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 .
Election/Restrictions
Applicant’s election without traverse of Group I, encompassing claims 21-32, in the reply filed on December 30, 2024 is acknowledged.
Applicant’s election with traverse of Group I, comprising claims 1-6, 9-14, and 17-20 in the reply filed on November 20, 2024 is acknowledged.
Although the inventions of Groups I and II do not share a special technical feature, upon further examination prior art found applicable to the elected invention of Group I was found to be applicable to Group II, and therefore, the examiner finds it is reasonable to rejoin the two groups. Thus, the restriction is withdrawn and the inventions of Groups I and II are rejoined. Claims 21-40 as filed on September 17, 2021 will be examined on the merits.
Because all claims previously withdrawn from consideration under 37 CFR 1.142 have been rejoined, the restriction requirement as set forth in the Office action mailed on September 20, 2024 is hereby withdrawn. In view of the withdrawal of the restriction requirement as to the rejoined inventions, applicant(s) are advised that if any claim presented in a divisional application is anticipated by, or includes all the limitations of, a claim that is allowable in the present application, such claim may be subject to provisional statutory and/or nonstatutory double patenting rejections over the claims of the instant application.
Once the restriction requirement is withdrawn, the provisions of 35 U.S.C. 121 are no longer applicable. See In re Ziegler, 443 F.2d 1211, 1215, 170 USPQ 129, 131-32 (CCPA 1971). See also MPEP § 804.01.
Claim Interpretation
Claim 21 recites a polypeptide comprising the sequence SEQ ID NO: 1 or a functionally equivalent variant thereof. Functionally equivalent variant thereof is defined on page 12 of the instant Specification as “any polypeptide which results from the insertion or addition of one or more amino acids and/or from the deletion of one or more amino acids and/or from the conservative substitution of one or more amino acids with respect to the polypeptide of SEQ ID NO: 1 and/or which results from the chemical modification of the polypeptide of SEQ ID NO: 1 and which substantially preserves the tumor suppressor activity of the SEQ ID NO: 1.” There is no limit to the number of amino acids which can inserted and/or deleted and/or conservatively substituted and there is no requirement that a minimum sequence identity to the length of SEQ ID NO: 1 be maintained. The only requirement of a functionally equivalent variant is that it demonstrate substantially preserved tumor suppressor activity of SEQ ID NO: 1. The Specification states that “preservation of the tumor suppressor activity requires that the variant can dimerize with Myc and/or its obligate partner p21/p22Max and inhibit Myc activity, that it is capable of translocating across the cell membrane and that it is capable of translocating across the nuclear envelope.” Claims 23 and 24 make clear that the sequence of SEQ ID NO: 1 is not capable of translocating the cell membrane and would have to be further fused to sequences responsible for such function.
Wang et al. (Oncogene. 38: 140-150; Published: August 3, 2018) teaches the sequence of OmoMyc which is 1005 identical to SEQ ID NO: 1; see Figure 1a. OmoMyc is a bHLH-Zip protein which mimics the bHLH-Zip domain of Myc by incorporating the following point mutations; E63T, E70I, R77Q, and R78N which inhibit Myc – Max binding; see page 142 right column. Soucek et al. (Oncogene. 17: 2463-2472; Published: October 12, 1998) teaches that residues E57, E64, R70, and R71, which corresponds with E63, E70, R77, and R78 in the Wang et al. reference, are critical to the dimerization of Myc; see page 2464 right column. Thus, Wang et al. and Soucek et al. combined provide a structure – function correlation for translocation across the nuclear envelope, dimerization with Myc or Max, and inhibition of Myc activity.
Further, the instant Specification provides further guidance on substitutions to the critical residues taught in Wang et al. and Soucek et al.; see page 14. Additionally, the instant Specification of discloses the subsequence within SEQ ID NO: 1 which is responsible for nuclear localization and the sequences of seven functionally equivalent variants (SEQ ID NO: 4-10); see pages 11 and 16.
