DETAILED ACTION
Applicant’s response filed on December 10, 2025 to the non-Final rejection mailed on February 27, 2025 is acknowledged.
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 filed on 02/21/2022 is a 371 of PCT/SG2020/050406 filed on 07/14/2020.
Status of claims
Claims 19-25, 30-37, and 41-44 are pending.
Information Disclosure Statement
No new information disclosure statement(s) (IDS) filed.
Response to Arguments
Applicant’s arguments over the 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph of claims 19-25, 30-37 is persuasive in part view of amendments made to the claim. The rejection is herewith modified.
Applicant’s arguments over the 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph of claim 19 is persuasive in view of amendments made to the claim. The rejection is herewith withdrawn.
Applicant’s arguments over the 35 U.S.C. 103 of claim 19-25, 30-37 of Daudt et. al. (Methylene Blue Protects Primary Rat Retinal Ganglion Cells from Cellular Senescence. Investigative Ophthalmology & Visual Science July 2012, Vol.53, 4657-4667. doi:https://doi.org/10.1167/iovs.12-9734) in view of Myung et al. (WO 2017132639 A1) is persuasive in view of amendments made to the claim. The rejection is herewith withdrawn.
Applicant’s arguments over the 35 U.S.C. 103 of claim 19-25, 30-37 of Fung et. al. (Methylene blue promotes survival and GAP-43 expression of retinal ganglion cells after optic nerve transection. Life Sci. 2020 Dec 1;262:118462. doi: 10.1016/j.lfs.2020.118462. Epub 2020 Sep 19. PMID: 32961228.) in view of Myung et al. (WO 2017132639 A1) is persuasive in view of amendments made to the claim. The rejection is herewith withdrawn.
Applicant’s arguments over the 35 U.S.C. 103 of claim 19-25, 30-37 of Rojas et. al. ( Methylene Blue Provides Behavioral and Metabolic Neuroprotection Against Optic Neuropathy. Neurotox Res 15, 260–273 (2009). https://doi.org/10.1007/s12640-009-9027-z) in view of Myung et al. (WO 2017132639 A1) is not persuasive. The rejection is herewith maintained. The Applicant argues the Rojas et al. reference relates to the CNS not PNS system. RGCs are not peripheral nerves.
The Examiner points out that Rojas et al. does not only relate to RGCs, but also discusses potential use in a number of genetic and acquired conditions associated with degeneration of the optic nerve and linked to mitochondrial dysfunction. The Examiners contention is while the optic nerve relates to the CNS, mitochondrial dysfunction relates both to the CNS and PNS. Furthermore, Rojas et. al. teaches genetic conditions featuring optic neuropathy and mitochondrial failure include Leber’s hereditary optic neuropathy, Leigh syndrome, Friedreich’s ataxia, myoclonic epilepsy ragged-red-fibers (MERRF), mitochondrial encephalomyopathy-lactic acidosis and stroke-like syndrome (MELAS), hereditary spastic paraplegia, and the deafness-dystonia-optic atrophy syndrome. Similarly, acquired diseases featuring optic neuropathy with an association with mitochondrial dysfunction include the tobacco–alcohol ambyopia, and intoxication with chloramphenicol, ethambutol, carbon monoxide, clioquinol, cyanide, hexachlorophene, isoniazide, lead, methanol, plasmocid, or triethyl tin. Even patients with Alzheimer’s disease, a common neurodegenerative disorder linked to mitochondrial dysfunction, show a reduction in the number of retinal ganglion cells and axons, compared to healthy individuals. Thus, the present results are not only relevant for several neuro-ophtalmological conditions, but also support a more general paradigm for the development of therapeutic approaches in neurodegeneration focusing on counteracting the immediate consequences of mitochondrial failure. The Examiner’s contention is that while most conditions listed do relate to CNS damage, an overlap in the listed conditions involve the PNS. The Applicant’s arguments are not persuasive.
