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 .
Claim Status
Claims 1-2, 4, 6, 8-9, 11-12, 19, 24, 26, 30, 39-41, and 48 are pending.
Claims 3, 5, 7, 10, 13-18, 20-23, 25, 27-29, 31-38, 42-47, and 49-122 are cancelled.
In response to species election, applicant elected (i) Tofacitinib to modulate BIN3 and a second agent of Erlotinib to modulate epidermal growth factor receptor. Thus, claims 26, 30, and 39-41 directed to a non-elected species are withdrawn.
Claims 1-2, 4, 6, 8-9, 11-12, 19, 24 and 48 have been examined.
Priority
This application is a 371 of PCT/US21/18716 02/19/2021
PCT/US21/18716 has PRO 63/027,852 05/20/2020
PCT/US21/18716 has PRO 62/978,776 02/19/2020
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 2/24/2026 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement has been considered by the examiner.
Non-Compliant Amendment
The correction of claim status identifier of claims 27-29 is in compliance with claim amendment.
Withdrawn Rejection
The rejection of claim claims 1-2, 4, 6, 8-9, 11, and 48 under 35 U.S.C. 102(a)(1) as being anticipated by Tan et al. (Nat Commun 10, 3601 (2019) and evidenced by (i) Kontzias et al. (Curr Opin Pharmacol. 2012 August ; 12(4): 464–470, previously cited 9/3/2025) and (ii) Tofacitinib product sold by MedChemExpress (https://www.medchemexpress.com/Tofacitinib. html? srsltid= AfmBOophuFvNAkDI34PMZyUimHcihgR6XlCpyjTxJWN47Do70h5CNbU) is withdrawn because Tan’s teachings the use of STAT3 inhibitors for treatment of glioblastoma, GBM (Abstract and p9, col 1, Discussion) are based on microarray data absence of an administration step of the drug to a subject. Thus, this 102(a)(1) rejection is withdrawn. However, Tan’s teachings is still valid as a 103 reference in view of other previously cited references.
Maintained Rejection
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.
Claims 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48 are rejected under 35 U.S.C. 103 as being unpatentable over Tan et al. (Nat Commun 10, 3601 (2019), previously cited 1/14/2026) and evidenced by (i) Kontzias et al. (Curr Opin Pharmacol. 2012 August ; 12(4): 464–470, previously cited 9/3/2025) and (ii) Tofacitinib product sold by MedChemExpress (https://www.medchemexpress.com/Tofacitinib. html?srsltid= AfmBOophuFvNAkDI34PMZyUimHcihgR6XlCpyjTxJWN47Do70h5CNbU, previously cited 1/14/2026) in view of He et al. (Sci Signal. 2013 Jul 9;6(283):ra55, previously cited 1/14/2026) and Wen et al. (Mol Cancer. 2015 May 1:14:100, previously cited 1/14/2026).
Claim 1 is drawn to a method for treating a subject for glioma, the method comprising administering to the subject an effective amount of an agent that modulates bridging integrator 3 (BIN3) signaling, or a pharmaceutically acceptable salt thereof.
Tan et al. teach “A STAT3-based gene signature stratifies glioma patients for targeted therapy” (Title). Tan et al. teach STAT3 has also been shown to regulate the self-renewal potential of glioma cells, suggesting that its inhibition would lead to a more curative and sustained outcome. Tan et al. teach the use of the JAK inhibitor Tofacitinib as a STAT3 inhibitor to block STAT3 activation in glioma patients (p2, col 1, para 3). Tan et al. further teach Janus kinase/STAT3 pathway is involved in the pathogenesis of many human malignancies in addition to glioma (p2, col 2, para 3). Thus, one of ordinary skill in the art would found it obvious to administer a JAK inhibitor of Tofacitinib (also STAT3 inhibitor) to treat a glioma patient. Since applicant elected the same compound of Tofacitinib as a modulator of BIN3 signaling, Tan’s JAK inhibitor of Tofacitinib is necessary modulate BIN3 signaling with EC50 of less than about 100 nM during treating a glioma, reading on claims 1-2 and 11. MPEP 2112.01 (I) states “Product and apparatus claims - When the
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structure recited in the reference is substantially identical to that of the claims, claimed properties or functions are presumed to be inherent”.
