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 .
Status of Claims
Claims 1-6 and 9-16 are pending following the Reply filed 11/03/2025. Claims 7-8 have been cancelled. Claims 1-6 and 9-16 have been amended without introducing new matter. All pending claims have been examined on the merits.
Information Disclosure Statement
The information disclosure statements (IDS) filed 11/03/2025 and 01/29/2026 have been considered by the examiner.
Withdrawn
The objection to the drawings has been withdrawn in light of the replacement drawings filed 11/03/2025 and the petition for color drawings granted 12/31/2025.
The objection to the specification has been withdrawn in light of the substitute specification filed 11/03/2025.
Any objection or rejection of claims 7-8 is moot because the claims have been cancelled.
The objections to claims 2, 6, 10, 13 and 15 are withdrawn in light of the amendments.
The rejections of claims 1-6 and 14 under 35 U.S.C. 112(b) are withdrawn in light of the amendments.
Claim Objections
Claim 3 is objected to because of the following informalities: it is understood that the dendritic cell is in an activated state when present in the composition, and the further limitation of the claim is a product-by-process step. For clarity, please amend claim 3 to recite “wherein the oncodriver pulsed dendritic cell [[is]] has been activated with IL-12.” Appropriate correction is required.
Claim 9 is objected to because of the following informalities: please amend the claim (1) by removing “and” in line 3 and (2) by adding “and” after “donor;” in lines 4-5. Appropriate correction is required.
Claim 16 is objected to because of the following informalities: please amend the claim by adding “and” after “donor;” in lines 4-5. Appropriate correction is required.
Maintained rejections and new rejections necessitated by amendment
Claim Rejections - 35 USC § 103
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.
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.
Claims 1-2, 4-6 and 9-16 are rejected under 35 U.S.C. 103 as being unpatentable over Czerniecki (US 2017/0216421 A1; previously cited), and further in view of Wargo (US 2022/0016188 A1; effectively filed 11/21/2018; previously cited) and Evans (US 2016/0115240 A1; previously cited).
Regarding claim 1, Czerniecki teaches a method of improving the migration and activity of immune cells in a tumor site of a subject, comprising administering to said subject a dendritic cell vaccine and an inhibitor of HER-2 in an effective amount to change the immune response in said tumor so that the immune cells in the tumor site are more effective in attacking tumor cells (see, e.g., claim 38). Czerniecki teaches the antigen-presenting capacity of dendritic cells (“DCs”) has led to enthusiasm for their use in anti-tumor vaccination and discloses the design of a HER2 peptide-pulsed autologous DC vaccine uniquely engineered to promote anti-HER2 Th1 sensitization and attraction (see pg. 25, para. [0296]). The “HER2 peptide-pulsed autologous DC vaccine” of Czerniecki meets the limitation of a composition comprising “i) at least one oncodriver pulsed dendritic cell” in view of dependent claim 2. Czerniecki teaches the dendritic cell vaccine and an inhibitor of HER-2 can be administered to the tumor site (see claim 51).
Czerniecki also teaches the treatment regimen is used in combination with an anti-tumor agent (see pg. 18, para. [0223]) that is a chemotherapeutic agent useful in the treatment of cancer (see pg. 18, para. [0224]) such as TAXOL (see pg. 19, para. [0224], col. 1). Czerniecki also discusses the state of the prior art, wherein previous therapies using Herceptin (trastuzumab) targeting HER2 are often used in combination with paclitaxel (sold under the trademark Taxol), and treatment with Herceptin results in the accumulation of Cdk inhibitors which lead to cancer cell death (see pg. 1, paras. [0005]-[0006]). Czerniecki discloses, however, that in spite of great promise, high doses of Herceptin or Taxol result in undesirable side effects, and the cancer often develops a resistance to both these therapeutics (see pg. 1, para. [0006]). Czerniecki discloses that there is therefore a need in the art to have additional immunotherapeutic approaches for treating or preventing breast cancer and other malignancies (see pg. 1, para. [0007]).
Czerniecki does not teach the composition further comprising ii) a fecal microbial transplant (FMT) from a pathologic complete response (pCR) donor.
Wargo teaches methods and compositions for treating cancer and/or for reducing toxicity to a therapy in a subject (see Abstract). Wargo discloses fecal microbiota transfer experiments using FMT samples from responders and non-responders of immunotherapy (see pg. 53, para. [0353]). Wargo teaches that a responsive patient may be one identified as having a complete response (CR), which is the disappearance of all target lesions (see pg. 22, para. [0106]). Wargo teaches a method of treating cancer and/or reducing toxicity of a therapy in a subject comprising administering to the subject a composition comprising fecal matter from a healthy patient or a patient determined to respond to immune checkpoint blockade combination therapy (see pg. 1, para. [0006]). Wargo teaches the method may find use in treating conditions where enhanced immunogenicity is desired such as increasing tumor immunogenicity for the treatment of cancer (see pg. 34, para. [0223]). Wargo teaches that intratumoral injection, or injection into the tumor vasculature is specifically contemplated for discrete, solid, accessible tumors (see pg. 33, para. [0213]).
Wargo teaches that current methods and compositions of the disclosure may include one or more additional therapies known in the art, including immunotherapies, such as dendritic cell therapy and chemotherapies (see pg. 28, paras. [0157]-[0158], [0162]; pg. 29, para. [0185]). Wargo teaches that dendritic cell therapy provokes anti-tumor responses by causing dendritic cells to present tumor antigens to lymphocytes, which activates them, priming them to kill other cells that present the antigen (see pg. 28, para. [0163]). Wargo teaches another strategy is to remove dendritic cells from the blood of a patient and activate them outside the body in the presence of tumor antigens, so when these cells (with optional adjuvants) are infused they invoke an immune response (see pg. 28, para. [0166]). Wargo teaches that suitable chemotherapeutic agents include Taxol (see pg. 29, para. [0186]).
