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 .
Priority
This application is a national stage entry of PCT/US2021/045231 filed on 08/09/2021, which claims priority to U.S. Provisional Application No. 63/062,874 filed on 08/07/2020.
Drawings
The drawings are objected to because Figures 1-9 are too small and illegible, as well as of poor quality and low resolution. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Election/Restrictions
Applicant’s election without traverse of Group II (claims 20-27 and 29) drawn to a method for reducing blood brain barrier permeability in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a 15-PGDH inhibitor; SW033291 as a species of a 15-PGDH inhibitor; and age-related dementia as a species of a subject in need thereof in the reply filed on February 4, 2026 is acknowledged.
Claims 11-19, 28 and 30 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected group, there being no allowable generic or linking claim.
Claims 20-27 and 29 are being examined as they read on the elected species.
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 20-22, 25-27 and 29 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 23-28 of copending Application No. 19/327,153 (U.S. Publication No. 2026/0007642). Although the claims at issue are not identical, they are not patentably distinct from each other because the cited claims of the instant application and the cited claims of copending ‘153 are drawn to the treatment of a patient with Alzheimer’s disease comprising the administration of a compound of formula (V) such as SW033291 having the following structure:
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Although copending ‘153 does not claim reducing blood brain barrier permeability in the subject as claimed, the method of copending ‘153 will inherently reduce blood brain barrier permeability in said subject as claimed in the instant claims.
It is not necessary that the prior art suggests the same advantage or result discovered by applicant when the steps of the claim are the same as those described or suggested by the prior art. See, e.g., In re Kahn, 441 F.3d 977, 987 (Fed. Cir. 2006). The discovery of a new use for an old structure based on unknown properties of the structure might be patentable to the discoverer as a process of using. In re Hack, 245 F.2d 246, 248, 114 USPQ 161, 163 (CCPA 1957). However, when the claim recites using an old composition or structure and the "use" is directed to a result or property of that composition or structure, then the claim is anticipated. In re May, 574 F.2d 1082, 1090, 197 USPQ 601, 607 (CCPA 1978) (Claims 1 and 6, directed to a method of effecting nonaddictive analgesia (pain reduction) in animals, were found to be anticipated by the applied prior art which disclosed the same compounds, as well as a method of using them for effecting analgesia but which was silent as to addiction. The court upheld the rejection and stated that the inventors had merely found a new property of the compound and such a discovery did not constitute a new use.
In the instant case, the use of the claimed compound in treating Alzheimer’s disease which is an age-related dementia is claimed in copending ‘153 and thus the effect or result of said method in reducing blood brain barrier permeability is also inherently present in the claims of copending ‘153. There is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003) (rejecting the contention that inherent anticipation requires recognition by a person of ordinary skill in the art before the critical date and allowing expert testimony with respect to post-critical date clinical trials to show inherency); see also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004) ("[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention."); Abbott Labs v. Geneva Pharms., Inc., 182 F.3d 1315, 1319, 51 USPQ2d 1307, 1310 (Fed. Cir. 1999).
Thus the cited claims of the instant application would be anticipated over the cited claims of copending ‘153.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 23 and 24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 23-28 of copending Application No. 19/327,153 (U.S. Publication No. 2026/0007642) as applied to claims 20-22, 25-27 and 29 above, and further in view of Wong et al. (Neurochemistry International, 1992, Volume 21, Issue 2, pages 197-202).
Claim 23 of the instant application claims the subject has a decrease or increase in the level of at least one of PGE2, 16-keto-PGE2, PGF2a, 6-keto-PGF1a, TXB2, PGD2, PGJ2, TN-E, 15-HETE, 12-HETE, 8-HETE, or 5-HETE brain tissue compared to a control.
Claim 24 of the instant application claims the subject has a decrease in the level of at least one, at least two, or at least three or more of PGF2a, 6-keto-PGF1a, TXB2, PGD2, PGJ2, TN-E, 15-HETE, 12-HETE, 8-HETE, or 5-HETE in brain tissue of the subject.
The claims of copending ‘153 do not specifically claim that the subject with Alzheimer’s disease has a decrease or increase of the proteins in brain tissue as claimed.
