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 .
All previous objections and rejections not reiterated herein were overcome by claim amendments and arguments, filed January 20th, 2026, have been fully considered and found persuasive. As such all objections and rejections not reiterated herein have been withdrawn.
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 112, 114 – 126, and 128 are rejected under 35 U.S.C. 103 as being unpatentable over International Publication Number WO 2016/022955 A1 to Copland III et. al. (herein after Copland’955; cited on the ISR form) in view of Ngiow et. al. ((2011), Anti-TIM3 Antibody Promotes T Cell IFN-g–Mediated Antitumor Immunity and Suppresses Established Tumors, Cancer Res, 71, 3540 – 3551; cited in the office action dated September 10th, 2025).
Regarding claims 112, 114– 126, and 128, Copland’955 teach a compound according to Formula (II)
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(page 4 lines 1 – 2). More specifically, Copland’955 teach the embodiment,
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that is SSI-4 (claim 112), (page 4 lines 16 – 17) in methods for inhibiting SCD1 in cells (page 4 lines 20 – 21). Furthermore, Copland’955 teach a method for treating cancer (claim 112) wherein the cancer is selected from the group consisting off a kidney cancer, a liver cancer, a breast cancer, a lung cancer, a pancreatic cancer, a bladder cancer, a colon cancer, a melanoma, a thyroid cancer, an ovarian cancer, and a prostate cancer (claim 128) (page 5 lines 15 – 18). Additionally, Copland’955 teach an embedment for the method of treating cancer comprising administering to the subject a therapeutically effective amount of an SCD1 inhibitor and a proteasome inhibitor, or pharmaceutically acceptable salts thereof, or a composition comprising the SCD1 inhibitor and the proteasome inhibitor (page 5 lines 27 – 31). Furthermore, Copland’955 teach in some embodiments, that the SCD1 inhibitor and the proteasome inhibitor are administered concurrently (claim 123) or sequentially (claim 124) (page 6 lines 2 – 4).
Moreover, Copland’955 teach that compounds of the disclosure can be administered orally (claim 125) or as intravenously (claim 126) (page 17 lines 19 – 22). Additionally, Copland’955 teach that although the dosage will vary depending on the symptoms, age and body weight of the subject, the nature and severity of the disorder to be treated or prevented, the route of administration and the form of the drug, in general, a daily dosage of from 0.01 to 2000 mg of the compound is recommended for an adult human subject, and this may be administered in a single dose or in divided doses (page 18 lines 3 – 8). Furthermore, Copland’955 teach that the compound s of the disclosure can be administered with an additional anticancer agent (page 28 lines 17 – 18). Specifically, Copland’955 teach some embodiments wherein the SCD1 inhibitors of this disclosure can be combined with nivolumab (claims 112, 114, and 118), pembrolizumab (claim 112, 114, and 118), or an immunomodulatory agent (page 30 lines 1 – 3, 10 – 11, and 20 – 21).
However, while Copland’955 teach the co-administration with an immunomodulatory agent (page 30 lines 20 – 21); Copland’955 fails to specifically teach a combination comprising at least two or three immune checkpoint inhibitors (claim 112) nor the inclusion of an anti-CTLA-4 antibody (claims 116, and 119 – 122) and/or an anti-TIM-3 antibody (claims 115 and 117).
Nevertheless Ngiow et. al. teach that strategies to activate and rescue exhausted tumor-specific T cells, including the use of monoclonal antibodies (mAb) that block the negative costimulatory receptors CTLA-4 and PD-1 (claims 116, and 119 – 122) are proving very effective, but TIM3 has been relatively neglected as a target (page 3540 abstract). Moreover Ngiow et. al. teach that given that TIM3 negatively regulates IFN-g-mediated Th1 responses, the use of anti-TIM3 monoclonal antibody (mAb) may complement therapies relieving T cell energy/exhaustion/ tolerance pathway [anti–PD-1 and anti-Cytotoxic T Lymphocyte Antigen-4 (CTLA-4)] (page 3540 column 2 paragraph 1). Furthermore, Ngiow et. al. teach that ipilimumab (anti-human CTLA-4) was reported at the 2010 American Society of Clinical Oncology annual meeting to extend the overall survival in patients with advanced melanoma by 10 months, and an important study showed the considerable therapeutic benefit in combining anti–CTLA-4 and anti–PD-1/PD-L1 in the early treatment of melanoma in the context of a tumor-cytokine vaccine (page 3540 column 2 paragraph 1).
