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
The preliminary amendment filed February 26, 2025 has been received and entered.
Claims 3-4 and 7 have been amended.
Claims 1-7 are pending and under consideration.
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. This application is a 371 of PCT/US2022/077630 filed October 5, 2022, which claims the benefit of U.S. Provisional Application No. 63/252,601 filed October 5, 2021.
Information Disclosure Statements
The information disclosure statements (IDSs) submitted on February 26, 2025 and March 6, 2026 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
Specification
The disclosure is objected to because of the following informalities:
The numbering of the paragraphs using indented numerals as the first item in each paragraph.
37 CFR 1.52(b)(6) states, other than in a reissue application or reexamination or supplemental examination proceeding, the paragraphs of the specification, other than in the claims or abstract, may be numbered at the time the application is filed, and should be individually and consecutively numbered using Arabic numerals, so as to unambiguously identify each paragraph. The number should consist of at least four numerals enclosed in square brackets, including leading zeros (e.g., [0001]). The numbers and enclosing brackets should appear to the right of the left margin as the first item in each paragraph, before the first word of the paragraph, and should be highlighted in bold. A gap, equivalent to approximately four spaces, should follow the number. See MPEP 608.01(I).
The heavy and light chain variable domain CDRs are recited as “CDR1, CDR2, and CDR2” throughout the specification, with CDR2 appearing twice.
Claim Objections
Claims 1, 3, 5, and 7 are objected to because of the following informalities:
Claims 1, 3, and 5 are drawn to the CDRs of the heavy or light chain variable regions. However, the claims recite “CDR1, CDR2, and CDR2”, instead of “CDR1, CDR2, and CDR3”.
Claim 7 (line 5) - recites “the IL-25 binding molecules”, however, should recite “the anti-IL25 binding molecules”.
Appropriate correction is required.
Claim Rejections - 35 USC § 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.
Claims 2-4 and 7 are rejected under 35 U.S.C. 112(b) as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor regards as the invention.
Claim 1 recites an isolated anti-IL25 binding molecule comprising a heavy chain variable domain comprising a CDR1, CDR2, and CDR3 as set forth in SEQ ID NO: 1, SEQ ID NO: 2, and SEQ ID NO: 3, respectively.
Claim 2 recites, “the isolated anti-IL25 binding molecule of claim 1, comprising a heavy chain variable domain comprising the sequence as set forth in SEQ ID NO: 4 or SEQ ID NO: 12.
However, the amino acid sequences for all three CDRs do no appear in either SEQ ID NO: 4 or SEQ ID NO: 12 as would be expected.
Specifically, sequence alignment of the heavy chain variable domain amino acid sequence of SEQ ID NO: 4 with the amino acid sequences of CDR1 (SEQ ID NO: 1), CDR2 (SEQ ID NO: 2), and CDR3 (SEQ ID NO: 3), shows that the recited amino acid sequences of CDR1 and CDR3 differ from the amino acid sequence of SEQ ID NO: 4 by one amino acid. An amino acid sequence 100% identical to that of CDR2 (SEQ ID NO: 2) is present in the amino acid sequence of SEQ ID NO: 4.
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Sequence alignment of the heavy chain variable domain amino acid sequence of SEQ ID NO: 12 with the amino acid sequences of CDR1 (SEQ ID NO: 1), CDR2 (SEQ ID NO: 2), and CDR3 (SEQ ID NO: 3), shows that the recited amino acid sequence of CDR2 differs from the amino acid sequence of SEQ ID NO: 4 by one amino acid. Amino acid sequences 100% identical to that of CDR1 (SEQ ID NO: 1) and CDR2 (SEQ ID NO: 2) are present in the amino acid sequence of SEQ ID NO: 12.
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This is in contrast to claim 3, which recites the CDRs of the anti-IL25 light chain variable domain. In this case, the recited sequences for CDR1 (SEQ ID NO: 5), CDR2 (SEQ ID NO: 6), and CDR3 (SEQ ID NO: 7) have 100% identity to the amino acid sequences found in both light chain variable domain amino acid sequences of SEQ ID NO: 8 and SEQ ID NO: 13.
