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 .
DETAILED ACTION
Applicant’s election without traverse of a) the heavy chain variable region (VH) of SEQ ID NO: 11, which comprises the CDRs 1-3 of SEQ ID NO(s): 1-3, respectively, and (b) the light chain variable region (VL) of SEQ ID NO: 16, which comprises the CDRs 1-3 of SEQ ID NO(s): 9, 4, and 5, respectively, in the reply filed on 07/21/2026 is acknowledged.
Claims 1-6, 8, 10, 12, and 14-24 are pending.
Claims 1-6, 8, 10, 12, and 14-24 are under examination on the merits.
Priority
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Claims 1-6, 8, 10, 12, 14-24 have an effective filing date of 05/04/2021, corresponding to EP21172160.0.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 01/26/2024, 04/04/2025, 05/12/2025, 06/20/2025, 07/21/2026, and 09/10/2026 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
Claim Rejections
35 U.S.C. 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Regarding claim 23, the phrase “for example” renders the claim indefinite because it is unclear whether the limitation(s) following the phrase are part of the claimed invention. See MPEP § 2173.05(d).
35 U.S.C. 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 2 and 18-22 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treating a disease or lung disorder, does not reasonably provide enablement for preventing a disease or lung disorder. It is noted that the recitation of a disease or lung disorder encompasses multiple types of cancer. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
MPEP § 2164.01 states:
The standard for determining whether the specification meets the enablement requirement was cast in the Supreme Court decision of Mineral Separation v. Hyde, 242 U.S. 261, 270 (1916) which postured the question: is the experimentation needed to practice the invention undue or unreasonable? That standard is still the one to be applied. In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988). Accordingly, even though the statute does not use the term “undue experimentation,” it has been interpreted to require that the claimed invention be enabled so that any person skilled in the art can make and use the invention without undue experimentation. In re Wands, 858 F.2d at 737, 8 USPQ2d at 1404 (Fed. Cir. 1988).
There are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is “undue.” These factors include but are not limited to:
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The breadth of the claims;
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The nature of the invention;
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The state of the prior art;
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The level of one of ordinary skill;
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The level of predictability in the art;
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The amount of direction provided by the inventor;
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The existence of working examples; and
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The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988). The factors most relevant to this rejection are 1) the amount of direction provided by the inventor and 2) the existence of working examples. In the instant case, the amount of direction provided by the inventor and existence of working examples disclosed in the specification, as filed, would not be sufficient to enable the skilled artisan to make and/or use the claimed invention at the time the application was filed without undue experimentation.
(1) The amount of direction provided by the inventor - The amount of guidance or direction needed to enable an invention is inversely related to the amount of knowledge in the state of the art as well as the predictability in the art. In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970). The “amount of guidance or direction” refers to that information in the application, as originally filed, that teaches exactly how to make or use the invention. The more that is known in the prior art about the nature of the invention, how to make, and how to use the invention, and the more predictable the art is, the less information needs to be explicitly stated in the specification. In contrast if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as to how to make and use the invention in order to be enabling. See, e.g., Chiron Corp. v. Genentech Inc., 363 F.3d 1247, 1254, 70 USPQ2d 1321, 1326 (Fed. Cir. 2004). Due to the high level of unpredictability in the area of disease or lung disorder prevention, particularly cancer prevention, the skilled artisan would need significant guidance in preventing cancer by practicing the claimed method. The skilled artisan recognizes that keeping individuals free of cancer indefinitely is an intractable proposition, if not now wholly impossible, given, for example, that cancers are widely heterogeneous diseases, having widely varying pathologies and etiologies, and with causes that are multifactorial and as yet only partially characterized and poorly understood. It is generally recognized that a disease cannot be prevented unless and until its causes are fully appreciated and understood to a degree that it becomes possible to intercede effectively to block its onset or development by any cause.
(2) The existence of working examples - Examples 2 and 3 of the specification demonstrate that the invention may be used to treat a disease or lung disorder, such as airway inflammation, by treating a subject in need thereof with the claimed antibody; however there is no showing in the specification of any means by which one skilled in the art could use the claimed methods to prevent any disease or lung disorder. Therefore one skilled in the art would be subject to undue experimentation to practice the instant invention as it is currently claimed.
