DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application is being examined under the pre-AIA first to invent provisions.
1. Claims 1-11 as filed on June 29, 2023 are pending and under consideration.
Priority
2. Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of the first paragraph of 35 U.S.C. 112. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, Application No. 60/611,797, fails to provide adequate support or enablement in the manner provided by the first paragraph of 35 U.S.C. 112 for one or more claims of this application. Examiner has established a priority date of 09/21/2005 for claims 1-11 because the claims as currently constituted recite vaccinating a patient against glioma which expresses EphA2 with a peptide comprising TLADFDPRV (SEQ ID NO: 6) and a review of the ‘797 application does not reveal the claimed limitations. Applicant is invited to submit evidence pointing to the serial number, page and line where support can be found establishing an earlier priority date.
Claim Rejections - 35 USC § 103
The following is a quotation of pre-AIA 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102 of this title, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negatived by the manner in which the invention was made.
This application currently names joint inventors. In considering patentability of the claims under pre-AIA 35 U.S.C. 103(a), the examiner presumes that the subject matter of the various claims was commonly owned at the time any inventions covered therein were made absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and invention dates of each claim that was not commonly owned at the time a later invention was made in order for the examiner to consider the applicability of pre-AIA 35 U.S.C. 103(c) and potential pre-AIA 35 U.S.C. 102(e), (f) or (g) prior art under pre-AIA 35 U.S.C. 103(a).
3. Claims 1-11 are rejected under pre-AIA 35 U.S.C. 103(a) as being obvious over US Patent App. Pub. No. 2007/0167375 (Okada, H., published 07/19/2007, effectively filed 09/21/2004, IDS), “Okada-375” in view of WO 03/091383 A2. (Kosmatopoulos et al. Nov. 06, 2003, IDS), “Kosmatopoulos” and in view of Debinski et al. (Neuro-Oncology 6, September 21, 2004 Abstract GE-02, pp. 308, 336-337, IDS), “Debinski”.
The applied reference has a common inventor with the instant application. Based upon the earlier effective U.S. filing date of the reference, it constitutes prior art under pre-AIA 35 U.S.C. 102(e). This rejection under pre-AIA 35 U.S.C. 103(a) might be overcome by: (1) a showing under 37 CFR 1.132 that any invention disclosed but not claimed in the reference was derived from the inventor of this application and is thus not an invention “by another”; (2) a showing of a date of invention for the claimed subject matter of the application which corresponds to subject matter disclosed but not claimed in the reference, prior to the effective U.S. filing date of the reference under 37 CFR 1.131(a); or (3) an oath or declaration under 37 CFR 1.131(c) stating that the application and reference are currently owned by the same party and that the inventor named in the application is the prior inventor under pre-AIA 35 U.S.C. 104 as in effect on March 15, 2013, together with a terminal disclaimer in accordance with 37 CFR 1.321(c). This rejection might also be overcome by showing that the reference is disqualified under pre-AIA 35 U.S.C. 103(c) as prior art in a rejection under pre-AIA 35 U.S.C. 103(a). See MPEP § 706.02(l)(1) and § 706.02(l)(2).
Okada-375 teaches administering WLPFGFILV (SEQ ID NO:2) or ELPFGFILV (SEQ ID NO:4) in a physiologically or acceptable carrier as a vaccine for glioma in humans under conditions sufficient of the patient to develop a CTL response. See ¶¶ [0008], [0020], [0024-0030], Examples 1-5 and claims 8, 10 and 17-22.
Okada-375 teaches that IL-13Ra2 is known to be expressed in the majority of human malignant gliomas but not in normal tissues. See ¶¶ 0005 and Examples 3-5.
Okada-375 teaches administering T-helper epitopes, including SEQ ID NO: 5, in combination with SEQ ID NO: 3. See ¶ [0025] and Example 5. Okada-375 teaches that glioma includes astrocytoma, oligodenroglioma, glioblastoma and mixed tumors comprising more than one glial cell type. See ¶ [0026].