Thus, while the limitation of functionally equivalent variant is broad, one of ordinary skill in the art would conclude that Applicant was in possession of the genus of functionally equivalent variants by both the disclosure of a structure – function correlation and a representative numbers of species.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 21-25, 30-37, 39, and 40 are rejected under 35 U.S.C. 103 as being unpatentable over Soucek et al. (WO 2014/180889 A1; Published: November 13, 2014) and Felsher et al. (WO 2017/152132 A1; Published: September 8, 2017) in view of the Pembrolizumab Approval Announcement (FDA; Published: May 10, 2017).
Regarding claims 21 and 32, Soucek et al. teaches a combination of a polypeptide 100% identical to instant SEQ ID NO: 1 with an anti-tumoral agent; see claim 15, the translated sequence on pages 8-9, and pages 25-28.
Regarding claim 22, Soucek et al. teaches the variant called Omomyc*LZArg, which comprises SEQ ID NO: 48, on page 15. Residues 1-92 of SEQ ID NO: 48 are 100% identical to SEQ ID NO: 4.
Regarding claims 23-25, Soucek et al. claims 6-9 teach that the polypeptide or functionally equivalent variant is a fusion protein comprising a cell penetrating peptide sequence selected from SEQ ID NOs: 28 and 29, which are 100% identical to instant SEQ ID NO: 37 and 38, and further comprises a nuclear localization signal.
Regarding claims 33 and 34, Soucek et al. teaches using the polypeptide of pharmaceutical composition comprising an anti-tumoral agent for the treatment of cancer and that lung cancer is the preferred embodiment; see claims 20 and page 16 lines 30-32.
Regarding claims 35 and 36, Soucek et al. teaches intranasal administration or instillation into the nose; see page 32 lines 29-32 and page 33 lines 5-8. Further, regarding claim 37, Soucek et al. teaches that the components of the composition may be formulated differently so that the components can be differently administered and exemplifies the second component being administered intravenously, or a form of systemic administration; see page 31 lines 9-13.
While Soucek et al. teaches combination regimens with the Myc inhibitor of SEQ ID NO: 1, Soucek et al. does not teach a combination or composition wherein the second component is an immune checkpoint inhibitor nor does Soucek et al. teach treating cancer with a combination or composition comprising an immune checkpoint inhibitor.
Felsher et al. teaches the method of identifying whether a subject having cancer will be responsive to an immune checkpoint inhibitor comprising determining from a sample that the cancer overexpresses a Myc oncogene, identifying the subject with Myc oncogene overexpression as responsive to immune checkpoint inhibition, and administering an immune checkpoint inhibitor, including a PD-1 inhibitor; see claims 1 and 6.
Regarding claims 21, 32, and 33, Felsher et al. suggests that a Myc inhibitor and immune checkpoint inhibitor may be used in combination to treat cancer; see Summary on page 2. Regarding the Myc inhibitor of claim 21, Felsher et al. teaches a Myc inhibitor with the sequence of SEQ ID NO: 19, which is 100% identical to instant SEQ ID NO: 1, or a variant thereof. Regarding the immune-oncology agent of claims 21, 30, and 31, Felsher et al. teaches several PD-1/PD-L1 pathway inhibitors, including pembrolizumab, an anti-PD-1 antagonist antibody.
Regarding claims 39 and 40, the recruitment of T cells to the tumor site, the expansion of T regulatory cells, and induction of IFN-gamma are all inherent properties of claim 33. The claim requires only that a therapeutically effective amount of the combination or composition of claim 21 be administered to a subject in need thereof and no additional steps are recited. Thus, these are outcomes which would inherently flow from the administration of the combination of the polypeptide and the immune-oncology agent.
