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 .
Application Status
The amended claims filed on August 11, 2025 are acknowledged. Claims 3, 5, 8, 16, and 21-22 are canceled. Claims 1-2, 6, 9-11, 14, 17-18, 23-24, 33, and 36-37 are amended. Claims 39-40 are newly added. Claims 1-2, 6, 9-11, 14, 17-18, 23-24, 33, and 36-40 are pending and under examination herein.
Claim Rejections Withdrawn
All prior rejections of claims 3, 5, 8, 16, and 21 are rendered moot by the cancelation of the claims.
The previous grounds of rejection of claims 6, 9, 11, 14, 17, and 37-38 under 35 U.S.C. § 112(b) are withdrawn in view of Applicant's claim amendments thereto.
The rejection of claim 9 under 35 U.S.C. § 112(d) is withdrawn in view of Applicant's claim amendments thereto.
The rejection of claims 1-2, 6, 11, and 38 under 35 U.S.C. § 101 is withdrawn in view of Applicant's amendments to claims 1 and 38.
The rejection of claims 1-2, 6, 9, 11, and 14 under 35 U.S.C. 102 as being anticipated by Hamana (Human Gene Therapy (2016) 27(11): 936-945; cited in IDS) as evidenced by Overwijk (Current Protocols in Immunology (2000) 20.1.1-20.1.29) is withdrawn in view of Applicant's amendments to claim 1.
The rejection of claims 1-2, 6, and 11 under 35 U.S.C. 102 as being anticipated by Westcott (Journal of Virology (2015) 89(15): 7944-7954) is withdrawn in view of Applicant's amendments to claim 1.
MAINTAINED REJECTIONS AND NEW REJECTIONS NECESSITATED BY AMENDMENT
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1-2, 6, 9, 11, 17-18, 23-24, 33, 36-38, and 40 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention. This is a new rejection necessitated by Applicant's claim amendments.
Claim 1 recites the limitation "the cell" in line 5. There is insufficient antecedent basis for this limitation in the claim. Because the claim recites several types of cells – “a modified human cancer cell” in list item (a) and “a dendritic cell, macrophage, B cell, T cell, or NK cell” in list item (b) – the claim scope is indefinite because “the cell” could be referring to any one of these cells.
Claims 6, 9, 11, 17-18, 23-24, 33, 36-38, and 40, which depend from claim 1, do not remedy this deficiency and are similarly rejected.
If Applicant is intending that “the cell” in the wherein clause refer to one of “a dendritic cell, macrophage, B cell, T cell, or NK cell” as recited in list item (b), it is suggested that the claim could be amended to recite, e.g., “…wherein said dendritic cell, macrophage, B cell, T cell, or NK
Claim 2 recites the limitation “wherein the IFN-β receptor agonist is … presented on the outer membrane of the cell". There is insufficient antecedent basis for this limitation in the claim. Both claim 2 and claim 1, from which the claim depends, recites several types of cells – “a modified human cancer cell” in list item (a) and “a dendritic cell, macrophage, B cell, T cell, or NK cell” in list item (b) – and it is unclear whether “the cell” in line 3 is meant to refer to the cell type as recited in list item (a) or to one of the many cell types as recited in list item (b).
Claim 18 recites the limitation "the cell expressing an interferon-β (IFN-β) receptor agonist and the tumour antigen" in lines 2-3. There is insufficient antecedent basis for this limitation in the claim. As previously stated, “the cell” may be referring back to one of several types of cells that are recited in claim 1. Furthermore, the wording of the claim is unclear because it recites that the “active or main ingredient” (singular) in the composition is “the cell expressing an interferon-β (IFN-β) receptor agonist and the tumour antigen”, which could either refer to two ingredients (i.e., a cell and a tumor antigen) or, alternatively, a single ingredient (i.e., a cell that both expresses an IFN-β receptor agonist and comprises a tumor antigen).
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
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 (i.e., changing from AIA to pre-AIA ) 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.
Claims 1-2, 6, 9-11, 17-18, 23, 24, 36-38, and 40 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Okano (EP 1690937 A1; published August 16, 2006; cited in IDS). This is a maintained rejection that has been updated in response to Applicant's claim amendments.
