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 .
Priority
This application filed on 10/19/2023, is a national phase application under 35 U.S.C. § 371 of International Application No. PCT/CN2022/087872, filed on 04/20/2022, which claims the priority of Chinese Patent Application No. 202110436177.6, filed on 04/22/2021.
Information Disclosure Statement
The information disclosure statement (IDS) filed on 10/19/2023, 01/29/2025, 05/27/2025 and 12/03/2025, complies with the provisions of 37 CFR 1.97, 1.98 and MPEP § 609. Accordingly, it has been placed in the application file and the information therein has been considered as to the merits, except where noted.
Status of claims
Applicant’s amendment and arguments filed on 06/21/2026 have been received and have been fully considered.
Claims 8 and 11 were amended, claims 9-10 and 12-15 were canceled, and claims 1-7 were previously cancelled. Claims 8 and 11 are pending.
Claim interpretation
Examination requires claim terms first be construed in terms in the broadest reasonable manner during prosecution as is reasonably allowed in an effort to establish a clear record of what applicant intends to claim. See MPEP § 2111. Under a broadest reasonable interpretation, words of the claim must be given their plain meaning, unless such meaning is inconsistent with the specification. See MPEP § 2111.01. It is also appropriate to look to how the claim term is used in the prior art, which includes prior art patents, published applications, trade publications, and dictionaries. MPEP § 2111.01 (III). However, specific embodiments of the specification cannot be imported into the claims, particularly where the subject claim limitation is broader than the embodiment. MPEP § 2111.01(II).
Claim interpterion for “ameliorating”
Claim 8 recites “A method for treating or ameliorating an autoimmune skin disease, comprising administering a JAK3/JAK1/TBK1 selective inhibitor in a dose of 20-600 mg/time/day to a subject in need thereof, …”.
The instant specification does not provide a definition for this term. Nevertheless, the instant specification recites:
“Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by those of ordinary skill in the art. [0043]”
As provided in MPEP 211.01 III, [T]he ordinary and customary meaning of a claim term is the meaning that the term would have to a person of ordinary skill in the art in question at the time of the invention, i.e., as of the effective filing date of the patent application." Phillips v. AWH Corp.,415 F.3d 1303, 1313, 75 USPQ2d 1321, 1326 (Fed. Cir. 2005) (en banc); Sunrace Roots Enter. Co. v. SRAM Corp., 336 F.3d 1298, 1302, 67 USPQ2d 1438, 1441 (Fed. Cir. 2003); Brookhill-Wilk 1, LLC v. Intuitive Surgical, Inc., 334 F.3d 1294, 1298, 67 USPQ2d 1132, 1136 (Fed. Cir. 2003) ("In the absence of an express intent to impart a novel meaning to the claim terms, the words are presumed to take on the ordinary and customary meanings attributed to them by those of ordinary skill in the art."). Where neither the claims, nor the specification, nor the prosecution history offer sufficient clarity on claim scope, extrinsic evidence may become a necessary part of claim interpretation. Moreover, MPEP 2111.01 stated that it is improper to “read limitations into a claim from the preferred embodiment described in the specification, even if it is the only embodiment described, absent clear disclaimer in the specification."
Thus, Claim 8 term “ameliorating” is given its plain meaning as described by medical dictionary as “lessened signs or symptoms of a disease.” (Ameliorate | definition of ameliorate by Medical dictionary, (2012) https://medical-dictionary.thefreedictionary.com/ameliorate).
Withdrawn Claim Rejections - 35 USC § 102
Rejection of claims 8-15 under 35 U.S.C. 102(a)(1) as being anticipated by S. Shan, et al. International Immunopharmacology, Volume 77, 2019, 105914, ISSN 1567-5769) as evidenced by Z. Xie et al. Journal of Medicinal Chemistry, January 22, 2021 Vol 64, Issue 3, P 1283- 1345), is withdrawn in view of Applicant’s amendment filed on 06/21/2026 that deleted “prevention”.
Withdrawn Double Patenting Rejection
Provisional rejection of claims 8 and 11 on the ground of nonstatutory double patenting as being unpatentable over claims 1, 9, 20 and 21 of Co-pending Application No. 17/780,284 (US PG-PUB 2023/0000863A1) in view of S. Shan, et al. International Immunopharmacology, Volume 77, 2019, 105914, ISSN 1567-5769), Z. Xie et al. Journal of Medicinal Chemistry, January 22, 2021 Vol 64, Issue 3, P 1283- 1345) H. He et al. American Journal of Clinical Dermatology (2019) 20:181–192), and C. Garcia-Melendo et al. (Actas Dermosifiliogr. 2021; 112:503-515), is withdrawn because Co-pending Application No. 17/780,284 was abandoned on 03/31/2026.
