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 .
Status of Claims
The amendment filed on 3/3/2026 amended claims 204, 208, and 212 and added new claims 220-223. Claims 204-223 will be examined on the merits.
Election/Restrictions
Applicant’s election of the anti-TL1A antibody with HCDRs defined by SEQ ID NO:1, 2, and 7, and LCDRs defined by SEQ ID NO: 10, 11, and 12, with heavy and light chain variable domain defined by SEQ ID NO: 104 and SEQ ID NO: 201, respectively, in the reply filed on 3/3/2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Priority
Provisional application 63/150,832 is acknowledged as disclosing the claimed invention and the effective filing date is 02/18/2021.
Information Disclosure Statement
The Information Disclosure Statements filed on 08/15/2025, 10/13/2025, and 03/03/2026 have been considered. Signed copies are enclosed.
The information disclosure statement filed 02/27/2024 fails to comply with 37 CFR 1.98(a)(2), which requires a legible copy of each cited foreign patent document; each non-patent literature publication or that portion which caused it to be listed; and all other information or that portion which caused it to be listed. There is no copy of non-patent literature references 042, 044, 074, 075, 136, and 139. It has been placed in the application file, but the information referred to therein has not been considered.
Claim Objections
Claim 214 is objected to because of the following informalities: line fifteen recites (292), as 292 options are not listed. Appropriate correction is required.
Claim Rejections - 35 USC § 112
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.
Claims 208, 220, and 221 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 208 recites the limitation "the sugar" in line 15, under (ix). There is insufficient antecedent basis for this limitation in the claim. As each numeral is considered a separate limitation, due to the presence of the “or” in line 36, each numeral must independently depend from claim 207. Claim 207 depends from claim 205, which depends on claim 204. None of claims 204, 205, and 207 recite a sugar. The only other line that recites a sugar is also in claim 208, line 13, under (viii). However, as (ix) must be read independently from (viii), there is no antecedent basis for “the sugar” on line 15, under (ix). Appropriate correction is required.
Claim 220 and 221 both recite the limitation "the heavy chain variable domain" and "the light chain variable domain" in lines 2 and 6, respectively. There is insufficient antecedent basis for these limitations in the claims. Claim 220 depends from claim 204, which recites “an antibody or antigen binding fragment” in line 3, and claim 221 depends from claim 211, which recites “an anti-TL1A antibody or antigen binding fragment” in line 3. While an antibody would normally only have one heavy and one light chain variable domain, the specification recites that an antigen binding fragment may be “multispecific antibodies formed from antibody fragments” in paragraph [00110]. A multispecific antibody would contain multiple heavy and light chain variable domains; therefore, the claims as written are indefinite, as “the heavy chain variable domain” and “the light chain variable domains” do not have antecedent basis in the claims they depend from. Appropriate correction is required.
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claim(s) 204-217 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by US 2015/0132311 A1 (Arch et al., publication date 05/14/2015) as evidenced by Distler et al., Semin Immunopathol 38, 87–95 (2016).
The instant claims are directed to methods of treating systemic sclerosis-associated interstitial lung disease in a subject in need thereof comprising administering to the subject an anti-TL1A antibody or antigen binding fragment. Arch et al. disclose a method for treating a disease, disorder, or condition mediated by TL1A, said method comprising administering to the subject in need thereof an effective amount of an anti-TL1A antibody or antigen binding fragment (paragraph [0517]). Paragraph [0520] of Arch discloses this disease, disorder, or condition may comprise scleroderma, which is another name for systemic sclerosis, as evidenced by Distler et al. Moreover, the same paragraph discloses treatment of asthma, which is a well-known condition of the lungs, indicating this treatment will also treat the lungs of individuals with systemic sclerosis-mediated interstitial lung disease. Therefore, Arch teaches a method of treating systemic sclerosis-associated interstitial lung disease comprising administering to an anti-TL1A antibody, meeting all limitations of instant claims 204. Furthermore, Arch recites administering an effective amount of antibody in paragraphs [0517] and [0844], anticipating claim 211.