Czerniecki and Wargo do not teach the therapy further comprising at least one immunoregulatory molecule inhibitor, wherein the immunoregulatory molecule being inhibited comprises Semaphorin (SEMA) 4D (SEMA4D), SEMA4A, SEMA4B, SEMA4C, SEMA4F, SEMA4G, SEMA3A, SEMA3B, SEMA3C, SEMA3D, SEMA3E, SEMA3F, SEMA3G, or VEGF.
Evans teaches methods for inhibiting, delaying or reducing tumor growth and metastases of plexin-B1-expressing cancer cells in a subject, comprising administering to the subject an effective amount of an isolated binding molecule which specifically binds to semaphorin-4D (SEMA4D) in combination with an effective amount of at least one other immune modulating therapy (see Abstract). Evans teaches the isolated binding molecule comprises an antibody (see pg. 3, para. [0012], lines 24-25) wherein the antibody is monoclonal antibody VX15/2503 (see pg. 3, para. [0012], lines 29-30). As set forth under Claim Interpretation in the previous office action, VX15/2503 is pepinemab, which meets the limitation of an “immunoregulatory molecule inhibitor” in view of dependent claim 6. Evans teaches that SEMA4D has been implicated in the development of certain cancers by promoting tumor angiogenesis and is over-expressed in a wide array of tumor types (see pg. 1, para. [0003]). Evans teaches the method to further comprise the administration of an effective amount of an anti-HER2 binding molecule (see pg. 3 para. [0013]), and the immune modulating therapy may comprise the administration of a cancer vaccine (see pg. 2, para. [0011]). Evans teaches the vaccine can comprise dendritic cells, especially autologous dendritic cells pulsed with tumor cells or tumor antigens (see pg. 16, para. [0126]), wherein the dendritic cells are exposed to natural or modified tumor antigens ex vivo that are re-infused into the patient (see pg. 16, para. [0132]). Evans teaches that the therapy can be combined with other low dose chemotherapy using low doses of a chemotherapeutic agent, such as paclitaxel (Taxol) (see pg. 17, para. [0138]).
Regarding the limitation of “iv) a pharmaceutically acceptable carrier”, Wargo teaches the bacterial composition further comprising a pharmaceutically acceptable excipient (see pg. 17, para. [0058]); and Evans teaches that compositions used in the disclosure comprise pharmaceutically acceptable carriers (see pg. 21, para. [0166]), including preparations for parental administration (see pg. 21, para. [0167]).
It would have been obvious at the time of filing for a person of ordinary of skill in the art to have arrived at the claimed invention by combining the teachings of Czerniecki, Wargo and Evans, because all references teach effective methods to treat cancer which can be used in combination with other therapies. One would have recognized that Czerniecki teaches combination therapies comprising the administration of oncodriver (HER2) pulsed dendritic cells with other agents, such as a CDK inhibitor (Taxol), and discloses the need for additional immunotherapeutic approaches in treating and preventing cancer, while Evans teaches the administration of anti-HER2 binding molecules and/or cancer vaccines in combination with a binding molecule, VX15/2503 (pepinemab), acting as an inhibitor of SEMA4D. One would have also recognized that Wargo teaches methods to treat cancer comprising administering fecal matter from pathologic complete response donors, which Wargo teaches can be combined with other therapies, including dendritic cell therapy, wherein dendritic cells are primed (i.e., pulsed) in the presence of tumor-associated antigens, similar to Czerniecki. Hence, each claimed element is taught by the combination of references, and each reference provides a suggestion to combine its teachings with other therapies. Accordingly, one would have recognized that each of these elements (i.e., pulsed DCs, FMT, SEMA-4D inhibitor, Taxol, pepinemab, etc.) could be combined using known methods and, as each element merely performs the same function in combination as it does separately, one would have recognized that the results of the combination would have been predictable. Finally, one would have been motivated to combine these teachings, because Czerniecki teaches there is a need in the art for more effective cancer therapies. Hence, the combination would have been readily apparent and deemed to be a mere (A) combining of prior art elements according to known methods to yield predictable results (see MPEP 2143(I): Rationales to support rejections under 35 U.S.C. 103).
Regarding claim 2, Czerniecki, as discussed above, teaches that the dendritic cells used in the therapy are HER2-pulsed.
Regarding claim 4, Wargo discloses species common to immunotherapy responsive mice to include Anaerosporobacter mobilis (see pg. 47, col. 1, Table 4). Wargo teaches a favorable microbiota profile comprises bacteria which include Anaerosporobacter mobilis (see pg. 7-8, para. [0040]), and also teaches compositions comprising an isolated or purified population that include Anaerosporobacter mobilis (see pg. 3-4, para. [0022]). Hence, it would have been obvious to have provided the FMT composition comprising enriched Anaerosporobacter.
Regarding claim 5, Czerniecki, Wargo and Evans each teach the cancer therapy may further include the administration of Taxol, as discussed above. Hence, it would have been obvious to include Taxol in the composition.
Regarding claim 6, Evans, as discussed above, teaches the cancer therapy to include VX15/2503, which is also known as pepinemab.
