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 .
DETAILED ACTION
Clams 87-98 are currently pending and under prosecution.
Specification
Applicant is reminded of the proper language and format for an abstract of the disclosure.
The abstract should be in narrative form and generally limited to a single paragraph on a separate sheet within the range of 50 to 150 words in length. The abstract should describe the disclosure sufficiently to assist readers in deciding whether there is a need for consulting the full patent text for details.
The language should be clear and concise and should not repeat information given in the title. It should avoid using phrases which can be implied, such as, “The disclosure concerns,” “The disclosure defined by this invention,” “The disclosure describes,” etc. In addition, the form and legal phraseology often used in patent claims, such as “means” and “said,” should be avoided.
The abstract of the disclosure is objected to because: (1) it contains over 150 words, (2) there is a missing period between “…to a subject. The subject may..”, (3) states “relates to a method” which can be implied, and (4) the abstract uses words such as “said composition” . A corrected abstract of the disclosure is required and must be presented on a separate sheet, apart from any other text. See MPEP § 608.01(b).
The title of the invention is not descriptive. A new title is required that is clearly indicative of the invention to which the claims are directed.
The current title does not describe the invention as there is no combination in the claims. The following title is suggested:
USE OF GAD65 FOR AUTOIMMUNE DIABETES
Claim Objections
Claims 89 and 90 are objected to because of the following informalities: There is a missing period at the end of the claims. Appropriate correction is required.
Claims 90 is objected to because of the following informalities: “the” is not capitalized in the beginning of the claim. Appropriate correction is required.
Claims 91 is objected to because of the following informalities: The claim recites “The method of claim 87, wherein the individual has GAD65 autoantibodies the GAD administered to the individual in step (b) is GAD65.” There is a grammatical error between GAD65 Autoantibodies and the GAD administered, the word “And” should be added between here. Appropriate correction is required.
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 87-98 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of reducing an autoimmune response in an individual that has autoimmune diabetes, such as type 1 diabetes, comprising administering GAD65, does not reasonably provide enablement for: (1) reducing or preventing any autoimmune response, (2) prevention of autoimmune diabetes, or (3) the use of any GAD isoform for the treatment of autoimmune diabetes. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
BREADTH OF THE CLAIMS: Claim 87 recites “A method for reducing or preventing an autoimmune response, comprising: administering GAD (glutamic acid decarboxylase) to an individual by injection directly into a lymph node.” Dependent claims 89 recites that the individual has autoimmune diabetes, and claim 90 recites that the autoimmune diabetes is selected from typ1 diabetes or latent autoimmune diabetes.
PRESENCE OR ABSENCE OF EXAMPLES: It is noted in the specification that autoimmune disorders often include autoimmune responses, thus it has been interpreted that the reduction of autoimmune responses is related to autoimmune disorders, such as type 1 diabetes. [see at least 0077 and 0153 of the published specification] The examples in the instant specification discloses the use of GAD65 (administered as Diamyd ® which is a vaccine with GAD65 in the Examples 1-4, 6 and 7 or recombinant human glutamic acid decarboxylase (rhGAD65) in Example 5. The instant specification does not disclose the use of other isoforms of GAD, such as GAD67 for the instantly claimed method, does not disclose Examples wherein the GAD prevents autoimmune diabetes, and does not disclose the treatment or any other reduction of other autoimmune responses/diseases.
STATE OF THE ART: It is well known in the art that glutamic acid decarboxylase (GAD) exists in two isoforms in mammals (GAD65 and GAD67), and that patients with autoimmune diabetes, such as Type 1 diabetes are primarily driven by autoantibodies against GAD65. A search of the prior art demonstrates the importance of GAD65 in specific autoimmune disease, autoimmune diabetes. Morales et al. (2011) (GAD-Alum Immunotherapy in Type 1 Diabetes Mellitus. Immunotherapy, 3(3), 323–332) teaches that glutamic acid decarboxylase is the enzyme that decarboxylates carboxylates glutamic acid to form GABA. Morales teaches that GAD65 and GAD67 reflects different molecular weight products of two independently regulated genes. Morales teaches that GAD65 is the isoform of the enzyme that exists in beta-cells of the human pancreas and that GAD65, not GAD67, is a major autoantigen in autoimmune diabetes. [pg 2, “Introduction to the compound] Furthermore, Jayakrishnan et al (“An analysis of the cross-reactivity of autoantibodies to GAD65 and GAD67 in diabetes.” PloS one vol. 6,4 e18411. 8 Apr. 2011) teaches that GAD65 is a key autoantigen in type 1 diabetes. Jayakrishnan teaches that GAD67 is 71% identical in amino acid sequence but is rarely an autoantigen in type 1 diabetes. [pg 1, Introduction] The prior art does not demonstrate that the use of GAD may be administered for reduction of any autoimmune response/diseases.