In conclusion upon careful consideration of the Wands factors that are used to determine whether undue experimentation is required to practice an invention, the amount of direction provided by the inventor and the working examples provided, as filed, is not deemed sufficient to enable the skilled artisan to make and/or use the invention commensurate in scope with the instant claims at the time the application was filed without undue experimentation.
Claims 19-22 are included in this rejection, because they depend from claim 18 but do not cure the deficiencies of claim 18 with respect to the enablement provision of 35 U.S.C. 112(a).
Applicant is informed that the instant rejection under 35 U.S.C. 112 (a) may be overcome by amending claims 2 and 18 to remove the “preventing” language.
35 U.S.C. 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.
Claims 1-6, 8, 10, 12, 14-20, and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Raats et al. (WO 2020/038963, international publication date: 02/27/2020, IDS), as evidenced by Mukherjee et al. (Frontiers in Immunology, 9: 1-10, 2018, IDS) and Quint et al. (J Allergy Clinical Immunol, 119(5): 1065-1071, 2017).
Raats et al. teach that “[i]nflammatory conditions, whether of a chronic or acute nature, represent a substantial problem in the healthcare industry. Briefly, chronic inflammation is considered to be inflammation of a prolonged duration (weeks or months) in which active inflammation, tissue destruction and attempts at healing are proceeding simultaneously. Although chronic inflammation can follow an acute inflammatory episode, it can also begin as an insidious process that progresses with time, for example, as a result of a persistent infection (e.g., tuberculosis, syphilis, fungal infection) that causes a delayed hypersensitivity reaction, prolonged exposure to endogenous (e.g., elevated plasma lipids) or exogenous (e.g., silica, asbestos, cigarette tar, surgical sutures) toxins, or autoimmune reactions against the body's own tissues (e.g., rheumatoid arthritis, systemic lupus erythematosus, vasculitis, multiple sclerosis, psoriasis)… One consequence of inflammation is the formation of Neutrophil Extracellular Traps (NETs). NETs are also known to cause inflammation. NETs are structures comprising DNA and histones that are produced by neutrophils as part of the host defense mechanism against pathogens. They can trap and kill various bacterial, fungal, viral and protozoal pathogens, and their release is one of the first lines of defense against pathogens. Following activation by microorganisms or cytokines, histones become hypercitrullinated and the neutrophil nucleus undergoes a process of chromatin decondensation that leads to the formation of NETs by NETosis, a form of neutrophil cell death… NETs play a pathological role in a variety of diseases, for example by causing aberrant inflammation. Thus, NETs are involved in the pathology of a variety of inflammatory conditions, such as systemic lupus erythematosus (SLE), lupus, sepsis, vasculitis, inflammatory arthritis, rheumatoid arthritis and osteoarthritis, psoriasis, Alzheimer's disease, autoimmune hepatitis, juvenile idiopathic arthritis, Bechet’s disease, spondylitis, spondyloarthropathy, multiple system atrophy, Parkinson's disease, Lewy body dementia asthma, allergic rhinovirus exacerbated asthma, cystic fibrosis and idiopathic pulmonary fibrosis… For example, NETs can cause autoantigen exposure to the extracellular space and the subsequent production of pathological autoantibodies by the subject. Furthermore, NETs and NET remnants harbor toxic histones, which induce vascular damage and subsequent organ damage and failure. Thus, in such diseases, interfering with NET formation, and inducing clearance of NETs and NET remnants from circulation and tissues, would have therapeutic benefits… Neutrophils are also increasingly being recognized as an important element in tumour progression. They have been shown to exert important effects at nearly every stage of tumour progression with a number of studies demonstrating that their presence is critical to tumour development. Studies have also implicated NETs as facilitators of tumour progression and metastasis. It has also been shown that neutrophils, through the generation of NETs, provide a scaffold and a stimulus for platelet adhesion, thrombus formation and coagulation in tumours… In addition, NETs have been implicated in reducing organ health after transplant. NETs contribute to primary graft dysfunction, contributing to early mortality after lung transplantation. It has been shown that NETs play a pathogenic role in solid organ transplantation… Thus, identifying therapeutic agents that could block NET formation, clear NETs, and/or prevent NETosis would have clinical benefit in inflammatory diseases such as inflammatory arthritis, rheumatoid arthritis and osteoarthritis, and other NET-associated pathologies such as systemic lupus erythematosus (SLE), lupus, sepsis, vasculitis, psoriasis, Alzheimer’s disease… The present inventors have created improved antibodies that bind to citrullinated epitopes on the amino terminus of histones 2A and/or histone 4. These antibodies can be used to treat diseases or pathologies associated with citrullination, such as NET-associated pathologies and inflammatory conditions (emphasis added).” See p. 1-4.
