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 .
Election/Restrictions
Applicant elected with traverse, Group IX, claims 61, 80, 87, 90, and 92 in the reply filed on 19 September 2025. The requirement was deemed proper and was made FINAL in the Official Action mailed on 04 November 2025.
All nonelected claims were canceled by applicant in the claim amendments received 04 February 2026.
Claim Status
Claim 61 is currently amended, claims 1-60, 62-79, 81-86, 88-89, 91, and 93-103 are canceled, claims 104-109 are new, and claims 61, 80, 87, 90, 92, and 104-109 have been considered on their merits.
Withdrawn Rejections
The claim objection of claim 90 has been withdrawn, the Examiner recognizes the claim does not recite the same two antigens.
The claim rejection under 35 U.S.C. § 112(b) directed to claim 61 and its dependent claims has been withdrawn due to Applicant’s amendments to the claims.
The claim rejections under 35 U.S.C. § 103 have been withdrawn due to Applicant’s amendments to the claims. However, new rejections are set forth below.
Claim Interpretation
The chemical structures disclosed in claims 61 and 107 are understood to represent Salvianolic acid A (Sal A) and Salvianolic acid C (Sal C), as that is how they are identified in the remarks filed by Applicant on 04 February 2026. Additionally, the claims identify a function of Sal A and Sal C as YTHDF1 attenuating agents.
Claim Rejections - 35 USC § 112
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.
Claim 80 is 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 repeated with regard to claim 80 for the same reason of record as set forth in the Official Action mailed 04 November 2025. The rejection was not traversed in the response filed 04 February 2026.
Claim 80 recites the limitation "wherein the subject is receiving, or will receive an anti-cancer treatment" in the second and third line of the claim. It is unclear whether this is the same anti-cancer treatment of claim 61 or if this is referring to a different anti-cancer treatment.
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.
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 61, 80, 87, 90, 92, and 105-106 are rejected under 35 U.S.C. 103 as being unpatentable over Han et al. (Nature, published 14 February 2019, of record) in view of Ma et al. (Life Science Research, 2017, 21(5): 437-441, IDS ref.), Zhang et al. (International Journal of Molecular Sciences, 2016, IDS ref., of record), and Zhang et al. (Cellular and Molecular Immunology, published 01 July 2020, of record) hereinafter Zhang 2020.
All citations for the Ma reference are from the translation found starting on page 7 of the copy of the reference provided by Applicant in the file wrapper.
This is a new rejection necessitated by Applicant’s amendment to the claims. A response to Applicant’s traversal follows the new rejection below.
Regarding claims 61, and 105-106, Han teaches neoantigen-specific immunity is regulated by mRNA N6-methyadenosine (m6A) methylation through the m6A-binding protein YTHDF1 (Abstract). Han teaches loss of YTHDF1 in classical dendritic cells (DCs) enhanced the cross-presentation of tumor antigens and the cross-priming of CD8+ T cells in vivo (Abstract). Han teaches binding of YTHDF1 to these transcripts increases the translation of lysosomal cathepsins in DCs (antigen presenting cell) (Abstract and p. 272, 2nd column). Han teaches the mouse model used in this study involved the inoculation of ovalbumin (OVA)-expressing B16 melanoma cells subcutaneously into wild-type and Ythdf1-/- mice (p. 270, 1st column). The B16 melanoma cells read as skin cancer (claim 106). Han teaches the in vivo antitumor response was markedly improved by cathepsin blockade in wild-type mice (Fig. 4b), suggesting cathepsins are critical factors for determining the antitumor response in this model, therefore, these data show that loss of YTHDF1 in DCs attenuates antigen degradation by restricting the expression of lysosomal proteases, leading to improved cross-presentation and better cross-priming of CD8+ T cells (p. 273, 1st column and Fig. 4b). Han teaches Ythdf1-/- mice showed a marked increase in IFNγ in CD8+ T cells, and IFNγ signaling upregulates the expression of PD-L1, the ligand for PD1 (p. 273, 1st column). Han teaches treating wild-type and Ythdf1-/- tumor-bearing mice with an anti-PD-L1 antibody, which showed 100% tumor regression (p. 273, 2nd column). Han teaches their data suggest combining checkpoint blockade with YTHDF1 depletion could be a potential new therapeutic strategy to improve outcomes in patients with low response to checkpoint blockades (p. 273, 2nd column).
