Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Status of Claims
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
This action is in response to the papers filed on July 29 2026. Claims 1 – 10, and 40 - 46 are currently pending. Claims 1 – 5, 7, 40, and 46 have been amended in the Applicant’s amendment filed July 29, 2026. No claims have been added or canceled in the Applicant’s amendment filed July 29, 2026
Information Disclosure Statement
The information disclosure statements (IDS) submitted on July 29, 2026. An initialed copy of the IDS accompanies this Office Action.
Priority
The present application filed October 10, 2024 is a CON of 17,042,030, filed October 25, 2020, (now US Patent 12144826) which is a 35 U.S.C. 371 national stage filing of PCT/US2019/025846, filed April 4, 2019, which claims the benefit of Provisional Application 62/722,681, filed August 24, 2018, which claims the benefit of Provisional Application 62/654,012, filed April 6, 2018.
Thus, the earliest possible priority for the instant application is April 06, 2018.
Withdrawn Objections/Rejections
Claim Rejection - 35 USC § 112(b)
The rejection of claims 40 - 46 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or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention is withdrawn.
Applicant has amended claim 40 to no longer be indefinite.
In view of the withdrawn rejection, Applicant’s arguments are moot.
Maintained Objections/Rejections
Nonstatutory Double Patenting
The rejection of claims 1 – 10, and 40 - 46 is maintained on the ground of nonstatutory double patenting as being unpatentable over allowed claims 1-8 of US Patent 12,144,826 Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims are wholly encompassed by, and significantly overlap in scope with claims 1-8 of US Patent 12,144,826.
Claim 1 of US Patent 12,144,826 is directed to a method of treating a subject for EGFRvIII positive glioblastoma, comprising administering an immune cell genetically modified with: (a) a nucleic acid sequence encoding a BTTS that bidns to EGFRvIII, (b) a nucleic acid sequence encoding a tandem CAR or TCR, wherein the tandem CAR or TCR comprises a first binding domain that recognizes EphA2 and a second binding domain that recognizes IL-13Rα2, and (c) a regulatory sequence operably linked to (b) that is responsive to BTTS, wherein binding of the BTTs to EGFRvIII on EGFRvIII positive glioblastoma cells activates expression of the tandem CAR or TCR, which binds to EphA2 and/or IL-13Rα2 in the glioblastoma and induces killing of glioblastoma cells. Claims 1 – 10 of the instant application also teaches a method of treating a subject for EGFRvIII positive glioblastoma, comprising administering a genetically modified immune cell.
Claims 1- 10 of the instant invention are directed to a method of treating a subject for an epidermal growth factor receptor variant III (EGFRvIII) positive glioblastoma. Specifically, claim 1 recites: A method of treating a subject for an epidermal growth factor receptor variant III (EGFRvIII) positive glioblastoma, the method comprising: administering to the subject an immune cell genetically modified with:(a) a nucleic acid sequence encoding a binding triggered transcriptional switch (BTTS) that binds to EGFRvIII;(b) a nucleic acid sequence encoding an antigen-specific therapeutic that binds to a killing antigen expressed by the glioblastoma; and (c) a regulatory sequence operably linked to (b) that is responsive to the BTTS; wherein binding of the BTTS to EGFRvIII activates expression of the antigen-specific therapeutic which binds the killing antigen thereby inducing killing of glioblastoma cells expressing the killing antigen.
Additionally, claim 40 - 46 of the instant invention are directed to an immune cell genetically modified with: (a) a nucleic acid sequence encoding a BTTS that binds to EGFRvIII, (b) a nucleic acid sequence encoding a tandem CAR or TCR, wherein the tandem CAR or TCR comprises a first binding domain that recognizes EphA2 and a second binding domain that recognizes IL-13Rα2, and (c) a regulatory sequence operably linked to (b) that is responsive to BTTS, wherein binding of the BTTs to EGFRvIII on EGFRvIII positive glioblastoma cells activates expression of the tandem CAR or TCR, which binds to EphA2 and/or IL-13Rα2 in the EGFRvIII positive glioblastoma and induces killing of tumor cells in a EGFRvIII positive glioblastoma.
