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 .
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
Priority
The instant application, filed 02/17/2023, is a 371 filing of PCT/US2021/047139, filed 08/23/2021, and claims domestic benefit to US provisional application 63/068,733, filed 08/21/2020.
Status of Application, Amendments, and/or Claims
Applicant’s amendment of 04/21/2026 is acknowledged. Claims 1-3, 5, and 8-13 are amended and claims 6-7 are cancelled. Claims 1-5 and 8-13 are currently pending and are examined on the merits herein.
Withdrawn Objections and Rejections
In the office action of 10/29/2025,
The drawings were objected to as being low resolution. Applicant’s submission of replacement drawings has overcome the objection and the objection is withdrawn.
The specification was objected to for having a registered trademark. Applicant’s amendment to the specification to amend “taxol” to “TAXOL®” has overcome the objection and the objection is withdrawn.
Claims 2 and 9 were objected to. Applicant’s correction to the claims to recite “(HER) 1 (HER1)” and “estrogen” has overcome the objections and the objections are withdrawn.
Claims 5 and 11 were rejected under 35 USC 112(b). Applicant’s amendment to the claims to remove “taxol” has overcome the rejections and the rejections are withdrawn.
Claim 7 was rejected under 35 USC 112(b). The cancellation of the claim has rendered the rejection moot and the rejection is withdrawn.
Claims 10 and 11 were rejected under 35 USC 112(b). Applicant’s amendment to the preamble of the claims to recite “the method of claim 8” has overcome the rejections and the rejections are withdrawn.
Claims 1-2 and 4-13 were rejected under 35 USC 103 over US’421 in view of Yu; and claim 3 was rejected under 35 USC 103 over US’421, Yu, and Grohmann. Applicant’s amendment to the independent claims to remove the limitation of “or a cyclin dependent kinase (CDK) inhibitor” has overcome the rejections and the rejections are withdrawn.
Claims 1-13 were rejected on the grounds of nonstatutory double patenting over copending application 18/021,847. Applicant’s amendment to the independent claims to remove the limitation of “or a cyclin dependent kinase (CDK) inhibitor” has overcome the rejections and the rejections are withdrawn.
The following grounds of objections and/or rejections are maintained or new as necessitated by applicant’s amendment to the claims..
Drawings
The drawings filed on 04/21/2026 are objected to for containing colored figures. It is noted that applicant has filed a petition for colored drawings on 04/21/2026. The instant objection is maintained until either the approval of the colored drawings petition or the filing of grayscale images.
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Specification Objection
The Figure 11 description in the specification references a purple line and a blue line (page 4, lines 2327). It is noted that applicant has filed colored drawings as well as a petition for colored drawings on 04/21/2026. The instant objection is maintained until either the approval of the colored drawings petition or the filing of grayscale images.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1-2, 4, 8-10, and 12 are rejected under 35 U.S.C. 103 as being unpatentable over US 2017/0216421A1 (Czerniecki, B.J. and G.K. Koski) 3 Aug 2017 in view of CA 3 120 709 (Wargo, J.A., et al) 28 May 2020, and Gopalakrishnan, V., et al (2018) The influence of the gut microbiome on cancer, immunity, and cancer immunotherapy Cancer cell 33(4; 57-580).
US’421 teaches that dendritic cells are white blood cells that acquire protein antigens from microbes or even cancerous cells and show, or “present” these antigens to T cells. The T cells, thus activated by the DCs, then initiate systemic immune response to challenge the threat (page 1, [0003]). Popular steps for cancer vaccines include: extracting DCs from cancer patients, loading them with tumor antigens in vitro, supplying unique activation signals to the cells, then re-administering them to the body. This ensures proper DC activation removed from the influence of the tumor microenvironment. When returned to the body, the DCs can then interact with T cells and initiate powerful anti-tumor immunity (page 1, [0004]).
