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 .
Election/Restrictions
Upon consideration, the restriction requirement filed 12/16/2025 has been withdrawn and all claims are hereby rejoined and fully examined for patentability under 37 CFR 1.104. Once the restriction requirement is withdrawn, the provisions of 35 U.S.C. 121 are no longer applicable.
Claims Status
Amendments filed 03/16/2026 are entered. Claims 7, 9-13, 16, 22-27, 29-33, 35, 37-40 are pending and under examination.
Priority
This application claims priority benefits from:
Provisional No. 63345365, filed 05/24/2022
Provisional No. 63367992, filed 07/08/2022
Provisional No. 63382382, filed 11/04/2022
The effective filing date for instant claims 7, 9-13, 16, 22-27, 29-32, 35, 37-40 is 05/24/2022, the filing date of the Provisional No. 63345365.
The effective filing date for instant claims 33 is 11/04/2022, the filing date of the Provisional No. 63382382. The subject matter regarding treating subjects less than 1 year of age is not found in earlier benefit documents.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 05/31/2023, 11/30/2023, 01/17/2024, and 03/16/2026 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 7, 22, 25, 35, 40 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 7 recites a “relative” of a patient with T1D but the specification does not define a “relative” and the commonly understood definition includes those connected legally (e.g. by adoption, marriage) and may not be significantly genetically similar. However, the specification discloses an example in which the subject is a first or second degree relative of a type-1 diabetic (p. 20, para 87), which is commonly understood as biological-related first or second degree relative. It is unclear if “relative” in the claims encompasses all relatives or only biological relatives, and what degree of relation.
Claim 22 recites the limitation "delays median time to clinical diagnosis of T1D". However, its parent claim recites “delaying the onset of Stage 3 type 1 diabetes (T1D)” in a subject with Stage 2 T1D. It is unclear if T1D in claim 22 is referring to the beginning of any stage of T1D in general, which would be Stage 1 T1D, or if it is referring to Stage 3 T1D, also known as clinical T1D, from its parent claim. There is insufficient antecedent basis for this limitation in the claim. For examination, T1D in claim 22 will be interpreted as Stage 3 T1D to be properly dependent on the parent claim.
The term “decrease” in claim 25 and “increase” in claim 40, respectively is a relative term which renders the claim indefinite. The terms “increase” and “decrease” are not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention.
Regarding “decrease” in claim 25, the specification discloses the method comprising determining, prior to or after the administration step, a “decrease” in the proliferation markers claimed (pp 36-37, para 144). However, it is unclear from the claims if the decrease should also occur between measurements taken prior to and after the 14-day course administration step. It is further unclear what degree of decrease is sufficient to show delay of onset of Stage 3 T1D as claimed.
Regarding “increase” in claim 40, the specification discloses examples where the increase in the claimed ratio is for prognosing responsiveness to preventing or delaying onset of type 1 diabetes in a non-diabetic patient (e.g. p.7 para 39). Therefore, it is unclear between what points in time, administration schedule, disease stage, or otherwise, the increase should occur and to what degree is needed to show delay of onset of Stage 3 T1D as claimed.
Claim 35 recites dysglycemia without “overt” hyperglycemia, but it is unclear what “overt” means in this situation, the specification does not provide a definition, and the commonly understood meaning would still make this claim indefinite. Is it dysglycemia without apparent hyperglycemia, meaning it is hypoglycemia? Is overt meant to indicate a threshold blood glucose level or a level of hyperglycemia, as in Burkly et al which teaches “overt hyperglycemia (i.e., fasting blood glucose levels > 250 mg/dL) (WO 9417828 A2, published 08/18/1994; p. 12, lines 11-13)?
Claim Rejections - 35 USC § 112(d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claims 7, 9-13, 16, 22-26 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
A series of singular dependent claims is permissible in which a dependent claim refers to a preceding claim which, in turn, refers to another preceding claim. A claim which depends from a dependent claim should not be separated by any claim which does not also depend from said dependent claim. It should be kept in mind that a dependent claim may refer to any preceding independent claim. In general, applicant's sequence will not be changed. See MPEP § 608.01(n).
