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 .
Remark
Preliminary amendment filed on 9/12/2024 has been acknowledged. Claims 2, 6-11 were canceled. Claims 1, 3 and 4-5 were amended. New claims 12-13 were assed. Claims 1, 3-5 and 12-13 are pending and considered.
Examiner’s notes: Cancer staging is generally considered from I to IV summarized published by Cancer Stage published by NIH NATIONAL CANCER INSTITUDE, October 24, 2022.
Stage
What it means
Stage 0
Abnormal cells are present but have not spread to nearby tissue. Also called carcinoma in situ, or CIS. CIS is not cancer, but it may become cancer.
Stage I, Stage II, and Stage III (may also be written as Stage 1, Stage 2, and Stage 3)
Cancer is present. The higher the number, the larger the cancer tumor and the more it has spread into nearby tissues.
Stage IV (may also be written as Stage 4)
The cancer has spread to distant parts of the body.
Hence, if any of the references cited below teaches the cancer received a recombinant Measles virus (rMV) treatment as a clinical surgical stage or advanced cancer or metastatic state, is considered to be in the state of II to IV. Therefore, it meets the limitation of claim 12.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1, 3, 4-5 and 12 are rejected under 35 U.S.C. 102 (a) (1) as being anticipated by Fujiyuki et al. (Molecular Therapy, Oncolytics, December 2020, Vol. 19, pp. 127-135).
Fujiyuki et al. teach a method using genetically modified oncolytic Measles virus, particularly , the recombinant SLAMblind Measles virus to treat a breast cancer that expresses Nectin-4, with rMV-SLAMblind to suppress the cancer growing, and then they maAdditionally, they also did intratumoral injection of rMV-SLAMblind to significantly decreased the viability in half of the analyzed cell lines in vitro. Additionally, intratumoral injection of rMV-SLAMblind suppressed tumor growth in xenografts of MDA-MB-468 and HCC70 cells. To assess treatment for metastatic breast cancer, they performed intravenous administration of the luciferase-expressing-rMV-SLAMblind to MDA xenografted mice. Virus replicated in the tumor and resulted in significant suppression of the tumor growth. The safety of the virus was tested by its intravenous injection into healthy cynomolgus monkeys, which did not cause any measles-like symptoms. These results suggest that rMV-SLAMblind is a promising candidate as a therapeutic agent for treating metastatic and/or TN type breast cancer (See Abstract and section of Results, Figs 1-5). Therefore, the cited reference anticipates claims 1, 3-4 and 5.
Claims 1, 3, 4-5 and 12 are rejected under 35 U.S.C. 102 (a) (1) or 102 (a) (2) as being anticipated by Kai et al. WO 2016/047645 (published on or US Patent Application publication No. 20170340726A1 (which was published on 03/13/2016) 11/13/2017) or US Patent No. 10,335,481B2.(which was published on 07/02/2019)
It is noted that All of them were published more than 1 year than the original filing date of the current Application on 03/16/2022).
Kai et al. teach composition and a method for using the same to treat cancer, wherein the composition comprising a recombinant genetically modified measles virus, particularly, named as rMV-V(−)-SLAM-blind. And the method comprises the steps of administering rMV-V(−)-SLAM-blind to a subject in need of treatment of cancer, wherein the cancer is refractory cancer, the cancer is metastatic cancer, the cancer is triple-negative breast cancer, pancreatic cancer, lung cancer, or colon cancer. wherein the composition is configured for intravenous as well as intratumoral formulation in addition to comprising a pharmaceutical acceptable carrier (Seel claims 1-14).
