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
Election/Restrictions
Applicant's election without traverse of species: a method for treating Alzheimer's discase in a patient comprising administering a combination of a recombinant p40 monomer protein and a monoclonal antibody against p40₂ homodimer in the reply filed 09/23/2024 is acknowledged.
Claims 9-16 are withdrawn from consideration pursuant to 37 CFR1.142(b) as being drawn to nonelected inventions and species, there being no allowable generic or linking claims. Election was made in the reply filed 09/23/2024.
Claims 1-3 and 5-6 are now under consideration in the instant Office Action.
Maintained 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 PTO-892 filed 11/28/2025).
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 filed 03/20/2026 have been fully considered but they are not persuasive.
Applicant argues “the claims are patentable over Griswold in view of Rush and Tan because 1) there is not suggestion or motivation to modify Griswold with Rush and Tan or to combine the teachings of Griswold with Rush and Tan and 2) there is no reasonable expectation of success when combining Griswold with Rush and Tan or modifying Griswold with Rush and Tan to arrive at the specific claimed invention” and “Griswold fails to suggest or teach replacing its antibody designed to specifically bind to Tau with an antibody that binds specifically to p40 homodimer.” This is not found persuasive.
In the obviousness rejection, Griswold-Prenner is used to elucidate the treatment of Alzheimer’s disease using antibodies that are administered intranasally via single or multiple doses. The Examiner selected this reference to recognize that the state of the prior art at the time of filing acknowledges that an effective method to administering antibodies to treat Alzheimer’s disease is via dosages administered intranasally. The antibody of Griswold-Prenner is an anti-Tau antibody, which is not the same as what is recited in the instant claims; however, Griswold-Prenner is not used in the rejection to teach the identity of the claimed antibody. Since the method of administration taught by Griswold-Prenner is well known in the art, one of ordinary skill would be motivated to modify Griswold-Prenner with Rush because the prior art shows that a number of antibodies which bind to a variety of proteins implicated in Alzheimer’s disease would have a reasonable expectation of success when administered in this manner. One of ordinary skill in the art would have a reasonable expectation of success because the antibody taught by Rush is also used in a method of treating diseases in a patient, particularly autoimmune diseases that impact the central nervous system like Alzheimer’s, that are afflicted by p40 monomer and homodimer proteins. Thus, the method by which the antibody is administered by Griswold-Prenner would have a reasonable expectation of success when substituted for the antibody of Rush because they are both drawn towards the same disease.
In regards to the Tan et al. reference, Applicant argues that the p40 homodimer and p40 monomer are distinct proteins and that the antibody of Tan et al. targets a different epitope than the one of the instant claims. Tan et al. teaches how IL-12/23 signaling impacts the production of p40. When knocked out, the p40 deficient mice experiences significantly decreased cerebral amyloid-β levels, reduced synaptic and neuronal loss, and reversed cognitive impairments which signals its role in Alzheimer’s disease. The Tan et al. reference is relied upon to teach that the p40 protein is implicated in Alzheimer’s disease and would provide guidance in combining Griswold-Prenner and Rush to arrive at the instant invention because the antibody of Rush would inhibit a major protein (p40) afflicting Alzheimer’s disease whilst using a method that is well known in the art to effectively deliver the targeted medication. The Tan et al. reference was not relied upon to conflate the p40 homodimer and p40 monomer, or argue that the p40 antibody taught by Tan was identical to the one of the instant claims. The reference was relied upon to show how an antibody against p40 can be used to treat Alzheimer’s disease by implicating the IL-12/23 pathway. In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Therefore, the rejection is maintained as obvious over Griswold-Prenner, Rush, and Tan.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/SELAM BERHANE/Examiner, Art Unit 1675
/AURORA M FONTAINHAS/Primary Examiner, Art Unit 1675
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