As such, one of ordinary skill in the art would not be able to discern the anti-IL25 heavy chain variable domain CDRs when all three CDRs recited in claim 1 are not present in the recited full length heavy chain variable domains.
Claims 3-4 and 7 are included in the rejection because they depend from and otherwise require all the limitations of the rejected claim
Claim 7 is drawn to administering “a therapeutically effective amount of any of the anti-IL25 binding molecules of claim 1”. However, claim 1 is drawn to a single anti-IL25 binding molecule. Therefore, there is no antecedent basis for more than one anti-IL25 binding molecule.
Claim Rejections - 35 USC § 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.
WRITTEN DESCRIPTION
Claims 1-2 and 5-7 are rejected under 35 U.S.C. 112(a), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, at the time the application was filed, had possession of the claimed invention.
The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus. See MPEP § 2163.
Claims 1-2 and 5-6 are drawn to an isolated anti-IL25 binding molecule. However, the claims define the binding molecule (i.e., antibody) by the heavy chain variable domain or the light chain.
Claim 1 discloses heavy chain variable domain CDR amino acid sequences SEQ ID NOs: 1, 2, and 3.
Claim 2 discloses heavy chain variable domain amino acid sequences SEQ ID NO: 4 or 12.
Claim 5 discloses light chain variable domain CDR amino acid sequences SEQ ID NOs: 5, 6, and 7.
Claim 6 discloses light chain variable domain amino acid sequences SEQ ID NO: 8 or 13.
Therefore, claims 1 and 2 are drawn to an anti-IL25 binding molecule heavy chain variable domain paired with any light chain variable domain, while claims 5 and 6 are drawn to an anti-IL25 binding molecule light chain variable domain paired with any heavy chain variable domain.
However, none of the claims provide all 6 CDRs for the recited anti-IL25 binding molecule.
Therefore, it can be considered that the claims encompass a large genus of binding molecules that bind to IL25, comprised of different combinations of heavy and light chain amino acid sequences, respectively, which represent structurally distinct polypeptides. The state of the art is such that antibody variable regions are composed of a heavy and light chain, each involved in providing for binding specificity. Variability in the antigen binding site is achieved by V(D)J recombination via heavy and light chain pairing, with the most diverse regions being the 6 CDR regions in the heavy and light chain. As taught by Janeway et al. (2001), the antibody repertoire in humans is at least 1011, with a large degree of diversity in both heavy and light chains. See also Rabia et al. (2018; pg. 4), which teaches that the maximal chemical diversity of antibody CDRs is unimaginably large and is extremely challenging to define the sequence determinant of antibody specificity.
The specification teaches that anti-IL25 binding molecules are a potential therapeutic for treating diseases associated with inflammation, such as asthma and IBS [pg. 1, lines 21-22]. To this end, Applicant developed four monoclonal antibodies against IL-25. Figure 3 shows a HT-29 cellular potency assay of monoclonal antibodies ABM109, ABM122, ABM124, and ABM125 (renamed, LNR109, LNR122, LNR124, and LNR125, respectively) against IL-25. Only two of the antibodies (ABM109 and ABM125) demonstrated the ability to neutralize IL-25 activity in a dose-dependent manner. ABM125 was selected for further development, including humanization. However, the amino acid sequences that correspond to the tested antibodies are not identified.
As presently written, however, the claims do not recite the amino acid sequences of all 6 CDRs that can bind to IL-25. While Applicant has provided examples of four anti-IL25 monoclonal antibodies and twelve humanized variants of ABM125 (see Table 5, pg. 40), such disclosure does not adequately represent the structural diversity of antibodies that bind to IL-25 and possess the functional properties recited in the instant claims.
