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 .
Applicant’s response of 12/15/2025, including a substitute specification and replacement drawing sheets, has been received and entered into the application file.
Claims 1-3, 6-9, 13, 21, and 23 were amended in the claim set filed 12/15/2025.
Claim 24 was added in the claim set filed 12/15/2025.
Accordingly, claims 1-13, 15-17, and 20-24 are pending and under consideration.
Status of Prior Objections/Rejections
RE: Specification
►The specification was previously objected to for various minor informalities, as well as embedded hyperlinks or other browser-executable code.
The substitute specification filed 12/15/2025 has obviated the basis of the prior objections. The objections of record are hereby withdrawn.
RE: Drawings
►Figures 4, 6, 8, 10, and 20A were previously objected to for being of insufficient quality to be clearly legible and interpretable.
The replacement drawing sheets filed 12/15/2025 have obviated the basis of the prior objections. The objections of record are hereby withdrawn.
RE: Claim Objections
►Claims 1, 10, 13, 21, and 23 were previously objected to for various minor informalities.
The amendments to the instant claim set filed 12/15/2025 have obviated the basis of most, but not all, of the prior objections. Those objections not repeated below are hereby withdrawn.
With specific regard to instant claim 21, the objection of record indicated that it would be remedial to amend the claim language to recite administration of the virus “at a dose of 1 x 105 to 5 x 109…” (bolded emphasis added). This correction was not incorporated into the claim set filed 12/15/2025. Accordingly, the objection of record regarding instant claim 21 is maintained. Furthermore, the amendments to the claim set filed 12/15/2025 have necessitated new grounds of objection, which are set forth below.
RE: Claim Rejections - 35 USC § 112(b)
►Claims 1-3, and 6-9 were previously 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.
The amendments to the claims filed 12/15/2025 have obviated the basis of the prior rejections. The rejections of record are hereby withdrawn.
RE: Claim Rejections - 35 USC § 103
►Claims 1-4, 8, 12, 13, 20 and 22 were previously rejected under 35 U.S.C. 103 as being unpatentable over WO 2009/111892 A1 (hereinafter Bell) in view of Senkevich et al., 2000.
►Claims 5, 9-11, 15-17, 21, and 23 were previously rejected under 35 U.S.C. 103 as being unpatentable over WO 2009/111892 A1 (hereinafter Bell) in view of Senkevich et al., 2000 as applied to claims 1, 3, and 20, and further in view of US 2013/0071430 A1 (hereinafter Nakamura) and Andorsky and Timmerman, 2008.
►Claim 6 was previously rejected under 35 U.S.C. 103 as being unpatentable over WO 2009/111892 A1 (hereinafter Bell) in view of Senkevich et al., 2000 as applied to claim 3, and further in view of Jiang and Doudna, 2017.
►Claim 7 was previously rejected under 35 U.S.C. 103 as being unpatentable over WO 2009/111892 A1 (hereinafter Bell) in view of Senkevich et al., 2000, US 2013/0071430 A1 (hereinafter Nakamura), and Andorsky and Timmerman, 2008 as applied to claim 5, and further in view of Jiang and Doudna, 2017.
Applicant has traversed the rejection of record, asserting that Bell does not disclose the term “essential gene” as set forth in the non-final rejection dated 09/19/2025. Applicant states that “Bell only teaches to specifically select a microRNA target gene, such that the corresponding protein has an essential role in viral growth and replication” (bolded emphasis from Applicant’s Remarks filed 12/15/2025). Applicant further asserts that Bell teaches that the function of the protein of the selected gene set forth above is to counteract antiviral responses. Applicant acknowledges that Senkevich et al., 2000 teaches that the E10R gene is essential for vaccinia virus replication but asserts that “it seems unlikely that [E10R] would be needed for the synthesis of viral DNA or late proteins.”
In response, this is not found persuasive. While the Examiner acknowledges that Bell does not disclose the term “essential gene,” the disclosure of Bell, as reflected in Applicant’s response, does explicitly state that “the microRNA target gene may be selected…by virtue of the fact that the protein has an essential role in viral growth and replication” (bolded emphasis added). As set forth in the non-final rejection dated 09/19/2025, Senkevich et al., 2000 discloses that the E10R gene is essential for vaccinia virus replication (page 245, column 1, paragraph 1; bolded emphasis added), which is consistent with the disclosure of Bell, as reflected in Applicant’s response. Furthermore, per the disclosure of Senkevich et al., 2000 which teaches the essential role of the E10R gene in vaccinia virus replication, the E10R gene must therefore necessarily counteract antiviral responses per the disclosure of Bell, as stated by Applicant. Thus, it is not found persuasive that the disclosure of Bell, when combined with the disclosure of Senkevich et al., 2000, would not render the claimed invention obvious to someone of ordinary skill in the art prior to the effective filing date of the claimed invention.
Applicant further asserts that the claimed invention achieves unexpected technical effects by selecting “a specific essential gene E10R from the genome of an oncolytic vaccinia virus” (bolded emphasis from Applicant’s Remarks filed 12/15/2025). While the Examiner acknowledges that Applicant has disclosed that the instantly claimed invention functions robustly, these same results would have been obtained from a person of ordinary skill in the art combining the disclosures of Bell and Senkevich et al., 2000, both of which were publicly available prior to the effective filing date of the claimed invention, as set forth in greater detail below.
Finally, Applicant asserts that Nakamura does not disclose or teach to incorporate a target sequence of a microRNA into the 3’ UTR of the E10R gene of an oncolytic vaccinia virus and that Andorsky and Timmerman, 2008 and Jiang and Doudna, 2017 do not involve a recombinant oncolytic vaccinia virus.
