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
2. The election without traverse filed 08/19/2026 in response to the Office Action of 07/23/2026 is acknowledged and has been entered.
Applicant has elected Group I, claims 87-96, drawn to a modified immune cell.
3. Claims 87-98 are pending in the application. Claims 97-98 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 08/19/2026.
4. Claims 87-96 are currently under prosecution.
Priority
5. Applicant’s claim under 35 U.S.C. §§ 120 and 365(c) for benefit of the earlier filing date of application, is acknowledged.
6. Receipt is acknowledged of papers submitted under 35 U.S.C. 119(a)-(d), which papers have been placed of record in the file.
7. 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 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.
Claim Rejections - 35 USC § 102
8. 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.
9. Claims 87-88 and 91-96 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by CN105153315A (published on 12/16/2015, IDS, hereafter ‘315 patent) evidenced by machine-translation of CN105153315A.
Claims 87-88 and 91-96 are herein drawn to a modified immune cell comprising:(a) a switch molecule comprising an extracellular domain (ECD) of a protein that, in an unmodified immune cell, elicits an immune cell inactivation signal upon binding to its ligand, wherein said ECD is fused to an intracellular domain (ICD) of co-stimulatory molecule that mediates an immune cell activation signal, and wherein binding of the switch molecule to the ligand yields an immune cell activation signal instead of said immune cell inactivation signal in said modified immune cell, and (b) a chimeric antigen receptor comprising (i) an antigen interacting domain capable of binding a B cell surface protein (e.g., CD19 or CD20); (ii) a transmembrane domain; and (iii) an intracellular signaling domain, wherein the modified immune cell is obtained from peripheral blood mononuclear cell and expresses endogenous PD1, or the modified immune cell specifically binds to a neoantigen.
‘315 patent teaches that immune cells are genetically modified to express chimeric antigen receptors (CAR); wherein CAR comprising immunosuppressive receptors (e.g. PD-1 extracellular domain) combined with tumor antigen chimeric receptors (e.g. binds to ERBB2) and the intracellular costimulatory signaling molecule (e.g. CD28); see entire document, e.g. claims 1-10, Fig.1, [0007-0025] and [0057] of machine-translation of CN105153315A.
For claims 88 and 91-93, ‘315 patent teaches TCR complex, and the tumor antigen is a neoantigen; see [0030] and [0033] of machine-translation of CN105153315A.
For claims 94-95, ‘315 patent teaches CD19 and CD20; see claim 2.
For claim 96, ‘315 patent teaches that engineered CAR receptors have better effector function and in vivo survival time; see [0005] of machine-translation of CN105153315A.
10. Claims 87, 89-90 and 94-96 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by CN103965361A (published on 08/06/2014, IDS, hereafter ‘361 patent) evidenced by machine-translation of CN103965361A.
Claims 87, 89-90 and 94-96 are herein drawn to a modified immune cell comprising:(a) a switch molecule comprising an extracellular domain (ECD) of a protein that, in an unmodified immune cell, elicits an immune cell inactivation signal upon binding to its ligand, wherein said ECD is fused to an intracellular domain (ICD) of co-stimulatory molecule that mediates an immune cell activation signal, and wherein binding of the switch molecule to the ligand yields an immune cell activation signal instead of said immune cell inactivation signal in said modified immune cell, and (b) a chimeric antigen receptor comprising (i) an antigen interacting domain capable of binding a B cell surface protein (e.g., CD19 or CD20); (ii) a transmembrane domain; and (iii) an intracellular signaling domain, wherein the modified immune cell is obtained from peripheral blood mononuclear cell and expresses endogenous PD1, or the modified immune cell specifically binds to a neoantigen.
‘361 patent teaches tumor infiltrating lymphocytes (TIL) expressing fused proteins epSCC and peSCC, comprising PD1-IGV (the ECD of PD-1), CD28IR (the ICD of CD28) and HERIN (which can bind to Her2 overexpressed in mammary cancer cells); see entire document, e.g. [0012-0058], Example 1, Fig. 1 of machine-translation of CN103965361A.
For claims 94-95, ‘361 patent teaches CD19 and CD20; see [0072] of machine-translation of CN103965361A.
Double Patenting
11. 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 claims at issue 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); and 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 a nonstatutory double patenting ground provided the reference application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
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12. Claims 87-96 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 11,866,731. Although the conflicting claims are not identical, they are not patentably distinct from each other for the following reasons:
Claims 87-96 are herein drawn to a modified immune cell comprising:(a) a switch molecule comprising an extracellular domain (ECD) of a protein that, in an unmodified immune cell, elicits an immune cell inactivation signal upon binding to its ligand, wherein said ECD is fused to an intracellular domain (ICD) of co-stimulatory molecule that mediates an immune cell activation signal, and wherein binding of the switch molecule to the ligand yields an immune cell activation signal instead of said immune cell inactivation signal in said modified immune cell, and (b) a chimeric antigen receptor comprising (i) an antigen interacting domain capable of binding a B cell surface protein (e.g., CD19 or CD20); (ii) a transmembrane domain; and (iii) an intracellular signaling domain, wherein the modified immune cell is obtained from peripheral blood mononuclear cell and expresses endogenous PD1, or the modified immune cell specifically binds to a neoantigen.
