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 .
DETAILED ACTION
The amendment filed February 5, 2026 in response to the Office Action of November 5, 2025 is acknowledged and has been entered.
Claim 1 has been amended.
Claims 7, 12, 15, 17, 20, 22, 48 and 49 have been cancelled.
Claims 1, 57, 62, 63, 65-67, 73, 76, 78, and 80 are pending.
Claims 62, 63, 65-67, 73, 76, 78, and 80 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected inventions or species, there being no allowable generic or linking claim.
Claims 1 and 57 are currently under consideration as drawn to the elected invention.
In view of cancelation of claim 22, the claim objection set forth in the previous Office Action is hereby withdrawn.
In view of cancelation of claims 12, 15, 17, 20 and 22, the 112(b) rejection set forth in the previous Office Action is hereby withdrawn.
Amended claim 1 introduced new limitations: the sequences for the HER2 inhibitor and ribociclib. In view of the amendment, the 112(a) rejection set forth in the previous Office Action is hereby withdrawn.
In view of claim amendments (the specific combination of amended claim 1), the 103 rejection set forth in the previous Office Action is hereby withdrawn.
In view of claim amendments, the Double Patenting rejection set forth in the previous Office Action is hereby withdrawn.
NEW REJECTION
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.
Claim 1 is rejected under 35 U.S.C. 103 as being unpatentable over Wei (Wei et al., Oncotarget, 2017, Vol. 8, No. 31, 51037-51049, Publication Date: 05/02/2017, of record) in view of Goel (Goel et al., Cancer Cell, 29, 255-269, Publication Date: 03/14/2016, cited in IDS of 09/27/2022) and Ribociclib-NCI (downloaded from: https://www.cancer.gov/news-events/cancer-currents-blog/2017/fda-ribociclib-palbociclib-breast-cancer, on 10/30/2025, Publication Date: 04/10/2017, of record), as evidenced by ANBENITAMAB (downloaded from: https://precision.fda.gov/ginas/app/ui/substances/890606e5-f01a-449c-b36e-909d0c3da902, on 10/30/2025, of record).
Wei teaches a bispecific antibody, termed KN026, targeting two distinct epitopes on HER2 derived from trastuzumab and pertuzumab (the bridging paragraph of cols 1-2 on page 51041).
Wei teaches that KN026 binds native HER2 on cell surface. More antibodies bind to HER2 on cell surface due to bi-specificity of KN026 where two KN026 molecules could bind one HER2 molecule on cells surface (the bridging paragraph of pages 51042-51043; and Fig. 3).
As evidenced by ANBENITAMAB, KN026 is also called anbenitamab (see § Names And Synonyms). Anbenitamab has four subunits. As shown below, Subunit 1 comprises SEQ ID NO: 14 of the instant application; Subunit 2 comprises SEQ ID NO: 13 of the instant application; Subunit 3 and Subunit 4 are identical and both comprise SEQ ID NO: 1 (the elected species) of the instant application.
Alignment of Subunit 1 and SEQ ID NO: 14:
KN026_SUBUNIT1
Query Match 100.0%; Score 645; DB 1; Length 450;
Best Local Similarity 100.0%;
Matches 120; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFNIKDTYIHWVRQAPGKGLEWVARIYPTNGYTRY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFNIKDTYIHWVRQAPGKGLEWVARIYPTNGYTRY 60
Qy 61 ADSVKGRFTISADTSKNTAYLQMNSLRAEDTAVYYCSRWGGDGFYAMDYWGQGTLVTVSS 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ADSVKGRFTISADTSKNTAYLQMNSLRAEDTAVYYCSRWGGDGFYAMDYWGQGTLVTVSS 120
Alignment of Subunit 2 and SEQ ID NO: 13:
KN026_SUBUNIT2
Query Match 100.0%; Score 634; DB 1; Length 449;
Best Local Similarity 100.0%;
Matches 119; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIY 60
Qy 61 NQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSS 119
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSS 119
Alignment of Subunit 3/4 and SEQ ID NO: 1:
KN026_SUBUNIT3_4
Query Match 100.0%; Score 557; DB 1; Length 214;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPS 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPS 60
Qy 61 RFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIK 107
Taken together, bispecific antibody KN026 reads on the HER2 inhibitor of instant claim 1.
Wei teaches that KN026 retains the strong ADCC activity (Fig. 4A; page 51043, col. 1, para. 2).
Wei teaches that KN026 shows anti-tumor activity to multiple tumor cell lines, including breast cancer cells BT474, gastric cancer cells NCI-N87, and lung cancer cells Calu-3 (Figs. 4B-4D).
Wei teaches that in treating NCI-N87 cells, KN026 is more potent at 1μg/ml concentration where it kills about 60% of the cells while trastuzumab plus pertuzumab kills about 40% (Fig. 4C; page 51043, col. 2, para. 1).