In response, the Examiner notes that the disclosure of Nakamura was applied to teach the advantages of engineering vaccinia viruses to further comprise an additional foreign, therapeutic gene that can be used in the treatment of cancer, such as interleukins. Furthermore, Andorsky and Timmerman, 2008, as well as Jiang and Doudna, 2017 were applied to teach specific therapeutic interleukin species, as well as methods of disrupting genes. These disclosures were not applied to teach a recombinant oncolytic vaccinia virus on their own, but rather to teach the claimed components, all of which would have been available to a person of ordinary skill in the art prior to the effective filing date of the claimed invention.
Accordingly, the rejections of record are hereby maintained.
RE: Double Patenting
►Claims 1, 3, 5-13, 15-17, and 20-23 were previously provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 6-12, and 15-18 of copending Application No. 16/650,076 (corresponds to US 20200289591 A1) in view of WO 2009/111892 A1 (hereinafter Bell) and Senkevich et al., 2000.
Applicant has traversed the rejection of record, asserting that copending Application No. 16/650,076 does not involve an isolated recombinant oncolytic vaccinia virus wherein a 3’ untranslated region of an E10R gene in the recombinant oncolytic vaccinia virus genome is integrated with a target sequence of the microRNA. Applicant asserts that Bell does not disclose or teach to incorporate a target sequence of a microRNA into the 3’ UTR of the E10R gene.
In response, this is not found persuasive. As set forth above regarding the claim rejections under 35 U.S.C. § 103, while the Examiner acknowledges that Bell does not disclose the term “essential gene,” the disclosure of Bell, as reflected in Applicant’s response, does explicitly state that “the microRNA target gene may be selected…by virtue of the fact that the protein has an essential role in viral growth and replication” (bolded emphasis added). As set forth in the non-final rejection dated 09/19/2025, Senkevich et al., 2000 discloses that the E10R gene is essential for vaccinia virus replication (page 245, column 1, paragraph 1; bolded emphasis added), which is consistent with the disclosure of Bell, as reflected in Applicant’s response. Furthermore, per the disclosure of Senkevich et al., 2000 which teaches the essential role of the E10R gene in vaccinia virus replication, the E10R gene must therefore necessarily counteract antiviral responses per the disclosure of Bell, as stated by Applicant. Thus, it is not found persuasive that the disclosure of Bell, when combined with the disclosure of Senkevich et al., 2000, would not render the instant and copending applications obvious over each other.
New/Maintained Grounds of Rejection/Objection
Claim Objections
Claims 7, 13, and 21 are objected to because of the following informalities:
Amended claim 7 recites “the exogenous IL-21 gene is inserted into a TK locus, thereby causing functional defect of the TK gene” (bolded emphasis added). The bolded “functional defect” does not comport with standard grammatical and/or linguistic conventions. It would be remedial to amend the instant claim such that it does comport with these conventions, for example by mirroring the recitations of instant claims 6 and 8. One example of such a recitation is ”the recombinant oncolytic vaccinia virus according to claim 5, wherein the exogenous IL-21 gene is inserted into a TK locus, thereby rendering the TK gene functionally deficient” (bolded emphasis added).
Amended claim 13 recites “the pharmaceutical composition comprises the recombinant oncolytic vaccinia virus at a dose of 1 ͯ 105 to 5 ͯ 109 plaque forming unit” (bolded emphasis added). While this amendment obviates the basis of the prior objections of record in that the acronym “pfu” is properly defined in the instant claim set, this recitation does not comport with standard grammatical and/or linguist conventions. The recited virus dose does not match the singular “unit” of “plaque forming unit.” While units of measurement are not conventionally pluralized when acronymized, they must match the recited numerical values. For example, a recitation of “30 mL” is proper, while a recitation of “30 milliliter” is improper and should instead be recited as “30 milliliters.” Similarly, it would be remedial in the instant claim to recite “the pharmaceutical composition comprises the recombinant oncolytic vaccinia virus at a dose of 1 ͯ 105 to 5 ͯ 109 plaque forming units” (bolded emphasis added).
Amended claim 21 recites “the recombinant oncolytic vaccinia virus is administered at dose of 1 ͯ 105 to 5 ͯ 109 plaque forming unit” (bolded and underlined emphasis added). As set forth in the previous action, the method recited at claim 21 is grammatically improper, as it lacks an such as “a” article preceding “dose.” It would be remedial to amend the instant claim to recite “administered at a dose” (bolded emphasis added), as previously indicated. Furthermore, as set forth above, while this amendment obviates the basis of one of the prior objections of record in that the acronym “pfu” is properly defined in the instant claim set, this recitation does not comport with standard grammatical and/or linguist conventions. The recited virus dose does not match the singular “unit” of “plaque forming unit.” While units of measurement are not conventionally pluralized when acronymized, they must match the recited numerical values. For example, a recitation of “30 mL” is proper, while a recitation of “30 milliliter” is improper and should instead be recited as “30 milliliters.” Similarly, it would be remedial in the instant claim to recite “the pharmaceutical composition comprises the recombinant oncolytic vaccinia virus at a dose of 1 ͯ 105 to 5 ͯ 109 plaque forming units” (bolded emphasis added).
Appropriate correction is required.
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, 3, 5-13, 15-17, and 20-23 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 6-12, and 15-18 of copending Application No. 16/650,076 (corresponds to US 20200289591 A1; of record) in view of WO 2009/111892 A1 (hereinafter Bell; of record) and Senkevich et al., 2000 (of record).
