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 is a continuation of application PCT/US23/61933 filed on 2/3/2023. Applicant’s claim for the benefit of a prior-filed application provisional application 63/306,950 filed 2/4/2022 under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 11/25/2024 is considered by the examiner.
Drawings
The drawings filed 8/5/2024 and 10/11/2024 are accepted.
Specification
The disclosure is objected to because of the following informalities: page 3 of the specification has a paragraph missing a paragraph number.
Appropriate correction is required.
Claim Interpretation
Claim 14 recites “a composition for treating or preventing metabolic dysfunction-associated steatohepatitis (MASH)”. The examiner notes that the recitation of “for treating or preventing metabolic dysfunction-associated steatohepatitis (MASH)” in the preamble is interpreted as an intended use of the claimed invention and not a limitation of the claimed invention. “For treating or preventing metabolic dysfunction-associated steatohepatitis (MASH)” does not limit the structure of the claimed invention; therefore, it does not provide significance to the claim construction. See MPEP § 2111.02.II.
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 1-21 are 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.
Claim 1 recites a method of treating or preventing metabolic dysfunction-associated steatohepatitis (MASH) in a subject in need thereof, the method comprising administering to the subject a composition targeting the hepatic TAZ pathway.
Claim 14 recites a composition for treating or preventing metabolic dysfunction-associated steatohepatitis (MASH), comprising an expression vector capable of targeting the hepatic TAZ pathway, wherein the composition increases MBOAT7 expression.
The composition may reduce or inhibit TAZ expression in the subject when compared to untreated subjects or to expression level of TAZ in the subject pre-treatment (claims 2).
The composition may comprise a TAZ siRNA (claim 3).
The composition may increase membrane bound O-acyltransferase domain containing 7 (MBOAT7) expression (claim 4).
The composition may comprise MBOAT7 mRNA (claims 5 and 15).
The composition may comprise an mRNA nanoparticle, viral vector, AAV, or AAV8 (claims 8-11 and 18-21).
The subject treated may be a human or a human expressing the rs641738 variant of the mBOAT7 gene (claim 13).
In analyzing whether the written description requirement is met for genus claims, it is first determined whether a representative number of species have been described by their complete structure. To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof. The disclosure of a single species is rarely, if ever, sufficient to describe a broad genus, particularly when the specification fails to describe the features of that genus, even in passing. (see In re Shokal 113USPQ283(CCPA1957); Purdue Pharma L.P. vs Faulding Inc. 56 USPQ2nd 1481 (CAFC 2000).
The court explained that “reading a claim in light of the specification, to thereby interpret limitations explicitly recited in the claim, is a quite different thing from ‘reading limitations of the specification into a claim,' to thereby narrow the scope of the claim by implicitly adding disclosed limitations which have no express basis in the claim.” The court found that applicant was advocating the latter, i.e., the impermissible importation of subject matter from the specification into the claim.). See also In re Morris, 127 F.3d 1048, 1054-55, 44 USPQ2d 1023, 1027-28 (Fed. Cir. 1997).
The claims are broad for reciting a genus of compositions targeting the hepatic TAZ pathway. Currently, the composition is claimed functionally rather than structurally and does not possess any structural limitations. As written, the claims are generic to compositions that have the function of targeting the hepatic TAZ pathway, inhibiting/reducing TAZ expression, and/or increasing MBOAT7 expression. Additionally, claim 14 recites the composition comprising an expression vector “capable of targeting the hepatic TAZ pathway”, wherein the composition increases MBOAT7 expression. The expression vector does not have any structural limitations.
The specification offers little guidance on this genera. For example, page 3 of the specification lists examples of other genes that the composition may reduce or inhibit expression of, which are assumed to be part of the hepatic TAZ pathway. However, [0011] recites inhibiting these factors to target a cholesterol targeting pathway. [0007] generically recites claim limits such as those found in claims 6 and 7. The working examples to not teach using any composition to treat or prevent MASH. Instead, the working examples are focused on inhibiting MBOAT7 in mice to demonstrate the role of MBOAT7 expression in MASH.