Rejection Maintained
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 8 and 11 remain rejected under 35 U.S.C. 103 as being unpatentable over S. Shan, et al. International Immunopharmacology, Volume 77, 2019, 105914, ISSN 1567-5769, “Shan” cited in the IDS dated 10/19/2023) in view of Z. Xie et al. Journal of Medicinal Chemistry, January 22, 2021 Vol 64, Issue 3, P 1283- 1345, “Xie” cited in the PTO-892 dated 03/25/2026) H. He et al. American Journal of Clinical Dermatology (2019) 20:181–192, “He” cited in the PTO-892 dated 03/25/2026), and C. Garcia-Melendo et al. (Actas Dermosifiliogr. 19 march 2021; 112:503-515, “Garcia-Melendo” cited in the IDS dated 01/29/2025).
Shan teaches a method of treating autoimmune disease by administering CS12192. [Abstract]. Shan teaches that CS12192 identified as a novel selective JAK inhibitor, with a potent inhibition on JAK3, and to a less extent on JAK1 and TBK1. [page 2, col. 1, 3rd para.].
Shan teaches that JAK3 is more restrictedly expressed in hematopoietic cells and mediates signals through the common γ chain shared by many immune related cytokine receptors [page 1, col. 2 last para.].
Shan teaches that “Considering that JAKs are essential signaling mediators downstream of many pro inflammatory cytokine receptors, small molecule inhibitors of JAKs have gained attraction as safe and efficacious options for the treatment of inflammation-driven pathologies such as Rheumatoid arthritis and psoriasis.” [page 2, col. 1, 1st para.].
Shan teaches that CS12192 showed more selective JAK3 inhibition with an IC50 of 11nM, and to a less extent of JAK1 inhibition with an IC50 of 105nM, and interestingly, CS12192 inhibited TBK1 and Flt4 with the IC50 of 162nM and 107nM, respectively. [page 4, col. 2, 1st para.]. Shan teaches that the results also showed that CS12192 is also a novel dual JAK/TBK1 inhibitor. [page 4, 2nd -3rd para.].
Shan teaches that CS12192 affects cytokine production of CD4+ T, and CS12192 significantly inhibited the serum levels of pro-inflammatory cytokines and/or differentiation-related cytokines. [page 6, col. 1, last para.].
Shan teaches that a novel selective JAK inhibitor, CS12192 is investigated for the treatment of Rheumatoid arthritis because several JAK inhibitors have been approved for the treatment of Rheumatoid arthritis such as tofacitinib, a JAK3/JAK1/JAK2 inhibitor, has been approved by FDA for the treatment of Rheumatoid arthritis patients, and JAK1/JAK2 inhibitor, baricitinib, was approved for the treatment of moderate-to-severe Rheumatoid arthritis patients. [page 2, col. 1, 1st and 3rd para.].
CS12192 is N-(3-((5-chloro-2-((4-fluoro-3-(N-methylacrylamido)phenyl) amino)-4-pyrimidinyl)amino)propyl)-4-cyanobenzamide, as explained in the 102 Rejection above:
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Shan’s administration of 80mg/kg of CS12192 twice a day is equivalent to 24mg/time/day (80mg/kg x 0.15kg1 (weight of rat in kg) = 12 mg x 2 (twice a day) = 24 mg per day, which reads on claim 8, 20-600 mg/day.
While Shan teaches the potency of CS12192 as selective JAK3/JAK1/TBK1 inhibitor, The effect of CS12192 on cytokine production of CD4+ T, and on inhibition of the pro-inflammatory cytokine serum levels, and the effectiveness of CS12192 in treating autoimmune disease and inflammation-driven pathologies such as Rheumatoid arthritis, Shan does not teach that the autoimmune disease is autoimmune skin disease, atopic dermatitis or alopecia areata.