Additionally, Ngiow et. al. teach the antitumor activity of anti-TIM3 and the critical role of both CD4+ and CD8+ T cell subsets and IFN-g in anti-TIM3 antitumor activity was also validated in the subcutaneous BALB/c CT26 colon adenocarcinoma (Supplementary Fig. S2A and B) and WTMCA2 fibrosarcoma (Supplementary Fig. S2C). Moreover, Ngiow et. al. teach that while each dual therapy combinations (claims 115 – 117) was more effective than any monotherapy (compare Fig. 6B with E) presented here
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when the 3 mAbs anti–CTLA-4, anti–PD-1, and anti-TIM3 (claims 115 and 117), were combined the combination produced further suppression of B16F10 tumor growth, significantly prolonging the survival of all mice in this group (Fig. 6E) as compared to the monotherapies and dual combination therapies.(page 3546 column 1 paragraph 1 and column 2 paragraph 1).
Therefore, it would been obvious before the effective filing date of the instant application to modify the method of Copland’955 for the administration of the SCD1 inhibitor SSI-4 in view of Ngiow et. al., that is to include at least two immune checkpoint inhibitors or three immune checkpoint inhibitors in the following combinations with an anti-PD-1/anti-TIM-3, anti-PD-1/anti-CTLA-4, anti-CTLA-4/anti-TIM-3, or anti-PD-1/anti-TIM-3/anti-CTLA-4. One of ordinary skill in the art would be motivated to make this modification to dismiss T cell energy/exhaustion/ tolerance pathways. Additionally, one of ordinary in the art would have a reasonable expectation of success because when the 3 mAbs, that is anti–CTLA-4, anti–PD-1, and anti-TIM3, were combined the combination produced further suppression of B16F10 tumor growth, significantly prolonging the survival of all mice in this group as compared to the monotherapies and dual combination therapies.
Claim 127 is rejected under 35 U.S.C. 103 as being unpatentable over International Publication Number WO 2016/022955 A1 to Copland III et. al. (herein after Copland’955; cited on the ISR form) and Ngiow et. al. ((2011), Anti-TIM3 Antibody Promotes T Cell IFN-g–Mediated Antitumor Immunity and Suppresses Established Tumors, Cancer Res, 71, 3540 – 3551; cited in the office action dated September 10th, 2025), as applied to claims 112 – 126, and 128 128 above, and further in view of Mason et. al. ((2012), SCD1 Inhibition Causes Cancer Cell Death by Depleting Mono-Unsaturated Fatty Acids, PLoS, 7, 1 – 8; cited on the IDS dated February 12th, 2024).
The teachings of Copland’955 and Ngiow et. al. as they relate to claims 112 are given previously in this office action and are fully incorporated here.
However, while Copland’955 does teach that although the dosage will vary depending on the symptoms, age and body weight of the subject, the nature and severity of the disorder to be treated or prevented, the route of administration and the form of the drug, in general, a daily dosage of from 0.01 to 2000 mg of the compound is recommended for an adult human subject, and this may be administered in a single dose or in divided doses (page 18 lines 3 – 8); Copland’955 does not express the dosage amount in mg/kg.
