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
Response to Amendment
Acknowledgment is made of the receipt and entry of the amendment filed on 04/20/2026, wherein claims 3, 6, 9-12, 14, and 16 are cancelled, and claims 1, 4, 13, 27, 29, 30 are amended.
Election/Restriction
Applicant elected without traverse : 1) Group I invention , drawn to a method of treating a patient with globoid cell leukodystrophy or Krabbe disease, comprising administration to a patient in need thereof an effective amount of a pharmaceutical composition comprising gemfibrozil and at least one pharmaceutically acceptable excipient or carrier ; 2) method species for inhibiting progression of the globoid cell leukodystrophy or Krabbe disease, in the reply filed on 12/04/2025.
Claims 17-26 and 28, remain withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention.
After searching prior art and further consideration, the elected method treatment species “inhibiting progression of the globoid cell leukodystrophy or Krabbe disease” recited in now cancelled claims 3, 6, 9 and 12 are considered as associated with other intended treatment outcome of administering gemfibrozil as recited in claims 1, 4, 7, 10, respectively. The requirement of species elections regarding the intended treatment outcome was withdrawn in last office action mailed on 01/20/2026 .
Status of Claims
Claims 1-2, 4-5, 7-8, 13, 15, 17-31 are pending in the instant application.
Claims 17-26 and 28 remain withdrawn.
Claims 1-2, 4-5, 7-8, 13, 15, 27, and 29-31 are currently under examination.
Priority
The instant application 18/261, 959 filed on 07/18/2023 is 371 of PCT/US2021/014124 filed on 01/20/2021.
Claim Interpretation
Independent claims are directed to a method of treating globoid cell leukodystrophy or Krabbe disease, comprising administration to a patient in need thereof an effective amount of a pharmaceutical composition comprising gemfibrozil and at least one pharmaceutically acceptable excipient or carrier. Regarding the limitation of intended treatment outcome recited in instant claims, e.g. “protecting myelin in the nervous system”(claim 1), “improving the locomotor activity of a patient with Krabbe disease” (claim 7) , etc. these recitations are construed as intended results of active method step of administering an effective amount of a pharmaceutical composition comprising gemfibrozil and pharmaceutical acceptable carrier to a patient in need thereof ( e.g. globoid cell leukodystrophy or Krabbe disease), which do not materially limit the claimed method since such limitations do not result in manipulative difference in method steps of the claims. Please note the biological activity of compound is the property of active compound and products of identical or similar composition cannot exert mutually exclusive properties when administered under the same or similar circumstances. “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer.” Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir.1999). If the prior art teaches and/or suggests the same or similar method step as instantly claimed (i.e. administering an effective amount of a pharmaceutical composition comprising gemfibrozil to a patient with globoid cell leukodystrophy or Krabbe disease), the method of the prior art would have achieved the intended results recited in instant claims and read on instant claimed methods. The burden of proof is shifted to the Applicant to show that the subject matter of the prior art does not possess the characteristic relied on whether the rejection is based on inherency under 35 U.S.C.102 or obviousness under 35 U.S.C. 103.
Action Summary/Response to Argument
Applicant's remarks filed 04/20/2026 have been fully considered. Any objection and rejection found in the previous Office Action and not repeated herein has been withdrawn in view of amendment and Applicant’s persuasive arguments .The text of those sections of Title 35 U.S. Code not included in this action can be found in a prior Office action.
35 USC §103:
Applicant's argument regarding 35 USC§103 have been fully considered, but NOT persuasive to overcome rejections over: 1) Pahan'666 (US20170354666A1), in view of Jana and Ghosh; 2) Pahan'000 (WO 2018126000A1); 3) Pahan'000, in view of Pahan'666 and Jana.
Applicant argues “ Krabbe disease is a leukodystrophy disorder, not a lysosomal storage disorder. Krabbe disease is a genetic disease caused by a mutation in the GALC gene resulting in demyelination of the nerve cells (CNS and PNS). This is a critical difference between the amended claims and the prior art cited by the Office” (Remarks, page 8).