US’421 teaches compositions and methods for producing an FDA-approved injectable multi-dose antigen pulsed dendritic cell vaccine for the personalized treatment of cancer or other disorders (page 4, [0033]). US’421 further teaches that the antigen suitable for loading into the APC is a tumor antigen including transformation related molecules, such as the oncogene HER-2/Neu/ErB-2 (pages 11-12, [0145]-[0147]). US’421 also exemplifies DCs pulsed with HER2 (page 20, [0236]).
US’421 teaches a method of enhancing the immune response in a mammal comprising the steps of: generating immature DCs from monocytes obtained from a mammal, e.g., a patient; pulsing the immature DCs with a composition comprising an antigenic composition; activating the antigen loaded DCs with at least one TLR agonist; cryopreserving the activated antigen loaded DCs; thawing the activated, antigen loaded DCs; and then administering the activated, antigen loaded DCs to a mammal in need thereof (page 15, [0189]). US’421 teaches that the embodiments include a cell that has been exposed or otherwise “pulsed” with an antigen. For example, an APC, such as a DC, may become Ag-loaded in vitro, for instance by culturing the cell ex vivo in the presence of an antigen, or in vivo by exposure to an antigen (page 10, [0128]). US’421 further teaches that the mammalian recipient may be a human and the cells can be autologous with respect to the recipient (page 16, [0190]).
US’421 further teaches that the present embodiments provide an effective therapy to treat cancer wherein the therapy includes changes in the immune response to the tumor so that the immune cells in the tumor site are more effective in attacking the tumor cells. In some instances, the effective therapy includes improving the migration and activity of immune cells in the tumor site (page 17, [0205]). US’421 further teaches that the disclosed methods can be used to treat breast cancer (page 17, [0210]).
US’421 teaches that the vaccines of the disclosure can be provided in a treatment regimen in combination with another cancer medicament for the treatment of cancer in subjects (page 17, [0208]).
US’421; however, does not disclose that the oncodriver pulsed dendritic cells are in combination with or administered in combination with a fecal microbial transplant from a pathologic complete response (pCR) donor.
CA’709 teaches methods 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, from a patient determined to respond to immune checkpoint blockade mono or combination therapy, or from a patient determined to have a non-toxic response to immune checkpoint blockade. CA’709 teaches that, in some embodiments, the fecal matter is transplanted into the colon or rectum of the subject (page 2, [0006]). CA’709 teaches that gut microbiome influences responses to anti-PD1 therapy in late stage melanoma patients through beneficial changes in the anti-tumor immune infiltrate and compared diversity between responders (R) and non-responders (NR) in the gut microbiome. CA’709 further teaches experimental design of studies in germ-free mice (page 45, [0073]; Fig 13A-F) and, in Figure 13D, teaches the use of fecal matter transplant (FMT) from R or NR human donors administered to subjects and the colonization of the subjects with donor microbiota. US’709 further teaches that a “responder” is a patient who benefits from the treatment and who is affected with a cancer and shows a clinically significant relieve in the cancer after treatment. For example, a responsive patient may be one identified as having a complete response, which is disappearance of all target lesions (page 53, [0104]).
CA’709 teaches microbial species common to CICB responding mice across MCA205 and RET tumor models, which include the species Anaerosporobacter mobilis among others (page 114, Table 4).
CA’709 teaches compositions comprising isolated or purified populations of at least one, at least two, or 3, 4, 5, 6, 7, 8, 9, 10, 15, or 20 of the disclosed bacteria (page 64, [0139]).
CA’709 further teaches that the methods and compositions disclosed may include one or more additional therapies known in the art, such as an additional cancer treatment. CA’709 teaches examples of such therapies including dendritic cell therapy (page 69, 2., [0156]-[0160]).
CA’709 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. Dendritic cells are antigen presenting cells (APCs) in the mammalian immune system. In cancer treatment, they aid in cancer antigen targeting (page 69, [0156]). Another strategy is to remove dendritic cells from the blood of a patient and activate them outside of the body. The dendritic cells are activated in the presence of tumor antigens which may be a single tumor-specific peptide/protein or a tumor cell lysate, which is a solution of lysed tumor cells. These cells, with optional adjuvants, are infused and provoke an immune response (page 69, [0159]).