The rejections are as below:
Claim Objections
Claim 33 is objected to because of the following informalities: misspelled word polyvinyl. Appropriate correction is required.
Claim Rejections –
35 USC § 112 Notice of Pre-AlA or AIA Status
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 19-25, 30-37 and 41-44 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treatment of dorsal root ganglion comprising administering the compound methylene blue, does not reasonably provide enablement for prevention of peripheral nerve damage. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The instant claims are drawn to a method of method of preventing and/or treating peripheral nerve damage comprising administering to a subject in need of preventing and/or treating peripheral nerve damage a topical preparation comprising (a) an effective amount of 3,7-bis(dimethylamino) phenothiazin-5-ium chloride. The instant specification fails to provide information that would allow the skilled artisan to practice the prevention of every single peripheral nerve.
[In re Sichert, 196 USPQ 209 (CCPA 1977)]
To be enabling, the specification of the patent must teach those skilled in the art how
to make and use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557, 1561 (Fed. Cir. 1993). Explaining what is meant by “undue experimentation,” the Federal Circuit has stated:
The test is not merely quantitative, since a considerable amount of experimentation is permissible, if it is merely routine, or if the specification in question provides a reasonable amount of guidance with respect to the direction in which the experimentation should proceed to enable the determination of how to practice a desired embodiment of the claimed invention. PPG v. Guardian, 75 F.3d 1558, 1564 (Fed. Cir. 1996).
The factors that may be considered in determining whether a disclosure would require undue experimentation are set forth by In re Wands, 8 USPQ2d 1400 (CAFC 1988) at 1404 where the court set forth the eight factors to consider when assessing if a disclosure would have required undue experimentation. Citing Ex parte Forman, 230 USPQ 546 (BdApls 1986) at 547 the court recited eight factors:
1) the quantity of experimentation necessary,
2) the amount of direction or guidance provided,
3) the presence or absence of working examples,
4) the nature of the invention,
5) the state of the prior art,
6) the relative skill of those in the art,
7) the predictability of the art, and
8) the breadth of the claims.
These factors are always applied against the background understanding that scope of enablement varies inversely with the degree of unpredictability involved. In re Fisher, 57 CCPA 1099, 1108, 427 F.2d 833, 839, 166 USPQ 18, 24 (1970). Keeping that in mind, the Wands factors are relevant to the instant fact situation for the following reasons:
1. The nature of the invention, state and predictability of the art, and relative
skill level
The invention relates to a method of preventing and/or treating peripheral nerve damage comprising administering to a subject in need of preventing and/or treating peripheral nerve damage
(a) an effective amount of 3,7-bis(dimethylamino) phenothiazin-5-ium chloride. The relative skill of those in the art is high, that of an MD or PHD. That factor is outweighed, however, by the unpredictable nature of the art. As illustrative of the state of the art, the examiner cites the fact that while Applicant demonstrated the use of the compound methylene blue in treating dorsal root ganglion, nowhere in the specification did applicant demonstrate the use of prevention of every single peripheral nerve damage utilizing 3,7-bis(dimethylamino) phenothiazin-5-ium chloride. Further, the predictability of treating peripheral nerve damage is relatively low given that the various types of conditions have different causative agents, involve different cellular mechanisms, and consequently, differ in treatment protocol. Thus, given that applicant has failed to demonstrate prevention of peripheral nerve damage utilizing 3,7-bis(dimethylamino) phenothiazin-5-ium chloride, the examiner maintains that applicant has not enabled the breadth of the claims.
2 The breadth of the claims
The claims are thus very broad insofar as they recite the “prevention peripheral nerve damage utilizing 3,7-bis(dimethylamino) phenothiazin-5-ium chloride. While such “treatment” might theoretically be possible for treating dorsal root ganglion utilizing methylene, as a practical matter it is nearly impossible to achieve prevention of any peripheral nerve damage with the 3,7-bis(dimethylamino) phenothiazin-5-ium chloride.