Wei teaches that KN026 shows stronger inhibition of tumor cell growth than trastuzumab plus pertuzumab for other tested cell lines, such as NCI-H2170, HCC1419 (Fig. 4F).
Wei teaches that KN026 also shows anti-tumor activity in HER2-overexpressing NSCLC and gastric tumor cell xenograft in vivo. The in vivo results show that KN026 could similarly inhibit tumor growth as trastuzumab and pertuzumab combination (Fig. 4G, 4H).
Wei teaches that in summary, KN026 retains the ADCC-mediated mechanism of trastuzumab and pertuzumab, and inhibits proliferation of HER2-over-expressing cancer cells with comparable or better activity as trastuzumab and pertuzumab combination in vitro and in vivo (page 51044, col. 1, para. 1).
Wei’s teachings are described above. However, Wei does not teach the bispecific antibody in combination with ribociclib.
Goel teaches that cyclin D1/CDK4 mediate resistance to targeted therapy for HER2-positive breast cancer. Inhibition of CDK4/6 not only suppresses Rb phosphorylation, but also reduces TSC2 phosphorylation and thus partially attenuates mTORC1 activity. This relieves feedback inhibition of upstream EGFR family kinases, resensitizing tumors to EGFR/HER2 blockade. Consequently, dual inhibition of EGFR/ HER2 and CDK4/6 invokes a more potent suppression of TSC2 phosphorylation and hence mTORC1/S6K/S6RP activity and enhanced anti-tumor activity (Abstract).
Goel teaches in vivo, CDK4/6 inhibitors sensitize patient-derived xenograft tumors to HER2-targeted therapies and delay tumor recurrence in a transgenic model of HER2-positive breast cancer (Abstract). In HER2-positive trastuzumab-refractory tumor models, the abemaciclib and trastuzumab combination resulted in tumor regression or a significantly greater growth delay (Fig. 7C and 7D; page 265, col. 2, para. 4).
Ribociclib-NCI teaches that the Food and Drug Administration (FDA) has approved both ribociclib for treating breast cancer (paragraphs 1 and 2 of page 1; and § Clinical Findings).
Ribociclib-NCI teaches that ribociclib work by inhibiting cyclin-dependent kinas (CDK) 4 and 6. These enzymes are commonly found in higher than normal amounts in breast cancer cells (paragraph 4 on page 1).
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to combine the teachings of Wei, Goel and Ribociclib-NCI and to treat HER2-positve breast cancer with a combination of KN026 and ribociclib, because Wei teaches the anti-HER2 bispecific antibody KN026 shows improved therapeutic activity to various HER2-positve tumors, Goel teaches CDK4/6 inhibitor can reverse the resistance to anti-HER2 antibody based therapy and improved the anti-tumor activity when combined with anti-HER2 antibody, Ribociclib teaches ribociclib is a FDA approved CDK4/6 inhibitor for cancer treatment. One of ordinary skilled in the art would have a reasonable expectation of success that the KN026 and ribociclib combination would reduce the resistance to the antibody KN026 and improve the therapeutic activity of the antibody. The motivation would have been to expand the options for the combinations and to develop a better combination for breast cancer treatment. One of ordinary skill in the art would have motivated to make a medical product comprising antibody KN026 and ribociclib for easy and stream-lined application.
Claim 57 is rejected under 35 U.S.C. 103 as being unpatentable over Wei (Wei et al., Oncotarget, 2017, Vol. 8, No. 31, 51037-51049, Publication Date: 05/02/2017, of record) in view of Goel (Goel et al., Cancer Cell, 29, 255-269, Publication Date: 03/14/2016, cited in IDS of 09/27/2022) and Ribociclib-NCI (downloaded from: https://www.cancer.gov/news-events/cancer-currents-blog/2017/fda-ribociclib-palbociclib-breast-cancer, on 10/30/2025, Publication Date: 04/10/2017, of record), as evidenced by ANBENITAMAB (downloaded from: https://precision.fda.gov/ginas/app/ui/substances/890606e5-f01a-449c-b36e-909d0c3da902, on 10/30/2025, of record), as applied to claim 1 above, and further in view of Nathan (Nathan et al., Oncol Ther (2017) 5: 17-29, Publication Date: 05/08/2017).
Wei, Goel and Ribociclin-NCI teach the medical product of claim 1 as set forth above. However, the references do not teach the medical product further comprises a fulvestrant.
Nathan teaches that fulvestrant is a selective estrogen receptor degrader that binds, blocks and degrades the estrogen receptor (ER), leading to complete inhibition of estrogen signaling through the ER (§ Abstract).
Nathan teaches that about 80% of breast cancers express ER, with their survival and proliferation driven by estrogen acting as the ligand and binding to the ER which is then translocated to the cancer cell nucleus. This is in turn initiates a signaling cascade, resulting in the propagation of breast cancer (the bridging paragraph of page 17-18).
