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 1-28, of record 4/18/24 are pending. Prosecution on the merits commences for claims 1-28.
PRIORITY
The instant application, filed 4/18/2024, is a CONTINUATION of US Patent No. 12,016,893 filed 12/13/2022, which is a CONTINUATION of PCT/US2022/026703, filed 04/28/2022, which claims priority to US Provisional Application No. 63/182,243, filed 4/30/2021. Thus, the earliest possible priority for the instant application is 4/30/2021.
CLAIMS
The claims are drawn to an oncolytic virus encoding an exogenous nucleic acid encoding an MHC I inhibitor, wherein the inhibitor is a dominant-negative interferon regulatory factor 7 (dnIRF7).
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Claim Rejections - 35 USC § 112b - indefinite
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 20 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 20 is rejected for the use of parentheticals. Claim 20 recites “a Western Reserve strain Vaccinia virus (ATCC VR-1354),” “a Wyeth strain (ATCC VR-325),” and an Ankara strain (ATCC VR-1508 or ATTC VR1566).” It is not clear whether the claim is requiring those specific strains recited within the parentheticals, or whether they are suggestions and thus encompass exemplary language. As such, a skilled artisan would not know if they are part of the claimed invention. MPEP 2173.05(d).
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, 9, 11, 13, 15-17, 19-22 and 25-28 are rejected under 35 U.S.C. 103 as being unpatentable over US Patent Application Publication No. 2017/0173092 to Mulvey, of record IDS dated 5/01/24 (12 pages) further in view of Zhang et al. Interferon Regulatory Factor 7 Mediates Activation of Tap-2 by Epstein-Barr Virus Latent Membrane Protein 1. Journal of Virology, 2001. 75(1): 341-350.
With regard to claim 1, Mulvey discloses oncolytic viruses encoding heterologous TAP inhibitors for the treatment of cancer (Abstract, paragraphs [0016]-[0019], [0031]-[0034]). Mulvey discloses inhibition of the transporter associated with antigen processing (TAP) in cells results in the down-regulation of MHC I surface expression of infected cells (paragraphs [0012]-[0013]). Mulvey discloses the decrease in MHC I-antigen complex display on infected cells allows for sufficient viral replication and spread before finally being cleared by host immune responses (paragraphs [0013]-[0014], [0046]). Mulvey discloses the heterologous TAP inhibitors include UL49.5, US6, US12, BNLF2a ICP47, CPXV12, but are not limited to those embodiments (paragraphs [0033]-[0036]). Thus, Mulvey discloses the oncolytic viruses encoding heterologous TAP inhibitors are oncolytic viruses encoding heterologous MHC I inhibitors.
However, Mulvey does not disclose wherein the exogenous TAP inhibitor is a dominant negative interferon regulatory factor 7 (dn-IRF7) as required by instant claim 1.
Zhang discloses Epstein Barr Virus LMP1 utilizes IRF7 in infected cells to induce TAP2 protein expression (Abstract). Zhang shows IRF7 can bind to, and activate the TAP2 promoter (FIG. 2), but both LMP1 and IRF7 are required to increase expression of TAP2 proteins (FIG. 4, 5, 6). Zhang shows IRF7 binds to the TAP2 promoter via it’s N- terminal DNA binding domain, showing variants which lack the DNA binding domain, isoform IRF-7C and a dominant-negative IRF7 protein (IRF-7DN), are unable to bind and activate TAP reporter constructs (FIG. 3). In addition, Zhang shows expression of IRF-7DN reduces Tap2 expression (page 345, FIG 4A, B).
It would have been obvious to combine the oncolytic viruses encoding heterologous TAP inhibitors which inhibit MHC I expression of Mulvey further with the TAP inhibitor dominant-negative IRF7 of Zhang to arrive at the instant claim. Mulvey teaches the TAP inhibitor is not limited, and Zhang shows the dominant-negative IRF7 is a TAP inhibitor. Combining prior art elements according to known methods to yield predictable results supports a conclusion of obviousness (MPEP2143 (I)(A). In the instant case, the prior art included each element claimed, that in combination, each element merely performs the same function as it does separately. In addition, the selection of a known material based on its suitability for its intended use supported a prima facie obviousness (MPEP 2144.07). Mulvey discloses that any TAP inhibitor can be encoded in the vector. A skilled artisan would have had a reasonable expectation of success in practicing the claimed invention as encoding heterologous TAP inhibitors which are MHC I inhibitors was known in the art at the time of the invention.