It is well established in the art that the formation of an intact antigen-binding site generally requires the association of the complete heavy and light chain variable regions of a given antibody, each of which consists of three complementarity determining regions (CDRs) which provide the majority of the contact residues for the binding of the antibody to its target epitope. Sela-Culang et al. (Fron lmmunol, 2013; 4:302) teaches six CDRs are widely assumed to be responsible for antigen recognition lie within each variable domain. The amino acid sequences and conformations of each of the heavy and light chain CDRs are critical in maintaining the antigen binding specificity and affinity which is characteristic of the parent immunoglobulin [Abstract, pg. 1].
Based on the state of the art, a full antibody binding site comprising six hypervariable loops (CDRs) within the VH and VL domains (with three CDRs on the heavy chain and three CDRs on the light chain), are required for IL-25 antigen binding. While the CDRs of the claimed invention are intended to bind IL-25 for the treatment of various inflammatory and respiratory diseases, artisans would not be able to envision the other CDR sequences or other variable domain based on recitation of three VH CDR sequences or three VL CDR sequences that would bind and inhibit IL-25.
Indeed, recent court decisions including AbbVie Deutschland GmbH v. Janssen Biotech. Inc. 759 F.3d 1285 (Fed. Cir. 2014) and Amgen v. Sanofi, (Fed Cir, 2017-1480. 10/5/2017) have clearly indicated that identification of the antigen or epitope to which an antibody binds is insufficient to provide adequate written description for antibodies binding said antigen or epitope. Additionally, when claiming a broad genus of antibodies, the accompanying specification should include a description of diverse species across the scope of genus. As illustrated by the AbbVie decision, a description of even 300 representative species may not be sufficient to satisfy the written description requirement if all 300 representative species are structurally and functionally similar.
Therefore, the claimed genus of anti-IL25 binding molecules lacks adequate written description because the claims fail to recite all six CDRs for the instantly claimed anti-IL25 binding molecule. Thus, one of ordinary skill in the art would reasonably conclude that the applicant was not in possession of the full breadth of the claimed genus of anti-IL25 binding molecules at the time the instant application was filed.
Claim 7 is included in the rejection as it depends from claim 1 and requires all the limitations of the rejected claim.
ENABLEMENT
Claim 7 is rejected under 35 U.S.C. 112(a), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
Claim 1 is rejected under 35 U.S.C. 112(a), first paragraph, because the specification, while being enabling for a method of treating a rhinoviral infection, coronavirus infection, airway inflammation, and asthma in a subject comprising administering to the subject a therapeutically effective amount of the instantly claimed anti-IL-25 binding molecule; does not reasonably provide enablement for treating rheumatoid arthritis, osteoarthritis, bone erosion, intraperitoneal abscesses and adhesions, inflammatory bowel disorder, allograft rejection, psoriasis, cancer, angiogenesis, atherosclerosis, cystic fibrosis or multiple sclerosis.
The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
As a general rule, enablement must be commensurate with the scope of claim language. MPEP § 2164.08 states, “The Federal Circuit has repeatedly held that “the specification must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation.” In re Wright, 999 F.2d 1557, 1561, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993)” (emphasis added). The “make and use the full scope of the invention without undue experimentation” language was repeated in 2005 in Warner-Lambert Co. v. Teva Pharmaceuticals USA Inc., 75 USPQ2d 1865, and Scripps Research Institute v. Nemerson, 78 USPQ2d 1019 asserts: “A lack of enablement for the full scope of a claim, however, is a legitimate rejection.” The principle was explicitly affirmed in Auto. Tech. Int’l, Inc. v. BMW of N. Am., Inc., 501 F.3d 1274, 84 USPQ2d 1108 (Fed. Cir. 2007), Monsanto Co. v. Syngenta Seeds, Inc., 503 F.3d 1352, 84 U.S.P.Q.2d 1705 (Fed. Cir. 2007), and Sitrick v. Dreamworks, LLC, 516 F.3d 993, 85 USPQ2d 1826 (Fed. Cir. 2008). See also In re Cortright, 49 USPQ2d 1464, 1466 and Bristol-Myers Squibb Co. v. Rhone-Poulenc Rorer Inc., 49 USPQ2d 1370.