Okano discloses methods for introducing a gene into a dendritic cell (DC) by contacting a minus-strand RNA virus with the dendritic cell, to produce dendritic cells having utility as a vaccine (Abstract). Okano teaches that DC vaccines are useful for immunotherapy against cancers due to the high ability of DCs for immune induction (¶ 0008). Said DC vaccines can be produced by introducing, e.g., a desired tumor antigen gene for tumor immunotherapy, by mixing DCs with the lysate of tumor cells, which Okano teaches would be expected to prolong the duration of in vivo tumor antigen presentation compared to tumor lysate and peptide pulse methods (¶ 0008; 0101-0105). Okano further teaches that the invention relates to the use of DCs in the induction of immune responses for anti-tumor immunotherapy, by expressing a cytokine (e.g., IFN-β) in the DC to stimulate the immune system against cancers (¶ 0105, 0107), relevant to instant claims 1-2, 6, 9, and 11. Okano discloses that DCs introduced with a minus-strand RNA viral vector carrying the IFN-β gene very strongly activate cytotoxic T lymphocytes to suppress tumor growth, rendering them an effective therapeutic agent for anti-tumor immunotherapy (¶ 0110, 0148-0151). Okano further discloses that DCs genetically modified using the minus-strand RNA viral vector are useful to stimulate T cells in patients in vivo, in vitro, and ex vivo (¶ 0116).
Relevant to instant claims 1, 17-18, 24, and 38, Okano teaches that the vector may be combined with desired pharmaceutically acceptable carriers in the production of compositions containing the vector (¶ 0099). Further, the compositions comprising a tumor antigen peptide and a cytokine may be useful as a vaccine administered for a tumor (¶ 0099, 0102).
Regarding instant claims 10, 23, 36-37, and 40, these claims set forth further limitations with respect to an immunogenic composition comprising a modified human cancer cell as recited in list item (a) of claim 1. These claims also retain the same limitations as previously set forth in claim 1, list item (b), for “a tumour antigen and a dendritic cell”. Because Okano anticipates claim 1 – in particular, the limitations set forth in list item (b) – Okano also anticipates instant claims 10, 23, 36-37, and 40.
Response to Arguments
Applicant's arguments filed August 11, 2025 have been fully considered but they are not persuasive.
Applicant asserts that Okano does not teach or suggest the features of claim 10, the features of which are newly incorporated into amended claim 1, and thus, does not anticipate the instantly claimed invention. For reference, claim 10 was previously drawn to “the immunogenic composition of claim 1, wherein the cell expressing an IFN-β receptor agonist is a human cancer cell that has been modified to express the IFN-β receptor agonist.” Remarks at pages 9-10.
In response, it is noted that claim 1 has also been amended to recite that the immunogenic composition comprises “a modified human cancer cell expressing an IFN-β (IFN-β) receptor agonist” or “a tumour antigen and a dendritic cell, macrophage, B cell, T cell, or NK cell”. By the recitation of “or” in the claim, only one of these two elements is required in order for a prior art reference to anticipate the instantly claimed immunogenic composition. In the present case, Okano expressly teaches a dendritic cell expressing a tumor antigen (and an IFN-β polypeptide), thereby anticipating the instant claims.
For these reasons, the rejection is maintained.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1-2, 6, 9-11, 14, 17-18, 23-24, 33, and 36-40 are rejected under 35 U.S.C. 103 as being unpatentable over Durda (US 2004/0253235 A1; cited in PTO-892 mailed April 9, 2025) in view of Hamana (Human Gene Therapy (2016) 27(11): 936-945; cited in IDS) and Keenan (Semin Oncol (2012) 39(3): 276-286; cited in IDS). This is a maintained rejection that has been updated to reflect Applicant's amendments to the claims.
Durda provides methods of modulating tumor antigen associated (TAA) expression to treat tumors and increase an immune response against tumor cells (Abstract). In embodiments of the invention, Durda discloses method that comprise administering to a subject with a tumor an amount of IFN-β receptor agonist and a TAA sufficient to increase an immune response against the tumor cell or to treat a tumor (Summary, ¶ 0006-0008; e.g., claims 1 and 14), relevant to instant claims 1 and 24. Relevant to instant claims 1, 14, and 40, the TAA is present on or in a cell, including a tumor cell or irradiated tumor cell that is incapable of growth but still able to induce an immune response (e.g., claims 7 and 23; ¶ 0040). Relevant to instant claims 1 and 9, Durda also teaches that TAAs can be loaded into dendritic cells or other antigen-presenting cells (¶ 0042). Durda teaches, “By combining IFN-β therapy with tumor-associated antigens, both enhanced immunity and enhanced tumor antigen expression leading to more effective tumor killing in vivo are expected” (Example 7, ¶ 0161). Relevant to instant claim 38, the treatment is administered as a vaccine in human patients (Example 7, ¶ 0193-0197).