Han does not teach the YTHDF1 attenuating agent is either Salvianolic acid A (Sal A) and Salvianolic acid C (Sal C).
However, Ma teaches the effect of salvianic acid A on cell phenotype and partial immune functions of dendritic cells (DCs) (Abstract). Ma discloses salvianic acid A (SML0045) and SML0045 is salvianolic acid A, therefore, it is understood that salvianic acid A is another name for salvianolic acid A. Ma teaches salvianolic acid A inhibits the secretion of cytokines in DC-induced T cells, wherein, a reduction in the ability of T cells to secrete the pro-inflammatory factor IFN-γ was significantly reduced and the ability to secrete the anti-inflammatory factor IL-10 was significantly enhanced in the salvianolic acid A treatment group (section 2.4).
Additionally, Zhang teaches Salvianolic acid A (Sal A) is a selective ETAR antagonist in both exogenous and endogenous cells lines and reveal the inhibitory effect of Sal A on the proliferation of multiple tumor cells lines (p. 10, Discussion, 1st para.). Zhang teaches the majority of cancer cell types, such as: prostate, ovarian, and lung cancers, show a reduction of ET-1-stimulated growth in response to ETAR antagonism (p. 10, Discussion, 3rd para.). Zhang suggests, based on their results, Sal A is a cardio-friendly anti-cancer leading compound (p. 11, Discussion, 4th para.). Zhang strongly suggests Sal A is a potential candidate for the development of an anti-cancer drug (p. 13, Conclusion).
Therefore, it would have been obvious to one of ordinary skill to combine the teachings and suggestions of Han with the Sal A of Ma and Zhang with a reasonable expectation of success because Han suggest YTHDF1 could be a therapeutic target for immunotherapy in combination with emerging checkpoint inhibitors or DC vaccines (p. 273, last para.) and Zhang strongly suggest Sal A is a potential candidate for the development of an anti-cancer drug (p. 13, Conclusion). Additionally, Han teaches Ythdf1-/- mice showed a marked increase in IFNγ in CD8+ T cells, and IFNγ signaling upregulates the expression of PD-L1, the ligand for PD1 (p. 273, 1st column) and Ma teaches salvianolic acid A inhibits the secretion of cytokines in DC-induced T cells, wherein, a reduction in the ability of T cells to secrete the pro-inflammatory factor IFN-γ was significantly reduced and the ability to secrete the anti-inflammatory factor IL-10 was significantly enhanced in the salvianolic acid A treatment group (section 2.4). One would be motivated to combine the teachings of Han with the Sal A of Ma and Zhang because Ma teaches when DCs are treated with Sal A the cells exhibit the same effects as the DCs of Han found in Ythdf1-/- mice which suggests Sal A would have the same effect as the genetically modified DCs. Additionally, the teachings of a Han suggest YTHDF1 deficiency enhances the cross-presentation of tumor antigens on DCs, leading to an improve antigen presenting DCs antitumor response (Han, Abstract). Therefore, the teachings of Han in view of Ma and Zhang suggest modified antigen presenting cells (mAPC) (claim 105) are treated with the TYHDF1 attenuating agent wherein the TYHDF1 attenuating agent is Sal A.
Han in view of Ma and Zhang are silent to specifically administering mAPC treated with the YTHDF1 attenuating agent.
