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 .
Claims 1-25, of record 9/23/24 are pending. Prosecution commences for claims 1-25.
PRIORITY
The instant application, filed 9/23/2024 is a CONTINUATION of US Patent No. 12,403,165, filed 2/3/2023, is a CONTINUATION of PCT/US21/59887, filed 11/18/2021, which claims priority to US Provisional Application No. 63/116,004, filed 11/19/2020. Thus, the earliest possible priority for the instant application is 11/19/2020.
CLAIMS
PNG
media_image1.png
200
400
media_image1.png
Greyscale
The claims of the instant application are drawn to methods of treating cancer comprising administering 1) a recombinant oncolytic virus comprising (at least) A) an exogenous fusion protein an IL-2 polypeptide and a leptin polypeptide, B) an exogenous CCR2 chemokine receptor, and C) a genetic mutation, and 2) an immune checkpoint inhibitor. Independent claim 1 is provided below:
Claim Objections
Claim 7 is objected to because of the following informalities:
Claim 7 should be amended to insert an article prior to every recited virus (“a measles virus, a poliovirus, a poxvirus, a vaccinia virus…”). Appropriate correction is required.
Claim Rejections - 35 USC § 103
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1-4, 6-15, and 19-25 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/089755 A1 to Thorne, of record, cited on Applicant’s IDS dated 10/7/24 (13 pages), further in view of WO2019/148109 A1 to Delgoffe, of record, cited on Applicant’s IDS dated 10/7/24 (13 pages).
The applied WO 2019/089755 Thorne reference and the applied WO2019/148109 A1 to Delgoffe have a common inventor with the instant application. Based upon the earlier publication date of the references, they constitute prior art under 35 U.S.C. 102(a)(1). The earliest priority date for the instant application is 11/19/2020. Thus, the 1-year exceptions provided for under 35 USC 102(b)(1) extend to 11/19/2019. The publication date of the WO 2019/089755 Thorne reference is May 9, 2019, and the publication date of the WO2019/148109 Delgoffe reference is August 1, 2019. Thus, the exceptions provided for under 35 USC 102(b)(1) are not available to overcome any rejection based on these references. See, generally MPEP § 717.02.
With regard to claim 1, Thorne discloses methods to treating cancer comprising administering a recombinant oncolytic viruses comprising genetic modifications, wherein the viruses encodes an exogenous nucleic acid encoding a chemokine receptor inserted into the viral genome, wherein the chemokine receptor is CCR2 (see, Abstract, paragraphs [0003], [0009]-[0035], [0037], [0042]-[0043], [0047]-[0072], [0080]-[0083], [0097]-[00100], [0125]-[0150], [0155]-[0158], [0166]-[0172], [0180]-[0182], [0185]-[0190], [0194]-[0204], and [0209]-[0237]). Thorne discloses the oncolytic viruses can further encode additional exogenous sequences, including IL-2 peptides (paragraphs [0209], [0214]). Thorne discloses the oncolytic viruses can comprise additional exogenous nucleic acids, including nucleic acids which encode metabolic modulating peptides (paragraphs [0013], [0048], [0210]).
Thorne discloses the method of treating cancer with the oncolytic virus further comprises further administering an additional therapeutic agent, including administering immunomodulators, including anti-CTLA4, anti-PD-1 or anti-PD-L1, which are checkpoint inhibitors (paragraphs [0099]-[00101]-[0103], [00213], [00274]-[0275], [00282]).
However, Thorne does not disclose wherein the additional exogenous nucleic acids which encode metabolic modulating peptides include a fusion protein comprising an IL-2 and leptin fusion protein, as required by instant claim 1.
Delgoffe discloses recombinant oncolytic viruses which encodes an exogenous nucleic acid encoding metabolic modulating peptides, wherein the metabolic modulating peptides include leptin, wherein leptin is encoded as a fusion protein with the immune stimulatory protein IL-2 and/or other cytokines (Abstract, pages 1-2, 10-11, 14-15, 19, 21-23, 25-29, 32-35, and 43-44). Delgoffe discloses leptin-cytokine (i.e. IL-2) fusion proteins expressed by oncolytic viruses simultaneously lyse tumor cells, increase T cell infiltration, while also simulating the immune system (pages 2, 20, and 22).
