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 .
This action is in response to the papers filed on 05/30/2024. Claims 1-12 are
currently pending. Claims 2-8 and 11 are currently amended.
Claims 1-12 are examined on their merits to which the following grounds of rejection are applicable. Claim 1 is an independent claim.
Sequence Compliance - 37 CFR 1.821-1.825
This application contains sequence disclosures that are encompassed by the
definitions for nucleotide and/or amino acid sequences set forth in 37 CFR 1.821(a)(1)
and (a)(2), see for example specification page 70-83 which lists SEQ ID Nos 1-52.
However, this application fails to comply with the requirements of 37 CFR 1.821 through
1.825 for the reason(s) set forth below and on the Notice to Comply With Requirements
For Patent Applications Containing Nucleotide Sequence And/Or Amino Acid Sequence
Disclosures which is attached to this communication.
The specification filed on 12/19/2024 discloses sequences that are missing corresponding sequence identifiers (i.e. SEQ ID Nos). On page 45 of the specification, para 00158 recites “The mouse HRH1 gRNA sequences are: gRNA1 (5'-
GCTCCACAACCCTTCCGAGTA-3'), and gRNA2 (5'-GTCCGTCTTCTCCACAACCCT-3') The human HRH1 gRNA sequences are: gRNA1 (5'-GTCTCCGTCCTCCTTAACCCC-3) and gRNA2 (5'-GATTCTCCGTCCTCCTTAAC-3).” Examiner requests sequence identifiers for the recited gRNAs for mouse HRH1 and human HRH1.
Applicant must amend the claims and specification and/or drawings to comply
with the sequence requirements.
APPLICANT IS GIVEN A THREE MONTH EXTENDABLE PERIOD WITHIN
WHICH TO COMPLY WITH THE SEQUENCE RULES, 37 CFR 1.821-1.825. Failure to
comply with these requirements will result in ABANDONMENT of this application under
37 CFR 1.821 (g). Extension of time may be obtained by filing a petition accompanied by the extension fee under the provisions of 37 CFR 1.136. In no case may an applicant
extend the period for response beyond the six month statutory period. Applicant is
requested to return a copy of the attached Notice to Comply with the response.
Required response – Applicant must provide:
• A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required sequence identifiers, including into the Brief Description of
the Drawings, consisting of:
o A copy of the previously-submitted specification, with deletions shown with
strikethrough or brackets and insertions shown with underlining (marked-
up version);
o A copy of the amended specification without markings (clean version); and
o A statement that the substitute specification contains no new matter.
Priority
The instant application is a 371 of PCT/US2022/080499 filed on 11/28/2022 which claims benefit of 63/284,424 filed on 11/30/2021. Thus, the earliest possible filing priority for the instant application is 11/30/2021.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 05/30/2024 and 02/04/2026, was filed before the mailing date of the non-final office action. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Objections
Claim 1 is objected to because abbreviations such as HRH1 should be spelled out at their first encounter in the claims. Appropriate correction is required.
Claim 7 is objected to because the phrase “subject is human” should recite “subject is a human”. Appropriate correction is required.
Claim 11 is objected to because abbreviations such as AAV should be spelled out at their first encounter in the claims. Appropriate correction is required.
Claim 11 is objected to because the phrase “guide (gRNA)” should recite “guide RNA (gRNA)”. Appropriate correction is required.
Claim 9 and 12 are in improper Markush form; a Markush group should be in the form “selected from the group consisting of A, B, and C”. Appropriate correction is requested.
Claim Interpretation
As stated above, it appears claim 12 should recite “SEQ ID NO: 31, 32, 33, and 34”. The examiner interprets the claim to read as “wherein the murine γ-synuclein promoter is selected from the sequence of SEQ ID NO: 31, 32, 33, and 34” since SEQ ID NO 3, 4, 5, 6, and 7 are directed to primers for GAPDH and ATF6 which are not murine γ-synuclein promoters.
Claim Rejections - 35 USC § 112
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 2, 5 and 12 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as failing to set forth 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.
Claim 2 recites the term “and/or” in line 6. It is unclear what the metes and bounds of this term, as “and” could be interpreted to include degeneration of axons and soma of retinal ganglion cells, or, “or” would imply that the cell features are in the alternative. Appropriate correction is required.