Regarding claim 9, Czerniecki, Wargo and Evans teach methods of treating cancer in a subject which may be combined with other anticancer therapies, as discussed above. Regarding limitation “i)”, Czerniecki teaches the method comprises administering a HER2 peptide-pulsed autologous DC vaccine (pg. 25, para. [0296]). Regarding limitation “ii)”, Wargo teaches the method comprises administering to the subject a composition comprising fecal matter from patients who have a pathologic complete response to immunotherapy (see pg. 1, para. [0006]; pg. 22, para. [0106]; and pg. 53, para. [0353]). Regarding limitation “iii)”, Evans teaches the method comprises administering to the subject an effective amount of an isolated binding molecule which specifically binds to semaphorin-4D (SEMA4D), specifically, VX15/2503 (i.e., pepinemab) (see Abstract; pg. 3, para. [0012], lines 24-30). It would have been obvious to have combined these teachings for the same reasons discussed regarding claim 1.
Regarding claim 10, Czerniecki teaches the dendritic cells administered in the method are HER2-pulsed, as discussed above.
Regarding claim 11, Wargo discloses species common to immunotherapy responsive mice to include Anaerosporobacter mobilis (see pg. 47, col. 1, Table 4). Wargo teaches a favorable microbiota profile comprises bacteria which include Anaerosporobacter mobilis (see pg. 7-8, para. [0040]), and also teaches compositions comprising an isolated or purified population that include Anaerosporobacter mobilis (see pg. 3-4, para. [0022]) and methods of detecting favorable bacteria in an FMT sample including Anaerosporobacter mobilis (see pg. 25, para. [0138]). Hence, a person of ordinary skill would have recognized that Wargo teaches species of the genus Anaerosporobacter are enriched in the stools of immunotherapy responsive donors and teaches methods to treat cancer comprising administering compositions comprising the fecal matter of immunotherapy responsive patients. Therefore, it would have been obvious to have administered an FMT comprising enriched Anaerosporobacter.
Regarding claim 12, Czerniecki, Wargo and Evans each teach the cancer therapy may further include the administration of Taxol, as discussed above.
Regarding claim 13, Evans, as discussed above, teaches the method comprising the administration of VX15/2503, which is also known as pepinemab.
Regarding claim 14, Czerniecki teaches that monocytic dendritic cell precursors were obtained from patients via tandem leukapheresis/countercurrent centrifugal elutriation and later pulsed with HER2-derived major histocompatibility complex (MHC) class II binding peptides (see pg. 26, para. [0308]). Hence, it is understood that the dendritic cells were removed from the subject and pulsed with the oncodriver ex vivo. Similarly, Wargo teaches dendritic cell therapy may involve removing dendritic cells from the blood of a patient and activating them outside the body in the presence of tumor antigens, so when these cells (with optional adjuvants) are infused they invoke an immune response (see pg. 28, para. [0166]). Similarly, Evans teaches the cancer vaccine can comprise dendritic cells, especially autologous dendritic cells pulsed with tumor cells or tumor antigens (see pg. 16, para. [0126]), wherein the dendritic cells are exposed to natural or modified tumor antigens ex vivo that are re-infused into the patient (see pg. 16, para. [0132]).
Regarding claim 15, Czerniecki teaches the dendritic cell vaccine and an inhibitor of HER-2 can be administered to the tumor site (see claim 51). Wargo teaches that intratumoral injection, or injection into the tumor vasculature is specifically contemplated for discrete, solid, accessible tumors (see pg. 33, para. [0213]), and the additional anticancer treatments may be administered intratumorally (see pg. 5, para. [0028]).
Regarding claim 16, Czerniecki teaches the method wherein the dendritic cell vaccine and HER-2 inhibitor are administered to the tumor site (see claim 51). Wargo teaches that intratumoral injection, or injection into the tumor vasculature is specifically contemplated for discrete, solid, accessible tumors (see pg. 33, para. [0213]), and the additional anticancer treatments may be administered intratumorally (see pg. 5, para. [0028]). Similarly, Evans teaches the therapeutics of the method (e.g., anti-SEMA4D binding molecules, antibodies, or antigen-binding fragments in combination with at least one other immune modulating therapy) can be delivered directly to the site of the adverse cellular population (see pg. 21, para. [0164]). Hence, it would have been obvious to have administered the limitations of i), ii) and iii) to a site of a primary tumor.
Czerniecki also teaches that the method to treat cancer includes metastatic cancers (see pg. 6, para. [0059]; pg. 15, para. [0182]). As discussed previously, Evans teaches the method can be used for inhibiting, delaying, or reducing tumor growth and metastases. Evans teaches the terms “metastasis” and “metastases” refer to cancer cells which spread or transfer from the site of origin (e.g., a primary tumor) to a new distant site where tumor growth and development occurs (see pg. 6, para. [0042]). Hence, a person of ordinary skill would have recognized from the prior art combination that these therapeutics could be administered to a site of a primary tumor, and, in doing so, there would be a reasonable expectation for the treatment to have an abscopal effect on secondary tumors. Furthermore, the limitation of the treatment having an “abscopal effect” is presumed to be an inherent effect of the claimed method, which would necessarily be present in the prior art combination. See MPEP 2112.
Claim 3 is rejected under 35 U.S.C. 103 as being unpatentable over Czerniecki, Wargo and Evans, as applied to claims 1-2, 4-6 and 9-16 above, and further in view of Grohmann et al (cited on Form 892), hereafter “Grohmann”.
