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
This action is written in response to applicant’s correspondence received 05/14/2026. Claims 19-42 are currently pending. Claims 24-25, 27-29 and 31-42 are withdrawn from prosecution as being drawn to non-elected subject matter. Accordingly, claims 19-23, 26 and 30 are examined herein.
Election/Restrictions
Applicant’s election of Species 1= siRNA; Species 2 = target location within exon 7; and Species 3 = chronic liver disease in the reply filed on 05/08/2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)). The requirement is still deemed proper and is therefore made FINAL.
Claims 19-23, 26, and 30 read upon the elected species. Claims 24-25, 27-29 and 31-42 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to nonelected species, there being no allowable generic or linking claim.
Clarity
Claim 19 recites the phrase, “administering an antisense molecule, an siRNA, or an shRNA that hybridizes to an HSD17B13 nucleic acid molecule to the subject”. The ‘to the subject’ immediately following ‘to an HSD 17B13 nucleic acid molecule” renders the phrase somewhat unclear. The clarity of the claim may be improved by amending the phrase to, “administering to the subject an antisense molecule, an siRNA, or an shRNA that hybridizes to an HSD17B13 nucleic acid molecule
Claim 21 recites “alcoholic liver fatty liver disease”. This appears to be a typographical error, and it is believed that the intended phrase was “alcoholic
Objections to the Specification
The disclosure is objected to because of the following informalities: The tables on pages 21-23 do not have titles/reference numbers. Appropriate correction is required.
Nucleotide and/or Amino Acid Sequence Disclosures
REQUIREMENTS FOR PATENT APPLICATIONS CONTAINING NUCLEOTIDE AND/OR AMINO ACID SEQUENCE DISCLOSURES
Items 1) and 2) provide general guidance related to requirements for sequence disclosures.
37 CFR 1.821(c) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.821(a) must contain a "Sequence Listing," as a separate part of the disclosure, which presents the nucleotide and/or amino acid sequences and associated information using the symbols and format in accordance with the requirements of 37 CFR 1.821 - 1.825. This "Sequence Listing" part of the disclosure may be submitted:
In accordance with 37 CFR 1.821(c)(1) via the USPTO patent electronic filing system (see Section I.1 of the Legal Framework for Patent Electronic System (https://www.uspto.gov/PatentLegalFramework), hereinafter "Legal Framework") as an ASCII text file, together with an incorporation-by-reference of the material in the ASCII text file in a separate paragraph of the specification as required by 37 CFR 1.823(b)(1) identifying:
the name of the ASCII text file;
ii) the date of creation; and
iii) the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(1) on read-only optical disc(s) as permitted by 37 CFR 1.52(e)(1)(ii), labeled according to 37 CFR 1.52(e)(5), with an incorporation-by-reference of the material in the ASCII text file according to 37 CFR 1.52(e)(8) and 37 CFR 1.823(b)(1) in a separate paragraph of the specification identifying:
the name of the ASCII text file;
the date of creation; and
the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(2) via the USPTO patent electronic filing system as a PDF file (not recommended); or
In accordance with 37 CFR 1.821(c)(3) on physical sheets of paper (not recommended).
When a “Sequence Listing” has been submitted as a PDF file as in 1(c) above (37 CFR 1.821(c)(2)) or on physical sheets of paper as in 1(d) above (37 CFR 1.821(c)(3)), 37 CFR 1.821(e)(1) requires a computer readable form (CRF) of the “Sequence Listing” in accordance with the requirements of 37 CFR 1.824.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed via the USPTO patent electronic filing system as a PDF, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the PDF copy and the CRF copy (the ASCII text file copy) are identical.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed on paper or read-only optical disc, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the paper or read-only optical disc copy and the CRF are identical. Please see Figures 7A and 7B.
Specific deficiencies and the required response to this Office Action are as follows:
Specific deficiency – Nucleotide and/or amino acid sequences appearing in the drawings are not identified by sequence identifiers in accordance with 37 CFR 1.821(d). Sequence identifiers for nucleotide and/or amino acid sequences must appear either in the drawings or in the Brief Description of the Drawings.
Required response – Applicant must provide:
Replacement and annotated drawings in accordance with 37 CFR 1.121(d) inserting the required sequence identifiers;
AND/OR
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required sequence identifiers into the Brief Description of the Drawings, consisting of:
A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
A copy of the amended specification without markings (clean version); and
A statement that the substitute specification contains no new matter.