Paragraph [0861] of Arch recites that the antibody has a solubility of at least 150 mg/mL, meeting the limitations of instant claim 205. In paragraph [1081], Arch recites that the anti-TL1A antibodies have a percentage aggregation of less than 2%, anticipating claim 206. Paragraph [0862] recites the composition may have a stabilizer, salts, buffers, and surfactants such as amino acids like glycine, methionine, arginine, and histidine, and sugars such as sucrose. Paragraph [0875] recites an embodiment containing sodium acetate buffer, polysorbate, ad sodium chloride at a pH of 5.0-6.0. Therefore, Arch anticipates the limitations of 207 and 208.
Paragraph [0888] of Arch recites that a weekly dose may be given at least 2.0 mg/kg or 10 mg/kg for 1-12 or more doses. Paragraph [0891] recites the dose may be a flat dose of .01 mg to 200 mg. These meet the limitations set forth in 209 and 210, and therefore Arch anticipates claims 209-210. Moreover, paragraph [0887] recites that dosing levels will fluctuate based on a variety of pharmacokinetic factors and population factors, accounting for the same principles as in instant claim 217. Additionally, the dosing parameters listed above meet the limitations for the induction and maintenance regimes recited in claims 212-214, and therefore the dosing of the method of Arch anticipates claims 212, 213, 214, and 217. Finally, the antibodies disclosed in the examples bind to monomeric and trimeric TL1A, and exhibit a KD of 1.16-19.4 pM, meeting the limitations of instant claims 215 and 216. Therefore, Arch et al., 2015, anticipates instant claims 204-217.
Claim(s) 204, 209-216, and 218-221 are is/are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by McGovern et al., US 2018/0305459 A1, publication date 10/25/2018, as evidenced by Distler et al., Semin Immunopathol 38, 87–95 (2016).
The instant claims are directed to methods of treating systemic sclerosis-associated interstitial lung disease in a subject in need thereof comprising administering to the subject an anti-TL1A antibody or antigen binding fragment. McGovern teaches a method of treating a subject with an inflammatory or fibrotic disease in need thereof, comprising administering an anti-TL1A antibody [paragraph 0014]. McGovern recites in paragraph [0016] that this disease or condition comprises both progressive systemic sclerosis and chronic asthma. Distler et al. recites that interstitial lung disease is a common component of systemic sclerosis. McGovern also discloses treatment of asthma, which is a well-known condition of the lungs, indicating the treatment will also treat the lungs of individuals with systemic sclerosis, and thus treat the systemic sclerosis-mediated interstitial lung disease. Therefore, McGovern teaches a method of treating systemic sclerosis-associated interstitial lung disease comprising administering to an anti-TL1A antibody, meeting all limitations of instant claims 204. Furthermore, McGovern recites administering an effective amount of antibody in paragraphs [0016], anticipating claim 211. McGovern discloses an antibody that has the CDRs of instant SEQ ID NO 1, 2, 7, 10, 11, and 12, respectively, as recited in instant claims 220 and 221, in McGovern SEQ ID NO: 148 and 149, and SEQ ID NO: 150 and 151, which are disclosed in paragraph [0062]. McGovern SEQ ID NO: 148 and 150 also have 97% sequence identity to instant SEQ ID NO: 104, and McGovern SEQ ID NO: 149 and 151 have 97% sequence identity to instant SEQ ID NO: 201. Together, these meet the limitations set forth in instant claim 218 (i) and (iii) and claim 219 (i) and (iii), anticipating these instant claims. Additionally, as an antibody’s binding affinity is determined by its CDRs, the antibodies of McGovern with SEQ ID NO: 148/149 and 150/151 would have the same dissociation equilibrium constant (KD) for both the monomer and trimer form of TL1A as the antibody of instant claims 220-221. As the KD for the antibody correlates with the CDRs of the antibody, it can be assumed that the antibody with identical CDRs, as recited in instant claims 220-221 and in McGovern paragraph [0062], has the same KD. The instant specification discloses the KD of the recited antibody in Table 2, and meets the limitations set forth in instant claims 215 and 216. As this is an inherent property of the recited antibody, the antibodies disclosed by McGovern with SEQ ID NO: 148/149 and 150/151 have the same KD, and thus also meets the limitations of instant claims 215 and 216. Therefore, McGovern teaches instant claims 215-216 and 218-221. Finally, McGovern teaches that the antibody can be administered in doses of 1, 3, 10, 30, 100, 300, 600, or 800 mg, and can be administered in multiple doses, meeting the limitations of instant claim 209. Paragraph [0184] recites that the dosing interval is every 2 weeks for 12 weeks, meeting all limitations of instant claim 209 and 210. Moreover, this dosing schema further meets the limitations of 213 and 214 when taken with this recitation as well, meaning that it includes both an induction and a maintenance regimen as defined by the instant claims, and thus meets the limitations of 212.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 204 and 209-221 are rejected under 35 U.S.C. 103 as being unpatentable over US 2018/0110855 A1 (Bilsborough et al., published 4/26/2018) in view of Clarke et al., MABS 2018, VOL. 10, NO. 4, 664–677.
