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 .
Claims 1-17 are pending in the present application.
Applicant’s election without traverse of Group III in the reply filed on 04/14/2025 is acknowledged.
Applicant also elected without traverse the following species: (i) a Zinc finger protein (ZFP); (ii) a repression domain; and (iii) intravenous route.
Accordingly, claims 1-11 and 17 are withdrawn from further consideration because they are directed to non-elected inventions.
Therefore, claims 12-16 are examined on the merits herein with the above elected species.
Claim Objections
Claim 12 is objected to because of its dependency on the unelected claim 1.
Claim Rejections - 35 USC § 112
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 12-16 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:
A method of modulating MAPT expression in a cell, the method comprises administering a vector comprising a polynucleotide sequence encoding a genetic modulator of MAPT, wherein the genetic modulator comprising: (i) a DNA-binding domain that binds to a target site of at least 12 nucleotides in the MAPT gene, and (ii) a transcriptional regulatory domain or nuclease domain; and
A method of treating a tauopathy in a subject, the method comprises administering intracerebroventricularly, intrathecally, retro-orbitally, or intracisternally to the subject an effective amount of a recombinant viral vector comprising a polynucleotide sequence encoding a genetic repressor of MAPT, or intravenously administering to the subject an effective amount of a recombinant AAV9 or AAV2/9 vector comprising a polynucleotide sequence encoding a genetic repressor of MAPT, wherein the genetic repressor comprising: (i) a DNA-binding domain that binds to a target site of at least 12 nucleotides in the MAPT gene, and (ii) a transcriptional repressor domain or nuclease domain, and wherein the treated subject has a reduced amount of tau;
does not reasonably provide enablement for a method of modulating MAPT expression in a cell, or a method of treating and/or preventing a tauopathy in a subject as claimed broadly. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
The factors to be considered in the determination of an enabling disclosure have been summarized as the quantity of experimentation necessary, the amount of direction or guidance presented, the state of the prior art, the relative skill of those in the art, the predictability or unpredictability of the art and the breadth of the claims. Ex parte Forman, (230 USPQ 546 (Bd Pat. Appl & Unt, 1986); In re Wands, 858 F.2d 731, 8 USPQ 2d 1400 (Fed. Cir. 1988)).
The instant specification is not enabled for the instant broadly claimed invention for the reasons discussed below.
1. The breadth of the claims
Claims 12-14 encompass a method of modulating MAPT expression in any cell in vitro or in vivo, the method comprises administering (e.g., intravenous, intraperitoneal, intramuscular, intracranial, intracerebroventricular administration) a genetic modulator of MAPT gene in any form (e.g., protein, mRNA, non-viral vector or viral vector such as an adenovirus vector, a lentiviral vector, or an AAV vector) to the cell, wherein the genetic modulator comprising: a DNA-binding domain that binds to a target site of at least 12 nucleotides in the MAPT gene, and a transcriptional regulatory domain or nuclease domain.
Claims 15-16 encompass a method for treating and/or preventing a tauopathy (e.g., Alzheimer’s disease, Frontotemporal dementia, Progressive supranuclear palsy and others) in a subject, the method comprises repressing MAPT expression by administering a genetic modulator of MAPT gene in any form (e.g., protein, mRNA, non-viral vector or viral vector such as an adenovirus vector, a lentiviral vector, or an AAV vector of any serotype) to the subject, wherein the genetic modulator comprising: a DNA-binding domain that binds to a target site of at least 12 nucleotides in the MAPT gene, and a transcriptional regulatory domain or nuclease domain; and wherein the administering is intracerebroventricular, intrathecal, intracranial, retro-orbital, intravenous (elected species) or intracisternal.
The term “genetic modulator” is defined by the present application to refer to any molecule that alters the expression and/or sequence of one or more genes, and a genetic modulator may be a genetic repressor or a genetic activator (paragraph [0078]).