Nevertheless, Mason et. al. teach the oral administration of 160 mg/kg (claim 127) twice daily of #28c, a commercially available SCD1 inhibitor, in nu/nu mice having passage five HCT116 colon tumors (page 8 column 1 paragraph 2), when tumors reached 200 mm3 (page 8 column 2 paragraph 2). Moreover, Mason et. al. teach that in Figure 4c provided here
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, SCD1 inhibitor #28c showed moderate growth delay of HCT116 tumors (page 5 column 1 paragraph 5).
While Mason et. al. fails to teach the administration of the specific SCD1 inhibitor SSI-4 of structure Mason et. al. does teach the administration of a known in the art SCD1 inhibitor for the treatment of cancer. Therefore, given that Copland’955 teach the use of SSI-4 as a SCD1 inhibitor in the treatment of cancer and Mason et. al. also teach the use of an SSI-4 inhibitor in the treatment of cancer it would have been obvious to one of ordinary skill in the art to substitute one SCD1 inhibitor for an alternative SCD1 inhibitor. One of ordinary skill in the art would have been motivated to make this modification because , as taught by Copland’955 and Mason et. al. both the SSI-4 and #28c are both SCD1 inhibitors useful in the treatment of cancer.
Furthermore, given that the prior art of Mason et. al. teach the oral administration of 160 mg/kg of the alternative #28c SCD1 inhibitor it would have been obvious to one of ordinary skill in the art the use a similar amount. Moreover, in the case where the claimed ranges "overlap or lie inside ranges disclosed by the prior art" a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990). Similarly, a prima facie case of obviousness exists where the claimed ranges or amounts do not overlap with the prior art but are merely close. Titanium Metals Corp. of America v. Banner, 778 F.2d 775, 783, 227 USPQ 773, 779 (Fed. Cir. 1985) (MPEP 2144.05(I)). Therefore, since the prior art of Mason et. al. teach the dosage of 160 mg/kg of an SCD1 inhibitor and given how close the value of 160 mg/kg is to “about 200 mg/kg, ” the prior art teaching of 160 mg/kg renders obvious the instant claim 127.
Therefore it would have been obvious before the effective filling date of the instant application to modify the method of Copland’955 for the administration of the SCD1 inhibitor SSI-4 in view of Ngiow et. al., that is to include at least two immune checkpoint inhibitors or three immune checkpoint inhibitors, and in further view of Mason et. al. to use a dosage amount of about 200 mg/kg. One of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because the SCD1 inhibitor #28c showed moderate growth delay of HCT116 tumors cells.
Response to Arguments
Applicant's arguments filed January 20th, 2026, with regards to the prior art rejections of the instant claims 112, and 114 – 128 have been fully considered but they are not persuasive.
Applicant argues neither Copland’955 alone or combination with Ngiow et. al. does not render obvious the method as recited in instant independent claim 112 (see applicant’s remarks page 6 paragraph 2). Moreover, applicant argues that the figures of Ngiow et. al. fails to demonstrate synergy between anti-TIM3 and anti-PD-1 in CT26 colon carcinomas (see applicant’s remarks page 6 paragraph 2). Furthermore, the applicant argues that with in the instant disclosure there was unexpected and synergistic effects between the SCD1 inhibitor and the antibodies (see applicant’s remarks page 6 paragraph 2).