It is noted that while Okada-375 teaches TLADFDPRV (SEQ ID NO: 6), see claims 23 and 24, SEQ ID NO: 6 does not have support in the priority document 60/611,797, the date on which the instant rejection is based. Thus, for the instant rejection SEQ ID NO: 6 is not taught by Okada-375.
The publication US 2006/0034856 A1 (Kosmatopoulos et al. Feb. 16, 2006, IDS), the US national stage filing under 35 USC 371 of the WO 03/091383 Kosmatopoulos application, is being used as the translation of WO 03/091383 and the citations refer to US 2006/0034856.
Kosmatopoulos teaches administrating an EphA2/883-891 peptide (p883, SEQ ID NO: 8, which is SEQ ID NO: 6) antitumor vaccine to a patient in a pharmaceutically acceptable carrier to elicit a cytotoxic T-cell immune response in combination with other EphA2 epitopes. See claims 1-13, ¶¶ [0032], [0040]-[0048], Examples 1 and 2 and Fig. 3. Kosmatopoulos teaches administering multi-epitope compositions, which would act as T-helper epitopes with the EphA2/883-891 peptide. See [0036] and [0037] and Examples 1-4. Kosmatopoulos teaches administrating an EphA2/883-891 peptide (p883) to a HLA-A*0201 patient, which is a human patient because HLA is a human leukocyte antigen. See claim 13.
Debinski teaches that EphA2 is widely overexpressed in human glioblastoma and EphA2 represents an attractive target for therapeutic applications for glioblastoma. See entire abstract.
It would have been prima facie obvious at the time the invention was made to combine the vaccine of SEQ ID NOs: 2 or 4 and SEQ ID NO: 5 taught by Okada-375 with SEQ ID NO: 8, TLADFDPRV, taught by Kosmatopoulos to vaccinate against gliomas because both Okada-375 and Kosmatopoulos teach using the peptides for antitumor vaccines against cancer or glioma and using the peptides in combination with other peptides for vaccination and treatment and Debinski teaches that EphA2 appears to be widely overexpressed in human glioblastoma and EphA2 represents an attractive target for therapeutic applications for glioblastoma. Thus, given that the art teaches that the peptides are used for the same purpose, i.e. vaccination to elicit a cytotoxic T-cell immune response against cancer or glioma and IL-13Ra2 and EphA2 are expressed in gliomas, one would have been motivated with a reasonable expectation of success of using the peptides in combination for vaccination against gliomas.
4. Claims 1-11 are rejected under pre-AIA 35 U.S.C. 103(a) as being obvious over WO 2006/034334 A2 (Storkus et al. published 07/19/2007, effectively filed 09/21/2004, IDS), “Storkus” in view of WO 03/091383 A2. (Kosmatopoulos et al. Nov. 06, 2003, IDS), “Kosmatopoulos” and in view of Debinski et al. (Neuro-Oncology 6, September 21, 2004 Abstract GE-02, pp. 308, 336-337, IDS), “Debinski”.
The applied reference has a common inventor with the instant application. Based upon the earlier effective U.S. filing date of the reference, it constitutes prior art under pre-AIA 35 U.S.C. 102(e). This rejection under pre-AIA 35 U.S.C. 103(a) might be overcome by: (1) a showing under 37 CFR 1.132 that any invention disclosed but not claimed in the reference was derived from the inventor of this application and is thus not an invention “by another”; (2) a showing of a date of invention for the claimed subject matter of the application which corresponds to subject matter disclosed but not claimed in the reference, prior to the effective U.S. filing date of the reference under 37 CFR 1.131(a); or (3) an oath or declaration under 37 CFR 1.131(c) stating that the application and reference are currently owned by the same party and that the inventor named in the application is the prior inventor under pre-AIA 35 U.S.C. 104 as in effect on March 15, 2013, together with a terminal disclaimer in accordance with 37 CFR 1.321(c). This rejection might also be overcome by showing that the reference is disqualified under pre-AIA 35 U.S.C. 103(c) as prior art in a rejection under pre-AIA 35 U.S.C. 103(a). See MPEP § 706.02(l)(1) and § 706.02(l)(2).
