DETAILED ACTION
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 .
Priority
The instant application, filed February 2nd 2024, is a 371 filing of PCT/US22/74383, filed August 1st, 2022, and claims domestic benefit to US provisional application 63/203,862, filed August 2nd, 2021.
Status of Claims/Application
Claims 1-16 filed on February 2nd, 2024 are currently pending and are examined on the merits herein.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on July 11th, 2025 and May 10th, 2024 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement has been considered by the examiner.
Claim Objections
Claim 15 is objected to because of the following informalities: A redundant phrase “one to one to two doses of ICT” was added to claim 15 and should be removed. Appropriate correction is required.
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.
Claims 1, 2, 3, 4, 5, 6, 7, 8, 12, 13, and 14 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2014/195852 A1 (listed in the IDS, filed 07/11/2025), published on December 11th, 2014, herein “Hoos”, and further in view of “Ribas” (Ribas, A., Algazi, A., Ascierto, P.A. et al. PD-L1 blockade in combination with inhibition of MAPK oncogenic signaling in patients with advanced melanoma. Nat Commun 11, 6262 (2020). https://doi.org/10.1038/s41467-020-19810-w, listed in the IDS filed on 05/10/2024).
Regarding instant claim 1, Hoos teaches a method of enhancing efficacy of MAPKi therapy or immune checkpoint therapy (ICT) (page 7, line 19-21, “combining therapeutic approaches for inhibiting proliferation of tumor cells and enhancing anti-tumor immunity”, line 24-25, “the current invention is directed to a combination of a BRAF inhibitor and/or a MEK inhibitor, and an anti-PD-L1 antibody in the treatment of cancer”). Hoos further teaches the method comprising: (a) Pretreating the subject in need of MAPKi therapy by administering one to two doses of ICT to the subject Subsequent to pretreating of (a), (b) administering to the subject a combination of MAPKi and ICT (page 42, line 33-36, “Suitably, an anti-PD-L 1 antibody will be administered first the sequence, in followed by an optional drug holiday, followed by administration of Compound followed B, by an optional drug holiday, followed by administration of Compound A.”, page 26, line 17-18, “Compound A is disclosed and claimed, along with pharmaceutically acceptable salts and solvates thereof, as being useful as an inhibitor of MEK activity,” and line 34-35, “Compound B is disclosed and claimed, along with pharmaceutically acceptable salts thereof, as being useful as an inhibitor of BRAF activity”, Drug holiday is defined in Hoos as “As used herein, a drug holiday is a period of days after the sequential administration of one of Compound A, Compound B and an anti-PD-L1 antibody and before the administration of the other component of the invention. Suitably the drug holiday will be a period of days selected from: 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, days, 11 days, 12 days, 13 days and 14 days.”). Further, Hoos teaches a combination of ICI and MAPKi (page 37, line 25-27, “one or more doses of Compound A are administered simultaneously or separately with one or more doses of Compound B and one or more doses of an anti-PD-L 1 antibody”).
Regarding instant claims 2 and 3, Hoos teaches the ICT comprises an anti-PD-1/anti-PD-L1 agent (page 16, line 4-15, [Hoos lists anti-PD-L1 antibodies]).
Regarding instant claim 5, Hoos teaches the subject has a NRAS, KRAS and/or NF1 mutant cancer (page 49, line 3-5, “method of treating or lessening the severity of a cancer that is either wild type or mutant for Raf and KRAS and either wild-type or mutant for Pl3K/Pten”) and as described prior Hoos teaches that the MAPKi is MEKi (page 62, line 12-13, “MAPK signaling inhibition by Compound A from CT 26 cells were determined by western blot analysis” and Compound A is defined by Hoos as an inhibitor of MEK activity (page 26, line 17-18)).
Regarding instant claim 6, 7, 8, and 12, Hoos teaches the pretreating of (a) consists of administering one to two doses over one to eight weeks (page 43, line 14-15, “an anti-PD-L1 antibody is administered once every two weeks for from 2 to 10 weeks”). Hoos further discloses administration of one to two doses of ICT (page 37, line 29-30, “multiple doses of Compound A are administered simultaneously or separately with multiple doses of Compound B and multiple doses of an anti-PD-L1 antibody”). Hoos further teaches that pretreating of (a) begins two to eight weeks prior to the administering of (b) and the administering of (b) begins two to eight weeks following the initiation of the pretreating of (a) (page 43, line 1-3, “by an optional drug holiday, followed by administration of Compound B for from 1 to 30 consecutive days, followed by an optional drug holiday, followed by administration of Compound A for from 1 to 30 consecutive days” and the drug holiday defined by Hoos is “Suitably the drug holiday will be a period of days selected from: 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, days, 11 days, 12 days, 13 days and 14 days.” (page 41, line 23-25)). It is noted however, that the phrase pretreatment is not disclosed by Hoos as recited in the instant claims but Hoos discloses administering anti-PD-L1 prior to the MAPKi inhibitor for at least 2 weeks.