Relatedly, Durda also discloses methods of treating a subject having a tumor or at risk of having a tumor, and of increasing effectiveness of anti-tumor therapy, comprising administering to the subject with a tumor an amount of an IFN-β receptor agonist and an immune cell that interacts with a tumor cell sufficient to treat the subject and increase the effectiveness of the therapy, wherein the cell is selected from a T cell, NK cell, or macrophage (e.g., ¶ 0095). Durda discloses that in an additional aspect the cell is pre-selected to bind to a TAA expressed by the tumor (¶ 0095).
Relevant to instant claim 6, Durda teaches that the TAAs are antigenic molecules for which expression thereof facilitates interaction of immune cells with tumor cells and include peptidic immunogenic fragments thereof (¶ 0033-0036, 0038, 0041).
Relevant to instant claims 11 and 39, Durda teaches that the IFN-β receptor agonist may be IFN-β peptide, an IFN-β mimic, or an IFN-β receptor antibody (¶ 0011, 0032, 0051-0053, 0057-0059; claims 2 and 9).
Relevant to instant claim 17-18, Durda teaches pharmaceutical compositions comprising an IFN-β receptor agonist and agents having a TAA-inducing activity in combination with pharmaceutically acceptable carriers or diluents (¶ 0103-0105).
Relevant to instant claim 33, Durda discloses that treatments of the invention may further include administering an immune enhancing therapy (e.g., an antibody that specifically binds to a TAA) (¶ 0015, 0047, and 0087).
However, Durda does not expressly teach that the IFN-β receptor agonist is comprised in a cell, nor a method of treatment with an IFN-β receptor agonist and a TAA that further comprises administering an immune checkpoint inhibitor.
Hamana teaches that IFN-β, a type of cytokine in the Type I IFN family, is used in cancer therapy and has highly potent anti-tumor effects (Introduction, page 936). However, several injections per week of IFN-β are required in patients in order to maintain an effective circulating concentration due to its rapid elimination from the circulation (Introduction, page 936). In view of this limitation, Hamana teaches that gene therapy is an attractive approach for continuous supply of IFN-β without decreasing its biological activity. Hamana constructed a plasmid vector encoding the murine IFN-β gene under control of the Mx promoter (pMx-IFN-β), which was transfected into B16-BL6 (mouse melanoma cell line) cells to achieve sustained long-term expression of IFN-β (Abstract; Introduction, page 937; Methods, page 938), relevant to instant claims 1 and 11. B16-BL6 cells secreted IFN-β polypeptide in culture media after transfection with pMx-IFN-β, with no detectable cytotoxicity (Results, page 939; Figure 1), relevant to instant claim 2.
Keenan reviews the design and implementation of whole cell cancer vaccines. Relevant to instant claims 10, 14, 16, and 36-38, Keenan teaches, “The advantage of whole tumor cells used as a vaccine rather than a specific protein or peptide tumor antigen is that the cells provide a source of all potential antigens, eliminating the need to identify the most optimal antigen to target in a particular type of cancer” (“Whole cell cancer vaccines”, page 2). Further, “Using autologous tumor cells in the generation of a whole cell cancer vaccine ensures that patients are vaccinated with cells containing the same tumor antigens that their tumor expresses. However, this approach is technically limited because harvesting tumor cells and generating a vaccine line which expresses a standardized amount of cytokine is not always feasible and can be financially costly and time consuming. Vaccines made from allogeneic cells circumvent the issue of individualizing each patient’s therapy and by using several cell lines derived from different tumors in the vaccine, there is an increased likelihood that the patient’s tumor will share antigens expressed by the vaccine cells, including important tumor antigens overexpressed or mutated in a high percentage of that particular cancer” (“Whole cell cancer vaccines”, page 2). Keenan also teaches that whole cell vaccines have been genetically modified to express cytokines to stimulate the immune response to the injected irradiated tumor cells, which has been shown to be safe in patients with many types of cancer in phase I and II trials (“Whole cell cancer vaccines”, page 2).
