CTNF 18/263,394 CTNF 81760 DETAILED ACTION Notice of Pre-AIA or AIA Status 07-03-aia AIA 15-10-aia The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA. This office action is in response to applicant’s communication of 7/28/2023. Currently claims 1-7, 11-12, 15-22, 24, 27, 29-31, 34-35, 37, 40, 42-48. Claim Rejections - 35 USC § 102 07-06 AIA 15-10-15 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. 07-07-aia AIA 07-07 The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action: A person shall be entitled to a patent unless – 07-12-aia AIA (a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention. 07-15-03-aia AIA Claim(s) 1-7, 11-12, 15-22, 24, 27, 29-31, 34-35, 37, 40, 42-48 is/are rejected under 35 U.S.C. 102(a)(2) as being anticipated by US 2019/282696 A1 (Biel et al.) . Concerning claim 1 Biel discloses a method for treating cancer in a subject, comprising:(a) administering to the subject a therapeutically effective amount of (i) one or more antibody-IR700 molecules (see para [0037]) wherein the antibody specifically binds to a tumor-specific protein on the surface of a cancer cell, wherein the tumor- specific protein comprises epidermal growth factor receptor (EGFR/HTER1), mesothelin, prostate specific membrane antigen (PSMA), HER2/ERBB2, CD3, CD 18, CD20, CD25 (IL-2Ra receptor), CD30, CD33, CD44, CD52, CD133, CD206, carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP), Lewis Y, tumor-associated glycoprotein 72 (TAG72), vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR), epithelial cell adhesion molecule (EpCAM), ephrin type-A receptor 2 (EphA2), glypican- 1, glypican-2, glypican-3, gpA33, a mucin, CAIX, a folate-binding protein, a ganglioside, integrin caVp3, integrin oa51, Erb-B2 Receptor Tyrosine Kinase 3 (ERBB3), MET Proto-Oncogene, Receptor Tyrosine Kinase (MET), insulin like growth factor 1 receptor (IGF1R), ephrin type-A receptor 3 (EPHA3), tumor necrosis factor-related apoptosis- inducing ligand receptor 1 (TRAILR1), TRAILR2, receptor activator of nuclear factor kappa-B ligand (RANKL), fibroblast activation protein (FAP), tenascin, BCR complex, gp72, HLA-DRHLA-DR antigen, IgE, CA 242, polymorphic epithelial mucin (PEM) antigen, SK-1 antigen, programmed death 1 (PD-i), (see para [0033]) or programmed death ligand 2 (PD-L2); and/or (ii) one or more immunoactivators(b) administering to the subject a therapeutically effective amount of one or more cytotoxic T-lymphocyte-associated protein 4 (CTLA4) antibody-IR700 molecules, one or more programmed death ligand 1 (PD-Li) antibody-IR700 molecules, or combinations thereof; and (c) subsequently irradiating the subject and/or irradiating cancer cells in the subject at a wavelength of 660 to 740 nm (see para [0005],[0014]) and at a dose of at least 1wherein the one or more antibody-I1R700 molecules, the one or more immunoactivators, the one or more CTLA4 antibody-IR700 molecules, and/or the one or more PD-Li antibody- I1R700 molecules, are administered sequentially or concurrently, thereby treating the cancer in the subject (see para [0044]). Examiner is of the position that the prior art does disclose the administration of the given Antibody-IR700 as this is also listed as an “and/or” and the use of this as an or would satisfy the claims. Concerning claim 2 and intravenous administration (see para [0007). Concerning claim 3 and a method for treating cancer in a subject, comprising:administering to the subject a therapeutically effective amount of one or more antibody- IR700 molecules(see para [0037]), wherein the antibody specifically binds to a tumor-specific protein on the surface of a cancer cell or to an immune cell-specific protein on the surface of an immune cell (see para [0033]); administering to the subject a therapeutically effective amount of one or more reducing agents (see para [0069] and immune modulating agent); and irradiating the subject and/or irradiating cancer cells in the subject at a wavelength of 660 to 740 nm and at a dose of at least 1 J/cm2(see para [0005-0014]);wherein the one or more antibody-IR700 molecules and the one or more reducing agents are administered sequentially or concurrently. Concerning claim 4 and the one or more antibody-IR700 molecules is administered intravenously and the one or more reducing agents is administered intraperitoneally (see para 0332-0333]). Concerning claim 5 and the irradiating is performed after both administering steps (see para [0005-0014]). Concerning claim 6 and the one or more reducing agents are administered prior to irradiating the subject and/or irradiating cancer cells in the subject (see para [0069] and “immune modulating agent” disclosure). Concerning claim 7 and the tumor- specific protein