DETAILED ACTION
This office action is intended to supersede the office action dated 7/1/2026 to respond to applicants’ arguments.
All other attached documents from 7/1/2026 similarly apply to this updated rejection.
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 21-27 and the gene IKZF1 in claim 21 along with the genes of claim 22 in the reply filed on 29 September 2025 is acknowledged. Claims 23-24 and 28-35 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected election and species (claims 23-24), there being no allowable generic or linking claim. Accordingly, claims 21-22 and 25-27 are pending and being examined on the merits. The search and examination was extended to the BTG2 gene.
Application Status
The Amendments and Remarks filed 11 March 2026 in response to the Office Action 12 December 2025 are acknowledged and have been entered. Claims 21-22 are amended, claims 1-20 have been cancelled, and claims 36-39 are newly added. Claims 21-22, 25-27, and 36-39 are pending and being examined on the merits.
Any objection or rejection nor reiterated herein has been overcome by applicant’s amendments.
Any new rejection set forth is necessitated by applicant’s claim amendments.
Priority
This application is a 371 PCT of KR2021/008524 filed 07/05/2021. Acknowledgment is made of applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d). Should applicant desire to obtain the benefit of foreign priority under 35 U.S.C. 119(a)-(d) prior to declaration of an interference, a certified English translation of the foreign application must be submitted in reply to this action. 37 CFR 41.154(b) and 41.202(e).
Failure to provide a certified translation may result in no benefit being accorded for the non-English application.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 21-22 is rejected under 35 U.S.C. 103 as being unpatentable over Zheng (Zheng et al. Cancer Letters 440-441 (2019); 1-10) in view of Sabir (US 20190125732A1), Gandhi (WO 2014/039960 A1) and Gramont (Gramont et al. Nature reviews Clinical oncology 12.4 (2015): 197-212).
Zheng teaches that IKZF1 is a transcription factor crucial for survival of myeloma cell [abstract}. Zheng teaches that treatment with a pan-PIM kinase inhibitor promoted degradation of IKZF1 and exhibit significant anti-myeloma activity [abstract]. Zheng does not the use of an inhibitor of expression of IKZF1 in a method for preventing or treating cancer in a subject in need, wherein the cancer is selected from the group consisting of breast cancer and pancreatic cancer.
Sabir teaches pharmaceutical composition containing an anticancer compound [abstract]. Sabir teaches that IKZF1 is a pancreatic cancer biomarker [0186]. Sabir teaches that BTG2 is an upregulated gene in breast cancer [Table 3].
Gandhi teaches methods of treating, preventing and/or managing locally advanced breast cancer [abstract]. Gandhi teach that IKZF1 expression can be used to stratify or select a subset of patients with locally advanced breast cancer for treatment decisions [pg. 31, lines 15-21].
Gramont teaches that while the overexpression of HER2/neu (ERBB2) was initially discovered as a prognostic biomarker associated with aggressive breast cancer, HER2 subsequently became the target of breast cancer therapy [Box 1; tables 2-3]
It would have been obvious to one ordinary skilled in the art before the effective filing date of the claimed invention that a composition that inhibits the expression of IKZF1 alone or in combination with BTG2 could be used to prevent or treat breast and pancreatic cancer. One of ordinary skill understands that biomarkers associated with cancer progression or clinically meaningful cancer subtypes frequently became candidates for targeted therapeutic intervention once their role in tumor biology was established, e.g. HER2. Accordingly, upon recognizing IKZF1 as a clinically relevant biomarker in breast cancer and pancreatic cancer, and in view of Zheng’s teaching that reduction in IKZF1 activity provides anti-cancer effects, a skilled artisan would have been motivated to investigate therapeutic inhibition of IKZF1 in cancers exhibiting clinically relevant IKZF1 expression, such as breast and pancreatic cancer.
Claims 25-27 and 36-38 are rejected under 35 U.S.C. 103 as being unpatentable over Zheng (Zheng et al. Cancer Letters 440-441 (2019); 1-10) in view of Sabir (US 20190125732A1), Gandhi (WO 2014/039960 A1) and Gramont (Gramont et al. Nature reviews Clinical oncology 12.4 (2015): 197-212) and as applied to claim 21 and further in view of Wagener (Wagener et al. British Journal of Cancer (2013) 108, 973–982) and Fidler (Fidler et al. Nature reviews cancer 3.6 (2003): 453-458).
