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
The status of the claims are as follows:
Claims 1-21 are pending.
Claims 1-21 are rejected.
Claim 11 is objected to.
Response to Restriction/Election
Applicant’s election without traverse of SSI-4 (2 - { [ 4- ( 2 - Chlorophenoxy ) piperidine 1 - carbonyl ] amino } -N - methylpyridine - 4 – carboxamide) as the SCD1 polypeptide inhibitor and lenvatinib as a species of tyrosine kinase inhibitor, drawn to claims 1-21, in the reply filed on 08/07/2026 is acknowledged.
Pursuant to MPEP 803.02, the Examiner expanded his search from lenvatinib to another specie. The expanded specie is sorafenib. The expanded search does not change the claims searched.
Priority
Acknowledgement is made that Instant Application 18631941, filed on 04/10/2024, claims priority from Provisional Application 63/458,627, filed on 04/11/2023.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 05/29/2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Objections
Claim 11 is objected to because it recites the limitation, “a SCD1 polypeptide and said tyrosine kinase inhibitor”, which should be corrected to “a SCD1 polypeptide inhibitor and said tyrosine kinase inhibitor”. Appropriate action nis required.
Claim Interpretations
Claim 11 recites the limitation, “a SCD1 polypeptide and said tyrosine kinase inhibitor”. The claims that depend therefrom refer to a “SCD1 polypeptide inhibitor”, therefore the recited limitation of “a SCD1 polypeptide” will be interpreted to mean “a SCD1 polypeptide inhibitor”.
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claim(s) 1, 3, 4-5, and 7-8 is/are rejected under 35 U.S.C. 102(a)(1) and under 35 U.S.C. 102(a)(2) as being anticipated by Copland (US 11,243,207 B2. Published 02/08/2022).
Claim 1 is directed to a method for treating cancer in a mammal, wherein said method comprises administering, to said mammal, a stearoyl CoA desaturase 1 (SCD1) polypeptide inhibitor and a tyrosine kinase inhibitor, wherein the number of cancer cells within said mammal is reduced.
Copland teaches methods and materials for identifying and/or treating mammals having a SCD1-associated cancer, wherein the mammal is treated with a SCD1 polypeptide inhibitor (abstract). The method further includes administering an additional therapeutic agent used to treat cancer to the mammal, wherein the additional therapeutic agent can be a chemotherapeutic agent, wherein the chemotherapeutic agent can be a kinase inhibitor, wherein the kinase inhibitor can be sorafenib (column 4, lines 21-29). Treating a mammal as described can be effective to reduce or eliminate the number of cancer cells within the mammal (column 19, lines 46-48).
Copland further teaches the SCD1 polypeptide inhibitor can be SSI-4 (2 - { [ 4- ( 2 - Chlorophenoxy ) piperidine 1 - carbonyl ] amino } -N - methylpyridine - 4 – carboxamide) with the following structure:
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Specifically, Copland teaches Example 1: targeting SCD1 in hepatocellular carcinoma (HCC) (column 27 lines 9-10). Using a xenograft (PDTX) mouse model, tumors were induced in mice until reaching a volume of ~100 mm3 and then were administered either 10 mg/kg SSI-4, 30 mg/kg sorafenib, or both in Nutra-gel diet (column 28, lines 6-18). The treatment resulted in the reduction of tumor volume, i.e., a reduction of the number of cancer cells within the mammal, as shown in Fig 7C (sheet 13/14), shown below for clarity.
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Claim 3 is directed to the method of claim 1, wherein said cancer is a liver cancer.
Copland teaches Fig 7A-7D demonstrate SSI-4 as a single anti-important agent and in synergy with sorafenib in HCC models (column 16, lines 43-45). Fig 7C shows the combination SSI-4 and sorafenib demonstrated prolonged durable response in a HLE HCC mouse model (column 16, lines 49-51).
Claims 4-5 are directed to the method of claim 1, wherein said SCD1 polypeptide inhibitor is a compound having Formula II or Formula IIa, or specifically is the compound SSI-4, (2 - { [ 4- ( 2 - Chlorophenoxy ) piperidine 1 - carbonyl ] amino } -N - methylpyridine - 4 – carboxamide), or a pharmaceutically acceptable salt thereof.
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Copland teaches tumor-induced mice were administered either 10 mg/kg SSI-4, 30 mg/kg sorafenib, or both in Nutra-gel diet (column 28, lines 6-18). Compound SSI-4 is derived from both Formula II and Formula IIa.