Xie teaches the use of JAK inhibitors for treatment of nononcologic diseases including autoimmune diseases, atopic dermatitis and alopecia areata. [Abstract], [Table 1]. Xie teaches that several JAK inhibitors have been approved for the treatment of autoimmune skin diseases. [page 1287, col. 1, 2nd para.]:
Ruxolitinib, a JAK1/JAK2 selective inhibitor, with effective, safe and well-tolerated profile for treating atopic dermatitis and alopecia areata, [page 1287, col. 1, 3rd para.].
Tofacitinib, a selective JAK3 inhibitor, approved by the U.S. FDA in 2012 to treat atopic dermatitis and alopecia areata, [page 1287, col. 1, last para.];
Oclacitinib, a JAK inhibitor, approved by the U.S. FDA in 2013 for the treatment of atopic dermatitis, [page 1287, col. 1, 2nd para.];
Delgocitinib, an effective and well tolerated JAK1/JAK2/JAK3 inhibitor, was developed for the treatment of atopic dermatitis, [page 1288, col. 2, 1st para.];
Baricitinib, a selective inhibitor of JAK1/JAK2, received a breakthrough therapy designation from the U.S. FDA to treat alopecia areata, [page 1287, col. 2, 2nd para.].
Baricitinib, JAK1/JAK2 inhibitor, approved by the U.S. FDA for treating atopic dermatitis, [page 1285, Table 1];
Upadacitinib, selective JAK1 inhibitor, approved by the U.S. FDA for treating atopic dermatitis, [page 1285, Table 1];
PF-06651600, selective JAK3 inhibitor, in clinical trials for treating alopecia areata, [page 1289, Table 2];
Abrocitinib, a selective JAK1 inhibitor, in clinical trials for treating atopic dermatitis, [page 1289, Table 2].
Xie teaches that CS12192, a possible irreversible JAK inhibitor is in phase 1 clinical trial. Xie teaches that CS12192 is superior to other JAK inhibitors because CS12192 selectively inhibits JAK3 (IC50 = 11nM) over JAK1, JAK2, and TYK2, demonstrated good therapeutic results, and has an IC50 value of 162nM against TANK-binding kinase1, which was found to play a role in RANKL-induced NF-κB activation. [page 1289, col. 1, 1st para.].
He teaches the use for JAK inhibitors for treating atopic dermatitis. [Title]. He efficacy of many different JAK inhibitors for the treatment of atopic dermatitis including Tofacitinib, selective against JAK1 and JAK3; Baricitinib, a JAK1 and JAK2 inhibitor; Upadacitinib, a selective JAK1 inhibitor; Abrocitinib, selective oral JAK1 inhibitor; ruxolitinib, JAK1/JAK2 inhibitor; Delgocitinib a JAK1/JAK2/JAK3/TYK2) inhibitor; and SNA-125, a JAK3/TrkA inhibitor. [page 183-185].
He teaches that Information regarding the safety of JAK inhibitors largely comes from studies in other inflammatory diseases, such as rheumatoid arthritis. [page 186, col. 1, 2nd para.]. He teaches that JAK inhibitors showed efficacy in treating atopic dermatitis with acceptable safety profiles. [page 186, col. 2, last para.].
One of He’s JAK inhibitor, is SNA-125, a selective JAK3 inhibitor. He teaches that because SNA-125 inhibiting JAK3, SNA-125 blocks signaling via IL-4 and other cytokines, and also blocks TrkA, a high affinity receptor for nerve growth factor (NGF), which mediates neurogenic inflammation and itch. [page 186, col. 1, 1st para.].
Garcia-Melendo teaches the use of JAK inhibitors for treating alopecia areata. [Abstract]. Garcia-Melendo teaches the connection between alopecia areata and JAK3, wherein analysis of skin biopsies from patients with alopecia areata has revealed overexpression of JAK3 and, albeit to a lesser extent, JAK1 and JAK2. [page 510, col. 2, 1st para.]. Garcia-Melendo teaches that the role of JAK in the pathogenesis of alopecia areata, the direct effect of JAK inhibitor on follicles during the telogen phase and promotion of anagen phase makes JAK inhibitors effective treatment for alopecia areata, [page 510, col. 2, 2nd para.].
Garcia-Melendo teaches many JAK inhibitors for the treatment of alopecia areata including tofacitinib, ruxolitinib, Baricitinib, delgocitinib, ritlecitinib and brepocitinib. [page 510- 511].