Given that Felsher et al. teaches the positive relationship between Myc expression and PD-L1 expression in human cancers, including non-small cell lung cancer, and suggests treating a subject, who has been identified as responsive to immune checkpoint inhibitors by Myc overexpression, with a Myc inhibitor and an immune checkpoint inhibitor, it would have been obvious to treat cancer using a combination of the Myc inhibitor comprising SEQ ID NO: 1 or a variant thereof as taught by Soucek et al. with the anti-PD-1 antibody, pembrolizumab, as taught by Felsher et al. Further, one would have been motivated to make the combination because Felsher et al. teaches that although the effects of Myc on the expression of CD47 and PD-L1 were modest, the consequences on tumor regression were dramatic suggesting that combining a Myc inhibitor and PD-1 inhibitor could have synergistic effects. Regarding the choice of pembrolizumab as the PD-1 inhibitor for the treatment of cancer, including lung cancer, because is pembrolizumab was the first FDA approved anti-PD-1 antibody and demonstrated significant survival benefit in patients with non-small cell lung cancer compared to chemotherapy alone; see Pembrolizumab Approval Announcement. Furthermore, one would have a reasonable expectation of success in treating cancer with the combination of the Myc inhibitor of SEQ ID NO: 1 as taught by Soucek et al. and pembrolizumab because each drug can be used alone for the treatment of cancer and because Felsher et al. teaches a possible synergistic relationship when inhibitors of Myc and the PD-1/PD-L1 pathway are administered in a combination.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art
before the effective filing date of the application, as evidenced by the references.
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 21-25, 30-37, 39, and 40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10 and 12-15 of U.S. Patent No. 10,370,434 B2 in view of Soucek et al. (WO 2014/180889 A1; Published: November 13, 2014), Felsher et al. (WO 2017/152132 A1; Published: September 8, 2017), and the Pembrolizumab Approval Announcement (FDA; Published: May 10, 2017).
Claims 21-25, 30-37, 39, and 40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 7-9, 11-13, 15, 18, 19, and 23 of U.S. Patent No. 11,339,205 B2 in view of Soucek et al. (WO 2014/180889 A1; Published: November 13, 2014), Felsher et al. (WO 2017/152132 A1; Published: September 8, 2017), and the Pembrolizumab Approval Announcement (FDA; Published: May 10, 2017).
Claims 21-25, 30-37, 39, and 40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 5-11, 17-20 of U.S. Patent No. 11,427,621 B2 in view of Soucek et al. (WO 2014/180889 A1; Published: November 13, 2014), Felsher et al. (WO 2017/152132 A1; Published: September 8, 2017), and the Pembrolizumab Approval Announcement (FDA; Published: May 10, 2017).
The following analysis applies to the nonstatutory double patenting rejections over claims U.S. Patent Nos. 10,370,434 B2; 11,339,205 B2; and 11,427,621 B2.
Regarding instant claims 21 and 32, U.S. 10,370,434 B2 teaches a combination of a polypeptide 100% identical to instant SEQ ID NO: 1 with an antitumoral agent; see issued claims 1, 2, 8, 10, 12, and 13. Similarly, U.S. 11,339,205 B2 teaches the method of treating cancer comprising administering a polypeptide comprising SEQ ID NO: 1, which is 100% identical to instant SEQ ID NO: 1, or a variant thereof in combination with an antitumoral agent; see issued claims 1, 7, 8, 11-13, 15, 18, 19, and 23. Additionally, issued claims 1-3, 17, and 18 of U.S. 11,427,621 B2 teach a functionally equivalent variant of instant SEQ ID NO: 1, which is nearly identical to instant SEQ ID NO: 1 except that the residue at position 89 may not be a cysteine. The polypeptide taught by the issued claims of U.S. 11,427,621 B2 is a functionally equivalent variant as defined on instant page 12 because it has the ability to dimerize with Myc and inhibiting its activity, translocate across the cell membrane, and translocate to the nucleus; see column 9 lines 32-38.
