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 .
Election/Restrictions
Applicant’s election without traverse of Group I (Claims 1-28 and 31-32; drawn to methods of inducing an inflating memory CD8+ T cell response/treating cancer) in the reply filed on November 4, 2024, is acknowledged.
Applicant further elected the following species:
a. Esophageal cancer for the alternative species of cancer
b. Multiple doses for the alternative species of dosing
In light of the Applicant’s elected species, claim 26 is withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.
DETAILED ACTION
The amended claims filed on May 22, 2026, have been acknowledged. Claims 14, 23, 29-30, and 33 were cancelled. Claims 1-2 and 28 were amended. Claims 35-42 are new. In light of the Applicant’s elected species, claim 26 is withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Claims 1-13, 15-22, 24-25, 27-28, 31-32, and 34-42 are pending and examined on the merits.
Applicant’s response has been considered. Rejections and/or objections not reiterated from the previous office action mailed November 25, 2025, are hereby withdrawn. The following rejections and/or objections are either newly applied or are reiterated and are the only rejections and/or objections presently applied to the instant application.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Priority
Applicant’s claim for the priority of a prior-filed application under 35 U.S.C. 119(a)-(d) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date as follows:
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of 35 U.S.C. 112(a) or the first paragraph of pre-AIA 35 U.S.C. 112, except for the best mode requirement. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed applications, Application No. GB19149848, filed October 16, 2019, and Application No. GB20094207, filed June 19, 2020, fail to provide adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. These foreign priority applications do not provide information related to SEQ ID NOs: 13-15, 18-19, and 33-34. However, Application No. PCT/GB2020/052620, filed on October 16, 2020, did provide the above information.
Therefore, claims 1-13, 15-18, 22, 24-25, 27-28, 31-32, and 34-42 receive foreign priority from foreign priority application GB19149848, filed October 16, 2019, while claims 19-21 receive foreign priority from application No. PCT/GB2020/052620, filed on October 16, 2020.
Information Disclosure Statement
The information disclosure statement (IDS) filed on May 22, 2026, has been considered.
New Claim Rejections - 35 USC § 112a
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-13, 15-22, 24-25, 27, 31-32, and 34 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for administering an adenovirus encoding the AH-1 single cancer-specific CD8+ T cell epitope to induce an inflating memory T cell response, does not provide enablement for any single cancer-specific CD8+ T cell epitope that is 8-15 amino acids in length and is not the NY-ESO-1 epitope. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. The applicant’s disclosure does not provide enough information for any person skilled in the art to administer an adenovirus encoding any cancer-specific CD8+ T cell epitope that is 8-15 amino acids in length and is not NY-ESO-1 and achieve the required inflating memory T cell response.
The factors to be weighed to evaluate whether a disclosure satisfies the enablement requirement and whether any necessary experimentation is undue are set forth in MPEP 2164.01(a).
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
Although all the factors have been considered, the relevant factors will be addressed below.
Breadth of the claims: Claim 1 recites the following claim language, “A method of inducing an inflating memory CD8+ T cell response comprising: administering a therapeutically effective amount of a pharmaceutical composition to a human subject with a tumor, wherein the pharmaceutical composition comprises an adenoviral vector comprising a nucleotide sequence encoding a polypeptide comprising a single cancer-specific CD8+ T cell epitope, wherein the polypeptide encoded by the nucleotide sequence consists of 8 to 15 amino acids, and wherein the adenoviral vector does not comprise a nucleic acid molecule encoding a cancer-specific T cell epitope other than the single cancer-specific CD8+ T cell epitope, wherein the single cancer-specific CD8+ T cell epitope is not an NY-ESO-1 epitope, wherein the inflating memory CD8+ T cell response (1) comprises production of CD8+/CX3CR1+/KLRG-1+ T cells and (2) persists in the human subject for at least 28 days after administration of the pharmaceutical composition, and wherein the single cancer specific CD8+ T cell epitope encoded by the adenoviral vector circumvents the normal antigen processing requirements for presentation on an MHC molecule.” The broadest reasonable interpretation is that any single cancer-specific CD8+ T cell epitope, wherein the polypeptide encoded by the nucleotide sequence consists of 8 to 15 amino acids that is not NY-ESO-1 can be used to generate the required inflating memory T cell response.
Nature of the invention: The subject matter of the invention relates to a method of inducing an inflating memory T cell response by administering a adenovirus encoding a single cancer-specific CD8+ T cell epitope, wherein the polypeptide encoded by the nucleotide sequence consists of 8 to 15 amino acids.
State of the prior art: Although Klyushnenkova et al. (J Immunother 35: 390-399. 2012) and Palmowski et al. (J Immunol 168: 4391-4398. 2002) teach administering viral vectors to induce a CD8 T cell response and Klyushnenkova teaches that vectors encoding PSA (65-73), a prostate specific epitope, showed greater tumor inhibition than CMV viruses encoding the full length PSA protein, neither teach the specific CD8+ T-cell inflating memory response required by claims 1 and 28.