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 19-23, 26 and 30 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 19 recites a method of treating a subject which has the steps of first determining whether the subject has a variant HSD17B13, and then, on the condition that the subject does not have the variant, administering an antisense molecule to the subject to decrease HSD17B13. The claim is conditional. However, the claim does not state what step should be taken if the subject does have the variant. As a result, the claim is missing a method step, and the ordinary artisan would not be apprised of the metes and bounds of the claimed method.
Claim 26 recites, “wherein the antisense molecule comprises an siRNA ”. This language is considered to be indefinite because it is unclear to which antisense molecule the claim refers. Claim 19, from which claim 26 ultimately depends, recites a group of alternatives which is an antisense molecule, an siRNA, or an shRNA. Claim 26 appears to recite the antisense molecule, not the siRNA. There are two possible interpretations. One is that the “antisense molecule” is intended to be a generic antisense molecule of which an antisense oligonucleotide, siRNA, and/or shRNA are species. In that case, claim 26 lacks antecedent basis because it does not recite a generic antisense molecule. The other interpretation is that the antisense molecule is an antisense oligonucleotide but does not encompass siRNA or shRNA. However, if that is the case, then claim 26 is indefinite because an siRNA, which is commonly understood in the art to be a double-stranded duplex, cannot also be an antisense oligonucleotide, which is commonly understood to be single-stranded. Because these two interpretations are mutually exclusive, and it is not clear which is intended, the ordinary artisan would not be apprised of the metes and bounds of the claimed invention.
Amending claim 19 to “administering an antisense molecule which is an antisense oligonucleotide, an siRNA or an shRNA”, to clearly establish antecedent for a generic antisense molecule encompassing an siRNA, would obviate this rejection.
Claim Rejections - 35 USC § 112(d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 30 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 30 recites the method of claim 19 wherein, “the antisense molecule, an siRNA, or an shRNA that hybridizes to an HSD 17B 13 nucleic acid molecule decreases expression of HSD17B13 in the subject.”. However, claim 19 already recites, “an antisense molecule, an siRNA, or an shRNA that hybridizes to an HSD 17B 13 nucleic acid molecule…thereby decreasing expression of HSD17B13 in a liver cell in the subject”. Claim 30 does not recite any other limitations which further limit the method.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 112(a) – Scope of Enablement
Claims 19-23, 26 and 30 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph.
The specification is enabling for:
A method of treating a subject having nonalcoholic fatty liver disease, alcoholic fatty liver disease, a chronic liver disease, comprising:
determining whether or not the subject carries a variant HSD17B13 gene;
wherein the determining comprises performing an assay on a biological sample obtained from the subject;
wherein the assay:
a) determines whether a thymine is inserted between positions corresponding to positions 12665 and 12666 of SEQ ID NO:1 of the wild type HSD17B13 gene, or whether a thymine is present at a position corresponding to position 12666 of SEQ ID NO:2 of a variant HSD17B13 gene; and wherein the subject does not carry the variant HSD17B13 gene when:
i) a thymine is not inserted between the positions corresponding to positions 12665 and 12666 of SEQ ID NO:1 of the wild type HSD17B13 gene,
ii) or if a thymine is not present at a position corresponding to position 12666 of SEQ ID NO:2 of the variant HSD17B13 gene;
b) determines the presence of an HSD17B13 Transcript D in the biological sample and wherein the subject does not carry the variant HSD17B13 gene when the HSD17B13 Transcript D is not present in the biological sample; or
c) determines the presence of an HSD17B13 Isoform D in the biological sample and wherein the subject does not carry the variant HSD17B13 gene when the HSD17B13 Isoform D is not present in the biological sample;
and, when the subject does not carry the variant HSD17B13 gene, administering an antisense molecule, an siRNA, or an shRNA that hybridizes to a sequence within exon 7 of SEQ ID NO: 12 (HSD17B13 Transcript A), thereby decreasing expression of HSD17B13 in a liver cell in the subject.
The specification is not enabling for the full breadth of methods of treating a subject having the full breadth of all chronic liver disease, including cirrhosis and hepatocellular carcinoma, for the full breadth of all variant HSD17B13 genes and targets for silencing. 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.
The test of enablement is whether one skilled in the art could make and use the claimed invention from the disclosures in the specification coupled with information known in the art without undue experimentation (United States v. Telectronics., 8 USPQ2d 1217 (Fed. Cir. 1988)). Whether undue experimentation is needed is not based upon a single factor but rather is a conclusion reached by weighing many factors. These factors were outlined in Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Inter. 1986) and again in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988), and the most relevant factors are indicated below:
Nature of the Invention
Breadth of the Claims
Guidance of the Specification
State of the Art
Experimentation Required
Nature of the Invention: The invention is the class of invention that the CAFC has characterized as “the unpredictable arts such as chemistry and biology.” Mycogen Plant Sci., Inc. v. Monsanto Co., 243 F.3d 1316, 1330 (Fed. Cir. 2001).