Regarding instant claim 22, U.S. 10,370,434 B2 teaches the variant called Omomyc*LZArg, which comprises SEQ ID NO: 48; see issued claims 7 and 12. Residues 1-92 of SEQ ID NO: 48 are 100% identical to SEQ ID NO: 4. Additionally, issued claims 18 and 23 of U.S. 11,339,205 B2 teach a variant comprising SEQ ID NO: 1, which is 100% identical to instant SEQ ID NO: 1, with a N-terminal methionine added and the resulting polypeptide is 100% identical to instant SEQ ID NO: 4. Additionally, issued claims 5 and 6 of U.S. 11,427,621 B2 teach that the polypeptide comprising SEQ ID NO: 1 has a serine or alanine at variable position 89 which is 100% identical to instant SEQ ID NO: 7 and that the polypeptide consists of SEQ ID NO: 4 which is 100% identical to instant SEQ ID NO: 6 when variable residue 90 is a serine.
Regarding instant claims 23-25, issued claims 2-6 U.S. 10,370,434 B2 teach that the polypeptide or functionally equivalent variant is a fusion protein comprising a cell penetrating peptide sequence selected from SEQ ID NOs: 28 and 29, which are 100% identical to instant SEQ ID NO: 37 and 38, and further comprises a nuclear localization signal. Issued claims 7-11 of U.S. 11,427,621 B2 teach that the polypeptide or functionally equivalent variant is a fusion protein comprising a cell penetrating peptide sequence selected from SEQ ID NOs: 38 and 39, which are 100% identical to instant SEQ ID NO: 37 and 38, and further comprises a nuclear localization signal.
Regarding instant claim 33, U.S. 10,370,434 B2 teaches using the polypeptide of pharmaceutical composition comprising an anti-tumoral agent for the treatment of cancer; see issued claims 10 and 13-15. Regarding instant claims 33 and 34, U.S. 11,339,205 B2 teaches that the combination of SEQ ID NO: 1 and an antitumoral agent is used for the treatment of cancer, including lung cancer; see issued claims 1, 2, and 13. Additionally, issued claims 19 and 20 of U.S. 11,427,621 B2 teach a method for treating cancer comprising administering the claimed polypeptide or conjugate.
Regarding instant claim 35, issued claim 9 of U.S. 11,339,205 B2 teaches that the first component, comprising SEQ ID NO: 1, is administered intranasally.
The issued claims of U.S. 10,370,434 B2 do not teach a combination or composition comprising SEQ ID NO: 1 or a variant thereof and an immune checkpoint inhibitor, including pembrolizumab, nor do the issued claims teach appropriate routes of administration or the use of the combination for the treatment of lung cancer.
The issued claims of U.S. 11,339,205 B2 do not teach a polypeptide further comprising a cell penetrating peptide or nuclear translation signal, a combination or composition comprising instant SEQ ID NO: 1 or a variant thereof and an immune checkpoint inhibitor, including pembrolizumab, nor do the issued claims teach appropriate routes of administration for each component.
The issued claims of U.S. 11,427,621 B2 do not teach a combination or composition comprising SEQ ID NO: 1 or a variant thereof and an immune checkpoint inhibitor, including pembrolizumab, nor do the issued claims teach appropriate routes of administration or the use of the combination for the treatment of lung cancer.
Similar to the issued claims of U.S. 10,370,434 B2, U.S. 11,339,205 B2, and U.S. 11,427,621 B2, Soucek et al. teaches a polypeptide 100% identical to instant SEQ ID NO: 1. Further, Soucek et al. teaches that that polypeptide may be used in combination with the immuno-oncology agent, IL-12; see claim 15, the translated sequence on pages 8-9, and page 27 lines 5.
Regarding instant claims 23-25, Soucek et al. claims 6-9 teach that the polypeptide or functionally equivalent variant is a fusion protein comprising a cell penetrating peptide sequence selected from SEQ ID NOs: 28 and 29, which are 100% identical to instant SEQ ID NO: 37 and 38, and further comprises a nuclear localization signal.
Regarding instant claim 34, Soucek et al. teaches that lung cancer is the preferred embodiment; see page 16 lines 30-32.