CA’709 further teaches that the cancers that can be treated include breast cancer (page 84, [0206]). CA’709 also teaches that the treatment can increase T cell priming, activation, proliferation, and/or infiltration (page 84, [0205]).
Gopalakrishnan teaches that there is mounting evidence supporting the role of the microbiome in response to cancer therapy, with several recent studies demonstrating the influence of the gut microbiome specifically on the responses to immune checkpoint blockade across cancer types (page 1, paragraph 1). Local immunity is promoted via recognition of pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide and flagellin, by pattern recognition of pathogen-associated-molecular patterns (RAMPs) by pattern recognition receptors (PRRs) such as TLRs present on IECs as well as innate immune effectors within the gut. Metabolites produced by bacteria may also impact local immunity via production of short chain fatty acids, which among a number of key activities, have been shown to augment immunity via IgA production by plasma cells (page 3, paragraph 2). RAMPs act to induce maturation of antigen-presenting cells such as dendritic cells as they sample antigen. Once activated, DCs travel to mLNs where they interact with and stimulate naïve T cells to form CD4+ T cells, specifically CD4+ T regulatory (Tregs) and Th17 cells, both of which have tropism for the gut. DCs may also directly stimulate CD8+ T cells (page 3, paragraph 3).
Gopalakrishnan further teaches that exemplification of the importance of eubiosis in preserving immunity is seen in the case of response to vaccination. A highly diverse microbiota has been associated with improved adaptive immune responses to a variety of vaccines in infants. Specific components of the microbiota can prime the immune system by activating TLR signaling pathways serving as a natural vaccine adjuvant. Thus, it is increasingly clear that the gut microbiota impacts not only local immunity, but also systemic immune responses (page 4, paragraph 3).
Gopalakrishnan also teaches that, in studies, supplementation with an oral probiotic containing Bifidobacterium restored anti-tumor efficacy of PDL1 blockade in mice with an “unfavorable” gut microbiota, which primarily occurred through enhanced dendritic cell maturation resulting in increased tumor-specific CD8+ T cell activity (page 8, paragraph 1).
Gopalakrishnan also teaches studies involving manipulation of the gut microbiome to enhance response to cancer immunotherapy including a study in breast cancer patients in which probiotics are being administered and the number of CD8+ cells changed from baseline is being evaluated (page 21, Table 1, row 5).
It would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to modify the composition and methods of treating cancer disclosed by US’421, in which oncogene pulsed DCs are used as anti-cancer vaccines, by further including in the compositions and methods the FMT therapies disclosed by CA’709 and as further supported by Gopalakrishnan. An ordinarily skilled artisan would have been motivated to further administer the FMT therapies of CA’709 because Gopalakrishnan teaches that there is mounting evidence that the gut microbiome influences responses to cancer therapy and that gut microbiota can act as vaccine adjuvant, enhancing dendritic cell maturation resulting in increased tumor-specific CD8+ T cell activity. An ordinarily skilled artisan would have had a reasonable expectation of success because CA’709 teaches the combination of the FMT compositions with additional anti-cancer agents, including dendritic cells manipulated outside of the body, which corresponds with the dendritic cells taught in the compositions and methods of US’421. Additionally, all three of US’421, CA’709, and Gopalakrishnan teach the treatment of cancer, including breast cancer.
Claim 3 is rejected under 35 U.S.C. 103 as being unpatentable over US 2017/0216421A1 (Czerniecki, B.J. and G.K. Koski) 3 Aug 2017 in view of CA 3 120 709 (Wargo, J.A., et al) 28 May 2020, and Gopalakrishnan, V., et al (2018) The influence of the gut microbiome on cancer, immunity, and cancer immunotherapy Cancer cell 33(4; 57-580) as applied to claim 1 above, and in further view of Grohmann, U., et al (1998) IL-12 acts directly on DC to promote nuclear localization of NF-κB and primes DC for IL-12 production Immunity 9; 315-323.
The combination of US’421, CA’709, and Gopalakrishnan teach the anti-cancer combination of claim 1 as discussed in detail above.