Moreover, Kai et al. also teach that PVRL4 (Poliovirus receptor related 4, which is also referred to as “Nectin-4”. The expression of PVRL4 is selectively increased in tumor cells including breast cancer cells, ovary cancer cells, and lung cancer cells (Non Patent Literature 10 to Non Patent Literature 13). In general, PVRL4 is expressed in human placenta, and the expression thereof is hardly observed in other tissues. The present inventors have conceived of using a wild-type measles virus strain to selectively target PVRL4. The receptor for the wild-type measles virus exhibiting pathogenicity is SLAM. SLAM is selectively expressed in immune cells and enables serious immunosuppression by the measles virus and diffusion of the virus to the entire body Hence, the inventors have produced a recombinant measles virus that does not recognize SLAM (rMV-SLAMblind), based on the wild-type measles virus strain HL When breast cancer cells are infected with rMV-SLAMblind in vitro or in vivo, the cancer cells can be killed. The antitumor activity of rMV-SLAMblind is higher than that of conventional measles virus vaccine strains. In addition, rMV-SLAMblind has been completely attenuated, and thus, it has been confirmed that rMV-SLAMblind does not cause the typical clinical symptoms of measles, when it is subcutaneously inoculated into a monkey, and thus that this recombinant virus is highly safe. As stated above, a recombinant measles virus that does not recognize SLAM, rMV-SLAMblind, is expected to be an extremely effective tool for cancer therapy. In particular, rMV-SLAMblind is greatly expected for the treatment of, not only primary cancer, but also metastatic cancer, and it is also greatly expected to have cytotoxic effects on cancer stein cells.
Hence, Kai et al. present an invention drawn to a pharmaceutical composition for use in the treatment of cancer, comprising rMV-SLAM-blind or rMV-V(−)-SLAM-blind. The pharmaceutical composition kills cancer stem cells, refractory cancer, metastatic cancer, triple-negative breast cancer, pancreatic cancer, lung cancer, or colon cancer. The pharmaceutical composition according to any one of the above (1) to (5), which is characterized in that it is used by intravenous administration of the rMV-SLAM-blind or the rMV-V(−)-SLAM-blin
FIG. 9 shows the expression states of PVRL4 in triple-negative breast cancer cell lines. FIG. 9(A) shows the results demonstrating the presence or absence of the expression of PVRL4 on the cell surface. FIG. 9(B) shows the results obtained by analyzing the infectivity of rMV-EGFP-SLAMblind to the triple-negative breast cancer cell line. FIG. 10 shows the results obtained by analyzing the cytotoxicity of rMV-SLAMblind to triple-negative breast cancer cells in vitro. Triple-negative breast cancer cells were infected with rMV-EGFP-SLAMblind and rMV-V(−)-EGFP-SLAMblind. FIG. 10(A): The viability of the triple-negative breast cancer cells HCC70 was measured at time points of 1 dpi, 3 dpi, 5 dpi, 7 dpi and 9 dpi according to a WST-1 assay. FIG. 10(B) shows the results obtained by measuring the viability of the control cells B95a that did not express PVRL4. The numerical value is shown as a mean value±SD of the values obtained from three times of experiments. Viability: survival rate; and dpi: days post first inoculation. FIG. 10(B) shows the results obtained by measuring the viability of the control cells B95a that did not express PVRL4. The numerical value is shown as a mean value±SD of the values obtained from three times of experiments. Viability: survival rate; and dpi: days post first inoculation.
Hence, the cited reference anticipates claims 1 and 3-5.
Claims 1, 3, 4-5 and 12 are rejected under 35 U.S.C. 102 (a) (1) as being anticipated by Awano et al. (Cancer Science, 25 August 2016, https://doi.org/10.1111/cas.13064Digital Object Identifier (DOI)
Awano et al. teach that pancreatic cancer is one of the most intractable cancers and has a devastating prognosis, which cancer cells also highly express Necti-4. As Nectin-4 is also a receptors for oncolytic recombinant measles virus (MV), rMV-SLAMblind, that had lost the ability to bind to its principal receptor, signaling lymphocyte activity molecule (SLAM), but which selectively infected and efficiently killed nectin-4-expressing pancreas etic cancer cells in addition to breast and lung cancer cells . In this study, they analyzed the antitumor effect of this virus against pancreatic cancer. Nectin-4 was expressed on the surface of 4/16 tested pancreatic cancer cell lines, which were efficiently infected and killed by rMV-SLAMblind in vitro. The intratumoral inoculation of rMV-SLAMblind suppressed the growth of KLM1 and Capan-2 cells xenografted in SCID mice. The sequence analysis of MV isolated from the tumor revealed that the designed mutation in the H protein of rMV-SLAMblind had been stably maintained for 47 days after the last inoculation. These results suggest that rMV-SLAMblind is a promising candidate for the novel treatment of pancreatic cancer for a subject suffering such type of pancreatic cancer. (Abstract and Results, e.g. Figs. 1-4). To this context, claims 1 and 3-5 are anticipated by Awano et al.
