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 the Claims
Claims 1, 3, 5, 7 – 8, 11, 14, 16 – 17, 21 – 23, 26, 29, 38 – 40, 44 and 48 are currently pending and are the subject of this Office Action. This is the first Office Action on the merits of the claims.
Information Disclosure Statement
No information disclosure statement has been filed in this case. The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1, 3, 5, 7 – 8, 11, 14, 16 – 17, 21 – 23, 26, 29, 38 – 40, 44 and 48 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Independent claim 1 recites a method of treating clinical type 1 diabetes (T1D), comprising administering to a subject in need thereof: a 12-day to 14-day course of teplizumab at a total dose of about 9000 µg/m2 to about 14000 µg/m2; and an effective amount of a DYRK1A inhibitor, optionally wherein the total teplizumab dose is about 9000 µg/m2 to about 9500 µg/m2. Similarly, independent claims 38 and 44 recite a method of preventing or delaying the onset of T1D or a method of treating T1D, respectively, comprising administering teplizumab and an effective amount of a DYRKIA inhibitor. However, the present specification does not provide an example in which a DYRK1A inhibitor is administered with teplizumab.
The Examples on pages 43 – 71 of the specification disclose the administration of teplizumab but only seem to provide broad possibilities of adding DYRK1 inhibitors in the teplizumab treatments (Examples 7 – 10, p. 69 – 71). No examples of any specific DYRK1A inhibitor used in a method of treating clinical T1D or in a method of preventing or delaying the onset of T1D or in a method of treating T1D are provided.
To provide evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof. Applicant is directed to MPEP 2163 for guidelines on compliance with the written description requirement.
Here, Applicant has not described a reasonable number of agents capable of inhibiting DYRK1A , i.e. the required starting materials for the claims, but rather, Applicant has presented the public with an idea of how to perform an assay that might identify some agents that fall within the scope of the claims. Of course, depending on what agents are used in the screening assay, it may well identify none. The Court of Appeals for the Federal Circuit addressed claims of this sort in great detail in University of Rochester v. G.D. Searle and Co. (69 USPQ 2nd 1886, CAFC 2004). In Rochester, the Federal Circuit upheld the district court's ruling that patent claims which recited administration of compounds not disclosed, but rather to be identified in a screening assay, were invalid on their face. Here the claimed agent, DYRK1A inhibitor, does not have any particular conserved structure. Moreover, the specification does not disclose a structure/function correlation. Agents claimed with no structure that are only defined by function are generally not considered described.
Functionally defined genus claims can be inherently vulnerable to invalidity challenge for lack of written description support, especially in technology fields that are highly unpredictable, where it is difficult to establish a correlation between structure and function for the whole genus or to predict what would be covered by the functionally claimed genus. Abbvie Deutschland GMBH & Co. v. Janssen Biotech, Inc. (759 F.3d 1285 (Fed. Cir. 2014). “When a patent claims a genus using functional language to define a desired result, the specification must demonstrate that the applicant has made a generic invention that achieves the claimed result and do so by showing that the applicant has invented species sufficient to support a claim to the functionally-defined genus." Capon v. Eshhar, 418 F.3d 1349 (Fed. Cir. 2005).
Consequently, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the claimed genus of administered agents nor guidance as to which of the myriad of molecules encompassed by the instant method claims would meet the limitations of the claims.
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111 (Fed. Cir. 1991), clearly states that “applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description’ inquiry, whatever is now claimed.” (See page 1117). The specification does not “clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed.” (See Vas-Cath at page 1116).
Furthermore, in Amgen Inc. et al. v. Sanofi et al., 598 U.S. 594, 2023 USPQ2d 602 (2023), the
Supreme Court, held that claims drawn to a genus of monoclonal antibodies, which were functionally claimed by their ability to bind to a specific protein, PCSK9, were invalid due to lack of enablement. The claims at issue were functional, in that they defined the genus by its function (the ability to bind to specific residues of PCSK9) as opposed to reciting a specific structure (the amino acid sequence of the antibodies in the genus). See MPEP 2164.01.
In the present claim 1, the DYRK1A inhibitor is only defined by functional properties, its ability to inhibit DYRK1A, with no specific structure recited in the claim. In view of the fact patterns detailed in Amgen Inc. et al. v. Sanofi et al., the applicant is not in possession of an inhibitor that binds to DYRK1A of claims 1, 38 and 44.