Claims 1-14 of U.S. Patent No. 11,866,731 are drawn to an isolated population of modified immune cells comprising modified immune cells that specifically binds to a tumor antigen, wherein each modified immune cell comprises a peripheral blood mononuclear cell (PBMC) expressing both endogenous PD1 and a chimeric stimulating molecule or a switch molecule, wherein said chimeric stimulating molecule or a switch molecule comprises: an extracellular domain (ECD) of a protein that, in an unmodified immune cell, elicits an immune cell inactivation signal upon binding to its ligand, wherein said ECD is fused to an intracellular domain (ICD) of a co-stimulatory molecule that mediates an immune cell activation signal, wherein binding of the chimeric stimulating molecule or the switch molecule to the ligand yields said immune cell activation signal in said modified immune cell instead of said immune cell inactivation signal and wherein the isolated population comprises a higher concentration of PBMCs endogenously expressing PD1 compared to a population of PBMCs in a subject, wherein each modified immune cell further expresses a chimeric antigen receptor comprising (i) an antigen interacting domain capable of binding a B cell surface protein; (ii) a transmembrane domain; and (iii) an intracellular signaling domain, wherein said B cell surface protein is selected from CD19, CD20, and CD22.
Additionally, it is noted that 35 USC § 121 does not provide protection for continuation or continuation in-part applications, and this application is a continuation of U.S. Patent No. 11,866,731. See 92 USPQ2d 1289 Amgen Inc. v. F. Hoffmann-La Roche Ltd. (Fed. Cir. 2009) and Pfizer, Inc. v. Teva Pharmaceuticals USA, Inc. 518 F.3d 1353 (Fed. Cir. 2008).
13. Claims 87-88 and 91-96 are provisionally rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 34-42 and 45-59 of copending Application No. 17/429835. Although the conflicting claims are not identical, they are not patentably distinct from each other for the following reasons:
Claims 87-88 and 91-96 are herein drawn to a modified immune cell comprising: (a) a switch molecule comprising an extracellular domain (ECD) of a protein that, in an unmodified immune cell, elicits an immune cell inactivation signal upon binding to its ligand, wherein said ECD is fused to an intracellular domain (ICD) of co-stimulatory molecule that mediates an immune cell activation signal, and wherein binding of the switch molecule to the ligand yields an immune cell activation signal instead of said immune cell inactivation signal in said modified immune cell, and (b) a chimeric antigen receptor comprising (i) an antigen interacting domain capable of binding a B cell surface protein (e.g., CD19 or CD20); (ii) a transmembrane domain; and (iii) an intracellular signaling domain, wherein the modified immune cell is obtained from peripheral blood mononuclear cell and expresses endogenous PD1, or the modified immune cell specifically binds to a neoantigen.
Claims 34-42 and 45-59 of copending Application No. 17/429835 are drawn to a method comprising a modified therapeutic immune cell (e.g. T cell), wherein the T cell is a tumor antigen-reactive T cell, wherein the T cell expresses (a) a CAR or exogenous TCR; and (b) an enhanced receptor, wherein the enhanced receptor is a transmembrane protein comprising an extracellular domain (ECD) and an intracellular domain, the ECD is a complete sequence of any one of a receptor, a ligand, an antibody of a membrane protein of the target cell of the immune cell, or other protein structure that can bind to the membrane protein, or a partial sequence comprising a binding domain thereof, and the ICD is any one of co-stimulatory signal proteins such as CD28 or 41BB or ICOS, and does not comprise CD3; wherein the ECD of the enhanced receptor generates an inhibitory signal on the T cells upon binding to its ligand, while an intact enhanced receptor generates an activating signal on the T cells upon binding to its ligand.
This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
14. Claims 87-88 and 91-96 are provisionally rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 87-97 of copending Application No. 18/518539. Although the conflicting claims are not identical, they are not patentably distinct from each other for the following reasons:
Claims 87-88 and 91-96 are herein drawn to a modified immune cell comprising: (a) a switch molecule comprising an extracellular domain (ECD) of a protein that, in an unmodified immune cell, elicits an immune cell inactivation signal upon binding to its ligand, wherein said ECD is fused to an intracellular domain (ICD) of co-stimulatory molecule that mediates an immune cell activation signal, and wherein binding of the switch molecule to the ligand yields an immune cell activation signal instead of said immune cell inactivation signal in said modified immune cell, and (b) a chimeric antigen receptor comprising (i) an antigen interacting domain capable of binding a B cell surface protein (e.g., CD19 or CD20); (ii) a transmembrane domain; and (iii) an intracellular signaling domain, wherein the modified immune cell is obtained from peripheral blood mononuclear cell and expresses endogenous PD1, or the modified immune cell specifically binds to a neoantigen.
