DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claims 88, 95 and 97-107 are pending.
Claims 99-107 have been withdrawn.
Claims 88, 95, 97 and 98 are currently under examination.
Applicant’s election without traverse of Group I in the reply filed on June 17, 2025 is acknowledged. Applicant’s election without traverse of the species, Myc inhibitor and St6galnac4 in the reply filed on June 17, 2025 is acknowledged. The species disialyl-T has been rejoined with the St6galnac4 because the art discloses that the only reaction ST6GALNAC4 is known to catalyze is the transfer of sialic acid a2-6 to GalNAc in sialyl- T to produce disialyl-T glycans
Objections to Specification
The objections to the specification are withdrawn in view of Applicant’s amendments to the Specification.
35 USC § 103 rejections withdrawn
The rejection of claims 88 and 95 under 35 U.S.C. 103 as being unpatentable over Kuo et al (US 2016/0022684, published January 28, 2016) in view of Chen et al (Signal Transduction and Targeted Therapy 3:5 pages 1-6, February 2018, cited previously) are withdrawn in view of Applicant’s amendments to claim 88.
35 USC § 112(a) rejections withdrawn
The rejection of claims 88, 95, 97 and 98 for failing to comply with the enablement requirement are withdrawn in view of Applicant’s arguments and Burchell’s disclosure that several cancer cells express sialylated core-1-MUCl glycoproteins recognized by the KL-6 antibody.
35 USC § 103 rejections maintained
The rejection of claims 88, 95, 97 and 98 under 35 U.S.C. 103 as being unpatentable over Kuo et al (US 2016/0022684, published January 28, 2016, cited previously) and Chen et al (Signal Transduction and Targeted Therapy 3:5 pages 1-6, February 2018, cited previously) in view of Burchell et al (US 2019/0211099, published July 11, 2019, effective filing date July 1, 2016, cited previously)), Ohyabu et al (J Am Chem Soc 131:17102-17109, 2009), Yamada et al (J Proteome Res 8:521-537, 2009, cited previously) in further view Harduin-Lepers (Biochem J 352:37-48, 2000, cited previously) are maintained.
Kuo teaches treating myc-driven B-cell malignancies having dysregulated Myc with BET inhibitors (paragraphs 3-8, 39, 40, 100, 101;Figs. 1-4). Kuo discloses that the BET inhibitor may be administered parenterally (paragraphs 167, 196).
Chen discloses multiple indirect Myc inhibitors including inhibitors of the BET inhibitor including JQ1, for the treatment of several cancers (page 1, 2nd column, to page 5, 1st column; Table 1).
One of ordinary skill in the art would have been motivated to apply Chen’s disclosure that the BET inhibitor is an indirect Myc inhibitor to Kuo’s method of treating leukemia having dysregulated Myc with the BET inhibitors because both Chen and Kuo disclose the treatment of cancers with dysregulated Myc, such as T-ALL. with indirect Myc inhibitors such at BET inhibitors. It would have been prima facie obvious to combine Kuo’s method of treating leukemia having dysregulated Myc with the BET inhibitors with Chen’s disclosure that the BET inhibitor is an indirect Myc inhibitor to have a method of enhancing immunogenicity of a cancer comprising dysregulated Myc, comprising administering an effective amount of an indirect Myc inhibitor.
Neither Kuo nor Chen teach assessing the levels of disialyl-T or St6galnac4 on the surface of cancer cells of the individual.
Burchell discloses that cancer cells in a subject that express certain sialylated core-1-MUCl glycoproteins not expressed by normal epithelial cells (paragraphs 7, 88). Burchell discloses the anti-MUC1 antibody KL-6 (paragraph 60).
Ohyabu discloses that the epitope of KL-6 antibody recognizes an MUC-1 epitope that includes disialyl-T (Abstract; page 17107, 2nd column).
Yamada discloses that leukemia cells generally showed simple glycan profiles and commonly contained sialyl-T and disialyl-T antigens as major O-glycans (page 524, 2nd column, page 535, 2nd column).
Given that Ohyabu discloses that KL-6 antibody recognizes a MUC1 epitope that includes disialyl-T, increased detection of MUC1 with the KL-6 antibody would indicate an increase in disialyl-T. This is consistent with what Yamada finds in that leukemia cell exhibit increased levels of disialyl-T. Thus, detecting higher levels of disialyl-T in a particular sample would indicate the presence of cancer, including leukemia.