3. The amount of direction or quidance provided and the presence or absence of working examples
The specification provides no direction or guidance for the use of 3,7-bis(dimethylamino) phenothiazin-5-ium chloride in preventing peripheral nerve damage. No reasonably specific guidance is provided concerning useful therapeutic protocols for 3,7-bis(dimethylamino) phenothiazin-5-ium chloride, other than example 1. The latter is corroborated by the working examples on pages 19-32 and table 1-6.
4. The quantity of experimentation necessary
Because of the known unpredictability of the art, and in the absence of experimental evidence, no one skilled in the art would accept the assertion that every instantly claimed compound 3,7-bis(dimethylamino) phenothiazin-5-ium chloride could be predictably used for the prevent peripheral nerve damage as inferred by the claims and contemplated by the specification. Accordingly, the instant claims do not comply with the enablement requirement of §112, since to practice the invention claimed in the patent a person of ordinary skill in the art would have to engage in undue experimentation, with no assurance of success.
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 33 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention. Applicant has included some carriers in parenthesis. It is unclear why the parenthesis is included in the claims.
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 of this title, 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 set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied 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.
Claims 19-25, 30-37 are rejected under 35 U.S.C. 103 as being unpatentable over Li et. al. (Methylene blue relieves the development of osteoarthritis by upregulating lncRNA MEG3. Exp Ther Med. 2018 Apr;15(4):3856-3864. doi: 10.3892/etm.2018.5918. Epub 2018 Mar 2. Retraction in: Exp Ther Med. 2024 May 08;28(1):274. doi: 10.3892/etm.2024.12562. PMID: 29581742; PMCID: PMC5863598.) in view of Myung et al. (WO 2017132639 A1).
Li et. al. teaches methylene blue (MB) is a long-term inhibitor of peripheral nerve axons. MB induces long-term analgesic effects and is extensively applied in the clinic. MB may be locally applied in the perianal area where it suppresses peripheral nerve conduction, thereby relieving the long-term pain caused by surgery. Local injection of 0.2% MB suppresses long-term peripheral nerve medulla pain to the treat neurodermatitis. It has also been revealed that the injection of MB into the fracture space of patients with pelvic fractures who were treated with in-screw augmented sacroiliac screw fixation, provided an analgesic effect for ~3 weeks.
While the reference teaches treatment of peripheral nerve with methylene blue, the reference fails to specifically teach the topical preparation as claimed, or corneal nerves i.e. peripheral nerve damage of neurotrophic keratopathy of claim 24.
Myung et al. teaches a crosslinking therapeutic factors to tissues in order to immobilize and concentrate therapeutic factors that promote wound healing at or under the surface of damaged tissue. The tissue damage comprises a diabetic ulcer, a neurotrophic ulcer, a burn, a chemical injury, a nerve injury, or damage to corneal tissue (e.g., neurotrophic keratopathy, recurrent corneal erosion, a corneal ulcer, exposure keratopathy, or physical trauma). Myung et al. teaches a method of treating damaged corneal tissue in a subject, the method comprising: a) contacting the damaged corneal tissue with effective amounts of a photosensitizer and one or more biomolecules capable of promoting tissue regeneration or repair, wherein the biomolecules are selected from the group consisting of epidermal growth factor (EGF), nerve growth factor (NGF), substance P (SP), insulin-like growth factor 1 (IGF-1), and netrin-1 b) exposing the tissue to light (e.g., UV or visible light) to induce a photocrosslinking reaction, whereby the one or more biomolecules are crosslinked directly to the damaged corneal tissue and to one another. Exemplary photosensitizers include riboflavin, rose bengal, eosin, and methylene blue, which upon exposure to light, produce reactive singlet oxygen and free radicals that generate covalent bonds between adjacent segments of macromolecules that