Keenan additionally instructs that rarely are single treatment agents effective in the treatment of cancer, and thus, combination therapy with immune checkpoint inhibitors in addition to whole cell vaccine vectors is used to stimulate the protective immune response and inhibit the suppressive immune response (Abstract), relevant to instant claim 33.
It would have been obvious to one of ordinary skill in the art, before the filing date of the instantly claimed invention, to arrive at an immunogenic composition comprising a modified (inactivated) human cancer cell expressing an IFN-β receptor agonist and a tumor antigen, and to administer such a composition in methods of treating cancer, based on the collective teachings of Durda, Hamana, and Keenan. The skilled artisan would have been motivated to do so because a composition comprising a combination of an IFN-β receptor agonist and a TAA would generate both enhanced immunity and enhanced tumor antigen expression leading to more effective tumor killing in vivo, as suggested by Durda. The skilled artisan would further have been motivated to incorporate the IFN-β receptor agonist into a cell (e.g., an irradiated tumor cell) because, as taught by Hamana, IFN-β is rapidly eliminated from the circulation after administration to patients. There would have been a reasonable expectation of success because one of ordinary skill in the art would have recognized that the genetic modification of irradiated tumor cells in whole cell vaccines, e.g., with a cytokine (as described by Keenan), and the genetic modification of the B16-BL6 tumor cells with pMx-IFN-β (as described by Hamana), are functionally equivalent modifications that achieve the common purpose of stimulating the immune response, and that this modification increases the efficacy of the anti-tumor therapy.
Response to Arguments
Applicant's arguments filed August 11, 2025 have been fully considered but they are not persuasive.
Applicant asserts that the combination of Durda, Hamana, and Keenan do not render claim 1 unpatentable. Applicant reiterates the position of the Office with respect to teachings of Durda, but does not appear to expressly articulate any specific deficiencies of Durda. Remarks at pages 12-13. Applicant states that the Office relies on Hamana for teaching the features of claim 1, but that Hamana (which Applicant asserts does not teach or suggest features which were previously included in claims 10 and 21) does not remedy the deficiencies of Durda. Remarks at pages 7-9 and 12-13. Applicant further argues that Keenan does not teach each of the features of claim 1 as presently amended and does not remedy the deficiencies of Durda and Hamana. Remarks at page 13.
Applicant further asserts that they surprisingly discovered that “the claimed immunogenic compositions are effective in protecting mice from cancer”, citing experimental evidence from Examples 2 and 3 of the specification. The cited experiments describe the injection of mice with B16 (murine-derived) melanoma expressing GFP ± IFNα1/β. Applicant states that the cited references do not teach or suggest these surprising results and that there would not have been a reasonable expectation of success in arriving at the instantly claimed composition. Remarks at pages 13-14.
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). It is held that Durda establishes the utility of the combination of at least an IFN-β receptor agonist in combination with either a tumor cell (e.g., an inactivated tumor cell) or dendritic cell expressing a tumor-associated antigen in the treatment of cancer. Based on the limitations noted by Hamana, namely that IFN-β is rapidly eliminated from the circulation when administered alone, it would have been obvious to implement the solution proposed by Hamana, specifically, modifying a cancer cell to express IFN-β to achieve long-term, sustained expression of IFN-β. As also noted by Hamana, IFN-β has potent anti-tumor properties. Keenan further sets forth that using irradiated human cancer cells (autologous or allogenic) which have been modified to express cytokines stimulates an immune response to the injected irradiated tumor cells and has been shown to be safe in human patients. Accordingly, the combination of cited references establishes that one of ordinary skill in the art would have had a reasonable expectation of success in generating the presently claimed composition comprising a human cancer cell modified to express IFN-β, and further, that such a composition would have utility in treating a cancer.
With respect to the surprising experimental results described by the Applicant, it is noted that the cited experimental findings are neither drawn to (a) a modified human cancer cell expressing an IFN-β receptor agonist or (b) a dendritic cell, macrophage, B cell, T cell, or NK cell and a tumor antigen. Accordingly, the arguments with respect to these surprising discoveries are not found persuasive.
For these reasons, the rejection is maintained.
Claims 1-2, 6, 9, 11, 17-18, 24, and 38 are rejected under 35 U.S.C. 103 as being unpatentable over Durda (US 2004/0253235 A1; supra) in view of Okano (EP 1690937 A1; cited in IDS; supra). This is a maintained rejection.