However, administering modified APC is a known technique for cancer treatment. Zhang 2020 teaches several types of immunotherapies, including adoptive cell transfer (ACT) and immune checkpoint inhibitors (ICIs), have obtained durable clinical responses in cancer patients (Abstract). Zhang 2020 teaches dendritic cell (DC)-based vaccination demonstrated significant clinical outcomes wherein after activation by tumor antigens, DCs can internalize, process, and subsequently present the processed epitopes to T cells and induce cytotoxic T lymphocyte (CTL) immune responses (p. 809, cancer vaccines, 1st column). Zhang 2020 teaches this process involves the reinfusion of isolated DCs pulsed with tumor antigens or tumor cell lysates and stimulated with a defined maturation cocktail ex vivo (p. 809, cancer vaccines, 1st column).
Therefore, it would have been obvious to one of ordinary skill in the art to combine the teachings of Zhang 2020 with the teachings of Han in view of Ma and Zhang with a reasonable expectation of success because Han suggests that YTHDF1 could be a therapeutic target for immunotherapy in combination with emerging DC vaccines (Han, p. 273, last para.). One would be motivated to combine the teachings of Zhang 2020 with the teachings of Han in view of Ma and Zhang because Zhang 2020 teaches DC-based vaccination demonstrated significant clinical outcomes highlighting the importance of antigen presenting cells in clinical applications of cancer treatment.
Regarding claim 80, the teachings of Han in view of Ma, Zhang, and Zhang 2020 read as the subject is receiving an anti-cancer treatment.
Regarding claims 87 and 90, Han teaches in Ythdf1-/- mice showed a marked increase in IFNγ in CD8+ T cells, and IFNγ signaling upregulates the expression of PD-L1, the ligand for PD1 (p. 273, 1st column). Han teaches neutralizing IFNγ diminished the expression of PD-L1 (p. 273, 1st column). Han teaches treating wild-type and Ythdf1-/- tumor-bearing mice with an anti-PD-L1 antibody in order to test the hypothesis that a PD-L1 blockade could potentiate the antitumor response in Ythdf1-/- mice (p. 273, 2nd column). Han suggests combining a checkpoint blockade (an additional anti-cancer treatment) with YTHDF1 depletion could be a potential new therapeutic strategy to improve outcomes in patients with low response to checkpoint blockade and further suggest the YTHDF1 expression may correlate with the T cell inflamed tumor microenvironment (p. 273, 2nd column). Therefore, Han teaches administration of an additional anti-cancer treatment (claim 87) comprising an anti-PD-L1 antibody (claim 90).
Regarding claim 92, the phrase “capable of causing an increase of tumor antigens in the subject”, is not considered limiting because it does not involve an active step, rather, this phrase reads as intended results. Therefore, this phrase does not limit the method of claim 87 and is interpreted as having the same limitations of claim 87 and is rejected for the same reasons.
If this phrase were limiting, Han teaches loss of YTHDF1 in DCs attenuates antigen degradation by restricting the expression of lysosomal proteases, leading to improved cross-presentation and better cross-priming of CD8+ T cells (p. 273, 1st column). The attenuation of antigen degradation reads as increased tumor antigens. Therefore, it would be reasonable to expect the additional cancer treatment would contribute to the increased tumor antigens in the subject because Han teaches 100% of anti-PD-L1 antibody treated Ythdf1-/- mice showed complete tumor regression (Fig. 4d and p. 273, 1st column).
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Response to Traversal
Applicant's arguments filed 04 February 2026, directed to the rejection of claim 61 have been fully considered but they are not persuasive.
In response to applicant's argument that the Han and Zhang references does not teach, suggest, or predict the claimed invention, the test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981).
Applicant has suggested the claimed invention produces unexpected results, however, the claims are not commensurate in scope with the experimental results cited by the Applicant. MPEP 716.02(d) discloses that whether the unexpected results are the result of unexpectedly improved results or a property not taught by the prior art, the "objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support." In other words, the showing of unexpected results must be reviewed to see if the results occur over the entire claimed range. In re Clemens, 622 F.2d 1029, 1036, 206 USPQ 289, 296 (CCPA 1980).