contain carbonyl functional groups. Also, this method can be used to create implantable tissue substitutes made from explanted tissue, cultured cells, encapsulated cells within matrices, bio-artificial polymers, proteins and/or peptides or some combination thereof. A gel, viscoelastic solution, putty, physical matrix or membrane can be configured from this invention to act as a wound dressing or overlay, similar to an amniotic membrane, but comprised of a specific and known formulation of biomolecules, and then crosslinked into place. Alternatively, the biomolecule formulation can change from one viscosity to another as a result of the crosslinking, or can change from a solution (or gel) to a formed (non- flowable) matrix as a result of the crosslinking. A physical membrane or matrix is performed as a gel or a sheet (in hydrated or dehydrated or partially dehydrated form) through the application of a chemical or photochemical reaction, then bonded to a tissue through a subsequent chemical or photochemical reaction. In yet another variation, combinations of biomolecules with other biomolecules, or hybrid gels combining biomolecules and synthetic polymers such as polyethylene glycol, polyvinyl alcohol, poly(lactic-co- glycolic acid) (PLGA), polycaprolactone, polyacrylic acid can be used as the encapsulating matrix. (reads on microparticle) The preparation can be in the form of a liquid solution or suspension immediately prior to administration. (reads on particles) Furthermore, the biomolecule formulation may have one or more thickening agents or other additives that contribute to the viscosity of the solution applied to a surface prior to crosslinking. The pharmaceutical compositions comprising biomolecules and/or other agents are in a sustained-release formulation The invention also provides kits comprising one or more containers holding compositions comprising therapeutic factors and/or photosensitizers, and optionally one or more other drugs for treating a wound or tissue damage.
It would have been obvious to one of ordinary skill in the art at the time of filing to incorporate the methylene blue in a topical formulation to treat surface peripheral nerve damage on the mucosal membrane, at varying viscosities in a gel for sustained release with additional compounds, in a kit to sustain treatment for a given number of days. The motivation comes from the teaching of Myung et al. that topical administration of methylene blue is used in a formulation for neurotrophic keratopathy. Hence, a skilled artisan would have reasonable expectation of successfully treating the mucosal membrane topically with methylene blue.
Claims 41-44 are rejected under 35 U.S.C. 103 as being unpatentable over Li et. al. (Methylene blue relieves the development of osteoarthritis by upregulating lncRNA MEG3. Exp Ther Med. 2018 Apr;15(4):3856-3864. doi: 10.3892/etm.2018.5918. Epub 2018 Mar 2. Retraction in: Exp Ther Med. 2024 May 08;28(1):274. doi: 10.3892/etm.2024.12562. PMID: 29581742; PMCID: PMC5863598.) in view of Myung et al. (WO 2017132639 A1), as applied to claims 19-25, 30-37, and further in view of Khan et al. (Chitosan coated PLGA nanoparticles amplify the ocular hypotensive effect of forskolin: statistical design, characterization and in vivo studies Int. J. Biol. Macromol., 116 (2018), pp. 648-663).
Li et. al. and Myung et al. are as discussed above.
While Myung et al. teaches the use of PLGA polymers, the reference fails to specify the coating of the particles with a mucoadhesive.
Khan et al. teaches chitosan (CS) coated poly lactic-co-glycolic acid (PLGA) nanoparticles (NP's) could be successfully formulated and are an excellent vehicle for forskolin in ocular delivery.
It would have been obvious to one of ordinary skill in the art at the time of filing to incorporate chitosan (CS) coated poly lactic-co-glycolic acid (PLGA) nanoparticles (NP's) in a topical formulation to treat surface peripheral nerve damage. The motivation comes from the teaching of Khan et al. that chitosan (CS) coated poly lactic-co-glycolic acid (PLGA) nanoparticles (NP's) could be successfully formulated and are an excellent vehicle for forskolin in ocular delivery. Hence, a skilled artisan would have reasonable expectation of successfully formulating an excellent vehicle for ocular delivery.
