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
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 04/28/2025 has been entered.
Claims 1-3 and 5-6 are now under consideration in the instant Office Action.
Withdrawn Rejections
Rejections of claims 1-3 and 5-6 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or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement are hereby withdrawn in view of the submission of a deposit made under the terms of the Budapest Treaty by Applicant.
Rejections of claims 1-3 and 5-6 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treating Alzheimer’s intranasally using a monoclonal antibody mAb-p40₂ a3-1d, does not reasonably provide enablement for using any antibody against the p40₂ homodimer or any recombinant p40 monomer protein as a treatment for Alzheimer’s disease as claimed are hereby withdrawn in view of the submission of a deposit made under the terms of the Budapest Treaty by Applicant.
Rejections of claims 1-3 and 5-6 under 35 U.S.C. 103 as being unpatentable over Rush, in view of Griswold-Prenner et al. are hereby withdrawn in view of Applicant’s arguments, which were persuasive.
New Rejections
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.
Claims 1-3 and 5-6 are rejected under 35 U.S.C. 103 as being unpatentable over Griswold-Prenner et al. (WO 2014/028777 A2, in PTO-892 filed 06/03/2025), in view of Rush (WO 2012/159100 A1, in IDS filed 04/27/2023) and Tan et al. (in instant PTO-892).
Griswold-Prenner teaches “methods of treating a tauopathy, involving administering an anti-Tau antibody”, see paragraph 0006. Griswold-Prenner defines “some examples of tauopathy include frontotemporal dementia (FTD), Alzheimer's disease, progressive supranuclear palsy, …”, see paragraph 0004. Griswold-Prenner teaches that the “administration of the suitable compositions may be effected by different ways, e.g., by … , intranasal, topical or intradermal administration or spinal or brain delivery. Aerosol formulations such as nasal spray formulations include purified aqueous or other solutions of the active agent with preservative agents and isotonic agents”, see paragraph 00152.
Griswold-Prenner also teaches in certain embodiments, “a subject antibody composition can be administered in a single dose or in multiple doses”, see paragraph 00341. Griswold-Prenner teaches that the administration of an anti-Tau antibody “prevents or delays the onset of at least one symptom of tauopathy that is a neurodegenerative disease in a subject” wherein “the symptom can be a neurological symptom, such as cognitive impairment, memory impairment, decreased motor function, and the like. In certain cases, anti-Tau antibodies of the invention can improve cognitive function. In certain cases, the anti-Tau antibodies of the invention can slow down the rate of cognitive decline. In certain cases, the anti-Tau antibodies of the invention can improve motor function. In some cases, the anti-Tau antibodies of the invention can slow down the rate of motor function decline”, see paragraph 00142.
However, Griswold-Prenner does not teach the antibody recited in the claims used in treating Alzheimer’s disease. Rush remedies this deficiency.
Rush teaches a method for treating a disease in a patient, the method comprising: administering a combination of a recombinant p40 monomer protein and at least one monoclonal antibody against p40₂ homodimer to the patient wherein the at least one monoclonal antibody against the p40₂ homodimer comprises mAb-p40₂ a3-1d; see Abstract, paragraphs 0012 and 0038, and claim 9. Rush further teaches a method for treating a disease wherein the recombinant p40 monomer protein is administered; see Abstract, paragraph 0012, and claim 9. Rush also teaches a method wherein the at least one monoclonal antibody against p40₂ homodimer is administered; see paragraph 0012 and claim 9. Rush teaches that a treatment for autoimmune diseases that impact the central nervous system includes at least one monoclonal antibody against p402 (mAb-p402 a3-ld); see paragraph 0006. This meets the limitations of instant claim 1 wherein a method of administering a combination of a recombinant p40 monomer protein and at least one monoclonal antibody against p40₂ homodimer.
However, Griswold-Prenner and Rush do not teach how the antibody used in the method is interchangeable dependent upon a specific target. Tan et al. remedies this deficiency.
Tan et al. teaches that increased proinflammatory cytokines are a major characteristic of the aging process and associated with age-related diseases such as Alzheimer's diseases (AD), see Abstract. To further examine whether the heightened activation of inflammatory cytokines may contribute to age-related brain dysfunction, Tan et al. employed direct in vivo infusion of nonviral small interfering RNA (siRNA) to knock down the common IL-12/23 signaling subunit p40 in the brain. Tan et al. found that these p40-deficient mice had significantly decreased cerebral amyloid-β levels, reduced synaptic and neuronal loss, and reversed cognitive impairments. Furthermore, in vivo delivery of a neutralizing p40-specific antibody likewise ameliorated AD-associated pathology and cognitive deficits in SAMP8 mice. Thus, the data collected by Tan et al. indicates that the upregulated cerebral IL-12/23 during aging is involved in age-associated brain dysfunction and point to the modulation of IL-12/23 signaling molecule p40 as a promising strategy for the development of an AD therapy, see Abstract.
The combination of references meets the limitations of instant claim 1 wherein the mAb- p40₂ a3-1d antibody is used in to treat an Alzheimer’s patient via intranasal administration, instant claim 2 wherein the recombinant p40 monomer protein is administered, instant claim 3 wherein the monoclonal antibody is administered in a single dose, instant claim 5 wherein one of the symptoms of Alzheimer’s disease that is memory loss is ameliorated, and instant claim 6 wherein the monoclonal antibody is administered in two or more doses.
It would have been obvious to a person of ordinary skill in the art at the time of the invention to modify the method taught by Griswold-Prenner, which teaches a method of treating Alzheimer’s disease using antibodies targeted for proteins implicated in its disease state that are administered intranasally to ameliorate symptoms associated with the disease, with the teachings of Rush which include the mAb- p40₂ a3-1d antibody and recombinant monomer proteins derived from a hybridoma in a method for treating a disease. One would be motivated to apply the antibody of Rush to the methods of Griswold-Prenner as guided by the teachings of Tan et al., which show that targeting the p40 subunit of proinflammatory cytokines related to Alzheimer’s disease “ameliorated AD-associated pathology and cognitive deficits” and is a promising strategy for new treatments for Alzheimer’s disease. Thus, one of ordinary skill in the art would have a reasonable expectation of success when using the antibody of Rush et al. to target the p40 subunit impact in Alzheimer’s disease in a method as disclosed by Griswold-Prenner because doing so would result in a targeted treatment with effective intranasal delivery for Alzheimer’s disease.
Therefore, claims 1-3 and 5-6 are rejected as obvious over Griswold-Prenner, Rush, and Tan et al.
Response to Arguments
Applicant’s arguments, see Remarks, filed 08/27/2025, with respect to the rejection(s) of claim(s) 1-3 and 5-6 under 35 U.S.C. 103 as being unpatentable over Rush, in view of Griswold-Prenner et al. have been fully considered and are persuasive. Therefore, the rejection has been withdrawn. However, upon further consideration, a new ground(s) of rejection is made in view of Griswold-Prenner et al., in view of Rush and Tan et al.
Conclusion
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/SELAM BERHANE/Examiner, Art Unit 1675
/AURORA M FONTAINHAS/Primary Examiner, Art Unit 1675