It would have been obvious to combine the disclosure of Thorne on methods of treating cancer comprising administering oncolytic viruses encoding a CCR2 receptor further with the disclosure of Delgoffe. A skilled artisan would have been motivated to include a leptin - IL-2 fusion protein because Thorne discloses the viruses can encode additional exogenous nucleic acids, including nucleic acids which encode metabolic modulating peptides (paragraphs [0013], [0048], [0210]), and Delgoffe discloses leptin-IL-2 fusion proteins encoded by oncolytic viruses simultaneously lyse tumor cells, increase T cell infiltration, while also simulating the immune system (pages 2, 20, 22). A skilled artisan would have had a reasonable expectation of success in practicing the claimed invention as oncolytic viruses encoding exogenous metabolic modulating peptides, including viruses encoding leptin-IL-2 fusion protein-encoding oncolytic viruses were known in the art at the time of the invention.
With regard to claims 2-4, Thorne discloses the immune checkpoint inhibitor comprises an anti- CTLA-4, anti-PD-1, or anti-PD-L1 antibody or antigen binding fragment thereof, including wherein the antibody is pembrolizumab or nivolumab (paragraphs [00101], [00275]).
With regard to claim 6, Thorne does not disclose a fusion protein, or a IL-2/leptin fusion protein. However, Delgoffe discloses oncolytic viruses which encodes an exogenous nucleic acid encoding metabolic modulating peptides, wherein the metabolic modulating peptides include leptin, wherein leptin is encoded as a fusion protein with the immune stimulatory protein IL-2 and/or other cytokines (Abstract, pages 1-2, 10-11, 14-15, 19, 21-23, 25-29, 32-35, and 43-44). Thus, claim 6 is obvious for the same reasons as stated above for claim 1.
With regard to claims 7-10, Thorne discloses wherein the oncolytic virus is a vaccinia virus, a poxvirus, including Copenhagen and Western Reserve strains (paragraphs [0172], [0228], [0323]).
With regard to claims 11-12, and 15, Thorne discloses wherein the oncolytic viruses comprise partial or complete deletions of the A52R gene and insertions of exogenous nucleic acids into the A52R locus (paragraphs [0068], [0220], [0233]-[0234], [0315], [0357]). Thus it would have been obvious to insert the exogenous chemokine receptor into the thymidine kinase gene as claimed.
With regard to claims 13-14, Thorne discloses wherein the oncolytic virus comprises a deletion of a thymidine kinase gene, wherein one or more of the exogenous nucleic acids are inserted into the loci of the deleted thymidine kinase gene (paragraph [0235]). Thus it would have been obvious to insert the IL-2/leptin fusion protein into the thymidine kinase gene as claimed.
With regard to claim 19, Thorne discloses the cancer treated includes melanoma, hepatocellular carcinoma, breast cancer, etc. (paragraph [00107]).
With regard to claim 20, Thorne discloses the oncolytic viruses are administered doses of about 105 PFU to about 1010 PFU (paragraph [00249]).
With regard to claims 21-22, Thorne discloses the oncolytic viruses are administered intravenously, intraperitoneally, or by intratumoral injection (paragraphs [00177], [00256]).
With regard to claim 23, Thorne discloses the subject is a human (paragraph [00123], [00163]).
With regard to claim 24, Thorne discloses the modified oncolytic virus is administered to the subject over a period of 1, 2, 3, 4, 5, 6, 7, or more days (paragraphs [00122], [00254]).
With regard to claim 25, Thorne discloses the further therapy, such as the immune checkpoint modulator, is administered to the subject over the period of about one week (paragraphs [00123], [00275], [00283]).
Claim 5 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/089755 A1 to Thorne, of record, and WO2019/148109 A1 to Delgoffe, of record, as applied to claims 1-4, 6-15, and 19-25 above, and further in view of WO2008/142479 to Moss, of record, cited on Applicant’s IDS dated 10/07/24 (13 pages). Claim 5 comprises an embodiment wherein the nucleic acid encoding the chemokine receptor comprises a codon optimized human coding sequence of the chemokine receptor.
The disclosures of Thorne and Delgoffe are applied as in the 103 rejection above, the content of which is incorporated herein in its entirety. Thorne and Delgoffe combine to render obvious a method of treating cancer comprising administering a modified oncolytic virus, including vaccinia virus, comprises exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide in combination with an immune checkpoint inhibitor. Thorne discloses the amino acid sequence encoding the CCR2 chemokine receptor is human (page 120; SEQ ID NO: 111). Thorne discloses the variants of the exogenous nucleic acids encoded by the oncolytic viruses therein include amino acid substitutions, deletions, additions, or other modifications (paragraph [0219]). Delgoffe discloses the variants of the exogenous nucleic acids encoded by the oncolytic viruses include silent mutations in the coding sequences wherein more than one codon can encode the same amino acid, in order to take advantage of the codon usage of the target species for whom the therapy is introduced (page 32).