With respect to claims 4, 6, and 8-9, Kontzias et al. is cited to show the inherent properties of Tofacitinib inhibiting all JAK1, JAK2, and JAK3 known in the art as follows (p8, Fig 1).
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Tofacitinib product introduction is further cited to show the inherent properties of Tofacitinib having EC50 for JAK3/2/1 as 1, 20, and 112 nM respectively shown as follows (p3).
With respect to claim 48, Tan et al. teach the treated glioma as glioblastoma/GBM (Title and Abstract; p2, col 1, para 1).
Tan et al. teach EGFR activation can contribute to STAT3 signaling in GBM cells (p12, col 1, last para), but did not teach administration of a second anti-cancer agent of erlotinib to treat GBM.
He et al. teach “Blockade of Glioma Proliferation Through Allosteric Inhibition of JAK2” (Title) because the epidermal growth factor receptor (EGFR) is frequently overexpressed or mutated in human cancers, including glioblastoma (Abstract). He et al. suggest inhibition of both EGFR and STAT3 by inhibiting JAK2 to treat glioblastoma (Abstract). Similarly, Wen et al. teach “Synergistic anti-tumor effect of combined inhibition of EGFR and JAK/STAT3 pathways in human ovarian cancer” (Title). Wen et al. further teach blockade of STAT3 pathway synergistically increased anti-tumor activity of gefitinib, as well as another EGFR inhibitor of erlotinib (p6, col 2, para 1). Because (i) Tan et al. teach the use of the JAK inhibitor Tofacitinib as a STAT3 inhibitor to block STAT3 activation in glioma patients (p2, col 1, para 3) and EGFR activation can contribute to STAT3 signaling in GBM cells (p12, col 1, last para), (ii) He et al. suggest inhibition of both EGFR and STAT3 pathways to treat glioblastoma (Abstract), and (iii) Wen et al. further teach blockade of STAT3 pathway synergistically increased anti-tumor activity of the EGFR inhibitor of erlotinib in glioma (p6, col 2, para 1), one of ordinary skill in the art would have found it obvious to beneficially combine Tan’s JAK2 and STAT3 inhibitor of Tofacitinib and Wen’s EGFR inhibitor of erlotinib with synergistically increased anti-tumor activity to treat glioma (p6, col 2, para 1).
One of ordinary skill in the art before the effective filing date of this invention would have found it obvious to beneficially combine (1) Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product and (2) He et al. in view of Wen et al. because (a) Tan et al. teach the use of the JAK inhibitor Tofacitinib as a STAT3 inhibitor to block STAT3 activation in glioma patients (p2, col 2, para 3) and EGFR activation can contribute to STAT3 signaling in GBM cells (p12, col 1, last para), (b) Kontzias et al. is cited to show the inherent properties of Tofacitinib inhibiting all JAK1, JAK2, and JAK3 known in the art (p8, Fig 1), (c) Tofacitinib product introduction is further cited to show the inherent properties of Tofacitinib having EC50 for JAK3/2/1 as 1, 20, and 112 nM respectively shown (p3), (d) He et al. suggest inhibition of both EGFR and STAT3 pathways to treat glioblastoma (Abstract), and (e) Wen et al. further teach blockade of STAT3 pathway synergistically increased anti-tumor activity of the EGFR inhibitor of erlotinib in glioma (p6, col 2, para 1). The combination would have reasonable expectation of success because Tan et al., He et al., and Wen et al. teach and/or suggest inhibition of EGFR and STAT3 pathways to treat glioma or glioblastoma/GBM patients.
With respect to claims 12, 19, and 24, He et al. suggest inhibition of both EGFR and STAT3 by inhibiting JAK2 to treat glioblastoma (Abstract). Similarly, Wen et al. teach “Synergistic anti-tumor effect of combined inhibition of EGFR and JAK/STAT3 pathways in human ovarian cancer” (Title). Wen et al. further teach blockade of STAT3 pathway synergistically increased anti-tumor activity of the EGFR inhibitor of erlotinib (p6, col 2, para 1).
Applicant’s Arguments
Tan does not say that Tofacitinib has been used in glioma patients. Neither does Tan say that Tofacitinib is a STAT3 inhibitor (Remarks, p6, para 2-4).
