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 .
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.
Claim(s) 1-6 and 11-16 are rejected under 35 U.S.C. 103 as being unpatentable over Goetzl (WO 2020/123884) in view of Gunther et al (Cell Reports, Vol 26, 2019, pp145-148).
Regarding Claim 1, Goetzl discloses a method of treating traumatic brain injury comprising (methods useful for treating acute TBI, Abstract) administering an effective amount of an agent to a human patient in need thereof (methods for treating a subject having a traumatic brain injury, comprising, administering an effective amount of a PrPc inhibitor to the subject, thereby treating the traumatic brain injury in the subject, Para. [0033]; the subject is a human subject, Para. [0069]).
Goetzl fails to explicitly disclose poly [4-styrenesulfonic acid-co-maleic acid] (PSCMA) or a pharmaceutically acceptable salt thereof.
Gunther teaches repairing synaptic damage (Pg. 152, right hand column, first full paragraph from top) and teaches poly [4-styrenesulfonic acid-co-maleic acid] (PSCMA) (polymers blocking Aßo binding to PrPC do so by competitive inhibition upon PrPC binding. We examined this for poly (4-styrenesulfonic acid-co-maleic acid) PSCMA directly binds PrPC PSCMA affinity for Aßo is undetectable by BLI and, when co-applied with full-length PrPC in solution, completely blocks PrPC binding to an Aßo-coated BLI sensor, Pg. 149, right hand column, first full paragraph from top; PSCMA exhibits selectivity for blockade of Aßo binding PrPC, Pg. 150, left hand column, first full paragraph from bottom; The PrPC antagonist, PSCMA, was administered orally to APP/ PS1 mice for 30 days at the 3 mg/kg twice daily dose treatment began at 12 months of age, after Ab accumulation, synapse loss, and learning and memory deficits are well established Oral PSCMA rescued mice from pre-existing phenotypic learning and memory impairment, Pg. 152, left hand column, first partial paragraph from bottom).
It would have been obvious to one of ordinary skill in the art to modify the method of Goetzl by an agent as taught by Gunther for the purpose of treating TBI by blocking Aßo binding to PrPC (Goetzl, Para. [0033]). See MPEP 2144.07.
Regarding Claim 2, Goetzl further discloses wherein the subject experienced a concussion and was unconscious for more than one second (the traumatic brain injury is acute TBI, Para. [0010]; Acute TBI was defined as having a concussion that met standard criteria for mild TBI, Para. [00101], See Gharibian, Pg. 5, first partial paragraph from bottom, which states an mTBI is the equivalent of a concussion and typical signs of an mTBI include loss of consciousness less than 30 minutes).
Regarding Claim 3, Goetzl further discloses wherein the subject experienced a concussion and was unconscious for more than 10 seconds (the traumatic brain injury is acute TBI, Para. [0010]; Acute TBI was defined as having a concussion that met standard criteria for mild TBI, Para. [00101], See Gharibian, Pg. 5, first partial paragraph from bottom, which states an mTBI is the equivalent of a concussion and typical signs of an mTBI include loss of consciousness less than 30 minutes).
Regarding Claim 4, Goetzl further discloses wherein the subject does not have a neurodegenerative disease (the subject has traumatic brain injury, Para. [0010]; Traumatic brain injury can increase the risk that a subject will subsequently develop a neurological disease the neurological disease is selected from the group consisting of: Alzheimer's disease, Para. [0068]; compositions used for preventing progression to a neurological disease, Para. [0089]; protocol is effective for preventing Alzheimer's disease, Para. [0031]).
Regarding Claim 5, Goetzl further discloses wherein the subject does not have Alzheimer's disease (the subject has traumatic brain injury, Para. [0010]; Traumatic brain injury can increase the risk that a subject will subsequently develop a neurological disease the neurological disease is selected from the group consisting of: Alzheimer's disease, Para. [0068]; compositions used for preventing progression to a neurological disease, Para. [0089]; protocol is effective for preventing Alzheimer's disease, Para. [0031]).
Regarding Claim 6, Goetzl further discloses wherein PSCMA is administered in combination with a second therapeutic agent (The administration of different combinations of anti-PrPc antibodies may be used to treat the traumatic brain injury, Para. [0094]).