Claims 7, 9-13, 16, 22-26 depend on independent claim 27. The claims are not numbered so that dependent claims refer only to a preceding claim.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 7, 9-11, 16, 22-27, 29-32, and 37 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Leon et al (US2020/0399368A1, published 12/24/2020).
To align terminology with the instant application, regarding claim 27, Leon et al teaches:
Clinical diabetes is synonymous with Stage 3 type I diabetes (para 6).
Stage 2 T1D is defined by the presence of diabetes-related autoantibodies and dysglycemia (p. 1, para 5) and that all subjects in their trial had 2 or more diabetes-related autoantibodies and dysglycemia as evidenced by abnormal glucose tolerance on OGTT (p. 10, para 102).
The 14-day course of teplizumab is counted from Day 0 – 13, instead of Day 1 – 14 (p. 10, para 105).
With these definitions, Leon et al therefore teaches:
a method of delaying the onset of Stage 3 type I diabetes (T1D) (Abstract),
comprising administering to a subject in need thereof with Stage 2 TlD a 14-day course of teplizumab comprising:
a first dose of about 65 μg/m2 teplizumab on day 1,
a second dose of about 125 μg/m2 teplizumab on day 2,
a third dose of about 250 μg/m2 teplizumab on day 3,
a fourth dose of about 500 μg/m2 teplizumab on day 4, and
one dose of about 1,030 μg/m2 teplizumab on each of days 5-14 (p. 10, para 105).
The instant specification teaches that “about” can be defined as within 30% of a value (p. 10, para 54). Therefore, the doses of Leon et al (p. 10, para 105) fall within the acceptable range and fulfill the limitations.
Day
(instant)
Dose (instant)
Acceptable range (+/- 30%)
Day
(Leon et al)
Dose
(Leon et al)
Dose x 0.7 (instant)
Dose x 1.3 (instant)
1
65
45.5
84.5
0
51
2
125
87.5
162.5
1
103
3
250
175
325
2
207
4
500
350
650
3
413
5-14
1030
721
1339
4-13
826
Regarding claim 7, Leon et al further teaches the subject is a relative of a patient with T1D, specifically children or siblings of patients with T1D (p. 11, para 117).
Regarding claim 9, Leon et al further teaches the subject has two or more autoantibodies (p. 11, para 117) and that these autoantibodies are selected from ICA, IAA, GAD, IA-2/ICA512 or ZnT8 (p. 1, para 11).
Regarding claims 10 and 11, Leon et al further teaches the subject has abnormal glucose tolerance on oral glucose tolerance test (OGTT) by the fasting plasma glucose level, 2 hour plasma, or intervening plasma glucose level claimed (p. 10, para 102).
Regarding claim 16, Leon et al further teaches the 14-day course of teplizumab is administered to the subject as a subcutaneous injection or as an intravenous infusion (p. 1, para 17), and specifically an intravenous infusion was reduced to practice in the trial (p. 10, para 105).
Regarding claim 22, Leon et al further teaches the method delays the median time to clinical diagnosis of T1D within the ranges instantly claimed. Specifically, the median times to T1D was 24.4 months in the placebo group versus 48.4 months in the teplizumab group, equating to a 24.2 month delay (p. 11, para 119).
Regarding claim 23, Leon et al further teaches determining the percentage of TIGIT+KLRG1+CD8+CD57- T cells after teplizumab administration (p. 12, para 123) and that drug treatment increased the proportion of TIGIT+KLRG1+CD8+CD57- T cells (p. 10, para 99). Figure 3A teaches there is at least 10 times more TIGIT+KLRG1+CD8+CD57- T cells in treated versus untreated subjects. Regarding claim 24, Leon et al further teaches determining of the percentage of TIGIT+KLRG1+CD8+ T cells is by flow cytometry (p. 11, para 111 and Figure 6). Regarding claim 25, since the drug treatment increased the proportion of TIGIT+KLRG1+CD8+CD57- T cells (p. 10, para 99), Leon et al inherently teaches determining a decrease in the percentage of CD8+ T cells expressing the CD57 marker after administration of the teplizumab course.
Regarding claim 26, Leon et al further teaches IV infusion of the 14-day course of teplizumab (p. 10, para 105) and that the subject is 8 years of age or older and has Stage 2 T1D (p. 10, para 102).