RESPONSE: Applicant's argument is fundamentally incorrect and NOT persuasive. Graziano 2015 (Gene 2015, 555, 2–13, http://dx.doi.org/10.1016/j.gene.2014.09.046 ) reviews history, genetic, and recent advances on Krabbe disease and explicitly states Krabbe disease or globoid cell leukodystrophy is one of the classic genetic lysosomal storage diseases with autosomal recessive inheritance that affects both central and peripheral nervous systems” (See abstract, page 2, left column, para 2). Won 2016( Journal of Neuroscience Research 94:990–1006) reviews biochemical, cell biological, pathological, and therapeutic aspects of Krabbe’s Disease and explicitly teaches “Krabbe disease is a fatal autosomal recessive lysosomal storage disorder (LSD) caused by genetic deficiency or abnormalities of galactocerebrosidase (GALC; EC 3.2.1.46) and, thus, accumulation of its substrates galactosylceramide (GalCer) and galactosylsphingosine (psychosine [PSY]) in macrophages and neural tissue, leading to progressive loss of myelin (See page 990, left column, last para). Ferreira (2017) reviews lysosomal storage diseases and explicitly teaches Krabbe disease is lysosomal storage diseases, along with Niemann-Pick disease, Gaucher disease, neuronal ceroid lipofuscinosis, Farber disease, Fabrydisease, Schindler disease, GM1 gangliosidosis, Tay-Sachs disease, Sandhoff disease, etc. (See abstract, Table 1-4; page 24, 2.4 Krabbe disease Section). Thus, a skilled artisan would have known Krabbe disease is a lysosomal storage disorder.
Applicant argues “ Pahan '666 is cited for administering gemfibrozil to treat a lysosomal storage disorder... Krabbe disease is not a lysosomal storage disorder... Pahan '000 teaches methods of treating lysosomal storage disorders and not a leukodystrophy disorder(Remarks, page 8-9)
RESPONSE: As elaborated above, Krabbe disease IS a lysosomal storage disorder. Both Pahan '666 and Pahan '000 teach method of treating lysosomal storage disorder with gemfibrozil. It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound as demonstrated in Pahan’ 666 and Pahan '000 treating variety of lysosomal storage disorder/disease with gemfibrozil alone or in combination with vitamin A. A skilled artisan would have known Krabbe disease is lysosomal storage disorder that belongs to the same group of disease taught by Pahan’ 666 and Pahan '000. It would have been obvious to one of the ordinary skilled in the art to further explore gemfibrozil alone or in combination with vitamin A for treating other lysosomal storage disease (e.g. Krabbe disease), based on combined beneficial teachings of prior art and general knowledge of treating neurological disorder (e.g. lysosomal storage disease).
Applicant argues Gosh studies late infantile Batten disease, which results from a mutation in the CLN2 gene. This disease is caused by a distinct mechanism in action because the cells are unable to make a working version of a TPP 1 enzyme, which when working breaks down the waste accumulated in the lysosomes. This pathway is distinct from GALC and there is nothing in Gosh to suggest that there is any cross interaction between these two molecular pathways. Accordingly, a person of skill in the art would not read Gosh or be motivated to modify Pahan '666 to arrive at the claimed methods( Remarks, page 8).
RESPONSE: Please note infantile Batten disease/ infantile Neuronal Ceroid Lipofuscinosis (LINCL) is also a lysosomal storage disorder as disclosed by Ghosh 2017(See Introduction). Instant claim 7 is directed to improve locomotor activity with gemfibrozil. Ghosh 2017 and its incorporated reference teach gemfibrozil treatment improves motor behavior, lowers the burden of storage material in the brain, prolongs the lifespan in Cln2(−/−) mice, and other benefit. Based on gemfibrozil’s beneficial effect on locomotor activity as taught by Ghosh 2017, a POSA would be motivated to explore gemfibrozil for improving locomotor activity in other patient/subjects with lysosomal storage disorder . The biological activity/ action of mechanism is the property of gemfibrozil. MPEP 2112 I states: “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art' s functioning, does not render the old composition patentably new to the discoverer.” Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus, the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977).”