With regard to claims 4-5, and 19 discloses the exogenous nucleic acid encoding the TAP inhibitor (MHC I inhibitor) is inserted into a genome of the oncolytic virus, including in the locus of a thymidine kinase gene resulting in the deletion of the thymidine kinase (paragraphs [0097], [0144]-[0162]).
With regard to claims 6, 9 and 11, Mulvey discloses the viruses can encode additional heterologous genes, including heterologous GM-CSF, which is a dendritic cell maturation factor, which increases MHC II presentation, interferon γ, or TNF-α (paragraphs [0037]-[0038], [0101], [0104]).
With regard to claims 13, 15 and 20, Mulvey discloses the oncolytic virus comprises an adeno- associated virus, an adenovirus, Newcastle disease virus (NDV), Reovirus (RV), a Myxoma virus (MYXV), Vaccinia virus (VV), and Vesicular Stomatitis virus (VSV), including Ankara and lister strains (paragraphs [0032], [0080]).
With regard to claims 16 and 17 Mulvey discloses the expression of the TAP inhibitor causes an inhibition or partial inhibition of MHC I presentation, which reduces the immune response to the cell and increases an immune response to the cells surrounding the virus-infected cell (paragraphs [0013], [0014], [0033]-[0038], [0049]-[0050]).
With regard to claims 21-22 and 24-28, Mulvey discloses the oncolytic virus is formulated as a pharmaceutical composition comprising a pharmaceutically acceptable excipient, diluent, carrier, including sterile water (paragraphs [0106]-[0113]), and if formulated as unit dosage forms, with a preservative (paragraph [0134]). The only mention of use of a preservative is when formulated as a unit dosage, as such, other formulations can be preservative free. Thus, generating a formulation that is preservative free is obvious over Mulvey. In addition, Mulvey further discloses the virus can be combined with additional therapeutic substances to treat cancer (paragraph [0114], [0122]-[0123], [0126]). Thus, it would have been obvious to include the additional therapeutics in the pharmaceutical composition.
Claims 2-3 are rejected under 35 U.S.C. 103 as being unpatentable over US Patent Application Publication No. 2017/0173092 to Mulvey, of record IDS dated 5/01/24 (12 pages) further in view of Zhang et al. Interferon Regulatory Factor 7 Mediates Activation of Tap-2 by Epstein-Barr Virus Latent Membrane Protein 1. Journal of Virology, 2001. 75(1): 341-350, as applied to claims 1, 4-6, 9, 11, 13, 15-17, 19-22 and 24-28 above, and further in view of Genbank Accession No. U73036, earliest publication date 10/21/1996, 2 pages.
Claim 2 is directed to an embodiment wherein the dnIRF7 comprises an amino acid sequence of SEQ ID NO: 37. The claimed recitation of “an” amino acid sequence of SEQ ID NO: 37 does not require full length SEQ ID NO: 37. Rather, the broadest reasonable interpretation of “an” amino acid sequence of SEQ ID NO: 37 minimally requires any two consecutive amino acids listed within SEQ ID NO: 37.
Claim 3 is directed to an embodiment wherein the dnIRF7 comprises a nucleic acid sequence of SEQ ID NO: 36. The claimed recitation of “a” nucleic acid sequence of SEQ ID NO: 36 does not require full length SEQ ID NO: 36. Rather, the broadest reasonable interpretation of “a” nucleic acid sequence of SEQ ID NO: 36 minimally requires any two consecutive nucleic acids listed within SEQ ID NO: 36.
The disclosures of Mulvey and Zhang are applied as in the 103 rejection above, the content of which is incorporated herein in its entirety. Mulvey and Zhang combine to render obvious an oncolytic virus encoding an MHC I inhibitor of dominant negative IRF7.
Zhang discloses the IRF7 are transcription factors in the IRF family, who all share a conserved N-terminal DNA binding domain, that are located in the cytoplasm until they are activated and translocate into the nucleus (pages 341, 348-349, FIG.8). Zhang’s work tests the ability of 3 isoforms of IRF7: IRF-7A (encoding full-length IRF7), IRF-7B and IRF-7C, in conjunction with the IRF-7 dominant negative, for their ability to activate TAP2. IRF-7B lacks 29 amino acids in the middle of the protein in comparison to IRF-7A, and IRF-7C comprises a truncated protein of the N-terminus, lacking C-terminus of the protein (page 344). Zhang does not disclose the specific sequences encoded on any vector or protein therein, but does disclose the dominant negative IRF-7A comprises amino acids 1-12 and 103-503 of IRF-7A, and provides a schematic of the IRF-7 variants tested. Alignment of IRF-7A and IRF-7ADN taken and modified from Zhang’s FIG. 3B:
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Genbank No. U73036.1 discloses the protein and nucleic acid sequence encoding IFR-7A.