Regarding claim 3, Czerniecki teaches that while a variety of strategies have been employed to mature dendritic cells (DCs) to a phenotype that optimizes sensitization of CD4+ and CD8+ T cells to recognize tumor epitopes and elicit antitumor immunity, further experiments were designed to utilize a method that employs the rapid maturation of monocytes in serum free media (SFM) using interferon gamma (IFN-γ), lipopolysaccharide (LPS), and a toll-like receptor (TLR) 4 agonist, resulting in mature DCs capable of polarizing the immune response to a Th1-type response and eliciting sensitization via an IL-12 dependent mechanism (see pg. 20, para. [0243]). Czerniecki also teaches a method of generating the antigen pulsed dendritic cell vaccine, wherein the DC is activated by a TLR agonist to produce an effective amount of IL-12 to generate a T cell response (see claims 1 and 12).
Evans teaches that examples of immune modulating agents include IL-12 (see pg. 6, para. [0041]), and the immune modulating agent of the disclosed therapy can include interleukins, such as IL-12, in combination with the anti-SEMA4D binding molecule, which can be provided in a single pharmaceutical formulation for administration (see pg. 17, para. [0139]).
Czerniecki, Wargo and Evans do not explicitly teach the therapy wherein the oncodriver pulsed dendritic cell has been activated with IL-12.
Grohmann teaches that previous work has shown that a significant proportion of murine splenic dendritic cells (DC) express a high affinity receptor for IL-12 (see Abstract), and it has been shown that IL-12 acts directly on DCs, presumably leading to increased maturation of the DC and enhanced antigen-presenting cell (APC) function (see pg. 3100, col. 1, para. 2). In Grohmann’s study, it is concluded that the CD8¯ cell fraction of splenic DCs is exquisitely sensitive to IL-12 and the adjuvanticity resulting from IL-12 action on these cells counteracts the suppressive effect of CD8+ DCs on presentation and/or recognition of the tumor peptide (see pg. 3100, col. 2, para. 1). In Grohmann’s results, it is reported that IL-12 in vitro confers priming ability on dendritic cells pulsed with a tumor peptide before transfer into recipient hosts (see pg. 3101, col. 2, para. 1). Grohmann discloses that the present data may be of importance for designing therapeutic approaches with DCs and synthetic peptides in antitumor immunotherapy (see pg. 3104, col. 2, para. 4).
It would have been obvious at the time filing for a person of ordinary skill in the art to have arrived at the claimed invention by combining the teachings of Czerniecki and Evans with Grohmann, because each reference discloses methodologies and/or experimental results that are useful in the design of anticancer immunotherapies. One of ordinary skill would have recognized that both Czerniecki and Grohmann teach the importance of maturing (i.e., priming or activating) antigen-pulsed dendritic cells prior to administration to a recipient in order to enhance their function as antigen-presenting cells and elicit an effective anti-tumor response by CD4+ and CD8+ T cells. Furthermore, one would have recognized that the combined teachings of Czerniecki and Evans would have included pharmaceutical compositions comprising IL-12 and HER2-pulsed dendritic cells, which would have inherently possessed the activity of dendritic cell activation by IL-12 in view of Grohmann. One would have been particularly motivated to combine IL-12 with the HER2-pulsed dendritic cells prior to administration, because Grohmann teaches that doing so may increase the maturation of the dendritic cells which is associated with enhanced APC function. Hence, one could have combined these teachings according to known methods with the reasonable expectation that it would have resulted in a more effective therapy. Hence, the combination would have been readily apparent and deemed to be a mere (A) combining of prior art elements according to known methods to yield predictable results (see MPEP 2143(I): Rationales to support rejections under 35 U.S.C. 103).
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 1-6 and 9-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 of U.S. Patent No. US 11,660,330 B2 (previously cited), hereafter “Czerniecki 2023”, in further view of Wargo.
Regarding instant claim 1, claim 1 of Czerniecki 2023 recites an anti-cancer combination therapy comprising at least one dendritic cell pulsed with a human epidermal growth factor receptor 2 (HER 2) oncodriver formulated for intratumoral administration and at least one immunoregulatory molecule inhibitor comprising an antibody or an antigen-binding fragment thereof that binds specifically to Semaphorin 4D (SEMA4D) formulated for systemic administration; and wherein administration of the combination therapy results in tumor shrinkage of injected and non-injected tumors.
Czerniecki 2023 does not teach the therapy comprising ii) a fecal microbial transplant (FMT) from a pathologic complete response (pCR) donor.
Wargo teaches methods and compositions for treating cancer and for predicting a subject’s response to combination checkpoint inhibitor therapy (see Abstract). Wargo discloses fecal microbiota transfer experiments using FMT samples from responders and non-responders of immunotherapy (see pg. 53, para. [0353]). Wargo teaches that a responsive patient may be one identified as having a complete response (CR), which is the disappearance of all target lesions (see pg. 22, para. [0106]). Wargo teaches a method of treating cancer and/or reducing toxicity of a therapy in a subject comprising administering to the subject a composition comprising fecal matter from a healthy patient or a patient determined to respond to immune checkpoint blockade combination therapy (see pg. 1, para. [0006]). Wargo teaches that intratumoral injection, or injection into the tumor vasculature is specifically contemplated for discrete, solid, accessible tumors (see pg. 33, para. [0213]).
Wargo teaches that current methods and compositions of the disclosure may include one or more additional therapies known in the art, including immunotherapies, such as dendritic cell therapy and chemotherapies (see pg. 28, paras. [0157]-[0158], [0162]; pg. 29, para. [0185]). Wargo teaches that dendritic cell therapy provokes anti-tumor responses by causing dendritic cells to present tumor antigens to lymphocytes, which activates them, priming them to kill other cells that present the antigen (see pg. 28, para. [0163]). Wargo teaches another strategy is to remove dendritic cells from the blood of a patient and activate them outside the body in the presence of tumor antigens, so when these cells (with optional adjuvants) are infused they invoke an immune response (see pg. 28, para. [0166]). Wargo teaches that suitable chemotherapeutic agents include Taxol (see pg. 29, para. [0186]). Wargo teaches the method may find use in treating conditions where enhanced immunogenicity is desired such as increasing tumor immunogenicity for the treatment of cancer (see pg. 34, para. [0223]).
