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 .
Application Status
The preliminary amendment filed December 3, 2024 is acknowledged. Claims 1, 10-12, 20-24, 27, 29-30, 33, 39, 41, 47, 54-55 and 58-59 are pending and under examination.
Specification
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code on page 51. Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
Claim Objections
Claim 23 is objected to because it is repetitive: “a promoter operably linked to a nucleotide sequence encoding the nucleotide sequence encoding the protein of interest”. It is suggested that claim 23 be amended to: “a promoter operably linked to the nucleic sequence encoding the proteins of interest”.
Claim Rejections - 35 USC § 112(b)
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 21 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.
Claim 21 recites “wherein the one or more gene regulator elements comprise binding sites for one or more transcription factors selected from the group consisting of Pit1 (POU Class 1 factors), Oct (POU Class 2 factors) …” The use of a specific gene/protein name with what appears to be a genus of factors in parentheses immediately following renders the claim indefinite. For instance, from GenBank it appears that there are several POU class 2 transcription factors including Oct1, Bob1 and Oct11. It is not clear if claim 3 is limited to transcription factor binding sites for Oct1 or if it can include transcription factors from any POU class 1 and POU class2 transcription factors.
Claim Rejections - 35 USC § 112(a) – Written Description
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 1, 10-12, 20-24, 27, 29-30, 33, 39, 41, 47, 54-55 and 58-59 rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
MPEP 2163.II.A3.(a).(i) states, “whether the specification shows that applicant was in possession of the claimed invention is not a single, simple determination, but rather is a factual determination reached by considering a number of factors. Factors to be considered in determining whether there is sufficient evidence of possession include the level of skill and knowledge in the art, partial structure, physical and/or chemical properties, functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and the method of making the claimed invention.”
For claims drawn to a genus, MPEP 2163.II.A3.(a).(ii) states, “written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species” where “representative number of species' means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus.”
Claims 1, 10 and 47 recite “a gene regulatory element sequence that has at least 85% identity to any one of SEQ ID NOs: 1-5, 17-22 or a fragment thereof.” A gene regulatory element (GRE) is defined by the Specification as “a variety of DNA sequences that are involved in the regulation of gene expression”. The Specification further describes a GRE as “rely[ing] on the interactions involving DNA, cellular proteins (e.g., histones), and/or transcription factors to regulate gene expression. A GRE can be a cis-regulatory element. Cis-regulatory elements are regions of non-coding DNA which regulate the transcription of nearby genes. Cis-regulatory elements are found in the vicinity of the genes that they regulate. Cis-regulatory elements typically regulate gene transcription by binding to transcription factors.” ([0024]). Therefore, a GRE is a piece of DNA that has the function of regulating the expression/transcription of a gene.
In addition to the functional requirements, claims 1, 10 and 47 recite a large genus of sequences. The recited SEQ ID NOs range from 179 nucleotides (SEQ ID NO 21) to 26185 nucleotides (SEQ ID NO 22) and originate from mouse or human chromosomal sequences. Except for SEQ ID NOs 1-2 and 17-18, the sequences share very little or no sequence identity. SEQ ID NOs 17-21 are fragments of SEQ ID NOs 1-5. Thus, the genus of sequences that are 85% identical to SEQ ID NOs 1-5 and 17-22 encompasses > 10133 sequences. SEQ ID NO 22 is much larger than the other claimed SEQ ID NOs. The genus of sequences that are at least 85% identical to SEQ ID NO 22 is > 106678 sequences. This does not include “fragments” thereof, and so the genus of sequences that are 85% identical to fragments of SEQ ID NOs 1-5 and 17-22 increase the size of the genus even more. Given the low level of sequence identity between SEQ ID NOs 1, 2, 17, 18 and the other SEQ ID NOs, the entire genus is quite diverse.
For the reasons that follow, Applicant did not sufficiently describe the genus of sequences having at least 85% identity to SEQ ID NOs 1-5 and 17-22 and fragments thereof that also have the function of regulating gene transcription.