Claim 2 recites the terms “reduces” and “ameliorates” and are relative terms which renders the claim indefinite. The terms “reduces” and “ameliorates” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention.
Claim 12 recites that SEQ ID NO 3, 4, 5, 6, and 7 are directed to the murine γ-synuclein promoter. The specification describes the murine γ-synuclein promoter as SEQ ID NO: 31, 32, 33, and 34 (Page 57-59) and SEQ ID NO 3, 4, 5, 6, and 7 are directed to primers for GAPDH and ATF6 (Para 00165, page 48). Appropriate correction is requested.
35 U.S.C. 112(a) - Scope of Enablement
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.
Claim 1-12 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:
a method of treating optic nerve (ON) crush (i.e. a traumatic ON neuropathy model system) in a mouse using the HRH1 antagonists amoxapine, desloratadine, and maprotiline by administering them intravitreally (para 00144-00145) and an AAV-vector based HRH1 antagonist with a pair of gRNAs (The mouse HRH1 gRNA sequences are: gRNA1 (5' -GCTCCACAACCCTT CCGAGTA-3') and gRNA2 (5'-GTCCGTCTTCTCCACAACCCT-3') (para 00158)) also administered intravitreally (para 00148),
does not reasonably provide enablement for treatment of any ON neuropathy including glaucoma, using any HRH1 antagonist or any guide RNA of 20-21 nucleotides within an AAV vector that targets histamine receptor H1. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention. The specification is not enabling for any route of administration to the optic nerve of a subject.
The factors to be considered in determining whether undue experimentation is required are summarized in In re Wands, 858 F.2d 731, 737, 8 U.S.P.Q.2d 1400, 1404 (Fed. Cir. 1988) (a) the breadth of the claims; (b) the nature of the invention; (c) the state of the prior art; (d) the level of one of ordinary skill; (e) the level of predictability in the art; (f) the amount of direction provided by the inventor; (g) the existence of working examples; and (h) the quantity of experimentation needed to make or use the invention based on the content of the disclosure.
While all of these factors are considered, a sufficient number are discussed below so as to create a prima facie case.
the breadth of the claims; the nature of the invention:
The claim 1 is directed to a method of treating a vast genus of optic nerve neuropathies in vast genus of mammalian subjects and a vast genus of HRH1 antagonists that can be administered any way to the optic nerve. Claim 2 further limits claim 1 to treating retinal ganglion cells. Claim 3 and 4 further limits claim 1 to systemic and intravitreally administered. Claim 5 and 6 limit claim 1 to glaucoma as the ON neuropathy. Claim 8-10 further limit claim 1 to the tricyclic compound maprotiline. Claim 11 and 12 further limit claim 1 to the HRH1 antagonist being an AAV vector that targets HRH1 with a murine γ-synuclein promoter linked to Cas9 and U6 promoter linked to at least one gRNA which precedes an -NGG protospacer and the promoter is selected from a group of SEQ ID NOs.
the amount of direction provided by the inventor; the existence of working
examples:
As recited above, claim 1 is broadly but reasonably interpreted as comprising a vast genus of optic nerve neuropathies in vast genus of mammalian subjects and a vast genus of HRH1 antagonists that can be administered any way to the optic nerve. The specification does not provide support for the genus of ON neuropathies in the genus of mammalian subjects and using a genus of HRH1 antagonists that would provide the claimed function of treating an ON neuropathy.