comprises HER1/EGFR, mesothelin, PSMA, HER2/ERBB2, CD3, CD18, CD20, CD25 (IL-2Ra receptor), CD30, CD33, CD44, CD52, CD133, CD206, CEA, AFP, Lewis Y, TAG7), VEGF, VEGFR, EpCAM, EphA2, glypican-1, glypican-2, glypican-3, gpA33, a mucin, CAIX, a folate-binding protein, a ganglioside, integrinERBB3, MET, IGF1R, EPHA3, TRAILR1, TRAILR2, RANKL, FAP, tenascin, BCR complex, gp72, HLA-DR 10(3, HLA-DRantigen, IgE, CA 242, PEM antigen, SK-1 antigen, PD-1, or PD-L2, and the immune cell specific protein comprises CTLA4 or PD-L1. (see para [0033]) Concerning claim 11 and the cancer or cancer cell is a cancer or cancer cell of the breast, liver, colon, ovary, prostate, pancreas, brain, cervix, kidney, bone, skin, head and neck, oropharynx or blood (see para [0095]). Concerning claim 12 and the CTLA4 antibody comprises ipilimumab or tremelimumab; and/or the anti-PD-L1 antibody is atezolizumab, avelumab, durvalumab, cosibelimab, KN035 (envafolimab), BMS-936559, BMS935559, MEDI-4736, MPDL-3280A, or MEDI-4737 (see paras [0036-0037]). Concerning claim 15 and wherein the subject and/or the cancer cells are irradiated at a wavelength of 680 nm or 690 nm at a dose of 10 to 60 J/cm2 (see para [0005-0014]). Concerning claim 16 and the cancer cells are in a subject's blood, and wherein irradiating the cancer cells comprises irradiating the blood by using a device worn by the subject, wherein the device comprises a near infrared (NIR) light emitting diode (LED) (see para [0108]). Concerning claim 17 and the method further comprises: selecting a subject with a cancer that expresses the tumor-specific protein that specifically binds to the antibody-IR700 molecule (see para [0037]). Concerning claim 18 and the method reduces the weight, volume or size of the cancer by at least 25% relative to the absence of treatment;reduces the weight, volume or size of a metastasis by at least 25% relative to the absence of treatment, wherein the metastasis is not irradiated at a wavelength of 660 to 740 nm and is located distant from the irradiated area of the tumor or lesion; increases survival time of the subject relative to the absence of treatment; increases progression-free survival time of the subject relative to the absence of treatment; increases disease-free survival time of the subject relative to the absence of treatment; or combinations thereof. (see para [0415]). Concerning claim 19 and the method selectively kills CD4+Foxp3+ Tregs;selectively depletes CTLA4+ cells from total live cell and T cell populations within the cancer but not within regional lymph nodes or the spleen; increases the CD8+/CD4+Foxp3+ ratio; increases the CD8+/Treg ratio; increases the CD4+Foxp3- cell:CD4+Foxp3+ cell ratio; decreases intra-tumoral blood perfusion; or combinations thereof. (see para [0061]). Concerning claim 20 and the method reduces edema and/or acute inflammatory reaction in the treated subject by at least 20% as compared to an amount of edema and/or acute inflammatory reaction in the absence of the one or more reducing agents. (see para [0364] and it is examiners position that the reaction would be at least 20% see figures 19A for example of efficacy). Concerning claim 21 and the cancer is a cancer in the airway or mediastinum (see para [0095]). Concerning claim 22 and the one or more reducing agents comprise L-sodium ascorbate, ascorbic acid, L-cysteine, glutathione or combinations thereof (See para 0263] and glutathione). Concerning claim 24 and administering to the subject a therapeutically effective amount of one or more CTLA4 antibody-IR700 molecules, one or more PD-L1 antibody-IR700 molecules, or combinations thereof (see para [0034]). Concerning claim 27 and the subject is administered two or more doses of the one or more one or more antibody-IR700 molecules that specifically bind to the tumor-specific protein on the surface of the cancer cell (see para [0337]). Concerning claim 19 and detecting the cancer cell with fluorescence lifetime imaging about 0 to 48 hours after the irradiating step (see para [0108]). Concerning claim 30 and the subject is administered two or more doses of the one or more CTLA4 antibody- IR700 molecules, and/or the one or more PD-L1 antibody-IR700 molecules (see para [0337]). Concerning claim 31 and administering to the subject a therapeutically effective amount of one or more immunoactivators (see para [0333]). Concerning claim 34 and a method for treating an EGFR-expressing cancer in a subject, comprising:administering to the subject a therapeutically effective amount of one or more anti- EGFR-IR700 molecules (see para [0037]); administering to the subject a therapeutically effective amount of one or more anti- CTLA4-IR700 molecules; and subsequently irradiating