Claims 19-25, 30-37 are rejected under 35 U.S.C. 103 as being unpatentable over Rojas et. al. ( Methylene Blue Provides Behavioral and Metabolic Neuroprotection Against Optic Neuropathy. Neurotox Res 15, 260–273 (2009). https://doi.org/10.1007/s12640-009-9027-z) in view of Myung et al. (WO 2017132639 A1).
Rojas et al. teaches “ The vitreous bodies of both eyes of each subject were injected with either: 1) Control group: the vehicle dimethylsulfoxide (DMSO) only as control (n = 5), 2) Rotenone group: 200 μg/kg rotenone in DMSO (n = 5), 3) Rotenone plus (0.5–25 μM) - MB group: 200 μg/kg rotenone in the vehicle DMSO, plus 70 μg/kg MB (n = 5), or 4) MB alone group: 70 μg/kg MB alone (n = 6). Rotenone (2 μM) and/or MB . Co-administration of MB prevented the changes in visual function and the retinal histopathology. Furthermore, rotenone induced a functional deafferentation of the visual system, as revealed by decreases in the metabolic activity of the retina, superior colliculus, and visual cortex. These metabolic changes were also prevented by MB. The results provided the first demonstration of MB’s behavioral and metabolic neuroprotection against optic neuropathy, and implicate MB as a candidate neuroprotective agent with metabolic-enhancing properties that may be used in the treatment of neurodegenerative diseases associated with mitochondrial dysfunction. Rojas et. al. teaches genetic conditions featuring optic neuropathy and mitochondrial failure include Leber’s hereditary optic neuropathy, Leigh syndrome, Friedreich’s ataxia, myoclonic epilepsy ragged-red-fibers (MERRF), mitochondrial encephalomyopathy-lactic acidosis and stroke-like syndrome (MELAS), hereditary spastic paraplegia, and the deafness-dystonia-optic atrophy syndrome. Similarly, acquired diseases featuring optic neuropathy with an association with mitochondrial dysfunction include the tobacco–alcohol ambyopia, and intoxication with chloramphenicol, ethambutol, carbon monoxide, clioquinol, cyanide, hexachlorophene, isoniazide, lead, methanol, plasmocid, or triethyl tin. Even patients with Alzheimer’s disease, a common neurodegenerative disorder linked to mitochondrial dysfunction, show a reduction in the number of retinal ganglion cells and axons, compared to healthy individuals. Thus, the present results are not only relevant for several neuro-ophtalmological conditions, but also support a more general paradigm for the development of therapeutic approaches in neurodegeneration focusing on counteracting the immediate consequences of mitochondrial failure.
While the reference teaches neuroprotective properties of methylene blue, the reference fails to specifically teach the topical preparation as claimed.
Myung et al. teaches a crosslinking therapeutic factors to tissues in order to immobilize and concentrate therapeutic factors that promote wound healing at or under the surface of damaged tissue. The tissue damage comprises a diabetic ulcer, a neurotrophic ulcer, a burn, a chemical injury, a nerve injury, or damage to corneal tissue (e.g., neurotrophic keratopathy, recurrent corneal erosion, a corneal ulcer, exposure keratopathy, or physical trauma). Myung et al. teaches a method of treating damaged corneal tissue in a subject, the method comprising: a) contacting the damaged corneal tissue with effective amounts of a photosensitizer and one or more biomolecules capable of promoting tissue regeneration or repair, wherein the biomolecules are selected from the group consisting of epidermal growth factor (EGF), nerve growth factor (NGF), substance P (SP), insulin-like growth factor 1 (IGF-1), and netrin-1 b) exposing the tissue to light (e.g., UV or visible light) to induce a photocrosslinking reaction, whereby the one or more biomolecules are crosslinked directly to the damaged corneal tissue and to one another. Exemplary photosensitizers include riboflavin, rose bengal, eosin, and methylene blue, which upon exposure to light, produce reactive singlet oxygen and free radicals that generate covalent bonds between adjacent segments of macromolecules that contain carbonyl functional groups. Also, this method can be used to create implantable tissue substitutes made from explanted tissue, cultured cells, encapsulated cells within matrices, bio-artificial polymers, proteins and/or peptides