Storkus teaches administering WLPFGFILV (SEQ ID NO:2) or ELPFGFILV (SEQ ID NO:4) in a physiologically or acceptable carrier as a vaccine for glioma in humans under conditions sufficient of the patient to develop a CTL response. See ¶¶ [0008], [0020], [0024-0030], Examples 1-5 and claims 8, 10 and 17-22. Storkus teaches administering T-helper epitopes, including SEQ ID NO: 5, in combination with SEQ ID NO: 3. See ¶ [0025] and Example 5.
Storkus teaches that IL-13Ra2 is known to be expressed in the majority of human malignant gliomas but not in normal tissues. See ¶¶ 0005 and Examples 3-5.
Storkus teaches that glioma includes astrocytoma, oligodenroglioma, glioblastoma and mixed tumors comprising more than one glial cell type. See ¶ [0026].
It is noted that while Storkus teaches TLADFDPRV (SEQ ID NO: 6), see claims 23 and 24, SEQ ID NO: 6 does not have support in the priority document 60/611,797, the date on which the instant rejection is based. Thus, for the instant rejection SEQ ID NO: 6 is not taught by Storkus.
The publication US 2006/0034856 A1 (Kosmatopoulos et al. Feb. 16, 2006, IDS), the US national stage filing under 35 USC 371 of the WO 03/091383 application, is being used as the translation of WO 03/091383 and the citations refer to US 2006/0034856.
Kosmatopoulos teaches administrating an EphA2/883-891 peptide (p883, SEQ ID NO: 8, which is SEQ ID NO: 6) antitumor vaccine to a patient in a pharmaceutically acceptable carrier to elicit a cytotoxic T-cell immune response in combination with other EphA2 epitopes. See claims 1-13, [0040]-[0046], Examples 1 and 2 and Fig. 3. Kosmatopoulos teaches administering multi-epitope compositions, which would act as T-helper epitopes with the EphA2/883-891 peptide. See [0036] and [0037] and Examples 1-4. Kosmatopoulos teaches administrating an EphA2/883-891 peptide (p883) to a HLA-A*0201 patient, which is a human patient because HLA is a human leukocyte antigen. See claim 13.
Debinski teaches that EphA2 is widely overexpressed in human glioblastoma and EphA2 represents an attractive target for therapeutic applications for glioblastoma. See entire abstract.
It would have been prima facie obvious at the time the invention was made to combine the vaccine of SEQ ID NOs: 2 or 4 and SEQ ID NO: 5 taught by Storkus with SEQ ID NO: 8, TLADFDPRV, taught by Kosmatopoulos to vaccinate against gliomas because both Storkus and Kosmatopoulos teach using the peptides for antitumor vaccines against cancer or glioma and using the peptides in combination with other peptides for vaccination and treatment and Debinski teaches that EphA2 appears to be widely overexpressed in human glioblastoma and EphA2 represents an attractive target for therapeutic applications for glioblastoma. Thus, given that the art teaches that the peptides are used for the same purpose, i.e. vaccination to elicit a cytotoxic T-cell immune response against cancer or glioma and IL-13Ra2 and EphA2 are expressed in gliomas, one would have been motivated with a reasonable expectation of success of using the peptides in combination for vaccination against gliomas.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
5. Claims 1-11 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 10,874,730 B2 in view of Debinski et al. (Neuro-Oncology 6, September 21, 2004 Abstract GE-02, pp. 308, 336-337, IDS), “Debinski and Debinski et al. (Mol. Med 6, 440-449, 2000, IDS), “Debinki-2”.
The ‘730 claims teach:.
1. A method for treating glioblastoma in a subject in need thereof, wherein the subject has failed prior therapy with temozolomide, radiation therapy, and surgery, the method comprising administering to the subject (a) bevacizumab and (b) a pharmaceutical composition, wherein the pharmaceutical composition is cell-free and comprises 250 to 400 μg of an IL-13Rα2 peptide, 250 to 400 μg of an EphA2 peptide, 250 to 400 μg of a survivin peptide, and 250 to 400 μg of a WT1 peptide; wherein the IL-13Rα2 peptide comprises the amino acid sequence of any one of SEQ ID NOs:1-4, the EphA2 peptide comprises the amino acid sequence of SEQ ID NO:6, the survivin peptide comprises the amino acid sequence of SEQ ID NO:7, and the WT1 peptide comprises the amino acid sequence of SEQ ID NO:8.