Regarding claims 29-32, Leon et al further teaches the subject is within the claimed age range (p. 10, para 102).
Regarding claim 37, Leon et al further teaches administering an effective amount of ibuprofen, which is a nonsteroidal anti-inflammatory drug (NSAID), and diphenhydramine, which is an antihistamine known as Benadryl, for at least the first 5 days of the 14-day course (p. 10, para 105).
Claim 35 is rejected under 35 U.S.C. 102(a)(1) as being anticipated by Leon et al (US2020/0399368A1, published 12/24/2020), as evidenced by Burkly et al (WO 9417828 A2, published 08/18/1994) and Lampasona et al (Lampasona et al, Islet Autoantibodies, Immunology and Transplantation, Vol 16, No 53; published 04/25/2016).
Regarding claim 35, Leon et al further teaches the patient has dysglycemia without overt hyperglycemia (p. 10, para 102), wherein overt hyperglycemia is interpreted to mean fasting blood glucose levels > 250 mg/dL, as evidenced by Burkly et al (p. 12, lines 11-13), and has two or more pancreatic islet autoantibodies, which encompass the autoantibodies taught by Leon et al (p. 1, para 11), as evidenced by Lampasona et al which teaches these claimed autoantibodies are islet autoantibodies (Abstract).
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 12-13 and 39 are rejected under 35 U.S.C. 103 as being unpatentable over Leon et al (US2020/0399368A1, published 12/24/2020).
Regarding claims 12 and 13, although Leon et al teaches a study including patients with and without ZnT8 autoantibodies, HLA-DR4, and HLA-DR3, they further explicitly envision the subject does not have ZnT8 autoantibodies, is HLA-DR4+, and is not HLA-DR3+ (Abstract).
Their findings that subjects without ZnT8 autoantibodies showed a greater response to the treatment than those with ZnT8 autoantibodies and that the presence of HLA-DR4 and absence of HLA-DR3 was associated with a more robust response to treatment (p. 12, para 124) and their subsequent teaching of treating this specific subject group (Abstract) makes it obvious to one skilled in the art, before the effective filing date, to apply this method to subjects without ZnT8 autoantibodies, with HLA-DR4, and without HLA-DR3. One skilled in the art, before the effective filing date, would be motivated to do so to get the greatest chance of a response to treatment, and would have a reasonable expectation of success due to the superior treatment response results.
Regarding claim 39, Leon et al further teaches the dose can be administered over a period of time, from about 5 minutes to about 22 hours; and in certain embodiments, by slow infusion over a period of 20 to 24 hours (p. 9, para 92); and in another specific embodiment, over a period of hours or days (p. 5, para 66). Leon et al further teaches all the doses are administered slowly by intravenous administration to reduce the possibility of cytokine release and other adverse effects (p. 9, para 92).
Leon et al does not explicitly teach administration over a period of at least 30 minutes as it teaches a range of times.
However, it would have been obvious to one skilled in the art, before the effective filing date of the instant application, to choose the higher range of time for infusion, such as the 20-24 hour embodiment. One skilled in the art, before the effective filing date of the instant application, would be motivated to administer the daily doses of teplizumab slowly for the advantage of reducing the risk of cytokine storm and adverse effects. A skilled artisan would have reasonable expectation of success due to the inverse relationship between infusion rate and risk of cytokine storm.
Claim 38 is rejected under 35 U.S.C. 103 as being unpatentable over Leon et al (US2020/0399368A1, published 12/24/2020) in view of Elliot et al (US11535679B2; filed 12/21/2021).
Leon et al further teaches administering an effective amount of ibuprofen, which is a nonsteroidal anti-inflammatory drug (NSAID), and diphenhydramine, which is an antihistamine known as Benadryl, for at least the first 5 days of the 14-day course (p. 10, para 105).
Leon et al does not explicitly teach the NSAID and antihistamine are administered orally.
However, Elliot et al teaches subjects to receive antibody infusions are pretreated with prophylaxis to attenuate infusion reactions, such as an oral dose of acetaminophen (column 50, line 30-35). Diphenhydramine can be administered orally or intravenously for the same purpose (column 50, line 30-35).