With regards to type 1 diabetes prevention, it is known in the art that there are no current agents that completely prevent the onset of Type 1 diabetes. Pande et (“Prevention of Type 1 Diabetes: Current Perspective.” Indian journal of endocrinology and metabolism vol. 27,4 (2023): 277-285) teaches that primary prevention may be possible for genetically predisposed persons via genetic testing, however the occurrence of T1D is still random and non-linear. Pande also teaches that there has been limited success if at all for primary prevention. [pg 279, 1st column-2nd column] Pande teaches when it comes to secondary prevention, which is delaying or preventing the onset of clinical disease, who already have T1D specific autoantibodies, there have been strategies, including proinsulin, insulin, GAD65. However, these strategies have not demonstrated promising outcomes. [pg 280; Figure 2, column 1, 4th paragraph, column 2, 1st paragraph] Pande also teaches that there is still a long way to go to prevent autoimmune diabetes. pg 284]
PREDICTABILITY: The specification lacks the critical steps necessary in presenting some type of predictable response in a population of hosts deemed necessary to (1) reduce or prevent any autoimmune response, (2) prevent autoimmune diabetes, or (3) the use of any GAD isoform for the treatment of autoimmune diabetes. There is no evidence in the instant application or the art that as noted in the prior art that demonstrates (1)-(3) as noted above. The amount of experimentation required to formulate such guidance would be enormous; one would have to demonstrate the efficacy of the combination in several models across several different types of autoimmune diseases, and determine the appropriate regimen (doses and frequency) for use of the composition in a preventative setting. Further, one would have to conduct population analysis to identify definitive characteristics which indicate that a subject is at risk of developing any autoimmune disease to a degree that would outweigh potential adverse effects of treatment with the claimed composition. Thus, considering the high level of skill in the art, the state of the art, the level of predictability, and the guidance and examples provided, the experimentation required to enable the full scope of the claimed invention would not be reasonable.
QUANTITY OF EXPERIMENTATION Undue experimentation would be required to determine what GAD is administered to which population of subjects could predictability function as noted in (1)-(3) above as claimed. MPEP 2164.01 recites that “The test of enablement is not whether any experimentation is necessary, but whether, if experimentation is necessary, it is undue. In re Angstadt, 537 F.2d 498, 504, 190 USPQ 214, 219 (CCPA 1976)”. The experimentation needed to practice this method is undue and unreasonable. A person skilled in the art will not be able to use the invention without undue experimentation. (In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988))
Accordingly, the instant claims do not comply with the enablement requirement of §112, since to practice the invention claimed in the patent a person of ordinary skill in the art would have to engage in undue experimentation, with no assurance of success.
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 91 recites the limitation “The method of claim 87, wherein the individual has GAD65 autoantibodies the GAD administered to the individual in step (b) is GAD65.” Claim 87 does not recite a step b. There is insufficient antecedent basis for this limitation in the claim.
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.
Claim 90 is 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. Claim 90 recites “The method of claim 89 wherein the autoimmune diabetes is selected from type 1 diabetes, autoimmune diabetes, and latent autoimmune diabetes. Claim 89 recites “The method of claim 87, wherein the individual has autoimmune diabetes.” Claim 90 fails to further limit claim 89 wherein it already recites autoimmune diabetes. 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.
Claim Rejections - 35 USC § 103
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.
