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 .
Response to Amendment
Applicant’s remarks and amendments to the claims filed 06/26/2026 have been acknowledged. Claims 1, 3-5, 7, 12, 15, and 30 have been amended. Claim 76 has been canceled. Claims 77-105 are newly added. The cancellation of claim 76 overcomes the claim objection previously set forth in the Non-Final Rejection of 05/13/2026.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-5, 11, 12, 15, 30, and 104 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of treating a GPC2-positive cancer comprising administering a polypeptide comprising a first antibody that targets GPC2 and a second antibody that targets a T cell antigen, engagement of which promotes T -cell mediated killing of cancers, does not reasonably provide enablement for a bispecific construct that engages any T cell antigen, including those that do not promote T cell activation/T-cell mediated tumor killing. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The nature of the invention relates to the fields of medicine, oncology, and immunotherapy; in particular, the development of agents useful for treating glypican 2 (GPC2)-positive cancers (see Field of Invention on Page 1 of Specification).
Claim 1 is broadly drawn to a method of treating a GPC2-positive cancer comprising administering a polypeptide comprising an anti-GPC2 antibody that “further comprises a second antibody that binds to a T cell”. Thus, the second antibody can bind to any T cell antigen, including those that do not promote T-cell mediated killing of tumor cells.
The specification teaches that three antibodies – m201, m202, and m203 – specifically targeting GPC2 were isolated from a phage display antibody library and affinity matured. Further in vitro characterization demonstrated that these antibodies possess therapeutic activity for use in CAR-T, antibody drug conjugate (ADC) and bispecific antibody formats for cancer therapy as stated in Example 1. Indeed, recent studies establish that D3-GPC2-PBD, a GPC2-targeted ADC that links a human GPC2 antibody (D3) to DNA-damaging pyrrolobenzodiazepine (PBD) dimers induces durable neuroblastoma and SCLC tumor regression via induction of DNA damage, apoptosis, and bystander cell killing, notably with no signs of ADC-induced in vivo toxicity (Raman et al, see Abstract). In addition, a GPC2-specific CAR T cell exhibited potent and durable eradication of neuroblastomas expressing clinically relevant GPC2 antigen densities, without toxicity (Heitzeneder et al, Abstract).
However, the specification does not provide evidence that a polypeptide comprising a tumor-associated antigen first antibody and a second antibody that binds to any T cell antigen can be used to treat cancer commensurate in scope with the claims. Further, the specification does not provide guidance for readily identifying T cell antigens that can be targeted by the claimed polypeptides in order to produce an antitumor effect.
The prior art teaches, for example, that bispecific T cell engagers (BiTE) are engineered antibodies that redirect T cells to mediate tumor cell killing by simultaneously binding to CD3 on T cells and tumor-associated antigens. In particular, the BiTE antibody constructs induce the formation of a cytolytic synapse between the T cell and the tumor cell; and target cell lysis occurs in the absence of regular major histocompatibility complex (MHC) class I/peptide antigen recognition and costimulation. Because the CD3ε target of BiTE antibody construct is invariant, both CD8+ and CD4+ T cells of any phenotype can be engaged, leading to a polyclonal T cell activation, expansion and tumor cell lysis (Ross et al, Introduction). The prior, however, does not establish that binding any and every T cell antigen can predictably produce the required antitumor response; rather, the therapeutic effect of a bispecific antibody construct appears to depend on the particular T cell targets, such as CD3, that are known to promote T cell activation and/or cytotoxicity.
A person of ordinary skill in the art at the time of filing would have had experience in antibody engineering and oncology. Even at this high level of skill, in the absence of further guidance, artisans would have to engage in undue trial-and-error experimentation (e.g. in vitro functional assays and animal tumor models) to determine the full scope of T cell antigens that can be targeted by the second antibody such that the claimed polypeptide effectively treats a GPC2-specific cancer in a subject. Claims 2-7, 11-12, 15, 30, and 104 depend either directly or indirectly on claim 1 but do not cure the deficiencies of claim 1 and thus are also rejected.