It would have been obvious to one skilled in the art, before the effective filing date of the instant application, that the premedication taught in Leon et al can also be administered orally, if they exist in oral form, and to choose oral administration of premedication, if the subject is able to orally intake. One skilled in the art, before the effective filing date of the instant application, would be motivated to choose the easier and less painful form of premedication administration to the advantage of minimizing pain and injections to the subject. One skilled in the art, before the effective filing date of the instant application, would have reasonable expectation of success since oral doses of premedication, such as acetaminophen, ibuprofen, and Benadryl, exist and are generally well-tolerated and used for premedication.
Claim 33 is rejected under 35 U.S.C. 103 as being unpatentable over Leon et al (US2020/0399368A1, published 12/24/2020) in view of Krischer et al (Krischer et al, The 6 year incidence of diabetes-associated autoantibodies in genetically at-risk children: the TEDDY study, Diabetologia 58, 980–987; published 02/10/2015) and Dayan et al (Dayan et al, Preventing type 1 diabetes in childhood, Science 373, 506-510; published 07/30/2021).
Leon et al teaches teplizumab was administered to subjects 8 years of age or older but does not explicitly exclude the possibility of treating younger patients. Leon et al further reports that the most common adverse effects were nausea and CRS (cytokine release storm), but only mild or moderate grades, which could be mitigated by premedication (column 60, line 60-67).
Krischer et al teaches that islet autoantibodies in young children have been reported to peak between 9 months and 2 years of age, with autoantibodies against insulin (IAA) typically appearing first (section: Introduction, para. 2).
Dayan et al teaches that although up to 90% of children with a single type of islet-specific autoantibody do not progress to clinical T1D, the presence of two or autoantibodies (which occurs at a median age of 2.1 years) indicates a high risk of developing clinical T1D later. Therefore, “[a] disease model of presymptomatic autoimmune β cell destruction identified by the presence of islet-specific autoantibodies offers the possibility of intervening early, before clinical diagnosis of T1D, to maximize the preservation of β cells” (section: Autoantibodies as biomarkers of early disease, paragraph 1).
It would have been obvious to one skilled in the art, before the effective filing date of the instant application, that autoantibodies implicated in the development of T1D can occur in infants under one year of age, and therefore, prevention of clinical T1D should occur as early as possible to protect insulin-producing beta cells, including for subjects under one year of age, especially when indicated by the presence of autoantibodies and other genetic and known risk factors for T1D. One skilled in the art, before the effective filing date of the instant application, would be motivated to protect against the destruction of insulin-producing beta cells as early as possible for the advantage of delaying or preventing the onset of type 1 diabetes, which can have dramatic impact on the overall lifespan of the subject. One skilled in the art, before the effective filing date of the instant application, would have reasonable expectation of success, in light of the safety and efficacy experienced by the child subjects in Leon et al and barring any known reasonable or definitive teachings contraindicating the use of teplizumab in infants under one year of age.
Claim 40 is rejected under 35 U.S.C. 103 as being unpatentable over Leon et al (US2020/0399368A1, published 12/24/2020) in view of Herold et al (A single course of anti-CD3 monoclonal antibody hOKT3y1(Ala-Ala) results in improvement in C-peptide response and clinical parameters for at least 2 years after onset of type 1 diabetes, Diabetes, 54(6):1763-1769; published 06/2005) and Ismail et al (Ismail et al, The shape of the glucose concentration curve during an oral glucose tolerance test predicts risk for type 1 diabetes, Diabetologia, 61:84-92; published 9/27/2017).
Regarding claim 40, Leon et al teaches determining the C-peptide AUC mean at baseline before treatment.
Leon et al does not explicitly teach determining the C-peptide AUC:glucose AUC ratio after the teplizumab course wherein an increase indicates responsiveness to the teplizumab course.
However, Herold et al teaches treatment of patients with recent onset type 1 diabetes with hOKT3γ1(Ala-Ala), i.e. teplizumab (Abstract), yielded increased C-peptide response compared to untreated (section: Effects of drug treatment on C-peptide response, para. 1), expressed as the total area under the response curve (AUC) (section: Assay measurements, para. 1), accompanied by improvement in glucose control (section: Discussion, para. 2), which means a decrease in glucose levels from the hyperglycemia of T1D.