Applicant provides evidence that three sequences called mPEP1_3 (SEQ ID NO 1), mNP9_3 (SEQ ID NO 3), and PEP_17 (SEQ ID NO 5) can regulate expression of a reporter gene when combined with a constitutive CMV promoter specifically in nociceptors in mouse cells ([00121]-[00124]). Thus, Applicant has evidence that three sequences out of the more than 106678 sequences have the claimed function. Applicant does not provide evidence from mutational studies or truncation studies that would indicate what nucleotides withing the ~500 nucleotide sequences are necessary or sufficient for gene expression in mouse cells. SEQ ID NOs 1, 3 and 5 are derived from sequences from mouse chromosomes 3, 9 and 17, respectively. It appears that SEQ ID NOs 2, 4 and 22 are derived from the human loci that are analogous to the mouse chromosomal loci from which SEQ ID NOs 1, 3 and 5 originate. However, Applicant fails to demonstrate the ability of SEQ ID NOs 2, 4 or 22 to function in gene regulation in human or mouse cells. It is noted that SEQ ID NOs 3 and 4 do not share any significant sequence identity as determined by a BLAST alignment. Applicant fails to disclose how or why they chose to evaluate SEQ ID NOs 1, 3 or 5 for regulatory control in dorsal root ganglion cells. As such, the skilled artisan has no instructions on how to evaluate what portions of SEQ ID NO 2, 4 and 22 could provide a gene regulatory function. Therefore, in view of the Specification, it was not predictable what additional sequences other than SEQ ID NOs 1, 3 and 5 would be capable of regulating gene expression in a cell.
Except for SEQ ID NO: 1, a thorough search of the prior and contemporary art found no evidence of the recited SEQ ID NOs residing in a gene regulatory area, such as promoter sequence, or having a gene regulatory function. SEQ ID NO 1 is derived from a sequence on mouse chromosome 3 that was previously discovered to have enhancer function in mouse embryonic stem cells (ESCs) (Peng et al., Genome Biology (2020), 21: 243). However, the sequence was not known to regulate gene expression specifically in nociceptors or dorsal root ganglion, as required by claim 11 and appears to be Applicant’s preferred embodiment. Importantly, Peng does not provide mutational studies or truncation studies that would indicate what nucleotides are necessary or sufficient for gene expression in mouse cells. SEQ ID NO 2 is located on human chromosome 1 between an uncharacterized protein ORF isoform and tubulin polyglutamylase TTLL7 isoform 1 gene. Other than having 94% sequence identity to SEQ ID NO 1 from mouse, there is nothing in the prior art to suggest that SEQ ID NO 2 could function as an enhancer in mouse or human cells. SEQ ID NO 3 is on mouse chromosome 9 just downstream of the Fli-1 gene. As indicated above SEQ ID NO 4 has no sequence similarity to SEQ ID NO 3. The only commonality with SEQ ID NO 3 is that it is near/within the human Fli-1 gene on chromosome 11. Likewise, SEQ ID NO 22 has no sequence similarity to SEQ ID NO 5, and their only commonality is their location relative to a known gene. In this case SEQ ID NOs 5 and 22 are within the mouse and human SMOC2 genes, respectively. There is no evidence from prior or contemporary art that the specific SEQ ID NOs or their chromosomal locations play any role in gene transcription regulation in general, or specifically in nociceptors or dorsal root ganglion cells. Therefore, in view of the prior art, it was not predictable what additional sequences other than SEQ ID NOs 1, 3 and 5 would be capable of regulating gene expression in a cell.
Given the lack of working examples demonstrating gene regulatory function of other sequences than SEQ ID NOs 1, 3 and 5, and the lack of understanding in the prior art as to the function of the mouse or human counterpart sequences, the skilled artisan would have reasonably concluded that Applicant did not possess the genus of claimed sequences that were capable of functioning as a gene regulatory element.
Dependent claims
Claims 11-12, 21-24, 27, 29-30, 33, 39, 41, 54-55 and 58-59 do not limit the genus of possible sequences and are rejected for the reasons outlined above for claims 1, 10 and 47.