the subject and/or irradiating and EGFR-expressing cancer cells in the subject at a wavelength of 670 to 700 nm (see para [0005],[0014]); and at a dose of 4 to 100 J/cm2;wherein the one or more anti-EGFR-IR700 molecules and the one or more anti-CTLA4- IR700 molecules are administered sequentially or concurrently, thereby treating the EGFR-expressing cancer in the subject (see paras [0033-0034]). Concerning claim 35 and the EGFR antibody comprises panitumumab or cetuximab (see para [0036-0037]). Concerning claim 37 and a method for treating cancer in a subject, comprising:administering to the subject a therapeutically effective amount of one or more anti-PD- L1-IR700 molecules (see para [0037]); administering to the subject a therapeutically effective amount of one or more immunoactivators (see para [0333]); and subsequently irradiating the subject and/or irradiating cancer cells in the subject at a wavelength of 670 to 700 nm and at a dose of 4 to 100 J/cm2 (see para [0005]-[0014]);wherein the one or more anti-PD-L1-IR700 molecules and the one or more immunoactivators are administered sequentially or concurrently, thereby treating the cancer in the subject (see para [0337]). Concerning claim 40 and further comprising administering to the subject a therapeutically effective amount of one or more antibody-IR700 molecules, wherein the antibody specifically binds to a tumor-specific protein on the surface of a cancer cell, wherein the tumor-specific protein comprises epidermal growth factor receptor HER1/EGFR, CTLA4, mesothelin, PSMA, HER2/ERBB2, CD3, CD18, CD20, CD25 (IL-2Ra receptor), CD30, CD33, CD44, CD52, CD133, CD206, CEA, AFP, Lewis Y, tumor-associated glycoprotein 72 (TAG72), VEGF, VEGFR, EpCAM, EphA2, glypican-3, gpA33, a mucin, CAIX, a folate-binding protein, a ganglioside, integrin aVf33, ERBB3, MET, IGF1R, EPHA3, TRAILR1, TRAILR2, RANKL, FAP, tenascin, BCR complex, gp72, HLA-DR 10(3, HLA-DR antigen, IgE, CA 242, PEM antigen, SK-1 antigen, PD-1, or PD-L2; (see para [0033]). Concerning claim 42 and a method for reducing edema resulting from cancer treatment in a subject, comprising:administering to the subject a therapeutically effective amount of one or more antibody- IR700 molecules (see para [0037]), wherein the antibody specifically binds to a tumor-specific protein on the surface of a cancer cell or binds to a protein on the surface of an immune cell; administering to the subject a therapeutically effective amount of L-sodium ascorbate; and irradiating the subject and/or irradiating cancer cells in the subject at a wavelength of 660 to 740 nm (see para [0005],[0014]); and at a dose of at least 1 J/cm2;wherein the one or more antibody-IR700 molecules and the one or more reducing agents are administered sequentially or concurrently, thereby reducing edema resulting from cancer treatment in a subject. (see para [0033]). Concerning claim 43 and the protein on the surface of an immune cell is CTLA4 and the tumor-specific protein comprises HER1/EGFR, PD-L1, mesothelin, PSMA, HER2/ERBB2, CD3, CD18, CD20, CD25 (IL-2Ra receptor), CD30, CD33, CD44, CD52, CD133, CD206, CEA, AFP, Lewis Y, tumor-associated glycoprotein 72 (TAG72), VEGF, VEGFR, EpCAM, EphA2, glypican-3, gpA33, a mucin, CAIX, a folate-binding protein, a ganglioside, integrin aV33, ERBB3, MET, IGF1R, EPHA3, TRAILRI, TRAILR2, RANKL, Page 9 of 11 FAP, tenascin, BCR complex, gp72, HLA-DR 10(3, HLA-DR antigen, IgE, CA 242, PEM antigen, SK-1 antigen, PD-1, or PD-L2 (see para [0033]). Concering claim 44 and the cancer is a highly or moderately immunogenic cancer (see para [0276]). Concerning claim 46 and the cancer is a low immunogenic cancer (see para 0487-0488]). Concerning claim 48 and the method has an abscopal effect (see para 0519]). Conclusion Any inquiry concerning this communication or earlier communications from the examiner should be directed to PHILLIP A GRAY whose telephone number is (571)272-7180. The examiner can normally be reached M-F 9-5 EST (FLEX). Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Michael Tsai can be reached at (571)270-5246. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. PHILLIP A. GRAY Primary Examiner Art Unit 3783 /PHILLIP A GRAY/ Primary Examiner, Art Unit 3783 Application/Control Number: 18/263,394 Page 2 Art Unit: 3783 Application/Control Number: 18/263,394 Page 3 Art Unit: 3783 Application/Control Number: 18/263,394 Page 4 Art Unit: 3783 Application/Control Number: 18/263,394 Page 5 Art Unit: 3783 Application/Control Number: 18/263,394 Page 6 Art Unit: 3783 Application/Control Number: 18/263,394 Page 7 Art Unit: 3783 Application/Control Number: 18/263,394 Page 8 Art Unit: 3783 Application/Control Number: 18/263,394 Page 9 Art Unit: 3783