or some combination thereof. A gel, viscoelastic solution, putty, physical matrix or membrane can be configured from this invention to act as a wound dressing or overlay, similar to an amniotic membrane, but comprised of a specific and known formulation of biomolecules, and then crosslinked into place. Alternatively, the biomolecule formulation can change from one viscosity to another as a result of the crosslinking, or can change from a solution (or gel) to a formed (non- flowable) matrix as a result of the crosslinking. A physical membrane or matrix is performed as a gel or a sheet (in hydrated or dehydrated or partially dehydrated form) through the application of a chemical or photochemical reaction, then bonded to a tissue through a subsequent chemical or photochemical reaction. In yet another variation, combinations of biomolecules with other biomolecules, or hybrid gels combining biomolecules and synthetic polymers such as polyethylene glycol, polyvinyl alcohol, poly(lactic-co- glycolic acid) (PLGA), polycaprolactone, polyacrylic acid can be used as the encapsulating matrix. (reads on microparticle) The preparation can be in the form of a liquid solution or suspension immediately prior to administration. (reads on particles) Furthermore, the biomolecule formulation may have one or more thickening agents or other additives that contribute to the viscosity of the solution applied to a surface prior to crosslinking. The pharmaceutical compositions comprising biomolecules and/or other agents are in a sustained-release formulation The invention also provides kits comprising one or more containers holding compositions comprising therapeutic factors and/or photosensitizers, and optionally one or more other drugs for treating a wound or tissue damage.
It would have been obvious to one of ordinary skill in the art at the time of filing to incorporate the methylene blue in a topical formulation to treat surface peripheral nerve damage on the mucosal membrane, at varying viscosities in a gel for sustained release with additional compounds, in a kit to sustain treatment for a given number of days. The motivation comes from the teaching of Myung et al. that topical administration of methylene blue is used in a formulation for neurotrophic keratopathy. Hence, a skilled artisan would have reasonable expectation of successfully treating the mucosal membrane topically with methylene blue.
Claims 41-44 are rejected under 35 U.S.C. 103 as being unpatentable over Rojas et. al. ( Methylene Blue Provides Behavioral and Metabolic Neuroprotection Against Optic Neuropathy. Neurotox Res 15, 260–273 (2009). https://doi.org/10.1007/s12640-009-9027-z) in view of Myung et al. (WO 2017132639 A1), as applied to claims 19-25, 30-37, and further in view of Khan et al. (Chitosan coated PLGA nanoparticles amplify the ocular hypotensive effect of forskolin: statistical design, characterization and in vivo studies Int. J. Biol. Macromol., 116 (2018), pp. 648-663).
Rojas et. al. and Myung et al. are as discussed above.
While Myung et al. teaches the use of PLGA polymers, the reference fails to specify the coating of the particles with a mucoadhesive.
Khan et al. teaches chitosan (CS) coated poly lactic-co-glycolic acid (PLGA) nanoparticles (NP's) could be successfully formulated and are an excellent vehicle for forskolin in ocular delivery.
It would have been obvious to one of ordinary skill in the art at the time of filing to incorporate chitosan (CS) coated poly lactic-co-glycolic acid (PLGA) nanoparticles (NP's) in a topical formulation to treat surface peripheral nerve damage. The motivation comes from the teaching of Khan et al. that chitosan (CS) coated poly lactic-co-glycolic acid (PLGA) nanoparticles (NP's) could be successfully formulated and are an excellent vehicle for forskolin in ocular delivery. Hence, a skilled artisan would have reasonable expectation of successfully formulating an excellent vehicle for ocular delivery.
Conclusion
The arguments are not persuasive and the rejection is made FINAL.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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 extension fee 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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/LAYLA SOROUSH/Primary Examiner, Art Unit 1622