Regarding the limitation of “iv) a pharmaceutically acceptable carrier”, Wargo teaches the bacterial composition further comprising a pharmaceutically acceptable excipient (see pg. 17, para. [0058]).
It would have been obvious at the time of filing for a person of ordinary of skill in the art to have arrived at the claimed invention by combining the teachings of Czerniecki 2023 and Wargo, because both references teach compositions and methods to treat cancer which can be used in combination with other therapies. One would have recognized that Wargo teaches methods to treat cancer comprising administering fecal matter from pathologic complete response donors, which Wargo teaches can be combined with other therapies, including dendritic cell therapy, wherein dendritic cells are primed (i.e., pulsed) in the presence of tumor-associated antigens, similar to Czerniecki 2023. Hence, each claimed element is taught by the combination of references, and Wargo provides a suggestion to combine its teachings with other therapies. Accordingly, one would have recognized that each of these elements (i.e., pulsed DCs, FMT, SEMA-4D inhibitor, Taxol, pepinemab, etc.) could be combined using known methods and, as each element merely performs the same function in combination as it does separately, one would have recognized that the results of the combination would have been predictable. Finally, one would have been motivated to combine these teachings, because Wargo teaches that administering FMTs from responsive patients may increase tumor immunogenicity for the treatment of cancer when combined with immunotherapies. Hence, the combination would have been readily apparent and deemed to be a mere (A) combining of prior art elements according to known methods to yield predictable results (see MPEP 2143(I): Rationales to support rejections under 35 U.S.C. 103).
Regarding instant claim 2, claim 1 of Czerniecki 2023 recites the oncodriver as a HER2 oncodriver.
Regarding instant claim 3, claim 2 of Czerniecki 2023 recites the anti-cancer combination therapy of claim 1, wherein the oncodriver pulsed dendritic cell is activated with interleukin-12 (IL-12) prior to administration.
Regarding instant claim 4, Wargo discloses species common to immunotherapy responsive mice to include Anaerosporobacter mobilis (see pg. 47, col. 1, Table 4). Wargo teaches a favorable microbiota profile comprises bacteria which include Anaerosporobacter mobilis (see pg. 7-8, para. [0040]), and also teaches compositions comprising an isolated or purified population that include Anaerosporobacter mobilis (see pg. 3-4, para. [0022]). Hence, it would have been obvious to have provided the FMT composition comprising enriched Anaerosporobacter.
Regarding instant claim 5, Czerniecki, as discussed above, teaches the cancer therapy to include Taxol.
Regarding instant claim 6, claim 3 of Czerniecki 2023 recites the anti-cancer combination therapy of claim 1, wherein the antagonist antibody that specifically binds to SEMA4D comprises pepinemab.
Regarding instant claim 9, claim 1 of Czerniecki 2023 recites the administration of the anti-cancer combination.
Regarding instant claim 10, claim 1 of Czerniecki 2023 recites the oncodriver as a HER2 oncodriver.
Regarding instant claim 11, Wargo discloses species common to immunotherapy responsive mice to include Anaerosporobacter mobilis (see pg. 47, col. 1, Table 4). Wargo teaches a favorable microbiota profile comprises bacteria which include Anaerosporobacter mobilis (see pg. 7-8, para. [0040]), and also teaches compositions comprising an isolated or purified population that include Anaerosporobacter mobilis (see pg. 3-4, para. [0022]) and methods of detecting favorable bacteria in an FMT sample including Anaerosporobacter mobilis (see pg. 25, para. [0138]). Hence, a person of ordinary skill would have recognized that Wargo teaches species of the genus Anaerosporobacter are enriched in the stools of immunotherapy responsive donors and teaches methods to treat cancer comprising administering compositions comprising the fecal matter of immunotherapy responsive patients. Therefore, it would have been obvious to have administered an FMT comprising enriched Anaerosporobacter.
Regarding instant claim 12, Wargo, as discussed above, teaches the cancer therapy may further include the administration of Taxol.
Regarding instant claim 13, claim 3 of Czerniecki 2023 recites the anti-cancer combination therapy of claim 1, wherein the antagonist antibody that specifically binds to SEMA4D comprises pepinemab.
Regarding instant claim 14, Wargo teaches dendritic cell therapy may involve removing dendritic cells from the blood of a patient and activating them outside the body in the presence of tumor antigens, so when these cells (with optional adjuvants) are infused they invoke an immune response (see pg. 28, para. [0166]). Hence, it would have been obvious to have removed the dendritic cells from the subject to pulse them with the oncodriver ex vivo.
Regarding instant claim 15, claim 1 of Czerniecki 2023 recites the HER2 oncodriver is formulated for intratumoral administration.
Regarding instant claim 16, claim 1 of Czerniecki 2023 recites the HER2 oncodriver is formulated for intratumoral administration, which reasonably includes administering to the site of a primary tumor. Similarly, Wargo teaches the cancer may be a recurrent metastatic cancer, wherein the recurrence of the cancer is in the area of a primary tumor (see pg. 5, para. [0026]). Further, claim 1 of Czerniecki 2023 recites, “wherein administration of the combination therapy results in tumor shrinkage of injected and non-injected tumors.” Hence, a person of ordinary skill would have recognized that when these therapeutics are administered to a site of a primary tumor (injected tumor), there would be a reasonable expectation for the treatment to have an abscopal effect on secondary tumors (non-injected tumors). Furthermore, the limitation of the treatment having an abscopal effect is merely an effect of the claimed method, and the only other difference with instant claim 9 is that the administration step is limited to the site of a primary tumor. Hence, the abscopal effect asserted in the claim is inherently present in the combination of Czerniecki 2023 and Wargo. See MPEP 2112.