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.
Claims 1, 3-5 and 12-13 are rejected under 35 U.S.C. 103 as being unpatentable over Claims 1, 3, 4-5 and 12 are rejected under 35 U.S.C. 102 (a) (1) or 102 (a) (2) as being anticipated by Kai et al. WO 2016/047645 (published on or US Patent Application publication No. 20170340726A1 (which was published on 03/13/2016) 11/13/2017) or US Patent No. 10,335,481B2.(which was published on 07/02/2019) as applied to claims 1, 3-5 above, and further in view of Lv et al. (Cancer Letters published in Sept. 2019, Vol. 460, pp. 108-118) for claims 12-13.
. Kai et al. teach composition and a method for using the same to treat cancer, wherein the composition comprising a recombinant genetically modified measles virus, particularly, named as rMV-V(−)-SLAM-blind. And the method comprises the steps of administering rMV-V(−)-SLAM-blind to a subject in need of treatment of cancer, wherein the cancer is refractory cancer, the cancer is metastatic cancer, the cancer is triple-negative breast cancer, pancreatic cancer, lung cancer, or colon cancer. wherein the composition is configured for intravenous as well as intratumoral formulation in addition to comprising a pharmaceutical acceptable carrier (Seel claims 1-14).
Moreover, Kai et al. also teach that PVRL4 (Poliovirus receptor related 4, which is also referred to as “Nectin-4”. The expression of PVRL4 is selectively increased in tumor cells including breast cancer cells, ovary cancer cells, and lung cancer cells (Non Patent Literature 10 to Non Patent Literature 13). In general, PVRL4 is expressed in human placenta, and the expression thereof is hardly observed in other tissues. The present inventors have conceived of using a wild-type measles virus strain to selectively target PVRL4. The receptor for the wild-type measles virus exhibiting pathogenicity is SLAM. SLAM is selectively expressed in immune cells and enables serious immunosuppression by the measles virus and diffusion of the virus to the entire body Hence, the inventors have produced a recombinant measles virus that does not recognize SLAM (rMV-SLAMblind), based on the wild-type measles virus strain HL When breast cancer cells are infected with rMV-SLAMblind in vitro or in vivo, the cancer cells can be killed. The antitumor activity of rMV-SLAMblind is higher than that of conventional measles virus vaccine strains. In addition, rMV-SLAMblind has been completely attenuated, and thus, it has been confirmed that rMV-SLAMblind does not cause the typical clinical symptoms of measles, when it is subcutaneously inoculated into a monkey, and thus that this recombinant virus is highly safe. As stated above, a recombinant measles virus that does not recognize SLAM, rMV-SLAMblind, is expected to be an extremely effective tool for cancer therapy. In particular, rMV-SLAMblind is greatly expected for the treatment of, not only primary cancer, but also metastatic cancer, and it is also greatly expected to have cytotoxic effects on cancer stein cells.
Hence, Kai et al. present an invention drawn to a pharmaceutical composition for use in the treatment of cancer, comprising rMV-SLAM-blind or rMV-V(−)-SLAM-blind. The pharmaceutical composition kills cancer stem cells, refractory cancer, metastatic cancer, triple-negative breast cancer, pancreatic cancer, lung cancer, or colon cancer. The pharmaceutical composition according to any one of the above (1) to (5), which is characterized in that it is used by intravenous administration of the rMV-SLAM-blind or the rMV-V(−)-SLAM-blin
FIG. 9 shows the expression states of PVRL4 in triple-negative breast cancer cell lines. FIG. 9(A) shows the results demonstrating the presence or absence of the expression of PVRL4 on the cell surface. FIG. 9(B) shows the results obtained by analyzing the infectivity of rMV-EGFP-SLAMblind to the triple-negative breast cancer cell line. FIG. 10 shows the results obtained by analyzing the cytotoxicity of rMV-SLAMblind to triple-negative breast cancer cells in vitro. Triple-negative breast cancer cells were infected with rMV-EGFP-SLAMblind and rMV-V(−)-EGFP-SLAMblind. FIG. 10(A): The viability of the triple-negative breast cancer cells HCC70 was measured at time points of 1 dpi, 3 dpi, 5 dpi, 7 dpi and 9 dpi according to a WST-1 assay. FIG. 10(B) shows the results obtained by measuring the viability of the control cells B95a that did not express PVRL4. The numerical value is shown as a mean value±SD of the values obtained from three times of experiments. Viability: survival rate; and dpi: days post first inoculation. FIG. 10(B) shows the results obtained by measuring the viability of the control cells B95a that did not express PVRL4. The numerical value is shown as a mean value±SD of the values obtained from three times of experiments. Viability: survival rate; and dpi: days post first inoculation.