Nathan teaches that fulvestrant has been widely tested in breast cancer clinical trials both as monotherapy or in combination with other therapy including CDK4/6 inhibitor ribociclib (Table 1). Fulvestrant is an important endocrine therapy that has demonstrated substantial clinical benefit in many phase 3 trials, either alone or in combination with other agents (§ CONCLUSIONS).
Nathan teaches that whilst fulvestrant is clearly an effective drug as monotherapy, we believe that its role in treatment of ER-positive breast cancer may be best reserved for combination therapy (§ ABSTRACT).
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to make the medicinal product of claim 1 for treating breast cancer based on the teachings of Wei, Goel and Ribociclib-NCI as set forth above, and to modify the medicinal product by adding fulvestrant as taught by Nathan, because Nathan teaches that most breast cancers (80%) are ER positive and fulvestrant is effective for treating ER positive breast cancer and is suitable for combination therapy. One of ordinary skilled in the art would have had a reasonable expectation of success that adding fulvestrant in the combination would further improve the therapeutic activity to ER positive breast cancer, because it brings another of anti-tumor mechanism into the medicinal product. Given all the components are well known in the art (as evidenced by the references), one of ordinary skill in the art would have known to make a product comprising the combination. The motivation would have been to expand the options for the combinations and to develop a better combination for breast cancer treatment.
Response to Arguments
For the 103 rejection, Applicant argues:
Firstly, the sequence information obtained from ANBENITAMAB was downloaded from 2025-10-30, which cannot be considered as prior art. Wei merely disclosed a biparatopic anti-Her2 antibody KN026, and neither mentioned any combination comprising the biparatopic anti-Her2 antibody nor the specific sequence of KN026.
Applicant’s arguments have been fully considered but they are not persuasive. ANBENITAMAB was not used as a prior art in the rejection. ANBENITAMAB was used to show that KN026 comprises the recited sequences of instant claim 1. Based on the prior art: Wei, Goel and Ribociclib-NCI, one of ordinary skilled in the art would have reached a medicinal product comprising combination of KN026 and ribociclib, which would read on the instant claim 1.
Applicant further argues about the unexpected results for the combination:
Specifically, it is verified that the combination of HER2 inhibitor of amend claim I
(having the variable region of first light chain and the second light chain has an identical amino acid sequence set forth as SEQ ID NO .1; the variable region of the first heavy chain and the second heavy chain are set forth as SEQ ID NO.13 and SEQ ID NO.14) and the CDK inhibitor Ribociclib can reduce the tumor volume significantly compared to administrating the HER2 inhibitor or Ribociclib alone.
Besides, according to Fig. 2 of the present application, there is still a 75% in tumor volume reduction, which is unexpected high. Therefore, the 75% of tumor volume reduction is an unexpected technical effect in tumor inhibition.
Applicant’s arguments have been fully considered but they are not persuasive. As shown be Goel, the combination of CDK4/6 and anti-HER2 antibody can significantly enhance the anti-tumor activity (Fig. 7C and 7D) compared to either agent alone. The tumor reduction under combination therapy is more than 75% in the in vivo study (Fig. 7C). Thus, the enhanced anti-tumor activity shown by the instant specification is not unexpected.
Double Patenting
The no statutory 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.
Patent No. US 11/396,557
Claims 1 and 57 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of U.S. Patent No. US 11/396,557 B2 (herein after Pat. 557, corresponding to Appl. 17/022,545, of record) in view of Wei (Wei et al., Oncotarget, 2017, Vol. 8, No. 31, 51037-51049, Publication Date: 05/02/2017, of record), Goel (Goel et al., Cancer Cell, 29, 255-269, Publication Date: 03/14/2016, cited in IDS of 09/27/2022), Ribociclib-NCI (downloaded from: https://www.cancer.gov/news-events/cancer-currents-blog/2017/fda-ribociclib-palbociclib-breast-cancer, on 10/30/2025, Publication Date: 04/10/2017, of record), and Nathan (Nathan et al., Oncol Ther (2017) 5: 17-29, Publication Date: 05/08/2017), as evidenced by ANBENITAMAB (downloaded from: https://precision.fda.gov/ginas/app/ui/substances/890606e5-f01a-449c-b36e-909d0c3da902, on 10/30/2025, of record).