Regarding the claim at issue, claim 61 encompasses a method of treating cancer in a subject by administering a mAPC treated with Sal A or Sal C. The claimed unexpected results appear to be directed to direct-priming function of Sal A treated APCs. As such, the claims as written are not commensurate in scope with the alleged unexpected results.
Additionally, it is not clear that these results would be unexpected as the teachings of Ma regarding Sal A support the suggested teaching of Han, in combining a checkpoint blockade with YTHDF1 depletion could be a potential new therapeutic strategy to improve outcomes in patients with low response to checkpoint blockade and further suggest the YTHDF1 expression may correlate with the T cell inflamed tumor microenvironment. Additionally, the teaching of Zhang demonstrate Sal A exhibits direct anti-cancer effects on multiple tumor lines, as indicated in the rejection above and in Applicant’s response on page 5.
Claims 104 and 106 are rejected under 35 U.S.C. 103 as being unpatentable over Han et al. (Nature, published 14 February 2019, of record) in view of Ma et al. (Life Science Research, 2017, 21(5): 437-441, IDS ref.), Zhang et al. (International Journal of Molecular Sciences, 2016, IDS ref., of record), and Zhang 2020 (Cellular and Molecular Immunology, published 01 July 2020, of record) as applied to claims 61, 80, 87, 90, 92, and 105-106 above, and further in view of Inman et al. (Clin Cancer Res; 23(8) April 15, 2017).
This is a new rejection necessitated by applicant’s amendments to the claims.
Regarding claims 104 and 106, Han in view of Ma, Zhang, and Zhang 2020 are silent to the specific anti-PD-L1 antibody. However, several anti-PD-L1 antibodies were known in the art to include atezolizumab.
Inman teaches atezolizumab (claim 104) is an FcyR binding-deficient, fully humanized IgG1 mAb designed to interfere with the binding of PD-L1 ligand (anti-PD-L1 antibody) to its two receptors, PD-1 and B7.1 (Abstract). Inman teaches atezolizumab was first evaluated in a phase I clinical trial for treating bladder cancer (claim 106), receiving breakthrough therapy designation status by the FDA in June 2014 (p. 1887, Efficacy Phase I). Inman teaches in a phase II clinical trial, the FDA approved atezolizumab for the treatment of bladder cancer in patients with locally advanced or metastatic urothelial carcinoma who have progressed (i) during/after platinum-based chemotherapy or (ii) within 12 months of neoadjuvant or adjuvant treatment with platinum-based chemotherapy (p. 1888, Efficacy Phase II).
Therefore, it would have been obvious to one of ordinary skill in the art to utilize the anti-PD-L1 antibody of Inman in the method of Han in view of Ma, Zhang, and Zhang 2020 with a reasonable expectation of success because both the method of Inman and Han in view of Ma, Zhang, and Zhang 2020 are used for the same purpose in treating cancer and it would be reasonable to expect the anti-PD-L1 antibody to work in the same manner. One would be motivated to utilize the anti-PD-L1 antibody of Inman in the method of Han in view of Ma, Zhang, and Zhang 2020 because Han and Inman are both teaching the use of an anti-PD-L1 antibody for the same purpose and substitution of one known element for another known element, the elements having equivalent effect, is considered to be obvious, absent a showing that the result of the substitution yields more than predictable results. See MPEP 2143(I).
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Claims 107 and 109 are rejected under 35 U.S.C. 103 as being unpatentable over Han et al. (Nature, published 14 February 2019, of record) in view of Zhang et al. (International Journal of Molecular Sciences, 2016, IDS ref., of record).
This is a new rejection necessitated by applicant’s amendments to the claims. A response to Applicant’s traversal follows the new rejection below.