However, Kai et al. do not teach using the genetically modified measles virus to treat Gastric cancer.
Lv et al. found that nectin-4, the other MV receptor on GC cells, was not localized in lipid rafts, thus viral entry through lipid raft-independent mechanism could not be excluded. A lot more details needs to be clarified before the mechanism of rMV-Hu191 viral entry can be revealed completely. In Fig. 6. They have shown that The oncolytic effect of intratumoral rMV-Hu191 in GC tumor models established in nude mice. (A) Tumor growth in mice bearing GC xenografts with or without intratumoral rMV-Hu191 injections. (B) Difference in tumor volume on post-implantation day 16. (C) The Kaplan-Meier survival curves of mice from rMV-Hu191 and mock-treated groups. (D) Monitoring of body weights of mice in the two groups after tumor implantation. (E) Detection of MV by tissue immunofluorescence of MV-P protein. Scale bar = 20 μm. (F) Formation of syncytia (a–b), expression of cleaved caspase 3 (c–d), and presence of in situ apoptosis (e–f) in tumor tissues from rMV-Hu191 and mock treated mice. Arrows indicate syncytia. Scale bar = 50 μm. (F) Levels of cleaved caspase 3 expression from tumor tissues of the two groups, and the quantitative densitometry analysis. **:P < 0.01,***:P < 0.001.
Finally, Lv et al. concluded that recombinant Chinese Hu191 MV vaccine strain has potent therapeutic efficacy against human GC both in vivo and in vitro. rMV-Hu191-induced apoptosis in GC cells is dependent on caspase activation and requires lipid raft integrity. Lipid rafts serve as a platform to facilitate entry of rMV-Hu191 into the GC cells at least in part, and CD46 could be involved. The characterization of the underlying mechanism may provide a theoretical basis for utilizing this attenuated virus as a novel oncolytic agent against human GC. (Last three paragraphs of the conclusion &. results at paragraph 3.1).
Therefore, it would have been obvious for a person with an ordinarily skilled in the art to be motivated by the cited references by Kai et al. and Lv et al. in combination to arrive the claimed method using the recombinant modified measles virus , such as rMV-SLAM-blind or rMV-V(−)-SLAM-blind top treat any or all cancels that can overexpress the Nectin-4 including GC in addition to the breast cancer, Pancreatic cancer especially metastatic cancer in the later state over 2 to 4 in order to obtain more effective cancer treatment by the genetic modified recombinant measles virus
As there are no unexpected results have been provided, hence the claimed invention as a whole is prima facie obvious absence unexpected results.
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 and 12-13 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 10,335,481B2 in view of Fujiyuki et al. (Molecular Therapy, Oncolytics, December 2020, Vol. 19, pp. 127-135) and Lv et al. (Cancer Letters published in Sept. 2019, Vol. 460, pp. 108-118) for claims 12-13.
In the instant case, the current claims 1,3-5are drawn to method for inducing a cell- mediated immunity against a tumor cell comprising: directly introducing an oncolytic gene-modified measles virus, rMV-SLAM-blind or rMV-V(-)-SLAM- blind, into a cell mass of a tumor cell expressing PVRL4/Nectin4 in a living body to cause cell death and induce a cell-medicated immunity against a tumor cell rMV-SLAM-blind or rMV-V(-)-SLAM- blind, which is a wild-type measles virus that has been genetically modified, wherein a tumor as a medical treatment target is breast cancer, lung cancer, colon cancer, or pancreatic cancer and furthermore, the remaining tumor cell is selected from the group consisting of a deep-seated tumor cell, a recurrent tumor cell, and a metastasized tumor cell.
