DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
2. A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on August 18, 2025 has been entered.
Claim Amendments
3. The Amendment filed August 18, 2025 was entered. Claims 1-32 were previously cancelled. Claim 33 was amended. Claims 34-39 were cancelled. Claims 33 and 40-44 are under consideration in this office action.
Maintained Grounds of Rejection
Claim Rejections - 35 USC § 103
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 (i.e., changing from AIA to pre-AIA ) 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.
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.
4. Claims 33 and 42-44 are rejected under 35 U.S.C. 103 as being unpatentable over Campana et al., (US PG PUB 20150139943 published May 15, 2015; priority to Oct. 17, 2013) in view of Olson et al., (WO2014093406 published June 2014; priority to Dec 2013).
The claims are drawn to a method for treating a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, wherein the chimeric antigen receptor comprises: a chlorotoxin comprising SEQ ID NO:1; a spacer domain comprising any of SEQ ID NOs:2-12; a transmembrane domain selected from: a CD4 transmembrane domain comprising SEQ ID NO:16, a CD8 transmembrane domain comprising SEQ ID NOs: 17, 18 or 19, and a CD28 transmembrane domain comprising SEQ ID NO:14 or 15; a co-stimulatory domain selected from a CD28 co-stimulatory domain comprising SEQ ID NO: 22 or 23 and a 41-BB co-stimulatory domain comprising SEQ ID NO:24; and a CD3z (zeta) signaling domain comprising SEQ ID NO: 21.
Campana et al., teach chimeric receptors comprising an extracellular domain with affinity and specific for the Fc portion of an immunoglobulin molecule (Ig) (e.g., an extracellular ligand-binding domain of F158 FCGR3A or V158 FCGR3A variant); a transmembrane domain (e.g., a transmembrane domain of CD8α); at least one co-stimulatory signaling domain (e.g., a co-stimulatory signaling domain of 4-1BB); and a cytoplasmic signaling domain comprising an immunoreceptor tyrosine-based activation motif (ITAM) (e.g., a cytoplasmic signaling domain of CD3ζ) [abstract]. Such immune cells can be used to enhance antibody-dependent cell-mediated cytotoxicity and/or to enhance antibody-based immunotherapy, such as cancer immunotherapy [abstract]. The methods are for enhancing antibody-dependent cell-mediated cytotoxicity (ADCC) in a subject. The method comprises administering to a subject in need of the treatment (e.g., a human cancer patient) an effective amount of host cells that express any of the chimeric receptors provided herein. The host cells are immune cells such as T cells [para 21].
Campana et al., teach a spacer domain comprising instant SEQ ID NOs:8, whereby Campana teach CD8-alpha protein hinge region/transmembrane domain consisting of amino acid sequence SEQ ID NO:58. Campana et al., teach a transmembrane domain selected from: a CD4 transmembrane domain comprising SEQ ID NO:16 whereby Campana et al., teach a CD4 Transmembrane domain as SEQ ID NO:14. Campana et al., teach a CD8 transmembrane domain comprising instantly claimed SEQ ID NO:19 within Campana et al’s CD8-alpha protein hinge region/transmembrane domain consisting of amino acid sequence SEQ ID NO:58.
Campana et al., teach a co-stimulatory domain selected from a CD28 co-stimulatory domain comprising instantly claimed SEQ ID NO: 23 at Campana et al’s SEQ ID NO;12 within Example 2. Campana et al., teach instantly claimed 41-BB co-stimulatory domain comprising SEQ ID NO:24; by disclosing 4-1BB (CD137) protein co-stimulatory/signaling domain, SEQ ID 59 [see also claim 8].Campana et al., teach the instantly claimed CD3z (zeta) signaling domain comprising SEQ ID NO: 21 by describing cytoplasmic signaling domain of CD3ζ consists of the amino acid sequence of SEQ ID NO: 60 [See claim 9]. Therefore, Campana et al., teach instant claim 33.
The subject may be a human patient suffering from a cancer and the therapeutic antibody is for treating the cancer. In some examples, the cancer is a head and neck cancer, glioma or glioblastoma [para 25]. It is noted that glioblastomas are the most aggressive and most common type of malignant glioma. The terms “treat”, “treatment”, and the like mean to relieve or alleviate at least one symptom associated with such condition, or to slow or reverse the progression of such condition. Within the meaning of the present disclosure, the term “treat” also denotes to arrest, delay the onset (i.e., the period prior to clinical manifestation of a disease) and/or reduce the risk of developing or worsening a disease. For example, in connection with cancer the term “treat” may mean eliminate or reduce a patient's tumor burden, or prevent, delay or inhibit metastasis, etc [para 55]. Thus teaching claims 42-44.