Breadth of the Claims:
Claim 19 is drawn to a method of treating chronic liver disease, comprising determining whether or not the subject carries any variant HSD17B13 gene, and if the subject does not carry any variant HSD17B13, administering an antisense molecule, an siRNA, or an shRNA that hybridizes to an HSD17B13 nucleic acid molecule to the subject, thereby decreasing expression of HSD17B13 in a liver cell in the subject. The instant specification does not explicitly define “treating” or “treatment”. The broadest reasonable interpretation of the term encompasses alleviation of symptoms, slowing of disease progression, and regression of the disease once the disease is present. The term is not interpreted as encompassing reducing the risk of developing the disease.
Regarding the dependent claims:
Claim 20 limits the subject to human. Claim 21 limits the diseases to NAFLD, alcoholic fatty liver disease, cirrhosis, and/or hepatocellular carcinoma. It is noted that the claim uses the open-ended term “comprises”. As a result, the broadest reasonable interpretation of the claim also encompasses any chronic liver disease beyond those recited. Claim 23, which depends from claim 19, specifies that the antisense RNA hybridizes to a sequence within exon 7 of SEQ ID NO: 12 (HSD17B13 Transcript A). The specification discloses that Transcript A is SEQ ID NO: 21, specifically an isoform (i.e., variant) which includes all seven exons, and that it is expressed in subjects with the wild type HSD17B13 gene (p. 20 ln 16-18). Therefore, claim 23 directs the ordinary artisan to inhibit a wild type variant if the subject does not have a variant. The term “variant” is interpreted as meaning any transcript or polypeptide which deviates from the canonical wild-type transcript(s)/isoforms. If there are multiple wild-type isoforms, these are not considered “variants”, because they do not deviate from what would be considered the canonical wild-type transcripts/isoforms.
Claim 22 provides determination/assay steps for detecting specific variants, but does not limit the scope of the diseases or the targets.
Claims 23 and 26 limit the target, but does not limit the scope of the variants or diseases.
Claim 30 does not further limit claim 19, as described above.
Guidance of the Specification:
The specification discloses the discovery of a loss-of-function splice variants of HSD17B13. These variants are characterized by a single-nucleotide polymorphism “rs72613567”, which is an “insertion of T at position 12666” of SEQ ID NO: 2 (p. 21 ln 16-21). These variants include Transcripts C, D, F, G and H (Id.). The SEQ ID NOs: of the variants are provided in the table on pages 21-22.
On page 144, lines 15-31, the specification further discloses that:
A splice variant (rs72613567:TA) in HSD17B13, encoding the hepatic lipid droplet protein 17-beta hydroxysteroid dehydrogenase 13, was reproducibly associated with reduced 20 ALT (P=4.2x10n¹²) and AST (P=6.2x10n¹n) levels. In DiscovEHR, this variant was associated with reduced risk of alcoholic and nonalcoholic liver disease (by 38%, 95% confidence interval (CI) 19%-52%; and by 16%, 95% CI 9%-22%, respectively, for each rs72613567:TA allele) and cirrhosis (by 44%, 95% CI 22-59%; and by 26%, 95% CI 12%-38% for alcoholic and nonalcoholic cirrhosis, respectively, for each rs72613567:TA allele) in an allele dosage- 25 dependent manner; associations were confirmed in two independent cohorts. rs72613567:TA was associated with decreased severity of histological features of nonalcoholic steatohepatitis (NASH) (23% reduction, 95% CI 10%-34% for each rs72613567:TA allele among individuals with fatty liver disease). rs72613567:TA results in an unstable and truncated protein with reduced enzymatic activity against steroid substrates.
A loss-of-function variant in HSD17B13 was associated with reduced risk of alcoholic and nonalcoholic liver disease, and progression from steatosis to NASH.
The invention may therefore be described as a method of detecting loss-of-function variants associated with a decreased risk of NAFLD, AFLD and cirrhosis. If those protective loss-of-function variants are not present, then expression of wild-type HSD17B13 is inhibited.
The specification does not reduce to practice any methods of treatment for any of the recited diseases. The specification especially does not show successful treatment of cirrhosis or hepatocellular carcinoma. The specification also does not disclose any other variants of HSD17B13 beyond Transcripts C-H, and it only discloses targeting nucleotides of a nucleic acid encoding HSD17B13 that would distinguish the canonical wild-type isoforms from the variants. For example, because Transcript D lacks exon 7, as shown in Figure 7A-B, an siRNA targeting exon 7 would be expected to bind and repress the wild-type isoform transcripts but would not bind Transcript D.
