DETAILED ACTION
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 the Claims
Claims 1-53 have been canceled.
Claims 54-75 are currently pending.
Election/Restrictions
Applicant’s election of Group I, Claims 54-73, and of species proinsulin, the individual has two or more autoantibodies against β-cell specific antigens, early stage pre-symptomatic T1D, the JAK inhibitor and pancreatic autoantigen or a derivative or variant thereof are provided simultaneously, Baricitinib, both the JAK inhibitor and pancreatic autoantigen or derivative thereof are administered in a pharmaceutical composition, in the reply filed on 3/6/2026 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 § 818.03(a)). Regarding species 5, during a telephone conversation with Katherine T. Wade on 4/22/2026 a provisional election was made without traverse to prosecute the species of JAK1 as species 5. Affirmation of this election must be made by applicant in replying to this Office action.
The requirement is still deemed proper and is therefore made FINAL.
Claims 57, 60-64, 66-68, and 73-75 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to nonelected inventions and species, there being no allowable generic or linking claims.
Claims 54-56, 58-59, 65, and 69-72 are being examined in this application, insofar as they read on the elected species of proinsulin, the individual has two or more autoantibodies against β-cell specific antigens, early stage pre-symptomatic T1D, the JAK inhibitor and pancreatic autoantigen or a derivative or variant thereof are provided simultaneously, JAK1, Baricitinib, both the JAK inhibitor and pancreatic autoantigen or derivative thereof are administered in a pharmaceutical composition.
Claim Objections
Claims 54 and 71 are objected to because of the following informalities:
Claim 54, line 3, the recitation of “JAK” is suggested to read “Janus Kinase”.
Claim 71, line 4-6, the recitation of “provided in the individual by administering to the individual a pharmaceutical composition comprising a pancreatic autoantigen or a derivative or variant thereof to the individual” is suggested to read “provided to the individual by administering to the individual a pharmaceutical composition comprising a pancreatic autoantigen or a derivative or variant thereof”.
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.
Claim 55 is 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 pre-AIA the applicant regards as the invention.
Claim 55, line 4, the recitation of “optionally” is indefinite as it is unclear if the limitation that follows is required to meet the scope of the invention. It is noted that the element follows the term “optionally” is already in the Markush group.
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 of this title, 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.
Claims 54-56, 58-59, 65, and 69-72 are rejected under 35 U.S.C. 103 as being unpatentable over Herold et al (WO 2005/076965 A2; 8/25/2005. Cited on IDS) in view of Insel et al (Diabetes Care. 2015;38:1964-1974.), Xi et al (US 2017/0081338 A1; 3/23/2017.), and Kubo et al (Annals of the Rheumatic Diseases. 2016;75:260.).
The instant claims recite a method of delaying the progression of type 1 diabetes (T1D) in an individual having T1D, the method comprising providing in the individual: an anti-inflammatory compound, wherein the anti-inflammatory compound is a JAK inhibitor; and a pancreatic autoantigen or a derivative or variant thereof; thereby delaying the progression of T1D in the individual.
Herold teaches a method for treating Type I diabetes (T1D), comprising administering to a subject an anti-CD3 antibody and a self-antigen in an amount sufficient to treat the underlying cause of T1D (para 0016) as well as one or more symptoms associated with T1D (Claim 16), wherein the self-antigen is proinsulin (a pancreatic autoantigen or a derivative or variant thereof) (para 0016, 0121), the anti-CD3 induces the activation/expansion of regulatory T-cells (an anti-inflammatory process, therefore, anti-CD3 is an anti-inflammatory compound) (para 0052), and the method prevents progression of autoimmunity (para 0050). Antigen-specific interventions to treat T1D have to be given early (during the pre-diabetic phase) (para 0094), the one or more symptoms associated with T1D includes reduced insulin production (Claim 17), abnormal levels of blood glucose (Claim 18), and destruction of insulin-producing islet cells (Claim 19), all of the above are indicators of early stage T1D. Before the effective filing date of the claimed invention, it was well-known in the art that early stage T1D is evidenced by the presence of two or more islet autoantibodies with normoglycemia and is presymptomatic, as evidenced by Insel (p.1964 para 1). The anti-CD3 antibody and the self-antigen are encountered at least at one time point essentially simultaneously by the subject’s immune system (para 0017). Anti-CD3 antibody and/or self-antigen can be administered on a dosing schedule (para 0068). The self-antigen is administered orally, subcutaneously, intramuscularly, or intravenously (para 0020).
Herold does not teach the method wherein the anti-inflammatory compound is a JAK inhibitor (claims 54, 59 and 71-72), the JAK inhibitor is selective for JAK1 (claim 65), and the JAK inhibitor is Baricitinib (claims 69-70).
However, Herold does teach the method for treating T1D comprises administering an anti-inflammatory compound and a self-antigen including proinsulin (a pancreatic autoantigen or a derivative or variant thereof) to a subject. Xi teaches protein kinase inhibitors have gathered attention as a new drug category for both immunosuppression and anti-inflammatory drug, new or improved agents which inhibit protein kinases such as Janus kinases (JAK) inhibitors are continually needed that act as agents for the prevention and treatment of autoimmune diseases including Type I diabetes (para 0029). In addition, Kubo teaches the JAK/STAT pathway is a potent therapeutic target in autoimmune diseases, baricitinib, a JAK1/2 inhibitor (p.260 col left – last para), characteristically inhibited the activation of IFN/STAT4 signal, and the different mode of action among JAK inhibitors may affect the clinical effects in patients not only with rheumatoid arthritis but other immune-mediated diseases (p.260 col right – para 5).