2. The method of claim 1, wherein the pharmaceutical composition further comprises an adjuvant.
3. The method of claim 2, wherein the adjuvant is Montanide ISA-51.
4. The method of claim 1, further comprising administering to the subject a helper T cell epitope, wherein the helper T cell epitope is a PADRE peptide, a Tetanus toxoid peptide, or the HBV 128-140 core peptide.
5. The method of claim 1, further comprising administering to the subject an immune response modifier, wherein the immune response modifier is poly-ICLC or imiquimod.
6. The method of claim 1, wherein the pharmaceutical composition is administered to the subject subcutaneously or intranodally.
7. The method of claim 1, wherein the subject is human.
8. A method for treating glioblastoma in a subject in need thereof, wherein the subject has failed prior therapy with temozolomide, radiation therapy, and surgery, the method comprising administering to a subject (a) bevacizumab and (b) a pharmaceutical composition, wherein the pharmaceutical composition is cell-free and comprises 250 to 400 μg of an IL-13Rα2 peptide, 250 to 400 μg of an EphA2 peptide, and 250 to 400 μg of a survivin peptide, wherein the IL-13Rα2 peptide comprises the amino acid sequence of any one of SEQ ID NOs:1-4, the EphA2 peptide comprises the amino acid sequence of SEQ ID NO:6, and the survivin peptide comprises the amino acid sequence of SEQ ID NO:7.
9. The method of claim 8, wherein the pharmaceutical composition further comprises an adjuvant.
10. The method of claim 9, wherein the adjuvant is Montanide ISA-51.
11. The method of claim 8, further comprising administering to the subject a helper T cell epitope, wherein the helper T cell epitope is a PADRE peptide, a Tetanus toxoid peptide, or the HBV 128-140 core peptide.
12. The method of claim 8, further comprising administering to the subject an immune response modifier, wherein the immune response modifier is poly-ICLC or imiquimod.
13. The method of claim 8, wherein the pharmaceutical composition is administered to the subject subcutaneously or intranodally.
14. The method of claim 8, wherein the subject is human.
SEQ ID NO: 2 is WLPFGFILV and SEQ ID NO: 4 is ELPFGFILV. See Table 1, column 47.
SEQ ID NO: 6 is TLADFDPRV. See column 3, line 16.
The HBV 128-140 core peptide is TPPAYRPPNAPIL (SEQ ID NO: 5). See column 49-line 60.
The claims do not teach that the glioblastoma expresses IL-13Ra2 and EphA2.
Debinski teaches that EphA2 is widely overexpressed in human glioblastoma and EphA2 represents an attractive target for therapeutic applications for glioblastoma. See entire abstract.
Debinki-2 teaches IL-13Ra2 (IL-13Ra) is overexpressed in high grade gliomas (HGG)/glioblastoma cells. See abstract, Fig. 1, p. 455-Gene Expression IL13 Receptors in Cells, Fig. 6, and p. 441-Materials and Methods.
Debinki-2 teaches that since IL-13Ra2 (IL-13Ra) is a cancer restricted protein its expression in gliomas make it a target for treatment.
It would have been prima facie obvious at the time the invention was made to combine the IL-13Ra2 peptides of SEQ ID NOs: 2 or 4 with the EphA2 peptide SEQ ID NO: 6 and SEQ ID NO: 5 (HBV 128-140 core peptide) helper T cell epitope taught by the ‘730 claims to vaccinate against gliomas which express IL-13Ra2 and EphA2, because the claims teach using the peptides for glioblastoma treatment and using the peptides in combination with the other peptides treatment Debinski teaches that EphA2 appears to be widely overexpressed in human glioblastoma and EphA2 represents an attractive target for therapeutic applications for glioblastoma and Debinki-2 teaches that IL-13Ra2 glioma/glioblastoma expression make it a target for treatment. Thus, given that the art teaches that glioma/glioblastoma express IL-13Ra2 and EphA2 one would have been motivated with a reasonable expectation of success of using the peptides antigens from IL-13Ra2 and EphA2 in combination for vaccination against glioma/glioblastoma which express IL-13Ra2 and EphA2.