State of the Art:
The prior art shows that while HSD17B13 had a known association with NAFLD, much of its function was unknown. Insofar as its function was known, it was involved in pathogenesis of NAFLD. Insofar as any variants were known, they also contributed to an increased, not decreased, risk of NAFLD.
Zhang (Omic studies reveal the pathogenic lipid droplet proteins in non-alcoholic fatty liver disease. Protein Cell. 2016 Oct 18;8(1):4–13.; of record, cited on an IDS) summarizes the state of the art shortly prior to the effective filing date of the claimed invention (01/23/2017), establishing the HSD17B13 was an excellent therapeutic target for NAFLD (p. 7):
Of the proteins of potential clinical interest identified in proteomic studies, 17β-hydroxysteroid dehydrogenase 13 (17β-HSD13) is possibly the most important. A comparative, quantitative proteomic study in humans detected a dramatic elevation of 17β-HSD13 in patients with NAFLD, compared with healthy controls (Su et al., 2014). Another independent study confirmed this result and also found a slight upregulation of 17β-HSD13 in patients with NASH without fatty liver (Kampf et al., 2014). In a study of fasted and refed mice, 17β-HSD13 was increased markedly on hepatic LDs of mice in the high-fat diet group compared with the low fat group (Crunk et al., 2013). In parallel, a GWAS study revealed that an intergenic SNP (rs6834314) near HSD17B13 (encoding 17β-HSD13) and MAPK10 (encoding mitogen-activated protein kinase 10, MAPK10) is strongly associated with the concentration of plasma alanine transaminase (ALT) (P = 3.1 × 10−9), the main marker of hepatocellular injury (possibly representing fatty liver disease) (Chambers et al., 2011). Overexpression of 17β-HSD13 in a mouse hepatocyte cell line induced liver steatosis and lipid accumulation. It also lead to increased expression of proteins involved in lipid synthesis such as mature SREBP-1 and FAS, suggesting that 17β-HSD13 is implicated in NAFLD development by promoting lipogenesis (Su et al., 2014). 17β-HSD13 is expressed primarily in the liver, with far less found in the gastrointestinal tract, muscle, spleen and uterus, making 17β-HSD13 an excellent potential therapeutic target.
Zhang further states that the gene was first cloned in 2007, but its real physiological function in vivo was still unknown (Id.).
The art does indicate an association between NAFLD and another gene variant involved in liver lipid metabolism, patatin-like phospholipase domain containing 3 (PNPLA3) 1148M , and that inhibition of PNPLA3 expression reduced triglycerides in vivo (paras [0004-0005] and [0098] of U.S. PGPUB 20170349903 A1 to Liu; of record, cited on an IDS). Given the art’s disclosures that HSD17B13 was an excellent potential therapeutic target, and the success of a similar therapeutic target as disclosed by Liu, the ordinary artisan might have had a reasonable expectation that methods of inhibiting wild-type HSD17B13 after verifying the absence of the instantly disclosed protective loss-of-function variants would be another good potential therapeutic approach.
Regarding the scope of diseases, the art shows that both cirrhosis and hepatocellular carcinoma have varying etiologies and treatments based on those etiologies. Sun states that, “Liver fibrosis is a significant health problem, which can ultimately lead to end stage cirrhosis and hepatocellular carcinoma” but that, “until today, there is no effective therapy available for liver fibrosis except the removal of underlying etiology or liver transplantation” (Sun et al. Reversibility of Liver Fibrosis. Clin Res Hepatol Gastroenterol. 2015 September ; 39(0 1): S60–S63.)(p. 1). Sun further states, “Liver fibrosis is a serious health problem with an unmet need for effective therapy...there are still many unanswered questions. The underlying mechanism of myofibroblast inactivation remains to be determined. The factors that determine the fate of myofibroblasts during liver fibrosis regression are still unknown. The switch between the two different phenotypes of macrophages is still hard to manipulate in vivo. Recent studies indicate that epigenetic regulation also affects the progression and resolution of liver fibrosis. Liver fibrosis is the consequence of a complex multicellular response to hepatic injury.” (p. 4). “The amount of guidance or direction needed to enable the invention is inversely related to the amount of knowledge in the state of the art as well as the predictability in the art.” (MPEP 2164.03). Given that no effective therapy existed for liver fibrosis, which precedes cirrhosis; considering the complexity of the disease; and given the many unanswered questions regarding its pathogenesis, the treatment of liver fibrosis and cirrhosis was a nascent technology with a low amount of knowledge and predictability.
