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 and species in the reply filed on January 12, 2026 is acknowledged.
Claims 1-60 are pending. Claims 41-60 are withdrawn. Claims 1-40 are examined.
Prior Art Rejections
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 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 of this title, 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.
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 1-39 are rejected under 35 U.S.C. 103 as being unpatentable over Benson et al. (US 8,221,760, 7/17/2012) in view of Shi et al. (J Gastroenterol (2018) 53:989-998), Ariaans et al (WO 2013/087911, Clinical Trial NCT03466411 (v28, 4/14/2020), and Sandborn et al. (Gastroenterology. 2020 Feb;158(3):537-549.e10. Epub 2019 Sep 4).
Benson discloses a human anti-IL-23p19 antibody, and a method for treating an IL-23 related disease including, among others, psoriasis, psoriatic arthritis, ulcerative colitis and Crohn's disease with a pharmaceutical composition comprising the anti-IL-23p19 antibody, wherein the antibody comprises the VH of SEQ ID NO: 106 and the VL of 116 (abstract; Column 40; column 44, lines 30-41; and claims 1, 4, 7 and 8), which are 100% identical to the present VH of SEQ ID NO:7 and the VL of SEQ ID NO:8, respectively. Benson antibody is the same as claimed and has the same structure. Benson does not teach administering to the patient anti-TNF inhibitor used to treat Crohn's disease. Benson does not teach clinical response.
Shi reviews various medications for the treatment of Crohn's disease including conventional medication and biologics, wherein the conventional medication includes, among others, corticosteroids and methotrexate, for example (page 991, 1st column to page 992, 1st column); and the biologics include, among others, anti-TNF agents (e.g., infliximab, adalimumab, and certolizumab) and ustekinumab (an antibody to IL-12/23), for example (page 992, 2nd column to page 994, 2nd column). Additionally, Shi teaches that up to 40% of patients show no clinical benefit (primary non-response) to anti-TNF therapy; and secondary loss of response refers to the clinical situation, in which a patient has an initial response to anti-TNF antibody, followed by a diminished or less durable response over time; and that secondary loss of response with therapeutic drug trough concentration is regarded as mechanistic failure, in which condition, patients may need to switch to a drug with an alternative mechanism of action (page 993, column 1, lines 1-5; and column 2, lines 1-4).
Ariaans et al teach numerous anti anti-TNF-α antibodies, including golimumab, (see pages 11, 14, SEQ ID Nos:6 and 7). The reference teaches that the anti-TNF-α antibodies are used to treat inflammatory bowel diseases, such as ulcerative colitis and Crohn’s disease at 0.01-1000 mg doses, (see table 2, and paragraphs 0090-0091, 0135). With respect to claims 10-12, the instant specification teaches that SEQ ID NO:11-18 are the heavy and light chain sequences for golimumab, and the Ariaans et al reference teaches said heavy and light variable chains for golimumab, (see SEQ ID NOs: 6, 7 and figures 2F and 2G of Ariaans et al). With respect to claim 2, the Ariaans et al reference teaches that analysis of a representative endoscopic picture of the colitis score is performed, (see 250, figure 14).
Clinical Trial NCT03466411 is a Phase 2/3 study of the efficacy and safety of guselkumab in participants with moderately to severely active Crohn's disease, wherein in Phase 2, safety and efficacy of guselkumab dose regimens were evaluated to support the selection of induction and maintenance dose regimens for confirmatory evaluation in Phase 3; and three groups of participants received guselkumab (Doses 1, 3 and 4, respectively) by intravenous (IV) infusion, followed by guselkumab (Doses 2, 2 and 5, respectively) by subcutaneous (SC) injection (see teachings under subtitles “Study Identification”, “Study Description”, and “Arms and Interventions” (1st three groups, for example)). In addition, NCT03466411 teaches various primary and secondary outcome measures, which include, for example, measuring change from baseline in the Crohn's Disease Activity Index (CDAI) score, and clinical remission at week 12, wherein the CDAI score will be assessed by collecting information on 8 different Crohn's disease-related variables, with scores ranging from 0 to approximately 600, and a decrease over time indicates improvement in disease activity; and clinical remission is defined as CDAI score less than (<) 150 points (see teachings under subtitles “Outcome Measures”). Further, NCT03466411 teaches the Inclusion Criteria, which include patients with demonstrated intolerance or inadequate response to conventional or to biologic therapy for CD (see teachings under subtitles “Eligibility”).
Sandborn reports a phase 2 clinical study of a monoclonal antibody against the IL-23 p19 subunit, mirikizumab, in patients with moderate to severe ulcerative colitis (UC), which study includes a 12-week induction period, followed by a 52-week maintenance period; wherein in the 12-week induction period, mirikizumab is administered intravenously at weeks 0, 4, and 8 at a dose of 50 mg or 200 mg (with exposure-based dosing) or 600 mg (fixed dosing); and wherein in the 52-week maintenance period, at week 12, mirikizumab is administered SC every 4 or 12 weeks at a dose of 200 mg (page 537, 1st column; paragraph bridging pages 538-539; and the paragraph bridging pages 539 and 541, for example).