Regarding claims 107 and 109, Han teaches neoantigen-specific immunity is regulated by mRNA N6-methyadenosine (m6A) methylation through the m6A-binding protein YTHDF1 (Abstract). Han teaches loss of YTHDF1 in classical dendritic cells (DCs) enhanced the cross-presentation of tumor antigens and the cross-priming of CD8+ T cells in vivo (Abstract). Han teaches binding of YTHDF1 to these transcripts increases the translation of lysosomal cathepsins in DCs (antigen presenting cell) (Abstract and p. 272, 2nd column). Han teaches the mouse model used in this study involved the inoculation of ovalbumin (OVA)-expressing B16 melanoma cells subcutaneously into wild-type and Ythdf1-/- mice (p. 270, 1st column). The B16 melanoma cells read as skin cancer (claim 109). Han teaches the in vivo antitumor response was markedly improved by cathepsin blockade in wild-type mice (Fig. 4b), suggesting cathepsins are critical factors for determining the antitumor response in this model, therefore, these data show that loss of YTHDF1 in DCs attenuates antigen degradation by restricting the expression of lysosomal proteases, leading to improved cross-presentation and better cross-priming of CD8+ T cells (p. 273, 1st column and Fig. 4b). Han teaches Ythdf1-/- mice showed a marked increase in IFNγ in CD8+ T cells, and IFNγ signaling upregulates the expression of PD-L1, the ligand for PD1 (p. 273, 1st column). Han teaches treating wild-type and Ythdf1-/- tumor-bearing mice with an anti-PD-L1 antibody, which showed 100% tumor regression (p. 273, 2nd column). Han teaches their data suggest combining checkpoint blockade with YTHDF1 depletion could be a potential new therapeutic strategy to improve outcomes in patients with low response to checkpoint blockades (p. 273, 2nd column).
Han does not teach the YTHDF1 attenuating agent is either Salvianolic acid A (Sal A) and Salvianolic acid C (Sal C).
Zhang teaches Salvianolic acid A (Sal A) is a selective ETAR antagonist in both exogenous and endogenous cells lines and reveal the inhibitory effect of Sal A on the proliferation of multiple tumor cells lines (p. 10, Discussion, 1st para.). Zhang teaches the majority of cancer cell types, such as: prostate, ovarian, and lung cancers (claim 109), show a reduction of ET-1-stimulated growth in response to ETAR antagonism (p. 10, Discussion, 3rd para.). Zhang suggests, based on their results, Sal A is a cardio-friendly anti-cancer leading compound (p. 11, Discussion, 4th para.). Zhang strongly suggests Sal A is a potential candidate for the development of an anti-cancer drug (p. 13, Conclusion).
Therefore, it would have been obvious to one of ordinary skill to combine the teachings and suggestions of Han and Zhang with a reasonable expectation of success because Han teaches administration of an additional anti-cancer treatment comprising an anti-PD-L1 antibody and Zhang strongly suggest Sal A is a potential candidate for the development of an anti-cancer drug. One would be motivated to combine the teachings of Han and Zhang because both references teach and/or suggest cancer treatments and the teachings of Han suggest combining checkpoint blockade (anti-PD-L1 antibody) with YTHDF1 depletion could be a potential new therapeutic strategy to improve outcomes in patients with low response to checkpoint blockades (p. 273, 2nd column).
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Response to Traversal
Applicant's arguments filed 04 February 2026, directed to the rejection of new claims 107-109 have been fully considered but they are not persuasive.
Applicant has asserted, Han's genetic knockout approach represents a research tool that is not clinically translatable to human patients, whereas applicant's claimed invention provides a pharmacologically-based combination therapy that can be readily implemented in clinical practice. However, the test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981). In this case the arguments are all directed to Han.