A search of the art returned multiple approaches to potentially treat MASH. However, the art overall did not touch on inhibition of TAZ or increasing MBOAT7 expression to treat or prevent MASH.
Wang et al. (Wang, Dekai, et al. "Research advances in the diagnosis and treatment of MASLD/MASH." Annals of Medicine 57.1 (2025): 2445780.) recently reviewed research advancements in the diagnosis and treatment of MASLD/MASH. Wang et al. teach that there are a number of treatment strategies being investigated and/or recommended, including pharmaceuticals such as THR-β agonists, FXR agonists, PPAR agonists, GLP-1 receptor agonists, and SGLT2 inhibitors, alongside lifestyle interventions like dietary changes, weight management, and exercise. Surgical options, including gastric bypass and liver transplantation, are effective, particularly for obese and advanced MASH patients. However, challenges remain in standardizing treatment protocols, validating long-term efficacy, and addressing patient-specific factors (Abstract). While research in drug therapy has made significant progress for treatment options, the long-term safety and efficacy of these drugs remain urgent issues to be addressed. Additionally, the diverse pathophysiology and clinical manifestations of MASLD/MASH, universally accepted and consistent standards have yet to be established. This leads to diagnostic inconsistencies between different medical institutions and professional domains, impacting the accurate diagnosis and treatment of patients. Wang et al. did not mention TAZ inhibitors as a treatment option.
Zhu et al. (Zhu, Yiwei, and Bishuang Cai. "Mechanisms and therapeutic insights into MASH-associated fibrosis." Trends in Endocrinology & Metabolism (2025).) recently reviewed mechanisms involved in MASH-associated fibrosis and potential therapeutics for the disease. Zhu et al. teaches that Indian hedgehog (IHH), has also emerged as a key profibrotic signal in this condition. Hepatocytes are the primary source of IHH, with TAZ shown to mediate its transcription and secretion in these cells [85]. Circulating IHH levels have been linked to fibrosis severity inpatients with MASLD/MASH[86]. Furthermore, hepatocyte-specific IHH knockout reduces fibrosis in both HFD-induced MASH and HFD/diethyl-nitrosamine-induced HCC models (pg. 408, para 5). Additionally, cholesterol is a critical upstream trigger of the TAZ–IHH axis. Excess cholesterol stabilizes TAZ in hepatocytes, upregulating IHH transcription and secretion (pg. 408, para 6). While Zhu et al. note the linkage of the TAZ pathway to MASH, they do not teach any therapeutic agents that have previously or are currently being developed to treat or prevent MASH that inhibit TAZ or increase MBOAT7 expression.
In summary, the art did not return any guidance on treating or preventing MASH by inhibiting TAZ or increasing MBOAT7 expression.
The specification fails to provide evidence or guidance that a generic composition targeting the hepatic TAZ pathway, or a composition that increases MBOAT7 expression (e.g., compositions described by function, not structure) would have the disclosed functions of treating or preventing MASH. Further, the specification fails to provide further guidance on the structures that would possess these functions.
Further, dependent claims 2 and 3 recite reducing or inhibiting TAZ expression in the subject when compared to untreated subjects or to expression level of TAZ in the subject pre-treatment, and increasing MBOAT7 expression, respectively.
Either these are inherent properties of (that naturally flows from) the method steps of claim 1/composition of claim 14, or they are not. The claims denote that not all of the structures/method steps of the independent claim are able to achieve the recited property(ies) recited in the dependent claim(s).
To the extent it is not an inherent property (that naturally flows) from the product/method of the independent claim, then something must change. The claim is considered to lack adequate written description for failing to recite the structure that is necessary and sufficient to cause the composition or active steps of the claimed method to possess the ability to treat or prevent MASH, target the hepatic TAZ pathway, inhibit TAZ expression, or increase MBOAT7 expression. For example, the dosage of the composition in the method of treating and preventing to be administered is recited at a high level of generality, e.g., no positively recited dosage(s) in any claims. The claim limitations recited above merely state functional characteristics without providing any indication about how the characteristic is provided. If the characteristic does not follow from (is not an inherent property of) the structure/active method steps recited in the claim, it is unclear whether the claim requires some other structure to be added to the composition to provide the characteristic.