Copending application ‘076 is drawn to isolated recombinant oncolytic vaccinia viruses, pharmaceutical compositions and uses thereof for drugs for treatment of tumors and/or cancers (paragraph [0001]). Claim 1 of copending application ‘076 recites “an isolated recombinant oncolytic vaccinia virus, wherein the recombinant oncolytic vaccinia virus is functionally deficient in the TK gene and the VGF gene, and comprises an exogenous IL-21 gene integrated into its genome, wherein the recombinant oncolytic vaccinia virus is capable of expressing the exogenous IL-21 gene in tumor cells, and wherein: the recombinant oncolytic vaccinia virus is a WR strain, and the exogenous IL-21 gene is inserted into the TK gene.” In comparison, claims 1, 3, and 5-9 of the instant application also recite “an isolated recombinant oncolytic vaccinia virus” (claim 1) of “the WR strain” (claim 9) “wherein the recombinant oncolytic vaccinia virus is functionally deficient in the TK gene and/or in the VGF gene” (claim 3) and “wherein the genome of the recombinant oncolytic vaccinia virus is integrated with an exogenous IL-21 gene…capable of being expressed in tumor cells” (claim 5). The instant application further recites that “the TK gene is rendered functionally deficient via the insertion of an exogenous nucleotide sequence into the TK locus” (claim 6) such as an “exogenous IL-21 gene…inserted into the TK locus” (claim 7). Additionally, the instant application recites that “the VGF gene is rendered functionally deficient by being knocked out” (claim 8).
While copending claim 1 does not recite the miRNA target sites integrated with the 3’-UTR of the vaccinia E10R gene, Bell discloses microRNA (miRNA)-mediated oncolytic virus targeting of cancer/tumor cells by integrating a target site for an miRNA into the 3’-UTR of an essential gene such that expression of the essential gene is inhibited in normal mammalian cells but not in mammalian tumor cells (paragraphs [0017], [0021], and [0023]), as claimed in copending application ‘076. Bell discloses that such oncolytic viruses may be vaccinia viruses (paragraph [0021]). While Bell does not disclose that the essential gene with an integrated target site for an miRNA in its associated 3’-UTR is E10R, this deficiency is cured by Senkevich et al., 2000, which discloses that the E10R gene is essential for vaccinia virus replication (page 245, column 1, paragraph 1). Thus, Bell and Senkevich et al., 2000, in combination with copending claim 1, collectively disclose an isolated recombinant oncolytic vaccinia virus capable of expressing IL-21 specifically in cancer cells, satisfying each and every limitation of instant claims 1, 3, and 5-9. It would have been obvious to someone of ordinary skill in the art prior to the effective filing date of the claimed invention to apply the teachings of Bell and Senkevich et al., 2000 regarding miRNA-mediated restriction of viral expression to the recombinant vaccinia virus of the copending application to predictably produce a recombinant vaccinia virus with its expression restricted to tumor cells, as claimed in both the instant and copending applications.
Claim 4 of copending application ‘076 recites “the VGF gene is rendered functionally deficient by being knocked out or via insertion of an exogenous nucleotide sequence into the VGF locus.” In comparison, instant claim 8 recites “the VGF gene is rendered functionally deficient by being knocked out or via insertion of an exogenous nucleotide sequence into the VGF locus.” Thus, claim 4 of copending application ‘076 anticipates each and every additional limitation of instant claim 8.
Claim 6 of copending application ‘076 recites “the genome of the recombinant oncolytic vaccinia virus further comprises an exogenous screening gene that includes the gpt gene, the LacZ gene, or combinations thereof.” In comparison, instant claim 10 recites “the genome of the recombinant oncolytic vaccinia virus is further integrated with an exogenous screening gene which includes [a] gpt gene and/or [a] LacZ gene.” Thus, claim 6 of copending application ‘076 anticipates each and every additional limitation of instant claim 10.
Claim 7 of copending application ‘076 recites “the exogenous IL-21 gene is derived from mouse or human.” In comparison, instant claim 11 recites “the exogenous IL-21 gene is derived from mouse or human.” Thus, claim 7 of copending application ‘076 anticipates each and every additional limitation of instant claim 11.
Claim 8 of copending application ‘076 recites “a pharmaceutical composition, wherein the pharmaceutical composition comprises the recombinant oncolytic vaccinia virus according to claim 1 as an active ingredient, and a pharmaceutically acceptable excipient.” In comparison, instant claim 12 recites “a pharmaceutical composition, wherein the pharmaceutical composition comprises the recombinant oncolytic vaccinia virus according to claim 1 as an active ingredient, and a pharmaceutically acceptable excipient.” Thus, claim 8 of copending application ‘076 anticipates each and every additional limitation of instant claim 12.
Claim 9 of copending application ‘076 recites “the pharmaceutical composition comprises the recombinant oncolytic vaccinia virus at a dose of 1 x 105-5 x 109 pfu.” In comparison, instant claim 13 recites “the pharmaceutical composition comprises the recombinant oncolytic vaccinia virus at a dose of 1 x 105 to 5 x 109 pfu.” Thus, claim 9 of copending application ‘076 anticipates each and every additional limitation of instant claim 13.
Claim 10 of copending application ‘076 recites “the recombinant oncolytic vaccinia virus is formulated for intratumoral or intravenous administration.” In comparison, instant claim 22 recites “the recombinant oncolytic vaccinia virus is administered by intratumoral injection or intravenous administration.” Thus, claim 10 of copending application ‘076 anticipates each and every additional limitation of instant claim 22.
Claim 11 of copending application ‘076 recites “a vector for preparing the recombinant oncolytic vaccinia virus…wherein the vector comprises an exogenous IL-21 gene under the control of a promoter.” In comparison, instant claims 15 and 16 respectively recite “a vector for preparing the recombinant oncolytic vaccinia virus” “wherein the vector comprises an exogenous IL-21 gene controlled by a promoter.” Thus, claim 11 of copending application ‘076 anticipates each and every additional limitation of instant claims 15 and 16.