Therefore, the specification is not enabling over the full scope of the claims.
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1-7, 11-12, 15, 104, and 105 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 1 recites a polypeptide comprising an antibody wherein the antibody “further comprises a second antibody”. The term “antibody” encompasses both monospecific and bispecific antibodies.
If the first “antibody” is monospecific, it is structurally impossible for it to “further comprise a second antibody” unless it is fused, conjugated, or linked to the second antibody in some manner.
If the first “antibody” is bispecific, it is unclear whether the “further comprising a second antibody” results in a trispecific polypeptide or if the limitation is a redundant description of the bispecific construct itself. Thus, the metes and bounds of the desired patent protection cannot be determined. Claims 2-7, 11-12, 15, and 30, depend directly or indirectly from claim 1 but do not cure the deficiencies of claim 1; thus claims 2-7, 11-12, 15, 30, 104, and 105 are also rejected.
Claims 12 and 15, which each depend on claim 1, recite the limitation “the antibody” in line 1. Claim 1 recites an antibody that selectively binds to Glypican 2 as well as an antibody that binds to a T cell. There is insufficient antecedent basis for the limitation because it is unclear whether ‘the antibody’ of claims 12 and 15 refer to the anti-Glypican 2 antibody or the anti-T-cell antibody. While the polypeptide of claim 1 can be, for example, a bispecific antibody and comprise a first antigen-binding domain (e.g. Fab or scFv) linked to a second antigen binding domain (e.g. Fab or scFv), an antibody that is a monospecific antibody cannot “further comprise” a second antibody.
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.
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Claims 77-103 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-30 of copending Application No. 19/711,665 (reference application) in view of June et al (US 20130288368 A1), hereinafter June, and Orentas et al (Orentas, Rimas J et al. “Identification of cell surface proteins as potential immunotherapy targets in 12 pediatric cancers.” Frontiers in oncology vol. 2 194. 17 Dec. 2012, doi:10.3389/fonc.2012.00194, of record), hereinafter Orentas.
The co-pending claims recite a CAR-T cell wherein the CAR comprises
a scFv that binds to human Glypican 2;
a hinge domain
a transmembrane domain;
an endodomain; and
wherein the scFv comprises:
(a) a VH chain comprising the CDRs of SEQ ID NOs: 5, 6, and 7 (corresponding to SEQ ID NOs: 5, 6, and 7 of the instant claims); and a VL chain comprising the CDRs of SEQ ID NOs: 8, 9, and 10 (corresponding to SEQ ID NOs: 8, 9, and 10 of the instant claims); or
(b) a VH chain comprising the CDRs of SEQ ID NOs: 15, 16, and 17 (corresponding to SEQ ID NOs: 15, 16, and 17 of the instant claims); and a VL comprising the CDRs of SEQ ID NOs: 18, 19, and 20 (corresponding to SEQ ID NOs: 18, 19, and 20 of the instant claims); or
(c) a VH chain comprising the CDRs of SEQ ID NOs: 25, 26, and 27 (corresponding to SEQ ID NOs: 25, 26, and 27 of the instant claims); a VL comprising the CDRs of SEQ ID NO: 28, 29, and 30 (corresponding to SEQ ID NOs: 28, 29, and 30 of the instant claims);
wherein the scFv is linked via its C-terminus to the hinge domain; the C-terminus of the hinge domain is linked to the N-terminus of the transmembrane domain; and the C-terminal of the transmembrane domain is linked to the N-terminus of the endodomain (co-pending claims 1, 6, 9, 13, 15, 18 19, 22, 23, 26, 28, and 30). In other embodiments, the anti-glypican 2 scFv has (d) VH/VL chains of SEQ ID NOs: 2 and 4, respectively (corresponding to SEQ ID NOs: 2 and 4 of the instant claims); (e ) VH/VL chains of SEQ ID NOs: 12 and 14, respectively (corresponding to SEQ ID NOs: 12 and 14 of the instant claims); or (f) the VH/VL chains of SEQ ID NOs: 22 and 24 respectively (corresponding to SEQ ID NOs: 22 and 24 of the instant claims) (co-pending claim 7, 8, and 9). In some embodiments, the hinge domain is from CD8 alpha (co-pending claim 2); and the endodomain comprises signaling domains from both 4-1BB and CD3 zeta (co-pending claim 3).