The instant claims require an antigen specific therapeutic that binds to a killing antigen expressed by a glioblastoma. Thus, the instantly recited “an antigen-specific therapeutic” is broader than a first binding domain that recognizes Ephrin type-A receptor 2 (EphA2) and a second binding domain that recognizes IL-13 receptor a2 (IL-13Ra2) in claim 1 of the US Patent 12,144,826 . Therefore, claim 1 of US Patent 12,144,826 recites “species” of the generic invention of instant application. It has been held that a generic invention is “anticipated” by a “species” within the scope of the generic invention. It is well established that a species of a claimed invention renders the genus obvious. In re Schaumann , 572 F.2d 312, 197 USPQ 5 (CCPA 1978).
Additionally, Claims 1-8 of US Patent 12,144,826 claim the method of treating a subject for EGFRvIII positive glioblastoma, comprising administering the genetically modified immune cell, while the instant application is directed to compositions and methods. However, double-patenting rejections of claims to a method of use based on a claimed composition are proper. This rejection is necessitated by the decision of the Court of Appeals for the Federal Circuit in Pfizer Inc. v Teva pharmaceuticals USA Inc., 86 USPQ2d 1001, at page 1008 (March 2008), which indicates that there is no patentable distinction between claims to a product and a method of using that product disclosed in the specification of the application and that the preclusion of such a double patenting rejection under 35 USC 121 does not apply where the present application is other than a divisional application of the patent application containing such patentably indistinct claims.
Response to Applicants’ Arguments as they apply to Double Patenting Rejection
At page 5 of the remarks filed on July 29, 2026, Applicants request that this rejection be held in abeyance, and a terminal disclaimer will be filed later, if necessary (pg. 5. Nonstatutory double patenting section). However, Applicant’s request is not a proper response to the rejections of record as it neither traverses the grounds of rejection by providing specific arguments, nor indicates that a terminal disclaimer has been filed to overcome the rejection. As such, the rejections of record stand.
Claim Rejection - 35 USC § 103
The rejection of claims 1 – 10 and 40 - 46 under 35 U.S.C. 103 as being unpatentable over Lim et al. (hereinafter referred to as “Lim”) (US Patent Application Publication, US 20180079812 A1, Published March 22, 2018), and further in view of Chow et al. (hereinafter referred to as “Chow”; or record) (Chow KK. et al. Mol Ther. 2013 Mar;21(3):629-37; of record).) is maintained.
Regarding claim 1 and 40, Lim teaches a method of treating cancer, comprising modifying T lymphocytes or NK cells with an expression vector encoding a chimeric Notch receptor polypeptide, and introducing the genetically modified cells into the individuals, wherein these genetically modified cells recognize and kill the cancer the cell (Paragraph [0529]). Lim teaches that the chimeric Notch receptor polypeptide is a binding triggered transcriptional switch (BTTS), wherein the BTTS comprises a first member of the first specific binding pair and a first member second specific binding pair (Paragraph [0028] and [0048] “wherein the cell expresses: i) a first binding-triggered transcriptional switch comprising an extracellular domain comprising a first member of the first specific binding pair, a binding-transducer and an intracellular domain; and ii) at least a second binding-triggered transcriptional switch comprising an extracellular domain comprising the first member of a second specific binding pair, a binding-transducer and an intracellular domain; wherein the intracellular domain of the first binding-triggered transcriptional switch provides a first effector function and the intracellular domain of the second binding-triggered transcriptional switch provides a second effector function” ). Lim teaches the second member of the specific binding pair is an antibody for EGFRvIII (Paragraph [0219]) (interpreted as a nucleic acid sequence encoding a BTTS that binds to EGFRvIII) and “Where the first member of the specific binding pair is an antigen” (para [0221]). Lim teaches that the antigen binding domain of the chimeric Notch polypeptide is specific for the antigen expressed by a glioblastoma, and more specifically EGFRvIII (Paragraph [0186] and [0188]) (interpreted as a method of treating EGFRvIII positive glioblastoma, wherein the immune cells is genetically modified and administered). Lim teaches that when the first member of the specific binding pair binds to the second member of the specific binding pair, the intracellular domain of the chimeric Notch receptor is released and induces production of a TCR (T cell receptor) in the cell (Paragraph [0438]) (interpreted as wherein the binding of the BTTS to EGFRvIII activates expression of the antigen-specific therapeutic).