The examiner contends in response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In this case the prior art both Copland’955 and Ngiow et. al. direct to methods of treating cancer. While Copeland’955 teach the embodiment,
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that is SSI-4 (claim 112), (page 4 lines 16 – 17) in methods for inhibiting SCD1 in cells with an immunomodulatory agent (page 30 lines 20 – 21); Copland’955 fails to specifically teach a combination comprising at least two or three immune checkpoint inhibitors. Ngiow et. al. teach that while each dual therapy combinations was more effective than any monotherapy (compare Fig. 6B with E) presented here
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when the 3 mAbs anti–CTLA-4, anti–PD-1, and anti-TIM3 (claims 115 and 117), were combined the combination produced further suppression of B16F10 tumor growth, a melanoma model, significantly prolonging the survival of all mice in this group (Fig. 6E) as compared to the monotherapies and dual combination therapies(page 3546 column 1 paragraph 1 and column 2 paragraph 1). Moreover, while the applicant had demonstrated unexpected results and synergy in breast cancer cell lines (see applicant’s remarks pages 6 – 7); the unexpected results are not commensurate in scope to cancer as broadly claimed in instant claim 112. Thus the prior art rejections of instant claims 112, and 114 – 128 is deemed proper, maintained, and made final.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 112, and 114 – 128 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 10 of U.S. Patent No. US 11596629 B2 to Copland, III et. al. (herein after Copland’629) in view of Mason et. al. ((2012), SCD1 Inhibition Causes Cancer Cell Death by Depleting Mono-Unsaturated Fatty Acids, PLoS, 7, 1 – 8; cited on the IDS dated February 12th, 2024) and Ngiow et. al. ((2011), Anti-TIM3 Antibody Promotes T Cell IFN-g–Mediated Antitumor Immunity and Suppresses Established Tumors, Cancer Res, 71, 3540 – 3551; cited in the office action dated September 10th, 2025).
Copland’629 recite a method of treating cancer in a subject, the method comprising administering to the subject a therapeutically effective amount of a compound of formula:
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(instant claim 112) or a pharmaceutically acceptable salt thereof, and a therapeutically effective amount of a checkpoint inhibitor selected from an antibody of cytotoxic T-lymphocyte-associated protein-4 (CTLA-4) and an antibody of T-cell immunoglobulin and mucin-domain containing-3 (TIM-3) (reference claim 1; instant claim 112).
However, Copland’629 fails to recite a combination comprising an anti-PD-L1 antibody (instant claim 112) nor a combination comprising at least two or three checkpoint inhibitor inhibitors (instant claims 112 and 119).
Nevertheless, the teachings of Mason et. al., and Ngiow et. al., as they related to the prior art rejections of instant 112, and 114 – 128, are given previously in this office action and are fully incorporated here.
Therefore, it would been obvious before the effective filing date of the instant application to modify the invention of Copland’629 to administer SSI-4 in a method for treating cancer in view of Mason et. al. and Ngiow et. al., that is in combination with an anti-PD-1/anti-TIM-3, anti-PD-1/anti-CTLA-4, anti-CTLA-4/anti-TIM-3, or anti-PD-1/anti-TIM-3/anti-CTLA-4 in a method of treating cancer. One of ordinary skill in the art would be motivated to make this modification to target the T cell energy/exhaustion/ tolerance pathways. Additionally, one of ordinary in the art would have a reasonable expectation of success because when the 3 mAbs, that is anti–CTLA-4, anti–PD-1, and anti-TIM3, were combined the combination produced further suppression of B16F10 tumor growth, significantly prolonging the survival of all mice in this group as compared to the monotherapies and dual combination therapies.
Claims 112, and 114 – 128 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 2, and 6 – 9 of U.S. Patent No. US 10301273 B2 to Copland, III et. al. (herein after Copland’273) in view of Mason et. al. ((2012), SCD1 Inhibition Causes Cancer Cell Death by Depleting Mono-Unsaturated Fatty Acids, PLoS, 7, 1 – 8; cited on the IDS dated February 12th, 2024) and Ngiow et. al. ((2011), Anti-TIM3 Antibody Promotes T Cell IFN-g–Mediated Antitumor Immunity and Suppresses Established Tumors, Cancer Res, 71, 3540 – 3551; cited in the office action dated September 10th, 2025).
Copland’273 recite a method for treating a cancer in a human subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound according to Formula (II)
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(reference claims 1 – 2, and 6 – 7) more specifically, the compound of (reference) claim 1 wherein the compound according to Formula (II) is
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(reference claim s 8 – 9; instant claim 112) wherein the cancer is selected from the group consisting of a kidney cancer, a liver cancer, a breast cancer, a lung cancer, a pancreatic cancer, a bladder cancer, a colon cancer, a melanoma, a thyroid cancer, an ovarian cancer, and a prostate cancer (reference claim 1 – 2; instant claim 128).