Regarding instant claim 13 and 14, Hoos teaches a method of suppressing melanoma metastasis in a subject (page 47, line 27 “metastatic forms”, line 28-29, “cancer is selected from: brain [….] melanoma (line 32)”). As described in claim 1 above, Hoos teaches the method comprising: (a) Pretreating a subject in need of treatment for melanoma metastasis by administering one to two doses of ICT to the subject (b) Subsequent to the pretreating of (a), administering to the subject a combination of MAPKi and ICI.
Regarding instant claim 4, while Hoos teaches that the MAPKi is a BRAF inhibitor (BRAFi) or a BRAF plus a MEK inhibitor (MEKi) (page 7, line 24-25, “the current invention is directed to a combination of a BRAF inhibitor and/or a MEK inhibitor, and an anti-PD-L1 antibody in the treatment of cancer”), Hoos does not teach the subject has a BRAF V600 mutant cancer. Ribas teaches the method of treating a subject that has BRAF V600 mutant cancer with the MAPKi inhibitor and anti-PD-L1 antibody (page 2, column 1, paragraph 2, “the phase 1 clinical trial testing triple therapy with dabrafenib [BRAF inhibitor (page 1, abstract)], trametinib [MEK inhibitor] (page 1, abstract)], and the anti-PD-L1 antibody durvalumab in patients with BRAFV600-mutant melanoma”). Ribas further teaches that “blocking oncogenic BRAFV600 signaling results in increased sensitivity of melanoma cells to immunotherapy and increasing antitumor activity in combination with immunotherapy in mouse models, while in patients it makes melanoma metastases permissive to immune cell infiltration” (page 2, column 1, paragraph 1). Finally, Ribas discloses that as a significant proportion of patients do not respond or progress after initial therapy, further treatment options are needed for patients with advanced melanoma“ (page 2, column 1, paragraph 1) and that the triplet combination is “feasible in patients with BRAF-mutant advanced melanoma and induces robust and sustained immune modulation” (page 8, column 1, paragraph 3). Therefore, it would have been obvious to the person of ordinary skill in the art to use the method of treating as taught by Hoos to treat subjects that have BRAF V600 mutant melanoma to increase sensitivity of melanoma cells to immunotherapy and advanced melanoma patients that do not respond or progress after initial therapy have better treatment options as taught by Ribas.
Regarding instant claim 3, Ribas teaches the ICI can be anti-CTLA-4 antibody (page 2, column 1, paragraph 1, “(ii) immune checkpoint inhibitors, with monoclonal antibodies targeting the programmed death receptor 1 (PD-1) and the cytotoxic T lymphocyte antigen-4 (CTLA-4)”).
Claims 9 and 10 are rejected under 35 U.S.C. 103 as being unpatentable over Hoos and Ribas as applied to claim 1 above, and further in view of “Oh” (Oh DS, Kim H, Oh JE, Jung HE, Lee YS, Park JH, Lee HK. Intratumoral depletion of regulatory T cells using CD25-targeted photodynamic therapy in a mouse melanoma model induces antitumoral immune responses. Oncotarget. 2017 Jul 18;8(29):47440-47453. doi: 10.18632/oncotarget.17663. PMID: 28537894; PMCID: PMC5564577).
While Hoos and Ribas do not teach the pretreating of (a) further comprises administering a modulator of regulatory T cells and the modulator is a CD25-depleting antibody. Oh teaches the method of using CD25 antibody to deplete T cells which help enhance anti-tumor responses to melanoma (title and page 47441, column 1, paragraph 2, “injected Chlorin e6 (Ce6) conjugated to an anti-CD25 monoclonal antibody (anti-CD25-Ce6) to locally deplete CD4+Foxp3+ Tregs”). Oh discloses that “Tregs are considered one of the most significant targets as they play a major role in maintaining immunosuppressive microenvironments within tumors” (page 47440, column 2, paragraph 1) and that “antibodies targeting immune cells could be exploited for selective depletion for target cells in tumor microenvironments to investigate their functions and therapeutic effects” (page 47441, column 1, paragraph 1). Oh further discloses that the “anti-CD25-Ce6-targeted PDT technique induced apoptosis and depletion of Tregs in tumors and inhibited tumor growth in a murine melanoma model” and that “the anti-CD25 Ce6-targeted PDT induced anti-tumoral immunity without altering systemic immune responses” (page 47441, column 1, paragraph 2). Therefore, it would have been obvious to the person of ordinary skill in the art to use anti-CD25 antibodies as taught by Oh to modulate T cells, specifically Tregs, that are important in maintaining immunosuppressive microenvironments within tumors. One of ordinary skill in the art would have used the anti-CD25 monoclonal antibody taught in Oh and added to the method of treating taught in Hoos to modulate T regs in tumors and inhibited tumor growth in a melanoma model as taught by Oh with reasonable expectation of success.