At p. 21, Raats et al. teach antibodies that bind to citrullinated epitopes on the amino terminus of histones 2A and/or histone 4 comprising the heavy chain variable region (VH) of SEQ ID NO: 11 (100% sequence homology with the instant SEQ ID NO: 11) and the light chain variable region (VL) of SEQ ID NO: 16 (100% sequence homology with the instant SEQ ID NO: 16). SEQ ID NO: 11 of Raats et al. comprises the CDRs 1-3 of SEQ ID NO(s): 1-3, respectively, which share 100% sequence homology with the instant SEQ ID NO(s): 1-3, respectively. SEQ ID NO: 16 of Raats et al. comprises the CDRs 1-3 of SEQ ID NO(s): 9, 4, and 5, respectively, which share 100% sequence homology with the instant SEQ ID NO(s): 9, 4, and 5, respectively.
At p. 1, Raats et al. teach that antibodies of the invention may be used to treat COPD and allergic asthma, and these diseases meet the limitations of a) diseases that include an eosinophil extracellular trap (EET)-associated pathology and b) eosinophilic diseases, as evidenced by Mukherjee et al. At p. 5 and at Table 1, Mukherjee et al. teach that EETs have been reported in several inflammatory disease tissues obtained by biopsy, including COPD and allergic asthma.
Based upon the teachings of Raats et al., one of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to administer the antibody of Raats et al., which meets the limitations of the antibody of claim 1, to COPD and allergic asthma patients, because there would have been a reasonable expectation that such a method would provide a therapeutic benefit to said patients. Furthermore since the method of Raats et al. comprises all of the active steps of the method of claim 1, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs. Also as indicated above, COPD and allergic asthma meet the limitations of a) diseases that include an eosinophil extracellular trap (EET)-associated pathology and b) eosinophilic diseases, as evidenced by Mukherjee et al., and as such the invention of Raats et al. meets the limitations of claims 1-6, 10, and 12.
With respect to claim 8, it is initially noted that the phrase “wherein the antibody or binding fragment thereof is for the ex vivo inhibition or detection of EET formation in a sample,” does not comprise any active steps. Furthermore at p. 1, Raats et al. teach that antibodies of the invention may be used to treat transplant organs ex vivo, which would involve administering the antibody of the invention to an organ under conditions suitable for binding.
With respect to claim 14, at p. 16, Raats et al. teach various antibody binding fragments, including Fabs, scFv fragments, diabodies, and triabodies.
With respect to claim 15, at p. 17, Raats et al. teach various antibody Fc region isotypes, including IgG1, IgG2, IGG3, and IgG4.
With respect to claim 16, at claim 17, Raats et al. teach that antibodies of the invention may comprise the heavy chain constant region of SEQ ID NO: 23, which shares 100% sequence homology with the instant SEQ ID NO: 23, and the light chain constant region of SEQ ID NO: 24, which shares 100% sequence homology with the instant SEQ ID NO: 24.
With respect to claim 17, since the method of Raats et al. comprises all of the active steps of the method of claims 1 and 17, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs and neutrophil extracellular traps (NETs).
With respect to claims 18 and 19, at p. 37 and 38, Raats et al. teach that antibodies of the invention may be used to treat inflammatory conditions, such as COPD and asthma, both of which are lung conditions.