The teachings of Zheng, Sabir, Gandhi, and Gramont are discussed above as applied to claim 1 and similarly apply to claims 25-27.
Zheng, Sabir, Gandhi, and Gramont do not teach where the cancer is cancer before production of circulating tumor cells (CTCs), and the composition inhibits the production of circulating tumor cells, and wherein the cancer Produces CTCs, and where the composition inhibits the colonization of the produced circulating tumor cells.
Wagener teaches that endogenous BTG2 expression contributes to the migratory potential of bladder cancer cells and that high levels of BTG2 in bladder cancers are linked to decreased cancer-specific survival [abstract]. Wagener teaches that BTG2 inhibition led to a slight decrease in bladder cancer cellular proliferation [pg. 978, col. 1, para 1]. Wagener teaches the that silencing of endogenous BTG2 expression markedly reduces the motility of bladder cancer cells (i.e., circulating bladder cancer tumor cells) and thus indicate that BTG2 substantially contributes to their migratory activity [pg. 978, col. 1, para 1]. The teaching that BTG2 reduces the motility of bladder cancer cells (i.e., circulating tumor cells) is a teaching that circulating tumor cells (CTCs) have been produced if they their motility can be inhibited. Wagener therefore teaches that inhibition of genes involved in migratory and metastatic cancer phenotypes can reduce dissemination of cancer cells and metastatic progression.
Fidler teaches that metastasis requires dissemination of tumor cells through the circulation followed by colonization of distant organs by those circulating tumor cells and that colonization of secondary sites represents a necessary step in the metastatic cascade [pg. 1, col. 3].
Regarding claims 25-26 and 36-38, it would have been obvious to one ordinary skilled in the art before the effective filing date of the claimed invention to administer an inhibitor of IKZF1 expression to subjects having breast cancer or pancreatic cancer prior to production of CTCs or in subjects in whom CTCs has already been detected in order to 1) inhibit production of circulating tumor cells because Zheng teaches that inhibition of IKZF1 provides anti-cancer activity, Gandhi and Sabir teach that IKZF1 is clinically relevant in breast and pancreatic cancers, respectively, and Wagener teaches that inhibition of genes associated with metastatic cellular phenotypes reduces migration and dissemination of tumor cells; and 2) because the presence of CTCs was recognized in the art as indicative of aggressive disease and metastatic progression and because anti-cancer therapies targeting clinically relevant biomarkers were routinely administered to such patient populations; thereby suppressing metastasis. One of ordinary skill in the art would have reasonable expected that inhibition of a clinically relevant cancer associated transcription factor, such as IKZF1, would reduce generation and dissemination of CTCs and thereby reduce metastatic progression.
Regarding claim 27, it would have been obvious to one of ordinary skilled in the art before the effective filing date of the claimed invention the inhibition of clinically relevant cancer associated factors, such as IKZF1, that are involved in tumor dissemination and CTC formation would inhibin colonization of CTC at secondary sites because prevention of metastatic colonization is an expected consequence of reducing CTC formation, survival and dissemination.
Response to Arguments
Applicant's arguments filed 03/11/2026 in regard to Zheng’s teachings have been fully considered but they are not persuasive. Applicant argues that Zheng related to survival of myeloma cells and therefore would not have suggested the presently claimed treatment of breast cancer, pancreatic cancer, or gastric cancer. Applicant further argues that amended claim 21 no longer encompasses blood cancers and therefore Zheng no longer renders the claims obvious.
While Zheng indeed teaches therapeutic inhibition of IKZF1 in multiple myeloma, Zheng nevertheless establishes that IKZF1 is a therapeutically actionable cancer-associated transcription factor whose inhibition produces anti-cancer effects. The presently applied rejection further relies on the combination of Gandhi and Sabir to establish the relevanct of IKZF1 to the claimed cancers. Therefore, Zheng’s teachings do not negate the motivation provided by the combined teachings as discussed above.
Applicant's arguments filed 03/11/2026 in regard to Wagener have been fully considered but they are not persuasive in view of the new rejections set forth above.
Allowable Subject Matter
The following is a statement of reasons for the indication of allowable subject matter: The limitation of “wherein the cancer is gastric cancer” was found allowable.
Claim 39 is objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Conclusion
No claims allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to TIFFANY N GROOMS whose telephone number is (571)272-3771. The examiner can normally be reached M-F 830-530.
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/TIFFANY NICOLE GROOMS/Examiner, Art Unit 1637
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