Claim 12 of copending application ‘076 recites “a host cell comprising the vector according to claim 11.” In comparison, instant claim 17 recites “a host cell comprising the vector according to claim 15.” As set forth above regarding copending claim 11 and instant claims 15 and 16, claim 11 of copending application ‘076 anticipates each and every additional limitation of instant claims 15 and 16. Thus, claim 12 of copending application ‘076 also reads on instant claim 17.
Finally, claims 15-18 of copending application ‘076 recite “a method for treating tumors and/or cancers, comprising administering the recombinant oncolytic vaccinia virus…to a tumor and/or cancer patient” (claim 15) “at a dose of 1 x 105-5 x 109 pfu/day, once a day, for 1-6 consecutive days” (claim 16) via intratumoral or intravenous administration (claim 17). This treatment regimen is recited to treat “lung cancer, melanoma, head and neck cancer, liver cancer, brain cancer, colorectal cancer, bladder cancer, breast cancer, ovarian cancer, uterus cancer, cervical cancer, lymphoma, stomach cancer, esophageal cancer, kidney cancer, prostate cancer, pancreatic cancer, leukemia, bone cancer, [and] testicular cancer” (claim 18). In comparison, instant claims 20-23 also recite “a method for treating tumors and/or cancers, comprising administering the recombinant oncolytic vaccinia virus…to a tumor and/or cancer patient” (claim 20) “at a dose of 1 x 105 to 5 x 109 pfu/day, once a day, for 1-6 consecutive days” (claim 21) via “intratumoral injection or intravenous administration” (claim 22). This treatment regimen is recited to treat “lung cancer, melanoma, head and neck cancer, liver cancer, intracranial tumor, colorectal cancer, bladder cancer, breast cancer, ovarian cancer, uterus cancer, cervical cancer, gastric cancer, esophageal cancer, kidney cancer, prostate cancer, pancreatic cancer, lymphatic cancer, leukemia, bone cancer, testicular cancer and osteosarcoma” (claim 23).
This is a provisional nonstatutory double patenting rejection.
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.
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, 8, 12, 13, 20 and 22 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2009/111892 A1 (hereinafter Bell; of record) in view of Senkevich et al., 2000 (of record).
With regard to amended instant claim 1, which recites “an isolated recombinant oncolytic vaccinia virus, wherein the recombinant oncolytic vaccinia virus is capable of being regulated by a microRNA which has a lower expression level in tumor cells of a mammal than in normal cells of the same mammal, wherein a 3’ UTR region of an E10R gene in the recombinant oncolytic vaccinia genome is integrated with a target sequence of the microRNA,” Bell discloses microRNA (miRNA)-mediated oncolytic virus targeting of cancer/tumor cells by integrating a target site for an miRNA into the 3’-UTR of an essential gene such that expression of the essential gene is inhibited in normal mammalian cells but not in mammalian tumor cells (paragraphs [0017], [0021], and [0023]). Bell discloses that such oncolytic viruses may be vaccinia viruses, such as a vaccinia virus with an miRNA target site engineered into a thymidine kinase (TK) gene (paragraphs [0021] and [0036]). While Bell does not disclose that the essential gene with an integrated target site for an miRNA in its associated 3’-UTR is E10R, this deficiency is cured by Senkevich et al., 2000. Senkevich et al., 2000 discloses that the E10R gene is essential for vaccinia virus replication (page 245, column 1, paragraph 1). Thus, Bell and Senkevich et al., 2000 collectively disclose an isolated recombinant oncolytic vaccinia virus meeting each and every limitation of instant claim 1, as set forth in greater detail below.
With regard to amended instant claim 2, which recites “the microRNA [of the recombinant oncolytic vaccinia virus according to claim 1] is selected from a group consisting of miR-9…”, Bell discloses that miRNAs such as miR-9 are expressed at very low levels in cancer cells as compared to non-cancer cells, facilitating expression of viral genes in selected host cells such as cancer cells (paragraphs [0016] and [0020]). Thus, Bell discloses that the microRNA associated with a therapeutic recombinant oncolytic virus (i.e. vaccinia virus) may be miR-9, as instantly claimed.
With regard to amended instant claim 3, which recites “the recombinant oncolytic vaccinia virus is functionally deficient in a TK gene and/or in a VGF gene,” Bell discloses that replication of viruses can be restricted to cancer cells with high TK activity by deleting the viral versions of TK, or other genes upregulated in cancer cells. Bell further discloses that vaccinia viruses with TK and VGF deletions to improve oncolytic and/or gene delivery capabilities were known in the art at the time of filing (paragraph [0008]). Thus, Bell discloses a recombinant oncolytic virus (i.e. vaccinia virus) with a non-functional endogenous TK gene and/or VGF gene, as instantly claimed.
With regard to claim 4, which recites “the target sequence of the microRNA [of the recombinant oncolytic vaccinia virus according to claim 1] is repeated and comprised of 2-8 repeats,” Bell further discloses that it may be desirable for the viruses taught therein to carry multiple repeats of, or repeats of different, miRNA target sites (paragraphs [0036]). Bell explicitly discloses engineered viruses comprising three repeats of an miRNA target sequence (paragraph [0066]). Thus, Bell discloses that the therapeutic recombinant oncolytic viruses (i.e. vaccinia viruses) taught therein comprises 2-8 repeated miRNA target sites, as instantly claimed.
With regard to amended instant claim 8, which recites “the VGF gene [of the recombinant oncolytic vaccinia virus according to claim 3] is rendered functionally deficient by being knocked out…”, as set forth above regarding instant claim 3, Bell discloses that vaccinia viruses with TK and VGF deletions to improve oncolytic and/or gene delivery capabilities were known in the art at the time of filing (paragraph [0008]). It is considered that these TK and VGF deletions read on the instantly claimed knockouts. Thus, Bell discloses a recombinant oncolytic virus (i.e. vaccinia virus) with a knocked out VGF gene, as instantly claimed.