The instant claims are directed to methods of treating systemic sclerosis-associated interstitial lung disease in a subject in need thereof comprising administering to the subject an anti-TL1A antibody or antigen binding fragment. Bilsborough teaches a method of treating inflammatory bowel disease (IBD) in a subject in need thereof, comprising administering an anti-TL1A antibody. Bilsborough does not teach administration of an anti-TL1A antibody in order to treat systemic sclerosis-associated interstitial lung disease. However, Clarke et al. teaches that the administration of an anti-TL1A antibody in an asthma model significantly reduces airway inflammation and fibrosis, as well as several aspects of disease pathology in colitis, or IBD, models (abstract). The instant specification teaches, in paragraph [0005], that the antibody may be administered to a subject in need thereof reduce fibrosis in the lung, and that the subject in need thereof may have systemic sclerosis-associated interstitial lung disease. Moreover, Xu et al. teaches that systemic sclerosis (SSc) is associated with fibrosis (Introduction, first paragraph), and shows that patients with SSc exhibit higher levels of TL1A compared to healthy controls, and that active disease is associated with higher levels of TL1A than less active disease (Introduction, last paragraph). Xu et al. also recite that similar increased TL1A levels are found in IBD patients (Discussion, second paragraph). Taken together, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to use the treatment methods of Watkins to treat patients with lung fibrosis from SSc. One would be motivated to do so as both IBD, in which the method of Watkins is used, and SSc are diseases characterized by fibrosis and increased TL1A expression, especially in active disease states. One would have a reasonable expectation of success because Clarke has shown that administration of a TL1A antibody can treat fibrosis and inflammation in both the lung and the gut. Therefore, the method of treating SSc associated interstitial lung disease of the instant claims is obvious over Watkins in view of Clarke and Xu.
Paragraph [0176] discloses that the dosage of the antibody can be 1, 3, 10, 30, 100, 300, 600 or 800 mg of antibody, paragraph [0177] discloses multiple doses, and paragraph [0184] of Bilsborough discloses the dosing interval of 2 weeks, meeting the limitations of claims 209 and 210. Instant claim 211 is drawn to a method of delivering an effective dose of the antibody. Paragraph [0129] of Bilsborough recites that the antibody may be delivered in a therapeutically effective amount, and that this amount will vary depending on a variety of factors, but could be determined by one skilled in the clinical and pathological arts by monitoring the subject’s response to the antibody and adjusting the dose accordingly. This description meets the limitations of claim 211, as the concept of comparing the concentration of TL1A after administration in diseased vs healthy tissue is a form of monitoring response and can be done by one skilled in the clinical and pathological arts. Therefore, Bilsborough meets the limitations of instant claim 211. Additionally, this determining of an effective dose is accounting for the same principles as in instant claim 217, and so meets the limitations of instant claim 217. Moreover, paragraph [0131] of Bilsborough also recites that the antibody should be administered until a diminution of the disease is achieved, and the duration of treatment depends on the subject’s clinical progress and responsiveness to therapy. This process of treating describes a maintenance regimen, meeting the limitations of 212. The dosing taught by Bilsborough above further meets the limitations of 213 and 214 when taken with this recitation as well.