Applicant argues “Sana studied healthy brain cells from humans and mice and the effects of gemfibrozil on genetically modified mice with knocked out PPAR-alpha and PPAR-beta genes ... Sana never looks at a system with a cell or animal model having GALC -/-, nor is there any suggestion to look at a knockout GALC model” ( Remarks, page 8).
RESPONSE: Instant claim 1 is directed to protecting myelin in the nervous system. Jana teaches novel myelinogenic property of gemfibrozil and gemfibrozil may be of therapeutic benefit in MS and other demyelinating diseases. Again, the biological activity/ action of mechanism is the property of gemfibrozil, no matter what animal model/assay is used. Based on gemfibrozil’s beneficial effect on myelin as taught by Jana, a POSA would be motivated to explore gemfibrozil for protecting myelin in other patient/subjects.
Non-statutory double patenting rejections
Applicant's argument regarding non-statutory double patenting rejections are similar as 35 USC 103 based on the incorrect conception that Krabbe disease is not a lysosomal storage disorder.
RESPONSE: As elaborated above, Krabbe disease is a lysosomal storage disorder. Reference claims are directed to method of treating neurogenerative disease, e.g. lysosomal storage disorder. It would be obvious for a skilled artisan to explore gemfibrozil alone or in combination with vitamin A for treating other lysosomal storage disease (e.g. Krabbe disease), based on combined beneficial teachings of reference claims and general knowledge of treating neurological disorder (e.g. lysosomal storage disease).
Claim Objections
Claim 7 remains objected to because of following informalities:
Independent claim 7 recites “improving the locomotor activity of a patient” and “ the administration to a patient in need thereof”. There is no antecedent basis for the locomotor activity and the administration, and article “the” is redundant and not necessary.
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 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 non-obviousness.
Claims 1-2, 4-5, 7-8, 13, 15, 27, and 29-31 are rejected under 35 U.S.C. 103 as being unpatentable over Pahan ( US20170354666A1, hereafter “Pahan’ 666”, Applicant’s IDS dated 03/27/2025), in view of Jana et al. ( The Journal of Biological Chemistry, 2012, Aug 9;287(41):34134–34148. doi: 10.1074/jbc.M112.398552, “Gemfibrozil, a Lipid-lowering Drug, Increases Myelin Genes in Human Oligodendrocytes via Peroxisome Proliferator-activated Receptor-β”) and Ghosh et al. (J. Neurochem, 2017, May;141(3):423-435, hereafter “ Ghosh’ 2017”, doi: 10.1111/jnc.13987. Epub 2017 Apr 3, “Gemfibrozil, food and drug administration-approved lipid-lowering drug, increases longevity in mouse model of late infantile neuronal ceroid lipofuscinosis”)(maintained/reiterated as necessitated by amendment).
Pahan’ 666 teaches a method for treatment of a lysosomal storage disorder, comprising administering to a subject in need thereof a therapeutically effective amount of composition comprising an active agent upregulation of Transcription Factor EB, e.g. lipid-lowering drug, fibrate/ gemfibrozil and vitamin A (See abstract, [0007], claims 1, 5-14, 27, 31-35).
Pahan’ 666 teaches embodiments wherein the composition further comprises a therapeutically effective amount of all-trans retinoic acid or vitamin A (See [0008], [0036]-[0037], claim 8).
Pahan’ 666 teaches embodiment wherein the composition comprises the fibrate (e.g. gemfibrozil) and all-trans retinoic acid/ vitamin A upregulating TFEB mRNA and protein levels in brain cells and other assays (See [0012]-[0019], [0041], claim 9-10, Fig 1-8.). Pahan’ 666 teaches combination of gemfibrozil fibrate and vitamin A may be a synergistic providing greater therapeutic effect in the subject than administration of vitamin A or the fibrate alone (See [0008]).
Pahan’ 666 teaches lysosomal storage disorder (LSDs) are a group of inherited metabolic disorders that result from defects in lysosomal function and exemplary neurodegenerative disorder selected from Tay-Sach's disease, Fabry disease, Niemann-Pick disease, Gaucher disease, Hunter Syndrome, Alpha-mannosidosis, Aspartylglucosaminuria, Cholesteryl ester storage disease, Chronic Hexosaminidase A Deficiency, Cystinosis, Danon disease, Farber disease, Fucosidosis, and Galactosialidosis (See [0005], [0010], claims 11 and 35).