Given that Bell discloses miRNA-mediated oncolytic viruses (i.e. vaccinia viruses) targeting of mammalian cancer/tumor cells by integrating multiple target sites for an miRNA (i.e. miR-9) into the 3’-UTR of an essential gene and deleting the endogenous TK and/or VGF genes such that expression of the essential gene is inhibited in normal mammalian cells but not in mammalian tumor cells, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to integrate multiple target sites for an miRNA (i.e. miR-9) into the essential E10R gene of vaccinia virus (as disclosed in Senkevich et al., 2000) to predictably generate a recombinant oncolytic vaccinia virus capable of selectively targeting mammalian cancer/tumor cells, thereby treating said cancer. One would have been motivated to make such a modification in order to receive the expected benefit of generating a recombinant oncolytic vaccinia virus capable of selectively targeting mammalian cancer/tumor cells, thereby treating said cancer.
With regard to claim 12, which recites “a pharmaceutical composition, wherein the pharmaceutical composition comprises the recombinant oncolytic vaccinia virus according to claim 1 as an active ingredient, and a pharmaceutically acceptable excipient,” as set forth above regarding instant claim 1, Bell and Senkevich et al., 2000 collectively disclose an isolated recombinant oncolytic vaccinia virus meeting each and every limitation of instant claim 1. Additionally, Bell discloses that the therapeutic recombinant oncolytic viruses (i.e. vaccinia viruses) taught therein may be delivered to patients in a pharmaceutical composition further comprising a pharmaceutically acceptable carrier or excipient (paragraph [0047]). Thus, Bell discloses a pharmaceutical composition comprising a recombinant oncolytic virus (i.e. vaccinia virus), as instantly claimed.
With regard to amended instant claim 13, which recites “the pharmaceutical composition [according to claim 12] comprises the recombinant oncolytic vaccinia virus at a dose of 1 x 105 to 5 x 109 plaque forming unit[s],” Bell further discloses that the therapeutic recombinant oncolytic viruses (i.e. vaccinia viruses) taught therein may be administered as “unit doses,” which contain a predetermined-quantity of the therapeutic composition and are described in terms of plaque forming units (pfu) for a viral construct ranging from 105 to 109 pfu and higher (paragraph [0056]). While Bell does not specifically disclose the instantly claimed dose range, as set forth in MPEP § 2144.05(II)(A), optimization of prior art conditions through routine experimentation is considered to be obvious to those of ordinary skill in the art. Therefore, given that Bell discloses therapeutic doses with pfus of the same order of magnitude of the instant application, it would have been obvious to someone of ordinary skill in the art to practice routine experimentation to optimize this therapeutic dose. Thus, Bell discloses the instantly claimed pharmaceutical composition.
Given that Bell and Senkevich et al., 2000 collectively disclose the recombinant oncolytic vaccinia virus of instant claim 1, and that Bell further discloses that this virus may be delivered in a pharmaceutical composition comprising unit doses containing a predetermined quantity of the virus taught therein ranging from 105 to 109 pfu and higher, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to practice routine experimentation to predictably optimize this therapeutic dose within the disclosed range of orders of magnitude. One would have been motivated to make such a modification in order to receive the expected benefit of optimizing this therapeutic dose within the disclosed range of orders of magnitude.
With regard to claim 20, which recites “a method for treating tumors and/or cancers, comprising administering the recombinant oncolytic vaccinia virus according to claim 1 to a tumor and/or cancer patient,” as set forth above regarding instant claim 1, Bell and Senkevich et al., 2000 collectively disclose an isolated recombinant oncolytic vaccinia virus meeting each and every limitation of instant claim 1. Additionally, Bell discloses that the recombinant oncolytic viruses (i.e. vaccinia viruses) taught therein may be administered to treat cancers (paragraphs [0021], [0047], and [0056]). Thus, Bell discloses a method for treating tumors and/or cancers, said method comprising administering recombinant oncolytic viruses (i.e. vaccinia viruses) to affected patients, as instantly claimed.
With regard to claim 22, which recites “the recombinant oncolytic vaccinia virus [of the method according to claim 20] is administered by intratumoral injection or intravenous administration,” Bell discloses that the recombinant oncolytic viruses (i.e. vaccinia viruses) taught therein may be administered to the host intravenously or intratumorally (paragraph [0023]). Thus, Bell discloses intratumoral or intravenous administration of recombinant oncolytic viruses (i.e. vaccinia viruses) to affected patients, as instantly claimed.
Given that Bell and Senkevich et al., 2000 collectively disclose the recombinant oncolytic vaccinia virus of instant claim 1, and that Bell further discloses that the recombinant oncolytic viruses (i.e. vaccinia viruses) taught therein may be administered to the host intravenously or intratumorally, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to administer recombinant oncolytic viruses (i.e. vaccinia viruses) to the host intravenously or intratumorally to predictably deliver the recombinant oncolytic viruses to patients in need thereof to treat diseases such as cancer. One would have been motivated to make such a modification in order to receive the expected benefit of delivering the recombinant oncolytic viruses to patients in need thereof to treat diseases such as cancer.
Claims 5, 9-11, 15-17, 21, 23, and 24 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2009/111892 A1 (hereinafter Bell; of record) in view of Senkevich et al., 2000 (of record) as applied to claims 1, 3, and 20 above, and further in view of US 2013/0071430 A1 (hereinafter Nakamura; of record) and Andorsky and Timmerman, 2008 (of record).