Regarding Claim 11, Goetzl discloses a method of treating chronic traumatic encephalopathy (compositions and methods useful for treating chronic traumatic encephalopathy, Para. [0002]; the methods of the present invention would be useful for treating neurological diseases, including. CTE, Para. [00113]) administering an effective amount of an agent to a human patient in need thereof (methods for treating a subject having a traumatic brain injury, comprising, administering an effective amount of a PrPc inhibitor to the subject, thereby treating the traumatic brain injury in the subject, Para. [0033]; the traumatic brain injury is chronic repetitive TBI, Para. [0010]; Subject suffering from a traumatic brain injury can progress to chronic traumatic encephalopathy, Para. [0065]; preventing neuronal cytotoxicity of Aß42o methods would be useful for treating neurological diseases, including CTE, Para. [00134]; treatment with anti-PrPc antibody to prevent neuron cytotoxicity of Aß42o, Para. [00130]; compounds that inhibit or reduce Abeta42 binding activity of neuronal prion protein, Para. [0098]; the subject is a human subject, Para. [0069]). Gunther is in the field of repairing synaptic damage (Pg. 152, right hand column, first full paragraph from top) and teaches poly [4-styrenesulfonic acid-co-maleic acid] (PSCMA) (polymers blocking Aßo binding to PrPC do so by competitive inhibition upon PrPC binding. We examined this for poly (4-styrenesulfonic acid-co-maleic acid) PSCMA directly binds PrPC PSCMA affinity for Aßo is undetectable by BLI and, when co-applied with full-length PrPC in solution, completely blocks PrPC binding to an Aßo-coated BLI sensor, Pg. 149, right hand column, first full paragraph from top; PSCMA exhibits selectivity for blockade of Aßo binding PrPC, Pg. 150, left hand column, first full paragraph from bottom; The PrPC antagonist, PSCMA, was administered orally to APP/ PS1 mice for 30 days at the 3 mg/kg twice daily dose treatment began at 12 months of age, after Ab accumulation, synapse loss, and learning and memory deficits are well established Oral PSCMA rescued mice from pre-existing phenotypic learning and memory impairment, Pg. 152, left hand column, first partial paragraph from bottom). It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl by an agent as taught by Gunther for the purpose of treating CTE by blocking Aßo binding to PrPC (Goetzl, Para. [0033]).
Regarding Claim 12, Goetzi further discloses wherein the subject experienced a concussion and was unconscious for more than one second (Features of CTE may appear after a single episode of moderately severe acute TBI or be imposed on a repetitive series of episodes of mild acute TBI, Para. [0065]; Acute TBI was defined as having a concussion that met standard criteria for mild TBI, Para. [00101], See Gharibian, Pg. 5, first partial paragraph from bottom, which states an mTBI is the equivalent of a concussion and typical signs of an mTBI include loss of consciousness less than 30 minutes).
Regarding Claim 13, Goetzl further discloses wherein the subject experienced head a concussion and was unconscious for more than 10 seconds (Features of CTE may appear after a single episode of moderately severe acute TBI or be imposed on a repetitive series of episodes of mild acute TBI, Para. [0065]; Acute TBI was defined as having a concussion that met standard criteria for mild TBI, Para. [00101], See Gharibian, Pg. 5, first partial paragraph from bottom, which states an mTBI is the equivalent of a concussion and typical signs of an mTBl include loss of consclousness less than 30 minutes).
Regarding Claim 14, Goetzl further discloses wherein the subject does not have a neurodegenerative disease (compositions used for preventing progression to a neurological disease, Para. [0089]; protocol is effective for preventing Alzheimer's disease, Para. [0031]).
Regarding Claim 15, Goetzl further discloses wherein the subject does not have Alzheimer's disease (compositions used for preventing progression to a neurological disease, Para. [0089]; protocol is effective for preventing Alzheimer's disease, Para. [0031]).
Regarding Claim 16, Goetzl further discloses wherein PSCMA is administered in combination with a second therapeutic agent (The administration of different combinations of anti-PrPc antibodies may be used, Para. [0094]).
Claims 7 and 8 are rejected under 35 U.S.C. 103 as being unpatentable over Goetzl (WO 2020/123884) in view of Gunther et al (Cell Reports, Vol 26, 2019, pp145-148) and Stein (US 8,614,203).
Regarding Claim 7, Goetzl fails to explicitly disclose wherein the second therapeutic agent is an anti-inflammatory agent.
Stein is in the field of traumatic brain injury (abstract) and teaches an anti-inflammatory agent (administration of a therapeutically effective amount of a progestin or progestin metabolite, Abstract).