Klyushnenkova teaches a method of inducing an inflating memory CD8+ T cell response comprising administering a recombinant mCMV viral vector encoding a CD8 T cell epitope (PSA65-73; a cancer specific CD8+ T cell epitope) to a subject before challenging it with a tumor (i.e. prophylactic administration to minimize development of cancer). Their results show that immunization with mCMV based vectors encoding a single PSA-specific CD8 T-cell epitope (PSA65–73) induced PSA-specific CD8 T-cell responses, which increased in time after immunization (termed “memory inflation”) and reduced tumor growth (page 391, column 1, paragraph 2 and column 2, paragraph 2 and Figure 4). Klyushnenkova teaches that CMV viruses encoding PSA (65-73; a 27 nucleotide sequence), a prostate specific antigen (i.e. not a viral immunogen), showed greater tumor inhibition than CMV viruses encoding the full length PSA protein (i.e. a subject not administered the pharmaceutical composition) (Figure 4).
Palmowski teaches a method of inducing a CD8+ T cell response comprising administering a vaccinia viral vector encoding the NY-ESO-1157-165 cancer epitope to a A2/Kb transgenic mouse. Their results show that immunization with vaccinia based vectors encoding a single NY-ESO-1157-165 cancer epitope induced an antigen-specific cytotoxic T lymphocyte [CTL] response including inducing CD8 T cell levels (page 4393, column 2, paragraph 3 and Figure 3).
Bolinger et al. (J Immuno 190: 4162-4174. 2013) teaches that to further understand the mechanism of CD8+ T cell memory inflation, which is still poorly understood, they developed a simpler and more tractable model using Ad-LacZ. In this study, they showed that Ad-LacZ, a nonreplicating AdV, induced a robust inflating CD8+ T cell population against the bgal96 epitope and a conventional CD8+ memory T cell response to the bgal497 epitope after a single i.v. injection in C57BL/6 mice. CD8+ T cell memory inflation after Ad-LacZ immunization revealed strong resemblance to that seen in MCMV infection, providing us with a novel, robust model for memory inflation that is internally controlled and allows dissection of the mechanism underpinning CD8+ T cell memory inflation (page 4170, column 1, paragraph 2).
Level of predictability in the art: Therefore, although vectors encoding single CD8 T-cell specific epitopes that could induce a CD8 T cell response were known in the art and adenoviruses encoding βGal epitopes can induce an inflating memory T cell response, the prior art does not identify any adenoviruses encoding cancer specific CD8+ epitopes that generate an inflating memory response in a human subject with a tumor. As such, one of skill in the art would neither expect nor predict which single cancer-specific CD8+ T cell epitopes would generate the required functional inflating memory T cell response when administered to human subjects with tumors.
Amount of direction provided by the inventor and existence of working examples:
Regarding the T cell response of claims 1 and 11, the instant specification discloses that administering an AdHu5 adenoviral vector encoding the AH-1 epitope leads to induction of CD8+/CX3CR1+/KLRG1+ cells in the tumor. Collection and expression was examined at the humane endpoint, which appears to have occurred at least 28 days after adenoviral administration based on the tumor growth data in Figure 2 (Examples 2-3 and Figures 2-3).
Applicant also has data regarding the E2F8 epitope. However, this epitope is 27 amino acids in length and would not fall within the limitations of claim 1.
Similarly, Applicant provides additional data regarding an adenovirus encoding the Mtch1 epitope (unclear which of the two Mtch1 epitopes references in Table 1). However, as this data was not part of the specification, it is not provided as part of a declaration, and the experimental methods are not clearly identified, this data has not been considered as part of this rejection.
Furthermore, the instant specification specifically identifies that the GSW11 epitope does not induce a CD8 T cell response in healthy immunocompetent mice, only achieving a CD8 T cell response when regulatory CD4 T cells are systematically depleted (Example 1).
Therefore, Applicant provides a single example of an epitope achieving the required CD8 T cell response of claim 1.
Regarding the additional limitations of claim 2, Applicant does provide evidence that adenoviral vectors encoding single cancer-specific CD8+ T cell epitopes AH1 and NY-ESO-1 produce the required T cell response and inhibits tumor growth to a greater extent than the full length gene in BALB/c mice and transgenic HHD mice, respectively (Examples and Figures 1-7 for AH1 and 8-9 for NY-ESO-1). However, these are the only two epitopes that were shown to have these properties when administered to mice and the NY-ESO-1 epitope is excluded from claims 1-2, as discussed above.
Therefore, the Applicant has provided a single example of an epitope that falls within the limitations of claim 2.
Regarding the T cell response limitations of claims 12-13, the AH-1 epitope is shown to induce CD8+/CX3CR1+/KLRG1+ cells in the tumor. It is unclear based on the percentage of CX3CR1+ and KLRG1+ cells in the spleen if any of those cells are CX3CR1+/KLRG1+ cells or if they are CX3CR1+/KLRG1- or CX3CR1-/KLRG1+ cells. Furthermore, These cells were examined in the spleen and the tumor and not in the circulating blood (Example 3 and Figure 3). Therefore, it is not clear what percentage of CD8+ T cells are CD8+/CX3CR1+/KLRG1+ cells and in circulation, as required by claims 12-13.
The only identified epitope that has been shown to cause the required T cell response of claims 12-13 is the NY-ESO-1 epitope as shown in Example 8 and Figure 8 of the instant application. Example 8 and corresponding Figure 8 of the instant specification disclose that they immunized HHD mice with AdHu5-NY-ESO-1(157-165) (an adenovirus 5 with E1 and E3 deleted). Following immunization, ~97% of CD8 T cells were CD44+ CD62L- 21 days post-immunization (Figure 8B). ~100% were CX3CR1+ and ~65% were KLRG-1+ at day 40 (Figures 8C and D). As such, there were at least 65% of cells that were CD8+/CX3CR1+/KLRG-1+ at day 40 (Claims 10-11). As shown in Figure 8A, these cell phenotypes at day 40 were only representative of ~12% of CD8+ T cells. As such, ~7% of CD8+ cells were CD8+/CX3CR1+/KLRG-1+ at day 40. Therefore, Applicant has not provided any examples of an epitope that is not NY-ESO-1 that has this T cell response.