The factors to be considered in determining whether a disclosure meets the enablement requirement of 35 U.S.C. 112, first paragraph, have been described in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988). Among these factors are: (1) the nature or the invention; (2) the state of the prior art; (3) the relative skill of those in the art; (4) the predictability or unpredictability of the art; (5) the breadth of the claims; (6) the amount of direction or guidance presented; (7) the presence or absence of working examples; and (8) the quantity of experimentation necessary. When the above factors are weighed, it is the examiner’s position that one skilled in the art could not practice the invention without undue experimentation. Some experimentation is not fatal; the issue is whether the amount of experimentation is “undue”; see In re Vaeck, 20 USPQ2d 1438, 1444.
(1) The nature of the invention and (5) The breadth of the claims:
Claim 7 is drawn to a method of treating a rhinoviral infection, coronavirus infection, airway inflammation, rheumatoid arthritis, asthma, osteoarthritis, bone erosion, intraperitoneal abscesses and adhesions, inflammatory bowel disorder, allograft rejection, psoriasis, cancer, angiogenesis, atherosclerosis, cystic fibrosis and multiple sclerosis in a subject comprising administering to the subject a therapeutically effective amount of the instantly claimed anti-IL-25 binding molecule.
The claims are broad and inclusive of numerous diseases. The breadth of the claim exacerbates the complex nature of the subject matter to which the present claims are directed. The claims are extremely broad due to the vast number of recited diseases, including cancer. However, cancer is not a single disease, or cluster of closely related disorders. There are hundreds of cancers, which have in common only some loss of controlled cell growth. Cancers are highly heterogeneous at both the molecular and clinical level, and can occur in most parts of the body. The following are examples of some of the major classes of cancer, each having numerous subclasses:
A. CNS cancers
B. Leukemias
C. Carcinomas of the liver
D. Lung and pleural cancers
E. Thyroid cancers
F. Melanomas
G. Colorectal cancers
H. Renal carcinomas
I. Prostate cancers
J. Breast cancers
K. Ovarian and uterine cancers
L. Testicular cancers
M. Esophageal cancers
N. Cervical cancers
O. Cardiothoracic cancers
P. Bladder cancers
(2) The state of the prior art and (4) The predictability or unpredictability of the art:
The current state of the art teaches that anti-IL25 immunotherapy is complex. For example, Liu et al. (J Immunol Res, 2018; 2018:6519465) teaches IL-25 can induce and enhance Th2-type immune responses and plays an important role in some allergic diseases. However, how IL-25 regulates the Th2 immune response is not fully understood. Some studies have suggested that IL-25 enhances the expression of Th2-type cytokines and induces Th2-type immune responses. In addition to promoting Th2-type immune responses, IL-25 can also inhibit the immune responses mediated by Th1/Th17 [Section 5].
Regarding rheumatoid arthritis, Liu et al. (Sci Rep, 2016; 6:36002) discloses current treatments for rheumatoid arthritis (RA) involve inhibition of IL-6 and/or TNFa and teaches away from treatment with an anti-IL-25 inhibitor. IL-25 acts as an anti-inflammatory regulator that helps suppress the disease progression of arthritis by downregulating harmful Th17 cell responses and reducing bone and cartilage [Abstract, Discussion]. Schett (Nat Rev Rheumatol, 2012; 8(11):656–664) teaches that bone erosion is a central feature of RA that results from excessive local bone resorption and inadequate bone formation. The main triggers of articular bone erosion are synovitis, including the production of proinflammatory cytokines [Abstract].