A link between treating a glioma and Tofacitinib is not provided by Tan (Remarks, p7, para 2-3).
He discloses that the "potential for developing anti-EGFR/EGFRvlll agents either as a
monotherapy or as a combination therapy remains high," but "therapeutic resistance leading to fatality" is an ongoing issue. He suggests that inhibition of JAK2 alone is not sufficient for glioblastoma treatment regimens. (Remarks, p7, last para to p8, para 1-4).
Wen, is specific to human ovarian cancer. He discloses that combining an EGFR inhibitor and a JAK2 inhibitor is not sufficient to treat a glioma, and because Wen only suggests that the combination may be useful for treating ovarian cancer, it would not have been obvious to combine Tofacitinib with an EGFR inhibitor as recited herein (Remarks, p9, para 1-2).
The instant application has surprisingly identified the EGFR-BIN3 signaling pathways as
"a major suppressor of invasiveness." See the instant application [00293], "tofacitinib is unlikely to upregulate BIN3 via inhibition of JAK/STAT pathways since ligand activation of the EGFR activates JAK/STATs and also upregulates BIN3." Id. So, it is not via inhibition of JAK that Tofacitinib confers its beneficial activity, but through activation of BIN3. Thus, not only was the relationship between BIN3 and glioma treatment unrecognized prior to the instant application, but the relationship between tofacitinib and BIN3 was also previously unrecognized. The success of the claimed treatment method is, therefore, even more surprising (Remarks, p9, para 1-2).
Response to Arguments
Applicant's arguments filed 2/13/2026 have been fully considered but they are not persuasive for the reasons as follows.
Applicant’s arguments (i) and (ii) are not persuasive under the 103 rejection for the reasons as follows.
Tan et al. teach “A STAT3-based gene signature stratifies glioma patients for targeted therapy” (Title). Tan et al. teach the use of the JAK inhibitor Tofacitinib as a STAT3 inhibitor to block STAT3 activation in glioma patients (p2, col 1, para 3), providing a link between treating a glioma and Tofacitinib. Tan et al. further teach Janus kinase/STAT3 pathway is involved in the pathogenesis of many human malignancies (p2, col 2, para 3). A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill in the art, including nonpreferred embodiments. Merck & Co. v. Biocraft Labs., Inc. 874 F.2d 804, 10 USPQ2d 1843 (Fed. Cir. 1989), cert. denied, 493 U.S. 975 (1989). See MPEP 2123(I).
Applicant argues no explicit teaching of using Tofacitinib to treat glioma by Tan et al.; thus, a link between treating a glioma and Tofacitinib is not provided by Tan et al. The arguments are not applied to this 103 rejection based on the combination of Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product sold by MedChemExpress, in view of He et al. and Wen et al. in the previous office action of record. In particular, He et al. teach blocking phosphorylation and activation of EGFR and STAT3 to treat glioblastoma (Abstract). Wen et al. suggest a combination therapy to inhibit EGFR and STAT3 can treat any EGFR and STAT3 sensitive cancers such as ovarian cancer explicitly taught by Wen et al. as well as glioblastoma (GBM) as taught by Tan et al. in view of He et al. The rationale to modify or combine the prior art does not have to be expressly stated in the prior art; the rationale may be expressly or impliedly contained in the prior art or it may be reasoned from knowledge generally available to one of ordinary skill in the art, established scientific principles, or legal precedent established by prior case law. 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). See MPEP 2144(I). A person of ordinary skill in the art is well defined as a person of ordinary creativity able to fit the teachings of multiple patents together like pieces of a puzzle.” Id. Office personnel may also take into account “the inferences and creative steps that a person of ordinary skill in the art would employ.” Id. at ___, 82 USPQ2d at 1396. See MPEP 2141.03 (I). In the present case, a person of ordinary creativity able to fit the teachings of the cited prior art references of record together like pieces of a puzzle without the need of explicitly teaching as argued by applicant.