Hepatocellular carcinoma (HCC) is likewise a disease with multiple risk factors, etiologies and treatments. Janevska notes that, “Almost 50% of all cases of HCC are associated with HBV infection and 25% are associated with HCV” (p. 733)(Janevska et al. Hepatocellular Carcinoma: Risk Factors, Diagnosis and Treatment. Open Access Macedonian Journal of Medical Sciences. 2015 Dec 15; 3(4):732-736.). However, there are many other risk factors. Lifestyle factors such as obesity, diabetes and alcohol consumption increase the risk of developing HCC (Id.). Genetic factors are also contributors to its pathogenesis. Janevska reports (Id.):
Point mutation of the c-KRAS gene and co amplification of the cyclin D1 gene are rare and are detected in 3% and 11% of HCCs respectively. Mutations of beta-catenin gene are detected in 26 41% of HCCs. Frequent allelic losses are reported at loci 1p, 4q, 5q, 8p, 11p, 13q, 16p, 16q and 17p and loss of heterozygosity (LOH) is reported on chromosome 16. Reduction of expression of p21WAF/CIP1 (universal CDK inhibitor), P16 protein loss, high level expression of transforming growth factor-beta (TGF-beta), high expression of DNA metiltransferase (DNMT1) mRNA are found in significant percentage of HCCs.
There is increased risk of developing HCC in several rare inherited disorders: glycogen storage disease, alpha-1-antitrypsin deficiency, metal storage disease and chronic cholestatic syndromes
Janevska goes on to describe treatment options, which include, “surgical resection, percutaneous ethanol injection (PEI), radiofrequency ablation (RFA), transarterial chemoembolization (TACE) and radio embolization” (p. 734). None of those treatments comprise administration of an antisense molecule, siRNA or shRNA to inhibit the expression of a gene. Additionally, a search of the prior art did not reveal a known role of HSD17B13 in hepatocellular carcinoma besides the instantly disclosed reduction in NAFLD risk and consequent reduction in the risk of developing diseases which may be caused by chronic NAFLD, such as cirrhosis and HCC.
In summary, the state of the art shows that there was a high degree of variability and unpredictability as well as a significant knowledge gap regarding the physiological function of HSD17B13 and any variants, and the causes and effective treatments for liver fibrosis, cirrhosis and HCC.
Experimentation Required:
Given the lack of any working example of a treatment in the specification, and the lack of knowledge and lack of guidance present in the prior art regarding the HSD17B13 gene, its role in liver fibrosis, cirrhosis, and HCC, and the lack of disease-modifying treatments for liver fibrosis/cirrhosis, further experimentation would be required. Considering that the additional experimentation would require de novo experimentation without a guarantee of success, and further considering that any positive results (e.g., reversal of fibrosis or cirrhosis) would amount to a significant advancement in the state of the art, the additional experimental required is considered undue.
Taking into consideration the factors outlined above, including the nature of the invention, the breadth of the claims, the state of the art, the guidance provided by the applicant and the specific examples, it is the conclusion that an undue amount experimentation would be required to make and use the invention as claimed.
Subject Matter Free of the Prior Art
The following subject matter is free of the prior art:
The art does not teach or suggest methods of treating NAFLD comprising determining whether a subject has any of the variant transcript C, D, F, G or H, and if the subject does not have those variants, administering to a subject an antisense molecule, siRNA or shRNA to inhibit HSD17B13 by targeting exon 7 of SEQ ID NO: 12 (wild-type transcript A).
As discussed in the above rejection of the claims under 35 U.S.C. 112(a) for lack of enablement, the function of HSD17B13 was largely unknown prior to the filing date of the instant invention. Insofar as it was known, it was involved in the pathogenesis of NAFLD. Only one variant was known, and that was also involved in the pathogenesis of NAFLD. The ordinary artisan, equipped with this knowledge, would have predicted that inhibition of HSD1713 would be a promising therapeutic avenue to treat NAFLD in a subject. However, the instant claims recite a step of first determining whether the subject has the disclosed variants before administering treatment. Those variants, and their protective role in NAFLD, were not known. Given the lack of knowledge regarding HSD17B13’s physiological functions, as well as the lack of knowledge of its variants and their functions, it would not have been obvious to one having ordinary skill in the art prior to the effective filing date of the invention to include a step of determining whether the subject has those variants prior to administering an HSD17B13 inhibitor.
Conclusion
No claim is allowed at this time.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to AMANDA M ZAHORIK whose telephone number is (703)756-1433. The examiner can normally be reached M-F 8:00-16:00 EST.
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/AMANDA M ZAHORIK/Examiner, Art Unit 1636
Prosecution Insights