Claim(s) 87-92 and 94-98 are rejected under 35 U.S.C. 103 as being unpatentable over Ludvigsson et al (US20090092637 A1; Published 4/9/2009), in view of Senti et al. (“Intralymphatic allergen administration renders specific immunotherapy faster and safer: a randomized controlled trial.” Proceedings of the National Academy of Sciences of the United States of America vol. 105,46, 2008) and Lobl et al (US20070255237 A1; Published 11/1/2007).
Ludvigsson teaches a method for reducing an autoimmune response, comprising administering GAD (glutamic acid decarboxylase) to an individual subcutaneously. [0009-0010, 0014] Regarding claim 88, Ludvigsson teaches further comprising identifying the individual as having GAD autoantibodies prior to administration of the GAD. [0057, 0107] Regarding claims 89 and 90, Ludvigsson teaches the individual has autoimmune diabetes, such as type 1 diabetes. [0010, 0015, 0020, 0043]
Regarding claim 91, Ludvigsson teaches, wherein the individual has GAD65 autoantibodies the GAD administered to the individual is GAD65. [0013, 0018, 0031, 0040, 0042, 0057-0059] Regarding claim 92, Ludvigsson teaches the GAD is administered in aluminum hydroxide (alum). [0017, 0020, 0030, 0057] Regarding claim 97, Ludvigsson teaches, wherein the GAD is administered to the individual at least 2 times, each administration being at least 14 days apart. Regarding claim 98, Ludvigsson teaches the GAD is administered to the individual at least 4 times, each administration being at least 30 days apart. [0020, 0037, 0059, 0109; claims 1-6] Ludvigsson teaches doses of GAD65 have been tested and range from 4 µg to 500 µg, and tested 20 µg. [0009]
However, Ludvigsson does not teach:
that the GAD is administered into the lymph node
the GAD is administered in an amount of 1-15 per injection (claim 94)
the GAD is administered in an amount of 2-10 µg per injection (claim 95); or
the GAD is administered in an amount of 2-5 µg per injection. (claim 96)
Senti teaches that intralymphatic administration for immunotherapy. Senti teaches that administering immunotherapy subcutaneously directly into lymph nodes is easy and safe. Senti also teaches that this administration mode allowed for enhanced safety and efficacy of immunotherapy and reduced treatment time. [Abstract] Senti also teaches that intralymphatic treatment also led to higher patient compliance as well. [pg 17911, 1st column] Senti also teaches that by administering directly into lymph nodes, lower doses were required. [pg 17911, 1st column, 1st paragraph, 2nd column, 4th paragraph]
Lobl teaches different administration routes, including direct injection of drugs into a lymph node. [0004, 0010] Lobl teaches immunotherapeutic and vaccines can be delivered to lymph nodes for treatment of autoimmune diseases to modulate immune response. [0055, 0067]
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to reduce an autoimmune response comprising administering GAD directly into the lymph nodes. One would have been motivated to, and have a reasonable expectation of success, because: (1). Ludvigsson teaches a method for reducing an autoimmune response, comprising administering GAD (glutamic acid decarboxylase) to an individual subcutaneously, (2) Senti teaches the known methods of administering an agent intralymphatically and teaches that this administration enhances the effect, is safe, and allows for higher patient compliance, and (3) Lobl teaches known methods of administering an immunotherapeutic and vaccines directly into lymph nodes for treatment of autoimmune diseases.
Given the known methods of administering an agent directly to lymph nodes as taught by the prior art, and given the known methods of administering GAD, one of skill in the art could have pursued administering the GAD of Ludvigsson directly into a lymph node, with a reasonable expectation of success.
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to reduce an autoimmune response comprising administering GAD directly into the lymph nodes, wherein the dose of GAD is administered in an amount of 1-15 µg per injection. One would have been motivated to, and have a reasonable expectation of success, because: (1). Ludvigsson teaches a method for reducing an autoimmune response, comprising administering GAD (glutamic acid decarboxylase) to an individual subcutaneously, wherein the dose ranges around 20 µg per injection, and (2) Senti teaches the known methods of administering an agent intralymphatically, wherein the administration directly into lymph nodes allowed for enhanced effects, as well as lower doses to be used.
