DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Status of the Claims
Claims 1, 3, 6-9, 11, 13, 16, 22, 43-44, 47-50, 52-54, 56-66 are pending.
Claims 1, 7-9, 11, 13, 43, 47-50, 52-54, and 61 are newly amended.
Claims 63-66 are newly added.
Claims 1, 3, 6-9, 11, 13, 16, 22, 43-44, 47-48, and 58-62 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 07/03/2025.
Claims 49-50, 52-54, 56-57, and 63-66 have been examined on their merits.
Withdrawn Objections & Rejections
The objections and rejections presented herein represent the full set of objections and rejections currently pending in the application. Any objections or rejections not specifically reiterated are hereby withdrawn.
The rejection of claims 49-50, 52-53, 56-57 under 35 U.S.C. 102(a)(1) or 35 U.S.C. 102(a)(2) as being anticipated Benson et al. (WO2019178422A1, 2019, on IDS 05/27/2022) is withdrawn due to amendment of the claims and Applicant’s persuasive arguments.
The rejection of claim 54 under 35 U.S.C. 103 as being unpatentable over Benson et al. (WO2019178422A1, 2019, on IDS 05/27/2022, previously cited) in view of Krishan et al. (Nat Chem Biol, 2014, previously cited) is withdrawn due to amendment of the claims and Applicant’s persuasive arguments.
Claim Objections
Claim 52 is objected to for the following informalities: claim 52 as amended recites “a Cas9 molecule complexed with agRNA.” While “agRNA” is a known molecule in the art (i.e., an antigene RNA), in this instance, this appears to be a typo for “a gRNA”, which is how it has been interpreted. Appropriate correction is required.
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 52 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.
Claim 52 contains the trademark/trade name “TALEN”. Where a trademark or trade name is used in a claim as a limitation to identify or describe a particular material or product, the claim does not comply with the requirements of 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph. See Ex parte Simpson, 218 USPQ 1020 (Bd. App. 1982). The claim scope is uncertain since the trademark or trade name cannot be used properly to identify any particular material or product. A trademark or trade name is used to identify a source of goods, and not the goods themselves. Thus, a trademark or trade name does not identify or describe the goods associated with the trademark or trade name. In the present case, the trademark/trade name is used to identify/describe “transcription activator-like effector nucleases” and, accordingly, the identification/description is indefinite. It is noted that while “TALEN” is a trademark, full phrase “transcription activator-like effector nucleases” is not, and therefore, writing out the full phrase would be ameliorative.
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 49-50, 52-53, 56-57, 63, and 65-66 are rejected under 35 U.S.C. 103 as being unpatentable over Benson et al. (WO2019178422A1, 2019, on IDS 05/27/2022, previously cited).
In regards to claim 49, Benson teaches methods for treating subjects with cell proliferative disorders, such as cancers, with compositions comprising gene-edited immune effector cells including CD8+ T cells (cytotoxic T cell or CTLs) specifically, to elicit anti-tumor immune responses and cause regression of cancer (Abstract; claims 1, 157, 160, 281-283, 293-294; paragraphs [0067, 00162, 00441]).
In regards to step a), Benson teaches that the cells are administered to subjects (claim 281; paragraph [0068]).
Benson also teaches that the cells are genetically edited to reduce function of the gene PTPN2 (claim 1; paragraph [00234]). Furthermore, Benson teaches that the editing is a partial or complete deletion of the gene (claims 101-103).
In regards to step b), Benson teaches that immune effector cells can be genetically edited to reduce function of PTPN1 (claims 1, 157, 160, 281-283, 293-294). It is well-known in the art that PTPN1 is the gene that encodes PTP1B.
Additionally, the instant specification explicitly states specification explicitly states that the inhibitor may including editing the gene encoding PTP1B (i.e., regulating expression of PTPN1).
Thus, the method of Benson reads on inhibiting PTP1B.
Additionally, Benson explicitly teaches that the cells may be edited in vivo (paragraph [00397]).
Furthermore, it is noted that changes in the sequence of adding ingredients or the selection of any order of performing process steps is prima facie obvious in the absence of new or unexpected results.” In re Burhans, 154 F.2d 690, 69 USPQ 330 (CCPA 1946).