As discussed in detail above, US’421 teaches methods in which DCs are supplied unique activation signals before re-administration to the body. US’421 further teaches that the DCs can be activated by a cytokine and/or a toll like receptor ligand (page 9, [0111]). Traditional DC-based vaccines comprise of matured DCs generated from using a cytokine cocktail mixture including combinations of TNF, IL-6, PGE2, and IL-1β. The embodiments disclosed by US’421 utilize TLR agonists to mature the DCs and stimulate production of signal (page 12, [0152]). The stimulation of DCs with a combination of TLR ligands leads to the production of increased amounts of IL-12 (page 12, [0153]).
The combination of US’421, CA’709, and Gopalakrishnan do not disclose that the DCs are activated with IL-12.
Grohmann teaches that DC are the most potent cellular initiators of the immune response and, in particular, are responsible for the induction of primary antigen-specific immune reactions. In keeping with this notion is their ability to secret IL-12 and to direct the development of Th1 cells from naïve CD4+ T cells. Based on previous findings that recombinant IL-12 will prime purified DC cultures pulsed with a tumor peptide in vitro for effective sensitization in vivo, the present study investigated the possible expression of an IL-12 receptor by DC. The results indicate that DC express an IL-12R and that IL-12 signaling in these cells may involve early events that differ from those operating in T lymphocytes, including nuclear localization of the NF-κB family. These events may ultimately lead to functional responses that are independent of the presence of IFNγ, including increased expression of MHC class II antigens and priming of DCs for LPS-induced production of IL-12 (paragraph bridging page 315).
The studies of Grohmann demonstrate that DC express a single class of high-affinity IL-12R on their surface and that IL-12 binding on DC transduces activation signals via nuclear localization of p50 and relB, two members of the NF-κB family. This unique feature of IL-12 effects on DC may confer unique actions on the target cells, including increased class II antigen expression and enhanced production of endogenous IL-12 (page 321, left column, paragraph 3).
It would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method taught by the combination of US’421, CA’709, and Gopalakrishnan for activating the DCs to either further include IL-12 with the disclosed cytokines and/or TLR ligand, or, alternatively, to substitute the disclosed cytokines and/or TLR ligand with IL-12, based on the teachings of Grohmann. An ordinarily skilled artisan would have been motivated to make these modifications as Grohmann teaches that DCs express a high-affinity IL-12R on their surface and that IL-12 increases antigen expression and enhances production of endogenous IL-12. An ordinarily skilled artisan would have had a reasonable expectation of success as US’421, CA’709, Gopalakrishnan, and Grohmann teach the activation of DCs and the expression of IL-12 by activated DCs.
Claims 5 and 11 are rejected under 35 U.S.C. 103 as being unpatentable over US 2017/0216421A1 (Czerniecki, B.J. and G.K. Koski) 3 Aug 2017 in view of CA 3 120 709 (Wargo, J.A., et al) 28 May 2020, and Gopalakrishnan, V., et al (2018) The influence of the gut microbiome on cancer, immunity, and cancer immunotherapy Cancer cell 33(4; 57-580) as applied to claims 1 and 8 above, and in further view of Schaer, D.A., et al (2018) The CDK4/6 inhibitor abemaciclib induces a T cell inflamed tumor microenvironment and enhances the efficacy of PD-L1 checkpoint blockade Cell Reports 22; 2978-2994.
The combination of US’421, CA’709, and Gopalakrishnan teach the anti-cancer combination of claim 1 and the method of treating cancer of claim 8 as discussed in detail above.
The combination of US’421, CA’709, and Gopalakrishnan do not disclose that the composition or method further include a CDK inhibitor comprising abemaciclib, ribociclib, palbociclib, or triaciclib.
Schaer teaches the immune modulating properties of abemaciclib that include upregulation of antigen presentation on tumor cells and increased T cell activation. These activities synergize with anti-PD-L1 therapy to further enhance immune activation, including macrophage and DC antigen presentation, and also lead to a reciprocal increased in abemaciclib dependent cell cycle gene regulation (Cover page, in brief).