The claims of Pat. 557 teach a method for preparing a bispecific antibody, wherein said bispecific antibody is comprised of two common light chains that are identical and two heavy chains that are different, wherein the preparing method comprises the following steps of: introducing expression vectors into a host cell, and inducing expression of said expression vectors to obtain said bispecific antibody, wherein said expression vectors encode for the two identical common light chains, and two heavy chains, and said host cells does not comprise an expression vector encoding for a light chain different from said common light chain; each of the two identical common light chains comprises a variable region having the sequence as set forth in amino acid positions 1-107 of a sequence selected from SEQ ID NO: 1, SEQ ID NO: 2, SEQ ID NO: 3, SEQ ID NO:4, SEQ ID NO: 5 or SEQ ID NO: 6;each of said two heavy chains has a variable region, and the sequence of one variable region of one of the heavy chains is as set forth in SEQ ID NO: 23 and the sequence of the other variable region of the other heavy chain is as set forth in SEQ ID NO: 24; wherein said method produces only a bispecific antibody comprising the two identical common light chains with the variable region as set forth in amino acid positions 1-107 of a sequence selected from SEQ ID NO: 1, SEQ ID NO: 2, SEQ ID NO: 3, SEQ ID NO: 4, SEQ ID NO: 5 or SEQ ID NO: 6 and the two different heavy chains with one heavy chain having the variable region as set forth in SEQ ID NO: 23 and the other heavy chain having the variable region as set forth in SEQ ID NO: 24 (claim 1), wherein the variable region of said common light chains comprises the sequence as set forth in amino acid positions 1-107 of SEQ ID NO: 1 (claim 3), wherein said common light chains comprise the sequence as set forth in SEQ ID NO: 1 (claim 7).
As shown below, SEQ ID NO: 1 of Pat. 557 comprises SEQ ID NO: 1 of the instant application; SEQ ID NO: 23 of Pat. 557 comprises SEQ ID NO: 14 of the instant application; SEQ ID NO: 24 of Pat. 557 comprises SEQ ID NO: 13 of the instant application.
SEQ ID NO: 1 of Pat. 557 alignment with SEQ ID NO: 1 of the instant application:
Query Match 100.0%; Score 557; Length 214;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPS 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPS 60
Qy 61 RFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIK 107
SEQ ID NO: 23 of Pat. 557 alignment with SEQ ID NO: 14 of the instant application:
Query Match 100.0%; Score 645; Length 120;
Best Local Similarity 100.0%;
Matches 120; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFNIKDTYIHWVRQAPGKGLEWVARIYPTNGYTRY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFNIKDTYIHWVRQAPGKGLEWVARIYPTNGYTRY 60
Qy 61 ADSVKGRFTISADTSKNTAYLQMNSLRAEDTAVYYCSRWGGDGFYAMDYWGQGTLVTVSS 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ADSVKGRFTISADTSKNTAYLQMNSLRAEDTAVYYCSRWGGDGFYAMDYWGQGTLVTVSS 120
SEQ ID NO: 24 of Pat. 557 alignment with SEQ ID NO: 13 of the instant application:
Query Match 100.0%; Score 634; Length 119;
Best Local Similarity 100.0%;
Matches 119; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIY 60
Qy 61 NQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSS 119
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSS 119
Thus, the bispecific antibody of Pat. 557 would read on the HER2 inhibitor of instant claims 1. It is noted that KN026 of Wei is a specie of bispecific antibody encompassed by the claims of Pat. 557.
The claims of Pat. 557 teach as set forth above. Although the claims of Pat. 557 is drawn to a method, the claims disclose the structure of the bispecific anti-HER2 antibody which reads on the HER2 inhibitor (a bispecific anti-HER2 antibody) of the instant application. However, the claims of Pat. 557 do not teach a medicinal product comprises a combination of the bispecific antibody with a CDK4 and/or CDK6 inhibitor: ribociclib.
As set forth above, Wei, as evidenced by ANBENITAMAB, teaches KN026 which comprises the light chains and variable regions of heavy chains with identical sequences as recited by the claims of Pat. 557 and the instant application. Wei teaches that KN026 has anti-tumor activity to various tumors (including breast cancers) both in vitro and in vivo. Goel teaches dual inhibition of EGFR/ HER2 and CDK4/6 invokes a more potent suppression of TSC2 phosphorylation and hence mTORC1/S6K/S6RP activity and enhanced anti-tumor activity. Ribociclib-NCI teaches that ribociclib is a CDK4/6 inhibitor and has been approved by FDA for cancer therapy.
Regarding instant claim 1, it would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to combine the teachings of the claims of Pat. 557, Wei, Goel and Ribociclib-NCI and to treat HER2-positve breast cancer with a combination of KN026 and ribociclib, because Wei teaches the anti-HER2 bispecific antibody KN026 shows improved therapeutic activity to various HER2-positve tumors, Goel teaches CDK4/6 inhibitor can reverse the resistance to anti-HER2 antibody based therapy and improved the anti-tumor activity when combined with anti-HER2 antibody, Ribociclib teaches ribociclib is a FDA approved CDK4/6 inhibitor for cancer treatment. One of ordinary skilled in the art would have a reasonable expectation of success that the KN026 and ribociclib combination would reduce the resistance to the antibody KN026 and improve the therapeutic activity of the antibody. The motivation would have been to expand the options for the combinations and to develop a better combination for breast cancer treatment. One of ordinary skill in the art would have motivated to make a medical product comprising antibody KN026 and ribociclib for easy and stream-lined application.