Moreover, a person of ordinary skill in the art would have been motivated to inhibit PTP1B by administration to a patient in order to inhibit a wider population of immune effector cells. Furthermore, because Benson explicitly teaches that in vivo gene modification is an embodiment of the method, it could have been done with predictable results and a reasonable expectation of success.
Furthermore, it is noted that Benson not only states that gene-regulating systems can be used to reduce expression of PTPN1 “or” PTPN2, which is inclusive, and therefore, necessarily suggests that PTPN1 and PTPN2 may be selected simultaneously, but also explicitly states that “one or more” of these genes may be selected (claim 1).
Therefore, the inhibition/editing of multiple genes/proteins is an embodiment envisioned by Benson.
In regards to claim 50, Benson teaches that the CD8+ T cells can be engineered to express a CAR (claims 150-151; paragraph [00134]).
In regards to claim 52, Benson teaches that PTPN2 is edited with a CRISPR/Cas9 system (paragraph [00234]), which requires a Cas9 molecule and a gRNA which complexes with the Cas9 (paragraph [00319-00322]).
In regards to claim 53, Benson teaches that the PTP1B inhibitor is a Cas9 that complexes with a gRNA directed to PTP1B (claims 52, 59; paragraphs [0030, 00101, 00234]).
In regards to claim 56, Benson teaches that the administration to a subject (which would comprise both PTPN2 edited cells and the PTP1B inhibitor) can be administered at one time (claims 1, 281-283; paragraph [00438]).
In regards to claim 57, Benson teaches that the CARs can be directed to HER2-specific tumor antigens (paragraph [00182]), and thus for HER2-positive cancers.
In regards to claim 63, Benson teaches that the gene-regulating system can comprise siRNA or shRNA (claim 21; paragraph [0015]).
In regards to claim 65, Benson teaches that the administration can be systemic (paragraph [00436]).
In regards to claim 66, as above, Benson teaches that cells at least, can be administered over multiple administrations (paragraph [00438]). Additionally, in regards to administrating the PTP1b inhibitor after the administration of the cytotoxic T cells, as above, changes in the sequence of adding ingredients or the selection of any order of performing process steps is prima facie obvious in the absence of new or unexpected results.” In re Burhans, 154 F.2d 690, 69 USPQ 330 (CCPA 1946).
Moreover, as above, a person of ordinary skill in the art would have been motivated to administer PTP1B after the administration of cytotoxic T cells in order to inhibit a wider population of immune effector cells, including both the transformed cytotoxic T cells and endogenous immune cells. Furthermore, because Benson explicitly teaches that in vivo gene modification is an embodiment of the method, it could have been done with predictable results and a reasonable expectation of success and because Benson teaches that patients may be treated over multiple steps, it could have been done with predictable results and a reasonable expectation of success.
Therefore, the teachings of Benson render obvious the invention as claimed.
Claims 54 and 64 are rejected under 35 U.S.C. 103 as being unpatentable over Benson et al. (WO2019178422A1, 2019, on IDS 05/27/2022, previously cited) as applied to claim 49 above, and further in view of Krishan et al. (Nat Chem Biol, 2014, previously cited).
In regards to claims 54 and 64, as above, Benson teaches that a patient may be administered a PTP1B inhibitor.
While Benson uses gene editing inhibition of PTP1B, a person of ordinary skill in the art would have been motivated to administer a small drug inhibitor of PTP1b such as MSI-1436 (trodusquemine) because Krishnan teaches that PTP1b plays a critical role in HER2 signaling in breast cancer, but that inhibition with small molecule inhibitor MSI-1436 (trodusquemine) antagonizes HER2 signaling, inhibits tumorigenesis, and abrogates metastasis of breast cancer in subjects (Abstract, p1-2; MSI-1436 attenuated HER2-mediated tumorigenesis, p7-8; MSI-1436 specifically targeted PTP1B in breast cancer models, p8). Furthermore, because Krishnan teaches that MSI-1436 (trodusquemine) effectively attenuated HER2 signaling, resulting in extensive inhibition of tumor growth and abrogation of metastasis (Introduction, p2-3) and because Benson teaches that drugs can be used in combination with the therapy (paragraph [00441]), it could have been done with predictable results and a reasonable expectation of success.