6. Claims 1-11 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 of U.S. Patent No. 10,434,155 (Okada et al. Oct. 8, 2019) in view of US Patent App. Pub. No. 2007/0167375 (Okada, H., published 07/19/2007, effectively filed 09/21/2004, IDS), “Okada-375” or WO 2006/034334 A2 (Storkus et al. published 07/19/2007, effectively filed 09/21/2004, IDS), “Storkus”.
The ’155 claims are drawn to:
1. A method of vaccinating a patient against glioma which expresses IL-13Rα2 and EphA2, the method comprising: (a) introducing into the patient (i) a peptide comprising TLADFDPRV (SEQ ID NO: 6) and (ii) a peptide comprising ALPFGFILV (SEQ ID NO: 3) under conditions sufficient for the patient to develop a cytotoxic T-cell lymphocyte (CTL) response against glioma cells in the patient which express IL-13Rα2 and EphA2; and administering chemotherapy or radiotherapy to the patient.
2. The method of claim 1, further comprising administering a T-helper epitope to the patient.
3. The method of claim 2, wherein the T-helper epitope is a peptide comprising the amino acid sequence TPPAYRPPNAPIL (SEQ ID NO: 5).
4. The method of claim 1, wherein the glioma is ependymoma, astrocytoma, oligodendroglioma, glioblastoma, or a mixed glioma.
5. The method of claim 1, wherein the patient is a mammal.
6. The method of claim 1, wherein the patient is human.
7. The method of claim 1, wherein the peptide of (i) consists of TLADFDPRV (SEQ ID NO: 6).
8. The method of claim 1, wherein the peptide of (ii) consists of ALPFGFILV (SEQ ID NO: 3).
9. The method of claim 7, wherein the peptide of (ii) consists of ALPFGFILV (SEQ ID NO: 3).
10. The method of claim 6, wherein the glioma is ependymoma, astrocytoma, oligodendroglioma, glioblastoma, or a mixed glioma.
11. The method of claim 7, wherein the glioma is ependymoma, astrocytoma, oligodendroglioma, glioblastoma, or a mixed glioma.
12. The method of claim 8, wherein the glioma is ependymoma, astrocytoma, oligodendroglioma, glioblastoma, or a mixed glioma
The ‘155 claims teach as set forth above, but do not teach vaccinating with SEQ ID NO: 2 or 4.
Okada-375 and Storkus teach set as forth above.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of the ‘155 claims and Okada-375 or Storkus and vaccinate with the IL-13Rα2 peptides WLPFGFILV (SEQ ID NO:2) or ELPFGFILV (SEQ ID NO:4) in place of the IL-13Rα2 peptide ALPFGFILV (SEQ ID NO: 3) of the ‘155 claims because Okada-375 or Storkus teaches administering the IL-13Rα2 peptides WLPFGFILV (SEQ ID NO:2) or ELPFGFILV (SEQ ID NO:4) in a physiologically or acceptable carrier as a vaccine for glioma in humans under conditions sufficient of the patient to develop a CTL response. Thus given that the IL-13Rα2 peptides WLPFGFILV (SEQ ID NO:2) or ELPFGFILV (SEQ ID NO:4) have the same function and are used for the same purpose as the IL-13Rα2 peptide ALPFGFILV (SEQ ID NO: 3) of the ‘155 claims, it would have been obvious to substitute the IL-13Rα2 peptides of Okada-375 or Storkus for the IL-13Rα2 peptide of the ‘155 claims.
7. Claims 1-11 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 8,859,488 (Okada et al. Oct. 14, 2014, IDS) in view of US Patent App. Pub. No. 2007/0167375 (Okada, H., published 07/19/2007, effectively filed 09/21/2004, IDS), “Okada-375” or WO 2006/034334 A2 (Storkus et al. published 07/19/2007, effectively filed 09/21/2004, IDS), “Storkus” and in view of Debinski et al. (Neuro-Oncology 6, September 21, 2004 Abstract GE-02, pp. 308, 336-337, IDS), “Debinski”.