Regarding claim 57, the claims of Pat. 557, Wei, Goel, Ribociclib-NCI, as evidenced by ANBENITAMAB, teach the medicinal product of instant claim 1 as set forth above. However, the cited references do not teach the medicinal product further comprising a fulvestrant.
Nathan’s teachings are described above in the 103 rejection. In particular, Nathan teaches that about 80% of breast cancers express ER; fulvestrant is an ER inhibitor and is effective to ER positive breast cancers alone or in combination with other agents; fulvestrant is suitable for combination therapy.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to make the medicinal product of claim 1 for treating breast cancer based on the teachings of the claims of Pat. 557, Wei, Goel and Ribociclin-NCI as set forth above, and to modify the medicinal product by adding fulvestrant as taught by Nathan, because Nathan teaches that most breast cancers (80%) are ER positive and fulvestrant is effective for treating ER positive breast cancer and is suitable for combination therapy. One of ordinary skilled in the art would have had a reasonable expectation of success that adding fulvestrant in the combination would further improve the therapeutic activity to ER positive breast cancer, because it brings another of anti-tumor mechanism into the medicinal product. Given all the components are well known in the art (as evidenced by the references), one of ordinary skill in the art would have known to make a product comprising the combination. The motivation would have been to expand the options for the combinations and to develop a better combination for breast cancer treatment.
Application No. 17/914,969
Claims 1 and 57 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 9, 16, 19, 20, 22, 24, 26, 29, 31, 34, 38, 41, 43, and 46 of copending Application No. 17/914,969 (hereinafter Appl. 969, US 2023/0151116 A1, of record) in view of Wei (Wei et al., Oncotarget, 2017, Vol. 8, No. 31, 51037-51049, Publication Date: 05/02/2017, of record), Goel (Goel et al., Cancer Cell, 29, 255-269, Publication Date: 03/14/2016, cited in IDS of 09/27/2022), Ribociclib-NCI (downloaded from: https://www.cancer.gov/news-events/cancer-currents-blog/2017/fda-ribociclib-palbociclib-breast-cancer, on 10/30/2025, Publication Date: 04/10/2017, of record), and Nathan (Nathan et al., Oncol Ther (2017) 5: 17-29, Publication Date: 05/08/2017), as evidenced by ANBENITAMAB (downloaded from: https://precision.fda.gov/ginas/app/ui/substances/890606e5-f01a-449c-b36e-909d0c3da902, on 10/30/2025, of record).
This is a provisional nonstatutory double patenting rejection.
The claims of Appl. 969 teach a formulation for use in preventing, alleviating or treating tumor or inhibiting tumor growth in a subject in need of, the formulation comprises at least 5 μg/mL of a HER2 bispecific antibody, wherein said HER2 bispecific antibody comprises a first light chain, a second light chain, a first heavy chain and a second heavy chain, wherein said first light chain and said second light chain is capable of assembling with a heavy chain of Pertuzumab and a heavy chain of Trastuzumab, respectively; wherein variable region of said first light chain and/or said second light chain comprises an amino acid sequence as set forth in any one of SEQ ID NO: 1-6 (claim 26). As shown below, SEQ ID NO: 1 of Appl. 969 is identical to SEQ ID NO: 1 of the instant application (the elected species):
US-17-914-969-1
Query Match 100.0%; Score 557; DB 1; Length 107;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPS 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPS 60
Qy 61 RFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIK 107
The claims of Appl. 969 teach that the formulation according to claim 26, wherein said first light chain comprises an amino acid sequence as set forth in any one of SEQ ID NO: 7-12, and/or, said second light chain comprises an amino acid sequence as set forth in any one of SEQ ID NO: 7-12 (claim 29).
The claims of Appl. 969 teach that the formulation according to claim 26, wherein variable region of said first heavy chain comprises an amino acid sequence as set forth in SEQ ID NO: 13; and variable region of said second heavy chain comprises an amino acid sequence as set forth in SEQ ID NO: 14 (claim 31). As shown below, SEQ ID NO: 13 and 14 of Appl. 969 are identical to SEQ ID NO: 13 and 14 of the instant application respectively:
US-17-914-969-13
Query Match 100.0%; Score 634; DB 1; Length 119;
Best Local Similarity 100.0%;
Matches 119; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIY 60
Qy 61 NQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSS 119
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSS 119
US-17-914-969-14
Query Match 100.0%; Score 645; DB 1; Length 120;
Best Local Similarity 100.0%;
Matches 120; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFNIKDTYIHWVRQAPGKGLEWVARIYPTNGYTRY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFNIKDTYIHWVRQAPGKGLEWVARIYPTNGYTRY 60
Qy 61 ADSVKGRFTISADTSKNTAYLQMNSLRAEDTAVYYCSRWGGDGFYAMDYWGQGTLVTVSS 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ADSVKGRFTISADTSKNTAYLQMNSLRAEDTAVYYCSRWGGDGFYAMDYWGQGTLVTVSS 120
Taken together, the bispecific antibody taught by the claims of Appl. 969 would read on the HER2 inhibitor of instant claim 1. It is noted that KN026 of Wei is a specie of bispecific antibody encompassed by the claims of Appl. 969.