Regarding the pharmaceutical composition, Pahan’ 666 explicitly teaches pharmaceutical composition comprising gemfibrozil and vitamin A (See 0041]).
Regarding the administration limitation, Pahan’ 666 teaches gemfibrozil or a combination thereof may be administered in a single daily dose or in multiple doses per day (See [0044]-[0045]) (which reads on instant claims 15, 27).
Regarding the dosage form of instant claims 29 and 31, Pahan’ 666 teaches pharmaceutical composition comprising active agent and commonly known excipients in the form of tablets, pills, aqueous or oily suspensions, syrups, alixiers, solid emulsions, solid dispersions, etc. (See [0042]-[0043])
Regarding claim 30, Pahan’ 666 teaches variety of administration route, e.g. oral, parenteral, etc.
Pahan’ 666 collectively teaches method of treating variety of lysosomal storage disease with a pharmaceutical composition comprising gemfibrozil alone or in combination with vitamin A and pharmaceutical excipient/carrier, wherein combination of gemfibrozil and vitamin A may be synergistic for treating lysosomal storage disease.
Pahan’ 666 is silent about Krabbe disease is lysosomal storage disorder and intended treatment outcome/result. As elaborate in the Claim Interpretation section, the biological activity of compound is the property of active compound and products of identical or similar composition cannot exert mutually exclusive properties when administered under the same or similar circumstances.
Further, Jana teaches gemfibrozil treatment restores the recruitment of PPAR-B to the mouse PLP promoter, inhibits demyelination in spinal cord, and suppresses EAE in PLP-TCR transgenic mice(See whole article, abstract, Fig 1). Jana collectively teaches a novel myelinogenic property of gemfibrozil and gemfibrozil may be of therapeutic benefit in MS and other demyelinating diseases (which reads on instant claim 1).
Ghosh 2017 teaches oral administration of gemfibrozil upregulates the expression of anti-inflammatory molecules like interleukin-1 receptor antagonist (IL-1Ra) and suppressor of cytokine
signaling 3 (SOCS3) in vivo in the brain of Cln2 null mice, an animal model of late infantile neuronal ceroid lipofuscinosis, leading to the suppression of neuronal apoptosis, increased survival and improved locomotor activity (See whole article, Graphical abstract; Results) (which reads on instant claims 4 and 7). Ghosh 2017 and its incorporated reference teach the mechanism of gemfibrozil treatment, e.g. prolongs the lifespan in Cln2(−/−) mice, improves motor behavior, lowers the burden of storage material in the brain and other benefit (See Results, page 5 to 8; Discussion). Neuronal apoptosis is a hallmark of most of the known neurodegenerative diseases including lysosomal storage disorders. Strong inhibition of neuronal apoptosis in different parts of the CNS of Cln2 (−/−) mice by gemfibrozil suggests that this anti-apoptotic property of gem may contribute to its lifespan-prolonging efficacy (See Discussion, page 8).
It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound as demonstrated in Pahan’ 666 treating variety of lysosomal disease with gemfibrozil alone or in combination with vitamin A. A skilled artisan would have known Krabbe disease is lysosomal storage disorder that belong to the same group of disease taught by Pahan’ 666. It would have been obvious to one of the ordinary skilled in the art before the effective filing date of instantly claimed invention to further explore gemfibrozil alone or in combination with vitamin A for treating other lysosomal storage disease (e.g. Krabbe disease), based on combined beneficial teachings of prior art and general knowledge of treating neurological disorder (e.g. lysosomal storage disease) and arrived instantly claimed invention with reasonable expectation of success. A skilled artisan would be motivated to explore gemfibrozil alone or in combination with vitamin A for treating Krabbe disease because Krabbe disease is a lysosomal storage disorder associated with lysosomal function as other lysosomal disease (e.g. Tay-Sach's disease, etc.).