As stated above, the working examples of the specification do not provide further guidance on how an Artisan would treat or prevent MASH with a composition targeting the hepatic TAZ pathway. The working examples are directed to inhibiting MBOAT7 (rather than increasing MBOAT7 expression, as recited in the claims).
The specification fails to disclose what structural changes to the method steps of claim 1/composition of the method and as claimed in claim 14 is necessary and sufficient to treat or prevent MASH in a subject, and thus the ordinary artisan would not know what modification(s) must be made in order to fulfill the instant recitation.
Claim Rejections - 35 USC § 112(a)- Enablement
Claims 1-21 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. 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 Examiner incorporates herein the analysis discussed above in the 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, written description rejection.
While determining whether a specification is enabling, one considers whether the claimed invention provides sufficient guidance to make and use the claimed invention. If not, whether an artisan would have required undue experimentation to make and use the claimed invention and whether working examples have been provided. When determining whether a specification meets the enablement requirements, some of the factors that need to be analyzed are: the breadth of the claims, the nature of the invention, the state of the prior art, the level of one of ordinary skill, the level of predictability in the art, the amount of direction provided by the inventor, the existence of working examples, and whether the quantity of any necessary experimentation to make or use the invention based on the content of the disclosure is “undue” (In re Wands, 858 F.2d 731, 737, 8 USPQ2ds 1400, 1404 (Fed. Cir. 1988)). Furthermore, USPTO does not have laboratory facilities to test if an invention will function as claimed when working examples are not disclosed in the specification. Therefore, enablement issues are raised and discussed based on the state of knowledge pertinent to an art at the time of the invention. And thus, skepticism raised in the enablement rejections are those raised in the art by artisans of expertise.
The Breadth of the Claims and The Nature of the Invention
The claims are directed to a method of treating or preventing MASH.
The claims are broad for defining the composition used in the method functionally, not structurally.
The State of the Prior Art, The Level of One of Ordinary Skill and The Level of Predictability in the Art
The art teaches the TAZ pathway being involved in the mechanism/development of MASH. However, the art does not teach treating or preventing MASH by administering an inhibitor of TAZ, or by administering a composition that increases MBOAT7 expression.
See 112(a) Written Description rejection above for discussion of what the art teaches in relation to TAZ and MASH treatment.
The closest art found that investigates altering MBOAT7 expression to treat MASH is Sharpe et al.:
Sharpe, Martin C., et al. "Enhancing hepatic MBOAT7 expression in mice with nonalcoholic steatohepatitis." Gastro hep advances 2.4 (2023): 558-572. (from IDS) fed mice a NASH diet, then injected the mice with an AAV expressing MBOAT7 or a control virus. Sharpe et al. noted that the murine NASH models displayed subtle changes in MBOAT7 expression, but
significantly decreased activity. After MBOAT7 overexpression, liver weights, triglycerides, and plasma alanine and aspartate transaminase were modestly improved by MBOAT7 overexpression, but NASH histology was not improved. Further, despite confirmation of increased activity with MBOAT7 overexpression, content of the main arachidonoylated PI species was not rescued by MBOAT7 although the abundance of many PI species was increased. Sharpe et al. concluded decreased MBOAT7 activity plays a role in NASH, but MBOAT7 overexpression fails to measurably improve NASH pathology potentially due to the insufficient abundance of its arachidonoyl-CoA substrate.
In summary, Sharpe et al. did not find increasing MBOAT7 expression effective in treating or preventing MASH.
The prior art appears to be entirely silent as to methods of treating or preventing MASH by administering a composition that inhibits TAZ or increases MBOAT7 expression in animal models for MASH, let alone in humans.