Claims 9, 11, 15 and 16 are rejected under 35 U.S.C. 103 as being unpatentable over Hoos and Ribas as applied to claim 1 above, and further in view of “Jaynes” (Jaynes et al. Mannose receptor (CD206) activation in tumor-associated macrophages enhances adaptive and innate antitumor immune responses. Sci Transl Med. 2020 Feb 12;12(530):eaax6337. doi: 10.1126/scitranslmed.aax6337. PMID: 32051227; PMCID: PMC7832040).
While Hoos and Ribas teach the method of treating using ICT and MAPKi to enhancing efficacy, Hoos and Ribas do not teach the pretreating of (a) further comprises administering a modulator of M2-like TAMs and the modulator is a peptide agonist of CD206 as recited in claims 9, 11, and 15.
Jaynes teaches a peptide “RP-182” that “triggers a conformational switch of the mannose receptor CD206 expressed on M2-like macrophages, induces endocytosis, phagosome-lysosome formation, and apoptosis in these cells, and shifts the population of TAMs from M2-like macrophages toward an M1 phenotype, increasing innate and adaptive antitumor immune responses and improving outcomes in a variety of human and murine cancer models” (page 4, paragraph 2). Jaynes further teach that “anti-TAM therapy via RP-182 might cooperate with PD-L1 immune checkpoint inhibition in pancreatic cancer not known to respond to single agent anti-PD-1/PD-L1 therapy, we combined RP-182 with anti PD-L1 treatment. Antitumor activity of the combination was enhanced compared to single agent therapy” (page 12, paragraph 1) and that the RP-182 reduced growth of B16 melanomas (page 12, paragraph 2, “RP-182 reduced growth of CT-26 colon tumors and murine B16 melanomas, where it showed equal efficacy to cytotoxic T lymphocyte-associated protein 4 (CTLA4) checkpoint inhibition”). Therefore, it would have been obvious to the person of ordinary skill in the art to use the peptide agonist of CD206, RP-182, to modulate TAMs from M2 to M1 phenotype and in combination with ICI as taught by Hoos to increase innate and adaptive immune responses to melanoma.
Regarding instant claim 16, Jaynes teaches the inhibiting of M2-like TAMs effects a selective upregulation of pro-inflammatory or M1-like TAMs in the subject (page 3, paragraph 1, “RP-182-mediated activation of this receptor in human and murine M2-like macrophages elicits a program of endocytosis, phagosome-lysosome formation, and autophagy and reprograms M2-like TAMs to an antitumor M1-like phenotype).
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
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Claim 1-16 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1, 5, 7, 9, 12, and 14, of copending Application No. 18/709,427, filed May 10th, 2024, herein “App’427”, in view of Hoos (cited previously), Oh (cited previously) and Jayden (cited previously).
Regarding instant claims 1 and 13, App’427 claim 1 recites a method of suppressing tumor-surface PD-L1 expression to thereby enhance anti-cancer therapy in a subject in need thereof, the method comprising administering to the subject an effective amount of a modulator of tumor cell-surface PD-L1/L2 and App’427 claim 5 recites the subject is treated with one or more MAPK inhibitors, and optionally, one or more immune checkpoint antibodies as anti-cancer therapy.
Regarding instant claims 4 and 5, App’427 claim 7 recites the MAPK inhibitor is selected from: Dabrafenib and Trametinib. As evidentiary reference, Ribas teaches that dabrafenib is a BRAF inhibitor and Trametinib is a MEK inhibitor (page 1, abstract).
Regarding instant claims 2 and 3, App’427 claim 9 recites the subject is treated with anti-CTLA-4 antibody, anti-PD1 antibody, and anti-PD-L1 antibody.
Regarding instant claims 13 and 14, App’427 claim 12 and 14 recites the subject is in need of treatment for melanoma.