Claim 20 recites the GRE comprises “a sequence that is identical to any one of SEQ ID NOs: 1-5 or 17-22” which is interpreted as requiring all of the nucleotides of the SEQ ID NOs without substitution, internal additions or truncations. SEQ ID NOs 17-21 are truncated versions of SEQ ID NOs 1-5, respectively. Although, Applicant demonstrates that SEQ ID NOs 1, 3 and 5 have a gene regulatory function, they did not do truncation studies to determine what portion(s) of SEQ ID NOs 1, 3 and 5 is necessary or sufficient for gene regulation. Thus, it was not predictable whether SEQ ID NOs 17, 19 and 21 had the necessary nucleotides to regulate gene expression. Additionally, Applicant does not test the presumably analogous human sequences to determine if they function the same in human cells as SEQ ID NOs 1, 3 and 5 do in mouse cells. A review published in 2017 underscores the unpredictability of using mouse studies to predict function of human sequences (Breschi et al., Nature Reviews Genetics (2017), 18: 425-440). Breschi states “Although many core biological processes and genetic elements are conserved between human and mouse, other biological features have diverged substantially, leading to phenotypic differences and poorly correlated physiological responses between species. Diverging features can be… regulatory differences that affect gene expression and, ultimately, protein levels (such as alternative splicing, enhancer activity, structural elements (for example, chromatin domains) and post-translational modifications)” (page 425, ¶4). Breschi goes on to explain that species-specific binding sites may arise from species-specific innovations or losses and novel transcription-factor binding sites and enhancers can arise from the transposition or repeated elements. For instance, 40% of the binding sites for CEBPa that are unbound in human but bound in mouse do not have any sequence differences between human and mouse. (page 433, ¶4). Additionally, only about 40% of the transcription factor regulatory connections are conserved between mice and humans (page 433, ¶4). Thus, it is more likely than not that a regulatory sequence identified in mice does not function in the same or any regulatory capacity in human cells. Because 1) Applicant did not verify that the SEQ ID NOs derived from human chromosomal sequences actually function in a regulatory capacity and 2) based on the understanding in the art of the conservation of regulatory sequences between mice and human, it is unpredictable whether SEQ ID NOs 2, 4, 18, 20 or 22 can function as gene regulatory elements as claimed.
Claim Rejections - 35 USC § 112(a) – Scope of Enablement
Claim 59 is 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 treating pain with an AAV vector comprising a GRE with SEQ ID NOs 1, 3 and 5 in mice does not reasonably provide enablement for the treatment of all neurological diseases in all subjects using the genus of claimed SEQ ID NOs. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
Exemplary 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. See MPEP 2164.01(a). All of these factors were considered, along with others, and a sufficient number are addressed below so as to create a prima facie case.
Nature of the Invention and Breadth of Claims
Claim 59 is drawn to a method of treating a “neurological disease or condition in a subject”. The genus of “neurological disorders” is vast and includes disorders affecting cells of the peripheral and central nervous systems, including cells of the spinal cord and brain. The Specification lists examples of neurological diseases including Alzheimer’s disease, glioblastomas and traumatic brain injury ([0039]). The specification does not provide a limiting definition for “subject” but does provide examples including any mammal ([00100]). However, the genus of “subjects” is larger than just mammals and also includes virtually any animal having a nervous system. “Treatment” is defined as application to a subject “with the purpose to cure, heal, alleviate, relieve, alter, remedy, ameliorate, improve, or affect the disease or condition, or a symptom of the disease or condition.” ([0040]). Finally, the genus of the GREs encompassed by claim 10 is incredibly vast and diverse, as explained above in paragraphs 12-13. Accordingly, enablement of the method requires one skilled in the art to be able to cure/alleviate/improve/affect the genus of all neurological diseases, including those that are not directly affected by or causing pain, by providing a nucleic acid that comprises an incredibly diverse set of nucleic acid sequences, in the genus of any animal having a nervous system. The analysis below will focus on lack of enablement for treating a neurological disease with nucleic acids comprising SEQ ID NO 1, 3 and 5.
Guidance in the Specification
The specification provides by way of a working example that an AAV vector comprising SEQ ID NOs 1, 3 or 5 can promote gene expression specifically in nociceptors, but not in Ab neurons, in neonatal mice ([00121]-[00123]). Applicant attests that “This property can be leveraged to target the treatment of pain and neuropathies to nociceptors” ([00121]-[00122]) and “the inclusion of the GREs [SEQ ID NOs 1, 3 and 5] in the AAV vector were able to restrict transgene expression in nociceptors in the DRG [dorsal root ganglion].” Thus, the Specification stresses that the claimed nucleic acids are for transgene expression only in the DRG and specifically in the nociceptors of the DRG. As such, it would be entirely unpredictable that GRE would have any effect on diseases that are not caused by and characterized by dysfunction of the DRG and/or nociceptors. Additionally, Applicant’s working examples only showed restricted gene expression in mice. Applicant did not test the claimed SEQ ID NOs in other model mammals (i.e., rats or non-human primates), let alone any other animal that has a nervous system. Accordingly, in light of the specification, it is highly unpredictable how the claimed nucleic acid could be used to treat the genus of all neurological diseases or conditions in the genus of all animals with a nervous system using the claimed nucleic acids that restrict gene expression to nociceptors of the DRG.