The co-pending claims do not recite a method of treating a glypican-2 positive cancer in a human subject comprising administering the CAR T cell.
However, June teaches that chimeric antigen receptors (CARs) combine antibody-based specificity for a desired antigen (e.g., tumor antigen) with a T cell receptor-activating intracellular domain to generate a chimeric protein that exhibits a specific anti-tumor cellular immune activity (Para. 0053). Disclosed are methods for treating cancer in a human subject including but not limited to hematologic malignancies and solid tumors comprising administering a genetically modified T cell to express a CAR wherein (1) the CAR comprises an antigen binding domain, a transmembrane domain, a costimulatory signaling region, and a CD3 zeta signaling domain (Abstract and Para. 0053) and (2) the antigen binding domain binds to a tumor antigen (Para. 0010). Types of solid tumors to be treated with the CARs of the invention include, but are not limited to breast cancer, prostate cancer, ovarian cancer, cervical cancer, skin cancer, pancreatic cancer, colorectal cancer, renal cancer, liver cancer lung cancer, and brain cancer. Adult tumors/cancers and pediatric tumors/cancers are also included (Para. 0200 and Para. 0202).
Orentas further teaches that glypican-2 (GPC2) is a tumor associated antigen expressed in several pediatric cancers such as acute lymphocytic leukemia, Ewing’s sarcoma, embryonal rhabdomyosarcoma, alveolar rhabdomyosarcoma, osteosarcoma, and neuroblastoma; and thus represents GPC2-expressing tumors can be the target of CAR or antibody-based therapies (see Abstract, “Tumors Analyzed” section under Results, and Figure 2).
It would have been obvious to one of ordinary skill in the art to administer the GPC2-specific CAR of the co-pending claims to a subject having a GPC2-expressing cancer such as pediatric acute lymphocytic leukemia, embryonal rhabdomyosarcoma or neuroblastoma. One of ordinary skill in the art would have been motivated to do so since June teaches that genetically-modified T cells expressing a chimeric antigen receptor that recognizes a tumor antigen can treat cancer in a subject, and GPC2 is expressed in several pediatric tumors such as acute lymphocytic leukemia, embryonal rhabdomyosarcoma or neuroblastoma and can thus be targeted and treated by CAR-based therapies as taught by Orentas, such as the GPC2-specific CAR of the co-pending claims. Therefore, one of ordinary skill in the art would reasonably expect the GPC2-specific CAR of the co-pending claims can be used to effectively treat GPC2-expressing cancers in a subject.