Bilsborough teaches an antibody with the CDRs of instant claim 220 and 221; namely, hCDRs with SEQ ID NO 1, 2, and 7, and lCDRs with SEQ ID NO 10, 11, and 12, in embodiment (a), paragraph [0137]. This antibody would subsequently meet the limitations of instant claims 218 and 219, which recite a broader class of anti-TL1A antibodies, but include the antibody of claims 220-221. Additionally, as an antibody’s binding affinity is determined by its CDRs, the antibody of Bilsborough [0137](a) would have the same dissociation equilibrium constant (KD) for both the monomer and trimer form of TL1A as the antibody of instant claims 220-221. As the KD for the antibody correlates with the CDRs of the antibody, it can be assumed that the antibody with identical CDRs, as recited in instant claims 220-221 and in Bilsborough [0137](a), has the same KD. The instant specification discloses the KD of the recited antibody in Table 2, and meets the limitations set forth in instant claims 215 and 216. As this is an inherent property of the recited antibody, the antibody recited in Bilsborough [0137](a) has the same KD, and thus also meets the limitations of instant claims 215 and 216. Therefore, claims 204-223 are obvious over Watkins in view of Clarke and Xu.
Claims 204-223 are rejected under 35 U.S.C. 103 as being obvious over US 2021/0122828 A1 (Watkins et al., EFD 12/2/2020) in view of Clarke et al., MABS 2018, 10:4, 664–677 and Xu et al., Clin Rheumatol (2017) 36:1317–1324.
The instant claims are directed to methods of treating systemic sclerosis-associated interstitial lung disease in a subject in need thereof comprising administering to the subject an anti-TL1A antibody or antigen binding fragment. Watkins teaches a method of treating inflammatory bowel disease (IBD) in a subject in need thereof, comprising administering an anti-TL1A antibody. Watkins teaches that this treatment works by reducing fibrosis in the gut (paragraph [0011]). Watkins does not teach administration of an anti-TL1A antibody in order to treat systemic sclerosis-associated interstitial lung disease. However, Clarke et al. teaches that the administration of an anti-TL1A antibody in an asthma model significantly reduces airway inflammation and fibrosis, as well as several aspects of disease pathology in colitis, or IBD, models (abstract). The instant specification teaches, in paragraph [0005], that the antibody may be administered to a subject in need thereof reduce fibrosis in the lung, and that the subject in need thereof may have systemic sclerosis-associated interstitial lung disease. Moreover, Xu et al. teaches that systemic sclerosis (SSc) is associated with fibrosis (Introduction, first paragraph), and shows that patients with SSc exhibit higher levels of TL1A compared to healthy controls, and that active disease is associated with higher levels of TL1A than less active disease (Introduction, last paragraph). Xu et al. also recite that similar increased TL1A levels are found in IBD patients (Discussion, second paragraph). Taken together, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to use the treatment methods of Watkins to treat patients with lung fibrosis from SSc. One would be motivated to do so as both IBD, in which the method of Watkins is used, and SSc are diseases characterized by fibrosis and increased TL1A expression, especially in active disease states. One would have a reasonable expectation of success because Clarke has shown that administration of a TL1A antibody can treat fibrosis and inflammation in both the lung and the gut. Therefore, the method of treating SSc associated interstitial lung disease of the instant claims is obvious over Watkins in view of Clarke and Xu.
Watkins also teaches that the antibody is administered in a composition of 170 mg/mL (paragraph [0012]), meeting the limitations of instant claim 205. The same paragraph teaches that the composition has a viscosity of 4 to 10 mPa-s, which is equivalent to 4-10 cP, meeting the limitation of instant claim 206. Paragraph [0272] of Watkins recites that the pharmaceutical composition may contain pharmaceutically acceptable salts, meeting the limitation of instant claim 207. This same paragraph recites that the composition may contain sucrose, which meets the limitations of claims 208 (vii)-(x), polysorbate, which meets the limitations of claim 208 (i) and (ii), and pH buffering agents, further meeting the limitations of claim 207 and 208. Paragraph [0274] discloses that the dosage of the antibody can be from .01 ug to 100 mg per kg of the body and can be administered once, or as a series of treatments lasting from several days to several months. The same limitation of .01 ug to 100 mg per kg is recited in the instant specification in paragraph [00352], so it is assumed that this limitation meets the parameter of up to 1000 mg per dose in claim 209. Moreover, the average human weighs between 60 and 70 kg, indicating a dose of 5-10 mg/kg, within the range recited by Watkins, meets the limitations of 209. Furthermore, table 15 in Watkins recites that the antibody will be given on Day 1, Day 15, and Day 29, meeting the limitations of timing present in claims 209 and 210. Therefore, Watkins meets the limitations of 209 and 210.