Campana et al., teach a method for treating a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, wherein the chimeric antigen receptor comprises: a spacer domain comprising any of SEQ ID NO: 8, a transmembrane domain selected from: a CD4 transmembrane domain comprising SEQ ID NO:16, a CD8 transmembrane domain comprising SEQ ID NO:19; a co-stimulatory domain selected from a CD28 co-stimulatory domain comprising SEQ ID NO: 23 and a 41-BB co-stimulatory domain comprising SEQ ID NO:24; and CD3z (zeta) signaling domain comprising SEQ ID NO: 21; but does not teach the inclusion of chlorotoxin.
Olson et al., teach methods are provided for treating a disease associated with cells expressing a chlorotoxin target, the method comprising: administering, to a subject in need thereof, a therapeutically effective amount of a pharmaceutical composition comprising a peptide according to the present disclosure or a composition comprising a peptide of the present disclosure, thereby treating the disease [para 13].
The disease comprises cancerous tissue associated with glioma [para 63]. Olson et al., teach treating gliomas and malignant gliomas such as astrocytomas ependymomas and other brain tumors [para 126]. Thus teaching claims 33 and 42-44. The peptides having D-amino acids and being based on a chlorotoxin scaffold, e.g., D-amino acid chlorotoxin and/or D-amino acid chlorotoxin variants. The peptides based on chlorotoxin can include varying amounts of D-amino acids [para 84]. The methods include administering a D-amino acid chlorotoxin and/or D-amino acid chlorotoxin variant described herein to a subject with a tumor such that the peptide selectively targets tumor tissue over normal tissue [para 127]. Olson et al., the targeting capability (e.g., tumor). Some selected properties include stability/oral bioavailability, 2) controllable/programmable pharmacokinetics, 3) ability to disrupt protein/protein interactions, 4) ability to cross the blood- brain barrier, 5) ability to penetrate cells, ability to penetrate specific organelles and/or cellular compartments, 6) potential for selectable tissue/organ targeting, 7) ability to be conjugated specifically to drugs, 8) "programmable diversity" 9) readily engineered and 10) potential for programmable intracellular targeting [para 53]. Olson et al., teach an IgK signal peptide (signaling domain) with linkers (spacers) and chlorotoxin fusion protein.
Campana et al., teach instantly recited SEQ ID NOs: 8, 16, 19, 21, 23 and 24 with 100% sequence identity. Olson et al., instantly claimed SEQ ID NO:1 with 100% sequence identity. Please see the office action mailed May 16, 2025 for the full sequence alignments.
Therefore, it would have been prima facie obvious to combine Campana et al’s treatment of a glioblastoma, a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, wherein the chimeric antigen receptor comprises: a spacer domain, a transmembrane domain selected from: a CD4 transmembrane domain, a CD8 transmembrane domain, a CD28 transmembrane domain, and a CD3 z transmembrane domain; a costimulatory domain; and CD3 z (zeta) signaling domain; and incorporate the chlorotoxin as taught by Olson et al., in order to treat malignant gliomas such as glioblastomas, astrocytomas and ependymomas. Taken all together, it would have been obvious to one of ordinary skill in this art before the filing of the instant application that the CAR of Campana et al., which treat glioma and malignant glioma cells, while also Olson’s chlorotoxin specifically treat malignant gliomas; thus teaching the same purpose. Such would provide the advantage of additivity or synergism between the CAR of Campana and Olson’s chlorotoxin. This is an inclusion CAR and chlorotoxin against glioblastoma to yield a predictably functional therapy with a very high expectation of success owed to the successes of Campana et al., and Olson et al., as discussed above.
Response to Arguments
5. Applicant’s arguments, filed August 18, 2025, with respect to the rejection of
claims 33 and 42-44 under Campana et al., in view of Olson et al., is maintained.
Applicants argue that no combination of Campana and Olson provide a reasonable expectation of success in practicing the claimed method because Campana does not teach or suggest that their CAR T cells target and kill cancer cells without the aid of an antibody- based immunotherapy. Figure 7, which Applicants pointed out teach The observation that CD16V-BB-ζ cross-linking provoked exocytosis of lytic granules implied that CD16V-BB-ζ T lymphocytes should be capable of killing target cells in the presence of specific antibodies. In the 4-hour in vitro cytotoxicity assays, CD16V-BB-ζ T lymphocytes were highly cytotoxic against the B-cell lymphoma cell lines. Applicants assert that Campana et al., requires the presence of an antibody. Campana et al., designed chimeric receptors comprising an extracellular domain with affinity and specificity for the Fc portion of an IgG antibody, a transmembrane domain, at least one co-stimulatory signaling domain, and a cytoplasmic signaling domain that comprises an immunoreceptor tyrosine-based activation motif (ITAM). Immune cells expressing such a chimeric receptor construct would enhance efficacy of immune therapy enhancing Antibody dependent cell-mediated cytotoxicity (ADCC) activity.