However, Copland’273 fails to recite a combination comprising an anti-PD-L1 antibody (instant claim 112), anti-CTLA-4 antibody (instant claims 116, and 119 – 122) and/or an anti-TIM-3 antibody (instant claims 115 and 117).
Nevertheless, the teachings of Mason et. al., and Ngiow et. al., as they related to the prior art rejections of instant claims 112, and 114 – 128, are given previously in this office action and are fully incorporated here.
Therefore, it would been obvious before the effective filing date of the instant application to modify the invention of Copland’273 to administer SSI-4 in a method for treating cancer in view of Mason et. al. and Ngiow et. al., that is in combination with an anti-PD-1/anti-TIM-3, anti-PD-1/anti-CTLA-4, anti-CTLA-4/anti-TIM-3, or anti-PD-1/anti-TIM-3/anti-CTLA-4 in a method of treating cancer. One of ordinary skill in the art would be motivated to make this modification to target the T cell energy/exhaustion/ tolerance pathways. Additionally, one of ordinary in the art would have a reasonable expectation of success because when the 3 mAbs, that is anti–CTLA-4, anti–PD-1, and anti-TIM3, were combined the combination produced further suppression of B16F10 tumor growth, significantly prolonging the survival of all mice in this group as compared to the monotherapies and dual combination therapies.
Claims 112, and 114 – 128 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 7 of U.S. Patent No. US 11325892 B2 to Copland, III et. al. (herein after Copland’892) in view of International Publication Number WO 2016/022955 A1 to Copland III et. al. (herein after Copland’955; cited on the ISR form), Mason et. al. ((2012), SCD1 Inhibition Causes Cancer Cell Death by Depleting Mono-Unsaturated Fatty Acids, PLoS, 7, 1 – 8; cited on the IDS dated February 12th, 2024) and Ngiow et. al. ((2011), Anti-TIM3 Antibody Promotes T Cell IFN-g–Mediated Antitumor Immunity and Suppresses Established Tumors, Cancer Res, 71, 3540 – 3551; cited in the office action dated September 10th, 2025).
Copland’892 recite a compound according to Formula (II)
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(reference claims 1 – 2) more specifically, the compound of (reference) claim 1 wherein the compound according to Formula (II) is
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(reference claim 6; instant claim 112).
However, Copland’892 fails to recite a method comprising the compound according to formula (II) (instant claim 112). Additionally, Copland’892 fails to specifically recite a combination comprising an anti-PD-L1 antibody (instant claim 112), anti-CTLA-4 antibody (instant claims 116, and 119 – 122) and/or an anti-TIM-3 antibody (instant claims 115 and 117).
Nevertheless, the teachings of Copland’955, Mason et. al., and Ngiow et. al., as they related to the prior art rejections of instant claims 112, and 114 – 128, are given previously in this office action and are fully incorporated here.
Therefore, it would been obvious before the effective filing date of the instant application to modify the invention of Copland’892 in view of Copland’955 to administer SSI-4 as a SCD1 inhibitor is in further view of Mason et. al. and Ngiow et. al., that is in combination with an anti-PD-1/anti-TIM-3, anti-PD-1/anti-CTLA-4, anti-CTLA-4/anti-TIM-3, or anti-PD-1/anti-TIM-3/anti-CTLA-4 in a method of treating cancer. One of ordinary skill in the art would be motivated to make this modification to target the T cell energy/exhaustion/ tolerance pathways. Additionally, one of ordinary in the art would have a reasonable expectation of success because when the 3 mAbs, that is anti–CTLA-4, anti–PD-1, and anti-TIM3, were combined the combination produced further suppression of B16F10 tumor growth, significantly prolonging the survival of all mice in this group as compared to the monotherapies and dual combination therapies.