Instant claim 211 is drawn to a method of delivering an effective dose of the antibody. Paragraph [0273] of Watkins recites that the pharmaceutical composition may be delivered in a therapeutically effective amount, and that this amount will vary depending on a variety of factors, but could be determined by one skilled in the clinical and pathological arts by monitoring the subject’s response to the antibody and adjusting the dose accordingly. This description meets the limitations of claim 211, as the concept of comparing the concentration of TL1A after administration in diseased vs healthy tissue is a form of monitoring response and can be done by one skilled in the clinical and pathological arts. Therefore, Watkins meets the limitations of instant claim 211. Additionally, this determining of an effective dose is accounting for the same principles as in instant claim 217, and so meets the limitations of instant claim 217. Moreover, paragraph [274] of Watkins also recites that the antibody should be administered until a diminution of the disease is achieved, and the duration of treatment depends on the subject’s clinical progress and responsiveness to therapy. This process of treating describes a maintenance regimen, meeting the limitations of 212. The dosing taught by Watkins above further meets the limitations of 213 and 214 when taken with this recitation as well.
Watkins teaches an antibody with the CDRs of instant claim 220 and 221; namely, hCDRs with SEQ ID NO 1, 2, and 7, and lCDRs with SEQ ID NO 10, 11, and 12., as well as heavy chain variable domain of instant SEQ ID NO 104 and light chain variable domain of instant SEQ ID NO 201, as recited in instant claim 222 and 223, in embodiment 343, paragraph [0219]. This antibody would subsequently meet the limitations of instant claims 218 and 219, which recite a broader class of anti-TL1A antibodies, but include the antibody of claims 220-223. Additionally, as an antibody’s binding affinity is determined by its CDRs, the antibody of embodiment 343 would have the same dissociation equilibrium constant (KD) for both the monomer and trimer form of TL1A as the antibody of instant claims 220-223. As the KD for the antibody correlates with the CDRs of the antibody, it can be assumed that the same antibody, as recited in instant claims 220-223 and in Watkins embodiment 343, has the same KD. The instant specification discloses the KD of the recited antibody in Table 2, and meets the limitations set forth in instant claims 215 and 216. As this is an inherent property of the recited antibody, the antibody recited in Watkins embodiment 343 has the same KD, and thus also meets the limitations of instant claims 215 and 216. Therefore, claims 204-223 are obvious over Watkins in view of Clarke and Xu.
The applied reference has a common applicant/assignee with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2).
This rejection under 35 U.S.C. 103 might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C.102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B); or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement. See generally MPEP § 717.02.
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 204-221 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7 of U.S. Patent No. US 10322174 B2 in view of US 2015/0132311 A1 (Arch et al., publication date 05/14/2015) and Distler. Claims 1-7 of ‘174 disclose an anti-TL1A antibody with recited CDRs that overlap with instant SEQ ID NOs 1, 2, 7, 10, 11, and 12, meaning the antibody of ‘174 claim 1 anticipates the antibody of instant claims 220 and 221. Additionally, as an antibody’s binding affinity is determined by its CDRs, the antibody of ‘174 claim 1 would have the same dissociation equilibrium constant (KD) for both the monomer and trimer form of TL1A as the antibody of instant claims 220-221. As the KD for the antibody correlates with the CDRs of the antibody, it can be assumed that the antibody with identical CDRs, as recited in instant claims 220-221 and in ‘174 claim 1 has the same KD. The instant specification discloses the KD of the recited antibody in Table 2, and meets the limitations set forth in instant claims 215 and 216. As this is an inherent property of the recited antibody, the antibody recited in ‘174 claim 1 has the same KD, and thus also meets the limitations of instant claims 215 and 216.