Regarding the T cell response limitations of claim 15, the AH-1 epitope does generate CD8+/CX3CR1+/KLRG-1+/CD44+/CD62L- T cells in the tumor as 69.2% of CD8+ T cells are CD44+/CD62L-, 79.3% are CX3CR1+, and 41.1% are KLRG1+. As there is an overlap between these markers, there will inevitably be some CD8+/CX3CR1+/KLRG-1+/CD44+/CD62L- T cells. However, this is the only epitope that falls within the claim limitations of claims 1 and 15 that produce the required T cell response of claim 15.
Regarding the T cell response limitations of claim 16, the AH-1 epitope does generate CD8+/CX3CR1+/KLRG-1+/CD44+/CD62L- T cells in the tumor as identified above. However, it is not clear that these cells are also CD27-(low) and CD127-(low). 23.3% are CD127+ and 68.9% are CD27+. As such, it is not known whether there are any cells that are CD8+/CX3CR1+/KLRG-1+/CD44+/CD62L-/CD27-(low)/CD127-(low) T cells. Therefore, the Applicant has not identified any epitope that falls within the claim limitations of claim 16.
Quantity of experimentation needed: In light of the above factors, the applicant provides enablement for an adenoviral vector encoding the AH-1 epitope as it relates to the T cell response of claims 1 and 15 and the tumor inhibition requirements of claim 2 but does not provide enablement for any epitope with the T cell response of claims 12-13 and 16. As such, there would be undue experimentation related to administering an adenovirus encoding any cancer-specific CD8+ T cell epitope that is 8-15 amino acids in length and is not NY-ESO-1 to achieve the required inflating memory T cell response to practice the full scope of the claim.
Claims 2-13, 15-22, 24-25, 27, 31-32, and 34 are also rejected because of their dependency on claim 1.
Response to Arguments
Applicant's arguments filed May 22, 2026, are acknowledged.
Applicant argues that the application as-filed contains sufficient information regarding the subject matter of the claims as to enable one skilled in the pertinent art to make and use the claimed invention with a reasonable amount of experimentations and cites to additional data (Figures 1-5 of the Remarks) to further evidence that Applicant is enabled (page 9, paragraph 1-page 14, paragraph 2).
Applicant's arguments and the cited additional data have been considered but they are not persuasive.
It is noted that the Applicant has supplied additional data in their remarks (Figures 1-5) to support that the AH-1, NY-ESO-1, and Mtch1 induce the required inflating memory T cell phenotypes of the claims. However, CFR 1.132 states that “When any claim of an application or a patent under reexamination is rejected or objected to, any evidence submitted to traverse the rejection or objection on a basis not otherwise provided for must be by way of an oath or declaration under this section.” (MPEP 716). Therefore, data that goes beyond what is found in the specification (as Figures 1-5 of the Remarks are) should be submitted as part of a Declaration. The fact that the data was not part of a Declaration is dispositive, in and of itself, in assessing the persuasiveness of the data presented in the Remarks. Furthermore, it is difficult to assess the applicability of the newly presented data as it compares to the data in the specification as there is limited explanation of the exact methods used for collecting the new data. For example, the Remarks (page 11, paragraph 4) states that Applicant has repeated the experiments provided in the application using AdHu5-AH1-MG vector and AdHu5-NY-ESO-1-MG vector to further validate the data and repeated the experiments with the Mtch1 epitope disclosed in Tabe 1 of the instant application (page 13, paragraph 2). However, the instant specification identifies multiple experimental setups as Figure 1 exemplifies administering AdHu5-AH1-MG alone or in combination with an Ad-Hu5-GSW-MG at 1 x108 IU while Figure 16 shows combinatorial administration of AdHu5-AH1-MG with anti-PD-L1 or an isotype. Furthermore, Table 2 identifies two Mtch1 epitopes and it is unclear which of these two epitopes is used as part of the newly presented experimental data. As such, the persuasiveness of Applicant’s newly presented data cannot be assessed at this point in time. For further consideration, Applicant should present the data as part of a Declaration with the detailed experimental methods used for each data set for proper assessment of the applicability of the newly cited data.
Claims 28 and 35-42 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for administering an adenovirus encoding the AH-1 or NY-ESO-1single cancer-specific CD8+ T cell epitope to induce an inflating memory T cell response, does not provide enablement for any single cancer-specific CD8+ T cell epitope that is 8-15 amino acids in length. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. The applicant’s disclosure does not provide enough information for any person skilled in the art to administer an adenovirus encoding any cancer-specific CD8+ T cell epitope that is 8-15 amino acids in length and achieve the required inflating memory T cell response.
The factors to be weighed to evaluate whether a disclosure satisfies the enablement requirement and whether any necessary experimentation is undue are set forth in MPEP 2164.01(a).
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
Although all the factors have been considered, the relevant factors will be addressed below.