One of ordinary skill in the art would have been motivated to apply Burchell, Ohyabu and Yamada disclosure that levels of diasyl-T are increased on cancer cells to Kuo and Chen’s method of enhancing immunogenicity of a cancer comprising dysregulated Myc, comprising administering an effective amount of a Myc inhibitor because Kuo teaches treating leukemia having dysregulated Myc with the BET inhibitor BRD4 while Burchell, Ohyabu and Yamada disclosure that diasyl-T is upregulated on leukemia cells. Once a cancer is detected it would have obvious to treat the leukemia having dysregulated Myc with the myc inhibitors listedin Chen, given that the majority of cancer have dysregulated myc.
Furthermore Harduin-Lepers discloses that ST6GALNAC4 is known to catalyze the transfer of sialic acid a2-6 to GalNAc in sialyl-T to produce disialyl-T glycans ( it would have been obvious to measure levels of ST6GALNAC4 to detect cancers including leukemia in a subject.
It would have been prima facie obvious to combine Kuo and Chen’s method comprising administering an effective amount of a Myc inhibitor with Burchell, Ohyabu and Yamada disclosure that levels of diasyl-T are increased on cancer cells including leukemia cells to have a method of enhancing immunogenicity of a cancer comprising dysregulated Myc, comprising administering an effective amount of a Myc inhibitor to an individual assessed as having elevated levels of disialyl-T or St6galnac4.
Applicant argues that Burchell, Ohyabu and Yamada taken individually or in
combination fail to teach, suggest or remotely contemplate administering an indirect Myc inhibitor to an individual on the basis of an assessment of Siglec-7 ligand levels on the surface of cancer cells of the individual to enhance the immunogenicity of the individual's cancer. Applicant argues that Burchell relates to the administration of Siglec-9 activity modulators that block interaction between Siglec-9 and sialylated Core-1-MUC1 glycoproteins. Applicant acknowledges that it was known in the prior art that sialylated Core-1-MUC1 glycoproteins reduce the immunogenicity of cancers via engagement with Siglecs as described in Burchell. Applicant argues that the therapeutic approach described in Burchell is entirely different from claimed methods in that Burchell relates exclusively to blocking interactions between Siglec-9 and Core-1-MUC1 glycoproteins already present on the surface of cancer cells but does not remotely contemplate administering an agent that enhances the immunogenicity of cancers by reducing the levels of Siglec ligands elevated on the surface of cancer cells in the first place. Applicant argues that Burchell was unaware that the levels of such ligands could be reduced via inhibition of Myc as an alternative therapeutic modality to the one taught by Burchell.
Applicant’s argument has been considered but is not persuasive. In response to Burchell, Chen, Ohyabu and Yamada individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). The active method steps of “administering an effective amount of a Myc inhibitor to an individual” and assessing levels of disialyl-T or St6galnac4” were known in the art. Burchel is used to demonstrate that disialyl-T and St6galnac4 were upregulated in many types of cancer. Thus, increased levels of disialyl-T and St6galnac4 may be used to diagnose cancer, including leukemia. Once a cancer had been diagnosed it would have been obvious to administer an effective amount of a Myc inhibitor as disclosed by Kuo and Chen, given that the majority of cancers have been shown to have dysregulated myc. Furthermore, as disclosed by Kuo and Chen, detecting dysregulated myc was well known in the art.
In response to Applicant’s argument that there is no evidence that Burchell’s KL-6 antibody binds Krebs von Lungen-6 (KL-H), Ishikawa et al (Respiratory Investigation 50:3-13, 2012) discloses that the KL-6 antibody was developed in a cooperative study with Eidia (page 4, 2nd column, 2nd paragraph, heading 2.) while Burchell discloses that the KL-6 antibody that they used was from Eidia (paragraph 60). Thus, as evidenced by Ishikawa, the KL-6 antibody used in Burchell was the same KL-6 antibody disclosed in Ohyabu.
NEW REJECTIONS: Based on the Amendment
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
Claims 88, 95, 97 and 98 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. Although the specification discloses specific indirect Myc inhibitors, the specification does not disclose the limitation “indirect Myc inhibitor”.
Summary
Claims 88, 95, 97 and 98 stand rejected
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 extension fee 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 date of this final action.
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/MARK HALVORSON/Primary Examiner, Art Unit 1646