Regarding inflammatory bowel disease (IBD), Liu et al. (J Immunol Res, 2018; 2018:6519465) teaches the etiology and pathogenesis of IBD are not completely clear, and recent studies suggest that IBD is caused by the interaction of several factors, including Th1/Th17-type reaction mediated by IL-12/23. However, studies have shown a dual role for IL-25 in IBD, with IL-25 promoting cell accumulation and cytokine production in type-2 driven colitis (Camelo et al., J Gastroenterol, 2012; 47(11):1198–1211), while other studies show that IL-25 helps suppress the aggressive Th1 and Th17 immune responses associated with IBD (Su et al., Inflamm Bowel Dis, 2013; 19(4):720-82013).
Regarding cancer, Shabgah et al. (Cancer Med, 2021; 10(15):5191–5202) teaches IL‐25 exerts a paradoxical role in cancer, including tumor supportive and tumor suppressive activities. IL‐25 exerts a tumor‐suppressive role through inducing infiltration of eosinophils and B cells into the tumor microenvironment and activating the apoptotic pathways. In contrast, the tumor‐supportive function has been implemented by activating inflammatory cascades, promoting cell cycle, and inducing type‐2 immune responses [Abstract].
Regarding atherosclerosis, Mantani et al. (PLoS One, 2015; 10(1):e0117255) teaches that IL-25 inhibits atherosclerosis [Title], which teaches away from inhibiting IL-25 as a course of treatment.
The state of the art is silent in regard to treatment of allograft rejection, psoriasis, cystic fibrosis, and multiple sclerosis.
Given the lack of predictability in treating diseases with an anti-IL25 binding molecule (i.e., antibody), one of ordinary skill in the art would have to engage in undue experimentation to identify subjects to which the instant method would apply.
6) the amount of direction or guidance provided by the inventor; 7) the existence of working examples;
The instant specification sets forth in vitro and in vivo examples with a single humanized anti-IL25 antibody (LNR125) that blocks type-2 immune and inflammatory responses. The specification discloses that airway epithelial cells are the primary site of respiratory viral infection and are critical to initiating anti-viral immunity. In the lungs, bronchial epithelial cells (BECs) induce an antiviral response through the production of type I interferon-b (IFN-b) and type III IFN-l which in turn induce expression of IFN-stimulated genes (ISGs) that directly interfere with viral replication, enhance viral antigen presentation, and activate the adaptive immunity. Deficient/delayed type I and type III IFN production by RV-infected BECs from patients with asthma contributes to enhanced airway inflammation and bronchoconstriction and more severe disease [0116].
LNR125 was tested in in vitro and in vivo models of viral infection in asthma, wherein LNR125 upregulated rhinovirus- and coronavirus-induced differentiated BECs from donors with asthma. Further, LNR125 IL-25 blockade enhanced ISG expression and down-regulated type-2 immune genes. Exogenous IL-25 protein treatment inhibited innate anti- viral immunity in RV-infected differentiated human BECs. Additionally, an established mouse model was used to determine effect of a single subcutaneous treatment with LNR125 on anti-viral immunity during RV-exacerbation of allergic airways disease. In additional to suppressing inflammation, antibody-mediated IL-25 blockade increased IFN-p expression in airways and reduced lung viral load [0116].
However, there are no examples wherein the anti-IL25 antibody was used to treat any other disease, including rheumatoid arthritis, osteoarthritis, bone erosion, intraperitoneal abscesses and adhesions, inflammatory bowel disorder, allograft rejection, psoriasis, cancer, angiogenesis, atherosclerosis, cystic fibrosis or multiple sclerosis as recited in the instant claims. Therefore, the only embodiment that is enabled is treating a rhinoviral infection, coronavirus infection, airway inflammation, and asthma in a subject comprising administering to the subject a therapeutically effective amount of the instantly claimed anti-IL25 binding molecule. One of skill in the art would be required to engage in extensive, difficult experimentation to identify the patient population that would benefit from said anti-IL25 blockade, which is known to be challenging as indicated above. This required experimentation is undue.