Breadth of the claims: Claim 28 recites the following claim language, “A method of treating cancer in a human subject with cancer, comprising: administering a therapeutically effective amount of a pharmaceutical composition to the human subject with cancer, wherein the pharmaceutical composition comprises an adenoviral vector comprising a nucleotide sequence encoding a polypeptide comprising a single cancer-specific CD8+ T cell epitope, wherein the polypeptide encoded by the nucleotide sequence consists of 8 to 15 amino acids, wherein the adenoviral vector does not comprise a nucleic acid molecule encoding a cancer-specific T cell epitope other than the single cancer-specific CD8+ T cell epitope, wherein the pharmaceutical composition induces an inflating memory CD8+ T cell response, wherein the inflating memory CD8+ T cell response comprises production of circulating CD8+/CX3CR1+ and CD8+/KLRG-1+ T cells that are specific to the single cancer specific CD8+ T cell epitope; wherein the method inhibits tumor growth to a greater extent compared to administration of a corresponding adenoviral vector comprising a nucleotide sequence encoding a full length protein containing the same single cancer-specific CD8+ T cell epitope: and wherein at least 70% of the circulating CD8+ T cells that are specific to the single cancer specific CD8+ T cell epitope are CD44+ and CD62L-.” The broadest reasonable interpretation is that any single cancer-specific CD8+ T cell epitope, wherein the polypeptide encoded by the nucleotide sequence consists of 8 to 15 amino acids can be used to generate the required inflating memory T cell response.
Nature of the invention: The subject matter of the invention relates to a method of inducing an inflating memory T cell response by administering a adenovirus encoding a single cancer-specific CD8+ T cell epitope, wherein the polypeptide encoded by the nucleotide sequence consists of 8 to 15 amino acids.
State of the prior art: Although Klyushnenkova et al. (J Immunother 35: 390-399. 2012) and Palmowski et al. (J Immunol 168: 4391-4398. 2002) teach administering viral vectors to induce a CD8 T cell response and Klyushnenkova teaches that vectors encoding PSA (65-73), a prostate specific epitope, showed greater tumor inhibition than CMV viruses encoding the full length PSA protein, neither teach the specific CD8+ T-cell inflating memory response required by claims 1 and 28.
Klyushnenkova teaches a method of inducing an inflating memory CD8+ T cell response comprising administering a recombinant mCMV viral vector encoding a CD8 T cell epitope (PSA65-73; a cancer specific CD8+ T cell epitope) to a subject before challenging it with a tumor (i.e. prophylactic administration to minimize development of cancer). Their results show that immunization with mCMV based vectors encoding a single PSA-specific CD8 T-cell epitope (PSA65–73) induced PSA-specific CD8 T-cell responses, which increased in time after immunization (termed “memory inflation”) and reduced tumor growth (page 391, column 1, paragraph 2 and column 2, paragraph 2 and Figure 4). Klyushnenkova teaches that CMV viruses encoding PSA (65-73; a 27 nucleotide sequence), a prostate specific antigen (i.e. not a viral immunogen), showed greater tumor inhibition than CMV viruses encoding the full length PSA protein (i.e. a subject not administered the pharmaceutical composition) (Figure 4).
Palmowski teaches a method of inducing a CD8+ T cell response comprising administering a vaccinia viral vector encoding the NY-ESO-1157-165 cancer epitope to a A2/Kb transgenic mouse. Their results show that immunization with vaccinia based vectors encoding a single NY-ESO-1157-165 cancer epitope induced an antigen-specific cytotoxic T lymphocyte [CTL] response including inducing CD8 T cell levels (page 4393, column 2, paragraph 3 and Figure 3).
Bolinger et al. (J Immuno 190: 4162-4174. 2013) teaches that to further understand the mechanism of CD8+ T cell memory inflation, which is still poorly understood, they developed a simpler and more tractable model using Ad-LacZ. In this study, they showed that Ad-LacZ, a nonreplicating AdV, induced a robust inflating CD8+ T cell population against the bgal96 epitope and a conventional CD8+ memory T cell response to the bgal497 epitope after a single i.v. injection in C57BL/6 mice. CD8+ T cell memory inflation after Ad-LacZ immunization revealed strong resemblance to that seen in MCMV infection, providing us with a novel, robust model for memory inflation that is internally controlled and allows dissection of the mechanism underpinning CD8+ T cell memory inflation (page 4170, column 1, paragraph 2).
Level of predictability in the art: Therefore, although vectors encoding single CD8 T-cell specific epitopes that could induce a CD8 T cell response were known in the art and adenoviruses encoding βGal epitopes can induce an inflating memory T cell response, the prior art does not identify any adenoviruses encoding cancer specific CD8+ epitopes that generate an inflating memory response in a human subject with a tumor. As such, one of skill in the art would neither expect nor predict which single cancer-specific CD8+ T cell epitopes would generate the required functional inflating memory T cell response when administered to human subjects with tumors.
Amount of direction provided by the inventor and existence of working examples: Regarding the T cell response of claim 28, the instant specification discloses that administering an AdHu5 adenoviral vector encoding the AH-1 epitope leads to induction of CD8+/CX3CR1+/KLRG1+ cells in the tumor (Examples 2-3 and Figures 2-3). Although this is not examined in the blood to assess whether any of these cells are in circulation, all that is required is that one of the cells from the tumor reach circulation which is highly likely to occur. Figure 1D shows that 96.6% of circulating CD8+ T cells are CD44+/CD62L- (Example 1).