Herold does not explicitly teach these measurements of response as a single C-peptide AUC:glucose AUC ratio.
However, Ismail et al teaches the AUC C-peptide/AUC glucose ratio is a known and validated index of beta cell function (section: Measures of beta cell function, para. 2).
It would have been obvious to one skilled in the art, before the effective filing date of the instant application, that an increase in AUC C-peptide/AUC glucose ratio, from an increase in C-peptide and decrease in glucose, is indicative of response to teplizumab as it confirms the ability of teplizumab to rescue the insulin-producing beta cells. One skilled in the art, before the effective filing date of the instant application, would be motivated to use this known and measurable biomarker for the advantage of quantifying response to treatment. One skilled in the art, before the effective filing date of the instant application, would have reasonable expectation of success due to the known relationship between AUC C-peptide/AUC glucose ratio and beta cell functions, which is an indicator of insulin production.
Double Patenting
Nonstatutory 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.
The double patenting reference claims that are relevant to each instant claim is mapped in the table below and will be discussed further.
Instant claims
19210427
18693879
US 11434291 B2
7
10
16
1, 17
9
11
16
1, 17
10
12
21
1, 17
11
13, 14, 15
21
5-8
12
23
18
1, 2
13
1
18
1, 2
16
2, 3, 16, 17
1, 4, 6, 9, 11, 14, 28
1, 17
22
16
26
1, 17
23
18
1, 4, 6, 9, 11, 14, 28
20
24
18
1, 4, 6, 9, 11, 14, 28
20
25
1
1, 4, 6, 9, 11, 14, 28
1, 17
26
1
1, 4, 6, 9, 11, 14, 28
1, 17
27
1
1, 4, 6, 9, 11, 14, 28
1, 17
29
1
1, 4, 6, 9, 11, 14, 28
28-19
30
1
1, 4, 6, 9, 11, 14, 28
1, 17
31
1
1, 4, 6, 9, 11, 14, 28
1, 17
32
1
1, 4, 6, 9, 11, 14, 28
1, 17
33
1
1, 4, 6, 9, 11, 14, 28
1, 17
35
1
1, 4, 6, 9, 11, 14, 28
1, 17
37
1
1, 4, 6, 9, 11, 14, 28
1, 17
38
1
1, 4, 6, 9, 11, 14, 28
1, 17
39
1
1, 4, 6, 9, 11, 14, 28
1, 17
40
1
1, 4, 6, 9, 11, 14, 28
1, 17
Patent No. US 11434291B2
Claim 27 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 17 and 1 of U.S. Patent No.11434291B2. Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding instant claim 27, claim 17 limitations on dosing, which depends on the method of claim 1 of Patent No. ‘291, teaches the same method of administering teplizumab to prevent or delay the onset of T1D.
Claims 7, 9-13, 16, 22-26, 29-33, 35, 37-40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 5-8, 17, 20, 28-29 of U.S. Patent No.11434291B2 in view of Leon et al (US2020/0399368A1, published 12/24/2020), Elliot et al (US11535679B2; filed 12/21/2021), Krischer et al (Krischer et al, The 6 year incidence of diabetes-associated autoantibodies in genetically at-risk children: the TEDDY study, Diabetologia 58, 980–987; published 02/10/2015), Dayan et al (Dayan et al, Preventing type 1 diabetes in childhood, Science 373, 506-510; published 07/30/2021), Herold et al (A single course of anti-CD3 monoclonal antibody hOKT3y1(Ala-Ala) results in improvement in C-peptide response and clinical parameters for at least 2 years after onset of type 1 diabetes, Diabetes, 54(6):1763-1769; published 06/2005), Ismail et al (Ismail et al, The shape of the glucose concentration curve during an oral glucose tolerance test predicts risk for type 1 diabetes, Diabetologia, 61:84-92; published 9/27/2017), as evidenced by Burkly et al (WO 9417828 A2, published 08/18/1994) and Lampasona et al (Lampasona et al, Islet Autoantibodies, Immunology and Transplantation, Vol 16, No 53; published 04/25/2016).
From the baseline method of delaying the onset of T1D from claim 17 of Patent US ‘291B2, it would be obvious to the skilled artisan to combine the claim of Patent US ‘291B2 and the teachings from the prior art references arrive at the limitations for instant claims 7, 9-13, 16, 22-26, 29-33, 35, 37-40, as discussed previously in the prior art rejection section.