The ’488 claims are drawn to:
1. A method of vaccinating a patient against glioma, comprising introducing into the patient (i) a peptide comprising TLADFDPRFV (SEQ ID NO:6) and (ii) a peptide comprising ALPFGFILV (SEQ ID NO:3)under conditions sufficient for said patient to develop a cytotoxic T-cell lymphocyte (CTL) response.
2. A method of vaccinating a patient against glioma, comprising introducing into the patient a composition comprising (i) a peptide comprising TLADFDPRV (SEQ ID NO:6), (ii) a peptide comprising ALPFGFILV (SEQ ID NO:3), and (iii) a physiologically acceptable carrier under conditions sufficient for said patient to develop a cytotoxic T-cell lymphocyte (CTL) response.
3. The method of claim 2 wherein said physiologically acceptable carrier is a pharmaceutically-acceptable carrier.
4. The use of claim 2, wherein said composition further comprises a T-helper epitope.
5. The method of claim 3, wherein said composition further comprises a T-helper epitope.
6. The use of claim 4, wherein the T-helper epitope is a peptide comprising the amino acid sequence TPPAYRPPNAPIL (SEQ ID NO:5).
7. The method of claim 5, wherein the T-helper epitope is a peptide comprising the amino acid sequence TPPAYRPPNAPIL (SEQ ID NO:5).
8. The method of claim 1 or 2, wherein the glioma is ependymoma, astrocytoma, oligodendroglioma, glioblastoma, or a mixed glioma.
9. The method of claim 1 or 2, wherein said patient is a mammal.
10. The method of claim 1 or 2, wherein said patient is human.
11. The method of claim 1, wherein the peptide of (i) consists of TLADFDPRV (SEQ ID NO:6).
12. The method of claim 2, wherein the peptide of (i) consists of TLADFDPRV (SEQ ID NO:6).
13. The method of claim 1, wherein the patient develops a CTL response against glioma cells in the patient.
14. The method of claim 2, wherein the patient develops a CTL response glioma cells in the patient.
The ‘488 claims teach as set forth above, but do not teach vaccinating with SEQ ID NO: 2 or 4 against a glioma which express IL-13Rα2 and EphA2.
Okada-375 , Storkus and Debinski teach set forth above.
It would have been prima facie obvious at the time the invention was filed given that the level of skill in the art was high to combine the teachings of the ‘488 claims, Okada-375 or Storkus, and Debinski and vaccinate gliomas, which express IL-13Ra2 and EphA2 as taught by Okada-375 and Debinski, with the IL-13Rα2 peptides WLPFGFILV (SEQ ID NO:2) or ELPFGFILV (SEQ ID NO:4) in place of the IL-13Rα2 peptide ALPFGFILV (SEQ ID NO: 3) of the ‘488 claims because Okada-375 or Storkus teaches administering the IL-13Rα2 peptides WLPFGFILV (SEQ ID NO:2) or ELPFGFILV (SEQ ID NO:4) in a physiologically or acceptable carrier as a vaccine for glioma in humans under conditions sufficient of the patient to develop a CTL response. Thus given that the IL-13Rα2 peptides WLPFGFILV (SEQ ID NO:2) or ELPFGFILV (SEQ ID NO:4) have the same function and are used for the same purpose as the IL-13Rα2 peptide ALPFGFILV (SEQ ID NO: 3) of the ‘488 claims, it would have been obvious to substitute the IL-13Rα2 peptides of Okada-375 or Storkus for the IL-13Rα2 peptide of the ‘488 claims to vaccinate gliomas which express IL-13Ra2 and EphA2.
Conclusion
8. No claims allowed.
9. Any inquiry concerning this communication or earlier communications from the examiner should be directed to PETER J REDDIG whose telephone number is (571)272-9031. The examiner can normally be reached M-F 8:30-5:30 Eastern Time.
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/PETER J REDDIG/ Primary Examiner, Art Unit 1646