The specification describes treatment of a crushed optic nerve using three compounds (amoxapine, desloratadine, or maprotiline) in a mouse (para 00144) wherein the compounds are administered intravitreally. Importantly, maprotiline was the only compound to show significantly higher survival of retinal ganglion cell (RGC) coma and axons in the ON crushed mouse model (para 00146; Fig 12a, Fig 5D,E). In regards to the AAV vector as an HRH1 antagonist for the treatment of ON neuropathy, the specification only discloses the use of gRNAs targeting mouse HRH1 and injected the mixture of AAV-mSncg-Cas9 + AAV-mouse HRH1-gRNAs (FIG. 15a) or AAV-control gRNAs intravitreally into mouse eyes (FIG. 15b) (para 00149). The specification discloses The mouse HRH1 gRNA sequences are: gRNA1 (5' -GCTCCACAACCCTT CCGAGTA-3') and gRNA2 (5'-GTCCGTCTTCTCCACAACCCT-3') (para 00158))
Therefore, the specification only provides details to use of the compounds amoxapine, desloratadine, and maprotiline and an AAV-vector with the specific gRNAs described above as HRH1 antagonists to treat a crushed ON in a mouse. Furthermore, while the specification describes several in vitro studies to determine the compounds to further validate in the mouse in vivo model (for example, para 00143 describes use of HEK293 cells to demonstrate inhibition of pathways induced by ER stress by the three compounds and para 00149 describes HRH1 knockdown by using Cas9 and HRH1 gRNAs in cell lines), it is unknown if the amoxapine, desloratadine, or any other HRH1 antagonist compound besides maprotiline would be able to elicit the claimed function of treating a ON neuropathy. Similarly, while the using a Cas9 and gRNA targeting HRH1 was shown in human cell lines, there is no indication that the HRH1 knockdown could be achieved in a human subject in vivo, if it would work in a AAV-vector, or if it would perform the claimed function of treating an ON neuropathy.
the state of the prior art; the level of predictability in the art:
Antagonists of histamine receptors have been used in prior art for treatment of ocular diseases such as glaucoma, however studies have shown that some histamine receptor antagonists have adverse ocular effects and the studies only provide proof-of-concept-level teachings of On neuropathy treatment. Sgambellone teaches that “Both H1R and H2R antagonists are capable of inducing glaucoma due to their anticholinergic activity; in fact, the H1R antago-nist promethazine has been shown to cause lens swelling and increase the risk of angle-closure glaucoma due to pupillary obstruction” (page 63, para 6), suggesting that not all HRH1 antagonists can elicit the function of treating the ON neuropathy glaucoma, but rather they may cause glaucoma. In regard to the use of AAV vector as an HRH1 antagonist, Wang teaches that “the specificity and potency of promoters from RGC-specific genes can be highly variable. This variability could be due to the particular characteristics of the promoter regions that we examined, or because RGCs contain additional enhancers that can affect specific promoter activity” (page 3910, right col, para 4, Discussion), hence not guaranteeing that AAV vector with a particular promoter will give functional activity. Wang further teaches that genomic modification of an endogenous gene Ddit3 in RGCs in vivo is only ~11%, thus despite the gene target being different than the instant application, results suggest that certain gene loci may be difficult to access by gRNAs/Cas9 (page 3912, left col, para 1).
the quantity of experimentation needed to make or use the invention based on the
content of the disclosure:
The skilled artisan would be required to perform under levels of experimentation
in order to practice the claimed invention. The instant specification does not reduce to
practice the claimed invention; the instant specification does not provide guidance on what HRH1 antagonists could be used to treat an ON neuropathy other than amoxapine, desloratadine, or maprotiline, at what dosage the HRH1 should be administered at, and the suitable period of time the HRH1 antagonist should be administered. The specification only describes methods for administering AAV into the into the peripheral retina just behind the ora serrata of a mouse and approximately 2 μl of the vitreous was removed to allow injection of 2 μl AAV into the vitreous chamber to achieve 3 X 109 vg/retina (page 46, para 00159), with no indication of timing interval of administration. Similarly, the specification only describes for compound treatment (i.e, amoxapine, desloratadine, or maprotiline treatment) each eye of the mouse received intravitreal injection with 2 μl of 2 mM test compounds once and intraperitoneal (i.p.) injection daily (15 mg/kg) for 14 days after optic nerve crush (page 49, para 00166). Thus, the skilled artisan would be forced to 1) determine which HRH1 antagonists to use for the mammalian subject, 2) which route of administration of the compound or AAV is appropriate for the mammalian subject, 3) which dose for both the AAV and compound would be necessary for proper treatment in a mammalian subject and 4) determine what result is sufficient to deem the method being capable of adequately treating the ON neuropathy in the mammalian subject.
the level of one of ordinary skill:
The level of one of ordinary skill is a PhD holder.