Regarding claim 48, although the claim recites specific DYRK1A inhibitors, claim 48 also recites derivatives. However, the present specification does not define the structures of the derivatives, and it is not clear what the boundaries of the derivatives are. A derivative is only described in terms of the source structure and not in terms of the structure of the derivative itself. Therefore, the derivatives are not described, only their sources are described.
The skilled artisan cannot envision the detailed chemical structure of the genus of claimed treatment agents, and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of identification. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it. The compound itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016 (Fed. Cir. 1991). Therefore, the instant claims do not meet the written description requirement.
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 48 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 applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 48 recites "e.g." in line 4 which is indefinite because it is unclear whether the limitation(s) following the phrase are part of the claimed invention. See MPEP § 2173.05(d).
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 (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 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 1, 3, 5, 7 – 8, 11, 14, 16 – 17, 21 – 23, 26, 29, 38 – 40, 44 and 48 are rejected under 35 U.S.C. 103 as being unpatentable over HEROLD (Herold, K. C., et al. (2019). An anti-CD3 antibody, teplizumab, in relatives at risk for type 1 diabetes. New England Journal of Medicine, 381(7), 603-613) in view of KUMAR (Kumar, K., et al. (2021). DYRK1A inhibitors as potential therapeutics for β-cell regeneration for diabetes. Journal of medicinal chemistry, 64(6), 2901-2922).
HEROLD is directed to a study where patients were randomly assigned to a single 14-day course of teplizumab or placebo, and follow-up for progression to clinical type 1 diabetes. See HEROLD at ABSTRACT: METHODS. HEROLD teaches that The median total dose of teplizumab administered was 9.14 mg per square meter (interquartile range, 9.01 to 9.37). See HEROLD at p. 606, RESULTS: PARTICIPANTS, second paragraph.
Furthermore, HEROLD teaches that in the disclosed phase 2 trial, a single course of teplizumab significantly slowed progression to clinical type 1 diabetes in high-risk, nondiabetic relatives of patients with diabetes who had at least two autoantibodies and abnormal results of an oral glucose-tolerance test at trial entry. The median delay in the diagnosis of diabetes was 2 years; at the conclusion of the trial, the percentage of diabetes-free persons in the teplizumab group (57%) was double that in the placebo group (28%). Thus, HEROLD’s method prevents or delays the onset of T1D.
However, HEROLD does not teach the administering of an effective amount of a DYRKIA inhibitor in addition to teplizumab.
KUMAR is directed to several small molecule DYRK1A inhibitors that have been identified that induce human β-cell proliferation in vitro and in vivo, have also been shown to synergize β-cell proliferation with other classes of drugs, such as TGFβ inhibitors and GLP-1 receptor agonists. KUMAR reviews the status of DYRK1A as a therapeutic target for β-cell proliferation and provide perspectives on technical and scientific challenges for future translational development. See KUMAR at the abstract.
Because KUMAR teaches that DYRK1A inhibitors have also been shown to synergize β-cell proliferation with other classes of drugs, it would have been obvious to combine DYRK1A inhibitors with HEROLD’s teplizumab in a method of treating clinical T1D of present claim 1 or in a method of preventing or delaying the onset of T1D of claim 38 or in a method of treating T1D of claim 44.
At the effective filing date of the present claims, it would have been prima facie obvious to the person of ordinary skill in the art to arrive at the claimed invention from the disclosures of HEROLD and KUMAR. The artisan would have been motivated to use the method of claims 1, 38 and 44 because HEROLD teaches that a 2-week course of treatment with teplizumab delayed the diagnosis of clinical type 1 diabetes in high-risk participants (see HEROLD at DISCUSSION, last sentence, p. 612) and KUMAR teaches that DYRK1A inhibitors have also been shown to synergize β-cell proliferation with other classes of drugs. Thus, the artisan would have a reasonable expectation of success from the combined teachings of HEROLD and KUMAR.
Regarding claims 3, 8 and 29, HEROLD teaches that teplizumab was given at a dose of 51 μg per square meter of body-surface area on day 0, a dose of 103 μg per square meter on day 1, a dose of 207 μg per square meter on day 2, and a dose of 413 μg per square meter on day 3, followed by a dose of 826 μg per square meter on each of days 4 through 13, as described previously. See HEROLD at TRIAL DESIGN and INTERVENTION, p. 605, left column. Although the dosing regimen is not exactly as recited in present claim 3, the regimen of claims 3, 8 and 29 can be arrived to routine experimentation. “[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 reAller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). Similarly, a prima facie case of obviousness exists where the claimed ranges or amounts do not overlap with the prior art but are merely close. Titanium Metals Corp. of Americav.Banner, 778 F.2d 775, 783, 227 USPQ 773, 779 (Fed. Cir. 1985)”. See MPEP 2144.05 (I) and (II).