Given the known methods of administering GAD, and given the known methods of administering via lymph nodes for enhanced efficacy and requirement of lower doses, one of skill in the art could have pursued administering the GAD of Ludvigsson directly into a lymph nodes at lower doses such as 1-15 µg, with a reasonable expectation of success.
Claim(s) 93 are rejected under 35 U.S.C. 103 as being unpatentable over Ludvigsson et al (US20090092637 A1; Published 4/9/2009), Senti et al. (“Intralymphatic allergen administration renders specific immunotherapy faster and safer: a randomized controlled trial.” Proceedings of the National Academy of Sciences of the United States of America vol. 105,46, 2008) and Lobl et al (US20070255237 A1; Published 11/1/2007).), as applied to claims 87-92 and 94-98 above, and further in view of Ludvigsson 2012 (Immune Intervention in Type I Diabetes Mellitus, Type 1 Diabetes Book, Published 2/27/2013)
The teachings of Ludvigsson, Senti and Lobl are recited above, however, they do not teach that the individual has a serum vitamin D level of above 50 nanomole/liter as recited in claim 93.
Ludvigsson (2012) teaches immune interventions in type 1 diabetes mellitus. Ludvigsson teaches the role of vitamin D in type 1 diabetes and teaches that experimental studies suggest that vitamin D play a role in the defense against type 1 diabetes. Ludvigsson teaches that epidemiological data suggest that there is a link between vitamin D deficiency and an increased incidence of Type 1 diabetes, and there is also increasing evidence suggesting that vitamin D also affects beta cells directly thereby rendering them more resistant to cellular stress. [page 504, section 12]
Ludvigsson teaches that GAD-alum may also be combined with Vitamin D-, to positively influence the dendritic cells and influence directly beta cell survival and insulin sensitivity. [page 501, section 9.6] Thus, Ludvigsson highlights the importance of having normal levels of vitamin D and its effect on enhancing immune interventions, such as GAD-alum.
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to administer GAD to an individual that has a serum vitamin D level above 40 nanomole/liter. One would have been motivated to, and have a reasonable expectation of success, because: (1) the prior art teaches a method for reducing an autoimmune response, comprising administering GAD (glutamic acid decarboxylase) to an individual intralymphatically, (2) Ludvigsson 2012 teaches that there is a link between vitamin D deficiency and an increased incidence of Type 1 diabetes, and there is also increasing evidence suggesting that vitamin D also affects beta cells directly thereby rendering them more resistant to cellular stress, and (3) Ludvigsson 2012 also teaches that when GAD-alum is combined with Vitamin D it can positively influence the dendritic cells and influence directly beta cell survival and insulin sensitivity.
Ludvigsson 2012 recognizes the importance of vitamin D in type 1 diabetes. Given the recognized role of vitamin D and its effect on immunotherapy against type 1 diabetes, and given the methods of administering GAD (with or without vitamin D to ensure the patient has normal levels of vitamin D), one of skill in the art could have pursued administering GAD-alum to an individual with normal serum vitamin D levels (that is above 50 nanomole/liter), with a reasonable expectation of success.
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 87-98 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-5 and 14-15 of U.S. Patent No. 12,605,432, in view of Ludvigsson et al (US20090092637 A1; Published 4/9/2009).
The U.S. Patent recites a method of treating type 1 diabetes comprising administering to a subject glutamic acid decarboxylase (GAD) directly into a lymph node. The referenced U.S. Patent and the instant application are claiming common subject matter, as follows:
Instant Application
U.S. Patent 12,605,432
Claim 87. A method for reducing or preventing an autoimmune response, comprising: administering GAD (glutamic acid decarboxylase) to an individual by injection directly into a lymph node.
Claim 89. The method of claim 87, wherein the individual has autoimmune diabetes.
Claim 90. The method of claim 89, wherein the autoimmune diabetes is selected from type 1 diabetes, autoimmune diabetes, and latent autoimmune diabetes.
Claim 92. The method of claim 87, wherein the GAD is administered in aluminum hydroxide (alum).
Claim 93. The method of claim 87, wherein the individual has a serum vitamin D level of above 50 nanomole/liter.