Claimed full length SEQ ID NO: 37 comprises 99.6% identity to amino acid sequences within IRF-7A (228-503) and IRF-7A DN (138 -413) of Zhang, wherein the only difference lies in the methionine
added to the 5’ end of the claimed SEQ ID (arrow):
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The nucleic acid sequences encoding the protein coding sequences of full length IRF-7A of U73036 =1512 nucleotides (1-1512 below). The nucleic acid sequences encoding the IRF-7A DN of Zhang (1-1242 below) are encompassed by nucleotides 1-36 and 307-1512 of those sequences of the full length IRF-7A. Claimed SEQ ID NO: 36 comprises 99% identity to nucleic acid sequences of U73036 of IRF-7A (678- 1512 nucleotides) and IRF-7A DN (414-1242) of Zhang, wherein the only difference lies in the atg encoding for methionine added to the 5’ end of claimed SEQ ID 36 (underlined at position):
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It would have been obvious to combine Mulvey and Zhang on an oncolytic virus encoding a dominant negative IRF-7 protein further with the known amino acid sequence and nucleotide sequence of IFR-7A, as disclosed by Genbank U73036. A skilled artisan would have been motivated to use the known protein and nucleic acid sequences to encode a dominant negative IRF-7 in the claimed oncolytic virus of Mulvey and Zhang. A skilled artisan would have had a reasonable expectation of success as dominant negative IRF-7 proteins were known in the art, and the sequences encoding the nucleic acids and the expressed proteins which could be used to generate them were known in the art at the time of the invention.
Claims 7-8, 12, 14 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over US Patent Application Publication No. 2017/0173092 to Mulvey, of record IDS dated 5/01/24 (12 pages) further in view of Zhang et al. Interferon Regulatory Factor 7 Mediates Activation of Tap-2 by Epstein-Barr Virus Latent Membrane Protein 1. Journal of Virology, 2001. 75(1): 341-350, as applied to claims 1, 4-6, 9, 11, 13, 15-17, 19-22 and 24-28 above, and further in view of WO2008/100292 to Frentzen, of record cited on Applicant’s IDS dated 5/1/24, and Rehm et al., Vaccinia Virus A35R Inhibits MHC Class II Antigen Presentation. Virology, 2010. 397: 176-186, of record, cited on Applicant’s IDS dated 05/01/24.
The disclosures of Mulvey and Zhang are applied as in the 103 rejection above, the content of which is incorporated herein in its entirety. Mulvey and Zhang combine to render obvious an oncolytic virus encoding an MHC I inhibitor of dominant negative IRF7.
With regard to claims 7-8, Mulvey discloses the viruses can encode additional heterologous genes which increases MHC II presentation (paragraph [0104]), but does not disclose wherein the oncolytic virus comprises a deletion of A35 or a WR158 in its genome which increases MHC II presentation, as required by instant claims 7-8.
Frentzen discloses recombinant oncolytic viruses comprising modifications of their genome, including deletions and/or insertions of one or more heterologous nucleic acids, wherein the viruses, or their encoded heterologous nucleic acids are capable generating immune responses towards tumor cells (Abstract, pages 5-6, 7-8, 10, 14-16, 18-20, 48-52, 64, 75, 81, 84-85, 92-95, 103, 107, 111-112, 121-127, 131-139, 149-150, 158-159, Examples). Frentzen discloses the viruses can be modified to cause altered expression of MHC presentation on tumor cells (page 108).
Frentzen discloses the viral genome comprises deletions including those that attenuate the viruses, including reducing toxicity or altering infectivity (page 49-50, 53-55, 62, 74-75, 103, 105, 158-159). Frentzen discloses deletion of the A35 gene from a virus attenuates the toxicity without affecting viral plaque size, viral replication, host range, or viral infectivity or spread (page 55). Frentzen generates poxviruses comprising a A35R gene deletion, wherein the deletion includes introduction of a multiple cloning site for insertion of heterologous nucleic acids, including strains: GLV-1j87, GLV-1j88 and GLV-1j89 (page 55, 173-174, 177, 187-189).