Regarding instantly claimed treatment outcome/ intended result, As elaborate in the Claim Interpretation section, the biological activity of compound is the property of active compound and products of identical or similar composition cannot exert mutually exclusive properties when administered under the same or similar circumstances. A skilled artisan would reasonably expect gemfibrozil alone or in combination with vitamin A administered to a subject with Krabbe disease might provide an alternative treatment for Krabbe disease based on the neuroprotective properties of gemfibrozil taught by prior art with instant claimed treatment outcome which is the property/biological activity of gemfibrozil.
One of ordinary skill in the art would have had reasonable expectation of success in producing the claimed invention based on the combined teachings of prior art and exploration/optimization of for intended treatment outcome based on the general knowledge of treating neurological disorder (e.g. lysosomal storage disease, Krabbe disease). Therefore, the invention as a whole is prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
Claims 4, 7, 13, 15, 27, and 29-31 are rejected under 35 U.S.C. 103 as being unpatentable over Pahan (WO 2018126000A1 , hereafter “Pahan’ 000”, patent family of US20190358188A1/ US11020366B2) (maintained/reiterated as necessitated by amendment).
Pahan’ 000 teaches a method for treatment of a neurodegenerative disease comprising administering to the subject a composition comprising a therapeutically effective amount of fibrate (e.g. gemfibrozil) (See abstract, [0005]-[0006], claims 1-22).
Pahan’ 000 teaches therapeutic efficacy of gemfibrozil in mouse model of LINCL wherein behavioral analysis and survival studies on Clnl2 mice showed increased longevity and improvement of motor behavior in gem-treated animals compared to vehicle (0.1% methyl cellulose)-treated controls. “The burden of storage materials and neuronal apoptosis were also found to be partially reduced in gem-treated animals with increase in levels of phospho- BCL2 Associated Agonist Of Cell Death (P-BAD), an anti-apoptotic molecule. Furthermore, levels of anti-inflammatory factors like suppressor of cytokine signaling 3 (SOCS3) and Interleukin-1 receptor antagonist (IL-IRa) was found to be elevated in gem- treated animals. Taken together, this study indicates a neuroprotective role of gemfibrozil”( See [0005]).
Regarding instant claim 4, Pahan’ 000 teaches a method of increasing levels of anti-inflammatory factors in a brain of a subject having neurodegenerative disease (e.g. late infantile neuronal ceroid lipofuscinosis) comprising administering to the subject a composition comprising a therapeutically effective amount of fibrate (e.g. gemfibrozil( See [0005], claims 18-21). Pahan’ 000 teaches increase in the levels of anti-inflammatory factors comprises an increase in the level of suppressor of cytokine signaling 3 (SOCS3) and Interleukin-1 receptor antagonist (IL-IRa) (See claim 21).
Regarding instant claim 7, Pahan’ 000 teaches a method of improving motor behavior of a subject having a neurodegenerative disease comprising administering to the subject a composition comprising a therapeutically effective amount of fibrate (e.g. gemfibrozil) (See [0010], [0013]-0015] claim 7)
Regarding instant claim 15 and 27, Pahan’ 000 teaches subject were treated daily with gemfibrozil (7.5 mg/kg body weight/day) (See [0051]).
Regarding claims 29-31, Pahan’ 000 teaches pharmaceutical composition in various forms, e.g. suspensions, solid emulsions, solid dispersions, etc. (See 0037]. Pahan’ 000 teaches the agent is for oral or parenteral administration (See Example 1- 6, claim 22). Pahan’ 000 also teaches "oral" refers to modes of administration which include oral, enteral, buccal, sublabial, sublingual, etc..
