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 .
Election/Restrictions
In the Remarks, filled on 10/21/2025, Applicant has identified that the Election/Restriction requirement, mailed on 7/22/25, was completed using the claim set filled on 11/03/2025 which did not include preliminary amendments. The correct claim set was also filled on 11/03/2025, however contained preliminary amendments. One such amendment was made onto claim 18, altering its dependency to depend from claim 13. The Election/Restriction requirement had grouped claim 18, and its current dependent claims 19-24, with the group of claim 1. Currently, claims 18-24 depend from claim 13, which remains part of a non-elected group. Due to the altered dependency of claim 18, the claim and its dependents must be grouped with the independent claim 13. Therefore, group I contains only claims 1, 2, and 5-8. If applicant desires claims 18-24 to be examined with group I, the dependency of the claims can be altered to depend from and include the independent requirements of the elected claim 1.
During a telephone conversation with Anusuya Das on 12/10/2025, the Applicant was notified of the corrected Groups which are outlined in the corrected Restriction Requirement presented below.
REQUIREMENT FOR UNITY OF INVENTION
As provided in 37 CFR 1.475(a), a national stage application shall relate to one invention only or to a group of inventions so linked as to form a single general inventive concept (“requirement of unity of invention”). Where a group of inventions is claimed in a national stage application, the requirement of unity of invention shall be fulfilled only when there is a technical relationship among those inventions involving one or more of the same or corresponding special technical features. The expression “special technical features” shall mean those technical features that define a contribution which each of the claimed inventions, considered as a whole, makes over the prior art.
The determination whether a group of inventions is so linked as to form a single general inventive concept shall be made without regard to whether the inventions are claimed in separate claims or as alternatives within a single claim. See 37 CFR 1.475(e).
When Claims Are Directed to Multiple Categories of Inventions:
As provided in 37 CFR 1.475 (b), a national stage application containing claims to different categories of invention will be considered to have unity of invention if the claims are drawn only to one of the following combinations of categories:
(1) A product and a process specially adapted for the manufacture of said product; or
(2) A product and a process of use of said product; or
(3) A product, a process specially adapted for the manufacture of the said product, and a use of the said product; or
(4) A process and an apparatus or means specifically designed for carrying out the said process; or
(5) A product, a process specially adapted for the manufacture of the said product, and an apparatus or means specifically designed for carrying out the said process.
Otherwise, unity of invention might not be present. See 37 CFR 1.475 (c).
Restriction is required under 35 U.S.C. 121 and 372.
This application contains the following inventions or groups of inventions which are not so linked as to form a single general inventive concept under PCT Rule 13.1.
In accordance with 37 CFR 1.499, applicant is required, in reply to this action, to elect a single invention to which the claims must be restricted.
Group I, claims 1-2 and 5-8, drawn to a method of promoting cardiomyocyte cell proliferation by providing a demethylase to the cardiomyocyte, designed to remove a methyl group from Bmp10.
Group II, claims 13-16 and 18-24, drawn to a method of inducing proliferation in a cardiomyocyte cell by providing an m6A methylation inhibitor or an engineered protein demethylase having at least 95% identity to SEQ ID NO: 2, which enhances Brg1 demethylation activity.
Group III, claims 29 and 32 drawn to a culture medium comprising a buffer and demethylase, which is effective to remove a methyl group from Bmp10 in a pharmaceutically acceptable carrier.
The groups of inventions listed above do not relate to a single general inventive concept under PCT Rule 13.1 because, under PCT Rule 13.2, they lack the same or corresponding special technical features for the following reasons:
Groups I-III lack unity of invention because even though the inventions of these groups require the technical feature of a demethylase, this technical feature is not a special technical feature as it does not make a contribution over the prior art in view of Akerberg et al (Dev Biol., 2017). Akerberg teaches the use of a demethylase, Kdm6b, which promotes cardiomyocyte proliferation (abstract).
Applicant’s election without traverse of Group I, currently drawn to claims 1-2 and 5-8, in the reply filed on 10/21/2025 is acknowledged.
Claims 13-16, 18-24, 29, and 32 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 10/21/2025.
Status of the Claims
Claims 1-2, 5-8, 13-16, 18-24, 29, and 32 are currently pending.
Claims 13-16, 18-24, 29, and 32 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected Invention, there being no allowable generic or linking claim.
Claims 3-4, 9-12, 17, 25-28, and 30-31 are cancelled.
Claims 1-2 and 5-8 have been considered on the merits.
Claim Rejections - 35 USC § 112(a)
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 1-2 and 5-8 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 specification does not reasonably provide enablement for providing a demethylase to a cardiomyocyte.