The combined disclosures of Bell and Senkevich et al., 2000 are described above and applied as before. However, these disclosures do not teach the expression of exogenous IL-21 of instant claims 5 and 11, the vaccinia virus strain of instant claim 9, the exogenous screening gene of instant claim 10, the vector and host cell comprising the same of instant claims 15-17, the treatment regimen of instant claim 21, or the cancers of instant claim 23 of instant claim.
With regard to claim 5, which recites “the genome of the recombinant oncolytic vaccinia virus [according to claim 3] is integrated with an exogenous IL-21 gene…capable of being expressed in tumor cells,” Nakamura discloses a vaccinia virus that specifically proliferates in a cancer cell, as controlled by miRNA targeting, and destroys the cancer cell, thereby treating the cancer (abstract). The vaccinia viruses disclosed in Nakamura are further disclosed to comprise an additional foreign, therapeutic gene that can be used in the treatment of cancer (paragraphs [0012], [0057], and [0059]). While Nakamura discloses a number of interleukins that may be said foreign, therapeutic gene (paragraph [0059]), they do not specifically disclose IL-21. However, Andorsky and Timmerman, 2008 disclose that IL-21 has potent antitumor effects against a variety of types of tumors, while also displaying acceptable clinical toxicity (page 1304, column 2, paragraph 2). Andorsky and Timmerman, 2008 further disclose that IL-21 has been utilized in a number of clinical trials to treat multiple cancers, including metastatic melanoma, renal cell carcinoma, and ovarian carcinoma, among others (Table 1).
With regard to amended instant claim 9, which recites “the recombinant oncolytic vaccinia virus [according to claim 1] is a WR strain or a Wyeth strain,” Nakamura discloses that vaccinia virus strains capable of producing the recombinant vaccinia virus taught therein include a Wyeth strain (paragraph [0038]), as instantly claimed.
With regard to amended instant claim 10, which recites “the genome of the recombinant oncolytic vaccinia virus [according to claim 1] is further integrated with an exogenous screening gene which includes a gpt gene and/or a LacZ gene,” Nakamura further discloses that the therapeutic recombinant vaccinia viruses taught therein may further comprise foreign marker/reporter genes such as the LacZ gene (paragraph [0057]), which reads on the instantly claimed exogenous screening gene LacZ.
With regard to claim 11, which recites “the exogenous IL-21 gene [of the recombinant vaccinia virus according to claim 5] is derived from mouse or human,” Andorsky and Timmerman, 2008 disclose that recombinant human IL-21 has been commercially developed for clinical testing against human cancers (section 2.3).
Given that Bell and Senkevich et al., 2000 collectively disclose the recombinant oncolytic vaccinia virus of instant claims 1 and 3 (as set forth above), that Nakamura discloses a vaccinia virus (i.e. of the Wyeth strain) that specifically proliferates and expresses a therapeutic and/or screening gene in cancer cells due to miRNA expression and binding, and that Andorsky and Timmerman, 2008 disclose that IL-21 (i.e. recombinant human IL-21) has potent antitumor effects against a variety of types of tumors, while also displaying acceptable clinical toxicity, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to modify the recombinant oncolytic vaccinia virus of Bell and Senkevich et al., 2000 to further express a therapeutic gene such as IL-21 in cancer cells (as disclosed in Nakamura and Andorsky and Timmerman, 2008) to predictably express IL-21 specifically in cancer cells, thereby treating the cancer. One would have been motivated to make such a modification in order to receive the expected benefit of expressing IL-21 specifically in cancer cells, thereby treating the cancer.
With regard to claim 15, which recites “a vector for preparing the recombinant oncolytic vaccinia virus according to claim 1,” as set forth above, Bell and Senkevich et al., 2000 collectively disclose the recombinant oncolytic vaccinia virus of instant claim 1, while Nakamura similarly discloses a vaccinia virus that specifically proliferates in a cancer cell, as controlled by miRNA targeting, and destroys the cancer cell, thereby treating the cancer (abstract). Nakamura further discloses the preparation of said recombinant oncolytic vaccinia virus via introduction of a transfer vector carrying the therapeutic foreign gene into vaccinia virus-infected cells (paragraph [0061]). Thus, Nakamura discloses a vector for preparing the recombinant oncolytic vaccinia virus, as instantly claimed.
With regard to claim 16, which recites “the vector [according to claim 15] comprises an exogenous IL-21 gene controlled by a promoter,” as set forth above, the vaccinia viruses disclosed in Nakamura are further disclosed to comprise an additional foreign, therapeutic gene that can be used in the treatment of cancer (paragraphs [0012], [0057], and [0059]), such as IL-21, as disclosed in Andorsky and Timmerman, 2008 (page 1304, column 2, paragraph 2; Table 1). Additionally, Nakamura discloses a vector for preparing the recombinant oncolytic vaccinia virus, said vector carrying the desired therapeutic foreign gene under the control of an appropriate promoter operably linked upstream of the foreign gene for introduction into vaccinia virus-infected cells (paragraphs [0061] and [0063]). Thus, Nakamura discloses a vector for preparing the recombinant oncolytic vaccinia virus, said vector comprising an exogenous IL-21 gene controlled by a promoter, as instantly claimed.
With regard to claim 17, which recites “a host cell comprising the vector according to claim 15,” as set forth above regarding claim 15, Nakamura discloses the preparation of a recombinant oncolytic vaccinia virus via introduction of a transfer vector carrying the therapeutic foreign gene into vaccinia virus-infected cells (paragraph [0061]). Given that the instant specification is silent as to any special definition of “a host cell,” it is considered that the vaccinia virus-infected cells into which the transfer vector carrying the therapeutic foreign gene is introduced (and ultimately integrated) read on the instantly claimed host cell. Thus, Nakamura discloses a host cell comprising a vector for preparing a recombinant oncolytic vaccinia virus, as instantly claimed.