Claims 7-8 are directed to the method of claim 1, wherein the tyrosine kinase inhibitor inhibits one or more polypeptides selected from the provided group, wherein the tyrosine kinase inhibitor is selected from the group consisting of cabozantinib, lenvatinib, sorafenib, sunitinib, and regorafenib.
Copland teaches a method of combination therapy of SSI-4 and sorafenib (column 28, lines 6-18).
Claim(s) 1, 6, 11-12 and 17 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by She (SCD1 is Required for EGFR-Targeting Cancer Therapy of Lung Cancer via Re-Activation of EGFR/PI3K/AKT Signals. Cancer Cell Int. 2019, 19:103. doi.org/10.1186/s12935-019-0809-y).
Claim 1 is directed to a method for treating cancer in a mammal, wherein said method comprises administering, to said mammal, a stearoyl CoA desaturase 1 (SCD1) polypeptide inhibitor and a tyrosine kinase inhibitor, wherein the number of cancer cells within said mammal is reduced.
She teaches a method of anti-tumor therapy of lung cancer, both in vitro and in vivo by administering the SCD1 inhibitor A939572 with the tyrosine kinase inhibitor gefitinib (Page 1, Background; Result). A549 and H1573 lung cancer cell lines were used for in vitro analysis due to their upregulation of SCD1 (page 4, left column, paragraph 1). It was found that cell vitality was inhibited by gefitinib (20 µM), but the inhibition was reversed when the cell lines were forced to express SCD1. Following the addition of A939572, cytotoxicity of gefitinib was restored (page 4, right column, paragraph 2. Fig 2a, b).
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She further teaches nude mice were administered with conditional tumor cells that are SCD1 overexpressed, or negative control (page 6, left column, paragraph 5). The mice were orally fed with A939572 (30 mg/kg, p.o.) or gefitinib (100 mg/kg, p.o., 3 days apart). It was found that gefitinib promoted tumor regression, but the mice with SCD1 overexpression abrogated the anti-tumor effects of gefitinib. However, tumor volume decreased in SCD1 overexpressed mice who were co-administered gefitinib and A939572 (page 6, right column, paragraph 1. Fig 5b).
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Therefore, She teaches a method for treating cancer in a mammal, comprising co-administering a SCD1 polypeptide inhibitor and a tyrosine kinase inhibitor, wherein the number of cancer cells within said mammal is reduced (Fig 5b, purple). Thus, claim 1 is anticipated.
Claim 6 is directed to the method of claim 1, wherein the SCD1 polypeptide inhibitor is selected from the group consisting of SSI-2, MF-438, and A939572, or pharmaceutically acceptable salts thereof.
She teaches the method comprises co-administering to the mammal the SCD1 polypeptide inhibitor A939572 with the tyrosine kinase inhibitor.
Claim 11 is directed to a method for treating cancer in a mammal, wherein cancer cells of said cancer have resistance to treatment with a tyrosine kinase inhibitor alone, wherein said method comprises administering, to said mammal, a SCD1 polypeptide and said tyrosine kinase inhibitor, wherein the number of cancer cells within said mammal is reduced.
The method of She is described above, in which mice having cancer cells with a high expression of SCD1 were resistant to treatment with tyrosine inhibitor alone (Fig 5b, blue). However, a reduction of cancer cells was observed when treatment included co-administration with a SCD1 polypeptide inhibitor (Fig 5b, purple). Thus, claim 11 is anticipated.
Claim 12 is directed to the method of claim 11, wherein the method comprises determining said cancers are resistant to treatment with said tyrosine kinase inhibitor alone.
She teaches a cohort of mice with tumor cells having a high expression of SCD1 were treated with a tyrosine inhibitor alone (Fig 5b, blue). It was determined that these tumors were resistant to treatment with the tyrosine kinase inhibitor alone because the tumor volume of this cohort was significantly larger than the cohort of treated mice whose tumor cells did not have a high expression of SCD1 (Fig 5b, red).
Claim 17 is directed to the method of claim 11, wherein the SCD1 polypeptide inhibitor is selected from the group consisting of: SSI-2, MF-438, or A939572, or pharmaceutically acceptable salts thereof.
The method of She comprises administering to the mammal the SCD1 polypeptide inhibitor A939572.