State of the Prior Art
The DRG carries sensory neural signals, including pain, pressure, proprioception and temperature to the central nervous system (CNS) from the peripheral nervous system (PNS) (Nascimento et al., Progress in Neurobiology (2018), 168: 86-103). Therefore, diseases that are characterized by the lack of or too much DRG signaling are ones that could potentially be treated using nucleic acids specific for DRG expression. These potentially include chronic pain, inflammation of the DRG, and fibromyalgia and ME/CFS. However, there is no evidence in the prior or contemporary art that gene therapy or modulating gene expression specifically in DRG neurons has any therapeutic value for diseases in which there is no connection to the DRG, like Alzheimer’s Disease or cancers of the brain. In fact, most of the neurological diseases and disorders listed in the Specification have no connection to DRG neurons. Thus, in view of the prior art, it would be highly unpredictable how one skilled in the art would treat the vast majority of neurological disorders or diseases with a nucleic acid whose function is to regulate gene expression in DRG neurons, specifically in nociceptors.
Experimentation Required
In order to practice the invention, one skilled in the art would need to develop models for each of the possible neurological diseases in several mammalian and non-mammalian animals, develop viral vectors to deliver nucleic acids to the neural tissues in each of the models, and determine if SEQ ID NOs 1, 3 and 5 had any activity in each of the model systems. Since development of such models and viral vectors to deliver nucleic acids would each constitute an invention, the skilled artisan would conclude that the experimentation required to practice the invention across its entire scope was undue.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 1, 10-12, 20-21, 23, 27, 29, 30, 41 and 55 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a judicial exception (i.e., a law of nature, a natural phenomenon, or an abstract idea) without significantly more. The claims are drawn to products that are natural products. However, the claims do not include elements, when considered separately and in combination, that are sufficient to amount to significantly more than the judicial exceptions as outlined below.
Subject Matter Eligibility Test for Products and Processes – Claims 1, 10 and 20
Step 1 - Is the Claim to a Process, Machine, Manufacture or Composition of Matter? YES
Claims 1, 10 and 20 are directed to nucleic acids. Thus, the claims are directed to a statutory category (e.g., a product).
Step 2A, Prong One - Does the Claim Recite a Natural Phenomenon? YES
Judicial exceptions have been identified by the courts by way of example, including natural products and natural correlations. The claims recite a single judicial exception – a nucleic acid, which is a natural phenomenon/product. For natural products, products that are not “markedly different” than their naturally occurring counterpart are judicial exceptions. See MPEP 2016.04((b). The courts have identified “isolated DNA” as one such natural product that may not be markedly different from their counterpart, DNA in cells. MPEP 2106.04(c) outlines the markedly different analysis.
The claims recite a nucleic acid comprising SEQ ID NOs 1-5 and 17-22. Claims 10 and 20 further require that the nucleic acid sequence also includes a nucleotide sequence that encodes a protein of interest. The specification defines “protein of interest” as protein or peptide that presents an interest in the treatment, management, or diagnosis of a medical disease, disorder, or condition, or in an experimental assay ([0041]). SEQ ID NO 2 is 100% identical to a sequence on human chromosome 1, coordinates 83769958 to 83770473 (see BLAST alignment in OA Appendix, pages 1-2). GenBank teaches that the sequence in the chromosome 1 is bordered on its 5’ side by an ORF encoding an uncharacterized protein loc107985043 isoform X1 and on its 3’ side by the gene encoding tubulin polyglutamylase ttII7 isoform 1 (i.e., a protein of interest). Thus, the closest naturally occurring counterpart to the claimed nucleic acid in claims 1, 10 and 20 is human chromosome 1, which comprises SEQ ID NO 2 and a nucleotide sequence encoding a protein of interest. The claimed nucleic acid is not markedly different than human chromosome 1 and therefore constitutes a judicial exception.
Step 2A, Prong Two - Does the Claim Recite an Additional Elements that Integrate the Judicial Exception into a Practical Application? NO
The Supreme Court has long distinguished between principles themselves, which are not patent eligible, and the integration of those principles into practical applications, which are patent eligible. The phrase "integration into a practical application" requires an additional element or a combination of additional elements in the claim to apply, rely on, or use the judicial exception in a manner that imposes a meaningful limit on the judicial exception, such that it is more than a drafting effort designed to monopolize the exception. In this case, the claims do not recite any additional elements and therefore the judicial exception is not integrated into a practical application.
Step 2B - Does the Claim Recite Additional Elements that Amount to Significantly More than the Judicial Exception? NO
The Supreme Court has identified a number of considerations for determining whether a claim with additional elements amounts to "significantly more" than the judicial exception(s) itself. The claim as a whole is evaluated as to whether it amounts to significantly more than the recited exception, i.e., whether any additional element, or combination of additional elements, adds an inventive concept to the claim (MPEP 2106.05). However, the claims do not recite any additional elements and therefore the claims do not amount to significantly more than the judicial exception.