Regarding claim 40, Lim also teaches that the when first member binds to the second member of the specific binding pair, it induces production of a CAR in a cell that expresses the chimeric Notch polypeptide (Paragraph [0440]). Lim teaches that CAR variants also include bispecific CARs, which include a secondary CAR binding domain that can either amplify or inhibit the activity of a primary CAR (Paragraph [0150]). Lim teaches that the second member of the specific binding pair is IL-13R-a2 (Paragraph [0219]) (interpreted as a nucleic acid encoding a tandem CAR, and a second binding domain that recognizes IL-13R-a2).
Lim teaches that the TCR is specific for antigens, including EphA2, IL13Ra2, EGFRvIII, which are all expressed in Glioma (Paragraph [0438]). Lim also teaches that there is first promoter that is responsive to the first binding-triggered transcriptional switch (Paragraph [0048]) (interpreted as a regulatory sequence operably linked to the TCR that is responsive to the BTTS).
Lim does not specifically exemplify that the binding of antigen-specific therapeutic to the killing antigen induces killing of glioblastomas expressing the killing antigen (instant claim 1 and 40), and that the killing antigen is expressed by all cells of the glioblastoma (instant claim 4).
Regarding claim 1 (in part), 40 (in part) and 4, Chow teaches EphA2 as an attractive target for immunotherapy of glioblastoma, as it is over expressed in glioma and promotes the malignant phenotype (Abstract) (interpreted as killing antigen (EphA2) is expressed by all cells of the glioblastoma, instant claim 4). Chow teaches the development of EphA2-specific CAR T cells that are able to recognize and kill EphA2 positive glioma cells in vitro and in vivo (Introduction, Paragraph 4) (interpreted as the expression of the antigen-specific therapeutic binds to the killing antigen, inducing killing of glioblastoma cells expressing the killing antigen, instant claim 1). Chow teaches EphA2 overexpression induces enhanced tumorigenesis and metastasis (Introduction, Paragraph 3). Chow teaches an in vivo experiment wherein the mice were administered EphA2 – CAR T cells, revealing a decrease in tumor progression after 40 days, when compared to the control mice (Figure 5A).
Therefore, in view of the benefits of targeting EphA2 for glioblastoma treatment as taught by Chow, it would have been prima facia obvious for one of ordinary skill in the art to use the genetically modified cells used for EGFRvIII glioblastoma treatment, wherein the TCR specific for EphA2 as taught by Lim in the in vivo experiments as described by Chow with a reasonable expectation of success in treating glioblastoma and decreasing the tumor size. It would have been prima facia obvious to combine the cited sources because Lim teaches the treatment for glioblastoma, the method of genetically modifying T cells to express the TCR and CAR specific for EphA2, and the administration of these genetically modified cells, and Chow teaches that EphA2 is overexpressed on the glioblastoma, and the method wherein EphA2 expressing CAR T cells recognize EphA2 on the glioblastoma, which then decreases tumor burden in vitro and in vivo.
Regarding claims 2 - 3, and 7, the combined teachings of Bedoya and Robin render obvious the teachings of claim 1. Moreover, Lim teaches that the EGFRvIII and EphA2 is expressed in the glioma (Paragraph [0472]) (interpreted as the EGFRvIII positive glioblastoma comprise cells that express the killing antigen (EphA2) and EGFRvIII).
Regarding claim 5 and 6, the combined teachings of Bedoya and Robin render obvious the teachings of claim 1. Moreover, Lim also teaches that EphA2 is also expressed in the lung (Paragraph [0438]).
Regarding claim 8 - 10, the combined teachings of Bedoya and Robin render obvious the teachings of claim 1. Moreover, Lim teaches that when the first member of the specific binding pair binds to the second member of the specific binding pair, the intracellular domain of the chimeric Notch receptor is released and induces production of a TCR (T cell receptor) in the cell (Paragraph [0438]) (interpreted as the antigen specific therapeutic is a TCR and is expressed on the surface of an immune cell, and is secreted by the immune cell).