2. The state and the unpredictability of the prior art
At about the effective filing date of the present application (12/01/2016), little was known about a method of modulating MAPT expression in a cell using the claimed genetic modulator of the present application; or a method of treating and/or preventing a tauopathy in a subject comprising repressing MAPT expression via administering the claimed genetic modulator of the present application to the subject as evidenced at least by the teachings of Flynn (US 2017/0035860; IDS), Hyman et al (WO2015/089375; IDS), Cox, III et al (US 6,534,261; IDS), Saraiva et al (J. Controlled Release 241:94-109, 2016) and Orr et al (Trends in Pharmacological Sciences 38: 637-648, 2017). In a 2017 brief review of tauopathy, Orr et al stated “There are currently no disease-modifying therapies for the treatment of tauopathies, a group of progressive neurodegenerative disorders that are pathologically defined by the presence of tau protein aggregates in the brain” (first sentence of the Abstract). Even in 2022, Zhang et al (Molecular Neurodegeneration 17:28; doi.org/10.1186/s13024-022-00533-z, 29 pages; 2022) still concluded “Since tauopathies are still untreatable diseases, efforts have been made to depict clinical and pathological characteristics, identify biomarkers, elucidate underlying pathogenesis to achieve early diagnosis and develop disease-modifying therapies” (See “Conclusions” section in the Abstract). Moreover, in a review of gene therapy for the CNS Saraiva et al stated “The success of CNS gene therapy approaches greatly depends on the selected delivery system. Non-viral vectors (e.g., liposomes, exosomes, polymeric nanoparticles) are considered a promising option, due to their simple and cost-effective production methods, as well as their safety profile [3,4]. However, they present a relative low efficiency and mediate a transient effect, requiring repeated administration with the potential risk of triggering an immune response” (page 95, left column, second paragraph); “Despite all the advantages of systemic AAV delivery, this method has been hindered by the fact that most serotypes cannot circumvent the BBB. As indicated in Table 1, IV administration does not induce an efficient CNS transduction for most of the known serotypes” (page 99, left column, last paragraph); and “However, AAV9 has been the most widely studied vector for IV delivery, since this serotype is among the best performers in both studies, showing high transgene expression and wide-spread transduction throughout the CNS in neonatal and adult mice” (page 101, left column, last sentence of first full paragraph). Furthermore, the physiological art is recognized as unpredictable (MPEP 2164.03).
3. The amount of direction or guidance provided
Apart from disclosing various MAPT-specific repressors in the form of engineered Zinc Finger Proteins operably linked to a KRAB repression domain (ZFP-TFs) in the form or recombinant AAV2/9 vectors, and these recombinant AAV2/9 vectors were shown to efficiently transduced neuronal targets when administered intracerebroventricularly or intravenously with the ZFP-TFs resulted in potent and sustained tau reduction throughout the CNS (brain and spinal cord, including in frontal cortex, anterior cortex, posterior cortex, hippocampus, brainstem, striatum, thalamus, midbrain, cerebellum, lumbar spinal cord, thoracic spinal cord and cervical spinal cord (see at least Examples 1-2 and 6); the specification fails to provide sufficient guidance for an ordinary skilled artisan on how to prevent any tauopathy in a subject, including the use of any MAPT genetic modulator as encompassed broadly by the instant claims. Particularly, in a 2022 review Zhang et al stated that tauopathies are still untreatable diseases, let alone tauopathies are preventable as encompassed by the instant claims. There is no evidence of record indicating or suggesting any genetic activator of MAPT is capable of repressing MAPT expression of any level to yield a desired therapeutic effect in a subject in need thereof as encompassed by the instant claims. Apart from disclosing the use of AAV2/9 vector and “SGMO” AAV vectors of the provisional application 62/503,121 which are not described in any detail in the present application for intravenous administration, the instant specification fails to provide sufficient guidance for an ordinary skill in the art on how to use any other recombinant adeno-associated viral vector of other serotypes such as AAV1, AAV2, AAV3, AAV4, AAV5, AAV6, or AAV7 to cross the blood brain barrier via intravenous administration to target the brain tissue in order to yield the desired therapeutic and prophylactic effects for a subject in need of tauopathy treatment, let