Additionally, the claims are not directed to human patients. In submitting evidence asserted to establish unobvious results, there is a burden on an applicant to indicate how the examples asserted to represent the claimed invention are considered to relate to the examples intended to represent the prior art and, particularly, to indicate how those latter examples do represent the closest prior art. See In re Borkowski, 595 F.2d 713, 184 USPQ 29 (CCPA 1974); In re Goodman, 339 F.2d 228, 144 USPQ 30 (CCPA 1964).
The evidence relied upon should also be reasonably commensurate in scope with the subject matter claimed and illustrate the claimed subject matter "as a class" relative to the prior art subject matter "as a class." In re Susi, 440 F.2d 442, 169 USPQ 423 (CCPA 1971 ); In re Hostettler, 429 F.2d 464, 166 USPQ 558 (CCPA 1970). See, also, In re Lindner, 457 F.2d 506, 173 USPQ 356 (CCPA 1972).
It should also be established that the differences in the results are in fact unexpected and unobvious and of both statistical and practical significance. In re Merck, 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986); In re Longi, 759 F. 2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Klosak, 455 F2d 1077, 173 UAPQ 14 (CCPA 1972); In re D'Ancicco, 429 F.2d 1244, 169 USPQ 303 (CCPA 1971 ). Ex parte Gelles, 22 USPQ2d 1318 (BPAI 1992).
In the rejection above, Han is utilized to demonstrate the effectiveness of the addition of an anti-PD-L1 antibody as it relates to cancer treatment, while Zhang is utilized to demonstrate the effectiveness of Sal A as an anticancer agent.
Claim 108 is rejected under 35 U.S.C. 103 as being unpatentable over Han et al. (Nature, published 14 February 2019, of record) in view of Zhang et al. (International Journal of Molecular Sciences, 2016, IDS ref., of record), as applied to claims 107 and 109 above, and further in view of Inman et al. (Clin Cancer Res; 23(8) April 15, 2017).
This is a new rejection necessitated by applicant’s amendments to the claims.
Regarding claim 108, Han in view of Zhang are silent to the specific anti-PD-L1 antibody. However, several anti-PD-L1 antibodies were known in the art to include atezolizumab.
Inman teaches atezolizumab is an FcyR binding-deficient, fully humanized IgG1 mAb designed to interfere with the binding of PD-L1 ligand (anti-PD-L1 antibody) to its two receptors, PD-1 and B7.1 (Abstract). Inman teaches atezolizumab was first evaluated in a phase I clinical trial for treating bladder cancer, receiving breakthrough therapy designation status by the FDA in June 2014 (p. 1887, Efficacy Phase I). Inman teaches in a phase II clinical trial, the FDA approved atezolizumab for the treatment of bladder cancer in patients with locally advanced or metastatic urothelial carcinoma who have progressed (i) during/after platinum-based chemotherapy or (ii) within 12 months of neoadjuvant or adjuvant treatment with platinum-based chemotherapy (p. 1888, Efficacy Phase II).
Therefore, it would have been obvious to one of ordinary skill in the art to utilize the anti-PD-L1 antibody of Inman in the method of Han in view of Zhang with a reasonable expectation of success because both the method of Inman and Han in view of Zhang are used for the same purpose in treating cancer and it would be reasonable to expect the anti-PD-L1 antibody to work in the same manner. One would be motivated to utilize the anti-PD-L1 antibody of Inman in the method of Han in view of Zhang because Han and Inman are both teaching the use of an anti-PD-L1 antibody for the same purpose and substitution of one known element for another known element, the elements having equivalent effect, is considered to be obvious, absent a showing that the result of the substitution yields more than predictable results. See MPEP 2143(I).
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Relevant prior art
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
Jia et al. (Evidence-Based Complementary and Alternative Medicine, Volume 2020, published 11 June 2020).
Jia teaches traditional Chinese medicine to treat liver cancer. Jia references studies utilizing bioactive compounds which posses immunostimulating properties, to include salvianolic acid C.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/N.A.H./Examiner, Art Unit 1631
/LAURA SCHUBERG/Primary Examiner, Art Unit 1631
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