Regarding instant claims 35 and 36, Soucek et al. teaches intranasal administration or instillation into the nose; see page 32 lines 29-32 and page 33 lines 5-8. Further, regarding claim 37, Soucek et al. teaches that the components of the composition may be formulated differently so that the components can be differently administered and exemplifies the second component being administered intravenously, or a form of systemic administration; see page 31 lines 9-13.
While Soucek et al. teaches combination regimens with the Myc inhibitor of SEQ ID NO: 1, Soucek et al. does not teach a combination or composition wherein the second component is an immune checkpoint inhibitor nor does Soucek et al. teach treating cancer with a combination or composition comprising an immune checkpoint inhibitor.
Felsher et al. teaches the method of identifying whether a subject having cancer will be responsive to an immune checkpoint inhibitor comprising determining from a sample that the cancer overexpresses a Myc oncogene, identifying the subject with Myc oncogene overexpression as responsive to immune checkpoint inhibition, and administering an immune checkpoint inhibitor, including a PD-1 inhibitor; see claims 1 and 6.
Regarding claims 21, 32, and 33, Felsher et al. suggests that a Myc inhibitor and immune checkpoint inhibitor may be used in combination to treat cancer; see Summary on page 2. Regarding the Myc inhibitor of claim 21, Felsher et al. teaches a Myc inhibitor with the sequence of SEQ ID NO: 19, which is 100% identical to instant SEQ ID NO: 1, or a variant thereof. Regarding the immune-oncology agent of claims 21, 30, and 31, Felsher et al. teaches several PD-1/PD-L1 pathway inhibitors, including pembrolizumab, an anti-PD-1 antagonist antibody.
Regarding claims 39 and 40, the recruitment of T cells to the tumor site, the expansion of T regulatory cells, and induction of IFN-gamma are all inherent properties of claim 33. The claim requires only that a therapeutically effective amount of the combination or composition of claim 21 be administered to a subject in need thereof and no additional steps are recited. Thus, these are outcomes which would inherently flow from the administration of the combination of the polypeptide and the immune-oncology agent.
Given that Felsher et al. teaches the positive relationship between Myc expression and PD-L1 expression in human cancers, including non-small cell lung cancer, and suggests treating a subject, who has been identified as responsive to immune checkpoint inhibitors by Myc overexpression, with a Myc inhibitor and an immune checkpoint inhibitor, it would have been obvious to treat cancer using a combination of the Myc inhibitor comprising SEQ ID NO: 1 or a variant thereof as taught by the issued claims of U.S. 10,370,434 B2, U.S. 11,339,205 B2, or U.S. 11,427,621 B2 with the anti-PD-1 antibody, pembrolizumab, as taught by Felsher et al. Further, one would have been motivated to make the combination because Felsher et al. teaches that although the effects of Myc on the expression of CD47 and PD-L1 were modest, the consequences on tumor regression were dramatic suggesting that combining a Myc inhibitor and PD-1 inhibitor could have synergistic effects. Regarding the choice of pembrolizumab as the PD-1 inhibitor for the treatment of cancer, including lung cancer, because is pembrolizumab was the first FDA approved anti-PD-1 antibody and demonstrated significant survival benefit in patients with non-small cell lung cancer compared to chemotherapy alone; see Pembrolizumab Approval Announcement. Furthermore, one would have a reasonable expectation of success in treating cancer with the combination of the Myc inhibitor of SEQ ID NO: 1 as taught by the issued claims of U.S. 10,370,434 B2, U.S. 11,339,205 B2, or U.S. 11,427,621 B2 and pembrolizumab because each drug can be used alone for the treatment of cancer, because Soucek et al. teaches that the same polypeptide or a functionally active variant thereof can be used in combination with an immune-oncology agent, and because Felsher et al. teaches a possible synergistic relationship when inhibitors of Myc and the PD-1/PD-L1 pathway are administered in a combination.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art
before the effective filing date of the application, as evidenced by the references.
Response to Arguments
Applicant’s amendments filed June 25, 2025 are acknowledged. Any rejection not repeated above is resolved by amendment.