Regarding claim 41 and 46, the combined teachings of Bedoya and Robin render obvious the teachings of claim 1. Moreover, Lim teaches the intracellular domain of chimeric Notch receptor polypeptide is the synNotch polypeptide (Paragraph [0441]). The first synNotch polypeptide is released upon binding of the first member to the second member of the specific binding pair, which induces production of a second synNotch polypeptide, (Paragraph [0441]) (interpreted as the BTTS is a SynNotch polypeptide, instant claim 41).
Regarding claim 45, the combined teachings of Bedoya and Robin render obvious the teachings of claim 1. Moreover, Lim teaches that the chimeric Notch receptor polypeptide comprises an antigen binding domain that can bind to EGFRvIII (Paragraph [0188]), transmembrane domain (TMD) that contains the γ-secretase cleavage site required for release of the Notch intracellular domain (Paragraph [0698]), and transcriptional activator (Paragraph [0294]).
Regarding claims 43 and 44, the combined teachings of Bedoya and Robin render obvious the teachings of claim 1. Moreover, Lim teaches that the cell is a cytotoxic T cell (Paragraph [0509]).
Response to Arguments as they apply to rejection of claims 1 – 10 and 40 - 46 under 35 USC § 103
Applicant’s arguments filed July 29, 2026 have been fully considered but they are not persuasive. Applicant essentially asserts (a) Lim can be disqualified as prior art because the subject matter owned by Lim and that claimed invention are owned by the same person (pg. 6, second paragraph), and (b) Chow teaches away from targeting EGFRvIII and IL-13Rα2, as EGFRvIII contributes to high risk of immune escape (pg. 6, third paragraph), and (c) the immune cell comprises a BTTS that binds to EGFRvIII is used to successfully treat glioblastomas (pg. 6, last paragraph).
Regarding (a), Applicant’s argument is not found persuasive.
Applicant is reminded that MPEP 718 teaches:
When any claim of an application or a patent under reexamination is rejected under 35 U.S.C. 103 as in effect on March 15, 2013, on a U.S. patent or U.S. patent application publication which is not prior art under 35 U.S.C. 102(b) as in effect on March 15, 2013, and the inventions defined by the claims in the application or patent under reexamination and by the claims in the patent or published application are not identical but are not patentably distinct, and the inventions are owned by the same party, the applicant or owner of the patent under reexamination may disqualify the patent or patent application publication as prior art. The patent or patent application publication can be disqualified as prior art by submission of:
(1) A terminal disclaimer in accordance with § 1.321(c); and
(2) An oath or declaration stating that the application or patent under reexamination and patent or published application are currently owned by the same party, and that the inventor named in the application or patent under reexamination is the prior inventor under 35 U.S.C. 104 as in effect on March 15, 2013.
Thus, the rejection of Lim in view of Chow is maintained.
Regarding (b) and (c), Applicant’s argument is not found persuasive.
As an initial matter, Applicant is reminded that none of the references has to teach each and every claim limitation. If they did, this would have been anticipation and not an obviousness-type rejection. One cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). The application of record is a combination of Lim and Chow.
Specifically, Lim teaches that the chimeric Notch receptor is a BTTS, which comprises a first member of the first specific binding pair and a first member second specific binding pair. Lim teaches when the first member of the specific binding pair binds to the second member of the specific binding pair, the intracellular domain of the chimeric Notch receptor is released and induces production of a TCR (T cell receptor) wherein the TCR is specific for EphA2, and IL-13Rα2 and EGFRvIII. Thus, Lim teaches that the use of the BTTS is used for treating the EGFRvIII positive glioblastomas.
While Chow does teach that targeting IL-13Rα2 and EGFRvIII is associated with the development of antigen loss variants, Chow also teaches that EphA2 has emerged as an attractive target for the immunotherapy of GBM as it is overexpressed in glioma and promotes its malignant phenotype (pg. 629, Abstract). Further, Chow teaches that EphA2 has emerged as an attractive target for GBM immunotherapy owing to recent findings that EphA2 signaling is involved in glioma cell proliferation, migration, and invasion (pg. 634, left column, second paragraph). Thus, one of ordinary skill in the art would target EphA2, and not IL-13Rα2 and EGFRvIII, for the treatment of glioblastomas.