Example 8 and corresponding Figure 8 of the instant specification disclose that they immunized HHD mice with AdHu5-NY-ESO-1(157-165) (an adenovirus 5 with E1 and E3 deleted). Following immunization, ~97% of CD8 T cells were CD44+ CD62L- 21 days post-immunization (Figure 8B). ~100% were CX3CR1+ and ~65% were KLRG-1+ at day 40 (Figures 8C and D). As such, there were at least 65% of cells that were CD8+/CX3CR1+/KLRG-1+ at day 40. Figure 8B shows that over 90% of circulating CD8+ T cells are CD44+/CD62L- (Example 8).
Applicant also has data regarding the E2F8 epitope. However, this epitope is 27 amino acids in length and would not fall within the limitations of claim 1.
Similarly, Applicant provides additional data regarding an adenovirus encoding the Mtch1 epitope (unclear which of the two Mtch1 epitopes references in Table 1). However, as this data was not part of the specification, it is not provided as part of a declaration, and the experimental methods are not clearly identified, this data has not been considered as part of this rejection.
Furthermore, the instant specification specifically identifies that the GSW11 epitope does not induce a CD8 T cell response in healthy immunocompetent mice, only achieving a CD8 T cell response when regulatory CD4 T cells are systematically depleted (Example 1). Additionally, Figure 22 shows that administering the AdHu5-AH1-MG followed by anti-PD-1 or isotype led to a reduction in the number of CD44+/CD62L- cells such that they are less than 70% of the circulating CD8+ T cells (Top left graph).
Therefore, Applicant provides two examples of an epitope achieving the required CD8 T cell response of claim 28. However, this is dependent on the method not including further administration of anti-PD1 or isotypes as the T cell response no longer falls within the requirements of claim 28.
Regarding the additional CD8 T cell response limitations of claims 35-41, these were also shown to occur in the AH-1 (Figures 1E and 7B) and NY-ESO-1 (Figures 8B-8D) epitopes.
Therefore, Applicant provides two examples of an epitope achieving the required CD8 T cell response of claims 34-41 and one (AH-1) based on the additional limitation that the epitope is not NY-ESO-1 in claim 42.
Quantity of experimentation needed: In light of the above factors, the applicant provides enablement for an adenoviral vector encoding the AH-1 epitope or NY-ESO-1 (except claim 42) epitope as it relates to the T cell response of claims 28 and 35-41 but does not provide enablement for any epitope that is 8 to 15 amino acids in length. As such, there would be undue experimentation related to administering an adenovirus encoding any cancer-specific CD8+ T cell epitope that is 8-15 amino acids in length to achieve the required inflating memory T cell response to practice the full scope of the claim.
Claims 35-42 are also rejected because of their dependency on claim 1.
Withdrawn Claim Rejections - 35 USC § 112b
The prior rejection of claim 2 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 is withdrawn in light of Applicant’s amendments to claim 2 to remove the language “inflating memory T cell response persists in a cell of the subject for at least 28 days”.
New Claim Rejections - 35 USC § 112b
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 15-16 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 rejection is a new rejection substantially similar to a previous rejection. Any aspect of Applicant’s traversal that is relevant to the rejection as newly written is addressed below.
The specification teaches that the designation (-) indicates low expression or no expression of the marker and wherein the (-) designation means low expression this may be further indicated by (low). As such, there are two different possible meanings for -, no expression or low expression. Therefore, the designation – as used in claim 15 is indefinite. It is not clear what the “-(low)” of claim 16 is supposed to mean and whether it is limiting. It is not clear whether one is supposed to read it as identifying that expression is supposed to be low and not absent.
Furthermore, even if it was supposed to be understood as identifying low expression of the markers, it is not clear how one would define low expression. The term “low” in claim 16 is a relative term which renders the claim indefinite. The term “low” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. It is unclear what level of expression of the markers would fall within low expression. Although the specification states that “low expression” may refer to cells wherein there is no expression or wherein there is low expression relative to other cells in the sample, these are not controlling definitions due to the “may” language. Furthermore, even if these were controlling definitions, it would still be considered indefinite as expression relative to other cells could lead to a cell that has expression above some cells but below others leading to a lack of clarity as to whether it is considered low expression or not.
Response to Arguments
Applicant's arguments filed May 22, 2026, are acknowledged.
Applicant argues that the specification as-filed at page 14, lines 29-31, states that "[t]he term 'low expression' may refer to cells wherein there is no expression of the markers, it may also refer to cells wherein there is low expression of the markers relative to other cells in the sample." Further, the specification notes that "the designation (-) indicates low expression or no expression of the marker. Wherein the (-) designation means low expression this may be further indicated by '(low)'." See Specification, p. 14, 1. 25-p.15, 11. 1-2. Thus, it would be clear to a skilled artisan that the designation of "-" refers to no expression of the biomarker and that "-(low)" refers to low expression of the biomarkers as determined relative to other cells in the sample. For at least this reason, Applicant respectfully submits that claims 15 and 16 are not indefinite. (page 14, paragraph 2).
Applicant's arguments have been fully considered but they are not persuasive.
As detailed above, as stated in the rejection above, the cited definitions are not controlling definitions as a result of the “may” language. Furthermore, even if these were controlling definitions, it would still be considered indefinite as expression relative to other cells could lead to a cell that has expression above some cells but below others leading to a lack of clarity as to whether it is considered low expression or not.
Therefore, the rejection is maintained.