Therefore, the combined teachings of Benson and Krishnan render obvious the invention as claimed.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 49-50, 52-54, 56-57, 63-66 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 6-7, 9, 11, 13, 15-18, 37, 41, 46, 50, 52-53, and 56-58 of copending Application No. 17/058,551 in view of over Benson et al. (WO2019178422A1, 2019, on IDS 05/27/2022, previously cited).
While the instant claims and the claims of copending Application No. 17/058,551, are not identical, the instant claims are not patentable distinct because both inventions are drawn to inducing an immune response in a subject comprising administering a PTP1B inhibitor and T cells, derived from a subject, to a subject for treating cancer.
Copending Application No. 17/058,551 does not explicitly teach that the T cells are cytotoxic T cells specifically or a step of editing the gene encoding PTPN2 in these cells.
However, a person of ordinary skill in the art would have been motivated to choose cytotoxic T cells because Benson teaches that CD8+ T cells (cytotoxic T cells or CTLs) can be used as immune effector cells for cancer immunotherapies (claims 1 and 281-283). A person of ordinary skill in the art would have been motivated to edit the gene encoding PTPN2 because Benson teaches that PTPN2-edited T cells are effective for treating cancers in subjects (claims 1 and 281-283; paragraphs [00219]).
Furthermore, because Benson teaches that gene-edited CD8+ T cells can be administered to tumorigenic subjects (paragraph [00485]), and teaches methods for editing the PTPN2 gene in T cells for treating cancer in subjects (Abstract; claims 1, 157, 281-283; paragraphs [0067, 00162, 00234, 00441]), it could have been done with predictable results and a reasonable expectation of success.
The copending Application also does not explicitly teach a step of administering the PTP1B to the subject.
However, Benson teaches that immune effector cells can be genetically edited to reduce function of PTPN1 (claims 1, 157, 160, 281-283, 293-294). It is well-known in the art that PTPN1 is the gene that encodes PTP1B. Additionally, the instant specification explicitly states specification explicitly states that the inhibitor may including editing the gene encoding PTP1B (i.e., regulating expression of PTPN1).Thus, the method of Benson reads on inhibiting PTP1B. Benson also teaches that the cells may be edited in vivo (paragraph [00397]).
A person of ordinary skill in the art would have been motivated to inhibit PTP1B by administration to a patient in order to inhibit a wider population of immune effector cells. Furthermore, because Benson explicitly teaches that in vivo gene modification is an embodiment of the method, it could have been done with predictable results and a reasonable expectation of success.
Additionally, in regards to the timings of administration, it is noted that changes in the sequence of adding ingredients or the selection of any order of performing process steps is prima facie obvious in the absence of new or unexpected results.” In re Burhans, 154 F.2d 690, 69 USPQ 330 (CCPA 1946).
This is a provisional nonstatutory double patenting rejection.
Response to Arguments
Applicant argues that Benson does not anticipate the claims under 35 USC 102(a) (Remarks, p9-10).
Applicant argues that the claims as amended no longer include the option of dual ex vivo inhibition (Remarks, p13).
In regards to the rejections under 35 USC 102, Applicant’s arguments filed 09/30/2025 have been fully considered and are persuasive. Therefore, the rejections under 35 USC 102 have been withdrawn.
However, in view of the amendment to the claims, a new ground of rejection under 35 USC 103 has been made as discussed above. Specifically, the claims are still prima facie obvious over Benson et al. (WO2019178422A1, 2019, on IDS 05/27/2022, previously cited) as discussed above.
Applicant argues that Benson does not disclose administration of a PRP1B inhibitor directly to a subject, and does not directly state that both PTP1B and PTPN2 should be specifically inhibited (Remarks, p9). As evidence, Applicant argues that claim 1 refers to a gene regulating system of which “PTPN1 OR PTPN2 may be selected” (emphasis by Applicant) (Remarks, p10). In regards to claim 281, Applicant argues that Benson simply defines a method of treatment comprising administering the effector cells of claim 1 (Remarks, p10). In regards to paragraph [0008]), Applicant argues that this paragraph only refers to modified immune effector cells comprising a genome editing system but does not disclose a method combining modified immune effector cells and systemic administration of a PTP1B inhibitor, while paragraph [00234] only mentions different types of genome editing systems available (Remarks, p10).
Applicant’s arguments filed 09/30/2025 have been fully considered but are not persuasive.