The teachings of Durda are recited in the 35 U.S.C. § 103 rejection above.
However, Durda does not expressly teach a composition comprising a cell expressing the IFN-β receptor agonist (and/or tumor antigen), wherein the cell is a dendritic cell, macrophage, or a B cell.
The teachings of Okano are recited in the 35 U.S.C. § 102 rejection above.
It would have been obvious to one of ordinary skill in the art, before the filing date of the instantly claimed invention, to arrive at an immunogenic composition comprising a dendritic cell expressing a TAA and an IFN-β receptor agonist, and to administer such a composition in methods of treating cancer, based on the collective teachings of Durda and Okano. The skilled artisan would have been motivated to do so because a composition comprising a combination of an IFN-β receptor agonist and a TAA would generate both enhanced immunity and enhanced tumor antigen expression leading to more effective tumor killing in vivo, as suggested by Durda. The skilled artisan would further have been motivated to incorporate the IFN-β receptor agonist into a cell (e.g., dendritic cell) because, as taught by Okano, DCs expressing IFN-β are highly effective in suppressing tumor growth, rendering them an attractive option for anti-tumor immunotherapy. There would have been a reasonable expectation of success because one of ordinary skill in the art would have recognized that the IFN-β receptor agonist administered in the methods taught by Durda and the IFN-β-expressing DCs taught by Okano both shared a common purpose (i.e., enhancing immune responses against tumors) and were functionally equivalent.
Response to Arguments
Applicant's arguments filed August 11, 2025 have been fully considered but they are not persuasive.
Applicant asserts that the combination of Durda and Okano do not render claim 1 unpatentable. Applicant states that the neither Durda or Okano, individually or in combination, teach or suggest the immunogenic composition as recited in presently amended claim 1. Remarks at page 15. Applicant reiterates the surprising discoveries exemplified in Examples 2-3 of the disclosure and states that the cited references do not teach or suggest such results or that one could arrive at the instantly claimed composition with a reasonable expectation of success. Remarks at page 15. Further, Applicant respectfully submits that some of the features of claim 10 (which was not previously included in this rejection) have been incorporated into presently amended claim 1.
In response, it is held that Durda establishes the utility of the combination of at least an IFN-β receptor agonist in combination with dendritic cell expressing (“loaded with”) a tumor-associated antigen in the treatment of cancer. Based on the further teachings of Okano, with respect to expressing a TAA and/or IFN-β in a dendritic cell, one of ordinary skill in the art would have had a reasonable expectation of success that one could express one or both peptides in a dendritic cell and furthermore use such a dendritic cell as a therapeutic agent for anti-tumor therapy.
With respect to the surprising experimental results described by the Applicant, it is noted that the cited experimental findings are neither drawn to (a) a modified human cancer cell expressing an IFN-β receptor agonist or (b) a dendritic cell and a tumor antigen (or a dendritic cell expressing a tumor antigen and an IFN-β receptor agonist). Accordingly, the arguments with respect to these surprising discoveries are not found persuasive.
With respect to the arguments regarding features of previous claim 10, it is noted that the immunogenic composition of claim 1 comprises “a modified human cancer cell expressing an IFN-β (IFN-β) receptor agonist” or “a tumour antigen and a dendritic cell, macrophage, B cell, T cell, or NK cell”. By the recitation of “or” in the claim, only one of these two elements is required in order for a prior art reference to anticipate or otherwise render obvious the instantly claimed immunogenic composition. In the present case, Durda expressly recites a dendritic cell “loaded with” a TAA peptide, and Okano expressly teaches a dendritic cell expressing a tumor antigen and an IFN-β polypeptide.
For these reasons, the rejection is maintained.
Citation of Relevant Art
The prior art made of record and not relied upon is considered pertinent to Applicant's disclosure:
Liu (US 2006/0165668 A1) discloses compositions comprising modified cancer cells and methods of use thereof in treating cancer (e.g., Abstract). The cancer cells are genetically modified to express one or more therapeutic proteins, e.g., IFN-β (e.g., ¶ 0021-0024). In embodiments of the invention, the cancer cells (autologous or allogenic) are inactivated by irradiation (e.g., ¶ 0032, 0068, 0084).
Conclusion
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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/ELIZABETH A SHUPE/Examiner, Art Unit 1643
/Brad Duffy/Primary Examiner, Art Unit 1643