Claims 77-103 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of copending Application No. 19718785 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the co-pending claims either anticipate or are obvious variants over the instant claims.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
The co-pending claims recite a method of treating a mammal having a disease associated with GPC2 overexpression, comprising administering to the mammal a genetically modified T cell comprising a chimeric antigen receptor (CAR), wherein the CAR comprises an anti-GPC2 antigen binding domain, a flexible hinge domain, a transmembrane domain, a costimualtiory domain, and an intracellular signaling domain (co-pending claims 11, 16, and 20). The GPC2-specific antigen binding domain comprises:
the VH chain of SEQ ID NO: 30 (corresponding to SEQ ID NO: 2 and fully comprising the CDRs of SEQ ID NOs: 5, 6, and 7 of the instant claims) and the VL chain of SEQ ID NO: 32 (corresponding to SEQ ID NO: 4 and fully comprising the CDRs of SEQ ID NOs: 8, 9, and 10 of the instant claims) (see Sequence Alignments_054 vs 580, OA.Appendix).;
the VH chain of SEQ ID NO: 34 (corresponding to SEQ ID NO: 12 and fully comprising the CDRs of SEQ ID NOs: 15, 16, and 17 of the instant claims) and the VL chain of SEQ IDNO: 36 (corresponding to SEQ ID NO: 14 and fully comprising the CDRs of SEQ ID NOs: 18, 19, and 20 of the instant claims) (see Sequence Alignments_054 vs 580, OA.Appendix).; or
the VH chain of SEQ ID NO: 38 (corresponding to SEQ ID NO: 22 and fully comprising SEQ ID NOs: 25, 26, and 27 of the instant claims) and the VL chain of SEQ ID NO: 40 (corresponding to SEQ ID NO: 24 and fully comprising the CDRs of SEQ ID NOs: 28, 29, and 30 of the instant claims) (co-pending claims 1 and 4) (see Sequence Alignments_054 vs 580, OA.Appendix) (Note: Sequence Alignments performed between the sequences of the parent application 17597580 and the instant application).
wherein the antigen binding domain is a Fab or single-chain variable fragment (scFv) (co-pending claims 12, 13, and 14). The disease associated with GPC2 overexpression is GPC2-expressing cancer, wherein the GPC2-expressing cancer is a solid tumor cell selected from the group consisting of sarcoma, neuroblastoma, rhabdoid cancer, neuroblastoma, retinoblastoma, medulloblastoma, small cell lung cancer, uterine carcinosarcoma, glioma, thymoma, a testicular germ cell tumor, glioblastoma multiforme, melanoma, hepatocellular carcinoma, thyroid cancer, renal clear cell carcinoma, renal papillary cell carcinoma, stomach adenocarcinoma, cholangiocarcinoma, adenoid cystic carcinoma, prostate adenocarcinoma, lung adenocarcinoma, head-neck squamous carcinoma, pancreatic adenocarcinoma, breast cancer, mesothelioma, colon and rectal adenocarcinoma, an esophageal carcinoma, ovarian cancer, lung squamous cell carcinoma, and bladder urothelial carcinoma. (co-pending claim 22).
The co-pending claims do not teach that the GPC2-expressing cancer is a pediatric cancer.
However, Orentas teaches that glypican-2 (GPC2) is a tumor associated antigen expressed in several pediatric cancers such as acute lymphocytic leukemia, Ewing’s sarcoma, embryonal rhabdomyosarcoma, alveolar rhabdomyosarcoma, osteosarcoma, and neuroblastoma; and thus represents GPC2-expressing tumors can be the target of CAR or antibody-based therapies (see Abstract, “Tumors Analyzed” section under Results, and Figure 2).
It would have been obvious to one of ordinary skill in the art to modify the method of the co-pending claims such that GPC2-expressing tumor is a pediatric cancer such as acute lymphocytic leukemia , embryonal rhabdomyosarcoma or neuroblastoma. One of ordinary skill in the art would have been motivated to do so since GPC2 is expressed in several pediatric cancers such as acute lymphocytic leukemia, embryonal rhabdomyosarcoma or neuroblastoma and can thus be targeted and treated by the GPC2-specific CAR of the co-pending claims. Therefore, one of ordinary skill in the art would reasonably expect the GPC2-specific CAR of the co-pending claims to effectively treat GPC2-expressing tumors in a subject.
Claims 77-103 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 5, 7, 9, 11, 15-23, 30, 33, 38, and 40 of copending Application No. 18716387 (reference application) in view of Orentas et al (Orentas, Rimas J et al. “Identification of cell surface proteins as potential immunotherapy targets in 12 pediatric cancers.” Frontiers in oncology vol. 2 194. 17 Dec. 2012, doi:10.3389/fonc.2012.00194, of record), hereinafter Orentas.
This is a provisional nonstatutory double patenting rejection.