With respect to claim 20, at p. 1065, Quint et al. teach that “[n]eutrophilic inflammation occurs in healthy lungs but is increased in many acute and chronic lung diseases, in particular acute bronchitis, adult respiratory distress syndrome, COPD, and severe asthma.” Furthermore at p. 1066, Quint et al. teach that “[t]here are increased numbers of neutrophils and CD8+ T lymphocytes infiltrating the smooth muscle in the peripheral airways of patients with COPD compared with smokers and nonsmoking controls.”
With respect to claim 24, at p. 31, Raats et al. teach that antibodies of the invention may be linked to another moiety.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art, as evidenced by Raats et al.
Claims 21 and 22 are rejected under 35 U.S.C. 103 as being unpatentable over Raats et al. (WO 2020/038963, international publication date: 02/27/2020, IDS), as evidenced by Mukherjee et al. (Frontiers in Immunology, 9: 1-10, 2018, IDS) and Quint et al. (J Allergy Clinical Immunol, 119(5): 1065-1071, 2017), as applied to claims 1-6, 8, 10, 12, 14-20, and 24, and further in view of Barnes et al. (The Lancet, 363: 731-733, 2004).
The teachings of Raats et al. are detailed above.
Based upon the teachings of Raats et al., one of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to administer the antibody of Raats et al., which meets the limitations of the antibody of claim 1, to COPD and allergic asthma patients, because there would have been a reasonable expectation that such a method would provide a therapeutic benefit to said patients. Furthermore since the method of Raats et al. comprises all of the active steps of the method of claim 1, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs. Also as indicated above, COPD and allergic asthma meet the limitations of a) diseases that include an eosinophil extracellular trap (EET)-associated pathology and b) eosinophilic diseases, as evidenced by Mukherjee et al., and as such the invention of Raats et al. meets the limitations of claims 1-6, 10, and 12.
With respect to claims 18 and 19, at p. 37 and 38, Raats et al. teach that antibodies of the invention may be used to treat inflammatory conditions, such as COPD and asthma, both of which are lung conditions. Raats et al. does not teach or suggest administering a corticosteroid to subjects suffering from a lung condition, such as asthma, nor do Raats et al. teach lung disorders that are not responsive to corticosteroids; however these deficiencies are remedied by Barnes et al.
At the Abstract, Barnes et al. teach that “[b]y contrast with patients with asthma, those with chronic obstructive pulmonary disease (COPD) are poorly responsive to the anti-inflammatory actions of corticosteroids, and these drugs provide little clinical benefit. In both diseases, multiple inflammatory genes are activated, which results from acetylation of core histones around which DNA is wound. This acetylation opens up the chromatin structure allowing gene transcription and synthesis of inflammatory proteins to proceed. Corticosteroids recruit histone deacetylase 2 (HDAC2) to the actively transcribing gene, which reverses this process and switches off inflammatory gene transcription. We propose that in patients with COPD, HDAC2 function is impaired by cigarette smoking and oxidative stress, leading to a pronounced reduction in responsiveness to corticosteroids.”
Based upon these teachings, one of ordinary skill in the art would have been motivated to modify the method of Raats et al. to comprise the administration of corticosteroids to asthma patients, because there would have been a reasonable expectation that the resultant method is effective in treating asthma. Furthermore based upon the teachings of Barnes et al., one of ordinary skill in the art would appreciate that COPD is poorly responsive to corticosteroids. The invention of Raats et al. and Barnes et al. meets the limitations of claims 21 and 22.
Therefore the invention as a whole was prima facie obvious to one of ordinary skill in the art, as evidenced by the references.
Nonstatutory 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 1-6, 8, 10, 12, 14-20, and 24 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 and 8-14 of U.S. Patent No. 11,345,750 in view of Raats et al. (WO 2020/038963, international publication date: 02/27/2020, IDS), as evidenced by Mukherjee et al. (Frontiers in Immunology, 9: 1-10, 2018, IDS) and Quint et al. (J Allergy Clinical Immunol, 119(5): 1065-1071, 2017).