Claims 1-6 and 9-16 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of copending Application No. 18/021,845, hereafter “Kodumudi”, in further view of Evans.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Regarding instant claim 1, claim 1 of Kodumudi recites an anti-cancer combination therapy comprising i) at least one oncodriver pulsed dendritic cell and ii) a fecal microbial transplant (FMT) from a pathologic complete response (pCR) donor or a cyclin-dependent kinase (CDK) inhibitor.
Kodumudi does not teach the therapy further comprising at least one immunoregulatory molecule inhibitor, wherein the immunoregulatory molecule being inhibited comprises Semaphorin (SEMA) 4D (SEMA4D), SEMA4A, SEMA4B, SEMA4C, SEMA4F, SEMA4G, SEMA3A, SEMA3B, SEMA3C, SEMA3D, SEMA3E, SEMA3F, SEMA3G, or VEGF.
Evans teaches methods for inhibiting, delaying or reducing tumor growth and metastases of plexin-B1-expressing cancer cells in a subject, comprising administering to the subject an effective amount of an isolated binding molecule which specifically binds to semaphorin-4D (SEMA4D) in combination with an effective amount of at least one other immune modulating therapy (see Abstract). Evans teaches the isolated binding molecule comprises an antibody (see pg. 3, para. [0012], lines 24-25) wherein the antibody is monoclonal antibody VX15/2503 (see pg. 3, para. [0012], lines 29-30). As set forth under Claim Interpretation, VX15/2503 is pepinemab, which meets the limitation of an “immunoregulatory molecule inhibitor” in view of dependent claim 6. Evans teaches that SEMA4D has been implicated in the development of certain cancers by promoting tumor angiogenesis and is over-expressed in a wide array of tumor types (see pg. 1, para. [0003]). Evans teaches the method to further comprise the administration of an effective amount of an anti-HER2 binding molecule (see pg. 3 para. [0013]), and the immune modulating therapy may comprise the administration of a cancer vaccine (see pg. 2, para. [0011]).
Regarding the limitation of “iv) a pharmaceutically acceptable carrier”, Evans teaches that compositions used in the disclosure comprise pharmaceutically acceptable carriers (see pg. 21, para. [0166]), including preparations for parental administration (see pg. 21, para. [0167]).
It would have been obvious at the time of filing for a person of ordinary of skill in the art to have arrived at the claimed invention by combining the teachings of Kodumudi and Evans, because both references teach anti-cancer combination therapies. One would have recognized that Kodumudi teaches combination therapies comprising the administration of oncodriver pulsed dendritic cells and a fecal microbial transplant (FMT) from a pathologic complete
response (pCR) donor or a cyclin-dependent kinase (CDK) inhibitor, while Evans teaches the administration of anti-HER2 binding molecules and/or cancer vaccines in combination with a binding molecule, VX15/2503 (pepinemab), acting as an inhibitor of SEMA4D. Accordingly, one would have recognized that each of these elements could be combined using known methods and that each element merely performs the same function as it does separately. Hence, one would have recognized that the results of the combination would have been predictable. Finally, one would have been motivated to combine these teachings, because Evans teaches that SEMA4D has been implicated in the development of certain cancers and promotes tumor angiogenesis. Hence, the combination would have been readily apparent and deemed to be a mere (A) combining of prior art elements according to known methods to yield predictable results (see MPEP 2143(I): Rationales to support rejections under 35 U.S.C. 103).
Regarding instant claim 2, claim 2 of Kodumudi recites the anti-cancer therapy of claim 1, wherein the oncodriver is selected from the group consisting of human epidermal growth factor receptor (HER) 1 (HER1), HER2, HER3, EGFR, c-MET, B-Rapidly Accelerated
Fibrosarcoma (BRAF), KIT, Androgen Receptor (AR), Estrogen Receptor (ER), KRAS, TP53, and APC.
Regarding instant claim 3, claim 3 of Kodumudi recites the anti-cancer combination therapy of claim 1, wherein the oncodriver pulsed dendritic cell is activated with IL-12 prior to administration.
Regrading instant claim 4, claim 4 of Kodumudi recites the anti-cancer combination therapy of claim 1, wherein the FMT comprises enriched Anaerosporobacter.
Regarding instant claim 5, claim 5 of Kodumudi recites the anti-cancer combination therapy of claim 1, wherein the CDK inhibitor comprises abemaciclib, ribociclib,
palbociclib, trilaciclib, or taxol.
Regarding instant claim 6, Evans, as discussed above, teaches the cancer therapy to include VX15/2503, which is also known as pepinemab.
Regarding instant claim 9, claim 8 of Kodumudi recites a method of treating a cancer in a subject comprising administering to the subject i) an oncodriver pulsed dendritic cell and ii) a fecal microbial transplant (FMT) from a pathologic complete response (pCR) donor or a cyclin-dependent kinase (CDK) inhibitor. As discussed regarding claim 1, Evans teaches a method of treating cancer comprising administering to the subject an effective amount of an isolated binding molecule which specifically binds to SEMA4D.
Regarding instant claim 10, claim 9 of Kodumudi recites the method of treating a cancer of claim 8, wherein the oncodriver is selected from the group consisting of human epidermal growth factor receptor (HER) 1 (HER1), HER2, HER3, EGFR, c-MET, B-Rapidly Accelerated Fibrosarcoma (BRAF), KIT, Androgen Receptor (AR), Estrogen Receptor (ER), KRAS, TP53, and APC.