Contrary to Applicants arguments, Campana et al., teach a method for treating a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, wherein the chimeric antigen receptor comprises: a spacer domain comprising any of SEQ ID NO: 8, a transmembrane domain selected from: a CD4 transmembrane domain comprising SEQ ID NO:16, a CD8 transmembrane domain comprising SEQ ID NO:19; a co-stimulatory domain selected from a CD28 co-stimulatory domain comprising SEQ ID NO: 23 and a 41-BB co-stimulatory domain comprising SEQ ID NO:24; and CD3z (zeta) signaling domain comprising SEQ ID NO: 21. The claims do not exclude any components taught by Campana et al. Therefore, taken all together, it would have been obvious to one of ordinary skill in this art before the filing of the instant application that the CAR of Campana et al., which treat glioma and malignant glioma cells, while also Olson’s chlorotoxin specifically target and treat malignant gliomas; thus teaching the same purpose.
Applicants argue that the CAR of Campana does not target the cancer cells, it is the antibody of Campana that targets the cancer cell, and this antibody-based combination immunotherapy is very different from the presently claimed methods, which features CAR T cells that directly target the cancer cell surface to kill the cancer cells. In response, Campana et al., teach targeting by the antibody or such other anti-tumor molecule comprising the Fc portion. Therefore Campana et al’s teaching is not limited to the full length antibody. Moreover, the instantly rejected claims do not exclude an antibody. Campana et al., in view of Olson et al., teach a method for treating a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, wherein the chimeric antigen receptor comprises: a spacer domain comprising any of SEQ ID NO: 8, a transmembrane domain selected from: a CD4 transmembrane domain comprising SEQ ID NO:16, a CD8 transmembrane domain comprising SEQ ID NO:19; a co-stimulatory domain selected from a CD28 co-stimulatory domain comprising SEQ ID NO: 23 and a 41-BB co-stimulatory domain comprising SEQ ID NO:24; and CD3z (zeta) signaling domain comprising SEQ ID NO: 21; and the inclusion of chlorotoxin.
Applicants argue that Campana in view of Olson do not directly target the cancer cells. In response to applicant's argument that the references fail to show certain features of the invention, it is noted that the features upon which applicant relies i.e., direct targeting of the cancer cells are not recited in the rejected claims. Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993).
The claims are drawn to a method for treating a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, wherein the chimeric antigen receptor comprises: a chlorotoxin comprising SEQ ID NO:1; a spacer domain comprising any of SEQ ID NOs:2-12; a transmembrane domain selected from: a CD4 transmembrane domain comprising SEQ ID NO:16, a CD8 transmembrane domain comprising SEQ ID NOs: 17, 18 or 19, and a CD28 transmembrane domain comprising SEQ ID NO:14 or 15; a co-stimulatory domain selected from a CD28 co-stimulatory domain comprising SEQ ID NO: 22 or 23 and a 41-BB co-stimulatory domain comprising SEQ ID NO:24; and a CD3z (zeta) signaling domain comprising SEQ ID NO: 21. Campana et al., clearly teach a method for treating a glioblastoma, a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, comprising a spacer domain; a transmembrane domain selected from: a CD4 transmembrane domain, a CD8 transmembrane domain, and a CD28 transmembrane domain; a co-stimulatory domain selected from a CD28 co-stimulatory domain; a 41-BB co-stimulatory domain; and a CD3z (zeta) signaling domain with the exact same sequences. Olson teach the chlorotoxin with the exact same sequence. The instant claims do not recite any specific targeting mechanism. Therefore, Applicants arguments regarding the targeting mechanism are not persuasive.