Enablement is considered in view of the Wands factors (MPEP 2164.01(a)). The court in Wands states: "Enablement is not precluded by the necessity for some experimentation such as routine screening. However, experimentation needed to practice the invention must not be undue experimentation. The key word is 'undue,' not 'experimentation.' " (Wands, 8 USPQ2d 1404). Clearly, enablement of a claimed invention cannot be predicated on the basis of quantity of experimentation required to make or use the invention. "Whether undue experimentation is needed is not a single, simple factual determination, but rather is a conclusion reached by weighing many factual considerations." (Wands, 8 USPQ2d 1404). The factors to be considered in determining whether undue experimentation is required include: (1) the quantity of experimentation necessary, (2) the amount of direction or guidance presented, (3) the presence or absence of working examples, (4) the nature of the invention, (5) the state of the prior art, (6) the relative skill of those in the art, (7) the predictability or unpredictability of the art, and (8) the breadth of the claims. While all of these factors are considered, a sufficient amount for a prima facie case are discussed below.
(1) The nature of the invention
The specification describes the invention as a method of promoting cardiomyocyte cell proliferation through providing a demethylase to a cardiomyocyte. Also provided are methods relating to the use of an engineered protein to demethylate BMP10 mRNA.
(2) the breadth of the claims:
Independent claim 1, broadly encompasses providing a demethylase to a cardiomyocyte, wherein the demethylase has enzymatic activity that removes a methyl group from region 2 of the BMP10 mRNA. Dependent claim 2 limits wherein the demethylase comprise an amino acid sequence having at least 95% sequence identity to one of the sequences selected from SEQ ID NOs: 3-5. Dependent claim 3 limits wherein the demethylase removes a methyl group from site M2+M3 of region 2. Dependent claim 4 limits wherein the M2 site has at least 95% identity to SEQ ID NO: 10, and dependent claim 5 limits wherein the M2 site comprises SEQ ID NO: 11. Dependent claim 8 limits wherein the demethylase is 95% identical to one of SEQ ID NOs: 3-5 and that Region 2 comprises a sequence 95% identical to SEQ ID NO: 10. The SEQ ID NO: 3 is listed in the specification as being the R/R and H/D motif of BRG1, SEQ ID NO: 4 is listed as specifically the R/R motif of BRG1, SEQ ID NO: 5 is listed as the H/D motif of BRG1. Thus, the claims taken together with the specification imply that BRG1 is and acts as a demethylase, which contradicts the art and is therefore unpredictable.
(3) The state of the prior art
The prior art shows that BRG1 does not act as a demethylase and is not recognized as a protein which performs demethylation. The prior art defines BRG1 as an ATP-dependent chromatin remodeler which plays a role in recruiting demethylase enzymes to specific sites, however does not itself possess an enzymatic property.
(4) the predictability or unpredictability of the art:
The claims embody a method of promoting cardiomyocyte cell proliferation comprising providing a demethylase to the cardiomyocyte, wherein the demethylase has enzymatic activity that removes a methyl group from Region 2 of the BMP10 mRNA, which is unpredictable.
The method is found unpredictable with regards to providing a demethylase to a cardiomyocyte, more specifically the method is unpredictable because dependent claim 2 and the specification exemplify that the “demethylase” provided to the cardiomyocyte is BRG1 or a sequence of BRG1, which is an ATPase subunit of the SWI/SNF chromatin remodeling complex, which is not known to have demethylation properties.
Huang et al (Chinese Medical Journal, 2021) teaches about the role of BRG1 in heart disease. Huang teaches that BRG1 is “a critical adenosine triphosphatase (ATP) catalytic subunit of the SWI/SNF complex, participates in several physiological and pathological processes by utilizing the energy generated by ATP hydrolysis to regulate gene transcription, DNA repair, and DNA replication” (pg. 1061, col. 1, para 1). Additionally, Huang details the many connections of BRG1 to various positive and negative outcomes in various studies in Fig. 1. Notably, BRG1 both promotes effects of JMJD2B, a histone H3K9 demethylase which leads to activation of PODXL, and KDM3A, a H3K9 lysine demethylase which leads to activation of NOX. However, promoting the effect of a demethylase, as described in Huang, would not lead a skilled person in the art to conclude that BRG1 is the protein which performs the act of demethylation. Huang concludes that “Brg1 plays critical role in heart disease through transcriptional activation, transcriptional repression, and the binding of cardiac transcription-related factors”. Therefore, Huang supports that the art does not currently consider BRG1 a protein capable of demethylation, and therefore the method is unpredictable.
Li et al (BBA- Molecular Basis of Disease, 2018) teaches that BRG1 regulates NOX gene transcription through the recruitment of a demethylase (abstract). Similar to Huang, Li teaches that “H3K9 demethylase KDM3A bound to the NOX promoters with kinetics similar to BRG1 and interacted with BRG1 to activate NOX transcription. KDM3A depletion ameliorated NOX induction and ROS production in endothelial cells exposed to [hypoxia-reoxygenation]” (abstract). Li exemplifies that together, BRG1 and the demethylase KDM3A activate NOX and further that BRG1 alone cannot activate NOX. Therefore, Li supports that BRG1 is not capable of acting as a demethylase. Additionally, Li states “Having observed that BRG1 deficiency resulted in recovery of demethylated H3K9, we hypothesized that BRG1 might interact with a specific demethylase dedicated to erasing H3K9 demethylation” and that “[s]ilencing of BRG1 significantly dampened the binding of KDM3A on the NOX promoters (Fig. 3D, E). Conversely, depletion of KDM3A also weakened the association of BRG1 with the NOX promoters (Fig. 3F, G). Collectively, these data suggest that a cooperation between BRG1 and KDM3A may be responsible for NOX trans-activation in endothelial cells” (pg. 3480, col. 2, last para spanning pg. 3482). Li is exemplifying that BRG1 acts as a recruiter for demethylases and is not capable of performing demethylation alone. Therefore, Li supports that the art does not currently consider BRG1 a protein capable of demethylation, and therefore the method is unpredictable.