In view of the foregoing discussion, it would have been prima facie obvious to one of ordinary skill in the prior to the effective filing date of instantly claimed invention to use JAK inhibitor, CS12192 for treating autoimmune skin diseases i.e., atopic dermatitis and alopecia areata. One of ordinary skill in the art would have been motivated to do so with reasonable expectation of success because: treating atopic dermatitis and alopecia areata with JAK inhibitors is well-known in the art as taught by the cited prior art of Xie, He and Garcia-Melendo, and CS12192 is a selective potent and safe JAK inhibitor as taught by Shan and Xie.
As discussed above, Xie, He and Garcia-Melendo teach many JAK inhibitors FDA approved/in clinical trials are used for the treatment of atopic dermatitis and alopecia areata including ruxolitinib, JAK1/JAK2 selective inhibitor, Tofacitinib, a selective JAK3 inhibitor, Oclacitinib, a JAK inhibitor, Delgocitinib, JAK1/JAK2/JAK3 inhibitor, Baricitinib, a selective inhibitor of JAK1/JAK2, Baricitinib, JAK1/JAK2 inhibitor, Upadacitinib, selective JAK1 inhibitor, PF-06651600, selective JAK3 inhibitor, Abrocitinib, a selective JAK1 inhibitor, which would motivate one of ordinary skill in the art to use another JAK inhibitor i.e., CS12192 for treating atopic dermatitis and alopecia areata. One of ordinary skill in the art would have been motivated to specifically utilize CS12192 in treating atopic dermatitis and alopecia areata because: Shan teaches using CS12192 in a method of treating autoimmune disease; Shan teaches that CS12192 identified as a novel selective JAK inhibitor; CS12192 showed more selective JAK3 inhibition with an IC50 of 11nM, and to a less extent of JAK1 inhibition with an IC50 of 105nM; CS12192 inhibited TBK1 and Flt4; CS12192 is a novel dual JAK/TBK1 inhibitor; CS12192 affects cytokine production of CD4+ T, and CS12192 significantly inhibited the serum levels of pro-inflammatory cytokines; Xie teaches that CS12192, a possible irreversible JAK inhibitor; CS12192 is superior to other JAK inhibitors because CS12192 selectively inhibits JAK3 (IC50 = 11nM) over JAK1, JAK2, and TYK2; CS12192 demonstrated good therapeutic results. Moreover, He teaches that the safety of JAK inhibitors largely comes from studies in other inflammatory diseases, such as RA and the safety and efficacy of CS12192 in RA is taught by Shan. Furthermore, Garcia-Melendo teaches the correlation between alopecia areata and overexpression of JAK3 and, albeit to a lesser extent, JAK1 and JAK2, which would motivate skilled artisan to use CS12192 because the potency and JAK3 selectivity of CS12192. Case law has established that it is prima facie obvious to substitute one known elementfor another to obtain predictable results. KSR Int'I Co. v. Teleflex, Inc., 550 U.S. 398 (2007). The cited prior arts provide one of ordinary skill in the art with the requisite predictability in using CS12192 for treating atopic dermatitis and alopecia areata.
Therefore, the combination of Shan, Xie, He, and Garcia-Melendo teaches each and every limitation of claims 8 and 11.
Response to Arguments
Applicant argues:
The applicant points out that autoimmune diseases are a common category of diseases, including at least dozens of diseases, whose names are derived only from manifestations, but the exact pathogenesis is mostly unknown. At present, the understanding of autoimmune diseases is still very limited, and there are great differences in the causes, influencing factors and treatment methods, and the predictability is very low. In addition, the applicant further points out that the examiner's view is actually formed by hindsight bias after reading the content of the present application and being influenced by the disclosure of the present invention. The examiner has acknowledged that Xie does not teach atopic dermatitis, or alopecia areata. While Xie et al. broadly lists various JAK inhibitors for skin diseases, they do not disclose the specific application of CS 12192 (the aforementioned compound) or its pharmaceutically acceptable salts in the treatment of alopecia areata. Other cited prior art (Xie, He, and Garcia- Melendo), while mentioning alopecia areata or atopic dermatitis, does not disclose the use of the specific compound CS 12192 for the treatment of atopic dermatitis or alopecia areata, nor does it provide any experimental data to demonstrate its feasibility. Applicant further points out that there are significant differences between rheumatoid arthritis (RA) mentioned by Shan and atopic dermatitis (AD) and alopecia areata (AA) as indications defined in this application, in terms of disease type, target organs, and clinical manifestations. For the above reasons, due to the limited understanding and unclear mechanisms of autoimmune diseases, an effect on one autoimmune disease does not necessarily mean an effect on another. In fact, the treatment of these diseases has always been a challenge in medicine. Applicant further provides prior art evidence (see attached) to show that the predictability of the treatment of various diseases under the concept of autoimmune diseases is very low. Therefore, for the compounds of the present application as JAK1/3 inhibitors, it is not reasonable to expect that they have good therapeutic effects on specific types of immune diseases (i.e., alopecia areata and atopic dermatitis)
