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 08/14/2026 amended claims 204, 208, 211, 213, and 214, and cancelled claims 218-223. Claims 1-203 were previously cancelled. Claims 204-217 are pending and will be examined on the merits.
Response to Amendment
The amendment filed 08/14/2026 in response to the office action mailed 04/17/2026 is acknowledged. The rejections set forth under 35 USC 112(b), 102, and 103 are withdrawn for the following reasons:
The amendments to claim 208 and the cancellation of claims 220 and 221 overcomes the 112(b) rejections over those claims. The amendment of claims 204 and 211 to recite the anti-TL1A antibody comprising a VH of SEQ ID NO: 104 and a VL of SEQ ID NO: 201 overcomes the art rejections in view of Arch et al., McGovern et al., and Bilsborough et al. in view of Clarke et al. and Xu et al., as well as the double patenting rejections over US Patents No. 10322174, 10689439, and 11292848.
Maintained or modified rejections are set forth below, as necessitated by the amendments. Responses to arguments follow.
Information Disclosure Statement
The Information Disclosure Statement filed on 08/14/2026 has been considered. Signed copies are enclosed.
Maintained Claim Rejections - 35 USC § 103 - Modified as Necessitated by Claim Amendments
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 204-217 are rejected under 35 U.S.C. 103 as being unpatentable 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 wherein the anti-TL1A antibody comprises a VH of SEQ ID NO: 104 and the VL of SEQ ID NO: 201.
Watkins teaches a method of treating inflammatory bowel disease (IBD) in a subject in need thereof, comprising administering an anti-TL1A antibody. Watkins teaches an antibody with the heavy chain variable domain of instant SEQ ID NO: 104 and light chain variable domain of instant SEQ ID NO: 201, in embodiment 343, paragraph [0219]. 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 to 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 using the anti-TL1A antibody 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 heavy chain variable domain of instant SEQ ID NO 104 and light chain variable domain of instant SEQ ID NO 201 in embodiment 343, paragraph [0219]. 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 the instant claims. As the KD for the antibody correlates with the CDRs of the antibody, it can be assumed that the same antibody, as recited in the instant claims 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 204-217 are obvious over Watkins in view of Clarke and Xu.
Response to Arguments
Applicant's arguments filed 08/14/2026 have been fully considered but they are not persuasive. Applicant disagrees with the Examiner’s statement that it would be obvious to one of ordinary skill in the art to use the treatment methods of Watkins to treat patients with SSc-ILD. Applicant argues that the cited references of Watkins, Clarke, and Xu et al. do not provide a motivation to treat SSc-ILD with the claimed antibody, nor that one of skill in the art would have a reasonable expectation of success in doing so. Applicant argues that the Examiner has not established a prima facie showing of obviousness, as therapeutic efficacy in one disease does not predict efficacy in another. Applicant argues that the examiner’s reasoning that IBD and SSc are characterized by fibrosis and increased TL1A expression, especially in active disease states, is based on impermissible hindsight that ignores fundamental differences in disease pathogenesis. Applicant does not detail what these fundamental differences are.
In response to applicant's argument that the examiner has not established a prima facie case of obviousness, Examiner has presented, and reiterated above, that there is motivation to use the method of Watkins to treat SSc-ILD, in that there are similarities in disease pathogenesis, such as fibrosis and increased TL1A expression. Applicant has not highlighted what fundamental differences in disease pathogenesis they believe would make the treatment of SSc-ILD not indicated by treatment with an antibody used in IBD that targets a common antigen between the disease states. Therefore, Examiner upholds that the two diseases have enough in common to provide motivation to treat SSc-ILD with the method of Watkins et al. Additionally, as Clarke et al. recite on page 669, left column, TL1A is known to be closely associated with mucosal immunity, which suggests that blocking TL1A activity would provide a benefit in inflammatory diseases involving mucosal surfaces, such as the gut and the lung. The similarities in mucosal immunology at these sites would indicate that a treatment for the gut may very well work for treatment in the lung, if the antigen is known to be the same. TL1A is known to play a role in both IBD (see Clarke et al.) and SSc (see Xu et al.). Therefore, there is, at the very least, motivation to try the methods of Watkins et al. as a treatment for SSc-ILD, as there is a reasonable expectation that the targeting of TL1A, which is successful in reducing fibrosis the gut (see Watkins et al., Clarke et al.), would be successful in reducing fibrosis in the lungs (as evidenced by Clarke et al. as well, as the treatment improves fibrosis caused by inflammation in asthma (see Figure 11C, page 669 left column, first paragraph, and page 671, right column, last paragraph)). Therefore, the combination of Watkins in view of Clarke et al. and Xu et al. is a prima facie case of obviousness to use the methods of Watkins et al. to teach SSc-ILD.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). At the time of filing, the similarities between IBD and SSc would be known, as demonstrated in Clarke et al., published in 2018, and Xu et al., published in 2017, thus providing both motivation and reasonable expectation of success before the effective filing date of the invention.