Abemaciclib is an inhibitor of CDK4/6 and had been recently approved for the treatment of hormone receptor-positive breast cancer. Schaer used murine syngeneic tumor models and in vitro assays to investigate the impact of abemaciclib on T cells and the tumor immune microenvironment. Abemaciclib monotherapy resulted in tumor growth delay that was associated with an increased T cell inflammatory signature in tumors. Combination with anti-PD-L1 therapy led to complete tumor regressions and immunological memory, accompanied by enhanced antigen presentation, a T cell inflamed phenotype, and enhanced cell cycle control. Schaer concludes that the data presented collectively supports the clinical investigation of abemaciclib with agents such as anti-PD-L1 that modulate T cell anti-tumor immunity (page 2978, Summary).
Schaer further studied the observed synergistic effects between abemaciclib and anti-PD-L1 and teaches that the top-scoring pathway by Ingenuity Pathway Analysis (IPA) was related to dendritic cell (DC) maturation; this observation indicates that phased abemaciclib and anti-PD-L1 combination treatment may affect immunological events beyond T cell activation and may modulate innate immune mechanisms resulting in enhanced antigen presentation and T cell priming (page 2985, paragraph bridging columns and right col. paragraph 2). Schaer teaches that during abemaciclib monotherapy, there was a notable trend towards the upregulation of MHC class II and/or antigen presentation, suggesting that the monotherapy directly or indirectly, has the potential to modulate innate immune and/or DC functions (page 2987, left column, paragraph 1).
Schaer teaches that the effects of abemaciclib appear to be the result of impact on multiple immune-related pathways, including the upregulation of innate immune pathways related to DC maturation, upregulation of genes associated with a T cell inflammatory and activated phenotype, and modulation of tumor-intrinsic antigen processing and presentation mechanisms. Together, these effects lead to immune cell activation and tumor clearance as well as direct effects on primary human T cells during their response profile without inhibiting their ability to proliferative signals (page 2990, paragraph bridging columns).
It would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to modify the anti-tumor combination and method taught by the combination of US’421, CA’709, and Gopalakrishnan by further including and administering the CDK inhibitor abemaciclib as taught by Schaer. An ordinarily skilled artisan would have been motivated to further include/administer abemaciclib as Schaer teaches that abemaciclib impacts multiple immune pathways including upregulation of immune pathways related to DC maturation, upregulation of genes associated with a T cell inflammatory and activated phenotype, and modulation of tumor-intrinsic antigen processing and presentation mechanisms. An ordinarily skilled artisan would have had a reasonable expectation of success as Schaer teaches that the data presented collectively supports the clinical investigation of abemaciclib with agents that modulate T cell anti-tumor immunity. Additionally, all of US’421, CA’709, Gopalakrishnan, Schaer teaches the treatment of cancer, including breast cancer.
Claim 13 is rejected under 35 U.S.C. 103 as being unpatentable over US 2017/0216421A1 (Czerniecki, B.J. and G.K. Koski) 3 Aug 2017 in view of CA 3 120 709 (Wargo, J.A., et al) 28 May 2020, and Gopalakrishnan, V., et al (2018) The influence of the gut microbiome on cancer, immunity, and cancer immunotherapy Cancer cell 33(4; 57-580) as applied to claim 8 above, and in further view of Yu, B., et al (2003) Effective combination of chemotherapy and dendritic cell administration for the treatment of advanced-stage experimental breast cancer Clinical Cancer Research 9; 285-294.
The combination of US’421, CA’709, and Gopalakrishnan teach the method of claim 8 as discussed in detail above.
The combination of US’421, CA’709, and Gopalakrishnan do not disclose that the dendritic cells are administered intratumorally.
Yu investigated the treatment of advanced stage breast cancer using a combination of chemotherapy and dendritic cell administration (abstract, purpose). Yu teaches that previous experiments established proof-of-concept that the combination of the intratumoral placement of ex vivo generated autologous DCs in concert with apoptosis inducing therapy might lead to a generation of systemic antitumor immunity. Yu used a tumor model of mammary adenocarcinoma DA3. DC administration was combined with 3 cycles of paclitaxel at a dose that induces apoptosis and moderate immune suppression. It was found that such combined treatment induces significant antitumor immune response that was associated with a marked antitumor effect (page 286, left column, paragraph 1).