Thus, as noted above, it would have been prima facia obvious for one of ordinary skill in the art to use the genetically modified cells used for EGFRvIII glioblastoma treatment, wherein the TCR specific for EphA2 as taught by Lim in the in vivo experiments as described by Chow with a reasonable expectation of success in treating glioblastoma and decreasing the tumor size. It would have been prima facia obvious to combine the cited sources because Lim teaches the treatment for glioblastoma, the method of genetically modifying T cells to express the TCR and CAR specific for EphA2, and the administration of these genetically modified cells, and Chow teaches that EphA2 is overexpressed on the glioblastoma, and the method wherein EphA2 expressing CAR T cells recognize EphA2 on the glioblastoma, which then decreases tumor burden in vitro and in vivo.
Thus, the rejection is maintained for the reasons of record.
Claim Rejection - 35 USC § 112(a) Scope of Enablement
The rejection of Claims 1 – 10, and 40 - 46 is maintained 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 subject for an epidermal growth factor receptor variant III (EGFRvIII) positive glioblastoma, the method comprising: administering to the subject an immune cell genetically modified with:(a) a nucleic acid sequence encoding a binding triggered transcriptional switch (BTTS) that binds to EGFRvIII;(b) a nucleic acid sequence encoding a CAR or TCR that binds to a killing antigen
expressed by the glioblastoma; and (c) a regulatory sequence operably linked to (b) that is responsive to the BTTS; wherein binding of the BTTS to EGFRvIII activates expression of the CAR or TCR which binds the killing antigen thereby inducing killing of glioblastoma cells expressing the killing antigen, wherein the tumor antigen is EphA2 or IL13Rα2,
does not reasonably provide enablement for any antigen-specific therapeutic or any killing antigen expressed by the EGFRvIII positive glioblastoma.
The Specification does not enable any person skill 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 claims, when given the broadest possible interpretation, encompass a method of treating a subject for an epidermal growth factor receptor variant III (EGFRvIII) positive glioblastoma, the method comprising: administering to the subject an immune cell genetically modified with:(a) a nucleic acid sequence encoding a binding triggered transcriptional switch (BTTS) that binds to EGFRvIII;(b) a nucleic acid sequence encoding an antigen-specific therapeutic that binds to a killing antigen expressed by the glioblastoma; and (c) a regulatory sequence operably linked to (b) that is responsive to the BTTS; wherein binding of the BTTS to EGFRvIII activates expression of the antigen-specific therapeutic which binds the killing antigen thereby inducing killing of glioblastoma cells expressing the killing antigen. 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 test of enablement is whether one skilled in the art could make and use the claimed invention from the disclosures in the patent coupled with information known in the art without undue experimentation (United States v. Telectronics, Inc., 8 USPQ2d 1217 (Fed. Cir. 1988)). Whether undue experimentation is required is not based on a single factor but is rather a conclusion reached by weighing many factors (See Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Inter, 1986) and In re Wands, 8USPQ2d 1400 (Fed. Cir. 1988); these factors include the following:
Nature of invention. The invention encompasses a method of treating a subject for an epidermal growth factor receptor variant III (EGFRvIII) positive glioblastoma, the method comprising: administering to the subject an immune cell genetically modified with:(a) a nucleic acid sequence encoding a binding triggered transcriptional switch (BTTS) that binds to EGFRvIII;(b) a nucleic acid sequence encoding an antigen-specific therapeutic that binds to a killing antigen expressed by the glioblastoma; and (c) a regulatory sequence operably linked to (b) that is responsive to the BTTS; wherein binding of the BTTS to EGFRvIII activates expression of the antigen-specific therapeutic which binds the killing antigen thereby inducing killing of glioblastoma cells expressing the killing antigen.
Scope of the invention. The invention encompasses a method of treating a subject for (EGFRvIII) positive glioblastoma.