Examiner response:
Applicant's arguments have been fully considered but they are not persuasive. Applicant argues that the predictability is very low for autoimmune diseases2, however, obviousness does not require absolute predictability, but a reasonable expectation of success. See MPEP 2143.02. Xie, He and Garcia-Melendo provide the ordinary skilled artisan with the requisite motivation to utilize Shan’s and Xie’s JAK inhibitor CS12192 to treat atopic dermatitis and alopecia areata, and obtain predictable results. One of ordinary skill in the art would predict that JAK inhibitor, CS12192 would treat atopic dermatitis and alopecia areata because Xie, He, and Garcia-Melendo teach many JAK inhibitors that are FDA approved/in clinical trials used for the treatment of atopic dermatitis and alopecia areata including ruxolitinib, JAK1/JAK2 selective inhibitor, Tofacitinib, a selective JAK3 inhibitor, Oclacitinib, a JAK inhibitor, etc. Moreover, Shan and Xie teach that CS12192 is a novel selective JAK inhibitor; CS12192 showed more selective JAK3 inhibition with an IC50 of 11 nM; CS12192 affects cytokine production of CD4+ T, CS12192 significantly inhibited the serum levels of pro-inflammatory cytokines; CS12192 is superior to other JAK inhibitors because CS12192 selectively inhibits JAK3 (IC50 = 11 nM); CS12192 demonstrated good therapeutic results. The teachings of Shan and Xie combined indicate that CS12192 is a potent JAK inhibitor, which would motivate skilled artisan to use CS12192 in treating a condition known in the art to be treated successfully with JAK inhibitors. Thus, the cited prior art would have motivated the ordinary skilled artisan to use CS12192 to treat atopic dermatitis and alopecia areata and have reasonable predictability and expectation of success.
Because Shan teaches using CS12192 for treating rheumatoid arthritis, Applicant argues the differences between rheumatoid arthritis (RA) atopic dermatitis (AD) and alopecia areata (AA), however, this argument is not persuasive when Shan is combined with Xie, He, and Garcia-Melendo because one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). See the rationale of the 103 rejection above.
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). The prior art of Shan and Xie clearly state that JAK inhibitor, CS12192, is a potent and selective JAK inhibitor, and Xie, He, and Garcia-Melendo teach the effectiveness of JAK inhibitor in treating atopic dermatitis and alopecia areata, thus it would have been reasonable for one of ordinary skill in the art to use the potent JAK inhibitor, CS12192, for treating atopic dermatitis and alopecia areata.
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.
Non-statutory Double Patenting over US Patent No. US 10,011,571 B2
Claims 8 and 11 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of US Patent No. 10,011,571 B2 in view of S. Shan, et al. International Immunopharmacology, Volume 77, 2019, 105914, ISSN 1567-5769, “Shan” cited in the IDS dated 10/19/2023), Z. Xie et al. Journal of Medicinal Chemistry, January 22, 2021 Vol 64, Issue 3, P 1283- 1345, “Xie” cited in the PTO-892) H. He et al. American Journal of Clinical Dermatology (2019) 20:181–192, “He” cited in the PTO-892), and C. Garcia-Melendo et al. (Actas Dermosifiliogr. 2021; 112:503-515, “Garcia-Melendo” cited in the IDS dated 01/29/2025). Although the claims at issue are not identical, they are not patentably distinct from each other because:
Instant claims 8 and 11 recites “a method for treating or ameliorating an autoimmune skin disease, by administering a JAK3/JAK1/TBK1 selective inhibitor in a dosage of 20-600 mg/time/day to a subject in need thereof, wherein the JAK3/JAK1/TBK1 selective inhibitor is N-(3-((5-chloro-2-((4-fluoro-3-(N-methylacrylamido)phenyl)amino)-4-pyrimidinyl)amino)propyl)-4-cyanobenzamide, or a pharmaceutically acceptable salt thereof, or a stereoisomer thereof, and the autoimmune skin disease is atopic dermatitis or alopecia areata.”