The Existence of Working Examples and The Amount of Direction Provided by the Inventor
The specification as filed does not provide any guidance or examples that would enable a skilled artisan to use the disclosed compound in a method of treating or preventing MASH as claimed. Additionally, a person skilled in the art would recognize that assessing the probability of achieving a treatment effect using heretofore uncharacterized polypeptides, vectors, nanoparticles, etc. is highly unpredictable. This is particularly true in view of the lack of guidance in the specification and known unpredictability in gene therapy.
The instant specification provided no working examples regarding the therapeutic outcomes of a composition that inhibits TAZ or increases MBOAT7 expression. The working examples instead assess the role of MBOAT7 in MASH by inhibiting MBOAT7 expression in mice and in vitro. As such, there is no evidence that the claimed composition would treat or prevent MASH.
Since the quantity of experimentation required to practice the invention as claimed is undetermined, one of skill in the art would have been unable to practice the invention without engaging in undue trial and error experimentation as presented in the specification over the scope claimed.
The Quantity of Any Necessary Experimentation to Make or Use the Invention
Thus, the quantity of necessary experimentation to make or use the invention as claimed, based upon what is known in the art and what has been disclosed in the specification, will create an undue burden for a person of ordinary skill in the art to necessarily and predictably use the claimed method comprising the broadly claimed genus of compositions that inhibit TAZ or lead to MBOAT7 expression to treat or prevent MASH.
In conclusion, the specification fails to provide any guidance as to how an artisan would have dealt with the art-recognized limitations of the claimed method commensurate with the scope of the claimed invention.
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.
Claims 12 and 15-21 are 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 15 recites “The composition of claim 13, wherein the composition comprises MBOAT7 mRNA.”. However, claim 13 recites “The method of claim 11, wherein the human expresses the rs641738 variant of the MBOAT7 gene.”
Claim 14 recites “A composition for treating or preventing metabolic dysfunction-associated steatohepatitis (MASH), comprising an expression vector capable of targeting the hepatic TAZ pathway, wherein the composition increases MBOAT7 expression.”
As such, it is unclear whether claim 15 is intended to further recite the method of claim 13, from which it depends, or further limit the composition of claim 13. It would be remedial to amend claim 15 to depend upon claim 14.
Claim 12 recites the limitation "the patient is a human". There is insufficient antecedent basis for this limitation in the claim. The recitation is indefinite because there is no prior reference to a patient in claim 12 or claim 1, of which claim 12 depends upon. Therefore, the metes and bounds of the claim is not clearly and precisely defined. It would be remedial to amend claim 12 to recite “the subject” instead of “the patient”.
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.
(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.
Claim(s) 1-3 and 12 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Tabas et al. (US20190255143, published 08/22/2019; by Applicant).
Regarding claim 1, Tabas et al. disclose a method of treating or preventing metabolic dysfunction-associated steatohepatitis (MASH) (e.g., also known as non-alcoholic Steatohepatitis (NASH)) in a subject in need thereof, the method comprising administering to the subject a composition targeting the hepatic TAZ pathway (e.g., inhibitor of TAZ) (e.g., claims 1, 4 of Tabas et al.).
Regarding claim 2, Tabas et al. discloses the composition reducing or inhibiting TAZ expression in the subject when compared to untreated subjects or to expression level of TAZ in the subject pre-treatment (e.g., [0115], claims 1, 4- an artisan would assume administering a therapeutically effective amount of a TAZ inhibitor would reduce TAZ expression in a subject and is thus anticipated).
Regarding claim 3, Tabas et al. discloses the composition comprising a TAZ siRNA (e.g., claims 1, 4, 9 of Tabas et al.).
Regarding claim 12, Tabas et al. discloses the patient being human (e.g., [0092]).
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) 1-5, 8-15, and 18-21 is/are rejected under 35 U.S.C. 103 as being unpatentable over Tabas et al. as applied to claims 1-3 and 12 above, and further in view of Meroni et al. (Meroni, Marica, et al. "MBOAT7 down-regulation by genetic and environmental factors predisposes to MAFLD." EBioMedicine 57 (2020)).
