the advantages of the chimeric sIL-6R/IL-6 of Revel for treating cancer, one would have been motivated to use it in the methods of the ‘888 claims.
Conclusion
11. All other objections and rejections recited in the Office Action of December 10, 2025 are withdrawn in view of Applicant’s amendments and arguments.
12. No claims allowed.
13. THIS ACTION IS MADE FINAL. 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 extension fee 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 date of this final action.
14. Any inquiry concerning this communication or earlier communications from the examiner should be directed to PETER J REDDIG whose telephone number is (571)272-9031. The examiner can normally be reached on M-F 8:30-5:30 Eastern Time
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/PETER J REDDIG/Primary Examiner, Art Unit 1646
APPENDIX
Alignment of SEQ ID NO: 3 with SEQ ID NO: 3 of Xiao
ALIGNMENT:
Query Match 100.0%; Score 232; Length 42;
Best Local Similarity 100.0%;
Matches 42; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 KRGRKKLLYIFKQPFMRPVQTTQEEDGCSCRFPEEEEGGCEL 42
||||||||||||||||||||||||||||||||||||||||||
Db 1 KRGRKKLLYIFKQPFMRPVQTTQEEDGCSCRFPEEEEGGCEL 42
Alignment of SEQ ID NO: 3 with SEQ ID NO: 28 of Xiao
PNG
media_image1.png
763
857
media_image1.png
Greyscale
Alignment of SEQ ID NO: 19 with SEQ ID NO: 20 of Brogdon.
ALIGNMENT:
Length: 112
Score: 593.00 Matches: 112
Percent Similarity: 100.0% Conservative: 0
Best Local Similarity: 100.0% Mismatches: 0
Query Match: 95.2% Indels: 0
Gaps: 0
US-17-091-741A-19 (1-339) x US-10-448-256-14 (1-112)
Qy 1 AGAGTGAAGTTCAGCAGGAGCGCAGACGCCCCCGCGTACCAGCAGGGCCAGAACCAGCTC 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 ArgValLysPheSerArgSerAlaAspAlaProAlaTyrGlnGlnGlyGlnAsnGlnLeu 20
Qy 61 TATAACGAGCTCAATCTAGGACGAAGAGAGGAGTACGATGTTTTGGACAAGAGGCGTGGC 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 21 TyrAsnGluLeuAsnLeuGlyArgArgGluGluTyrAspValLeuAspLysArgArgGly 40
Qy 121 CGGGACCCTGAGATGGGGGGAAAGCCGAGAAGGAAGAACCCTCAGGAAGGCCTGTACAAT 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 41 ArgAspProGluMetGlyGlyLysProArgArgLysAsnProGlnGluGlyLeuTyrAsn 60
Qy 181 GAACTGCAGAAAGATAAGATGGCGGAGGCCTACAGTGAGATTGGGATGAAAGGCGAGCGC 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GluLeuGlnLysAspLysMetAlaGluAlaTyrSerGluIleGlyMetLysGlyGluArg 80
Qy 241 CGGAGGGGCAAGGGGCACGATGGCCTTTACCAGGGTCTCAGTACAGCCACCAAGGACACC 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 81 ArgArgGlyLysGlyHisAspGlyLeuTyrGlnGlyLeuSerThrAlaThrLysAspThr 100
Qy 301 TACGACGCCCTTCACATGCAGGCCCTGCCCCCTCGC 336
||||||||||||||||||||||||||||||||||||
Db 101 TyrAspAlaLeuHisMetGlnAlaLeuProProArg 112
Alignment of SEQ ID NO: 35 with SEQ ID NO: 8 of Revel.
US-11-688-640-8
Sequence 8, US/11688640
Publication No. US20070172455A1
GENERAL INFORMATION
APPLICANT: REVEL, Michel
APPLICANT: CHEBATH, Judith
APPLICANT: LAPIDOT, Tsvee
APPLICANT: KOLLET, Orit
TITLE OF INVENTION: CHIMERIC INTERLEUKIN-6 SOLUBLE RECEPTOR/LIGAND PROTEIN, ANALOGS
TITLE OF INVENTION: THEREOF AND USES THEREOF
FILE REFERENCE: REVEL=15
CURRENT APPLICATION NUMBER: US/11/688,640
CURRENT FILING DATE: 2007-03-20
PRIOR APPLICATION NUMBER: PCT/IL98/00321
PRIOR FILING DATE: 1998-07-09
PRIOR APPLICATION NUMBER: IL 121284
PRIOR FILING DATE: 1997-07-10
PRIOR APPLICATION NUMBER: IL 122818
PRIOR FILING DATE: 1997-12-30
NUMBER OF SEQ ID NOS: 13
SEQ ID NO 8
LENGTH: 471
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: synthetic
Query Match 100.0%; Score 1071; Length 471;
Best Local Similarity 100.0%;
Matches 212; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 MNSFSTSAFGPVAFSLGLLLVLPAAFPAPVPPGEDSKDVAAPHRQPLTSSERIDKQIRYI 60
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Db 1 MNSFSTSAFGPVAFSLGLLLVLPAAFPAPVPPGEDSKDVAAPHRQPLTSSERIDKQIRYI 60
Qy 61 LDGISALRKETCNKSNMCESSKEALAENNLNLPKMAEKDGCFQSGFNEETCLVKIITGLL 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 LDGISALRKETCNKSNMCESSKEALAENNLNLPKMAEKDGCFQSGFNEETCLVKIITGLL 120
Qy 121 EFEVYLEYLQNRFESSEEQARAVQMSTKVLIQFLQKKAKNLDAITTPDPTTNASLLTKLQ 180
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Db 121 EFEVYLEYLQNRFESSEEQARAVQMSTKVLIQFLQKKAKNLDAITTPDPTTNASLLTKLQ 180
Qy 181 AQNQWLQDMTTHLILRSFKEFLQSSLRALRQM 212
||||||||||||||||||||||||||||||||
Db 181 AQNQWLQDMTTHLILRSFKEFLQSSLRALRQM 212
Prosecution Insights