Applicant's arguments filed June 25, 2025 have been fully considered but they are not persuasive.
Applicant asserts that Felsher et al. teaches administering Myc inhibitors or immune checkpoint inhibitors as monotherapies.
Examiner disagrees. Felsher et al. teaches “methods of identifying whether a subject having cancer will be responsive to agents” and “methods of treating a subject having cancer” and such methods comprise “administering an agent, e.g., an immune checkpoint inhibitor and/or a MYC inhibitor, to the subject to treat the cancer”; see Abstract, Summary, and Detailed Description. Felsher et al. teaches that Myc inhibitors inhibit the production, function or activity of Myc; see page 27 lines 22-23. Further, Felsher et al. exemplifies the Myc inhibitor comprising instant SEQ ID NO: 1; Felsher et al. SEQ ID NO: 19. Of immune checkpoint inhibitors, Felsher et al. teaches that they inhibit the production, function, or activity. Felsher et al. exemplifies immune checkpoint inhibitors on pages 28-31 and encompasses antagonistic PD-1 antibodies.
Applicant alleges that because Felsher et al. does not provide experimental data administering the immune checkpoint inhibitor, there is no support for stating “an immune checkpoint inhibitor and/or a MYC inhibitor”.
Examiner disagrees. Felsher et al. claims a method of identifying whether a cancer will be responsive to an immune checkpoint inhibitor, wherein a responsive cancer overexpresses Myc, and administering an immune checkpoint inhibitor to treat the cancer; see claims 1-10. Similarly, Felsher et al. claims a method of treating cancer comprising administering a Myc inhibitor when the cancer overexpresses CD47, PD-L1, or both; see claim 11. Pages 65 and 66 teach that oncogenic levels of Myc or Myc overexpression results in CD47 and PD-L1 overexpression. Felsher et al. concludes that “MYC regulates CD47 and PD-L1 expression in multiple human tumor types”; see page 66 line 2. Thus, depending on the tumor type, the cancer which overexpresses Myc and should be treated with an immune checkpoint inhibitor (Felsher et al. claim 10) is likely the same cancer which overexpresses CD47, PD-L1, or both and should be treated with a Myc inhibitor (Felsher et al. claim 11). Only instant claim 34 restricts the tumor type to lung cancer. Indeed, Felsher et al. highlights lung cancer, including NSCLC, as a relevant cancer; see pages 16, 18, Figure 2B, and claims 9 and 24.
Because Felsher et al. states administering “an immune checkpoint inhibitor and/or a MYC inhibitor”, contemplating the combination therapy to the same degree as instantly claimed, the rejection is maintained.
Conclusion
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure: Soucek et al. (Oncogene. 17: 2463-2472; Published: October 12, 1998) teaches OmoMyc varaints and suggests the use of such variants for the treatment of cancer. Wang et al. (Oncogene. 38: 140-150; Published: August 3, 2018) teaches OmoMyc having the sequence identical to SEQ ID NO: 1 and suggests combining with chemotherapy for the treatment of cancer. Annibali et al. (Nature Communications. 5: 4632; Published: August 18, 2014) teaches OmoMyc as a possible treatment for glioma. Casey et al. (Science. 352(6282): 227-231; Published: March 10, 2016) teaches that Myc regulates the expression of CD47 and PD-L1. Ock et al. (Nature Communications. 8: 1050; Published: October 19, 2017) teaches that Myc is activated in patients who were non-responders to anti-CTLA-4 immunotherapy. Kim et al. (Lung Cancer. 110: 63-67; Published: June 20, 2017) teaches the correlation between Myc and PD-L1 expression in non-small cell lung cancer.
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 KATHERINE ANN HOLTZMAN whose telephone number is (571)270-0252. The examiner can normally be reached Monday - Friday 7:30am - 5:00pm.
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/KATHERINE ANN HOLTZMAN/Examiner, Art Unit 1646
/JULIET C SWITZER/Primary Examiner, Art Unit 1682