The claims of ‘174 do not teach a method of using the recited antibody. However, in view of Arch, it would be obvious to use this anti-TL1A antibody to treat systemic sclerosis-mediated lung disease. Arch recites a method for treating a disease, disorder, or condition mediated by TL1A, said method comprising administering to the subject in need thereof an effective amount of an anti-TL1A antibody or antigen binding fragment (paragraph [0517]). Paragraph [0520] of Arch discloses this disease, disorder, or condition may comprise scleroderma, which is another name for systemic sclerosis, as evidenced by Distler et al. Moreover, the same paragraph discloses treatment of asthma, which is a well-known condition of the lungs, indicating this treatment will also treat the lungs of individuals with systemic sclerosis-mediated interstitial lung disease. Therefore, Arch teaches a method of treating systemic sclerosis-associated interstitial lung disease comprising administering to an anti-TL1A antibody, meeting all limitations of instant claims 204. Furthermore, Arch recites administering an effective amount of antibody in paragraphs [0517] and [0844], anticipating claim 211. Paragraph [0861] of Arch recites that the antibody has a solubility of at least 150 mg/mL, meeting the limitations of instant claim 205. In paragraph [1081], Arch recites that the anti-TL1A antibodies have a percentage aggregation of less than 2%, anticipating claim 206. Paragraph [0862] recites the composition may have a stabilizer, salts, buffers, and surfactants such as amino acids like glycine, methionine, arginine, and histidine, and sugars such as sucrose. Paragraph [0875] recites an embodiment containing sodium acetate buffer, polysorbate, ad sodium chloride at a pH of 5.0-6.0. Therefore, Arch anticipates the limitations of 207 and 208. Paragraph [0888] of Arch recites that a weekly dose may be given at least 2.0 mg/kg or 10 mg/kg for 1-12 or more doses. Paragraph [0891] recites the dose may be a flat dose of .01 mg to 200 mg. These meet the limitations set forth in 209 and 210, and therefore Arch anticipates claims 209-210. Moreover, paragraph [0887] recites that dosing levels will fluctuate based on a variety of pharmacokinetic factors and population factors, accounting for the same principles as in instant claim 217. Additionally, the dosing parameters listed above meet the limitations for the induction and maintenance regimes recited in claims 212-214, and therefore the dosing of the method of Arch anticipates claims 212, 213, 214, and 217.
It would be obvious to one of ordinary skill in the art to use the antibody of ‘174 with the methods recited by Arch et al. One would be motivated to do so to provide a treatment for systemic sclerosis, which is needed, as recited in Distler (abstract). One would have a reasonable expectation of success as Arch discloses a method of treating systemic sclerosis and asthma with an anti-TL1A antibody. Therefore, claims 204-221 are obvious over ‘174 claims 1-7 in view of Arch and Distler.
Claims 204-221 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of U.S. Patent No. US 10689439 B2 in view of Arch and Distler. Claims 1, 2, 4, 6, and 12 of ‘439 disclose an anti-TL1A antibody with recited CDRs that overlap with instant SEQ ID NOs 1, 2, 7, 10, 11, and 12, meaning the antibody of ‘439 anticipates the antibody of instant claims 220 and 221. Additionally, as an antibody’s binding affinity is determined by its CDRs, the antibody of ‘439 would have the same dissociation equilibrium constant (KD) for both the monomer and trimer form of TL1A as the antibody of instant claims 220-221. As the KD for the antibody correlates with the CDRs of the antibody, it can be assumed that the antibody with identical CDRs, as recited in instant claims 220-221 and in ‘439 has the same KD. The instant specification discloses the KD of the recited antibody in Table 2, and meets the limitations set forth in instant claims 215 and 216. As this is an inherent property of the recited antibody, the antibody recited in ‘439 has the same KD, and thus also meets the limitations of instant claims 215 and 216.
The claims of ‘439 do not teach a method of using the recited antibody. However, in view of Arch, it would be obvious to use this anti-TL1A antibody to treat systemic sclerosis-mediated lung disease. Arch recites a method for treating a disease, disorder, or condition mediated by TL1A, said method comprising administering to the subject in need thereof an effective amount of an anti-TL1A antibody or antigen binding fragment (paragraph [0517]). Paragraph [0520] of Arch discloses this disease, disorder, or condition may comprise scleroderma, which is another name for systemic sclerosis, as evidenced by Distler et al. Moreover, the same paragraph discloses treatment of asthma, which is a well-known condition of the lungs, indicating this treatment will also treat the lungs of individuals with systemic sclerosis-mediated interstitial lung disease. Therefore, Arch teaches a method of treating systemic sclerosis-associated interstitial lung disease comprising administering to an anti-TL1A antibody, meeting all limitations of instant claims 204. Furthermore, Arch recites administering an effective amount of antibody in paragraphs [0517] and [0844], anticipating claim 211. Paragraph [0861] of Arch recites that the antibody has a solubility of at least 150 mg/mL, meeting the limitations of instant claim 205. In paragraph [1081], Arch recites that the anti-TL1A antibodies have a percentage aggregation of less than 2%, anticipating claim 206. Paragraph [0862] recites the composition may have a stabilizer, salts, buffers, and surfactants such as amino acids like glycine, methionine, arginine, and histidine, and sugars such as sucrose. Paragraph [0875] recites an embodiment containing sodium acetate buffer, polysorbate, ad sodium chloride at a pH of 5.0-6.0. Therefore, Arch anticipates the limitations of 207 and 208. Paragraph [0888] of Arch recites that a weekly dose may be given at least 2.0 mg/kg or 10 mg/kg for 1-12 or more doses. Paragraph [0891] recites the dose may be a flat dose of .01 mg to 200 mg. These meet the limitations set forth in 209 and 210, and therefore Arch anticipates claims 209-210. Moreover, paragraph [0887] recites that dosing levels will fluctuate based on a variety of pharmacokinetic factors and population factors, accounting for the same principles as in instant claim 217. Additionally, the dosing parameters listed above meet the limitations for the induction and maintenance regimes recited in claims 212-214, and therefore the dosing of the method of Arch anticipates claims 212, 213, 214, and 217.