Rehm discloses vaccinia virus A35R gene inhibits MHC-II presentation and function in cells (Abstract, page 177, second column; 178, second column; page 180, FIG 1, 3D, 7, 8). Rehm discloses deletion of the A35R gene in vaccinia virus increases MHC-II presentation and function on infected cells (page 180, FIGs 7, 8). Rehm shows deletion of A35R increases anti-viral antigen production in infected cells (page 180, second column; page 183, first column). Rehm also discloses the vaccinia virus A35 gene is also known as the Western Reserve WR 158 gene (page 176, second column).
It would have been obvious to combine the oncolytic virus encoding an MHC I inhibitor, wherein the virus can increase MHC II expression of Mulvey in view of Zhang, with the disclosures of Frentzen and Rehm. A skilled artisan would be motivated to delete A35/WR158 in the viruses of Mulvey and Zhang because Frentzen discloses deletion attenuates the toxicity without affecting viral plaque size, viral replication, host range, or viral infectivity or spread, and Rehm shows that deletion of A35R increases MHC-II expression on infected cells, but also increases anti-viral antigen presentation on infected cells. A skilled artisan would have had a reasonable expectation of success because deleting A35 from the genome of an oncolytic virus to increase MHC II presentation was known at the time of the invention.
With regard to claim 12, wherein the oncolytic virus encodes for an interferon-gamma or dendritic cell maturation activation that is fused to a secretion sequence, Mulvey discloses the viruses encode additional heterologous genes, including heterologous GM-CSF, which is a dendritic cell maturation factor, which increases MHC II presentation, and interferon γ (paragraphs [0037]-[0038], [0101], [0104]). However, Mulvey does not disclose wherein the proteins are fused to a secretion signal as required by instant claim 12.
Frentzen discloses the oncolytic viruses encode heterologous proteins, wherein the proteins are fused to a secretion signal, and operably linked to an inducible promoter, so secretion from the tumor can be controlled (pages 14, 20, 163-167, and 263).
It would have been obvious to combine the oncolytic viruses encoding heterologous proteins of Mulvey in view of Zhang, with the disclosures of Frentzen, and operably link the heterologous protein to secretion sequences that are inducible, in order to control for their secretion, as taught by Frentzen.
With regard to claim 14, Mulvey discloses the oncolytic virus comprises an adeno- associated virus, an adenovirus, Newcastle disease virus (NDV), Reovirus (RV), a Myxoma virus (MYXV), Vaccinia virus (VV), and Vesicular Stomatitis virus (VSV), including Ankara and lister strains (paragraphs [0032], [0080]). However, Mulvey does not disclose the viruses include the poxviruses listed in the claim.
Frentzen discloses the oncolytic viruses can be adenovirus, Newcastle disease virus, vesicular stomatitis virus, reovirus, or a pox virus (page 17, 64). Frentzen discloses pox viruses include vaccinia viruses (page 49), as well as a pox viruse including a yatapoxvirus, a leporipoxvirus, a suipoxvirus, a molluscipoxvirus, an alphaentomopoxvirus, a capripoxvirus, an avipoxvirus, or a parapoxvirus (page 96). It would have been obvious to use a different pox virus for the oncolytic virus of Mulvey because Frentzen discloses other pox viruses can be used instead of vaccinia virus in oncolytic viruses.
With regard to claim 18, Mulvey discloses the oncolytic viruses comprise deletions in the genome wherein heterologous sequences are inserted (paragraph [0096]-[0097], [0105], [0144]). However, Mulvey nor Zhang disclose wherein the deletion are those listed in claim 18.
Frentzen discloses the insertions of heterologous nucleic acids can occur by replacing endogenous genes, including at N1L or K1L genes (pages 8-9, 18, 69). It would have been obvious to delete endogenous N1L or K1L when inserting heterologous genes in the genome of Mulvey, as Frentzen discloses such locations can be the site of deletion in an oncolytic virus.
Claim 10 is rejected under 35 U.S.C. 103 as being unpatentable over US Patent Application Publication No. 2017/0173092 to Mulvey, of record IDS dated 5/01/24 (12 pages) further in view of Zhang et al. Interferon Regulatory Factor 7 Mediates Activation of Tap-2 by Epstein-Barr Virus Latent Membrane Protein 1. Journal of Virology, 2001. 75(1): 341-350, as applied to claims 1, 4-6, 9, 11, 13, 15-17, 19-22 and 24-28 above, and further in view of Wang et al. An Optimized HMGB1 Expressed by Recombinant Rabies Virus Enhances Immunogenicity Through Activation of Dendritic Cells in Mice. Oncotarget, 2017. 8(48): 83539-83554, of record, cited on Applicant’s IDS dated 5/01/24. Claim 10 is drawn to wherein the heterologous nucleic acid encoding enhanced activation of MHC-II is HMGB1.