alone the use of other viral or non-viral delivery vectors for crossing the blood brain barrier. Zincarelli et al (Molecular Therapy 16:1073-1080, 2008) analyzed AAV serotypes 1-9 mediated gene expression and tropism in mice after systemic injection, and they found that AAV9 had the best viral genome distribution and highest protein level, including one of only two AAV serotypes (AAV8 and AAV9) that are capable of expressing luciferase protein expression in brain (see Abstract; and Figure 4). Moreover, in a 2016 review of gene therapy for the CNS Saraiva et al stated “The success of CNS gene therapy approaches greatly depends on the selected delivery system. Non-viral vectors (e.g., liposomes, exosomes, polymeric nanoparticles) are considered a promising option, due to their simple and cost-effective production methods, as well as their safety profile [3,4]. However, they present a relative low efficiency and mediate a transient effect, requiring repeated administration with the potential risk of triggering an immune response” (page 95, left column, second paragraph); “Despite all the advantages of systemic AAV delivery, this method has been hindered by the fact that most serotypes cannot circumvent the BBB. As indicated in Table 1, IV administration does not induce an efficient CNS transduction for most of the known serotypes” (page 99, left column, last paragraph); and “However, AAV9 has been the most widely studied vector for IV delivery, since this serotype is among the best performers in both studies, showing high transgene expression and wide-spread transduction throughout the CNS in neonatal and adult mice” (page 101, left column, last sentence of first full paragraph). The instant specification also fails to provide any guidance for a skill in the art on how to deliver a MAPT genetic modulator in the form of a protein and/or naked mRNA encoding a MAPT genetic modulator to the central nervous system of a subject in need of tau treatment via any of the administration routes recited in claim 14, and particularly via an intravenous administration, such that they can be delivered intact and in sufficient amount inside brain and spinal cord cells to yield the desired therapeutic and/or prophylactic effects.
With respect to claims 12-14, the instant specification also fails to provide sufficient guidance for an ordinary skill in the art on how to deliver a MAPT genetic modulator in the form of a protein and/or a naked mRNA, such that they can be entered into a cell without the help of a vector (e.g., liposome, non-viral or viral vectors) in a sufficient amount to modulate MAPT expression in said cell, particularly they are administered systemically via an intravenous administration (elected species as recited in dependent claim 14) and are not subjected to any proteolysis and/or mRNA degradation. Although tau/MAPT proteins are expressed primarily in the brain, and more precisely, in neurons; tau expression has been reported in tissues other than the brain that include the muscles of patients suffering from inclusion body myositis, or an inflammatory muscle disease; and cancers affecting various tissues such as breast, prostate, ovary, bladder and stomach cancers (Caillet-Boudin et al Molecular Neurodegeneration 10:28; DOI 10.1186/s13024-015-025-8, 14 pages; 2015).
Since the prior art at the effective filing date of the present application failed to provide sufficient guidance regarding to the aforementioned issues, it is incumbent upon the present application to do so. Given the state of the prior art discussed above, coupled with the lack of sufficient guidance provided by the present application, it would have required undue experimentation for a skilled artisan to make and/or use the instant treatment method as claimed broadly.
As set forth in In re Fisher, 166 USPQ 18 (CCPA 1970), compliance with 35 USC 112, first paragraph requires:
That scope of claims must bear a reasonable correlation to scope of enablement provided by specification to persons of ordinary skill in the art; in cases involving predictable factors, such as mechanical or electrical elements, a single embodiment provides broad enablement in the sense that, once imagined, other embodiments can be made without difficulty and their performance characteristics predicted by resort to known scientific laws; in cases involving unpredictable factors, such as most chemical reactions and physiological activity, scope of enablement varies inversely with degree of unpredictability of factors involved.
Moreover, the courts have also stated that reasonable correlation must exist between scope of exclusive right to patent application and scope of enablement set forth in the patent application (27 USPQ2d 1662 Ex parte Maizel.).