It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl with an agent as taught by Stein for the purpose of treating traumatic brain injury (Stein, Abstract). MPEP 2144.06
Regarding Claim 8, Goetzl fails to explicitly disclose wherein the second therapeutic agent is a glucocorticoid, dexamethasone, progesterone, or methylprednisolone.
Stein is in the field of traumatic brain injury (abstract) and teaches an a glucocorticoid, dexamethasone, progesterone, or methylprednisolone (administration of a therapeutically effective amount of a progestin or progestin metabolite, Abstract; the term progesterone refers to a member of the progestin family, Col. 4, Lns. 61-62).
It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl with progesterone as taught by Stein for the purpose of treating traumatic brain injury (Stein, Abstract).
Claims 17 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Goetzl (WO 2020/123884) in view of Gunther et al (Cell Reports, Vol 26, 2019, pp145-148) and Dennis (US 2015/0329636).
Regarding Claim 17, Goetzl fails to explicitly disclose wherein the second therapeutic agent is an anti-inflammatory agent.
Dennis is in the field of antibodies targeting prion protein (Para. [0010]) and teaches an anti-inflammatory agent (the low affinity anti-BBB-R antibody herein is coupled with a label and/or neurological disorder drug, Para. [0115]; a neurological drug may be. a nonsteroidal anti-inflammatory drug.. i.e., ibuprofen, Para. [0118]).
It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl with an agent as taught by Dennis for the purpose of treating brain injury (Dennis, Para. [0153]).
Regarding Claim 18, Goetzl fails to explicitly disclose wherein the second therapeutic agent is a glucocorticoid, dexamethasone, progesterone, or methylprednisolone.
Dennis is in the field of antibodies targeting prion protein (Para. [0010]) and teaches the second therapeutic agent is dexamethasone (the low affinity anti-BBB-R antibody herein is coupled with a label and/or neurological disorder drug, Para. [0115]; a neurological drug may be... dexamethasone, Para. [0118]).
It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl with an agent as taught by Dennis for the purpose of treating brain injury (Dennis, Para. [0153]).
Claims 9, 10, 19, and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Goetzl (WO 2020/123884) in view of Gunther et al (Cell Reports, Vol 26, 2019, pp145-148) and Ashton (US 2011/0183944).
Regarding Claim 9, Goetzl fails to explicitly disclose wherein the second therapeutic agent is a non-steroidal antiinflammatory drug, indomethacin, ibuprofen, carprofen, or celecoxib.
Ashton is in the field of formulations for preventing neurological disorders, Para. [0059]) and teaches the second therapeutic agent is a non-steroidal antiinflammatory drug or ibuprofen (celecoxib, Para. [0014]).
It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl with an agent as taught by Ashton for the purpose of treating traumatic brain injury (Ashton, Para. [0059]).
Regarding Claim 10, Goetzl fails to explicitly disclose wherein the second therapeutic agent is a statin, simvastatin, atorvastatin, or lovastatin.
Ashton is in the field of formulations for preventing neurological disorders, Para. [0059]) and teaches the second therapeutic agent is a statin, simvastatin, atorvastatin, or lovastatin (simvastatin, Abstract). It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl with an agent as taught by Ashton for the purpose of treating traumatic brain injury (Ashton, Para. [0059]).
Regarding Claim 19, Goetzl fails to explicitly disclose wherein the second therapeutic agent is a non-steroidal antiinflammatory drug, indomethacin, ibuprofen, carprofen, or celecoxib.
Ashton is in the field of formulations for preventing neurological disorders, Para. [0059]) and teaches the second therapeutic agent is a non-steroidal antiinflammatory drug or ibuprofen (celecoxib, Para. [0014]).
It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl with an agent as taught by Ashton for the purpose of treating neurological injury (Ashton, Para. [0059]).
Regarding Claim 20, Goetzl fails to explicitly disclose wherein the second therapeutic agent is a statin, simvastatin, atorvastatin, or lovastatin.
Ashton is in the field of formulations for preventing neurological disorders, Para. [0059]) and teaches the second therapeutic agent is a statin, simvastatin, atorvastatin, or lovastatin (simvastatin, Abstract).
It would have been obvious to one of ordinary skill in the art before the priority date to modify the method of Goetzl with an agent as taught by Ashton for the purpose of treating neurological injury (Ashton, Para. [0059]).
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to BENJAMIN J PACKARD whose telephone number is (571)270-3440. The examiner can normally be reached Mon 2-6pm and Tues-Fri 9:30am-6:30pm + mid-day flex.
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/BENJAMIN J PACKARD/ Primary Examiner, Art Unit 1612
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