Applicant additionally argues that the amendments to the claim overcome the rejection. The sequence alignment of instant SEQ ID NO: 104 with Watkins SEQ ID NO: 104 and instant SEQ ID NO:201 with Watkins SEQ ID NO: 201 are provided below, and are attached to this office action, showing 100% sequence identity between the VH and VL regions of the antibody of Watkins et al. and the antibody recited by the instant claims.
Sequence alignment 1: Instant SEQ ID NO: 104 with Watkins SEQ ID NO: 104
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Sequence alignment 2: Instant SEQ ID NO: 201 with Watkins SEQ ID NO: 201
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Maintained Double Patenting - Modified as Necessitated by Claim Amendments
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 204-217 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 US 2015/0132311 A1 (Arch et al., publication date 05/14/2015) and Distler et al., Semin Immunopathol 38, 87–95 (2016).
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 the instant claims (see Sequence alignment below), meaning the antibody of ‘789 claim 1 anticipates the antibody of instant claims. 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 the instant claims. As the KD for the antibody correlates with the variable regions of the antibody, it can be assumed that an antibody with identical variable regions, as recited in the instant claims 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 the limitations of the method of instant claims 204. Furthermore, Arch recites administering an effective amount of antibody in paragraphs [0517] and [0844], teaching 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, and sodium chloride at a pH of 5.0-6.0. Therefore, Arch teaches 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 teaches the limitations of 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 teaches the limitations of 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 and compositions 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, which broadly includes the antibody of ‘789. Therefore, claims 204-217 are obvious over ‘789 claims 1-7 in view of Arch and Distler.
Response to Arguments
Applicant's arguments filed 08/14/2026 have been fully considered but they are not persuasive. Applicant argues that the amendment of claims 204 and 211 to recite the anti-TL1A antibody comprising a VH of SEQ ID NO: 104 and the VL of SEQ ID NO: 201. The sequence alignment of instant SEQ ID NO: 104 with Watkins SEQ ID NO: 104 and instant SEQ ID NO:201 with Watkins SEQ ID NO: 201 are provided below, and are attached to this office action, showing 100% sequence identity between the VH and VL regions of the antibody of Watkins et al. and the antibody recited by the instant claims.
Sequence alignment 3: Instant SEQ ID NO: 104 with ‘789 SEQ ID NO: 104
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Sequence alignment 4: Instant SEQ ID NO: 201 with ‘789 SEQ ID NO: 201
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Double Patenting (New)
Claims 204-217 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 13, 20, 25, 26, 39, 42, 47, 54, 62, 66, 70, 74, 113, 114, 118, 125, 128, 131, 138, 139, 145, 178, 181, 221, and 225-227 of copending Application No. 19/157,176 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the method of the instant claims and the methods of '176 would both treat both SSc-ILD and SSc skin fibrosis.
Claims 1, 113, 118, and 178 of ‘176 are drawn to methods of treating skin inflammation or fibrosis of the skin comprising administering an anti-TL1A antibody. The anti-TL1A antibody is defined, in at least claims 221 and 225-227, as having a VH chain with at least 96% identity to that of SEQ ID NO:104 and a VL chain with at least 96% identity to that of SEQ ID NO: 201. These are 100% identical to the instantly claimed antibody (see sequence alignments below). Additionally, ‘176 names systemic sclerosis as a disease that can be treated via administration of the claimed antibody, in at least claim 114, 145, and 178. ‘176 also discloses administration in similar amounts, compositions, and dosing regimens as the instant claims, in at least claims 26, 29, 66, 70, 74, 128, 131, 138, 139, and 145. Therefore, treatment with the method of the instant claims would treat the diseases named in ‘176, and treatment with the methods of ‘176 would treat SSc-ILD, as recited in the instant claims. Therefore, claims 204-216 are substantially the same as those of Application ‘176. Finally, claim 178 of ‘176 recites administration of the effective does as determined by the same parameters as instant claim 217, and therefore teaches claim 217 as well. Together, claims 204-217 are taught by and teach the instant claims of Application ‘176.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Sequence alignment 5: Instant SEQ ID NO: 104 with ‘176 SEQ ID NO: 104
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Sequence alignment 6: Instant SEQ ID NO: 201 with ‘176 SEQ ID NO: 201
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Conclusion
No claim is allowed.
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure. Herro et al., Journal of Immunology, . Herro et al. disclose the role of TL1A in lung fibrosis, present in diseases such as asthma and systemic sclerosis. Herro et al. emphasizes that treatments that target fibrosis for these diseases are limited (abstract, discussion). Herro et al. provides further motivation to treat SSc-ILD with an anti-TL1A antibody before the effective filing date of the claimed invention.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Amelia Stephens whose telephone number is (571)272-1006. The examiner can normally be reached M-F 8-5 EST.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Anne Gussow can be reached at (571) 272-6047. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/AMELIA STEPHENS/Examiner, Art Unit 1645
/ANNE M. GUSSOW/Supervisory Patent Examiner, Art Unit 1683
Prosecution Insights