Both the instant and the conflicting claims recite an antibody that binds to citrullinated epitopes on the amino terminus of histones 2A and/or histone 4 comprising the heavy chain variable region (VH) of SEQ ID NO: 11 (100% sequence homology with the instant SEQ ID NO: 11) and the light chain variable region (VL) of SEQ ID NO: 16 (100% sequence homology with the instant SEQ ID NO: 16). SEQ ID NO: 11 of Raats et al. comprises the CDRs 1-3 of SEQ ID NO(s): 1-3, respectively, which share 100% sequence homology with the instant SEQ ID NO(s): 1-3, respectively. SEQ ID NO: 16 of Raats et al. comprises the CDRs 1-3 of SEQ ID NO(s): 9, 4, and 5, respectively, which share 100% sequence homology with the instant SEQ ID NO(s): 9, 4, and 5, respectively.
The teachings of Raats et al., Mukherjee et al., and Quint et al. are detailed above. Based upon the teachings of Raats et al., one of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to administer the antibody of the conflicting claims, which meets the limitations of the antibody of claim 1, to COPD and allergic asthma patients, because there would have been a reasonable expectation that such a method would provide a therapeutic benefit to said patients. Furthermore since the method of the conflicting claims and Raats et al. comprises all of the active steps of the method of claim 1, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs. Also as indicated above, COPD and allergic asthma meet the limitations of a) diseases that include an eosinophil extracellular trap (EET)-associated pathology and b) eosinophilic diseases, as evidenced by Mukherjee et al., and as such the invention of the conflicting claims and Raats et al. meets the limitations of claims 1-6, 10, and 12.
With respect to claim 8, it is initially noted that the phrase “wherein the antibody or binding fragment thereof is for the ex vivo inhibition or detection of EET formation in a sample,” does not comprise any active steps. Furthermore at p. 1, Raats et al. teach that antibodies of the invention may be used to treat transplant organs ex vivo, which would involve administering the antibody of the invention to an organ under conditions suitable for binding.
With respect to claim 14, at p. 16, Raats et al. teach various antibody binding fragments, including Fabs, scFv fragments, diabodies, and triabodies.
With respect to claim 15, at p. 17, Raats et al. teach various antibody Fc region isotypes, including IgG1, IgG2, IGG3, and IgG4.
With respect to claim 16, at claim 17, Raats et al. teach that antibodies of the invention may comprise the heavy chain constant region of SEQ ID NO: 23, which shares 100% sequence homology with the instant SEQ ID NO: 23, and the light chain constant region of SEQ ID NO: 24, which shares 100% sequence homology with the instant SEQ ID NO: 24.
With respect to claim 17, since the method of Raats et al. comprises all of the active steps of the method of claims 1 and 17, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs and neutrophil extracellular traps (NETs).
With respect to claims 18 and 19, at p. 37 and 38, Raats et al. teach that antibodies of the invention may be used to treat inflammatory conditions, such as COPD and asthma, both of which are lung conditions.
With respect to claim 20, at p. 1065, Quint et al. teach that “[n]eutrophilic inflammation occurs in healthy lungs but is increased in many acute and chronic lung diseases, in particular acute bronchitis, adult respiratory distress syndrome, COPD, and severe asthma.” Furthermore at p. 1066, Quint et al. teach that “[t]here are increased numbers of neutrophils and CD81 T lymphocytes infiltrating the smooth muscle in the peripheral airways of patients with COPD compared with smokers and nonsmoking controls.”
With respect to claim 24, at p. 31, Raats et al. teach that antibodies of the invention may be linked to another moiety.
Therefore the invention as a whole was prima facie obvious over the conflicting claims in view of the references cited.
Claims 21 and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 and 8-14 of U.S. Patent No. 11,345,750 in view of Raats et al. (WO 2020/038963, international publication date: 02/27/2020, IDS), as evidenced by Mukherjee et al. (Frontiers in Immunology, 9: 1-10, 2018) and Quint et al. (J Allergy Clinical Immunol, 119(5): 1065-1071, 2017, IDS), as applied to claims 1-6, 8, 10, 12, 14-20, and 24, and further in view of Barnes et al. (The Lancet, 363: 731-733, 2004).