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 text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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(s) 2 is/are rejected under 35 U.S.C. 103 as being unpatentable over Copland as evidenced by Isidan (Development and Characterization of Human Primary Cholangiocarcinoma Cell Lines. The American Journal of Pathology, 2002, 192(9), 1200-1217. doi.org/10.1016/j.ajpath.2022.05.007).
Claim 1, from which claim 2 depends, is rejected under 35 U.S.C. 102 as being anticipated by Copland. The teachings described therein are incorporated herein by reference.
Claim 2 is directed to the method of claim 1, wherein said mammal is human.
Copland teaches co-administration of the SCD1 inhibitor and tyrosine kinase inhibitor is synergetic in reducing tumor volume in mice (Fig 7C) and further teaches the disclosed methods and materials can be used in treating humans having cancer (e.g., a SCD1-associated cancer) (column 1, lines 35-37). Copland further teaches compound SSI-4 inhibits cell proliferation in human (CX-004T2 and HUCCT1) and mouse (M1-1a and M6-1b) cholangiocarcinoma (CAA) cell lines at 1 µM (Fig 8).
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CAA cell lines are derived from intrahepatic and extrahepatic cancers and have been used for almost 50 years to better understand CCA properties, investigate treatment options, model the disease in vitro, and generate in vivo xenograft models (see Isidan). Thus, their inhibition would have motivated one of ordinary skill in the art to use the method of Copland to treat cancer in humans.
Claim(s) 6 and 9-10 is/are rejected under 35 U.S.C. 103 as being unpatentable over Copland.
Claim 1, from which claims 6 and 9-10 depend, is rejected under 35 U.S.C. 102 as being anticipated by Copland. The teachings described therein are incorporated herein by reference.
Claim 6 is directed to the method of claim 1, wherein the SCD1 polypeptide inhibitor is selected from the group consisting of: SSI-2, MF-438, or A939572 or a pharmaceutically acceptable salt thereof.
The difference between the teaching of Copland and the Instant Application is that Copland fails to teach an explicit embodiment wherein the SCD1 polypeptide inhibitor is, SSI-2, MF-438, or A939572.
However, Copland teaches the method may include SSI-2, or a pharmaceutically acceptable salt thereof as the SCD1 polypeptide inhibitor (column 4, line 1).
By applying the prong (B) rationale of In re KSR Int’l Co., 550 U.S. 398 (2007), in which obviousness entails simple substitution of one known element for another to obtain predictable results, it would have been obvious for a person of ordinary skill in the art to substitute SSI-4 for SSI-2 to achieve the desired result with a reasonable expectation of success.
Claim 9 is directed to the method of claim 1, wherein the method comprises administering two or more SCD1 polypeptide inhibitors to said mammal.
The difference between Copland and the Instant Application is that Copland fails to teach an explicit embodiment wherein two or more SCD1 polypeptide inhibitors are administered to the mammal.
However, Copland teaches treating cancer in a mammal using one or more SCD1 polypeptide inhibitors (abstract) and further teaches representative examples of SCD1 polypeptide inhibitors include, without limitation, SSI-1, SSI-2, SSI-3, and/or SSI-4 (column 21, line 50 to column 23, line 48).
Combining equivalents known for the same purpose is prima facie obvious according to MPEP 2244.06, which states
“It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art.”
Therefore, one of ordinary skill in the art would have found it prima facie obvious to formulate a composition comprised of, for example, at least any two or more of the disclosed SCD1 polypeptide inhibitors to administer to a mammal for the treatment of cancer.
Claim 10 is directed to the method of claim 1, wherein the method comprises administering two or more tyrosine kinase inhibitors to said mammal.
The difference between Copland and the Instant Application is that Copland fails to teach an explicit embodiment wherein two or more tyrosine kinase inhibitors are administered to the mammal.
However, Copland teaches in some cases, when treating a mammal (e.g., human) identified as having cancer, said mammal can be administered or instructed to self-administer one or more additional therapeutic agents, wherein the additional therapeutic agent includes kinase inhibitors (e.g., sorafenib, regorafenib, bortezomib, erlotinib, gefitinib, imatinib, vemurafenib, and vismodegib) (column 24, lines 1-18).
Combining equivalents known for the same purpose is prima facie obvious (see MPEP 2144.06). Therefore, one of ordinary skill in the art would have found it prima facie obvious to formulate a composition comprised of, for example, at least any two or more of the disclosed kinase inhibitors to administer to a mammal for the treatment of cancer.