The disclosures of Mulvey and Zhang are applied as in the 103 rejection above, the content of which is incorporated herein in its entirety. Mulvey and Zhang combine to render obvious an oncolytic virus encoding an MHC I inhibitor of dominant negative IRF7, and wherein the oncolytic virus encodes heterologous transgenes, including GM-CSF which increases MHC II upregulation (paragraphs [0037], [0104]).
However, neither Mulvey nor Zhang disclose wherein the heterologous nucleic acid that increases MHC II presentation is HMGB1, as required by claim 10.
Wang discloses HMGB1 is a proinflammatory cytokine, and an immune stimulant (page 83540, second column). Wang shows over-expression of a secreted form of HMGB1 is capable of upregulating MHC-II on cells (page 83541, FIGs 1-3).
It would have been obvious to combine the disclosures of Mulvey and Zhang of an oncolytic virus encoding a heterologous MHC-I inhibitor, and a heterologous MHC-II enhancer, further with the disclosure of Wang. Mulvey discloses the expression of GM-CSF increases an anti-tumor immune response via MHC II upregulation (paragraphs [0037], [0104]). Wang discloses HMGB1 functions as a chemokine and can be used to increase MHC-II expression on cells. Thus, a person of ordinary skill in the art would have had a reasonable expectation of success in substituting HMGB1for GM-CSF because both explicitly taught as being useful for increasing MHC-II expression on cells. Therefore, these compositions are functional equivalents in the art, and substituting one for the other would have been obvious at the time of the invention. “When a patent ‘simply arranges old elements with each performing the same function it had been known to perform’ and yields no more than one would expect from such an arrangement, the combination is obvious.” See KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 (U.S. 2007) at 1395-1396, quoting Sakraida v. AG Pro, Inc., 425 U.S. 273 (1976) and In re Fout, 675 F.2d 297, 301 (CCPA 1982) (“Express suggestion to substitute one equivalent for another need not be present to render such substitution obvious”).
Claim 23 is rejected under 35 U.S.C. 103 as being unpatentable over US Patent Application Publication No. 2017/0173092 to Mulvey, of record IDS dated 5/01/24 (12 pages) further in view of Zhang et al. Interferon Regulatory Factor 7 Mediates Activation of Tap-2 by Epstein-Barr Virus Latent Membrane Protein 1. Journal of Virology, 2001. 75(1): 341-350, as applied to claims 1, 4-6, 9, 11, 13, 15-17, 19-22 and 24-28 above, and further in view of, US Patent Application Publication No. 2020/0268831 to Tobin, of record, cited on Applicant’s IDS dated 5/01/24. Claim 23 is drawn to wherein the pharmaceutical composition comprising the oncolytic virus comprises sorbitol.
The disclosures of Mulvey and Zhang are applied as in the 103 rejection above, the content of which is incorporated herein in its entirety. Mulvey and Zhang combine to render obvious a pharmaceutical composition comprising an oncolytic virus encoding an MHC I inhibitor of dominant negative IRF7 and an excipient.
However, neither Mulvey of Zhang disclose wherein the excipient includes sorbitol.
Tobin discloses administration of MHC class II inducing agents can be used to treat cancer (paragraphs [0030], [0037], [0040], [0074]-[0078] ). Tobin discloses MHC class II inducing agents include GM-CSF, IFN-gamma, or TNF-alpha (paragraphs [0030], [0076]). Tobin discloses the formulations can be administered as viral vectors (paragraph [0129]). Tobin discloses the formulations comprise pharmaceutically acceptable excipients, including antioxidants, preservatives, dextrose or sorbitol (paragraphs [0117], [0127]).
A person of ordinary skill in the art would have had a reasonable expectation of success in substituting excipients such as sorbitol for excipients such as dextrose because both explicitly taught as being useful excipients for pharmaceutical compositions. Therefore, these compositions are functional equivalents in the art, and substituting one for the other would have been obvious at the time of the invention. “When a patent ‘simply arranges old elements with each performing the same function it had been known to perform’ and yields no more than one would expect from such an arrangement, the combination is obvious.” See KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 (U.S. 2007) at 1395-1396, quoting Sakraida v. AG Pro, Inc., 425 U.S. 273 (1976) and In re Fout, 675 F.2d 297, 301 (CCPA 1982) (“Express suggestion to substitute one equivalent for another need not be present to render such substitution obvious”).
Conclusion
No claims are allowed.
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KAA
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633
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