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to treat Crohn's disease with an anti-IL23 antibody such as Benson’s anti-IL23 antibody (or guselkumab) in combination with an additional drug used to treat Crohn's disease such as anti-TNF antibodies. When a biologic therapy failure or intolerance for Crohn's disease such as being failed to the treatment of an anti-TNF agent with an anti-IL23 antibody such as Benson’s anti-IL23 antibody (or guselkumab) following the teachings of Benson and Shi. The person of ordinary skill in the art would have been motivated to do so for disease treatment and for the potential additive effect of the combination therapy, and reasonably would have expected success because both the anti-IL-23 antibody and other agents for CD can be used for treating CD; and they have different modes of action.
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to treat Crohn's disease with an anti-IL23 antibody such as Benson’s anti-IL23 antibody or guselkumab following Shie anti-TNF antibody treatment with Sandborn’s regimens with some adjustment/optimization as needed, and measuring the efficacy or responsiveness (using CDAI score, for example) at different treatment time points such as at week 38, wherein the patient may have intolerance or inadequate response to conventional or biologic therapy, following the teachings of Benson, Clinical Trial NCT03466411, and Sandborn. The person of ordinary skill in the art would have been motivated to for disease treatment, and reasonably would have expected success because, like guselkumab, mirikizumab also is an anti-IL23 antibody; and both UC and CD are inflammatory bowel disease and therapies effective for one often are effective for the other.
The claimed antibodies are anti-TNF-α antibody, (golimumab) and anti-IL-23 antibody, (guselkumab) according to the specification.
Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made.
Claim(s) 1-39 is/are rejected under 35 U.S.C. 103 as being unpatentable over Shi et al. (J Gastroenterol (2018) 53:989-998), Ariaans et al (WO 2013/087911, Clinical Trial NCT03466411 (v28, 4/14/2020), and Sandborn et al. (Gastroenterology. 2020 Feb;158(3):537-549.e10. Epub 2019 Sep 4) as applied to claims 1-39 above, and further in view of Bedi et al. (WO2018218215A1, 11/29/2018).
Teaching of Benson, Shi, Ariaans, and Sandborn are discussed above.
Benson does not teach the H and L chain sequences of the anti-IL-23p19 antibody of SEQ ID NO: 9-10.
Bedi teaches multifunctional antibody-ligand traps including, among others, an anti-IL23 antibody (guselkumab) - TEVI3 ECD antibody-ligand trap comprising the guselkumab heavy chain + TEVI3 ECD fusion protein of SEQ ID NO: 130, and the guselkumab light chain of SEQ ID NO: 131, wherein the heavy chain (HC) of guselkumab comprises amino acids 1-447 of SEQ ID NO:130 (which is a fusion protein comprising the HC of guselkumab, a peptide linker (GGGGS)3, and TIM3 ECD (Fig. 97A); and wherein amino acids 1-447 of SEQ ID NO:130 and SEQ ID NO:131 are 100% identical to the present HC of SEQ ID NO:9 and LC of SEQ ID NO:10, respectively (see attached sequence search result below).
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to use an anti-IL23 antibody such as guselkumab for treating Crohn's disease following the teachings of Benson and Bedi. The person of ordinary skill in the art would have been motivated to do so for disease treatment, and reasonably would have expected success because Benson expressly teaches that the anti-IL23 antibody comprising the VH of SEQ ID NO: 106 and the VL of 116 (the VH and VL of guselkumab) can be used for treating Crohn's disease.
Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made.
Claims 40 is rejected under 35 U.S.C. 103 as being unpatentable over Benson et al. (US 8,221,760, 7/17/2012), Shi et al. (J Gastroenterol (2018) 53:989-998), Ariaans et al (WO 2013/087911, Clinical Trial NCT03466411 (v28, 4/14/2020), and Sandborn et al. (Gastroenterology. 2020 Feb;158(3):537-549.e10. Epub 2019 Sep 4) as applied to claims 1-39 above, and further in view of Randazzo et al. (US 2018/0094052, 4/5/2018).
The teachings of Benson, Clinical Trial NCT03466411, and Sandborn are reviewed above. None of the references teaches the formulation recited in claim 10.
Randazzo teaches a pharmaceutical composition comprising an isolated anti-IL-23 specific antibody having the guselkumab heavy chain variable region amino acid sequence of SEQ ID NO: 106 and the guselkumab light chain variable region amino acid sequence of SEQ ID NO: 116 at 100 mg/mL; 7.9% (w/v) sucrose, 4.0 mM Histidine, 6.9 mM L-Histidine monohydrochloride monohydrate; 0.053% (w/v) Polysorbate 80; wherein the diluent is water at standard state; and a method of treatment using the pharmaceutical composition (page 4, [0014]; and claims 18, 19 and 28, for example).
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to treat Crohn's disease with Randazzo’s pharmaceutical composition comprising said anti-IL-23 or guselkumab following Sandborn’s regimens, following the teachings of Benson, Clinical Trial NCT03466411, Sandborn, and Randazzo. The person of ordinary skill in the art would have been motivated to for disease treatment, and reasonably would have expected success because Randazzo teaches that the pharmaceutical composition can be used for disease treatment.
Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made.
Double Patenting Rejections:
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 claims at issue 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); and 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 a nonstatutory double patenting ground provided the reference application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The USPTO internet Web site contains terminal disclaimer forms which may be used. Please visit http://www.uspto.gov/forms/. The filing date of the application will determine what form 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 http://www.uspto.gov/patents/process/file/efs/guidance/eTD-info-I.jsp.
Claims 1-40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7 of U.S. Patent No. 12258393. Although the claims at issue are not identical, they are not patentably distinct from each other for the following reasons:
Claims 1-7 of U.S. Patent No. 12258393 teach all the claim limitations of pending claims. Therefore, the conflicting claims are not patentably distinct from each other.
Claims 1-40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-42 of U.S. Patent No. 11780911. Although the claims at issue are not identical, they are not patentably distinct from each other for the following reasons:
Claims 1-42 of U.S. Patent No. 11780911 teach all the claim limitations of pending claims. Therefore, the conflicting claims are not patentably distinct from each other.
Claims 1-3 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of copending Application No. 17/308,302 (reference application) ioin view of Clinical Trial NCT03466411 (v28, 4/14/2020), and Sandborn et al. (Gastroenterology. 2020 Feb;158(3):537-549.e10. Epub 2019 Sep 4). Although the claims at issue are not identical, they are not patentably distinct from each other for the following reasons:
Claims 1-16 of copending Application No. 17/308,302 (reference application) teach the administration of IL-23 inhibitor and TNF inhibitor to treat Crohn disease. ‘302 does not teach the 38 week after initial treatment.
Clinical Trial NCT03466411 is a Phase 2/3 study of the efficacy and safety of guselkumab in participants with moderately to severely active Crohn's disease, wherein in Phase 2, safety and efficacy of guselkumab dose regimens were evaluated to support the selection of induction and maintenance dose regimens for confirmatory evaluation in Phase 3; and three groups of participants received guselkumab (Doses 1, 3 and 4, respectively) by intravenous (IV) infusion, followed by guselkumab (Doses 2, 2 and 5, respectively) by subcutaneous (SC) injection (see teachings under subtitles “Study Identification”, “Study Description”, and “Arms and Interventions” (1st three groups, for example)). In addition, NCT03466411 teaches various primary and secondary outcome measures, which include, for example, measuring change from baseline in the Crohn's Disease Activity Index (CDAI) score, and clinical remission at week 12, wherein the CDAI score will be assessed by collecting information on 8 different Crohn's disease-related variables, with scores ranging from 0 to approximately 600, and a decrease over time indicates improvement in disease activity; and clinical remission is defined as CDAI score less than (<) 150 points (see teachings under subtitles “Outcome Measures”). Further, NCT03466411 teaches the Inclusion Criteria, which include patients with demonstrated intolerance or inadequate response to conventional or to biologic therapy for CD (see teachings under subtitles “Eligibility”).
Sandborn reports a phase 2 clinical study of a monoclonal antibody against the IL-23 p19 subunit, mirikizumab, in patients with moderate to severe ulcerative colitis (UC), which study includes a 12-week induction period, followed by a 52-week maintenance period; wherein in the 12-week induction period, mirikizumab is administered intravenously at weeks 0, 4, and 8 at a dose of 50 mg or 200 mg (with exposure-based dosing) or 600 mg (fixed dosing); and wherein in the 52-week maintenance period, at week 12, mirikizumab is administered SC every 4 or 12 weeks at a dose of 200 mg (page 537, 1st column; paragraph bridging pages 538-539; and the paragraph bridging pages 539 and 541, for example).
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to modify Claims 1-16 of copending Application No. 17/308,302 (reference application) with Sandborn’s regimens with some adjustment/optimization as needed, and measuring the efficacy or responsiveness (using CDAI score, for example) at different treatment time points such as at week 38, wherein the patient may have intolerance or inadequate response to conventional or biologic therapy, following the teachings of Benson, Clinical Trial NCT03466411, and Sandborn. The person of ordinary skill in the art would have been motivated to for disease treatment, and reasonably would have expected success because, like guselkumab, mirikizumab also is an anti-IL23 antibody; and both UC and CD are inflammatory bowel disease and therapies effective for one often are effective for the other.
Therefore, the conflicting claims are not patentably distinct from each other.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to MICHAEL D PAK whose telephone number is (571)272-0879. The examiner can normally be reached on flexible time.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Vanessa Ford can be reached on 571-272-0857. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of an application may be obtained from the Patent Application Information Retrieval (PAIR) system. Status information for published applications may be obtained from either Private PAIR or Public PAIR. Status information for unpublished applications is available through Private PAIR only. For more information about the PAIR system, see http://pair-direct.uspto.gov. Should you have questions on access to the Private PAIR system, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative or access to the automated information system, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/MICHAEL D PAK/Primary Examiner, Art Unit 1674
Prosecution Insights