Given that Bell and Senkevich et al., 2000 collectively disclose the recombinant oncolytic vaccinia virus of instant claim 1 (as set forth above), that Andorsky and Timmerman, 2008 disclose that IL-21 (i.e. recombinant human IL-21) has potent antitumor effects against a variety of types of tumors, while also displaying acceptable clinical toxicity, and that Nakamura discloses preparation of a vaccinia virus (i.e. of the Wyeth strain) that specifically proliferates and expresses a therapeutic and/or screening gene in cancer cells by introducing a vector comprising a foreign gene under the control of a promoter into vaccinia virus-infected cells, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to prepare the recombinant oncolytic vaccinia virus of instant claim 1 using the vector methodology of Nakamura to predictably produce a recombinant oncolytic vaccinia virus that specifically proliferates and expresses a therapeutic and/or screening gene in cancer cells due to miRNA binding and expression patterns. One would have been motivated to make such a modification in order to receive the expected benefit of producing a recombinant oncolytic vaccinia virus that specifically proliferates and expresses a therapeutic and/or screening gene in cancer cells due to miRNA binding and expression patterns.
With regard to amended instant claim 21, which recites “the recombinant oncolytic vaccinia virus [of the method of claim 20] is administered at [a] dose of 1 x 105 to 5 x 109 plaque forming unit[s], once per day for 1-6 days, or once every two days for 1-6 consecutive times,” as set forth above regarding instant claim 13, Bell discloses that the therapeutic recombinant oncolytic viruses (i.e. vaccinia viruses) taught therein may be administered as “unit doses,” which contain a predetermined-quantity of the therapeutic composition and are described in terms of plaque forming units (pfu) for a viral construct ranging from 105 to 109 pfu and higher (paragraph [0056]). While Bell does not specifically disclose the instantly claimed dose range, as set forth in MPEP § 2144.05(II)(A), optimization of prior art conditions through routine experimentation is considered to be obvious to those of ordinary skill in the art. Therefore, given that Bell discloses therapeutic doses with pfus of the same order of magnitude of the instant application, it would have been obvious to someone of ordinary skill in the art to practice routine experimentation to optimize this therapeutic dose. While Bell discloses continuous perfusion of these recombinant oncolytic vaccinia viruses (paragraph [0055]), Nakamura discloses administration of 107 pfu of the viruses taught therein into murine tumors at days 0, 3, and 6 for a total of three times (paragraph [0079]). Thus, while Nakamura also does not specifically disclose the instantly claimed dosing regimen, as set forth above, optimization of prior art conditions through routine experimentation is considered to be obvious to those of ordinary skill in the art (MPEP § 2144.05(II)(A)). Thus, it is considered that Bell and Nakamura collectively disclose the instantly claimed treatment regimen.
With regard to amended instant claim 23, which recites “the tumors and/or cancers [treated by the method according to claim 20] include lung cancer, melanoma, head and neck cancer, liver cancer, intracranial tumor, colorectal cancer, bladder cancer, breast cancer, ovarian cancer, uterine cancer, cervical cancer, gastric cancer, esophageal cancer, kidney cancer, prostate cancer, pancreatic cancer, lymphatic cancer, leukemia, bone cancer, testicular cancer and osteosarcoma,” Nakamura discloses that the recombinant oncolytic vaccinia viruses taught therein can target multiple cancer types, including gastric cancer, liver cancer, esophageal cancer, leukemia, osteosarcoma, and pancreatic cancer (paragraph [0055]). Thus, Nakamura discloses treatment of multiple types of cancer, as instantly claimed.
With regard to new claim 24, which recites “the microRNA [of the recombinant oncolytic vaccinia virus according to claim 1] is selected from a group consisting of miR-199a and miR-199b,” Nakamura further discloses that the recombinant oncolytic vaccinia viruses for treating cancer taught therein are controlled by microRNAs in that the microRNA is less expressed in a cancer cell than in a normal cell, thereby facilitating specific proliferation in cancer cells to destroy said cancer cells (abstract; paragraph [0009]). Suitable microRNAs for use in said therapeutic recombinant oncolytic vaccinia viruses are disclosed to include miR-199a (paragraphs [0009] and [0046]) and miR-199b (paragraph [0046]). Per Nakamura, miR-199a is particularly relevant to the treatment of cancers such as hepatocellular carcinoma, while miR-199b is particularly relevant to the treatment of cancers such as lung cancer (paragraph [0046]). Thus, Nakamura discloses selection of miR-199a or miR-199b for use in recombinant oncolytic vaccinia viruses, as instantly claimed.
Given that Bell and Senkevich et al., 2000 collectively disclose the recombinant oncolytic vaccinia virus of instant claim 1 (as set forth above), that Andorsky and Timmerman, 2008 disclose that IL-21 (i.e. recombinant human IL-21) has potent antitumor effects against a variety of types of tumors, while also displaying acceptable clinical toxicity, and that Nakamura discloses administration of several doses (107 pfu) of recombinant oncolytic vaccinia virus over several days to treat multiple types of cancer, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to administer the recombinant oncolytic vaccinia virus collectively disclosed in Bell, Senkevich et al., 2000, Nakamura, and Andorsky and Timmerman, 2008 per the regimen disclosed in Bell and Nakamura to predictably treat multiple types of cancer, including gastric cancer, liver cancer, esophageal cancer, leukemia, osteosarcoma, and pancreatic cancer. One would have been motivated to make such a modification in order to receive the expected benefit of treating multiple types of cancer, including gastric cancer, liver cancer, esophageal cancer, leukemia, osteosarcoma, and pancreatic cancer.