In conclusion, the claimed invention does not provide enablement for treating rheumatoid arthritis, osteoarthritis, bone erosion, intraperitoneal abscesses and adhesions, inflammatory bowel disorder, allograft rejection, psoriasis, cancer, angiogenesis, atherosclerosis, cystic fibrosis or multiple sclerosis with the instantly claimed anti-IL25 binding molecule. Thus for the reasons outlined above, the specification is not considered to be enabling for one skilled in the art to make and use the claimed invention as the amount of experimentation required is undue, due to the broad scope of the claims, the lack of guidance and working examples provided in the specification. Therefore, the specification is not representative of the instant claims and the specification is not fully enabled for the instant claims. In view of the above, one of skill in the art would be forced into undue experimentation to practice the claimed invention.
Prior Art
There is no prior art that teaches an anti-IL25 binding molecule comprising a heavy chain variable domain CDR1, CDR2, and CDR3 comprising the amino acid sequences of SEQ ID NO: 1, SEQ ID NO: 2, and SEQ ID NO: 3, respectively. Furthermore, there is no prior art that teaches an anti-IL25 binding molecule comprising a light chain variable domain CDR1, CDR2, and CDR3 comprising the amino acid sequences of SEQ ID NO: 5, SEQ ID NO: 6, and SEQ ID NO: 7, respectively.
The closest prior art, WO 2017/160587, teaches isolated anti-IL25 antibodies, however, none of the anti-IL25 antibodies disclosed by the ‘587 publication teach or suggest the heavy chain or light chain CDR amino acid sequences as recited in the instant claims.
Double Patenting
Pursuant to 37 CFR 1.78(f), when two or more applications filed by the same applicant or assignee contain patentably indistinct claims, elimination of such claims from all but one application may be required in the absence of good and sufficient reason for their retention during pendency in more than one application. Applicant is required to either cancel the patentably indistinct claims from all but one application or maintain a clear line of demarcation between the applications. See MPEP § 822.
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 1-7 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 5-8 of copending Application No. 18/488,848.
Although the claims at issue are not identical, they are not patentably distinct from each other because they are coextensive in scope. Copending claim 1 is drawn to a method of treating cancer in a subject in need thereof comprising administering an anti- IL-25 binding molecule to the subject. Copending claim 5 recites the anti-IL25 heavy chain variable domain CDR amino acid sequences. Copending claim 6 recites the anti-IL25 heavy chain variable domain amino acid sequence. Copending claim 7 recites the anti-IL25 light chain variable domain CDR amino acid sequences. Copending claim 8 recites the anti-IL25 light chain variable domain amino acid sequence.
The amino acid sequences (SEQ ID NOs) of the anti-IL25 antibody disclosed in the copending application are 100% identical to those recited in the instant claims.
The methods of the copending claims read on the instant invention as they are drawn to the identical anti-IL25 antibody for use in treating cancer as recited in the instant claims. As such, the instant claimed invention is an obvious modification of the claims of the copending application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Similarly, claims 1-7 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over one or more claims of the following copending applications.
Application No.
Brief Description of the Invention
Pertinent Claims
18/841,520
A method of treating pneumonitis comprising administering an IL-25 antagonist comprising heavy chain variable domain and light chain variable domain CDRs of SEQ ID NOs: 1- 3 and SEQ ID NOs: 5-7, respectively.
147-151, 160-163
19/472,473
A method for treating cancer comprising administering an anti-IL25 antibody comprising heavy chain variable domain and light chain variable domain CDRs of SEQ ID NOs: 1- 3 and SEQ ID NOs: 4-6, respectively.
1-15, 19-20, 23
The above-listed copending applications at a minimum read on the identical anti-IL25 antibody recited in the instant claims for the treatment of cancer and pneumonitis. As such, the instant claimed invention is an obvious modification of the claims of the copending applications.
These are provisional nonstatutory double patenting rejections.
Conclusion
No claim is allowed.
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 MAUREEN DRISCOLL whose telephone number is (571) 270-0730. The examiner can normally be reached Monday through Friday.
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/MAUREEN VARINA DRISCOLL/ Examiner, Art Unit 1642 /SAMIRA J JEAN-LOUIS/Supervisory Patent Examiner, Art Unit 1642
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