The reference claims are directed to a composition and a method for using the same to treating cancer, comprising administering rMV-V(−)-SLAM-blind to a subject in need of treatment of cancer, wherein the cancer is refractory cancer, the cancer is metastatic cancer, the cancer is triple-negative breast cancer, pancreatic cancer, lung cancer, or colon cancer. wherein the composition is configured for intravenous administration of the rMV-V(−)-SLAM-blind.
However, the issued reference claims does not explitely indicates that the refractory cancer, the metastatic cancer, the triple-negative breast cancer, pancreatic cancer, lung cancer, or colon cancer are the cancer cells more likely the cells expressing PVRL4/Nectin4.
Fujiyuki et al. teaches that one of the most refractory breast cancer types is triple negative (TN) breast cancer, in which cells are resistant to both hormone and Herceptin treatments and, thus, often cause recurrence and metastasis. Effective treatments are needed to treat TN breast cancer. They previously demonstrated that rMV-SLAMblind, are recombinant measles virus, showed anti-tumor activity against breast cancer cells. Here, we examined whether rMV-SLAMblind is effective for treating TN breast cancer. Nectin-4, a receptor for rMV-SLAMblind, was expressed on the surface of 75% of the analyzed TN breast cancer cell lines. rMV-SLAMblind infected the nectin-4-expressing TN breast cancer cell lines and significantly decreased the viability in half of the analyzed cell lines invitro. Additionally, intratumoral of rMV-SLAMblind suppressed tumor growth in xenografts of MDA-MB-468 and HCC70 cells. To assess treatment for metastatic breast cancer, we performed intravenous administration of the luciferase-ex pressing-rMV-SLAMblind to MDA xenografted mice. Virus replicated in the tumor and resulted in significant suppression of the tumor growth. The safety of the virus was tested by its intra venous injection into healthy cynomolgus monkeys, which did not cause any measles-like symptoms. These results suggest that rMV-SLAM blind is a promising candidate as a therapeutic agent for treating metastatic and/or TN type breast cancer.(Abstract).
Lv et al. found that nectin-4, the other MV receptor on GC cells, was not localized in lipid rafts, thus viral entry through lipid raft-independent mechanism could not be excluded. A lot more details needs to be clarified before the mechanism of rMV-Hu191 viral entry can be revealed completely. In Fig. 6. They have shown that The oncolytic effect of intratumoral rMV-Hu191 in GC tumor models established in nude mice. (A) Tumor growth in mice bearing GC xenografts with or without intratumoral rMV-Hu191 injections. (B) Difference in tumor volume on post-implantation day 16. (C) The Kaplan-Meier survival curves of mice from rMV-Hu191 and mock-treated groups. (D) Monitoring of body weights of mice in the two groups after tumor implantation. (E) Detection of MV by tissue immunofluorescence of MV-P protein. Scale bar = 20 μm. (F) Formation of syncytia (a–b), expression of cleaved caspase 3 (c–d), and presence of in situ apoptosis (e–f) in tumor tissues from rMV-Hu191 and mock treated mice. Arrows indicate syncytia. Scale bar = 50 μm. (F) Levels of cleaved caspase 3 expression from tumor tissues of the two groups, and the quantitative densitometry analysis.
Finally, Lv et al. concluded that recombinant Chinese Hu191 MV vaccine strain has potent therapeutic efficacy against human GC both in vivo and in vitro. rMV-Hu191-induced apoptosis in GC cells is dependent on caspase activation and requires lipid raft integrity. Lipid rafts serve as a platform to facilitate entry of rMV-Hu191 into the GC cells at least in part, and CD46 could be involved. The characterization of the underlying mechanism may provide a theoretical basis for utilizing this attenuated virus as a novel oncolytic agent against human GC. (Last three paragraphs of the conclusion &. results at paragraph 3.1).
Therefore, in view of the well-known factor that refractory cancer, the metastatic cancer, the triple-negative breast cancer, pancreatic cancer, lung cancer, or colon cancer or GC are the cancer cells expressing PVRL4/Nectin4, the current claims are not considered to be distinct but obvious version to the issued claims for any person with an ordinary skilled in the art.
Conclusion
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BAO Q. LI
Examiner
Art Unit 1671
/BAO Q LI/ Primary Examiner, Art Unit 1671
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