However, App’427 claims do not recite the subject has BRAF V600 mutant cancer (claim 4) and that the subject has NRAS, KRAS and/or NF1 mutant cancer (claim 5). Ribas teaches the method of treating a subject that has BRAF V600 mutant cancer with the MAPKi inhibitor and anti-PD-L1 antibody (page 2, column 1, paragraph 2, “the phase 1 clinical trial testing triple therapy with dabrafenib [BRAF inhibitor (page 1, abstract)], trametinib [MEK inhibitor] (page 1, abstract)], and the anti-PD-L1 antibody durvalumab in patients with BRAFV600-mutant melanoma”). Ribas further teaches that “blocking oncogenic BRAFV600 signaling results in increased sensitivity of melanoma cells to immunotherapy and increasing antitumor activity in combination with immunotherapy in mouse models, while in patients it makes melanoma metastases permissive to immune cell infiltration” (page 2, column 1, paragraph 1). Finally, Ribas discloses that as a significant proportion of patients do not respond or progress after initial therapy, further treatment options are needed for patients with advanced melanoma“ (page 2, column 1, paragraph 1) and that the triplet combination is “feasible in patients with BRAF-mutant advanced melanoma and induces robust and sustained immune modulation” (page 8, column 1, paragraph 3). Therefore, it would have been obvious to the person of ordinary skill in the art to use the method of treating as recited by App’427 claims to treat subjects that have BRAF V600 mutant melanoma to increase sensitivity of melanoma cells to immunotherapy and advanced melanoma patients that do not respond or progress after initial therapy have better treatment options as taught by Ribas. Regarding instant claim 5, Ribas teaches the subjects in need of treatment have NRAS mutation (page 4, column 1, paragraph 3, “Among the 11 patients with NRAS-mutant disease across cohorts B and C, 3 (27.2%) had PRs.”).
However, App’427 claims do not recite the method of administering ICI prior to MAPKI and or combination with ICI as recited in instant claims 1, 6, 7, 8, 12, 13, 15, 16. As described prior, Hoos teaches a method of combining therapeutic approaches for inhibiting proliferation of tumor cells and enhancing anti-tumor immunity using BRAF inhibitors, MEK inhibitors and anti-PD-L1 antibody (page 7, line 19-22 and line 24-25). Hoos further teaches the method comprising: (a) Pretreating the subject in need of MAPKi therapy by administering one to two doses of ICT to the subject Subsequent to pretreating of (a), (b) administering to the subject a combination of MAPKi and ICT (page 42, line 33-36, “Suitably, an anti-PD-L 1 antibody will be administered first the sequence, in followed by an optional drug holiday, followed by administration of Compound followed B, by an optional drug holiday, followed by administration of Compound A.”, page 26, line 17-18, “Compound A is disclosed and claimed, along with pharmaceutically acceptable salts and solvates thereof, as being useful as an inhibitor of MEK activity,” and line 34-35, “Compound B is disclosed and claimed, along with pharmaceutically acceptable salts thereof, as being useful as an inhibitor of BRAF activity”, Drug holiday is defined in Hoos as “As used herein, a drug holiday is a period of days after the sequential administration of one of Compound A, Compound B and an anti-PD-L1 antibody and before the administration of the other component of the invention. Suitably the drug holiday will be a period of days selected from: 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, days, 11 days, 12 days, 13 days and 14 days.”). Further, Hoos teaches a combination of ICI and MAPKi (page 37, line 25-27, “one or more doses of Compound A are administered simultaneously or separately with one or more doses of Compound B and one or more doses of an anti-PD-L 1 antibody”).
Hoos teaches the pretreating of (a) consists of administering one to two doses over one to eight weeks (page 43, line 14-15, “an anti-PD-L1 antibody is administered once every two weeks for from 2 to 10 weeks”). Hoos further discloses administration of one to two doses of ICT (page 37, line 29-30, “multiple doses of Compound A are administered simultaneously or separately with multiple doses of Compound B and multiple doses of an anti-PD-L1 antibody”). Hoos further teaches that pretreating of (a) begins two to eight weeks prior to the administering of (b) and the administering of (b) begins two to eight weeks following the initiation of the pretreating of (a) (page 43, line 1-3, “by an optional drug holiday, followed by administration of Compound B for from 1 to 30 consecutive days, followed by an optional drug holiday, followed by administration of Compound A for from 1 to 30 consecutive days” and the drug holiday defined by Hoos is “Suitably the drug holiday will be a period of days selected from: 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, 7 days, 8 days, 9 days, days, 11 days, 12 days, 13 days and 14 days.” (page 41, line 23-25)). It is noted however, that the phrase pretreatment is not disclosed by Hoos as recited in the instant claims but Hoos discloses administering anti-PD-L1 prior to the MAPKi inhibitor for at least 2 weeks.