Subject Matter Eligibility Test for Products and Processes – Dependent Claims
Claims 11-12 and 21 recite functional limitations for the GREs which comprise SEQ ID NO 2. Although Genbank does not disclose the function of SEQ ID NO 2, MPEP 2112.01.I states “Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established”. As applied to §101 subject matter eligibility, the structure of the claimed nucleic acid is not markedly different than the nucleic acids of chromosome 1. As such, the nucleic acids of naturally occurring human chromosome 1, but also inherently have the claimed feature, and the claimed nucleic acid is still not markedly different than its natural counterpart. Claims 11-12 do not recite any additional element other than the nucleic acid and therefore the claims do not integrate the judicial exception into a practical application or amount to something more than the judicial exception.
Claim 23 recites the nucleic comprises a promoter operably linked to the protein of interest. GenBank shows the gene encoding tubulin polyglutamylase TTLL7 isoform 1 as being expressed, and therefore the coding sequence must inherently be operably linked to a promoter sequence. As such, the claimed nucleic acid still constitutes a judicial exception that is not markedly different than human chromosome 1. Claim 23 does not recite any additional element other than the nucleic acid and therefore the claim does not integrate the judicial exception into a practical application or amount to something more than the judicial exception.
Claim 27 recites the protein of interest encoded by the nucleic acid is a pro-neurogenic protein, which is described by the Specification as a protein that stimulates neurogenesis and/or enhances neuron formation. Human chromosome 1 also encodes the PROX1, a master transcription factor that promotes the transition of neural stem cells into mature neurons (see OA Appendix, pages 3). As such, the claimed nucleic acid still constitutes judicial exceptions that is not markedly different than human chromosome 1. Claim 27 does not recite any additional element other than the nucleic acid and therefore the claim does not integrate the judicial exception into a practical application or amount to something more than the judicial exception.
Claims 29-30 recite the protein of interest encoded by the nucleic acid is a membrane protein and specifically an ion channel. Human chromosome 1 also encodes the voltage-gated potassium channels, KCNA2 and KNCA3 (see OA Appendix, pages 4-5). As such, the claimed nucleic acids still constitute judicial exceptions that are not markedly different than human chromosome 1. Claims 29-30 do not recite any additional element other than the nucleic acid and therefore the claims do not integrate the judicial exception into a practical application or amount to something more than the judicial exception.
Claim 41 recites a vector comprising the nucleic acid of claim 10. The Specification defines “vector” as including any genetic element which is capable of replication when associated with the proper controls elements and which can transfer gene sequences between cells ([0036]). A chromosome is encompassed by the definition of “vector”. As such, the claimed vector still constitutes a judicial exception that is not markedly different than human chromosome 1. Claim 41 does not recite any additional element other than the vector and therefore the claim does not integrate the judicial exception into a practical application or amount to something more than the judicial exception.
Claim 55 recites a pharmaceutical composition comprising the nucleic acid of claim 10 and a pharmaceutically acceptable carrier. The specification defines “pharmaceutically acceptable carriers” as molecular entities and compositions that do not produce an allergic or similar untoward reaction when administered to a host ([0037]). A human cell comprising human chromosome 1 is encompassed by the claimed pharmaceutical composition. When ex vivo human cells are administered to the original cell donor, they do not elicit an allergic reaction. As such, the claimed composition still constitutes a judicial exception that is not markedly different than a human cell comprising chromosome 1. Claim 55 does not recite any additional element other than the composition and therefore the claim does not integrate the judicial exception into a practical application or amount to something more than the judicial exception.
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)(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 1 and 47 are rejected un20der 35 U.S.C. 102(a)(1) as being anticipated by Furness (US 6673549 B1).
Regarding claim 1 and 47, Furness teaches a cDNA comprising SEQ ID NO 412, which is 100% identical to SEQ ID NO 4 of the examined application. Although Furness only teaches that SEQ ID NO 412 is a cDNA expressed in liver cells upon steroid treatment (column 4, line 53), MPEP 2112.01.I states “Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established”. Because Furness’s SEQ ID NO 412 is structurally identical to examined SEQ ID NO 4, it must inherently have the claimed gene regulatory function. Further regarding claim 47, Furness teaches the sequences can be included in AAV vectors for gene delivery purposes (column 22, lines 12-15).
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Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CATHERINE KONOPKA whose telephone number is (571)272-0330. The examiner can normally be reached Mon - Fri 7- 4.
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/CATHERINE KONOPKA/Primary Examiner, Art Unit 1635
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