US Patent No. 10,011,571 B2 recites in claims 1 and 17-20 a compound of formula (I) and a method of using a compound of formula (I) in treating a disease related to abnormal activities of JAK3 and/or JAK1 kinases, wherein the disease is selected from the group consisting of autoimmune diseases, rheumatoid arthritis, psoriasis, and claim 8 recites N-(3-((5-chloro-2-((4-fluoro-3-(N-methylacrylamido)phenyl)amino)-4-pyrimidinyl) amino)propyl)-4- cyanobenzamide (claimed compound) as species of formula (I).
While US Patent No. 10,011,571 B2 recites using N-(3-((5-chloro-2-((4-fluoro-3-(N-methylacrylamido)phenyl)amino)-4-pyrimidinyl) amino)propyl)-4- cyanobenzamide (claimed compound) in treating a disease related to abnormal activities of JAK3 and/or JAK1 kinases, and recites that the disease is an autoimmune disease, US Patent No. 10,011,571 B2 does not recite that the autoimmune disease is an autoimmune skin disease. The court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Sun Pharm. Indus., Ltd. v. Eli Lilly & Co., 611 F.3d 1381, 95 USPQ2d 1797 (Fed. Cir. 2010); Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003). US Patent No. 10,011,571 B2’s specification recites that compound of formula (I) are JAK3 and/or JAK1 inhibitors.
Shan, Xie, He and Garcia-Melendo teach as discussed above, and said teachings are incorporated herein by reference.
The obviousness rationale is the same as the rationale of the 103 Rejection above, at pages 9-10.
US Patent No. 10,011,571 B2 recites in claims 15 and 21, a pharmaceutical composition comprising the compound of formula (I) in an amount ranging from 0.0001 to 200 mg.
US Patent No. 10,011,571 B2 recites overlapping amounts of the recited amount of the same JAK3/JAK1/TBK1 selective inhibitor of 20-600mg/time/day. As described in MPEP 2144.05, in the case where the claimed ranges "overlap or lie inside ranges disclosed by the prior art" a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990). "[A] prior art reference that discloses a range encompassing a somewhat narrower claimed range is sufficient to establish a prima facie case of obviousness." In re Peterson, 315 F.3d 1325, 1330, 65 USPQ2d 1379, 1382-83 (Fed. Cir. 2003). See also In re Harris, 409 F.3d 1339, 74 USPQ2d 1951 (Fed. Cir. 2005) (claimed alloy held obvious over prior art alloy that taught ranges of weight percentages overlapping, and in most instances completely encompassing, claimed ranges; furthermore, narrower ranges taught by reference overlapped all but one range in claimed invention). Moreover, "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955).
Response to Argument
Applicant argues:
As mentioned above, the technical solution of the amended claims 8 and 11 are not obvious. Therefore, there is no issue of double patenting of claims 8 and 11 of the present application overUS10011571B2.
Examiner response:
Applicant's arguments have been fully considered but they are not persuasive for the reasons stated in the examiner response above.
Conclusion
Claims 8 and 11 are rejected. No claim is allowed.
THIS ACTION IS MADE FINAL. 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 MANAHIL MIRGHANI ALI ABDALHAMEED whose telephone number is (571)272-1242. The examiner can normally be reached M-F 7:30 am - 5:00 pm.
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/M.M.A./Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
1 Weight of rat in kg (S. Reagan-Shaw et al. (2008), The FASEB Journal, 22: 659-661, page 660, Table 1, cited in the PTO-892 dated 03/25/2026).
2 Applicant asserted that evidences 1-5 are attached, with Evidence 1 showing the complete failure of the Phase II clinical trial of the JAK inhibitor izencitinib in the treatment of ulcerative colitis. Evidence 2 shows that itacitinib, a JAK1 inhibitor, failed in a key phase III trial for first-line treatment of acute graft-versus-host disease. Evidence 3 shows Aclaris' JAK1/3 inhibitor ATI-502 failed in Phase II clinical trial for alopecia areata. Evidence 4 shows that not all AA (alopecia areata) patients respond to JAK1 treatment, the relationship between JAKi selectivity and clinical effectiveness is unknown. Evidence 5 shows that the negative results of the JAK1 inhibitor filgotinib in Crohn's disease. However, these evidences 1-5 are not provided. Thus, argument with respect to these evidences is not considered.
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