Accordingly, due to the lack of sufficient guidance provided by the specification regarding to the issues set forth above, the state and unpredictability of the relevant gene therapy art to attain the desired therapeutic effects, and the breadth of the instant claims, it would have required undue experimentation for one skilled in the art to make and use the instant broadly claimed invention.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale or otherwise available to the public before the effective filing date of the claimed invention.
Claims 12-13 are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Flynn (US 2017/0035860; IDS).
The instant claims encompass a method of modulating a microtubule associated protein tau (MAPT) expression in a cell, the method comprises administering to the cell a genetic modulator of MAPT gene, wherein the genetic modulator comprising: a DNA-binding domain that binds to a target site of at least 12 nucleotides in the MAPT gene, and a transcriptional regulatory domain or nuclease domain.
Flynn already disclosed at least a medical composition for treating a neurodegenerative disorder (e.g., Alzheimer disease, Frontotemporal dementia), comprising: a CRISPR/Cas9 nuclease component and a guide polynucleotide targeting MAPT (microtubule-associated protein tau) gene, including a catalytically inactive programmable RNA-dependent DNA binding protein (dCas9) fused to VP16 tetramer activation domain or a Krueppel-associated box (KRAB) repressor domain to enhance or repress expression of MAPT, respectively; the gene editing or modification composition can be in the form of a single vector or multiple vectors such as adeno-associated virus (AAV) vectors, plasmid vectors; and patient-derived stem cells or human embryonic stem cells comprising the same gene editing or modification composition (Summary of the Invention; particular paragraphs 21-26, 33-38, 42-43, 49-51, 93-96, 100-103, 108, 110, 111-114, 142-147, 150-151; Examples 1-3, 6-7; Tables 1-2, 5; Figure 1; and claims 26-34, 36-41 and 50-57). In addition to an active CRISPR-Cas9 nuclease, Flynn discloses that other targeted nucleases such as TALEN and ZFN can be used to create a double-stranded break in the target sequence (paragraphs 76, 103). In an exemplification, Flynn disclosed a MAPT CRISPR guide RNA design in exon 2 with 3 disclosed 23-nucleotide target sequences (Table 5). Flynn also taught a method of delivering into a target cell in vitro and/or in vivo (e.g., a human patient suffering from a neurodegenerative disorder) using the above disclosed medical composition (Abstract; and at least claims 1-3).
Accordingly, the teachings of Flynn meet every limitation of the instant claims. Therefore, the reference anticipates the instant claims.
Claims 12-16 are rejected under 35 U.S.C. under 35 U.S.C. 102(a)(1) as being anticipated by Hyman et al (WO2015/089375; IDS) and evidenced at least by WO 2010/076939 (IDS).
Claims 12-14 encompass a method of modulating a microtubule associated protein tau (MAPT) expression in a cell, the method comprises administering to the cell a genetic modulator of MAPT gene, wherein the genetic modulator comprising: a DNA-binding domain that binds to a target site of at least 12 nucleotides in the MAPT gene, and a transcriptional regulatory domain or nuclease domain; while claims 15-16 encompass a method for treating and/or preventing a tauopathy in a subject using the same method for repressing MAPT expression and wherein the administration is intracerebroventricular, intrathecal, intracranial, retro-orbital, intracisternal, or intravenous (elected species).