Claim(s) 13 is/are rejected under 35 U.S.C. 103 as being unpatentable over She in view of Copland as evidenced by Isidan.
Claim 11, from which claim 13 depends, is rejected under 35 U.S.C. 102 as being anticipated by She. The teachings described therein are incorporated herein by reference.
Claim 13 is directed to the method of claim 11 wherein said mammal is a human.
The difference between the teaching of She and the Instant Application is that She fails to teach wherein the mammal is a human.
However, Copland as evidenced by Isidan teaches co-administration of the SCD1 inhibitor and tyrosine kinase inhibitor is synergetic in reducing tumor volume in mice (Fig 7C) and further teaches the disclosed methods and materials can be used in treating humans having cancer (e.g., a SCD1-associated cancer) (column 1, lines 35-37). Copland further teaches compound SSI-4 inhibits cell proliferation in human (CX-004T2 and HUCCT1) cholangiocarcinoma (CAA) cell lines at 1 µM (Fig 8).
Therefore, one of ordinary skill in the art would have had a reasonable expectation of success in applying the method taught by She, whereby mice were co-administered an SCDI inhibitor and tyrosine kinase inhibitor, to humans.
Claim(s) 14 and 18-21 is/are rejected under 35 U.S.C. 103 as being unpatentable over She in view of Copland.
Claim 11, from which claims 14 and 18-19 depend, is rejected under 35 U.S.C. 102 as being anticipated by She. The teachings described therein are incorporated herein by reference.
Claim 14 is directed to the method of claim 11, wherein the cancer is liver cancer.
The difference between the teaching of She and the Instant Application is that She fails to teach wherein the cancer is liver cancer and instead teaches wherein the cancer is lung cancer.
However, Copland teaches a method of administering a SCD1 inhibitor in combination with a tyrosine kinase inhibitor to treat HCC (liver cancer) (column 27 lines 9-10).
One of ordinary skill in the art would have been motivated to combine the above teachings because Copland teaches the disclosed methods can be used in treating lung cancer (column 4, lines 36-39) and further teaches the tyrosine kinase inhibitor can be gefitinib (column 4, lines 26-28). Additionally, She teaches the SCD1 is a highly expressed oncogene in various types of cancers including hepatocarcinoma (page 2, left column, paragraph 2). Therefore, it would have been prima facie obvious for a skilled artisan to utilize the method of She in treating HCC (liver cancer).
Claims 18-19 are directed to the method of claim 11, wherein the tyrosine kinase inhibitor inhibits one or more polypeptides selected from the provided group, wherein the tyrosine kinase inhibitor is selected from the group consisting of cabozantinib, lenvatinib, sorafenib, sunitinib, and regorafenib.
The difference between the teaching of She and the Instant Application is that She fails to teach the use of one of the recited tyrosine kinase inhibitors.
However, Copland teaches the use of the tyrosine kinase inhibitor sorafenib in combination with a SCD1 inhibitor.
One of ordinary skill in the art would have been motivated to combine the above teachings because the two are linked by the disclosed effective tyrosine kinase inhibitors. For example, She teaches the use of gefitinib in combination with a SCD1 inhibitor in treating cancer and Copland teaches effective kinase inhibitors include sorafenib and gefitinib (column 4, lines 26-29).
Therefore, one of ordinary skill in that art could have applied the prong (B) rationale of In re KSR Int’l Co., 550 U.S. 398 (2007), in which obviousness entails simple substitution of one known element for another to obtain predictable results, it would have been obvious for a person of ordinary skill in the art to substitute gefitinib for sorafenib to achieve the desired result with a reasonable expectation of success.
Claim 20 is directed to the method of claim 11, wherein the method comprises administering two or more SCD1 polypeptide inhibitors to said mammal.
The difference between the teaching of She and the Instant Application is that She fails to teach an embodiment wherein the mammal is administered two or more SCD1 polypeptide inhibitors.
However, Copland teaches treating cancer in a mammal using one or more SCD1 polypeptide inhibitors (abstract) and further teaches representative examples of SCD1 polypeptide inhibitors include, without limitation, SSI-1, SSI-2, SSI-3, and/or SSI-4 (column 21, line 50 to column 23, line 48).