Again, Applicants point to Campana et al., use of Rituximab and other antibodies. Campana et al., teach examples of therapeutic Fc-containing therapeutic proteins [para 133]. Campana et al., an effective amount refers to the amount of the respective agent (e.g., the host cells expressing chimeric receptors, Fc-containing therapeutic agents, or compositions thereof) that upon administration confers a therapeutic effect on the subject. Determination of whether an amount of the compositions achieved the therapeutic effect would be evident to one of skill in the art [para 134]. Again, the instantly claimed method does not exclude an antibody, Fc-fusion protein, Fc -portion of an antibody or other FC-containing molecules or fragments. The chimeric receptor refers to a non-naturally occurring molecule that can be expressed on the surface of a host cell (T cell) and comprises an extracellular domain capable of binding to a target molecule containing an Fc portion and one or more cytoplasmic signaling domains for triggering effector functions of the immune cell expressing the chimeric receptor [para 52]. Campana et al., teach therapeutic antibodies such as trastuzumab, infliximab, and adalimumab. Olson et al., teach fusions with trastuzumab, infliximab, adalimumab, which are the same antibodies taught by Campana et al. Therefore, the combination of Campana et al., in view of Olson et al., would clearly function, when both references teach their composition targeting and treating malignant glioma cells. Therefore Applicants arguments regarding the antibodies are not persuasive because the claims do not exclude antibodies.
Applicants urge that nothing in Campana shows that administering a CAR T cell immune therapy can directly target and kill cancer cells. Therefore, Applicants are reminded that the instant claims do not require direct killing of cancer cells. The instant claims recite a method for treating a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor. At best the claims are required to treat a malignant glioma. Campana et al., teach administration and treatment of a glioblastoma; while Olson et al., teach administration and treatment of astrocytomas and ependymomas. Campana et al., and Olson et al., similarly define treatment to include eliminate or reduce a patient's tumor burden, or prevent, delay or inhibit metastasis and/or treatment improves or a treatment may delay worsening of a progressive disease in an individual, or prevent onset of additional associated diseases. Therefore, the instantly rejected claims recite treatment and the prior art references teach treatment. Therefore this argument is not persuasive.
Applicants argue that Olson does not show that chlorotoxin, let alone a CAR construct comprising a chlorotoxin, directly targets and kills any cancel cells or a glioma. In response, the Office points to the instant claims which do not direct targeting and killing of any malignant glioma cells. First, Applicant is reminded that reduction to practice is not required. Additionally, MPEP section 2123 teaches that patents are relevant as prior art for all they contain, “The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain.” In re Heck, 699 F.2d 1331, 1332-33, 216 USPQ 1038, 1039 (Fed. Cir. 1983) (quoting In re Lemelson, 397 F.2d 1006, 1009, 158 USPQ 275, 277 (CCPA 1968)). A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill the art, including nonpreferred embodiments. Merck & Co. v. Biocraft Laboratories, 874 F.2d 804, 10 USPQ2d 1843 (Fed. Cir.), cert. denied, 493 U.S. 975 (1989).
In this case, Olson et al., teach methods are provided for treating astrocytomas and/or ependymomas with cells expressing a chlorotoxin target. Olson et al., teach a method comprising administering an effective dose of a composition including fusion proteins, peptides, or conjugates thereof to a subject with cancerous tissue (e.g., a tumor) such that the peptide selectively targets cancerous tissue (e.g., tumor tissue) over normal tissue [par 108]. Campana et al., teach treatment of a glioblastoma, a malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, wherein the chimeric antigen receptor comprises: a spacer domain, a transmembrane domain selected from: a CD4 transmembrane domain, a CD8 transmembrane domain, a CD28 transmembrane domain, and a CD3 z transmembrane domain; a costimulatory domain; and CD3 z (zeta) signaling domain; and incorporating the chlorotoxin as taught by Olson et al., in order to improve bioavailability and target malignant cancers like malignant gliomas. Thus, the argument is not persuasive.
Applicants assert that neither Campana nor Olson demonstrated that a CAR or a CAR comprising a chlorotoxin could successfully target and treat a malignant glioma. The Office directs Applicants attention to MPEP 2138.05 which states
“…The filing of a patent application serves as conception and
constructive reduction to practice of the subject matter described
in the application. Thus, the inventor need not provide evidence of
either conception or actual reduction to practice when relying on the
content of the patent application. Hyatt v. Boone, 146 F.3d 1348, 1352,
47 USPQ2d 1128, 1130 (Fed. Cir. 1998). A reduction to practice can be
done by another on behalf of the inventor. De Solms v. Schoenwald,
15 USPQ2d 1507, 1510 (Bd. Pat. App. & Inter. 1990). "
Therefore scientific experiments as a form of reduction to practice are not required. Furthermore, MPEP 2123 teaches that patents are relevant as prior art for all they contain. A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill the art, including nonpreferred embodiments. In this case, Campana et al., in view of Olson et al., is relevant because the references teach a method for treating malignant glioma comprising administering a therapeutically effective dose of T cells expressing a chimeric antigen receptor, wherein the chimeric antigen receptor comprises: a chlorotoxin comprising SEQ ID NO:1; a spacer domain comprising any of SEQ ID NO:8; a transmembrane domain selected from: a CD4 transmembrane domain comprising SEQ ID NO:16, a CD8 transmembrane domain comprising SEQ ID NO:19, and a CD28 transmembrane domain comprising SEQ ID NO:14 or 15; a co-stimulatory domain selected from a CD28 co-stimulatory domain comprising SEQ ID NO:23 and a 41-BB co-stimulatory domain comprising SEQ ID NO:24; and a CD3z (zeta) signaling domain comprising SEQ ID NO: 21. The teaching teach each and every claimed limitation.