Conclusion:
When all of the Wands factors are considered together, they establish a prima
facie case that the specification is not enabling for the claims. The Specification only provides details for a method of treating optic nerve (ON) crush (i.e. a traumatic ON neuropathy model system) in a mouse using the HRH1 antagonists 1) compounds amoxapine, desloratadine, and maprotiline by administering them intravitreally (para 00144-00145) or intraperitoneally at 2 mM concentration and 2) an AAV-vector based HRH1 antagonist with a pair of gRNAs wherein the gRNA sequences are: gRNA1 (5' -GCTCCACAACCCTT CCGAGTA-3') and gRNA2 (5'-GTCCGTCTTCTCCACAACCCT-3'), a murine γ-synuclein promoter, and the vector is also administered intravitreally (para 00148) and at a concentration of 3 X 109 vg/retina.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claim(s) 1-12 are rejected under 35 U.S.C. 103 as being unpatentable over He et al (WO 2021222507 A1; as cited in IDS) and further in view of Firkusny et al (Br J clin Pharmac ,1994; pages 383-388), Sgambellone et al (biomolecules, 11 Aug 2021, pages 1-10), and Wang et al (The Journal of Neuroscience, 2020, pages 3896–3914) and as evidenced by NCBI (Human HRH1 DNA sequence GenBank: AB041380.1, published first on April 18 2000).
Regarding claims 1-4 and 7, He teaches a method of treating a human subject (page 9, line 7) having a disease associated with Myelination failure (e.g. an optic nerve injury/neuropathy) by administering to the subject an agent which can be clemastine fumarate which is a small molecule having histamine H1 [receptor] antagonistic properties (page 19, para 3 line 4-8). He teaches that the agent, when contacted with the optic nerve (which comprises retinal ganglion cells), regenerates an axon (i.e. reduces degeneration of an axon) (page 5, lines 16-24). He teaches that an agent can be intravitreally injected (Fig 4J; page 40, line 30-31) or administered systemically (page 23, line 9), rendering obvious a method of treating an optic nerve (ON) neuropathy in a human subject in need thereof, the method comprising: administering an effective dose of an HRH1 antagonist to the optic nerve of the subject, thereby treating the ON neuropathy, wherein the administration of an HRH1 antagonist reduces or ameliorates degeneration of axons of retinal ganglion cells and the composition is administered intravitreally and systemically.
Regarding claims 5, 6, and 8-10, the teachings of He render obvious claim 1.
He does not teach the ON neuropathy is glaucoma, the HRH1 antagonist is a tricyclic compound selected from the plurality of compounds listed in claim 9, and the agent is maprotiline formulated for ocular delivery.
However, one of ordinary skill in the art would have considered the teachings of Sgambellone and Firkusny as these references are analogous prior art pertaining to the pathophysiology of glaucoma, histamine ligands and receptors expression in the eye, and maprotiline as an antagonist of histamine receptors.
Sgambellone teaches that glaucoma is characterized by the progressive degeneration of retinal ganglion cells (abstract), glaucoma can be cause by optic nerve damage (page 1, para 3), and the histamine H1 [receptor] has been localized to the inner later of ganglion cells and that circuits involved with vision may be altered by histamine release (page 4, para 1). Sgambellone also teaches that the dysregulation of histamine secretion may contribute to the pathophysiology of Glaucoma (page 2, para 1).
Firkusny teaches maprotiline show direct antagonism at pulmonary histamine receptors (page 386, Discussion, para 1) and histamine-induced bronchoconstriction was abolished after a single dose of maprotiline and this effect persisted throughout multiple dose treatment (abstract), suggesting a histamine antagonistic property of maprotiline.
It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of a method to treat an ON neuropathy wherein the treatment regenerates axons of the retinal ganglion cells by administering an HRH1 antagonist such as clemastine fumarate from He with the teachings of Sgambellone pertaining histamine’s role in glaucoma and presence of HRH1 in the retinal ganglion cells and with the teachings of Firkusny pertaining to maprotiline having histamine antagonistic properties. With Sgambellone’s teaching that glaucoma may be caused by histamine dysregulation and HRH1 is expressed in RGCs, one would combine this with the teaching from Firkusny disclosing that maprotiline is antagonistic to histamine receptors to arrive at the claimed invention of a method to treat the ON neuropathy glaucoma by administering maprotiline as the HRH1 antagonist to the optic nerve. As use of maprotiline for histamine-related disorders has been shown and treatment of ON neuropathies such as glaucoma with HRH1 antagonists for regenerating axons has been shown, one would be motivated to combine the teachings to have an alternative treatment option for ON neuropathy and would have a reasonable expectation of success.