New Claim Rejections - 35 USC § 112d
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 15-16 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claims 15-16 are dependent on claim 14 which has been cancelled.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Withdrawn Claim Rejections - 35 USC § 103
The prior rejection of claims 1-18, 22-23, 27, 32, and 34 under 35 U.S.C. 103 as being unpatentable over Palmowski et al. (J Immunol 168: 4391-4398. 2002) and further in view of Jager et al. (PNAS 39: 14453-14458. 2006), Weiser et al. (Journal of Immunotherapy 24: 151-161. 2001), Klyushnenkova et al. (J Immunother 35: 390-399. 2012), Geiben-Lynn et al. (Clinical and Vaccine Immunology: 691–696. 2008), and Sorensen et al. (Eur. J. Immunol. 39: 2725–2736. 2009) as evidenced by Bolinger et al. (Cell Reports 13: 1578-1588. 2015) and Jackson Laboratories (NSG-HLA-A2/HHD). is withdrawn in light of Applicant’s amendments to claim 1 to recite the limitation “wherein the single cancer-specific CD8+ T cell epitope is not an NY-ESO-1 epitope.”
New Claim Rejections - 35 USC § 103
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.
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 28 and 35-41 are rejected under 35 U.S.C. 103 as being unpatentable over Palmowski et al. (J Immunol 168: 4391-4398. 2002) and further in view of Jager et al. (PNAS 39: 14453-14458. 2006), Weiser et al. (Journal of Immunotherapy 24: 151-161. 2001), Klyushnenkova et al. (J Immunother 35: 390-399. 2012), Geiben-Lynn et al. (Clinical and Vaccine Immunology: 691–696. 2008), and Sorensen et al. (Eur. J. Immunol. 39: 2725–2736. 2009) as evidenced by Bolinger et al. (Cell Reports 13: 1578-1588. 2015) and Jackson Laboratories (NSG-HLA-A2/HHD). This is a new rejection made in response to Applicant’s amendments to claim 28. Any aspect of Applicant’s traversal that is relevant to the rejection as newly written is addressed below.
Regarding claims 1, Palmowski teaches a method of inducing a CD8+ T cell response comprising administering a vaccinia viral vector encoding the NY-ESO-1157-165- cancer epitope to a A2/Kb transgenic mouse. Their results show that immunization with vaccinia based vectors encoding a single NY-ESO-1157-165- cancer epitope (9 amino acids long and 27 nucleotides long) induced an antigen-specific cytotoxic T lymphocyte [CTL] response including inducing CD8 T cell levels (page 4393, column 2, paragraph 3 and Figure 3). Palmowski teaches that recombinant vaccines encoding tumor-derived peptides are currently being designed for use against cancer (abstract).
Palmowski does not teach wherein the vector is administered to a subject with a tumor.
However, Jager teaches that they administered vaccinia viruses expressing the full length NY-ESO-1 in cancer patients (abstract). CD8 T cell responses were observed in 19 of 23 evaluable patients and were directed against the p157–170 region (page 14455, column 1, paragraph 4). Jager teaches that they treated patients with tumor bearing cancers, including lung metastases (Table 1).
Weiser teaches that lung cancer cells (H-1355) were transduced with an adenovirus expressing full length NY-ESO-1. Although high levels of NY-ESO-1 were expressed following transduction, cancer cell death did not occur likely due to deficient antigen processing which is commonly observed in lung cancer (page 156, column 1, paragraph 1 and Table 2).
Klyushnenkova teaches a method of inducing an inflating memory CD8+ T cell response comprising administering a recombinant mCMV viral vector encoding a CD8 T cell epitope (PSA65-73; a cancer specific CD8+ T cell epitope) to a subject before challenging it with a tumor. Their results show that immunization with mCMV based vectors encoding a single PSA-specific CD8 T-cell epitope (PSA65–73) induced PSA-specific CD8 T-cell responses, which increased in time after immunization (termed “memory inflation”) (page 391, column 1, paragraph 2 and column 2, paragraph 2 and Figure 4). Klyushnenkova teaches that CMV viruses encoding PSA (65-73), a prostate specific antigen, showed greater tumor inhibition than CMV viruses encoding the full length PSA protein (Figure 4).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have combined the vector of Palmowski with the method of treating cancer of Jager to arrive at the instantly claimed invention. One of ordinary skill in the art would have a reason to substitute with a reasonable expectation of success because Jager teaches vaccinia viruses expressing NY-ESO-1 can be used to treat cancer in patients and Weiser teaches that although high levels of NY-ESO-1 were expressed following transduction with an adenovirus expressing full length NY-ESO-1, cancer cell death did not occur likely due to deficient antigen processing which is commonly observed in lung cancer. Furthermore, Klyushnenkova teaches that CMV viruses encoding PSA (65-73), a prostate specific antigen, showed greater tumor inhibition than CMV viruses encoding the full length PSA protein. As such, it would have been obvious that one of ordinary skill in the art would have used a viral vector encoding the NY-ESO-1157-165 peptide as Jager successfully reduced to practice using vectors expressing NY-ESO-1 to treat cancer, Weiser taught that the full length protein failed likely due to a common deficiency in antigen processing in lung cancer cells, and Klyushnenkova teaches that encoding a single epitope compared to the full length protein improved tumor growth inhibiton. Therefore, using the NY-ESO-1157-165- epitope expressing vector would get around this issue. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
Palmowski does not teach wherein the viral vector is an adenovirus.