Wong et al. demonstrates that as compared to control patients, patients with Alzheimer’s disease have a significant reduction in prostanoid levels in the post-mortem frontal cortex as compared to control (page 199 and abstract). Wong et al. teaches that as compared to control, post-mortem brains of patients with AD had a 46% downregulation in AA metabolism measured by total prostanoid production (page 199). Overall, the production of PGE2 (45% reduction), PGF2α (48% reduction) and PGD2 (63% reduction) were significantly lower in the frontal cortex of patients with AD compared to control (page 199).
Accordingly, claims 23 and 24 of the instant application are rendered obvious since patients with Alzheimer’s disease as claimed in copending ‘153 are known in the art as taught by Wong et al. to have decreased levels of PGE2, PGF2α, and PGD2 in brain tissue. Thus treating a subject having a decrease in the level of at least one of PGE2, 16-keto-PGE2, PGF2a, 6-keto-PGF1a, TXB2, PGD2, PGJ2, TN-E, 15-HETE, 12-HETE, 8-HETE, or 5-HETE in brain tissue of the subject with Alzheimer’s disease as claimed is rendered obvious.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
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.
Claims 20-22, 25-27 and 29 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Markowitz et al. WO 2018/017582 A1 (Provided on IDS dated 10/18/2023).
Claims 20-22, 25-27 and 29 of the instant application claim a method reducing blood brain barrier permeability in a subject in need thereof comprising administering to the subject a therapeutically effective amount of a 15-PGDH inhibitor, wherein the subject has age-related dementia, and the 15-PGDH inhibitor is SW033291 having the following structure:
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Markowitz et al. teaches compositions and methods that promote the generation or the survival of neurons in the mammalian brain as well as to compositons and methods of treating diseases, disorders, and/or conditions of the nervous system [0005]. Markowitz et al. teaches that it was found that compounds that inhibit, reduce, and/or antagonize short-chain dehydrogenase activity, such as 15-PGDH inhibitors, can be used to increase PGE2 levels in the nervous system (e.g., brain) of a mammal, wherein PGE2 elevates cyclic AMP via binding to EP2 and EP4 receptors, which are highly expressed in the cerebral cortex, hippocampus, and striatum [0005]. Markowitz et al. teaches that stimulation of these receptors with PGE2 by administration of a compound that inhibits, reduces, and/or antagonizes 15-PGDH acivity, such as with a 15-PGDH inhibitor described therein, can promote neuroprotection in a subject from axonal degeneration, neuronal cell death, and/or glia cell damage after injury, augment neuronal signaling underlying learning and memory, stimulate neuronal regeneration after injury, and/or treat diseases, disorders, and/or conditions of the nervous system [0005].
Markowitz et al. teaches the disease, disorder, and/or condition of the nervous system, which can be treated with the 15-PGDH inhibitors, can include at least one of a neurological disorder, a neuropsychiatric disorder, a neural injury, a neural toxicity disorder, a neuropathic pain, or a neural degenerative disorder, such as at least one of Alzheimer's disease, dementias related to Alzheimer's disease, Parkinson's, Lewy diffuse body diseases, senile dementia, Huntington's disease, Gilles de Ia Tourette's syndrome, multiple sclerosis, amyotrophic lateral sclerosis, hereditary motor and sensory neuropathy, diabetic neuropathy, progressive supranuclear palsy, epilepsy, or Jakob- Creutzfieldt disease [0006]-[0007].
Markowitz et al. teaches that the 15-PGDH inhibitors can be administered to a subject or neurons of the subject to promote the survival, growth, development and/or function of the neurons, particularly, the central nervous system (CNS), brain, cerebral, and hippocampal neurons, and in particular, the 15-PGDH inhibitors can be used stimulate hippocampal neurogenesis, for the treatment of neuropsychiatric and neurodegenerative diseases, including Alzheimer's disease [0009].
Markowitz et al. teaches that the 15-PGDH inhibitors can be administered to a subject at an amount effective to increase prostaglandin levels in the nervous system (e.g., brain), wherein the 15-PGDH inhibitor can include a compound having formula (V) having the same structure as the compounds as claimed in claim 29 of the instant application ([0010]-[0011] and [00128]). Markowitz et al. teaches that the 15-PGDH inhibitors can inhibit the enzymatic activity of recombinant 15-PGDH at an IC50 of less than 1 mM [00137]. Markowitz et al. teaches that the 15-PGDH inhibitor can increase the cellular levels of PGE2 [00138].