Therefore, it would have been obvious to the person of ordinary skill in the art to combine the method as taught by Hoos with the App’427 claims to arrive at the claimed invention as Hoos teaches that the combination treatment of ICI and MAPKi will allow inhibiting proliferation of tumor cells and enhancing anti-tumor immunity that are more effective for individuals suffering the effects for cancer (page 7, line 17-20).
However, App’427 claims do not recite administering a modulator of regulatory T cells is a CD25-depleting antibody as recited in instant claims 9 and 10. Oh teaches the method of using CD25 antibody to deplete T cells which help enhance anti-tumor responses to melanoma (title and page 47441, column 1, paragraph 2, “injected Chlorin e6 (Ce6) conjugated to an anti-CD25 monoclonal antibody (anti-CD25-Ce6) to locally deplete CD4+Foxp3+ Tregs”). Oh discloses that “Tregs are considered one of the most significant targets as they play a major role in maintaining immunosuppressive microenvironments within tumors” (page 47440, column 2, paragraph 1) and that “antibodies targeting immune cells could be exploited for selective depletion for target cells in tumor microenvironments to investigate their functions and therapeutic effects” (page 47441, column 1, paragraph 1). Oh further discloses that the “anti-CD25-Ce6-targeted PDT technique induced apoptosis and depletion of Tregs in tumors and inhibited tumor growth in a murine melanoma model” and that “the anti-CD25 Ce6-targeted PDT induced anti-tumoral immunity without altering systemic immune responses” (page 47441, column 1, paragraph 2). Therefore, it would have been obvious to the person of ordinary skill in the art to use anti-CD25 antibodies as taught by Oh to modulate T cells, specifically Tregs, that are important in maintaining immunosuppressive microenvironments within tumors. One of ordinary skill in the art would have used the anti-CD25 monoclonal antibody taught in Oh and added to the method of treating recited in App’427 to modulate T regs in tumors and inhibited tumor growth in a melanoma model as taught by Oh with reasonable expectation of success.
However, App’427 claims do not recite administering a modulator of M2-like TAMS which is a peptide of CD206 as recited in instant claims 9, 11, 16. Jaynes teaches a peptide “RP-182” that “triggers a conformational switch of the mannose receptor CD206 expressed on M2-like macrophages, induces endocytosis, phagosome-lysosome formation, and apoptosis in these cells, and shifts the population of TAMs from M2-like macrophages toward an M1 phenotype, increasing innate and adaptive antitumor immune responses and improving outcomes in a variety of human and murine cancer models” (page 4, paragraph 2). Jaynes further teach that “anti-TAM therapy via RP-182 might cooperate with PD-L1 immune checkpoint inhibition in pancreatic cancer not known to respond to single agent anti-PD-1/PD-L1 therapy, we combined RP-182 with anti PD-L1 treatment. Antitumor activity of the combination was enhanced compared to single agent therapy” (page 12, paragraph 1) and that the RP-182 reduced growth of B16 melanomas (page 12, paragraph 2, “RP-182 reduced growth of CT-26 colon tumors and murine B16 melanomas, where it showed equal efficacy to cytotoxic T lymphocyte-associated protein 4 (CTLA4) checkpoint inhibition”). Therefore, it would have been obvious to the person of ordinary skill in the art to use the peptide agonist of CD206, RP-182, to modulate TAMs from M2 to M1 phenotype and in combination with ICI as recited in App’427 claims to increase innate and adaptive immune responses to melanoma.
Regarding instant claim 16, Jaynes teaches the inhibiting of M2-like TAMs effects a selective upregulation of pro-inflammatory or M1-like TAMs in the subject (page 3, paragraph 1, “RP-182-mediated activation of this receptor in human and murine M2-like macrophages elicits a program of endocytosis, phagosome-lysosome formation, and autophagy and reprograms M2-like TAMs to an antitumor M1-like phenotype).
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Lam Thuy Vi Tran Ho whose telephone number is (571)272-9135. The examiner can normally be reached Monday-Friday 7:30-3.
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/LAM THUY VI TRAN HO/Examiner, Art Unit 1647 /L.T./Examiner, Art Unit 1647 /JOANNE HAMA/Supervisory Patent Examiner, Art Unit 1647
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