Claim 6 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2009/111892 A1 (hereinafter Bell; of record) in view of Senkevich et al., 2000 (of record) as applied to claim 3 above, and further in view of Jiang and Doudna, 2017 (of record).
The combined disclosures of Bell and Senkevich et al., 2000 are described above and applied as before. However, these disclosures do not teach the insertion of an exogenous nucleotide sequence into the TK locus, thereby rendering it functionally deficient, of instant claim 3.
With regard to amended instant claim 6, which recites “the TK gene [of the recombinant oncolytic vaccinia virus according to claim 3] is rendered functionally deficient via an insertion of an exogenous nucleotide sequence into a TK locus,” while Bell discloses that replication of viruses can be restricted to cancer cells with high TK activity by deleting the viral versions of TK (or other genes upregulated in cancer cells; paragraph [0008]), Bell does not disclose that the viral version of TK is rendered functionally deficient by via the insertion of an exogenous nucleotide sequence. However, insertion of an exogenous nucleotide sequence, for example by methods such as CRISPR/Cas9, is a known technique to generate precise gene knockouts (reviewed in Jiang and Doudna, 2017; see especially Figure 2), which render the affected gene(s) functionally deficient, as instantly claimed.
Given that Bell and Senkevich et al., 2000 collectively disclose the recombinant oncolytic vaccinia virus with a functionally deficient TK gene of instant claim 3 (as set forth above), and that Jiang and Doudna, 2017 disclose that precise gene knockouts (which render the affected gene(s) functionally deficient) may be generated by insertion of an exogenous nucleotide sequence using CRISPR/Cas9, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to generate the recombinant oncolytic vaccinia virus with a functionally deficient TK gene of Bell and Senkevich et al., 2000 using the CRISPR/Cas9 knock-in methodology disclosed in Jiang and Doudna, 2017 to predictably knock out (i.e. render functionally deficient) the viral TK gene, thereby restricting replication of said recombinant oncolytic vaccinia virus to cancer cells with endogenously high TK activity. One would have been motivated to make such a modification in order to receive the expected benefit of restricting replication of said recombinant oncolytic vaccinia virus to cancer cells with endogenously high TK activity.
Claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2009/111892 A1 (hereinafter Bell; of record) in view of Senkevich et al., 2000 (of record), US 2013/0071430 A1 (hereinafter Nakamura; of record), and Andorsky and Timmerman, 2008 (of record) as applied to claim 5 above, and further in view of Jiang and Doudna, 2017 (of record).
The combined disclosures of Bell, Senkevich et al., 2000, Nakamura, and Andorsky and Timmerman, 2008 are described above and applied as before. However, these disclosures do not teach the insertion of an exogenous IL-21 sequence into the TK locus, thereby rendering it functionally deficient, of instant claim 5.
With regard to amended instant claim 7, which recites “the exogenous IL-21 gene [of the recombinant oncolytic vaccinia virus according to claim 5] is inserted into a TK locus, thereby causing functional defect of the TK gene,” while Bell discloses that replication of viruses can be restricted to cancer cells with high TK activity by deleting the viral versions of TK (or other genes upregulated in cancer cells; paragraph [0008]) and Nakamura and Andorsky and Timmerman, 2008 collectively disclose therapeutic recombinant vaccinia viruses that further comprise a foreign, therapeutic gene such as IL-21 (Andorsky and Timmerman, 2008: page 1304, column 2, paragraph 2) that can be used in the treatment of cancer (Nakamura paragraphs [0012], [0057], and [0059]), none of these disclosures teach rendering the viral TK gene functionally deficient by inserting an exogenous IL-21 gene into the TK locus. However, insertion of an exogenous nucleotide sequence, for example by methods such as CRISPR/Cas9, is a known technique to generate precise gene knockouts (reviewed in Jiang and Doudna, 2017; see especially Figure 2), which render the affected gene(s) functionally deficient, as instantly claimed.
Given that Bell and Senkevich et al., 2000 collectively disclose the recombinant oncolytic vaccinia virus with a functionally deficient TK gene of instant claim 3 (as set forth above), that Nakamura and Andorsky and Timmerman, 2008 collectively disclose therapeutic recombinant vaccinia viruses that further comprise a foreign, therapeutic gene such as IL-21 to be used in treating cancer, and that Jiang and Doudna, 2017 disclose that precise gene knockouts (which render the affected gene(s) functionally deficient) may be generated by insertion of an exogenous nucleotide sequence using CRISPR/Cas9, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to generate the recombinant oncolytic vaccinia virus with a functionally deficient TK gene of Bell and Senkevich et al., 2000 and expressing exogenous IL-21 (as disclosed in Nakamura and Andorsky and Timmerman, 2008) using the CRISPR/Cas9 knock-in methodology disclosed in Jiang and Doudna, 2017 to insert exogenous IL-21, predictably knocking out (i.e. render functionally deficient) the viral TK gene, thereby restricting replication of said recombinant oncolytic vaccinia virus to cancer cells with endogenously high TK activity. One would have been motivated to make such a modification in order to receive the expected benefit of restricting replication of said recombinant oncolytic vaccinia virus expressing therapeutic IL-21 to cancer cells with endogenously high TK activity.
Conclusion
No claims are allowed.
Claims 7, 13, and 21 are objected to.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Sarah E Allen whose telephone number is (571)272-0408. The examiner can normally be reached M-Th 8-5, F 8-12.
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, Jennifer Dunston can be reached at 571-272-2916. 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.
/SARAH E ALLEN/ Examiner, Art Unit 1637
/J. E. ANGELL/ Primary Examiner, Art Unit 1637
Prosecution Insights