Yu teaches that combined treatment resulted in the induction of HA-specific CD8-mediated responses in all nine of the tested mice, and CD4-mediated responses in four of six treated mice. These effects were only observed if DCs were injected into the tumor site, but not when injected by i.v. No specific responses were found in mice treated with either chemotherapy or DCs alone (abstract, results). Yu further teaches that combined treatment increased median survival from 29 days in the control group to 45 days (page 291, right column, paragraph 2; Figure 6).
It would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method taught by the combination of US’421, CA’709, and Gopalakrishnan by administering the pulsed dendritic cells intratumorally based on the teachings of Yu. An ordinarily skilled artisan would have been motivated to administer the DC intratumorally as Yu teaches anti-tumor response was more significant when DCs were administered intratumorally comped to, for instance, injection by i.v. An ordinarily skilled artisan would have had a reasonable expectation of success because, like US’421, CA’709, and Gopalakrishnan, Yu teaches DC administration for the treatment of breast cancer.
Response to Arguments
Applicant’s arguments in the response filed 04/21/2026 have been fully considered in so far as they apply to the rejections of the instant office action, but are not persuasive.
Applicant argues that the previously applied references US’421 (referenced by applicant in the response as “Czerniecki”) and Yu does not disclose or enable a combination therapy including a FMT from a pCR donor.
In the rejections of the instant office action, the references CA’709 and Gopalakrishnan are applied to demonstrate that combination therapies with complete response donor FMT were taught by the prior art, including with dendritic cells, and that the art recognized that the gut microbiome impacts anti-cancer immunotherapy and immune response.
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.
18/021,847
Claims 1-5 and 8-13 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 and 9-15 of copending Application No. 18/021,847. Although the claims at issue are not identical, they are not patentably distinct from each other.
App’847 claims pharmaceutical composition comprising i) at least one oncodriver pulsed dendritic cell and ii) a FMT from a pCR donor; further comprising an immunoregulatory molecule (claim 1). The claims further recite that the oncodriver is selected from HER1, HEr2, HER3, EGFR, c-MET, BRAF, KIT, AR, ER, KRAS, TP53, and APC (claim 2) and that the oncodriver pulsed dendritic cell is activated with IL-12 prior to administration. App’847 further claims that the FMT is enriched Anaerosporobacter, and that the CDK inhibitor is abemaciclib, ribociclib, palbociclib, Trilaciclib, or Taxol (claims 4-5). App’847 further clams a method of treating cancer comprising administering the anti-cancer combination and that the DC is administered intratumorally (claim 15). App’847 claims that the DC are removed from the subject and pulsed with the oncodriver ex vivo (claim 14).
The claims of App’847 differ from the instant claims in that App’847 claims an additional immunoregulatory molecule in the combination/treatment.
The instant claims are drawn to combinations and methods using “comprising” language. The instant specification defines “comprising” as meaning that the compositions, methods, etc. include the recited elements, but do not exclude others (page 8, lines 7-16). A definition which is consistent with that of MPEP 2111.03 I. As the instant claims encompass combinations and methods that include the recited elements as well as additional, unrecited elements, the claims of App’847 are a species of the instantly claimed combination and method and; therefore, anticipate the instant claims.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Arguments
In the response filed 04/21/2026, applicant requests that the nonstatutory double patenting rejection be held in abeyance until the indication of allowable subject matter.
As no subject matter is indicated as allowable in the instant office action, the rejection is maintained.
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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to AUDREY L BUTTICE whose telephone number is (571)270-5049. The examiner can normally be reached M-Th 8:00-4:00.
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, Joanne Hama can be reached on 571-272-2911. 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.
/AUDREY L BUTTICE/Examiner, Art Unit 1647
/SCARLETT Y GOON/Supervisory Patent Examiner
Art Unit 1693
Prosecution Insights