The claims of Appl. 969 teach as set forth above. However, the claims of Appl. 969 do not teach a medicinal product comprises a combination of the bispecific antibody with a CDK4 and/or CDK6 inhibitor: ribociclib.
As set forth above, Wei, as evidenced by ANBENITAMAB, teaches KN026 which comprises the light chains and variable regions of heavy chains with identical sequences as recited by the claims of Appl. 969 and the instant application. Wei teaches that KN026 has anti-tumor activity to various tumors (including breast cancers) both in vitro and in vivo. Goel teaches dual inhibition of EGFR/HER2 and CDK4/6 invokes a more potent suppression of TSC2 phosphorylation and hence mTORC1/S6K/S6RP activity and enhanced anti-tumor activity. Ribociclib-NCI teaches that ribociclib is a CDK4/6 inhibitor and has been approved by FDA for cancer therapy.
Regarding instant claim 1, it would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to combine the teachings of the claims of Appl. 969, Wei, Goel and Ribociclib-NCI and to treat HER2-positve breast cancer with a combination of KN026 and ribociclib, because Wei teaches the anti-HER2 bispecific antibody KN026 shows improved therapeutic activity to various HER2-positve tumors, Goel teaches CDK4/6 inhibitor can reverse the resistance to anti-HER2 antibody based therapy and improved the anti-tumor activity when combined with anti-HER2 antibody, Ribociclib teaches ribociclib is a FDA approved CDK4/6 inhibitor for cancer treatment. One of ordinary skilled in the art would have a reasonable expectation of success that the KN026 and ribociclib combination would reduce the resistance to the antibody KN026 and improve the therapeutic activity of the antibody. The motivation would have been to expand the options for the combinations and to develop a better combination for breast cancer treatment. One of ordinary skill in the art would have motivated to make a medical product comprising antibody KN026 and ribociclib for easy and stream-lined application.
Regarding instant claim 57, the claims of Appl. 969, Wei, Goel, Ribociclib-NCI, as evidenced by ANBENITAMAB, teach the medicinal product of instant claim 1 as set forth above. However, the cited references do not teach the medicinal product further comprising a fulvestrant.
Nathan’s teachings are described above in the 103 rejection. In particular, Nathan teaches that about 80% of breast cancers express ER; fulvestrant is an ER inhibitor and is effective to ER positive breast cancers alone or in combination with other agents; fulvestrant is suitable for combination therapy.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to make the medicinal product of claim 1 for treating breast cancer based on the teachings of the claims of Appl. 969, Wei, Goel and Ribociclin-NCI as set forth above, and to modify the medicinal product by adding fulvestrant as taught by Nathan, because Nathan teaches that most breast cancers (80%) are ER positive and fulvestrant is effective for treating ER positive breast cancer and is suitable for combination therapy. One of ordinary skilled in the art would have had a reasonable expectation of success that adding fulvestrant in the combination would further improve the therapeutic activity to ER positive breast cancer, because it brings another of anti-tumor mechanism into the medicinal product. Given all the components are well known in the art (as evidenced by the references), one of ordinary skill in the art would have known to make a product comprising the combination. The motivation would have been to expand the options for the combinations and to develop a better combination for breast cancer treatment.
Application No. 18/454,006
Claims 1 and 57 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 18/454,006 (herein after Appl. 006, US 2024/0101707 A1, of record), in view of Wei (Wei et al., Oncotarget, 2017, Vol. 8, No. 31, 51037-51049, Publication Date: 05/02/2017, of record), Goel (Goel et al., Cancer Cell, 29, 255-269, Publication Date: 03/14/2016, cited in IDS of 09/27/2022), Ribociclib-NCI (downloaded from: https://www.cancer.gov/news-events/cancer-currents-blog/2017/fda-ribociclib-palbociclib-breast-cancer, on 10/30/2025, Publication Date: 04/10/2017, of record), and Nathan (Nathan et al., Oncol Ther (2017) 5: 17-29, Publication Date: 05/08/2017), as evidenced by ANBENITAMAB (downloaded from: https://precision.fda.gov/ginas/app/ui/substances/890606e5-f01a-449c-b36e-909d0c3da902, on 10/30/2025, of record).