As discussed above, in regards to step b), Benson teaches that immune effector cells can be genetically edited to reduce function of PTPN1 (claims 1, 157, 160, 281-283, 293-294). It is well-known in the art that PTPN1 is the gene that encodes PTP1B.
Additionally, the instant specification explicitly states specification explicitly states that the inhibitor may including editing the gene encoding PTP1B (i.e., regulating expression of PTPN1).
Thus, the method of Benson reads on inhibiting PTP1B.
Additionally, Benson explicitly teaches that the cells may be edited in vivo (paragraph [00397]).
Furthermore, it is noted that changes in the sequence of adding ingredients or the selection of any order of performing process steps is prima facie obvious in the absence of new or unexpected results.” In re Burhans, 154 F.2d 690, 69 USPQ 330 (CCPA 1946).
Moreover, a person of ordinary skill in the art would have been motivated to inhibit PTP1B by administration to a patient in order to inhibit a wider population of immune effector cells. Furthermore, because Benson explicitly teaches that in vivo gene modification is an embodiment of the method, it could have been done with predictable results and a reasonable expectation of success.
Furthermore, it is noted that Benson not only states that gene-regulating systems can be used to reduce expression of PTPN1 “or” PTPN2, which is inclusive, and therefore, necessarily suggests that PTPN1 and PTPN2 may be selected simultaneously, but also explicitly states that “one or more” of these genes may be selected (claim 1).
Therefore, the inhibition/editing of multiple genes/proteins is an embodiment envisioned by Benson.
Benson teaches that the administration can be systemic (paragraph [00436]).
Applicant argues that Krishnan does not renders the claims obvious (Remarks, p10-12). Applicant argues that selection of the information in Krishnan is purely arbitrary and uses hindsight reasoning (Remarks, p13). In particular, Applicant argues that the references do not consider the scenario where it may be desirable or beneficial to inhibit both phosphatases (Remarks, p13).
Applicant’s arguments filed 09/30/2025 have been fully considered but are not persuasive.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
In regards to Krishnan, as discussed above, While Benson uses gene editing inhibition of PTP1B, a person of ordinary skill in the art would have been motivated to administer a small drug inhibitor of PTP1b such as MSI-1436 (trodusquemine) because Krishnan teaches that PTP1b plays a critical role in HER2 signaling in breast cancer, but that inhibition with small molecule inhibitor MSI-1436 (trodusquemine) antagonizes HER2 signaling, inhibits tumorigenesis, and abrogates metastasis of breast cancer in subjects (Abstract, p1-2; MSI-1436 attenuated HER2-mediated tumorigenesis, p7-8; MSI-1436 specifically targeted PTP1B in breast cancer models, p8). Furthermore, because Krishnan teaches that MSI-1436 (trodusquemine) effectively attenuated HER2 signaling, resulting in extensive inhibition of tumor growth and abrogation of metastasis (Introduction, p2-3) and because Benson teaches that drugs can be used in combination with the therapy (paragraph [00441]), it could have been done with predictable results and a reasonable expectation of success.
In regards to considering the scenario where it may be desirable or beneficial to inhibit both phosphatases, as discussed above, Benson discloses that both PTPN1 and PTPN2 can be knocked out (claim 1). Moreover, the claim does not require beneficial effects of eliminating both phosphatases.
Thus, in response to applicant's argument that the references fail to show certain features of the invention, it is noted that the features upon which applicant relies (i.e., beneficial effects) are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993).
Applicant argues that there are unexpected results Remarks, p11-12). Specifically, Applicant argue that the claimed invention involves using a PTPN2 inhibitor (such as CRISPR, etc.) to target T cels. Once CAR T cells or transgenic T cells have been generated (Remarks, p12).
Continuing, Applicant argues that the treatment with PTP1B inhibitors ensures that inhibition of PTP1B can be terminated once CAR T cells have repressed tumor growth, thus preventing toxicities or autoreactivity (Remarks, p12).
Applicant’s arguments filed 09/30/2025 have been fully considered but are not persuasive.
In regards to Applicant’s allegations of unexpected results, 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) (see MPEP 716.02(d)).
In the instant case, the claims do not require any specific result.
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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/JOSEPH PAUL MIANO/Examiner, Art Unit 1631
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