Pahan’ 000 teaches variety of neurodegenerative disease, e.g. neuronal ceroid lipofuscinosis, Alzheimer's disease, Huntington's disease, Amyotrophic lateral sclerosis (ALS), Parkinson's disease, including Parkinson's plus diseases such as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) or dementia with Lewy bodies (DLB)…The neurodegenerative disease may be caused by a lysosomal storage disorder, for example, Tay-Sach's disease, Fabry disease, Niemann-Pick disease, Gaucher disease, Hunter Syndrome, Alpha-mannosidosis, Aspartylglucosaminuria, Cholesteryl ester storage disease, Chronic Hexosaminidase A Deficiency, Cystinosis, Danon disease, Farber disease, Fucosidosis, or Galactosialidosis (See [0006])
Pahan’ 000 teaches a method for treatment of a neurodegenerative disease comprising administering to the subject a composition comprising a therapeutically effective amount of gemfibrozil wherein the intended treatment outcome, e.g. of prolonging a lifespan, improving motor behavior in the subject, read on instant intended treatment outcome.
Pahan’ 000 is silent about treating Krabbe disease and intended treatment outcome.
It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound. It would have been obvious to one of the ordinary skilled in the art before the effective filing date of instantly claimed invention to further explore gemfibrozil for treating other neurodegenerative disease (e.g. Krabbe disease), based on combined teachings of prior art and general knowledge of neurological disorder and arrived instantly claimed invention with reasonable expectation of success. A skilled artisan would be motivated to explore gemfibrozil for treating other neurodegenerative disease (e.g. Krabbe disease) since Krabbe disease is lysosomal storage disease that belongs to the same group of neurological disorder as taught by Pahan’ 000.
One of ordinary skill in the art would have had reasonable expectation of success in producing the claimed invention based on the combined teachings of prior art and exploration/optimization of for intended treatment outcome based on the general knowledge of treating neurological disorder (e.g. lysosomal disease, Krabbe disease). Therefore, the invention as a whole is prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
Claims 1-2, 4-5, 7-8, 13, 15, 27, and 29-31 are rejected under 35 U.S.C. 103 as being unpatentable over Pahan ( WO 2018126000A1 , “Pahan’ 000”), in view of Pahan ( US20170354666A1, “Pahan’ 666”, Applicant’s IDS dated 03/27/2025), and Jana et al. ( The Journal of Biological Chemistry, 2012, Aug 9;287(41):34134–34148. doi: 10.1074/jbc.M112.398552, “Gemfibrozil, a Lipid-lowering Drug, Increases Myelin Genes in Human Oligodendrocytes via Peroxisome Proliferator-activated Receptor-β”) (maintained/reiterated as necessitated by amendment).
The collective teachings of Pahan’ 000, Pahan’ 666 and Jana are elaborated in preceding 103 rejections and applied as before.
Pahan’ 000 teaches a method for treatment of a neurodegenerative disease comprising administering to the subject a composition comprising a therapeutically effective amount of gemfibrozil wherein the intended treatment outcome, e.g. of prolonging a lifespan, improving motor behavior in the subject, read on instant intended treatment outcome.
Pahan’ 000 is silent about vitamin A in combination with gemfibrozil.
Pahan’ 666 teaches combination of gemfibrozil and vitamin A may be a synergistic providing greater therapeutic effect in the subject than administration of vitamin A or the fibrate alone for treating lysosomal storage disorder.
Jana collectively teaches a novel myelinogenic property of gemfibrozil and gemfibrozil may be of therapeutic benefit in demyelinating diseases (which reads on claim 1).
It would have been obvious to one of the ordinary skilled in the art before the effective filing date of instantly claimed invention to further explore gemfibrozil for treating other neurodegenerative disease (e.g. Krabbe disease), based on combined teachings of prior art and general knowledge of neurological disorder and arrived instantly claimed invention with reasonable expectation of success. A skilled artisan would be motivated to explore gemfibrozil for treating other neurodegenerative disease (e.g. Krabbe disease) since Krabbe disease is lysosomal storage disease that belongs to the same group of neurological disorder as taught by Pahan’ 000 and Pahan’ 666.
Regarding instantly claimed treatment outcome/ intended result, the biological activity of compound is the property of active compound and products of identical or similar composition cannot exert mutually exclusive properties when administered under the same or similar circumstances. A skilled artisan would reasonably expect gemfibrozil alone or in combination with vitamin A administered to a subject with Krabbe disease might provide an alternative treatment for Krabbe disease based on the neuroprotective properties of gemfibrozil taught by prior art with instant claimed treatment outcome which is the property/biological activity of gemfibrozil.