Applicant’s arguments (iii) is not persuasive because a therapeutic drug resistance is related to a subset patient population and He’s teaching is still relevant for one of ordinary skill in the art to combine Tan’s JAK2 and STAT3 inhibitor of Tofacitinib and Wen’s EGFR inhibitor for the same purpose to treat any EGFR and STAT3 sensitive cancers such as ovarian cancer explicitly taught by Wen et al. as well as glioblastoma (GBM) as taught by Tan et al. in view of He et al. "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." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980). See MPEP 2144.06(I).
Applicant’s arguments (iv) is not persuasive because Applicant argues a single reference of Wen et al. whereas the rejection is based on Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product sold by MedChemExpress, in view of He et al. and Wen et al. In particular, Tan et al. teach the use of the JAK inhibitor Tofacitinib as a STAT3 inhibitor to block STAT3 activation in glioma patients (p2, col 1, para 3) and EGFR activation can contribute to STAT3 signaling in GBM cells (p12, col 1, last para). Consistently, He et al. suggest inhibition of both EGFR and STAT3 by inhibiting JAK2 to treat glioblastoma (Abstract). Wen et al. further teach blockade of STAT3 pathway synergistically increased anti-tumor activity of gefitinib, as well as another EGFR inhibitor of erlotinib consistent with previous reports in some other tumors, including glioma (p6, col 2, para 1), not limited to ovarian cancer as argued by applicant.
Applicant’s arguments (v) is not persuasive because applicant failed to provide data to show surprising or unexpected result of the pathway as argued by applicant. See MPEP 716.02(b). The evidence relied upon should establish "that the differences in results are in fact unexpected and unobvious and of both statistical and practical significance." Ex parte Gelles, 22 USPQ2d 1318, 1319 (Bd. Pat. App. & Inter. 1992). Furthermore, Tan’s JAK/STAT3 inhibitor of Tofacitinib is the same modulator of BIN3 signaling in the instant claim 11. MPEP 2112.01 (II) states "Products of identical chemical composition cannot have mutually exclusive properties." In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present.
Applicant’s arguments (vi) is not persuasive because (a) applicant’s argument does not commensurate in scope with the rejected claim as the argued limitation of "a major suppressor of invasiveness" is not found in the rejected claims and (b) the base claim 1 does not require EGFR inhibitor as argued by applicant. Furthermore, applicant’s opinion of combining tofacitinib (in the instant claim 11) and erlotinib (I the instant claim 19) to treat glioma is unrecognized does not overcome the 103 rejection of record. See the maintained 103 rejection above not repeated here.
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 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2 of U.S. Patent No. 11, 285,154 (the ‘154 patent) in view of Tan et al. (Nat Commun 10, 3601 (2019) , previously cited 1/14/2026) and evidenced by (i) Kontzias et al. (Curr Opin Pharmacol. 2012 August ; 12(4): 464–470, previously cited 9/3/2025) and (ii) Tofacitinib product sold by MedChemExpress (https://www.medchemexpress.com/Tofacitinib. html?srsltid=AfmBOophuFvNAkDI34PMZyUimHcihgR6XlCpyjTxJWN47Do70h5CNbU, previously cited 1/14/2026) in view of He et al. (Sci Signal. 2013 Jul 9;6(283):ra55, previously cited 1/14/2026) and Wen et al. (Mol Cancer. 2015 May 1:14:100, previously cited 1/14/2026).
Claim 1 of the ‘154 patent disclosed a method for treating a malignant brain cancer comprising administering an effective amount of an EGFR inhibitor and a JNK inhibitor.
Claim 2 of the ‘154 patent disclosed the EGFR inhibitor is gefitinib.
The relevancy of Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product in view of He et al. and Wen et al. is described above not repeated here. In particular, Wen et al. teach blockade of STAT3 pathway synergistically increased anti-tumor activity of gefitinib, as well as another EGFR inhibitor (erlotinib) as applied to 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48 described above not repeated here.
Because Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product in view of He et al. and Wen et al. teach beneficial combination a JNK inhibitor of Tofacitinib and an EGFR inhibitor of gefitinib as suggested by claims 1-2 of the ‘154 patent to treat glioblastoma, claims 1-2 of the ‘154 patent in view of Tan et al. He et al., Wen et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product are obvious to the instant claims 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48.