Markowitz et al. specifically teaches that the 15-PGDH inhibitor is a compound of formula (IX) having the following structure:
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[00144]. Markowitz et al. specifically teaches that the 15-PDGH inhibitor having formula (IX) was found to: i) inhibit recombinant 15-PGDH at 1 nM concentration; ii) inhibit 15-PGDH in cell lines at 100 nM concentration, iii) increase PGE2 production by cell lines; iv) is chemically stable in aqueous solutions over broad pH range; v) is chemically stable when incubated with hepatocyte extracts, vi) is chemically stable when incubated with hepatocyte cell lines; vii) shows 253 minutes plasma half-life when injected IP into mice; and viii) shows no immediate toxicity over 24 hours when injected IP into mice at 0.6 mmole/per mouse and at 1.2 mmole/per mouse and also no toxicity when injected IP into mice at 0.3 mmole/per mouse twice daily for 21 days [00145].
Markowitz et al. specifically demonstrates the effects of formula (IX) also called SW033291 in the brain and on learning and memory (Example 2 pages 143-145). Markowitz et al. specifically demonstrates that SW033291 administration increases the level of PGE2 in the brain and improves learning and memory [00327]-[00330].
Markowitz et al. specifically demonstrates 15-PGDH mRNA expression in the neurons of the mouse hippocampus, a region of the brain involved in learning and memory, and that is an early site of damage in Alzheimer’s disease and that the 15-PGDH enzyme activity can be readily inhibited in the brain following IP injection of the 15-PGDH inhibitor [00331]-[00333].
Markowitz et al. demonstrates that PGE2 levels are elevated in rat brain cortex 30, 120, and 180 minutes following a single IP injection of (+)-SW033291 at the noted doses [00334].
Markowitz et al. further demonstrates increases in the levels of 15-PGDH in brain tissue of subjects with Alzheimer’s disease relative to age matched control subjects without Alzheimer’s disease and markedly elevated levels of 15-PGDH enzyme in brain tissue (occipital and frontal cortex) of patients with Alzheimer’s disease (average age 85), relative to age matched (average age 85) control subjects without Alzheimer’s disease [00335].
Claims 12, 17 and 19 of Markowitz et al. specifically claim a method of treating Alzheimer’s disease in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a 15-PGDH inhibitor, wherein the 15-PGDH inhibitor is formula (V); and wherein the 15-PGDH inhibitor is formula (IX).
The cited claims of the instant application are anticipated since Markowitz et al. specifically teaches and claims administering to a subject having an age-related dementia which is Alzheimer’s disease, a therapeutically effective amount of a 15-PGDH inhibitor, wherein the 15-PGDH inhibitor is SW033291 having the following structure:
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, and therefore the method of Markowitz et al. will inherently reduce blood brain barrier permeability in said subject as claimed in the instant claims.
It is not necessary that the prior art suggests the same advantage or result discovered by applicant when the steps of the claim are the same as those described or suggested by the prior art. See, e.g., In re Kahn, 441 F.3d 977, 987 (Fed. Cir. 2006). The discovery of a new use for an old structure based on unknown properties of the structure might be patentable to the discoverer as a process of using. In re Hack, 245 F.2d 246, 248, 114 USPQ 161, 163 (CCPA 1957). However, when the claim recites using an old composition or structure and the "use" is directed to a result or property of that composition or structure, then the claim is anticipated. In re May, 574 F.2d 1082, 1090, 197 USPQ 601, 607 (CCPA 1978) (Claims 1 and 6, directed to a method of effecting nonaddictive analgesia (pain reduction) in animals, were found to be anticipated by the applied prior art which disclosed the same compounds, as well as a method of using them for effecting analgesia but which was silent as to addiction. The court upheld the rejection and stated that the inventors had merely found a new property of the compound and such a discovery did not constitute a new use.