It would be obvious to one of ordinary skill in the art to use the antibody of ‘439 with the methods recited by Arch et al. One would be motivated to do so to provide a treatment for systemic sclerosis, which is needed, as recited in Distler (abstract). One would have a reasonable expectation of success as Arch discloses a method of treating systemic sclerosis and asthma with an anti-TL1A antibody. Therefore, claims 204-221 are obvious over ‘439 claims 1-18 in view of Arch and Distler.
Claims 204-214 and 217 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. US 11292848 B2 in view of Arch and Distler. Claims 1-20 of ‘848 disclose anti-TL1A antibodies with recited modifications to the framework regions of both the heavy and light chains. As instant claim 204 is directed to treatment with any anti-TL1A antibody, the antibodies of claim 1 of ‘848 can be used via the method of Arch to treat systemic sclerosis-mediated lung disease. Arch recites a method for treating a disease, disorder, or condition mediated by TL1A, said method comprising administering to the subject in need thereof an effective amount of an anti-TL1A antibody or antigen binding fragment (paragraph [0517]). Paragraph [0520] of Arch discloses this disease, disorder, or condition may comprise scleroderma, which is another name for systemic sclerosis, as evidenced by Distler et al. Moreover, the same paragraph discloses treatment of asthma, which is a well-known condition of the lungs, indicating this treatment will also treat the lungs of individuals with systemic sclerosis-mediated interstitial lung disease. Therefore, Arch teaches a method of treating systemic sclerosis-associated interstitial lung disease comprising administering to an anti-TL1A antibody, meeting all limitations of instant claims 204. Furthermore, Arch recites administering an effective amount of antibody in paragraphs [0517] and [0844], anticipating claim 211. Paragraph [0861] of Arch recites that the antibody has a solubility of at least 150 mg/mL, meeting the limitations of instant claim 205. In paragraph [1081], Arch recites that the anti-TL1A antibodies have a percentage aggregation of less than 2%, anticipating claim 206. Paragraph [0862] recites the composition may have a stabilizer, salts, buffers, and surfactants such as amino acids like glycine, methionine, arginine, and histidine, and sugars such as sucrose. Paragraph [0875] recites an embodiment containing sodium acetate buffer, polysorbate, ad sodium chloride at a pH of 5.0-6.0. Therefore, Arch anticipates the limitations of 207 and 208. Paragraph [0888] of Arch recites that a weekly dose may be given at least 2.0 mg/kg or 10 mg/kg for 1-12 or more doses. Paragraph [0891] recites the dose may be a flat dose of .01 mg to 200 mg. These meet the limitations set forth in 209 and 210, and therefore Arch anticipates claims 209-210. Moreover, paragraph [0887] recites that dosing levels will fluctuate based on a variety of pharmacokinetic factors and population factors, accounting for the same principles as in instant claim 217. Additionally, the dosing parameters listed above meet the limitations for the induction and maintenance regimes recited in claims 212-214, and therefore the dosing of the method of Arch anticipates claims 212, 213, 214, and 217.