The teachings of Raats et al., Mukherjee et al., Quint et al., and Barnes et al. are detailed above. Based upon the teachings of Raats et al., one of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to administer the antibody of the conflicting claims, which meets the limitations of the antibody of claim 1, to COPD and allergic asthma patients, because there would have been a reasonable expectation that such a method would provide a therapeutic benefit to said patients. Furthermore since the method of the conflicting claims and Raats et al. comprises all of the active steps of the method of claim 1, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs. Also as indicated above, COPD and allergic asthma meet the limitations of a) diseases that include an eosinophil extracellular trap (EET)-associated pathology and b) eosinophilic diseases, as evidenced by Mukherjee et al., and as such the invention of the conflicting claims and Raats et al. meets the limitations of claims 1-6, 10, and 12.
With respect to claims 18 and 19, at p. 37 and 38, Raats et al. teach that antibodies of the invention may be used to treat inflammatory conditions, such as COPD and asthma, both of which are lung conditions.
Based upon the teachings of Barnes et al., one of ordinary skill in the art would have been motivated to modify the method of the conflicting claims and Raats et al. to comprise the administration of corticosteroids to asthma patients, because there would have been a reasonable expectation that the resultant method is effective in treating asthma. Furthermore based upon the teachings of Barnes et al., one of ordinary skill in the art would appreciate that COPD is poorly responsive to corticosteroids. The invention of the conflicting claims, Raats et al., and Barnes et al. meets the limitations of claims 21 and 22.
Therefore the invention as a whole was prima facie obvious over the conflicting claims in view of the references cited.
Claims 1-6, 8, 10, 12, 14-20, and 24 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 12,590,143 in view of Raats et al. (WO 2020/038963, international publication date: 02/27/2020, IDS), as evidenced by Mukherjee et al. (Frontiers in Immunology, 9: 1-10, 2018, IDS) and Quint et al. (J Allergy Clinical Immunol, 119(5): 1065-1071, 2017).
Both the instant and the conflicting claims recite an antibody that binds to citrullinated epitopes on the amino terminus of histones 2A and/or histone 4 comprising the heavy chain variable region (VH) of SEQ ID NO: 11 (100% sequence homology with the instant SEQ ID NO: 11) and the light chain variable region (VL) of SEQ ID NO: 16 (100% sequence homology with the instant SEQ ID NO: 16). SEQ ID NO: 11 of Raats et al. comprises the CDRs 1-3 of SEQ ID NO(s): 1-3, respectively, which share 100% sequence homology with the instant SEQ ID NO(s): 1-3, respectively. SEQ ID NO: 16 of Raats et al. comprises the CDRs 1-3 of SEQ ID NO(s): 9, 4, and 5, respectively, which share 100% sequence homology with the instant SEQ ID NO(s): 9, 4, and 5, respectively.
The teachings of Raats et al., Mukherjee et al., and Quint et al. are detailed above. Based upon the teachings of Raats et al., one of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to administer the antibody of the conflicting claims, which meets the limitations of the antibody of claim 1, to COPD and allergic asthma patients, because there would have been a reasonable expectation that such a method would provide a therapeutic benefit to said patients. Furthermore since the method of the conflicting claims and Raats et al. comprises all of the active steps of the method of claim 1, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs. Also as indicated above, COPD and allergic asthma meet the limitations of a) diseases that include an eosinophil extracellular trap (EET)-associated pathology and b) eosinophilic diseases, as evidenced by Mukherjee et al., and as such the invention of the conflicting claims and Raats et al. meets the limitations of claims 1-6, 10, and 12.
With respect to claim 8, it is initially noted that the phrase “wherein the antibody or binding fragment thereof is for the ex vivo inhibition or detection of EET formation in a sample,” does not comprise any active steps. Furthermore at p. 1, Raats et al. teach that antibodies of the invention may be used to treat transplant organs ex vivo, which would involve administering the antibody of the invention to an organ under conditions suitable for binding.