However, neither Thorne nor Delgoffe disclose wherein a transgene encoding a human transgene is codon optimized, as required by the instant claim 5.
Moss discloses recombinant vaccinia viruses encoding exogenous genes useful for medical or vaccines, including the treatment of cancer (Abstract; page 12). Moss discloses exogenous genes inserted into the vaccinia virus genome can be stabilized using codon optimization by introducing silent mutations into the exogenous sequences to remove runs of 4-6 G or C sequences without altering the amino acid sequence of the exogenous sequence (pages 37-38, 42, claim 30). Moss discloses the vaccinia viruses can encode multiple exogenous genes, including proteins, peptides, and/or selection markers (page 12).
It would have been obvious to combine the disclosures of Thorne and Delgoffe on a modified oncolytic virus, including vaccinia virus, comprises exogenous nucleic acid encoding a human CCR2 chemokine receptor, further with the disclosure of Moss. A skilled artisan would have been motivated to codon-optimize the gene encoding the human CCR2 chemokine receptor within the vaccinia virus in order to stabilize the gene, as taught by Moss. A skilled artisan would have had a reasonable expectation of success in practicing the claimed invention as codon optimizing exogenous nucleic acids in vaccinia virus to stabilize the transgene was known at the time of the invention.
Claim 16 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/089755 A1 to Thorne, of record, and WO2019/148109 A1 to Delgoffe, of record, as applied to claims 1-4, 6-15, and 19-25 above, and further in view of EP0119621 to Bhatt, of record, cited on Applicant’s IDS dated 10/07/2024 (13 pages). Claim 16 encompasses an embodiment wherein the nucleic acid sequence encoding the IL-2 peptide is at least 75% identity to SEQ ID NO: 5.
The disclosures of Thorne and Delgoffe are applied as in the 103 rejection above, the content of which is incorporated herein in its entirety. Thorne and Delgoffe combine to render obvious a method of treating cancer comprising administering a modified oncolytic virus, including vaccinia virus, comprises exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide in combination with an immune checkpoint inhibitor.
However, neither Thorne nor Delgoffe teach a nucleic acid sequence encoding IL-2, nor wherein the nucleic acid sequence encoding the IL-2 peptide comprises at least 75% identity to SEQ ID NO: 5, as required by instant claim 16.
PNG
media_image2.png
541
637
media_image2.png
Greyscale
Bhatt discloses a vector comprising a nucleotide sequence encoding mature human IL-2 (Abstract, pages 2-3). The DNA sequence encoding the human IL-2 of Bhatt is 100% identical to instant SEQ ID NO: 5:
It would have been obvious to combine the disclosures of Thorne and Delgoffe on a modified oncolytic virus, including vaccinia virus, comprising an exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide, further with the disclosure of Bhatt on nucleic acids which encode human IL-2. Combining prior art elements according to known methods to yield predictable results supports a prima facie case of obviousness (MPEP 2143(I)(A)). In the instant case, the prior art included each element claimed, and in combination, each element merely performs the same function as it does separately. A skilled artisan would have had a reasonable expectation of success in encoding the nucleic acids encoded by Bhatt in the viruses of Thorne and Delgoffe as the nucleic acids encoding the human IL-2 protein were known in the art at the time of the invention.
Claim 17 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/089755 A1 to Thorne, of record, and WO2019/148109 A1 to Delgoffe, of record, as applied to claims 1-4, 6-15, and 19-25 above, and further in view of Genbank Accession No. NM_000586.4, Homo Sapiens Interleukin 2 (IL2), mRNA. Earliest publication date 1992, 4 pages, of record, cited on Applicant’s IDS dated 10/07/24 (p ages). Claim 17 encompasses an embodiment wherein the nucleic acid sequence encoding the leptin- IL-2 fusion protein comprises at least 75% identity to SEQ ID NO: 1.
The disclosures of Thorne and Delgoffe are applied as in the 103 rejection above, the content of which is incorporated herein in its entirety. Thorne and Delgoffe combine to render obvious a method of treating cancer comprising administering a modified oncolytic virus, including vaccinia virus, comprises exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide in combination with an immune checkpoint inhibitor.