This is a provisional nonstatutory double patenting rejection.
The claims of Appl. 006 teach a method of preventing, alleviating or treating tumor or inhibiting tumor growth in a subject, comprising: administrating to the subject a HER2 inhibitor, …, wherein said HER2 inhibitor is a bispecific antibody or an antigen binding portion thereof, and is capable of binding to different epitopes of human HER2 (claim 1).
The claims of Appl. 006 teach that the HER2 inhibitor is a bispecific antibody or the antigen binding portion thereof, and said bispecific antibody or the antigen binding portion thereof has a first heavy chain and a second heavy chain, and wherein said first heavy chain and said second heavy chain are capable of correctly assembling with said light chains respectively under physiological conditions or during in vitro protein expression, wherein variable region of said first light chain and/or said second light chain comprises an amino acid sequence as set forth in any one of SEQ ID NO: 91-96, wherein said first light chain comprises an amino acid sequence as set forth in any one of SEQ ID NO: 65-70, and/or, said second light chain comprises an amino acid sequence as set forth in any one of SEQ ID NO: 65-70, wherein variable region of said first heavy chain comprises an amino acid sequence as set forth in SEQ ID NO: 87; and variable region of said second heavy chain comprises an amino acid sequence as set forth in SEQ ID NO: 88, and/or, wherein two heavy chains thereof comprise a sequence as set forth in any one of SEQ 1D NO: 80-81, 83-84, 97-100 (claim 2).
As shown below, SEQ ID NO: 65 of Appl. 006 comprises SEQ ID NO: 1 of the instant application; SEQ ID NO: 97 of Appl. 006 comprises SEQ ID NO: 13 of the instant application; SEQ ID NO: 98 of Appl. 006 comprises SEQ ID NO: 14 of the instant application.
SEQ ID NO: 65 of Appl. 006 alignment with SEQ ID NO: 1 of the instant application:
US-18-454-006A-65
Query Match 100.0%; Score 557; DB 1; Length 214;
Best Local Similarity 100.0%;
Matches 107; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPS 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPS 60
Qy 61 RFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIK 107
|||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIK 107
SEQ ID NO: 97 of Appl. 006 alignment with SEQ ID NO: 13 of the instant application:
US-18-454-006A-97
Query Match 100.0%; Score 634; DB 1; Length 449;
Best Local Similarity 100.0%;
Matches 119; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIY 60
Qy 61 NQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSS 119
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSS 119
SEQ ID NO: 98 of Appl. 006 alignment with SEQ ID NO: 14 of the instant application:
US-18-454-006A-98
Query Match 100.0%; Score 645; DB 1; Length 450;
Best Local Similarity 100.0%;
Matches 120; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLVESGGGLVQPGGSLRLSCAASGFNIKDTYIHWVRQAPGKGLEWVARIYPTNGYTRY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLVESGGGLVQPGGSLRLSCAASGFNIKDTYIHWVRQAPGKGLEWVARIYPTNGYTRY 60
Qy 61 ADSVKGRFTISADTSKNTAYLQMNSLRAEDTAVYYCSRWGGDGFYAMDYWGQGTLVTVSS 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 ADSVKGRFTISADTSKNTAYLQMNSLRAEDTAVYYCSRWGGDGFYAMDYWGQGTLVTVSS 120
Thus, the claims of Appl. 006 teach the HER2 inhibitor of the instant claim 1. It is noted that KN026 of Wei is a specie of bispecific antibody encompassed by the claims of Appl. 006.
The claims of Appl. 006 teach as set forth above. Although the claims of Appl. 006 is drawn to a method, the claims disclose the structure of the bispecific anti-HER2 antibody which reads on the HER2 inhibitor (a bispecific anti-HER2 antibody) of the instant application. However, the claims of Appl. 006 do not teach a medicinal product comprises a combination of the bispecific antibody with a CDK4 and/or CDK6 inhibitor: ribociclib.
As set forth above, Wei, as evidenced by ANBENITAMAB, teaches KN026 which comprises the light chains and variable regions of heavy chains with identical sequences as recited by the claims of Pat. 557 and the instant application. Wei teaches that KN026 has anti-tumor activity to various tumors (including breast cancers) both in vitro and in vivo. Goel teaches dual inhibition of EGFR/ HER2 and CDK4/6 invokes a more potent suppression of TSC2 phosphorylation and hence mTORC1/S6K/S6RP activity and enhanced anti-tumor activity. Ribociclib-NCI teaches that ribociclib is a CDK4/6 inhibitor and has been approved by FDA for cancer therapy.