With respect to claim 14, at p. 16, Raats et al. teach various antibody binding fragments, including Fabs, scFv fragments, diabodies, and triabodies.
With respect to claim 15, at p. 17, Raats et al. teach various antibody Fc region isotypes, including IgG1, IgG2, IGG3, and IgG4.
With respect to claim 16, at claim 17, Raats et al. teach that antibodies of the invention may comprise the heavy chain constant region of SEQ ID NO: 23, which shares 100% sequence homology with the instant SEQ ID NO: 23, and the light chain constant region of SEQ ID NO: 24, which shares 100% sequence homology with the instant SEQ ID NO: 24.
With respect to claim 17, since the method of Raats et al. comprises all of the active steps of the method of claims 1 and 17, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs and neutrophil extracellular traps (NETs).
With respect to claims 18 and 19, at p. 37 and 38, Raats et al. teach that antibodies of the invention may be used to treat inflammatory conditions, such as COPD and asthma, both of which are lung conditions.
With respect to claim 20, at p. 1065, Quint et al. teach that “[n]eutrophilic inflammation occurs in healthy lungs but is increased in many acute and chronic lung diseases, in particular acute bronchitis, adult respiratory distress syndrome, COPD, and severe asthma.” Furthermore at p. 1066, Quint et al. teach that “[t]here are increased numbers of neutrophils and CD81 T lymphocytes infiltrating the smooth muscle in the peripheral airways of patients with COPD compared with smokers and nonsmoking controls.”
With respect to claim 24, at p. 31, Raats et al. teach that antibodies of the invention may be linked to another moiety.
Therefore the invention as a whole was prima facie obvious over the conflicting claims in view of the references cited.
Claims 21 and 22 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 12,590,143 in view of Raats et al. (WO 2020/038963, international publication date: 02/27/2020, IDS), as evidenced by Mukherjee et al. (Frontiers in Immunology, 9: 1-10, 2018) and Quint et al. (J Allergy Clinical Immunol, 119(5): 1065-1071, 2017, IDS), as applied to claims 1-6, 8, 10, 12, 14-20, and 24, and further in view of Barnes et al. (The Lancet, 363: 731-733, 2004).
The teachings of Raats et al., Mukherjee et al., Quint et al., and Barnes et al. are detailed above. Based upon the teachings of Raats et al., one of ordinary skill in the art would have been motivated with a reasonable expectation of success at the effective filing date of the invention to administer the antibody of the conflicting claims, which meets the limitations of the antibody of claim 1, to COPD and allergic asthma patients, because there would have been a reasonable expectation that such a method would provide a therapeutic benefit to said patients. Furthermore since the method of the conflicting claims and Raats et al. comprises all of the active steps of the method of claim 1, both methods would be expected to exhibit the same functional characteristics, such as inhibiting the formation of EETs. Also as indicated above, COPD and allergic asthma meet the limitations of a) diseases that include an eosinophil extracellular trap (EET)-associated pathology and b) eosinophilic diseases, as evidenced by Mukherjee et al., and as such the invention of the conflicting claims and Raats et al. meets the limitations of claims 1-6, 10, and 12.
With respect to claims 18 and 19, at p. 37 and 38, Raats et al. teach that antibodies of the invention may be used to treat inflammatory conditions, such as COPD and asthma, both of which are lung conditions.
Based upon the teachings of Barnes et al., one of ordinary skill in the art would have been motivated to modify the method of the conflicting claims and Raats et al. to comprise the administration of corticosteroids to asthma patients, because there would have been a reasonable expectation that the resultant method is effective in treating asthma. Furthermore based upon the teachings of Barnes et al., one of ordinary skill in the art would appreciate that COPD is poorly responsive to corticosteroids. The invention of the conflicting claims, Raats et al., and Barnes et al. meets the limitations of claims 21 and 22.
Therefore the invention as a whole was prima facie obvious over the conflicting claims in view of the references cited.
Conclusion
No claims are allowed.
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/NELSON B MOSELEY II/Primary Examiner, Art Unit 1642
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