One of ordinary skill in the art would have been motivated to combine the above teachings because they are in the same field of endeavor of treating cancer in a mammal by administering a combination SCD1 polypeptide inhibitor and a tyrosine kinase inhibitor. Said artisan could have used the teaching of Copland as guidance to administer a second or more of SCD1 polypeptide inhibitor to the subject in the case that, for example, the cancer was not responding to treatment with a single SCD1 polypeptide inhibitor in combination with a tyrosine kinase inhibitor. Furthermore, combining equivalents known for the same purpose is prima facie obvious according to MPEP 2244.06, which states
“It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art.”
Therefore, one of ordinary skill in the art would have found it prima facie obvious to formulate a composition comprised of, for example, at least any two or more of the disclosed SCD1 polypeptide inhibitors to administer to a mammal for the treatment of cancer, wherein the cancer is resistant to treatment with a tyrosine kinase inhibitor alone.
Claim 21 is directed to the method of claim 11, wherein the method comprises administering two or more tyrosine kinase inhibitors to said mammal.
The difference between the teaching of She and the Instant Application is that She fails to teach an embodiment wherein the mammal is administered two or more tyrosine kinase inhibitors.
However, Copland teaches in some cases, when treating a mammal (e.g., human) identified as having cancer, said mammal can be administered or instructed to self-administer one or more additional therapeutic agents, wherein the additional therapeutic agent includes kinase inhibitors (e.g., sorafenib, regorafenib, bortezomib, erlotinib, gefitinib, imatinib, vemurafenib, and vismodegib) (column 24, lines 1-18).
One of ordinary skill in the art would have been motivated to combine the above teachings because they are in the same field of endeavor of treating cancer in a mammal by administering a combination SCD1 polypeptide inhibitor and a tyrosine kinase inhibitor. Said artisan could have used the teaching of Copland as guidance to administer at least a second or more of the disclosed tyrosine kinase inhibitors to the subject in the case that, for example, the cancer which is resistant to treatment with a tyrosine kinase inhibitor alone, was not responding to treatment with a single tyrosine kinase inhibitor in combination with a SCD1 polypeptide inhibitor.
Combining equivalents known for the same purpose is prima facie obvious (see MPEP 2244.06). Therefore, one of ordinary skill in the art would have found it prima facie obvious to formulate a composition comprised of, for example, at least any two or more of the disclosed tyrosine kinase inhibitors to administer to a mammal for the treatment of cancer, wherein the cancer is resistant to treatment with a tyrosine kinase inhibitor alone.
Claim(s) 15-16 is/are rejected under 35 U.S.C. 103 as being unpatentable over She in view of von Roemeling (Accelerated Bottom-Up Drug Design Platform Enables the Discovery of Novel Stearoyl-CoA Desaturase 1 Inhibitors for Cancer Therapy. Oncotarget. 2017, 9(1), 3-20. Doi: 10.18632/oncotarget.21545).
Claim 11, from which claims 15-16 depend, is rejected under 35 U.S.C. 102 as being anticipated by She. The teachings described therein are incorporated herein by reference.
Claims 15-16 are directed to the method of claim 11, wherein the SCD1 polypeptide inhibitor is a compound of Formula II or Formula IIa, wherein the compound is SSI-4.
The difference between the teaching of She and the Instant Application is that She fails to teach the use of the SCD1 inhibitor SSI-4 and instead teaches the use of the SCD1 inhibitor A939572.
However, von Roemeling teaches an innovative method of computational-based drug discovery strategy, coupled with machine-based learning and functional assessment, for the rational design of novel small molecule inhibitors of SCD1 (abstract). The method comprises decomposing known SCD1 inhibitors, including A939572, into de novo ligands to generate novel chemical structures (page 4, left column, paragraph 4). One of the top inhibitors identified was SSI-4 (page 4, right column, paragraph 1), which showed SCD1 IC50 = 1.9 nM (page 10, Fig 3c).
One of ordinary skill in the art would have been motivated to combine the above teachings because they are both in the same field of endeavor of SCD1 polypeptide inhibitors. Furthermore, said artisan would expect compounds that have similar structures to also exhibit similar properties.
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Therefore, one of ordinary skill in the art would have had a reasonable expectation of success in using the SCD1 inhibitor SSI-4 in place of A939572 in the method of She, thus arriving at the current invention.
Conclusions
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Paul Arcoria whose telephone number is (571)272-8719. The examiner can normally be reached Mon-Fri 8:00-5:00 EST.
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/P.A./Examiner, Art Unit 1621
/CLINTON A BROOKS/Supervisory Patent Examiner, Art Unit 1621
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