Hyman et al already disclosed various agents selected to inhibit the expression levels of endogenous, intracellular tau protein that can disrupt expression of MAPT (microtubule-associated protein tau) gene and/or inhibit transcription of the MAPT gene; and such agents include at least a nuclease which is not limited to a zinc finger nuclease (ZFN), transcription activator-like effector nuclease (TALEN), a CRISPR/Cas system, a transcriptional repressor, a nucleic acid inhibitor such as RNAi, siRNA, anti-miR, antisense oligonucleotides, ribozymes; and others; and a method for treating tau-associated neurodegeneration in a subject using the same agents, and wherein the agents can be administered to a brain of a subject via a carrier, with an exemplary carrier be an adeno-associated virus (see at least Summary; particularly paragraphs 23-24, 27-28, 37-42, 103, 153-157, 163-167, 191-195, 203-204, 218, 236). Hyman et al stated explicitly “In some embodiments, the soluble HMW tau species present in the brain interstitial fluid and/or cerebrospinal fluid of the subject can be selectively reduced by administering to the brain of the subject an antagonist of soluble HMW tau species, e.g., by intracranial injection, intracortical injection, or intracerebroventricular injection, or via peripheral administration of a molecule that crosses the blood brain barrier in sufficient quantities” (paragraph 167); and “Specifically contemplated herein are active zinc finger nuclease proteins specific for MAPT and fusion proteins, including zinc finger protein transcription factors (ZFP-TFs) or zinc finger nucleases (ZFNs), comprising these MAPT-specific zinc finger proteins. The proteins comprising MAPT-specific zinc finger proteins can be used for therapeutic purposes, including for treatment of tau-associated neurodegeneration or tauopathy. For example, zinc finger nuclease targeting of the MAPT locus in neurons can be used to disrupt or delete the MAPT sequence. Zinc finger nucleases have been used to target different genes, e.g., as described in International Patent Application Nos. WO 2010/007639…..(each hereby incorporated by reference), and can be adapted to disrupt or inhibit expression and/or activity of MAPT gene” (paragraph 155). Thus, at least the MAPT-specific ZFN contemplated by Hyman et al include a ZFN consisting of 3 or more tandemly arrayed zinc finger modules, each of which recognizes 3bp sub-sites, with a preferred ZFN containing 4 zinc finger modules which target successfully 26% of potential cleavage sites relative to ZFN containing a 3-zinc finger module as evidenced at least by paragraph 51 on page 7 of the incorporated-by-referenced WO 2010/007639. Hyman et al also stated “In some embodiments, neurons transduced with a vector encoding a soluble HMW tau species antagonist described herein and/or a tau antagonist described herein can be included in the pharmaceutical compositions and stored frozen” (first sentence of paragraph 236).
Accordingly, the teachings of Hyman et al meet every limitation of the instant claims. Therefore, the reference anticipates the instant 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, 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.
Claims 12-16 (for the embodiment containing the elected intravenous administration) are rejected under 35 U.S.C. 103 as being unpatentable over Hyman et al (WO2015/089375; IDS) in view of Zincarelli et al (Molecular Therapy 16:1073-1080, 2008) and evidenced by WO 2010/076939 (IDS).
Hyman et al already disclosed various agents selected to inhibit the expression levels of endogenous, intracellular tau protein that can disrupt expression of MAPT (microtubule-associated protein tau) gene and/or inhibit transcription of the MAPT gene; and such agents include at least a nuclease which is not limited to a zinc finger nuclease (ZFN), transcription activator-like effector nuclease (TALEN), a CRISPR/Cas system, a transcriptional repressor, a nucleic acid inhibitor such as RNAi, siRNA, anti-miR, antisense oligonucleotides, ribozymes; and others; and a method for treating tau-associated neurodegeneration in a subject using the same agents, and wherein the agents can be administered to a brain of a subject via a carrier, with an exemplary carrier be an adeno-associated virus (see at least Summary; particularly paragraphs 23-24, 27-28, 37-42, 103, 153-157, 163-167, 191-195, 203-204, 218, 236). Hyman et al stated explicitly “In some embodiments, the soluble HMW tau species present in the brain interstitial fluid and/or cerebrospinal fluid of the subject can be selectively reduced by administering to the brain of the subject an antagonist of soluble HMW tau species, e.g., by intracranial injection, intracortical injection, or intracerebroventricular injection, or via peripheral administration of a molecule that crosses the blood brain barrier in sufficient quantities” (paragraph 167); and “Specifically contemplated herein are active zinc finger nuclease proteins specific for MAPT and fusion proteins, including zinc finger protein transcription factors (ZFP-TFs) or zinc finger nucleases (ZFNs), comprising these MAPT-specific zinc finger proteins. The proteins comprising MAPT-specific zinc finger proteins can be used for therapeutic purposes, including for treatment of tau-associated neurodegeneration or tauopathy. For example, zinc finger nuclease targeting of the MAPT locus in neurons can be used to disrupt or delete the MAPT sequence. Zinc finger nucleases have been used to target different genes, e.g., as described in International Patent Application Nos. WO 2010/007639…..