Claims 112, and 114 – 128 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5, 7 – 16, and 18 – 21 of copending Application No. 18/631941 to Copland et. al. (herein after Copland’941) in view of Mason et. al. ((2012), SCD1 Inhibition Causes Cancer Cell Death by Depleting Mono-Unsaturated Fatty Acids, PLoS, 7, 1 – 8; cited on the IDS dated February 12th, 2024) and Ngiow et. al. ((2011), Anti-TIM3 Antibody Promotes T Cell IFN-g–Mediated Antitumor Immunity and Suppresses Established Tumors, Cancer Res, 71, 3540 – 3551; cited in the office action dated September 10th, 2025).
Copland’941 recite a method for treating cancer (instant claims 112) in a mammal, wherein said method comprises administering, to said mammal, a stearoyl CoA desaturase I (SCD 1) polypeptide inhibitor and a tyrosine kinase inhibitor, wherein the number of cancer cells within said mammal is reduced (reference claim 1). Moreover, Copland’941 recite a method wherein said cancer is a liver cancer (reference claim 3; instant claims 112 and 128); wherein said SCD1 polypeptide inhibitor is a compound having Formula (II) or Formula (Ila):
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(reference claim 31); more specifically, wherein said SCD I polypeptide inhibitor is SSI-4, 2-{ [ 4-(2-Chlorophenoxy )piperidine-1-carbonyl] amino }-N-methylpyridine-4-carboxamide (reference claim 5; instant claim 112).
However, while Copland’941 recite the co-administration with an immune checkpoint inhibitor; Copland’941 fails to specifically recite a combination comprising an anti-PD-L1 antibody (instant claim 112), anti-CTLA-4 antibody (instant claims 116, and 119 – 122) and/or an anti-TIM-3 antibody (instant claims 115 and 117).
Nevertheless, the teachings of Mason et. al. and Ngiow et. al., as they related to the prior art rejections of instant claims 112, and 114 – 128, are given previously in this office action and are fully incorporated here.
Therefore, it would been obvious before the effective filing date of the instant application to modify copending Copland’941 to administer the SCD1 inhibitor is SSI-4 in view of Mason et. al. and Ngiow et. al., that is in combination with an anti-PD-1/anti-TIM-3, anti-PD-1/anti-CTLA-4, anti-CTLA-4/anti-TIM-3, or anti-PD-1/anti-TIM-3/anti-CTLA-4 in a method of treating cancer. One of ordinary skill in the art would be motivated to make this modification to target the T cell energy/exhaustion/ tolerance pathways. Additionally, one of ordinary in the art would have a reasonable expectation of success because when the 3 mAbs, that is anti–CTLA-4, anti–PD-1, and anti-TIM3, were combined the combination produced further suppression of B16F10 tumor growth, significantly prolonging the survival of all mice in this group as compared to the monotherapies and dual combination therapies.
This is a provisional nonstatutory double patenting rejection.
Response to Arguments
Applicant's arguments filed January 20th, 2026, with regards to the provisional nonstatutory double patent (NSDP) and NSDP rejections of instant claims 112, and 114 – 128 have been fully considered but they are not persuasive.
Applicants’ arguments are similar to the arguments presented against the prior art rejections above (see applicants’ remarks pages 9 – 12).
Therefore, the examiner’s response to the arguments against the provisional NSDP and NSDP rejections of instant claims 112, and 114 – 128 have been addressed above in the response to the prior art rejections. Thus the provisional NSDP and NSDP rejections of instant claims 112, and 114 – 128 are deemed proper, maintained, and made final.
Conclusion
Claims 112, and 114 – 128 are rejected.
THIS ACTION IS MADE FINAL. 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 DAWANNA S WHITE whose telephone number is (703)756-4687. The examiner can normally be reached 7:00 am - 5:00 pm [EST] M - Th.
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/DAWANNA SHAR-DAY WHITE/Examiner, Art Unit 1627
/JULIET C SWITZER/Primary Examiner, Art Unit 1682