Thorne does not disclose a leptin-IL-2 fusion protein. Delgoffe discloses recombinant oncolytic viruses which encodes an exogenous nucleic acid encoding a leptin and IL-2 fusion protein, wherein the fusion protein comprises leptin-linker-IL2 or leptin-IL-2 (pages 2, 28, 44). Delgoffe discloses the protein linkers are at least 5 to 50 amino acids in length (page 12), which encompasses 0 to 150 nucleotides in length. Delgoffe’s SEQ ID NO:1 comprises nucleotides 57-577 therein that are 100% identical to instantly claimed SEQ ID NO:4 nucleotides 57-557 encoding leptin.
Thus, Thorne in view of Delgoffe disclose a Leptin-IL-2 fusion protein, encoded by a nucleic acid construct accordingly:
PNG
media_image3.png
106
711
media_image3.png
Greyscale
However, neither Thorne nor Delgoffe disclose a nucleic acid sequence encoding IL-2, or wherein the nucleic acid sequence encoding the Leptin-IL-2 peptide comprises at least 75% identity to SEQ ID NO: 1.
Genbank Accession No. NM_000586.4 encodes human IL-2 mRNA. Genbank Accession No. NM_000586.4 discloses the mature IL-2 peptide is encoded by nucleotides 346-744 of the nucleic acid sequence therein.
PNG
media_image4.png
97
702
media_image4.png
Greyscale
Insertion of the nucleic acids encoding the mature IL-2 into a 3’ position of the fusion protein disclosed by Thorne in view of Delgoffe, without any linker sequences results in a fusion protein schematically shown as:
The composite nucleotide sequence encoding a leptin- IL-2 fusion peptide is the following 900 nucleotide sequence (human IL-2 is underlined):
PNG
media_image5.png
314
1024
media_image5.png
Greyscale
Nucleotides 1-502 and 500-900 of the above sequence have 100% identity with nucleotides 1-502 and 566-966 of instantly claimed SEQ ID NO:1 (which has 966 nucleotides):
PNG
media_image6.png
218
975
media_image6.png
Greyscale
PNG
media_image7.png
662
660
media_image7.png
Greyscale
PNG
media_image8.png
497
660
media_image8.png
Greyscale
It would have been obvious to combine the disclosures of Thorne and Delgoffe on a modified oncolytic virus, including vaccinia virus, comprising an exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide, further with the disclosure of NM_000586.4 on nucleic acids which encode human IL-2. Combining prior art elements according to known methods to yield predictable results supports a prima facie case of obviousness (MPEP 2143(I)(A)). In the instant case, the prior art included each element claimed, and in combination, each element merely performs the same function as it does separately. A skilled artisan would have had a reasonable expectation of success in encoding the nucleic acids encoded by NM_000586.4 in the viruses of Thorne and Delgoffe as the nucleic acids encoding the human IL-2 protein were known in the art at the time of the invention.
Claim 18 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2019/089755 A1 to Thorne, of record, and WO2019/148109 A1 to Delgoffe, of record, as applied to claims 1-4, 6-15, and 19-25 above, and further in view of Genbank Accession No. NM_001123041.3 Human CCR2 mRNA, of record, cited on Applicant’s IDS dated 10/07/24 (9 pages). Earliest priority 1988. 5 pages, of record. Claim 18 encompasses an embodiment wherein the nucleic acid sequence encoding the CCR2 receptor comprises at least 75% identity to SEQ ID NO: 2.
The disclosures of Thorne and Delgoffe are applied as in the 103 rejection above, the content of which is incorporated herein in its entirety. Thorne and Delgoffe combine to render obvious a method of treating cancer comprising administering a modified oncolytic virus, including vaccinia virus, comprises exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide in combination with an immune checkpoint inhibitor. Thorne discloses the amino acid sequence encoding the CCR2 chemokine receptor is human, having accession number P41597 (page 120; SEQ ID NO: 111).
However, neither Thorne nor Delgoffe disclose wherein the nucleic acid sequence encoding the CCR2 receptor comprises at least 75% identity to SEQ ID NO: 2, as required by instant claim 16.