Regarding claims 5 and 7, HEROLD teaches that the drug was given for only one course but repeated dosing may provide additional benefits and capture more persons with active disease or prolong the therapeutic effect. See HEROLD at DISCUSSION, second to last paragraph of left column, p. 612.
Regarding claim 11, HEROLD teaches the monitoring of KLRG1+TIGIT+CD8+ T cells (see ABSTRACT: RESULTS) and further teaches that repeated dosing may provide additional benefits and capture more persons with active disease or prolong the therapeutic effect (see HEROLD at DISCUSSION, second to last paragraph of left column, p. 612).
Regarding claim 14, HEROLD teaches that KLRG1-TIGIT-CD8+ T cells at over 10% and measurement of the frequency of at 0, 3, 6 and 18 months. See HEROLD at Supplementary Appendix Figure S3A. Thus, HEROLD teaches monitoring the patients’ KLRG1-TIGIT-CD8+ T cells one year after the 6-month measurement.
Regarding claim 16, KUMAR teaches that the development of DYRK1A kinase inhibitors for β-cell proliferation, alone or in combination with other drugs, shows unequivocal promise and merits further drug development with the potential reward to end insulin dependence for hundreds of millions of people with both T1D and T2D. See KUMAR at the last sentence, p. 2917, right column. Thus, because KUMAR teaches that the disclosed method can end insulin dependence, the treatment likely results in reduction of exogenous insulin use, HbAlc levels, hypoglycemic episodes, or combinations thereof by at least 10% as compared to pre-treatment levels.
Regarding claims 17 and 39, HEROLD teaches that teplizumab or saline was administered intravenously in a clinical research center. See HEROLD at TRIAL DESIGN AND INTERVENTION, p. 605, top of left column.
Regarding claim 21, KUMAR teaches the oral dosage of the DYRK1A GNF4877. See p. 2908, top of left column and Figure 5, p. 2907.
Regarding claim 22, KUMAR teaches the administration of DYRK1A in combination with other drugs. For example, the DYRK1A inhibitor CC-401 and TGFβ inhibitor combination increased both rat and human β-cell proliferation. See KUMAR at p. 2910, right column, under DYRK1A INHIBITORS IN COMBINATION WITH TGFβ INHIBITORS.
Regarding claim 23, HEROLD teaches that eligible participants were nondiabetic relatives of patients with type 1 diabetes and were at least 8 years of age at the time of randomization and at high risk for development of clinical diabetes. See HEROLD at p. 604, right column, second paragraph. Furthermore, HEROLD teaches that the effects of teplizumab treatment in participants whose C-peptide area under the curve during the oral glucose tolerance test at randomization had a median of 1.75 nmol/L (see HEROLD at Supplemental Appendix, Figure S8) or 1.75 pmol/mL, which is greater than 0.2 pmol/mL as recited. Although the c-peptide is from an oral glucose tolerance test, HEROLD’s c-peptide of 1.75 nmol/L is significantly is greater than 0.2 pmol/mL as recited and thus, the c-peptide value will likely be greater than 0.2 pmol/mL during a mixed meal tolerance test.
Regarding claim 26, HEROLD teaches the effects of teplizumab treatment in participants whose C-peptide area under the curve for 60 months. See HEROLD at Supplemental Appendix, Figure S8.
Regarding claims 29 and 40, HEROLD teaches that teplizumab was given at a dose of 51 μg per square meter of body-surface area on day 0, a dose of 103 μg per square meter on day 1, a dose of 207 μg per square meter on day 2, and a dose of 413 μg per square meter on day 3, followed by a dose of 826 μg per square meter on each of days 4 through 13. See HEROLD at Trial Design and Intervention, p. 605, top of left column. Although the dosing regimen is not exactly as recited in present claims 29 and 40, it would have been obvious to arrive the recited dosing regimen from the teachings HEROLD by routine experimentation. See MPEP 2144.05 (I) and (II).
Regarding claim 48, KUMAR teaches the DYRK1A inhibitors harmine, 5-IT, CC-401, harmine analogue, GNF7156, GNF4877, GNF2133 and 1,5-naphthridine. See KUMAR at Table 1, p. 2902.
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 1, 3, 5, 7 – 8, 11, 14, 16 – 17, 21 – 23, 26, 29, 38 – 40, 44 and 48 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 20 of U.S. Patent No. 11,434,291 in view of HEROLD and KUMAR.