Claims 87-97 of copending Application No. 18/518539 are drawn to a method of expanding a T cell population, comprising: (a) introducing a nucleic acid encoding a chimeric antigen receptor (CAR) into the T cell population, thereby producing a first CAR-expressing cell population, wherein the CAR comprises (i) an antigen interacting domain capable of binding a B cell surface protein; (ii) a transmembrane domain; and (iii) an intracellular signaling domain; and (b) contacting the first CAR-expressing cell population with a B cell surface protein, thereby producing an expanded and/or activated immune cell population, wherein said B cell surface protein is selected from CD19, CD20, and CD22.
In Pfizer, Inc., v. Teva Pharamaceutical USA, inc. (Fed. Cir, 2008), the Court concluded that the safe harbor of section 121 is limited to divisional applications only. The instant application is not filed as a result of a restriction requirement of copending Application No. 18/518539. The T cell population claimed in the claims of the copending Application No. 18/518539 is the same as the instantly claimed modified immune cell.
This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
15. Claims 87-88 and 91-96 are provisionally rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 19 and 21-30 of copending Application No. 18/033483. Although the conflicting claims are not identical, they are not patentably distinct from each other for the following reasons:
Claims 87-88 and 91-96 are herein drawn to a modified immune cell comprising: (a) a switch molecule comprising an extracellular domain (ECD) of a protein that, in an unmodified immune cell, elicits an immune cell inactivation signal upon binding to its ligand, wherein said ECD is fused to an intracellular domain (ICD) of co-stimulatory molecule that mediates an immune cell activation signal, and wherein binding of the switch molecule to the ligand yields an immune cell activation signal instead of said immune cell inactivation signal in said modified immune cell, and (b) a chimeric antigen receptor comprising (i) an antigen interacting domain capable of binding a B cell surface protein (e.g., CD19 or CD20); (ii) a transmembrane domain; and (iii) an intracellular signaling domain, wherein the modified immune cell is obtained from peripheral blood mononuclear cell and expresses endogenous PD1, or the modified immune cell specifically binds to a neoantigen.
Claims 19 and 21-30 of copending Application No. 18/033483 are drawn to a method for treating or preventing diseases or symptoms related to viral infections, or preventing recurrence of diseases or symptoms related to viral infections in a subject, comprising administering to the subject the a composition comprising a cell population of claim 18, wherein the cell population comprises a modified immune cell, wherein the modified immune cell is a PD-1-positive T (PD-1+T) cell derived from peripheral blood, and is capable of targeting to a target cell in the subject, wherein the target cell is a virus-infected cell; wherein the diseases or symptoms related to viral infections are not cancer; and wherein the modified immune cell comprises an enhanced receptor (ER) comprising an extracellular domain (ECD) and an intracellular domain (ICD), wherein the ECD is capable of binding to the target cell of the modified immune cell, and the ICD comprises a costimulatory molecule or a fragment thereof that elicits an immune cell activation signal.
In Pfizer, Inc., v. Teva Pharamaceutical USA, inc. (Fed. Cir, 2008), the Court concluded that the safe harbor of section 121 is limited to divisional applications only. The instant application is not filed as a result of a restriction requirement of copending Application No. 18/033483. The modified immune cell claimed in the claims of the copending Application No. 18/033483 is the same as the instantly claimed modified immune cell.
This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
16. Claims 87-96 are provisionally rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-2 and 9-20 of copending Application No. 17/793771. Although the conflicting claims are not identical, they are not patentably distinct from each other for the following reasons:
Claims 87-96 are herein drawn to a modified immune cell comprising: (a) a switch molecule comprising an extracellular domain (ECD) of a protein that, in an unmodified immune cell, elicits an immune cell inactivation signal upon binding to its ligand, wherein said ECD is fused to an intracellular domain (ICD) of co-stimulatory molecule that mediates an immune cell activation signal, and wherein binding of the switch molecule to the ligand yields an immune cell activation signal instead of said immune cell inactivation signal in said modified immune cell, and (b) a chimeric antigen receptor comprising (i) an antigen interacting domain capable of binding a B cell surface protein (e.g., CD19 or CD20); (ii) a transmembrane domain; and (iii) an intracellular signaling domain, wherein the modified immune cell is obtained from peripheral blood mononuclear cell and expresses endogenous PD1, or the modified immune cell specifically binds to a neoantigen.
Claims 1-2 and 9-20 of copending Application No. 17/793771 are drawn to a composition comprising (i) an enhanced receptor for improving the function of an immune cell comprising an enhanced transmembrane receptor protein expressed across a membrane of the immune cell, wherein the receptor protein comprises an extracellular domain (ECD) and an intracellular domain (ICD); (ii) a naturally unmodified T cell receptor (TCR), an artificially modified engineered TCR, or a CAR (chimeric antigen receptor).
This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
Conclusion
17. No claim is allowed.
18. Any inquiry concerning this communication or earlier communications from the examiner should be directed to YAN XIAO whose telephone number is (571)270-3578. The examiner can normally be reached M-F 8-5 EST.
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/YAN XIAO/Primary Examiner, Art Unit 1642