Response to Arguments
Applicant's arguments of the claim scope of ‘154 patent different from the instant claims and none of the cited references teaching Tofacitinib with activity toward JNK filed 2/13/2026 have been fully considered but they are not persuasive because claims 1-2 of the ‘154 patent in combination with Tan et al. in view of He et al., Wen et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product are obvious to the instant claims 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48. See the maintained 103 rejection above in details. Furthermore, Tan’s Tofacitinibis identical to the claimed compound as argued by applicant. "Products of identical chemical composition cannot have mutually exclusive properties." See MPEP 2112.01 (II).
Claims 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 6 of copending Application No. 17/800,208 (the ‘208 application, 2025-9-22) in view of Tan et al. (Nat Commun 10, 3601 (2019) and evidenced by (i) Kontzias et al. (Curr Opin Pharmacol. 2012 August ; 12(4): 464–470, previously cited 3/16/2026) and (ii) Tofacitinib product sold by MedChemExpress (https://www.medchemexpress.com/Tofacitinib.html?srsltid= AfmBOophuFvNAkDI34PMZyUimHcihgR6XlCpyjTxJWN47Do70h5CNbU) in view of He et al. (Sci Signal. 2013 Jul 9;6(283):ra55) and Wen et al. (Mol Cancer. 2015 May 1:14:100.).
Claims 1 and 6 of the ‘208 application disclosed an EGFR inhibitor of erlotinib
Claims 1 and 6 of the ‘208 application did not disclose a combination of Tofacitinib with erlotinib to treat glioblastoma.
The relevancy of Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product in view of He et al. and Wen et al. is described above not repeated here. In particular, Wen et al. teach blockade of STAT3 pathway synergistically increased anti-tumor activity of gefitinib, as well as another EGFR inhibitor (erlotinib) as applied to 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48 described above not repeated here.
Because Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product in view of He et al. and Wen et al. teach beneficial combination a JNK inhibitor of Tofacitinib and an EGFR inhibitor of gefitinib as suggested by claims 1 and 6 of the ‘208 application to treat glioblastoma, claims 1 and 6 of the ‘208 application in view of Tan et al. He et al., Wen et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product are obvious to the instant claims 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48.
This is a provisional nonstatutory double patenting rejection.
Claims 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2 and 4 of copending Application No. 17/910,637 (the ‘637 application, 2025-12-05) in view of Tan et al. (Nat Commun 10, 3601 (2019) and evidenced by (i) Kontzias et al. (Curr Opin Pharmacol. 2012 August ; 12(4): 464–470, previously cited 9/3/2025) and (ii) Tofacitinib product sold by MedChemExpress (https://www.medchemexpress.com/Tofacitinib.html?srsltid= AfmBOophuFvNAkDI34PMZyUimHcihgR6XlCpyjTxJWN47Do70h5CNbU) in view of He et al. (Sci Signal. 2013 Jul 9;6(283):ra55) and Wen et al. (Mol Cancer. 2015 May 1:14:100.).
Claims 1-2 of the ‘637 application disclosed administering a combination therapy comprising an EGFR inhibitor to treat glioma.
Claim 4 of the ‘637 application disclosed the EGFR inhibitor as erlotinib.
Claims 1-2 and 4 the ‘637 application dis not teach the combination further comprising Tofacitinib.
The relevancy of Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product in view of He et al. and Wen et al. is described above not repeated here. In particular, Wen et al. teach blockade of STAT3 pathway synergistically increased anti-tumor activity of gefitinib, as well as another EGFR inhibitor (erlotinib) as applied to 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48 described above not repeated here.
Because Tan et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product in view of He et al. and Wen et al. teach beneficially combine Tofacitinib with an EGFR inhibitor of erlotinib taught by claims 1-2 and 4 the ‘637 application to treat glioblastoma, claims 1-2 and 4 the ‘637 application in view of Tan et al. He et al., Wen et al. and evidenced by (i) Kontzias et al. and (ii) Tofacitinib product, are obvious to the instant claims 1-2, 4, 6, 8-9, 11-12, 19, 24, and 48.
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claim is allowed.
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.
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/J.L/Examiner, Art Unit 1658
08-May-2026
/Melissa L Fisher/ Supervisory Patent Examiner, Art Unit 1658
Prosecution Insights