Weiser teaches that lung cancer cells (H-1355) were transduced with an adenovirus expressing full length NY-ESO-1. Although high levels of NY-ESO-1 were expressed following transduction, cancer cell death did not occur likely due to deficient antigen processing which is commonly observed in lung cancer (page 156, column 1, paragraph 1 and Table 2).
Geiben-Lynn teaches that mice vaccinated with vaccinia viruses (replication competent or replication incompetent) led to early animal death (replication competent) or short term expression (~48 hours for immunocompetent and immunocompromised mice; replication incompetent) while the adenovirus vaccine (recombinant adenovirus 5 with E1 and E3 deleted maintained for ~10 days in immunocompetent mice and at least 100 days in immunocompromised mice (page 691, column 2, paragraph 3 and page 692, column 2, paragraph and Figures 1-3).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have substituted the vaccinia viral vector backbone of Palmowski with the adenoviral vector backbone of Weiser to arrive at the instantly claimed invention. One of ordinary skill in the art would have a reason to substitute with a reasonable expectation of success because Geiben-Lynn teaches that mice vaccinated with vaccinia viruses (replication competent or replication incompetent) led to early animal death (replication competent) or short term expression (~48 hours for immunocompetent and immunocompromised mice; replication incompetent) while the adenovirus vaccine maintained for ~10 days in immunocompetent mice and at least 100 days in immunocompromised mice. As such, the adenovirus backbone would have been an obvious substitute for expressing the epitope. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
Palmowski, Weiser, and Geiben-Lynne silent as to which promoter is used in their vectors. However, Sorensen teaches an adenoviral vector lacking E1 and E3
With a CMV promoter was used to express a tumor-associated immunodominant epitope for vaccination purposes against tumors (abstract and page 2733, column 2, paragraph 2 and Figure 7).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have used a CMV promoter. One of ordinary skill in the art would have a reason to use a CMV promoter with a reasonable expectation of success because Sorensen has successfully reduced to practice that CMV reporters can be used to express tumor-associated immunodominant epitopes and NY-ESO-1157-165 is a known tumor-associated immunodominant epitope. Furthermore, CMV promoters are known to be constitutively active ensuring continued expression of the epitope over time and have been used extensively within the field. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
Regarding whether the vector of the combined teachings of Palmowski, Jager, Weiser, Klyushnenkova, Geiben-Lynn, and Sorenson causes the required inflating memory T cell response, Palmowski teaches the vector encodes NY-ESO-1157-165, Geiben-Lynn teaches that the adenoviral vector is a recombinant adenovirus 5 with E1 and E3 deleted, Palmowski teaches that the vaccination can occur in HHD mice (Jackson Laboratory evidence that HHD mice are immunodeficient mice (page 1), and Sorenson teaches that a CMV promoter can be used to express the epitope. Examples 8-9 of the instant specification discloses that they immunized HHD mice with AdHu5-NY-ESO-1(157-165) (an adenovirus 5 with E1 and E3 deleted). Following immunization, ~97% of CD8 T cells were CD44+ CD62L- 21 days post-immunization (Figure 8B). ~100% were CX3CR1+ and ~65% were KLRG-1+ at day 40 (Figures 8C and D). As such, there were at least 65% of cells that were CD8+/CX3CR1+/KLRG-1+ at day 40. As the combined method of Palmowski, Jager, Weiser, Klyushnenkova, Geiben-Lynn, and Sorenson is the same as the example of the instant specification, it naturally flows that their combined method would also have the same properties.
Regarding the method inhibiting tumor growth to a greater extent than a corresponding adenoviral vector encoding a full length protein containing the epitope, Palmowski teaches the vector encodes NY-ESO-1157-165, Geiben-Lynn teaches that the adenoviral vector is a recombinant adenovirus 5 with E1 and E3 deleted, Palmowski teaches that the vaccination can occur in HHD mice (Jackson Laboratory evidence that HHD mice are immunodeficient mice (page 1), and Sorenson teaches that a CMV promoter can be used to express the epitope. Examples 8-9 of the instant specification discloses that they immunized HHD mice with AdHu5-NY-ESO-1(157-165) (an adenovirus 5 with E1 and E3 deleted) and saw that the epitope vector performed better than the vector encoding the full length protein (i.e. a subject not administered the pharmaceutical composition). As the combined method of Palmowski, Jager, Weiser, Klyushnenkova, Geiben-Lynn, and Sorenson is the same as the example of the instant specification, it naturally flows that their combined method would also have the same property.
Response to Arguments
Applicant's arguments filed August 8, 2025, are acknowledged.
Applicant argues that one of ordinary skill in the art would have no motivation to combine the references cited by the Office action to arrive at the present claims. Applicant cites to Klyushnenkova as identifying that they used CMV-based vectors and identifies multiple reasons why they used a CMV vector instead of an adenovirus as it can replicate and may show improved distribution for controlling prostate cancer (page 17, paragraph 5-page 18, paragraph 3).
Applicant's arguments have been fully considered but they are not persuasive.
As an initial matter, the rejection above is related to substituting a vaccinia viral backbone with an adenoviral backbone based on the teachings of Weiser and Geiben-Lynn.
Weiser teaches that lung cancer cells (H-1355) were transduced with an adenovirus expressing full length NY-ESO-1. Although high levels of NY-ESO-1 were expressed following transduction, cancer cell death did not occur likely due to deficient antigen processing which is commonly observed in lung cancer (page 156, column 1, paragraph 1 and Table 2).