Number of working examples and guidance. In the instant case, Applicant teaches one relevant working examples pertaining to the use of the killing antigen. In Example 1, the Applicant teaches that the IL13 Mutein-EphA2 CAR and the EphA2 CAR were only expressed when synNotch CAR T cells engaged with the priming antigen, EGFRvIII (Paragraph [0326]). The as-Filed Specification teaches the sequences of the EphA2 CAR (Paragraph [0345]), IL13Rα2 CAR (Paragraph [0346]), and EphA2/ IL13Rα2 CAR (Paragraph [0347]).
State of the art. Although the field of treating a subject with cancer is highly developed, the
method of treating a subject for an epidermal growth factor receptor variant III (EGFRvIII) positive glioblastoma by administering to the subject an immune cell genetically modified with:(a) a nucleic acid sequence encoding a binding triggered transcriptional switch (BTTS) that binds to EGFRvIII;(b) a nucleic acid sequence encoding an CAR or TCR that binds to a EphA2 or IL13Rα2 expressed by the glioblastoma is not highly developed. The art must therefore be considered to be poorly developed.
Unpredictability of the art. Before the effective filing date of the claimed invention, it was
known in the art that the simultaneous targeting of Eph receptors is used to treat glioblastomas, as evidenced by Ferluga et al. (Ferluga S. et al. Simultaneous targeting of Eph receptors in glioblastoma. Oncotarget. 2016 Sep 13;7(37):59860-59876. doi: 10.18632/oncotarget.10978. PMID: 27494882; PMCID: PMC5312354.) (Title). Ferluga et al. teaches the ephrinA5 (eA5) is a ligand that binds EphA3, EphA2 and EphB2 receptors, and used it to construct a novel targeted anti-glioblastoma cytotoxin, which targets different compartments of glioblastoma tumors and mitigates tumor heterogeneity (Abstract).
Additionally, it was known in the art that knockout of the EGFR/EGFRvIII, via CRISPR/Cas9 provides benefit for treatment in vitro and in vivo (as evidenced by Huang et al. (Huang K. et al. The CRISPR/Cas9 system targeting EGFR exon 17 abrogates NF-κB activation via epigenetic modulation of UBXN1 in EGFRwt/vIII glioma cells. Cancer Lett. 2017 Mar 1;388:269-280. doi: 10.1016/j.canlet.2016.12.011. Epub 2016 Dec 18. PMID: 27998759.) (Abstract).
These references teach the variability in the target genes that can be targeted for treatment of glioblastomas.
Amount of Experimentation Required. Given the unpredictability of the art, and the many
different target genes that can be targeted for the treatment of glioblastoma, the skilled artisan would have to conduct undue, and unpredictable experimentation to practice the claimed invention using the killing antigen to treat EGFRvIII positive glioblastoma.
Response to Arguments as they apply to rejection of claims 1 – 10 and 40 - 46 under 35 USC § 112 (a)
Applicant’s arguments filed July 29, 2026 have been fully considered but they are not persuasive. Applicant essentially asserts (a) there is no reason why other tumor antigens, which are known in the art, would not be successful in combination with the EGFRvIII priming antigen to treat glioblastoma (pg. 7, last paragraph).
Regarding (a), Applicant’s argument is not found persuasive. Earlier in the remarks, Applicant argues that Choe tested CAR T cells that express a BTS that binds to EGFRvIII and an antigen-specific therapeutic that binds to a tumor antigen showed complete and long term remission, and that Choe teaches that an anti-EGFRvIII CAR showed consistent tumor recurrence (pg. 6, last paragraph). However, Choe teaches the use of a tandem CAR that simultaneously targets the two killing antigens, EphA2 OR IL13Rα2 (pg. 4, first paragraph). Choe does not teach the use of any killing antigen (tumor antigen) for the treatment of the glioblastoma. Choe further notes that EGFRvIII is an ideal tumor specific antigen target, as it is found in a subset of patient, EGFRvIII expression in the tumors is highly heterogeneous, and EGFRvIII− tumor cells can escape and grow (pg. 3, first paragraph). Thus, not all tumor antigens expressed by the glioblastoma can be targeted for treatment.
Conclusion
Claims 1 – 10, and 40 - 46 remain rejected.
THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicants are 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 mailing date of this final action.
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/VYOMA SHUBHAM TIWARI/Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634
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