It would be obvious to one of ordinary skill in the art to use the antibody of ‘848 with the methods recited by Arch et al. One would be motivated to do so to provide a treatment for systemic sclerosis, which is needed, as recited in Distler (abstract). One would have a reasonable expectation of success as Arch discloses a method of treating systemic sclerosis and asthma with an anti-TL1A antibody. Therefore, claims 204-214 and 217 are obvious over ‘848 claims 1-20 in view of Arch and Distler.
Claims 204-223 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-7 of U.S. Patent No. US 11999789 B2 in view of Arch and Distler. Claims 1-7 of ‘789 disclose an anti-TL1A antibody with defined heavy and light chain variable regions that are 100% identical to the antibodies of instant claim 222, meaning the antibody of ‘789 claim 1 anticipates the antibody of instant claims 222 and 223, as well as 220 and 221. Additionally, as an antibody’s binding affinity is determined by its CDRs, the antibody of ‘789 claim 1 would have the same dissociation equilibrium constant (KD) for both the monomer and trimer form of TL1A as the antibody of instant claims 220-221. As the KD for the antibody correlates with the CDRs of the antibody, it can be assumed that the antibody with identical CDRs, as recited in instant claims 220-221 and in ‘789 claim 1 has the same KD. The instant specification discloses the KD of the recited antibody in Table 2, and meets the limitations set forth in instant claims 215 and 216. As this is an inherent property of the recited antibody, the antibody recited in ‘789 claim 1 has the same KD, and thus also meets the limitations of instant claims 215 and 216.
The claims of ‘789 do not teach a method of using the recited antibody. However, in view of Arch, it would be obvious to use this anti-TL1A antibody to treat systemic sclerosis-mediated lung disease. Arch recites a method for treating a disease, disorder, or condition mediated by TL1A, said method comprising administering to the subject in need thereof an effective amount of an anti-TL1A antibody or antigen binding fragment (paragraph [0517]). Paragraph [0520] of Arch discloses this disease, disorder, or condition may comprise scleroderma, which is another name for systemic sclerosis, as evidenced by Distler et al. Moreover, the same paragraph discloses treatment of asthma, which is a well-known condition of the lungs, indicating this treatment will also treat the lungs of individuals with systemic sclerosis-mediated interstitial lung disease. Therefore, Arch teaches a method of treating systemic sclerosis-associated interstitial lung disease comprising administering to an anti-TL1A antibody, meeting all limitations of instant claims 204. Furthermore, Arch recites administering an effective amount of antibody in paragraphs [0517] and [0844], anticipating claim 211. Paragraph [0861] of Arch recites that the antibody has a solubility of at least 150 mg/mL, meeting the limitations of instant claim 205. In paragraph [1081], Arch recites that the anti-TL1A antibodies have a percentage aggregation of less than 2%, anticipating claim 206. Paragraph [0862] recites the composition may have a stabilizer, salts, buffers, and surfactants such as amino acids like glycine, methionine, arginine, and histidine, and sugars such as sucrose. Paragraph [0875] recites an embodiment containing sodium acetate buffer, polysorbate, ad sodium chloride at a pH of 5.0-6.0. Therefore, Arch anticipates the limitations of 207 and 208. Paragraph [0888] of Arch recites that a weekly dose may be given at least 2.0 mg/kg or 10 mg/kg for 1-12 or more doses. Paragraph [0891] recites the dose may be a flat dose of .01 mg to 200 mg. These meet the limitations set forth in 209 and 210, and therefore Arch anticipates claims 209-210. Moreover, paragraph [0887] recites that dosing levels will fluctuate based on a variety of pharmacokinetic factors and population factors, accounting for the same principles as in instant claim 217. Additionally, the dosing parameters listed above meet the limitations for the induction and maintenance regimes recited in claims 212-214, and therefore the dosing of the method of Arch anticipates claims 212, 213, 214, and 217.
It would be obvious to one of ordinary skill in the art to use the antibody of ‘789 with the methods recited by Arch et al. One would be motivated to do so to provide a treatment for systemic sclerosis, which is needed, as recited in Distler (abstract). One would have a reasonable expectation of success as Arch discloses a method of treating systemic sclerosis and asthma with an anti-TL1A antibody. Therefore, claims 204-221 are obvious over ‘789 claims 1-7 in view of Arch and Distler.
Conclusion
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/AMELIA STEPHENS/Examiner, Art Unit 1645
/ANNE M. GUSSOW/Supervisory Patent Examiner, Art Unit 1683
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