Thus, before the effective filing date of the claimed invention, it would have been obvious to one of ordinary skill in the art to incorporate a JAK inhibitor such as Baricitinib as an anti-inflammatory compound, and to provide the JAK inhibitor and a pancreatic autoantigen simultaneously, since Herold discloses a method for treating T1D comprises administering an anti-inflammatory compound and a self-antigen including proinsulin (a pancreatic autoantigen) simultaneously to a subject, Xi discloses that new or improved agents which inhibit protein kinases such as JAK inhibitors are continually needed that act as agents for the prevention and treatment of autoimmune diseases including Type I diabetes, and Kubo discloses that baricitinib, a JAK1/2 inhibitor, characteristically inhibited the activation of IFN/STAT4 signal, and may affect the clinical effects in patients not only with rheumatoid arthritis but other immune-mediated diseases. Moreover, before the effective filing date of the claimed invention, one of ordinary skill in the art would have been motivated by the cited references to incorporate a JAK inhibitor such as Baricitinib as an anti-inflammatory compound, and to provide the JAK inhibitor and a pancreatic autoantigen simultaneously, with a reasonable expectation for successfully treating Type I diabetes (T1D).
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 claims at issue 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); and 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 a nonstatutory double patenting ground provided the reference application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The USPTO internet Web site contains terminal disclaimer forms which may be used. Please visit http://www.uspto.gov/forms/. The filing date of the application will determine what form 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 http://www.uspto.gov/patents/process/file/efs/guidance/eTD-info-I.jsp.
Claims 54-56, 58-59, 65, and 69-72 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-2, 4-8 and 10-11 of U.S. Patent No 11,806,386 B2 (referred to as the ‘386 patent) in view of Xi et al (US 2017/0081338 A1; 3/23/2017.) and Kubo et al (Annals of the Rheumatic Diseases. 2016;75:260.).
Claims 1-2, 4-8 and 10-11 of the ‘386 patent recite a method of delaying the onset of type 1 diabetes (T1D) in an individual having or at risk of having T1D, the method comprising providing in the individual: an anti-inflammatory compound; and a pancreatic autoantigen or a derivative or variant thereof; thereby delaying the onset of T1D in the individual; wherein the anti-inflammatory compound is Ruxolitinib, and wherein the pancreatic autoantigen is proinsulin or a derivative or variant thereof. The individual at risk of developing type 1 diabetes has 2 or more autoantibodies against β-cell specific antigens. The T1D is early-stage type 1 diabetes. The anti-inflammatory compound and pancreatic autoantigen or a derivative or variant thereof are provided simultaneously. The pancreatic autoantigen or derivative or variant thereof is administered orally, by inhalation, subcutaneously, intravenously, intranasally, intramuscularly or intradermally.
‘386 patent does not teach the method wherein the JAK inhibitor is Baricitinib (claims 69-70).
However, ‘386 patent does teach the method for treating T1D comprises administering a JAK inhibitor and proinsulin to a subject. Xi teaches protein kinase inhibitors have gathered attention as a new drug category for both immunosuppression and anti-inflammatory drug, new or improved agents which inhibit protein kinases such as Janus kinases (JAK) inhibitors are continually needed that act as agents for the prevention and treatment of autoimmune diseases including Type I diabetes (para 0029). In addition, Kubo teaches the JAK/STAT pathway is a potent therapeutic target in autoimmune diseases, baricitinib, a JAK1/2 inhibitor (p.260 col left – last para), characteristically inhibited the activation of IFN/STAT4 signal, and the different mode of action among JAK inhibitors may affect the clinical effects in patients not only with rheumatoid arthritis but other immune-mediated diseases (p.260 col right – para 5).
Thus, before the effective filing date of the claimed invention, it would have been obvious to one of ordinary skill in the art to incorporate Baricitinib as a JAK inhibitor, since ‘386 patent discloses a method for treating T1D comprises administering a JAK inhibitor and proinsulin to a subject, Xi discloses that new or improved agents which inhibit protein kinases such as JAK inhibitors are continually needed that act as agents for the prevention and treatment of autoimmune diseases including Type I diabetes, and Kubo discloses that baricitinib, a JAK1/2 inhibitor, characteristically inhibited the activation of IFN/STAT4 signal, and may affect the clinical effects in patients not only with rheumatoid arthritis but other immune-mediated diseases. Moreover, before the effective filing date of the claimed invention, one of ordinary skill in the art would have been motivated by the cited references to incorporate Baricitinib as a JAK inhibitor with a reasonable expectation for successfully treating Type I diabetes (T1D).
Conclusion
No claims are allowed.
Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to LYNN Y FAN whose telephone number is (571)270-3541. The examiner can normally be reached on M-F 7am-4pm.
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/Lynn Y Fan/
Primary Examiner, Art Unit 1759
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