Regarding instant claim 11, claim 10 of Kodumudi recites the anti-cancer combination therapy of claim 8, wherein the FMT comprises enriched Anaerosporobacter.
Regarding instant claim 12, claim 11 of Kodumudi recites the anti-cancer combination therapy of claim 8, wherein the CDK inhibitor comprises abemaciclib, ribociclib, palbociclib, trilaciclib, or taxol.
Regarding instant claim 13, Evans, as discussed above, teaches the method comprising the administration of VX15/2503, which is also known as pepinemab.
Regarding instant claim 14, claim 12 of Kodumudi recites the method of treating a cancer of claim 8, wherein the dendritic cells are removed from the subject and pulsed with oncodriver ex vivo.
Regarding instant claim 15, claim 13 Kodumudi recites the method of treating a cancer of claim 8, wherein the pulsed dendritic cells are administered intratumorally.
Regarding instant claim 16, Kodumudi and Evans teach methods of treating cancer in a subject comprising administering to the subject a combination of the claimed therapeutics, as discussed above. Evans teaches the therapeutics of the method (e.g., anti-SEMA4D binding molecules, antibodies, or antigen-binding fragments in combination with at least one other immune modulating therapy) can be delivered directly to the site of the adverse cellular population (see pg. 21, para. [0164]). Similarly, claim 13 of Kodumudi recites the pulsed dendritic cells as being administered intratumorally, which reasonably includes administering to the site of a primary tumor. As discussed previously, Evans teaches the method can be used for inhibiting, delaying, or reducing tumor growth and metastases. Evans teaches the terms “metastasis” and “metastases” refer to cancer cells which spread or transfer from the site of origin (e.g., a primary tumor) to a new distant site where tumor growth and development occurs (see pg. 6, para. [0042]). Hence, a person of ordinary skill would have recognized from the combination of Kodumudi and Evans that these therapeutics could be administered to a site of a primary tumor, and, in so doing, there would be a reasonable expectation for the treatment to have an abscopal effect on secondary tumors. Furthermore, the limitation of the treatment having an abscopal effect is merely an effect of the claimed method, and the only other difference with instant claim 9 is that the administration step is limited to the site of a primary tumor. Hence, the abscopal effect asserted in the claim is inherently present in the combination of Kodumudi and Evans. See MPEP 2112.
Response to Arguments
Regarding the rejections under 35 U.S.C. 103 in view of Czerniecki and Evans, Applicant argues that there is no disclosure nor enabled teaching in either Czerniecki or Evans of a composition comprising a fecal microbial transplant (FMT) from a pathologic complete response (pCR) donor. Therefore, the combination of references cannot account for all the features of the present claims.
Applicant’s arguments with respect to claim(s) 1-2, 5-6, 9-10, 12-14 and 16 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. In the instant case, Applicant’s amendment now requires “a fecal microbial transplant (FMT) from a pathologic complete response (pCR donor)” which Wargo is relied upon in the present rejection.
Regarding the rejection of claim 3 under 35 U.S.C. 103 in view of Czerniecki, Evans and Grohmann, Applicant argues that Grohmann also does not disclose nor suggest a composition comprising an FMT from a pCR donor. Therefore, the combination of references cannot account for all the features of the present claims.
Applicant’s arguments with respect to claim(s) 3 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. In the instant case, Applicant’s amendment now requires “a fecal microbial transplant (FMT) from a pathologic complete response (pCR donor)” which Wargo is relied upon in the present rejection.
Regarding the rejections of claims 4, 11 and 15 under 35 U.S.C. 103 over Czerniecki and Evans in further view of Chen and Wargo, Applicant argues that there is no disclosure not enabled teaching in either Czerniecki or Evans of a combination therapy comprising a fecal microbial transplant from a pathologic complete response donor.
Applicant’s arguments have been fully considered but they are not persuasive for the following reasons.
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). In the instant case, the Wargo reference is relied upon for its teaching of a therapy to treat cancer comprising a fecal microbial transplant from a pathologic complete response donor.
Applicant further argues that Chen makes no mention of using dendritic cell vaccines in combination with fecal microbial transplant (FMT) therapy.
Applicant’s arguments with respect to claim(s) 4, 11 and 15 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. In the instant case, the Chen reference is not used in the present rejection.
Applicant further argues that “Separately” Wargo highlights FMT experiments in combination with immune checkpoint inhibitors. There is no indication that the gut microbiome would influence therapeutic outcomes in a subject to an oncodriver pulsed dendritic cell and/or an immunoregulatory molecule inhibitor, nor that combining FMT with an oncodriver pulsed dendritic cell and an immunoregulatory molecule inhibitor would be effective at treating cancer based on the teachings of Wargo alone or in combination with Czerniecki, Evans, and Chen.
Applicant’s arguments have been fully considered but they are not persuasive for the following reasons.
First, Applicant is reminded that one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). In the instant case, Applicant’s argument that the Wargo reference does not teach the claimed invention when taken “separately” is not a valid argument for overcoming the rejection under 35 U.S.C. 103.
Furthermore, Czerniecki, Wargo and Evans all teach dendritic cell based immunotherapies which may be used in combination with other anticancer therapies, as discussed in the present rejection. Wargo specifically teaches combining FMT therapy with dendritic cell therapy, and Evans specifically teaches the use of an immunoregulatory molecule inhibitor (pepinemab) in combination with a dendritic cell vaccine, as discussed regarding claim 1. Further, each reference describes pulsing or activating the dendritic cells with tumor antigens, and Czerniecki specifically teaches using the oncodriver, HER2, as discussed in the present rejection of claim 1.