Claim 1. A method for treatment of type 1 diabetes comprising administering to a subject having a serum vitamin-D level above 50 nanomole/liter a therapeutic composition comprising glutamic acid decarboxylase (GAD) formulated in alum by injection directly into a lymph node of the subject.
Claim 94. The method of claim 87, wherein the GAD is administered in an amount of 1-15 µg per injection.
Claim 95. The method of claim 87, wherein the GAD is administered in an amount of 2-10 µg per injection.
Claim 96. The method of claim 87, wherein the GAD is administered in an amount of 2-5 µg per injection.
Claim 2. The method according to claim 1, wherein GAD is administered in an amount of 1-15 μg, 2-10 μg, 2-5 μg, or 4 μg per injection.
Claim 97. The method of claim 87, wherein the GAD is administered to the individual at least 2 times, each administration being at least 14 days apart.
Claim 98. The method of claim 87, wherein the GAD is administered to the individual at least 4 times, each administration being at least 30 days apart.
Claim 3. The method according to claim 1 comprising administering the composition comprising glutamic acid decarboxylase two or more times, each administration being 14 or more days after the administering step before it.
Claim 4. The method according to claim 1 comprising administering the composition comprising glutamic acid decarboxylase two or more times, each administration being 30 or more days after the administering step before it.
Claim 5. The method according to claim 1 comprising administering the composition comprising glutamic acid decarboxylase three or more times.
Claim 91. The method of claim 87, wherein the individual has GAD65 autoantibodies the GAD administered to the individual in step (b) is GAD65
Claim 14. The method according to claim 1, wherein the glutamic acid decarboxylase (GAD) is GAD-65.
However, the U.S. Patent does not recite that the individual has GAD autoantibodies as recited in claim 88.
Ludvigsson teaches a method for reducing an autoimmune response, comprising administering GAD (glutamic acid decarboxylase) to an individual subcutaneously. [0009-0010, 0014] Regarding claim 88, Ludvigsson teaches further comprising identifying the individual as having GAD autoantibodies prior to administration of the GAD. [0057, 0107] Regarding claims 89 and 90, Ludvigsson teaches the individual has autoimmune diabetes, such as type 1 diabetes. [0010, 0015, 0020, 0043]
Regarding claim 91, Ludvigsson teaches, wherein the individual has GAD65 autoantibodies the GAD administered to the individual is GAD65. [0013, 0018, 0031, 0040, 0042, 0057-0059] Regarding claim 92, Ludvigsson teaches the GAD is administered in aluminum hydroxide (alum). [0017, 0020, 0030, 0057] Regarding claim 97, Ludvigsson teaches, wherein the GAD is administered to the individual at least 2 times, each administration being at least 14 days apart. Regarding claim 98, Ludvigsson teaches the GAD is administered to the individual at least 4 times, each administration being at least 30 days apart. [0020, 0037, 0059, 0109; claims 1-6] Ludvigsson teaches doses of GAD65 have been tested and range from 4 µg to 500 µg, and tested 20 µg. [0009]
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention to identify the individual as having GAD autoantibodies prior to administration of the GAD. One would have been motivated to, and have a reasonable expectation of success, because: (1) Ludvigsson teaches a method for reducing an autoimmune response, comprising administering GAD (glutamic acid decarboxylase) to an individual subcutaneously, wherein the individual has type 1 diabetes, (2) Ludvigsson teaches further comprising identifying the individual as having GAD autoantibodies prior to administration of the GAD, and (3) The U.S. Patent recites a method of reducing an autoimmune response, wherein the individual has type 1 diabetes. Given the known methods of administering GAD, and given the known methods of identifying if the individual has GAD autoantibodies prior to administration of the GAD, one of skill in the art could have pursued identifying if the individual has GAD autoantibodies prior to administration of GAD, with a reasonable expectation of success.
Conclusion
Conclusion: Claims 89-91 are objected to. Claims 87-98 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SARAH A ALSOMAIRY whose telephone number is (571)272-0027. The examiner can normally be reached Monday-Friday 7:30 AM to 5:30 PM.
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/SARAH A ALSOMAIRY/ Examiner, Art Unit 1646
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