One of ordinary skill in the art would have had reasonable expectation of success in producing the claimed invention based on the combined teachings of prior art and exploration/optimization of for intended treatment outcome based on the general knowledge of treating neurological disorder (e.g. lysosomal disease, Krabbe disease). Therefore, the invention as a whole is prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
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 1-2, 4-5, 7-8, 13 and 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-11 of U.S. Patent No. 9750712 B2(maintained/reiterated as necessitated by amendment).
Reference claims are directed to a method of for treatment of a neurodegenerative disease, comprising administering to a subject in need of such treatment a composition comprising a therapeutically effective amount of an agent that mediates upregulation of TPP1, the agent comprising a lipid-lowering drug, wherein the neurodegenerative disease is neuronal ceroid lipofuscinosis, wherein the lipid lowering drug is a fibrate.
Reference claims 2, 8 and 11 further recite the fibrate is gemfibrozil .
Reference claim 5 recites all-trans retinoic acid (which reads on vitamin A) .
Reference claim 6 recites administering all-trans retinoic acid and a fibrate provides a greater therapeutic effect in the subject than administration of all-trans retinoic acid or the fibrate alone.
The difference of instant claims and reference claims are targeted disease: Krabbe disease vs neuronal ceroid lipofuscinosis and intended treatment outcome.
It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound. A skilled artisan would have known both neuronal ceroid lipofuscinosis and Krabbe disease are lysosomal storage disease. It would have been obvious to one of the ordinary skilled in the art to further explore gemfibrozil alone or in combination with vitamin A for treating other lysosomal storage disease (e.g. Krabbe disease), based on combined beneficial teachings of reference claims and general knowledge of treating neurological disorder (e.g. lysosomal storage disease). A skilled artisan would be motivated to explore gemfibrozil alone or in combination with vitamin A for treating Krabbe disease because Krabbe disease is a lysosomal storage disorder associated with lysosomal function as neuronal ceroid lipofuscinosis.
Regarding instantly claimed treatment outcome/ intended result, the biological activity of compound is the property of active compound and products of identical or similar composition cannot exert mutually exclusive properties when administered under the same or similar circumstances. A skilled artisan would reasonably expect gemfibrozil alone or in combination with vitamin A administered to a subject with Krabbe disease might provide an alternative treatment for Krabbe disease based on the neuroprotective properties of gemfibrozil taught by reference claims.
The instant application shares at least one common inventor/applicant with the reference patent. Further, the continuing data of instant application is not related to the reference patent and thus no 35 USC 121 shield exists. See MPEP 804.01.
Claims 1, 7, 13 and 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-15 of U.S. Patent No. 11020366 B2 (maintained/reiterated as necessitated by amendment).
Reference claims are directed to a method of decreasing neuronal apototic cell death in a subject having neuronal ceroid lipofuscinosis, comprising administering to the subject a composition comprising a therapeutically effective amount of gemfibrozil.
Reference claim 5 recites method of prolonging a lifespan of a subject having neuronal ceroid lipofuscinosis. Reference 7 recites a method of improving motor behavior of a subject having neuronal ceroid lipofuscinosis.
Reference claims are silent about Krabbe disease as targeted disease and intended treatment outcome thereof.
It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound. It would have been obvious to one of the ordinary skilled in the art to further explore gemfibrozil alone or in combination with vitamin A for treating other lysosomal storage disease (e.g. Krabbe disease), based on combined beneficial teachings of reference claims and general knowledge of treating neurological disorder (e.g. lysosomal storage disease). A skilled artisan would be motivated to explore gemfibrozil for treating Krabbe disease because Krabbe disease is a lysosomal storage disorder associated with lysosomal function as neuronal ceroid lipofuscinosis.
The instant application shares at least one common inventor/applicant with the reference patent. Further, the continuing data of instant application is not related to the reference patent and thus no 35 USC 121 shield exists. See MPEP 804.01.
Claims 1-2, 4-5, 7-8, 13, 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of U.S. Patent No. 11351142 B2(maintained/reiterated as necessitated by amendment).