In response to applicant's argument that “there is no indication that the gut microbiome would influence outcomes in a subject to an oncodriver pulsed dendritic cell and/or an immunoregulatory molecule inhibitor”, the fact that the inventor has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious. See Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985). In the instant case, all three references teach combining efficacious methods to treat cancer including, FMT + dendritic cell therapy (Wargo) and dendritic cell therapy + pepinemab (Evans). Hence, whether or not each reference teaches the combination to achieve the same results as the present inventors, each reference teaches or suggests combining at least one of the claimed treatments (FMT, pepinemab, taxol) with dendritic cell therapy to treat cancer.
Applicant further argues that the Examiner has identified the various parts of the claimed invention, but has not provided “any scientifically credible evidence as to an apparent reason” for one of ordinary skill in the art to combine FMT with an oncodriver pulsed dendritic cell and an immunoregulatory molecule inhibitor, and thereby enhancing the treatment of cancer, for example breast cancer. The Examiner has merely alleged that Czerniecki, Evans, and/or Wargo provide the elements of the claim and the teachings therein could be combined. However, the mere fact that elements can theoretically be combined does not necessarily mean that it would be obvious to one of ordinary skill in the art to actually combine them. It was only with the benefit of improper hindsight reasoning after review of the disclosure of the present disclosure that a rejection was formulated.
Applicant’s arguments have been fully considered but they are not persuasive for the following reasons.
(1) In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). In the instant case, all facts presented in the rejections are from the prior art of record, including those used in the rationale for their combination.
(2) In response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In this case, each reference (e.g., Evans, Wargo) teaches elements of the claims (e.g., pepinemab, FMT) which are explicitly taught and/or suggested to be used in combination with the other claimed elements (e.g., pulsed dendritic cells) as further taught by the other reference (e.g., Czerniecki), wherein each reference teaches these elements to have the same purpose (i.e., compositions and methods for treating cancer).
Therefore, the examiner disagrees with Applicant’s allegation that the rationale for combining these teachings is based on a purely “theoretical” reasoning outside of what is expressly taught in the references themselves or that this rationale lacks any “scientifically credible evidence” to prove that the references actually teach and/or suggest what they disclose. It is apparent that each reference teaches combination therapies for treating cancer in a subject, wherein each reference teaches tumor antigen-pulsed dendritic cells may be included in the therapy. An “apparent reason” to combine these therapies would be to treat cancer, which a person of skill would have clearly recognized from these disclosures, along with the suggestion to combine these treatments (e.g., every reference teaches dendritic cell therapy and/or taxol may be combined for each treatment).
In response to applicant's argument that the references fail to show certain features of the invention, it is also noted that the features upon which applicant relies (i.e., “enhancing the treatment of cancer, for example breast cancer”) are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993).
Regarding the nonstatutory double patenting rejections over US Patent No. 11,660,330 B2 and co-pending Application No. 18/021,845, Applicant only states: “Applicant respectfully requests that this rejection be held in abeyance until allowable claims are found.”
Applicant's arguments do not comply with 37 CFR 1.111 because they do not clearly point out the patentable novelty which he or she thinks the claims present in view of the state of the art disclosed by the references cited or the objections made. Further, they do not show how the amendments avoid such references or objections.
Per CFR 1.111(b):
In order to be entitled to reconsideration or further examination, the applicant or patent owner must reply to the Office action. The reply by the applicant or patent owner must be reduced to a writing which distinctly and specifically points out the supposed errors in the examiner’s action and must reply to every ground of objection and rejection in the prior Office action. The reply must present arguments pointing out the specific distinctions believed to render the claims, including any newly presented claims, patentable over any applied references. If the reply is with respect to an application, a request may be made that objections or requirements as to form not necessary to further consideration of the claims be held in abeyance until allowable subject matter is indicated. The applicant’s or patent owner’s reply must appear throughout to be a bona fide attempt to advance the application or the reexamination proceeding to final action. A general allegation that the claims define a patentable invention without specifically pointing out how the language of the claims patentably distinguishes them from the references does not comply with the requirements of this section. (Emphasis added)
Per MPEP 804:
A complete response to a nonstatutory double patenting (NSDP) rejection is either a reply by applicant showing that the claims subject to the rejection are patentably distinct from the reference claims, or the filing of a terminal disclaimer in accordance with 37 CFR 1.321 in the pending application(s) with a reply to the Office action (see MPEP § 1490 for a discussion of terminal disclaimers). Such a response is required even when the nonstatutory double patenting rejection is provisional. As filing a terminal disclaimer, or filing a showing that the claims subject to the rejection are patentably distinct from the reference application’s claims, is necessary for further consideration of the rejection of the claims, such a filing should not be held in abeyance. Only compliance with objections or requirements as to form not necessary for further consideration of the claims may be held in abeyance until allowable subject matter is indicated. (Emphasis added)
Accordingly, Applicant is hereby reminded that Applicant must reply to every ground of objection and rejection in the prior Office action. Only objections or requirements as to form not necessary to further consideration of the claims may be requested to be held in abeyance. As the aforementioned reply appears to be a bona fide attempt to advance prosecution, the examiner has updated the nonstatutory double patenting rejections to reflect the amendments made to the claims.
Conclusion
No claims are allowed.
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.
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/DENNIS IGNATIUS ARMATO JR/Examiner, Art Unit 1651
/MELENIE L GORDON/Supervisory Patent Examiner, Art Unit 1651