Geiben-Lynn teaches that mice vaccinated with vaccinia viruses (replication competent or replication incompetent) led to early animal death (replication competent) or short term expression (~48 hours for immunocompetent and immunocompromised mice; replication incompetent) while the adenovirus vaccine (recombinant adenovirus 5 with E1 and E3 deleted maintained for ~10 days in immunocompetent mice and at least 100 days in immunocompromised mice (page 691, column 2, paragraph 3 and page 692, column 2, paragraph and Figures 1-3).
As identified in the rejection above, one of ordinary skill in the art would have a reason to substitute with a reasonable expectation of success because Geiben-Lynn teaches that mice vaccinated with vaccinia viruses (replication competent or replication incompetent) led to early animal death (replication competent) or short term expression (~48 hours for immunocompetent and immunocompromised mice; replication incompetent) while the adenovirus vaccine maintained for ~10 days in immunocompetent mice and at least 100 days in immunocompromised mice. As such, the adenovirus backbone would have been an obvious substitute for expressing the epitope. Because the prior art teaches all of the elements of the claimed invention, there is a reasonable expectation of success.
As such, there was an obvious reason to make the substitution to avoid killing the patient.
Regarding the teachings of Klyushnenkova, these teachings were related to the benefit of using a single epitope versus the full length gene as Klyushnenkova teaches that CMV viruses encoding PSA (65-73), a prostate specific antigen, showed greater tumor inhibition than CMV viruses encoding the full length PSA protein. Although Klyushnenkova discusses some potential benefits for using a CMV vector compared to an adenoviral vector, this is in part due to the cancer that they are treating which is prostrate cancer. Additionally, Klyushnenkova also identifies potential benefits to using an adenovirus such as generating TCM responses which have greater proliferative potential.
Furthermore, in order to complete the art of record and rebut Applicant’s arguments, it is worth noting that Klyushnenkova cites a Phase I clinical trial that used an adenovirus/Prostate-Specific Antigen Vaccine to treat prostate cancer (Lubaroff et al. (Clin Cancer Res 15: 7375-7380. 2009; previously cited art). Lubaroff discloses that the adenovirus/PSA vaccine was proven safe with no serious vaccine related adverse events. The majority of vaccinated patients produced anti-PSA T-cell responses and over half survived longer than predicted by nomogram. Furthermore, Lubaroff directly addresses that pre-existing immunity is found in most humans and can be overcome by immunization of mice with Ad/PSA in a matrix as the vector can induce anti-PSA responses even in the presence of high-titer anti-Ad antibodies. Furthermore, although this is an issue in humans with pre-existing immunity to adenovirus, it is not in naïve patients. Additionally, the method of claim 28 doesn’t require multiple doses of the adenovirus. Therefore, although pre-existing immunity to adenoviruses were known in the art, the art also recognized ways of getting around this problem (either using a matrix as cited by Lubaroff or by treating naïve patients).
Additionally, Bolinger et al. (J Immuno 190: 4162-4174. 2013; previously cited art) discloses that although MCMV is a good model to study CMV infection, there are limitations in examining the mechanisms of memory inflation, because it is a complex system, both virologically with its longterm low-grade persistence, its latency and stochastic reactivation at diverse sites, as well as immunologically, with multiple immunologic mechanisms required to establish and maintain control, and a wide range of CD8+ T cell epitopes. Thus, to further understand the mechanism of CD8+ T cell memory inflation, which is still poorly understood, they developed a simpler and more tractable model using Ad-LacZ. In this study, they showed that Ad-LacZ, a nonreplicating AdV, induced a robust inflating CD8+ T cell population against the bgal96 epitope and a conventional CD8+ memory T cell response to the bgal497 epitope after a single i.v. injection in C57BL/6 mice. CD8+ T cell memory inflation after Ad-LacZ immunization revealed strong resemblance to that seen in MCMV infection, providing us with a novel, robust model for memory inflation that is internally controlled and allows dissection of the mechanism underpinning CD8+ T cell memory inflation (page 4170, column 1, paragraph 2).
Bolinger et al. (Cell Reports 13: 1578-1588. 2015; previously cited art) discloses that when examining adenoviral and mCMV viral vaccines, they observed similar transcriptional profiles. In humans, an adenovirus vaccine induced similar CMV-like phenotypes and transcription factor regulation. These data clarify the core features of CD8+ T cell memory following vaccination with adenovectors and indicate a conserved pathway for memory development shared with persistent herpesviruses (abstract).
Bolinger (2015) discloses that in humans, an adenovirus vaccine induced similar CMV-like phenotypes and transcription factor regulation, showing that there is a conserved pathway for CD8+ T cell memory development between mCMV and adenoviruses (abstract). Furthermore, Bolinger (2015) specifically states that adenovirus-vaccine-induced responses in humans are dominated by effector memory populations. These are high in Tbet and relatively low in Eomes, similar to CMV-specific responses from the same individuals (page 1582, column 2, paragraph 3). Therefore, adenoviral vaccines and CMV vaccines were known to have a similar affect on producing effector memory T cells.
As adenoviruses represent a simpler system and induces a similar effector memory T cell response to CMV based vectors and there were known means to address pre-existing immunity to adenovirus, it would have been well understood that adenoviral vectors can be used for the backbone and multiple benefits compared to a CMV backbone.
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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/KEENAN A BATES/Examiner, Art Unit 1631
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