(each hereby incorporated by reference), and can be adapted to disrupt or inhibit expression and/or activity of MAPT gene” (paragraph 155). Thus, at least the MAPT-specific ZFN contemplated by Hyman et al include a ZFN consisting of 3 or more tandemly arrayed zinc finger modules, each of which recognizes 3bp sub-sites, with a preferred ZFN containing 4 zinc finger modules which target successfully 26% of potential cleavage sites relative to ZFN containing a 3-zinc finger module as evidenced at least by paragraph 51 on page 7 of the incorporated-by-referenced WO 2010/007639. Hyman et al also stated “In some embodiments, neurons transduced with a vector encoding a soluble HMW tau species antagonist described herein and/or a tau antagonist described herein can be included in the pharmaceutical compositions and stored frozen” (first sentence of paragraph 236).
Hyman et al did not teach explicitly using intravenous administration for administering to the brain of the subject an antagonist of soluble HMW tau species.
Before the effective filing date of the present application (12/01/2016), Zincarelli et al already analyzed AAV serotypes 1-9 mediated gene expression and tropism in mice after tail vein/intravenous injection, and they found that AAV9 had the best viral genome distribution and highest protein level, including one of only two AAV serotypes (AAV8 and AAV9) that are capable of expressing luciferase protein expression in brain (see at least the Abstract; and Figure 4).
It would have been obvious for an ordinary skilled artisan to modify the teachings of Hyman et al by also utilizing intravenous administration for administering to the brain of the subject an antagonist of soluble HMW tau species in the form of a recombinant AAV9, in light of the teachings Zincarelli as presented above.
An ordinary skilled artisan would have been motivated to carry out the above modification because Zincarelli et al already analyzed AAV serotypes 1-9 mediated gene expression and tropism in mice after tail vein/intravenous injection, and they found that AAV9 had the best viral genome distribution and highest protein level in the brain among the tested AAV serotypes. Moreover, please note that the primary Hyman reference already taught that agents can be administered to a brain of a subject via a carrier, with an exemplary carrier be an adeno-associated virus, and administering to the brain of the subject an antagonist of soluble HMW tau species, e.g., by intracranial injection, intracortical injection, or intracerebroventricular injection, or via peripheral administration of a molecule that crosses the blood brain barrier in sufficient quantities.
An ordinary skilled artisan would have a reasonable expectation of success in light of the teachings of Hyman et al and Zincarelli et al; coupled with a high level of skill for an ordinary skilled artisan in the relevant art.
The modified method resulting from the combined teachings of Hyman et al and Zincarelli et al as set forth above is indistinguishable and encompassed by the presently claimed invention.
Therefore, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
Cox, III et al (US 6,534,261; IDS) already taught using at least recombinant zinc finger proteins comprising KRAB repression domain form the human KOX-1 protein or KAP-1 to modulate expression of endogenous cellular genes (Abstract; Summary of the Invention; particularly col. 21, line 17 continues to line 7 on col. 22; and issued claims 1-85).
Conclusion
No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Quang Nguyen, Ph.D., at (571) 272-0776.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s SPE, James Douglas (Doug) Schultz, Ph.D., may be reached at (571) 272-0763.
To aid in correlating any papers for this application, all further correspondence regarding this application should be directed to Group Art Unit 1631; Central Fax No. (571) 273-8300.
Any inquiry of a general nature or relating to the status of this application or proceeding should be directed to (571) 272-0547.
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/QUANG NGUYEN/Primary Examiner, Art Unit 1631
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