via a chlorotoxin-drug conjugate to, e.g., tumors in the brain of a subject.
In response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). Applicants attention is directed to MPEP 2144.06. In this case, "It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (citations omitted) (Claims to a process of preparing a spray-dried detergent by mixing together two conventional spray-dried detergents were held to be prima facie obvious.). See also In re Crockett, 279 F.2d 274, 126 USPQ 186 (CCPA 1960) (Claims directed to a method and material for treating cast iron using a mixture comprising calcium carbide and magnesium oxide were held unpatentable over prior art disclosures that the aforementioned components individually promote the formation of a nodular structure in cast iron.); Ex parte Quadranti, 25 USPQ2d 1071 (Bd. Pat. App. & Inter. 1992) (mixture of two known herbicides held prima facie obvious); and In re Couvaras, 70 F.4th 1374, 1378-79, 2023 USPQ2d 697 (Fed. Cir. 2023) (That the two claimed types of active agents, GABA-a agonists and ARBs, were known to be useful for the same purpose—alleviating hypertension—alone can serve as a motivation to combine). Taken all together, it would have been obvious to one of ordinary skill in this art before the filing of the instant application that the CAR of Campana et al., which treat glioma and malignant glioma cells, while also Olson’s chlorotoxin specifically treat malignant gliomas; thus teaching the same purpose. Such would provide the advantage of additivity or synergism between the CAR of Campana and Olson’s chlorotoxin. This is an inclusion CAR and chlorotoxin against glioblastoma to yield a predictably functional therapy with a very high expectation of success owed to the successes of Campana et al., and Olson et al., as discussed above. Therefore the rejection is maintained.
Claim Objections
6. Claims 40-41 are objected to because of the following informalities: Claims 40-41 depend upon rejected claim 33. Appropriate correction is required.
Pertinent Art
7. The prior art made of record and not relied upon is considered pertinent to applicant’s disclosure. Caligiuri et al., (WO 2016164370 published Oct. 13, 2016; priority to April 6, 2015).
Forman et al., (WO2015105522 published July 16, 2015; priority to March 14, 2014) teach 100% sequence identity to at least instantly claimed SEQ ID NO:2 (IgG4 Fc region CH2 domain mutant, SEQ ID:20); 3 (IgG4 Fc region CH2 domain mutant, SEQ ID:20); 4 (IgG4 Fc region mutant (N79Q), SEQ ID:17); 5(IgG4 Fc region CH2 domain mutant, SEQ ID:20); 10, 11 (IgG4 Fc region mutant (S10P/L17E/N79Q), SEQ ID:19) and 12 (IgG4 Fc region CH2 domain mutant, SEQ ID:20).
Alvarez et al., (US Pat Pub 20110311445 published May 2011; priority to June 2003). Cooper et al., (WO2015123642) teach chimeric antigen receptors (CAR) to treat gliomas. Hallahan et al., (WO2015031645) teach antibody specifically binds 14-3-3 epsilon and comprises a heavy chain CDR3 to treat brainstem gliomas, brain tumors (cerebellar astrocytoma, cerebral astrocytoma/malignant glioma, ependymoma, medulloblastoma, supratentorial primitive neuroectodermal tumors, visual pathway and hypothalamic gliomas).
Conclusion
8. No claims allowed. However SEQ ID NOs:26-40 are free of the prior art.
9. Any inquiry concerning this communication or earlier communications from the examiner should be directed to JA-NA A HINES whose telephone number is (571)272-0859. The examiner can normally be reached Monday thru Thursday.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor Vanessa Ford, can be reached on 571-272-0857. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/JANA A HINES/Primary Examiner, Art Unit 1645