In regard to the recitation “wherein the tricyclic agent is maprotiline formulated for ocular delivery” as required in claim 10, It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of using maprotiline for as a clinical treatment from Firkusny to be formulated for ocular delivery as reformulation of pharmaceuticals for alternative regions of interest of the body is known technique in the art. One would be motivated to do so to ensure effective usage of maprotiline to treat an eye disease and have a reasonable expectation of success.
Regarding claims 11 and 12, the teachings of He render obvious claim 1.
The teachings of He do not teach wherein the HRH1 antagonist comprises an AAV vector, comprising: a murine y-synuclein promoter in operable linkage with a nucleic acid encoding a Cas9 nuclease; and a U6 promoter in operable linkage with at least one guide (gRNA) 20-21 nucleotides in length, wherein each gRNA precedes an -NGG protospacer, and wherein each gRNA targets histamine receptor H1 (HRH1) and wherein the murine γ-synuclein promoter is selected from the sequence of SEQ ID NO:3, 4, 5, 6, 7, or a variant thereof.
However, one of ordinary skill in the art would have considered the teachings of Wang, Wu, and NCBI as this reference is analogous prior art pertaining to the use of AAVs for gene expression and editing in mammalian retinal ganglion cells and guide RNA design.
Wang teaches “the success of adeno-associated virus (AAV)-mediated gene replacement in treating inherited retinal disease makes RGC-specific gene expression and editing by AAV a promising gene therapy strategy for optic neuropathies” (page 3897, left col, para 1). Wang teaches there is a need for retinal ganglion cell targeting with AAVs and identified γ-Synuclein Promoter as a good promoter for humans and when combined with AAV and CRISPR/Cas9, it provides effective neuroprotection in optic neuropathies (abstract). Wang teaches a gRNA to mouse Ddit3 and Sarm1 genes that is 20-nucleotides and preceded by a 5’-NGG protospacer-adjacent motif (page 3902, right col, para 1) and the vector carried a SpCas9 with mSncg-0.27K (murine γ-Synuclein) promotor (page 3901, left col, Para 1).
It would have been prima facie obvious to one of ordinary skill, in the art at the time of the effective filing date, to modify the teachings of a method to treat an ON neuropathy wherein the treatment regenerates axons of the retinal ganglion cells by administering an HRH1 antagonist such as clemastine fumarate from He with the teachings of Wang to instead use a AAV vector comprising a murine γ-Synuclein Promoter with a nucleic acid encoding Cas9 nuclease and a U6 promoter operably linked to a gRNA as the HRH1 antagonist. One would be motivated to combine these teachings as use of AAV vectors for targeting retinal diseases would be an alternative option to treating ON neuropathies since they can be RGC-specific, hence a more efficient, specific, and potent treatment option compared to treating with a compound.
While Wang and He do not explicitly disclose that each gRNA targets the HRH1, one of ordinary skill in the art would consider the teachings of NCBI who teaches the gene sequence of HRH1 (i.e. the target sequence) and Wu who teaches that several tools (eleven tools are cited in Wu; page 66, left col, para 2) have been developed for designing guide RNAs such that off-target effects are mitigated. Wu teaches that the tools take into consideration the input sequence, a genomic region, or a gene and predicts guide RNAs with minimal off-target effects. Wu teaches that these tools can also consider the presence of SNPs and secondary structures, the genomic context of the guide, and GC content, all of which can impact the effectiveness of the gRNA (page 66, left col, para 2-3). As the gene sequence of HRH1 was known at the time of filing of the instant application, as evidenced by the gene sequence disclosed by NCBI, one of ordinary skill in the art would be able to design gRNAs using Wu’s teachings for Wang’s method
Wang also teaches a murine γ-synuclein promoter (mSncg-1.45kb, in Fig 1-1 extended data) that has 100% sequence alignment to SEQ ID NO: 31 in the instant application claim 12. See alignment below:
Qy = SEQ ID NO 31 from instant application, Db = Wang’s mSncg-1.45kb sequence
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Conclusion
Claims 1-12 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Juliana Candelaria whose telephone number is (571)272-5488. The examiner can normally be reached Monday - Friday 8am - 5pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Maria Leavitt can be reached at (571) 272-1085. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/JULIANA IRENE CANDELARIA/ Examiner, Art Unit 1634
/MARIA G LEAVITT/ Supervisory Patent Examiner, Art Unit 1634
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