Reference claims are directed to a method for treatment of a neurodegenerative disease, comprising administering to a subject in need of such treatment a composition comprising a therapeutically effective amount of an agent that mediates upregulation of TPP1, the agent comprising a lipid-lowering drug, wherein the neurodegenerative disease is a lysosomal storage disorder, and wherein the lipid-lowering drug is a fibrate, and wherein the lysosomal storage disease is Tay-Sach's disease.
Reference claim 2 and 7 recite the fibrate is gemfibrozil.
Reference claim 4 recites composition further comprises a therapeutically effective amount of all-trans retinoic acid (which reads on vitamin A) .
Reference claim 5 recites administering all-trans retinoic acid and a fibrate provides a greater therapeutic effect in the subject than administration of all-trans retinoic acid or the fibrate alone.
Reference claims are silent about Krabbe disease as targeted disease and intended treatment outcome thereof.
It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound. A skilled artisan would have known Krabbe disease are lysosomal storage disease. It would have been obvious to one of the ordinary skilled in the art to further explore gemfibrozil alone or in combination with vitamin A for treating other lysosomal storage disease (e.g. Krabbe disease), based on combined beneficial teachings of reference claims and general knowledge of treating neurological disorder (e.g. lysosomal storage disease). A skilled artisan would be motivated to explore gemfibrozil alone or in combination with vitamin A for treating Krabbe disease because Krabbe disease is a lysosomal storage disorder associated with lysosomal function as Tay-Sach's disease.
The instant application shares at least one common inventor/applicant with the reference patent. Further, the continuing data of instant application is not related to the reference patent and thus no 35 USC 121 shield exists. See MPEP 804.01.
Claims 1-2, 4-5, 7-8, 13, 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of U.S. Patent No. 11844767 B2(maintained/reiterated as necessitated by amendment).
Reference claims are directed to method for reducing amyloid-β protein aggregates in the brain of comprising administering to the subject in need of such treatment a composition comprising a therapeutically effective amount of a combination of vitamin A or a derivative thereof and an agonist of proliferator-activated receptor α (“PPARα”).
Reference claim 9 and 16 recite PPARα agonist is gemfibrozil.
Reference claims 14 and 15 recite Alzheimer's disease and Parkinson’s Disease.
Reference claims are silent about Krabbe disease as targeted disease and intended treatment outcome thereof. It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound. A skilled artisan would be motivated to explore gemfibrozil alone or in combination with vitamin A for treating Krabbe disease based on the beneficial teaching of reference claims with reasonable expectation that gemfibrozil alone or in combination with vitamin A might provide an alternative treatment for Krabbe disease with the intended treatment outcome/result.
The instant application shares at least one common inventor/applicant with the reference patent. Further, the continuing data of instant application is not related to the reference patent and thus no 35 USC 121 shield exists. See MPEP 804.01.
Claims 1-2, 4-5, 7-8, 13, 15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of U.S. Patent No. 11135180 B2(maintained/reiterated as necessitated by amendment).
Reference claims are directed to method for reducing amyloid-β protein aggregates in the brain of a subject, the method comprising administering to the subject in need of such treatment a composition comprising a therapeutically effective amount of a combination of vitamin A or a derivative thereof and an agonist of proliferator-activated receptor α (“PPARα”), wherein the agonist of PPARα is gemfibrozil.
Reference claim 7 recites Alzheimer’ disease.
Reference claims are silent about Krabbe disease as targeted disease and intended treatment outcome thereof. It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound. A skilled artisan would be motivated to explore gemfibrozil alone or in combination with vitamin A for treating Krabbe disease based on the beneficial teaching of reference claims with reasonable expectation that gemfibrozil alone or in combination with vitamin A might provide an alternative treatment for Krabbe disease with the intended treatment outcome/result.
The instant application shares at least one common inventor/applicant with the reference patent. Further, the continuing data of instant application is not related to the reference patent and thus no 35 USC 121 shield exists. See MPEP 804.01.
Conclusion
No claims are allowed.
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/L.M./Examiner, Art Unit 1628
/JARED BARSKY/Primary Examiner, Art Unit 1628
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