In the instant case, the use of the claimed compound in treating Alzheimer’s disease which is an age-related dementia is known in the art and thus the effect or result of said method in reducing blood brain barrier permeability is also inherently present in the prior art. There is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003) (rejecting the contention that inherent anticipation requires recognition by a person of ordinary skill in the art before the critical date and allowing expert testimony with respect to post-critical date clinical trials to show inherency); see also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004) ("[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention."); Abbott Labs v. Geneva Pharms., Inc., 182 F.3d 1315, 1319, 51 USPQ2d 1307, 1310 (Fed. Cir. 1999).
Thus the cited claims of the instant application are rejected.
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.
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 23 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Markowitz et al. WO 2018/017582 A1 as applied to claims 20-22, 25-27 and 29 above, and further in view of Wong et al. (Neurochemistry International, 1992, Volume 21, Issue 2, pages 197-202).
Claim 23 of the instant application claims the subject has a decrease or increase in the level of at least one of PGE2, 16-keto-PGE2, PGF2a, 6-keto-PGF1a, TXB2, PGD2, PGJ2, TN-E, 15-HETE, 12-HETE, 8-HETE, or 5-HETE brain tissue compared to a control.
Claim 24 of the instant application claims the subject has a decrease in the level of at least one, at least two, or at least three or more of PGF2a, 6-keto-PGF1a, TXB2, PGD2, PGJ2, TN-E, 15-HETE, 12-HETE, 8-HETE, or 5-HETE in brain tissue of the subject.
Markowitz et al. is as set forth above.
Markowitz et al. does not specifically teach that the subject with age-related dementia such as Alzheimer’s disease has a decrease or increase of the proteins in brain tissue as claimed.
However, Markowitz et al. demonstrates that increases in the levels of 15-PGDH in brain tissue of subjects with Alzheimer’s disease relative to age matched control subjects without Alzheimer’s disease and markedly elevated levels of 15-PGDH enzyme in brain tissue (occipital and frontal cortex) of patients with Alzheimer’s disease (average age 85), relative to age matched (average age 85) control subjects without Alzheimer’s disease [00335]. Furthermore, Markowitz et al. demonstrates that PGE2 levels are elevated in rat brain cortex 30, 120, and 180 minutes following a single IP injection of (+)-SW033291 at the noted doses [00334]. Thus Markowitz et al. demonstrates that 15-PGDH inhibition leads to elevated PGE2 levels in the brain.
Accordingly, it would have been obvious to a person of ordinary skill in the art that subjects with Alzheimer’s disease having markedly elevated levels of 15-PGDH enzyme in brain tissue as demonstrated by Markowitz et al. would also have markedly reduced levels of PGE2 levels in the brain since the 15-PGDH enzyme leads to PGE2 degradation. Thus a subject having a decrease of the level of PGE2 as claimed in claim 23 of the instant application is rendered obvious.
In addition, Wong et al. demonstrates that as compared to control patients, patients with Alzheimer’s disease have a significant reduction in prostanoid levels in the post-mortem frontal cortex as compared to control (page 199 and abstract). Wong et al. teaches that as compared to control, post-mortem brains of patients with AD had a 46% downregulation in AA metabolism measured by total prostanoid production (page 199). Overall, the production of PGE2 (45% reduction), PGF2α (48% reduction) and PGD2 (63% reduction) were significantly lower in the frontal cortex of patients with AD compared to control (page 199).
Accordingly, claim 24 is rendered obvious since patients with Alzheimer’s disease as taught in Markowitz et al. are known in the art as taught by Wong et al. to have decreased levels of PGE2, PGF2α, and PGD2 in brain tissue as compared to control. Thus treating a subject having a decrease in the level of at least one of PGF2a, 6-keto-PGF1a, TXB2, PGD2, PGJ2, TN-E, 15-HETE, 12-HETE, 8-HETE, or 5-HETE in brain tissue of the subject with Alzheimer’s disease as claimed is rendered obvious.
Thus claims 23 and 24 of the instant application are rendered obvious in view of the cited prior art teachings.
Conclusion
Claims 1-10 are canceled. Claims 11-19, 28 and 30 are withdrawn. Claims 20-27 and 29 are rejected. No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KARA R. MCMILLIAN whose telephone number is (571)270-5236. The examiner can normally be reached Tuesday-Friday 12:00 PM-6:00 PM.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Adam C. Milligan can be reached at (571)270-7674. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/KARA R. MCMILLIAN/Primary Examiner, Art Unit 1623
KRM
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