As shown above, the base claims are obvious over the base art.
Tabas et al. is silent on whether the discloses composition increases MBOAT7 expression.
An Artisan, interested in NASH/MASH, would be aware of Meroni et al. for reviewing predispositions to developing metabolic associated fatty liver disease (MAFLD), which encompasses a broad spectrum of hepatic disorders, including steatosis, nonalcoholic steatohepatitis (NASH), fibrosis and cirrhosis,
Regarding claims 4, 5, 9, and 13-15, Meroni et al. teaches that the rs641738 variant is associated with liver damage and hampered gene and protein expression of MBOAT7. Additionally, the rs641738 T allele seems to be associated with reduced MBOAT7 expression in human hepatocytes and in immune cells (e.g., pg. 4, col 2; Fig. 2). In studies where MBOAT7 knock-out mice were fed high fat diets, the mice spontaneously develop steatosis and hepatic fibrosis. MBOAT7 specifically plays a role in NASH/MASH formation by modulating LPI lipid levels. Evidence has shown MBOAT7 depletion leading to the accumulation of LPI lipids, an MBOAT7 substrate. In turn, increased circulating LPI lipid levels are found in obese NASH patients (e.g., pg. 6, col 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to combine the teachings of Meroni et al. (e.g., the role of MBOAT7 in MASH) and Tabas et al. (e.g., methods of treating MASH) to administer a composition comprising an MBOAT7 sequence in order to treat MASH and arrive at the claimed invention. It was previously known in the art that decreased MBOAT7 expression leads to NASH/MASH, and the combination of Meroni et al. and Tabas et al. would require nothing more than employing well known genetic engineering methods (e.g., upregulating a gene of choice). Thus, one of ordinary skill in the art would have had a reasonable expectation of success in making and using the methods as claimed. One would be motivated to increase MBOAT7 expression to treat MASH because as taught by Meroni et al., the restoration of MBOAT7 activity or a reduction of its effectors may constitute possible therapeutic strategies to improve liver damage in NAFLD patients (e.g., pg. 7, col 1, para 1).
Regarding claims 8 and 18, Tabas et al. teaches the composition comprising an mRNA nanoparticle (e.g., [0110]).
Regarding claims 10, 11, and 19-21, Tabas et al. teaches the composition comprising a viral vector, including AAV8 (e.g., [0173]).
Claim(s) 1-21 is/are rejected under 35 U.S.C. 103 as being unpatentable over Tabas et al. and Meroni et al. as applied to claims 1-5, 8-15, and 18-21 above, and further in view of GenBank Accession AK055908 (www.ncbi.nlm.nih.gov/nuccore/AK055908, published 01/09/2008).
As shown above, the base claims are obvious over the base art.
Tabas et al. and Meroni et al. do not teach the composition comprising either SEQ ID NO: 1 or 2, or mRNA encoding either SEQ ID NO: 3 or 4 (e.g., would still read on SEQ ID NO: 1 or 2, as the mRNA sequence, not amino acid sequence, is claimed).
An Artisan, interested in MBOAT7 sequences, would be aware of GenBank as an online tool to find nucleotide sequences for genes of interest.