Patented claim 1 recites a method of preventing or delaying the onset of clinical type I diabetes (T1D), comprising: providing a non-diabetic subject who is (1) in an immunospecific assay, free of antibodies against zinc transporter 8 (ZnT8), (2) HLA-DR4+, and (3) not HLA-DR3+; and administering an agent comprising a prophylactically effective amount of teplizumab to the non-diabetic subject.
Patented claim 9 recites that the prophylactically effective amount comprises a 10 to 14 day course of subcutaneous (SC) injection or intravenous (IV) infusion or oral administration of teplizumab at from about 10 to about 1000 micrograms/meter squared (μg/m2).
The main difference between the present claims and the patented claims is that the present claims recite the administration of an effective amount of a DYRK1A inhibitor. However, KUMAR teaches this difference. The teachings of HEROLD and KUMAR, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims recite a method of preventing or delaying the onset of clinical type I diabetes (T1D), comprising: administering an agent comprising a prophylactically effective amount of teplizumab and KUMAR teaches that DYRK1A inhibitors have also been shown to synergize β-cell proliferation with other classes of drugs, it would have been obvious to one having ordinary skill in the art to add KUMAR’s DYRK1A inhibitors to the method of the patented claims.
Claims 1, 3, 5, 7 – 8, 11, 14, 16 – 17, 21 – 23, 26, 29, 38 – 40, 44 and 48 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 23 of U.S. Patent No. 12,006,366 in view of HEROLD and KUMAR.
Patented claim 1 recites a method of preventing or delaying the onset of clinical type 1 diabetes (T1D), comprising: administering a prophylactically effective amount of teplizumab to a non-diabetic subject who is at risk for T1D, wherein the prophylactically effective amount of teplizumab comprises a 10 to 14 day course of teplizumab, wherein at three months or more after the administration of the 10 to 14 day course of teplizumab, the subject has a frequency of from about 5% to about 50% T Cell Immunoreceptor With Ig And ITIM Domains (TIGIT)+ killer cell lectin like receptor G1 (KLRG1)+ cluster of differentiation 8 (CD8)+ T-cells in all cluster of differentiation 3 (CD3)+ T-cells, indicative of successful prevention or delay of the onset of clinical T1D.
Patented claim 9 recites administering by subcutaneous injection the 10 to 14 day course of teplizumab at a daily dose of 10-1000 micrograms/meter squared (μg/m2).
The main difference between the present claims and the patented claims is that the present claims recite administering an effective amount of a DYRKIA inhibitor. However, KUMAR teaches this difference. The teachings of HEROLD and KUMAR, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims recite recites a method of preventing or delaying the onset of clinical type I diabetes (T1D), comprising: administering a prophylactically effective amount of teplizumab to a non-diabetic subject who is at risk for T1D and KUMAR teaches that DYRK1A inhibitors have also been shown to synergize β-cell proliferation with other classes of drugs, it would have been obvious to one having ordinary skill in the art to add KUMAR’s DYRK1A inhibitors to the method of the patented claims.
Claims 1, 3, 5, 7 – 8, 11, 14, 16 – 17, 21 – 23, 26, 29, 38 – 40, 44 and 48 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 66 of U.S. Patent No. 12,565,529 in view of HEROLD and KUMAR.
Patented claim 1 recites a method of delaying progression of Stage 3 type 1 diabetes (T1D) in a patient diagnosed with Stage 3 T1D, comprising administering to the patient two 12-day courses of teplizumab, wherein each 12-day course comprises a first dose of 106 μg/m2 teplizumab on day 1, a second dose of 425 μg/m2 teplizumab on day 2, and one dose of 850 μg/m2 teplizumab on each of days 3-12.
The main difference between the present claims and the patented claims is that the present claims recite administering an effective amount of a DYRKIA inhibitor. However, KUMAR teaches this difference. The teachings of HEROLD and KUMAR, and how they relate to the claims, are set forth in the rejections under 35 U.S.C. 103 above.
Because the patented claims recite recites a method of delaying progression of Stage 3 type 1 diabetes (T1D) in a patient diagnosed with Stage 3 T1D, comprising administering teplizumab and KUMAR teaches that DYRK1A inhibitors have also been shown to synergize β-cell proliferation with other classes of drugs, it would have been obvious to one having ordinary skill in the art to add KUMAR’s DYRK1A inhibitors to the method of the patented claims.
Conclusion
No claim is allowed.
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/ESTELLA M. GUSTILO/Examiner, Art Unit 1646
/GREGORY S EMCH/Supervisory Patent Examiner, Art Unit 1678
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