Genbank Accession No. NM_001123041.3 encodes human CCR2 mRNA, encoding the human CCR2 protein, which is 100% identical to the P41597 CCR2 protein sequence in Thorne:
PNG
media_image9.png
478
703
media_image9.png
Greyscale
Instant SEQ ID NO:2, comprising the nucleic acids encoding the CCR2 protein (nucleotides 1-1125) is 100% identical to nucleotides 119-1243 of NM_001123041.3 which comprises the nucleic acids encoding the CCR2 protein:
PNG
media_image10.png
228
584
media_image10.png
Greyscale
PNG
media_image11.png
836
587
media_image11.png
Greyscale
It would have been obvious to combine the disclosures of Thorne and Delgoffe on a modified oncolytic virus, including vaccinia virus, comprising an exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide, wherein the amino acid sequence encoding the CCR2 chemokine receptor is human, having accession number P41597 (page 120; SEQ ID NO: 111), further with the disclosure of NM_001123041.3 which comprises the nucleic acids encoding the identical CCR2 protein. Combining prior art elements according to known methods to yield predictable results supports a prima facie case of obviousness (MPEP 2143(I)(A)). In the instant case, the prior art included each element claimed, and in combination, each element merely performs the same function as it does separately. A skilled artisan would have had a reasonable expectation of success in using the nucleic acids encoded by NM_001123041.3 in the viruses of Thorne and Delgoffe as the nucleic acids encoding the human CCR2 protein were known in the art at the time of the invention.
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.
Claims 1-25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-27 of U.S. Patent No. 12,403,165 in view of WO 2019/089755 A1 to Thorne, of record. The instant application is a CONTINUATION of the ‘165 Patent.
The disclosure of Thorne is applied as in the 103 rejections above, the content of which is incorporated herein in their entirety.
Independent claim 1 of the ‘165 Patent is drawn to an oncolytic virus (composition) comprising a exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide.
Independent claim 1 of the instant application is drawn to a method of treating cancer by administering an oncolytic virus comprising a exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide, in combination with administering a checkpoint inhibitor.
Thus, the instant claims are directed to methods of using the virus claimed in the parent patent. The claims of the parent patent do not require the oncolytic virus is administered in a method of treating cancer as claimed.
However, Thorne discloses methods of treating cancer by administering oncolytic virus encoding exogenous sequences, including CCR2, and further administering checkpoint inhibitors was known (paragraphs [0099]-[00103], [00213], [00274]-[0275], [00282]).
Thus, it would have been obvious to modify the claims of the ‘165 Patent, in combination with Thorne, into methods of use claims directed to methods of treating cancer, comprising administering the oncolytic virus in combination with a checkpoint inhibitor.
Instant claims 2-25 are obvious variants over patented claims 2-27 OR are obvious over the disclosure of Thorne for the reasons stated above in the 103 rejections of record.
Claims 1-25 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of copending Application No. 18/892,953 in view of WO 2019/089755 A1 to Thorne, of record. The instant application and copending Application No. 18/892,953 both claim priority to U.S. Patent No. 12,403,165, share the same specification and effective filing dates.
The disclosure of Thorne is applied as in the 103 rejections above, the content of which is incorporated herein in their entirety.
Independent claim 1 of the ‘953 Application is drawn to a method of treating cancer by administering an oncolytic virus comprising a exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide, in combination with administering a chemotherapeutic agent.
Independent claim 1 of the instant Application is drawn to a method of treating cancer by administering an oncolytic virus comprising a exogenous nucleic acid encoding a human CCR2 chemokine receptor, and an exogenous nucleic acid encoding a leptin and IL-2 fusion peptide, in combination with administering a checkpoint inhibitor.
Thus, the instant claim differs from the claim in the cited application only by administering a different additional therapeutic agent (checkpoint inhibitor vs. chemotherapeutic agent).
However, Thorne discloses methods of treating cancer by administering oncolytic virus encoding exogenous sequences, including CCR2, and further administering one or more additional therapies was known, including A) checkpoint inhibitors or B) chemotherapeutic agents (paragraphs [0099]-[00103], [00109]-[00111], [00213], [00274]-[0275], [00282]).
Thus, it would have been obvious to modify the claims of the ‘953 Application, in combination with Thorne, and substitute the chemotherapeutic agent with a checkpoint inhibitor.
Instant claims 2-25 are obvious variants over application claims 2-21 OR are obvious over the disclosure of Thorne for the reasons stated above in the 103 rejections of record.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KIMBERLY A ARON whose telephone number is (571)272-2789. The examiner can normally be reached Monday-Friday 9AM-5PM.
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, Christopher Babic can be reached at 571-272-8507. 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.
KAA
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633
Prosecution Insights