Regarding instant claim 1, it would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to combine the teachings of the claims of Pat. 557, Wei, Goel and Ribociclib-NCI and to treat HER2-positve breast cancer with a combination of KN026 and ribociclib, because Wei teaches the anti-HER2 bispecific antibody KN026 shows improved therapeutic activity to various HER2-positve tumors, Goel teaches CDK4/6 inhibitor can reverse the resistance to anti-HER2 antibody based therapy and improved the anti-tumor activity when combined with anti-HER2 antibody, Ribociclib teaches ribociclib is a FDA approved CDK4/6 inhibitor for cancer treatment. One of ordinary skilled in the art would have a reasonable expectation of success that the KN026 and ribociclib combination would reduce the resistance to the antibody KN026 and improve the therapeutic activity of the antibody. The motivation would have been to expand the options for the combinations and to develop a better combination for breast cancer treatment. One of ordinary skill in the art would have motivated to make a medical product comprising antibody KN026 and ribociclib for easy and stream-lined application.
Regarding instant claim 57, the claims of Appl. 006, Wei, Goel, Ribociclib-NCI, as evidenced by ANBENITAMAB, teach the medicinal product of instant claim 1 as set forth above. However, the cited references do not teach the medicinal product further comprising a fulvestrant.
Nathan’s teachings are described above in the 103 rejection. In particular, Nathan teaches that about 80% of breast cancers express ER; fulvestrant is an ER inhibitor and is effective to ER positive breast cancers alone or in combination with other agents; fulvestrant is suitable for combination therapy.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to make the medicinal product of claim 1 for treating breast cancer based on the teachings of the claims of Appl. 006, Wei, Goel and Ribociclin-NCI as set forth above, and to modify the medicinal product by adding fulvestrant as taught by Nathan, because Nathan teaches that most breast cancers (80%) are ER positive and fulvestrant is effective for treating ER positive breast cancer and is suitable for combination therapy. One of ordinary skilled in the art would have had a reasonable expectation of success that adding fulvestrant in the combination would further improve the therapeutic activity to ER positive breast cancer, because it brings another of anti-tumor mechanism into the medicinal product. Given all the components are well known in the art (as evidenced by the references), one of ordinary skill in the art would have known to make a product comprising the combination. The motivation would have been to expand the options for the combinations and to develop a better combination for breast cancer treatment.
Response to Arguments
For the Double Patenting rejection, Applicant argues:
Firstly, US 11396557B2 and USI 7/914,969 did not teach a medical product comprises a combination of the bi specific antibody with ribociclib as recited in amended claim 1, or the combination further including fulvestrant as recited in claim 57.
Applicant’s arguments have been fully considered but they are not persuasive. Although the claims of Pat. 557 or Appl. 969 do not teach a medical product comprises a combination of the bispecific antibody with ribociclib as recited in amended claim 1, the claims disclose the structure of the bispecific anti-HER2 antibody which reads on the HER2 inhibitor (a bispecific anti-HER2 antibody) of the instant application. Combining teachings from Wei, Goel, Ribociclin-NCI and Nathan, one of ordinary skill in the art would reach the claimed invention, as set forth above.
Applicant further argues:
The sequence information obtained from ANBENITAMAB cannot be considered as prior art. Hence, the sequence of KN026 cannot be obtained by combining the sequence information of ANBENITAMAB and Wei. Wei merely disclosed a biparatopic anti Her2 antibody KN026, and neither mentioned any combination comprising the biparatopic anti Her2 antibody nor the specific sequence of KN026.
In addition, the medicinal product of the application provided exerted unexpected technical effect set forth above.
Applicant is reiterating the arguments set forth above (see Response to Arguments in 103 session). Thus for the reasons set forth above the rejection is maintained.
Applicant further argues:
US 18/454,006 merely disclosed a medicinal product comprising a bi specific antibody
which comprise the sequence as set forth in SEQ ID NO: 1, 13 and 14 of this application and a
multiple CDK inhibitor, and wherein the CDK inhibitors is selected from a group consisting of:
THZ53 l, Dinaciclib and SR-3029.
In view of claim amendments, the rejection is rewritten and new references are used. As set forth above, the claims of Appl. 006 disclose the structure of the bispecific anti-HER2 antibody which reads on the HER2 inhibitor (a bispecific anti-HER2 antibody) of the instant application. Combining teachings from Wei, Goel, Ribociclin-NCI and Nathan, one of ordinary skill in the art would reach the claimed invention, as set forth above.
Conclusion
No claims are allowed.
All other objections and rejections set forth in the previous Office Action are hereby withdrawn in view of the claim amendments and applicant’s arguments.
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 CHENG LU whose telephone number is (571)272-0334. The examiner can normally be reached Monday-Friday 8-5.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Samira Jean-Louis can be reached at (571)270-3503. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/CHENG LU/ Examiner, Art Unit 1642
/SAMIRA J JEAN-LOUIS/Supervisory Patent Examiner, Art Unit 1642