Application No. 19210427
Claims 7-12, 16-24, and 27 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 10-18 of copending Application No. 19210427. Although the claims at issue are not identical, they are not patentably distinct from each other. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Regarding instant claims 7-12, 16-24, and 27, the claims from copending App. No. ‘427 that teach the limitations are outlined above in the table. In summary, claim 1 teaches the same method of instant independent claim 27 (see prior art rejection for analysis of dose ranges) and the other reference claims teach the specific limitations of the instant method.
Claims 13, 25-26, 28-40 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3, 10-18 of copending Application No. 19210427 in view of Leon et al (US2020/0399368A1, published 12/24/2020), Elliot et al (US11535679B2; filed 12/21/2021), Krischer et al (Krischer et al, The 6 year incidence of diabetes-associated autoantibodies in genetically at-risk children: the TEDDY study, Diabetologia 58, 980–987; published 02/10/2015), Dayan et al (Dayan et al, Preventing type 1 diabetes in childhood, Science 373, 506-510; published 07/30/2021), Herold et al (A single course of anti-CD3 monoclonal antibody hOKT3y1(Ala-Ala) results in improvement in C-peptide response and clinical parameters for at least 2 years after onset of type 1 diabetes, Diabetes, 54(6):1763-1769; published 06/2005), Ismail et al (Ismail et al, The shape of the glucose concentration curve during an oral glucose tolerance test predicts risk for type 1 diabetes, Diabetologia, 61:84-92; published 9/27/2017), as evidenced by Burkly et al (WO 9417828 A2, published 08/18/1994) and Lampasona et al (Lampasona et al, Islet Autoantibodies, Immunology and Transplantation, Vol 16, No 53; published 04/25/2016). This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
From the baseline method of delaying the onset of T1D from claim 1 of App. No. ‘427, the teachings from the prior art references arrive at the limitations for instant claims 13, 25-26, 28-40, as discussed previously in the prior art rejection section.
Application No. 18693879
Claims 7, 9-13, 16, 22-27, 29-33, 35, 37-40 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 6, 9, 11, 14, 16, 18, 26, and 28 of copending Application No. 18693879 in view of Leon et al (US2020/0399368A1, published 12/24/2020), Elliot et al (US11535679B2; filed 12/21/2021), Krischer et al (Krischer et al, The 6 year incidence of diabetes-associated autoantibodies in genetically at-risk children: the TEDDY study, Diabetologia 58, 980–987; published 02/10/2015), Dayan et al (Dayan et al, Preventing type 1 diabetes in childhood, Science 373, 506-510; published 07/30/2021), Herold et al (A single course of anti-CD3 monoclonal antibody hOKT3y1(Ala-Ala) results in improvement in C-peptide response and clinical parameters for at least 2 years after onset of type 1 diabetes, Diabetes, 54(6):1763-1769; published 06/2005), Ismail et al (Ismail et al, The shape of the glucose concentration curve during an oral glucose tolerance test predicts risk for type 1 diabetes, Diabetologia, 61:84-92; published 9/27/2017), as evidenced by Burkly et al (WO 9417828 A2, published 08/18/1994) and Lampasona et al (Lampasona et al, Islet Autoantibodies, Immunology and Transplantation, Vol 16, No 53; published 04/25/2016).This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Regarding instant claims 7-13, 22, 27, and 40, the claims from copending App. No. ‘879 that teach the limitations are outlined above in the table. From the baseline method of prognosis or assessing responsiveness of a therapeutic or prophylactic agent for treating or preventing the onset of claim 1 of T1D, which includes steps regarding the therapeutic or prophylactic administration, of App. No. ‘879, the teachings from the prior art references arrive at the limitations for instant claims 7-13, 22, 27, and 40 and further for claims 16, 23-26, and 29-39, as discussed previously in the prior art rejection section.
Conclusion
No claims are allowed.
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BONIRATH CHHAY
Examiner
Art Unit 1645
April 13, 2026
/BAO-THUY L NGUYEN/Supervisory Patent Examiner, Art Unit 1677 April 14, 2026
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