The co-pending claims recite a method of treating cancer in a patient comprising administering a cell comprising a polynucleotide encoding a CAR having a GPC2-specific single chain antibody variable region (co-pending claims 1, 33, and 40). The GPC2 single chain antibody comprises the VH chain of SEQ ID NO: 1 (corresponding to SEQ ID NO: 2 and thus fully comprising the CDRs of SEQ ID NOs: 5, 6, and 7 of the instant claims) and the VL chain of SEQ ID NO: 2 (corresponding to SEQ ID NO: 4 and thus fully comprising SEQ ID NOs: 8, 9, and 10 of the instant claims) (co-pending claim 15) (see Sequence Alignments_054 vs 387, OA.Appendix). Further recited in the co-pending claims is a cell comprising the polynucleotide encoding the GPC2-speicfic CAR (co-pending claim 33). The CAR comprises an ectodomain having the GPC2-specific single chain antibody, a CD28 hinge, CD28 transmembrane domain, a CD28, 4-1BB, or CD3 zeta costimulatory domain (co-pending claims 2, 3, 5, 7, 9, and 11).
The co-pending claims do not specifically recite that the cancer treated is a GPC2-expressing cancer.
However, Orentas teaches that glypican-2 (GPC2) is a tumor associated antigen expressed in several pediatric cancers such as acute lymphocytic leukemia, Ewing’s sarcoma, embryonal rhabdomyosarcoma, alveolar rhabdomyosarcoma, osteosarcoma, and neuroblastoma; and thus represents GPC2-expressing tumors can be the target of CAR or antibody-based therapies (see Abstract, “Tumors Analyzed” section under Results, and Figure 2).
It would have been obvious to one of ordinary skill in the art to modify the method of the co-pending claims such that the cancer treated is a GPC2-expressing cancer such as acute lymphocytic leukemia , embryonal rhabdomyosarcoma or neuroblastoma. One of ordinary skill in the art would have been motivated to do so since GPC2 is expressed in several pediatric cancers such as acute lymphocytic leukemia , embryonal rhabdomyosarcoma or neuroblastoma and can thus be targeted and treated by the GPC2-specific CAR of the co-pending claims. Therefore, one of ordinary skill in the art would reasonably expect the GPC2-specific CAR of the co-pending claims to effectively treat GPC2-expressing tumors in a subject.
Response to Arguments
Applicant's arguments filed 06/26/2026 have been fully considered but they are not fully persuasive.
With respect to the 35 USC 112(a) rejection, Applicant argues that claim 1 as amended incorporates subject matter indicated as compliant with the enablement requirement.
In response to Applicant’s arguments, the Examiner notes that claim 1, as amended, is broadly drawn to a method of treating a GPC2-positive cancer comprising administering a polypeptide comprising an anti-GPC2 antibody that “further comprises a second antibody that binds to a T cell” without limitation on the T cell antigen engaged. Thus, the second antibody can bind to any T cell antigen, including those that do not promote T-cell mediated killing of tumor cells as discussed further in the Enablement rejection above. Additionally, claim 1 as amended introduces issues under 35 USC 112(b) as discussed further above.
With respect to double patenting rejections, Applicant argues that the present application has an earliest "patent term filing date" for the purpose of non-statutory double patenting of November 8, 2016, which is earlier than that of U.S. Appl. No. 17/597,580 (July 17, 2020) and that of U.S. Appl. No.18/716,387 (December 5, 2022). In this situation, if the only remaining rejection against the present application is a provisional non-statutory double patenting rejection, it should be withdrawn.
In response to Applicant’s arguments, the Examiner notes that the amendments to the claims introduced new issues under 35 USC 112(a) enablement and 35 USC 112(b). Therefore, the double patenting rejections are not the only remaining rejections and are thus maintained here.
Conclusion
No claims are allowable.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/LIA E TAYLOR/Examiner, Art Unit 1641
/MISOOK YU/Supervisory Patent Examiner, Art Unit 1641
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