GenBank entry AK055908 shares 99.9% identity with instant SEQ ID NO: 2 (see SEQ ID NO: 2 ABSS sequence search results- us-18-795-070-2.rge; GenEmbl database search, result #1). Both sequences represent human MBOAT7 mRNA sequences (as noted in GenBank, BB1 is another term for MBOAT7). AK055908 is 2529 base pairs in length, encompassing instant SEQ ID NO: 2, which is 2294 base pairs in length.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the current invention to substitute the human MBOAT7 nucleotide sequence taught by GenBank for the MBOAT7 sequence used in the method of treating MASH taught by Tabas et al. and Meroni et al. with a reasonable expectation of success because the simple substitution of one known element for another would have yielded predictable results to one of ordinary skill in the art at the time of the invention. M.P.E.P. §2144.07 states "The selection of a known material based on its suitability for its intended use supported a prima facie obviousness determination in Sinclair & Carroll Co. v. Interchemical Corp., 325 U.S. 327, 65 USPQ 297 (1945).” “When substituting equivalents known in the prior art for the same purpose, an express suggestion to substitute one equivalent component or process for another is not necessary to render such substitution obvious. In re Fout, 675 F.2d 297, 213 USPQ 532 (CCPA 1982).” M.P.E.P. §2144.06. Further, an artisan would have a reasonable expectation for success because replacing
one sequence with another has long been done in the molecular biology art and would be routine.
One would be motivated to make this substitution in order to express a human MBOAT7 gene/protein, compared to a different species, such as a mouse MBOAT7 gene/protein.
Additionally, in the case where the claimed ranges "overlap or lie inside ranges disclosed by the prior art" a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990). It is routine procedure to optimize component amounts to arrive at an optimal product that is superior for its intended use, since it has been held where the general conditions of a claim are disclosed in the prior art, discovering the optimum or workable ranges involves only routine skill in the art. Similarly, a prima facie case of obviousness exists where the claimed ranges or amounts do not overlap with the prior art but are close enough that one skilled in the art would have expected them to have the same properties. See M.P.E.P. §2144.05(I).
As mentioned above, AK055908 shares 99.9% identity with instant SEQ ID NO: 2, with only 2 base pairs being mismatched out of the 2294 nucleotides of instant SEQ ID NO: 2 when comparing the two sequences. Since the specification of the claimed invention permits the MBOAT7 sequence to be at least 99% identical to SEQ ID NO: 2 in various embodiments, the AK055908 would substantially overlap with the instantly claimed MBOAT7 nucleotide sequence.
Further, the instant application fails to disclose an element of criticality for instant SEQ ID NO: 2 (e.g., why must the composition comprise instant SEQ ID NO:2, specifically the two nucleotides that differ between AK055908 and the instant human MBOAT7 sequence? Would a composition comprising AK055908 not produce the same result?) as opposed to the human MBOAT7 nucleotide sequence previously known in the art as taught by GenBank.
The "mere existence of differences between the prior art and an invention does not establish the invention's nonobviousness." Dann v. Johnston, 425 U.S. 219, 230, 189 USPQ 257, 261 (1976). The gap between the prior art and the claimed invention may not be "so great as to render the [claim] nonobvious to one reasonably skilled in the art."
It is proper to "take account of the inferences and creative steps that a person of ordinary skill in the art would employ." KSR Int'l Co. v. Teleflex Inc., 127 S. Ct. 1727, 1741,82 USPQ2d 1385, 1396 (2007). See also Id. At 1742, 82 USPQ2d 1397 ("A person of ordinary skill is also a person of ordinary creativity, not an automaton.").
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-3 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 12285464. Although the claims at issue are not identical, they are not patentably distinct from each other because the reference patent is a species of the instant application.
Claims 1 and 2: claim 1 of the reference patent recites a method for treating or preventing progression of steatosis to non-alcoholic steatohepatitis (NASH) in a patient in need thereof, the method comprising administering to the patient in need thereof a therapeutically effective amount of an inhibitor of TAZ, where the inhibitor of TAZ is a nucleic acid comprising a sequence complementary to a sequence encoding human TAZ.
Claim 3: claim 4 of the reference patent recites the nucleic acid being an siRNA.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ALLISON M JOHNSON whose telephone number is (703)756-1396. The examiner can normally be reached Monday-Friday 9am-5pm.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Tracy Vivlemore can be reached at (571) 272-2914. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
ALLISON M. JOHNSON
Examiner
Art Unit 1638
/ALLISON MARIE JOHNSON/ Examiner, Art Unit 1638
/ROBERT M KELLY/ Primary Examiner, Art Unit 1638
Prosecution Insights