Alexander et al (UCSF Theses and Dissertations, 2012) teaches about H3K27me3 demethylases, Jmjd3 and Kdm6a, and their relation to BRG1. Alexander teaches that BRG1 has been implicated in regulating H3K27me3 demethylase levels in embryonic stem cells. Alexander states that “We looked at genome-wide levels of H3K27me3 in normal and Brg1-depleted mesodermal differentiations by ChIP-seq. This analysis revealed a clear reduction in H3K27me3 at genes derepressed upon loss of Brg1 (Figure 3.12a). Interestingly, this was not observed for genes downregulated by loss of Brg1, which supports a specific requirement for Brg1 in H3K27me3 enrichment at derepressed genes.” (pg. 119-120, Section 3.4.5 spans both pgs.). Alexander supports that BRG1 is an important regulator of demethylase activity, but does not possess the demethylation capabilities. Additionally, Alexander supports that BRG1 is specifically a regulator of the activity of the demethylases and not a regulator of the presence of demethylase through stating “Moreover, H3K27me3 demethylases Jmjd3 and Kdm6a were not significantly altered by loss of Brg1. These findings support an important role for Brg1 in H3K27me3 enrichment at developmental regulators.” (pg. 120, para 1). Therefore, Alexander supports that the art does not currently consider BRG1 a protein capable of demethylation, and therefore the method is unpredictable.
Therefore, Huang, Li, and Alexander support that BRG1 is not considered a demethylase in the art and therefore the method is unpredictable without specific guidance as to how a skilled person might perform the method of promoting cardiomyocyte cell proliferation using a demethylase.
Turning to the Specification, the contents of examples 1-46 are detailed under “(6) the amount of direction or guidance presented” below. However, Examples 28 and 38 appear to be of the most importance regarding the alleged demethylation activity of BRG1.
Example 28 describes “examining m6A marks of polyadenylated RNAs in mouse embryonic hearts with or without BRG1 in cardiomyocytes”. The example details creating a BRG1 knockout model in which BRG1 knockout occurs at day 8.5-9.5 of embryonic development. The results are a 44% increase of methylated to demethylated ratio of m6A methylation, which is interpreted as “consistent with BRG1 functioning as an m6A demethylase in the embryonic hearts”. However, the example also states that “such m6A changes occurred in the absence of protein changes of m6A reader (YTHDF2), methyltransferases (METTL3 and 14), or demethylases (FTO, ALKBH5) (data not shown)”. Due to the in vitro nature of the experiment, one could not be certain there is no background activity from the demethylases which are inherently present. Additionally, as stated above, Alexander et al teaches demethylases, including kdm6a, an m6A demethylase are not significantly altered by loss of BRG1 (pg. 120, para 1). Based on this information, it is entirely plausible that the 44% increase in methylation to demethylation ratio was caused by the inability of BRG1 to recruit a demethylase to perform its function, and not because the BRG1 is directly responsible for demethylation. Further, this interpretation is supported by the state of the art presented above through Huang, Li and Alexander. Therefore, it appears that Example 28 does not necessarily support that BRG1 is capable of demethylase activity, and the method is found unpredictable.
Example 38 is described as testing “whether BRG1 was in itself an m6A demethylase”. In this example, recombinant protein and synthetic RNA probes were employed to examine the biochemical activity of BRG1 which was quantitated by a dot blot analysis. The example states “We found that both full-length Brg1 proteins and the helicase domain (MBP-D1D2) (SEQ ID NO 27 coupled to SEQ ID NO 2) effectively erased the m6A mark from Bmp10 (Fig. 15), whereas the subdomain D1 (amino acid 774-913) (SEQ ID NO 6) or D2 (amino acid 1075-1202) (SEQ ID NO 7) alone was incapable of doing that (Fig. 16)”. However, dot blots are not capable of directly demonstrating that a specific m6A mark is erased, rather they are capable of demonstrating the relative amount of the anti- m6A antibody which did or did not bind a m6A. In other words, the results obtained can be interpreted as the full length BRG1 containing the complete helicase subunit and the full helicase subunit was capable of binding to the RNA probe and this blocked the anti- m6A antibody from identifying the m6A mark due to steric hinderance. It is entirely plausible another distinct reasoning applies, however the data are consistent with steric hinderance and do not uniquely require demethylation. Additionally, the result that each subunit of helicase alone did not cause a decrease in the ability of anti- m6A antibody to find and bind the m6A mark, is also supported by the concept of stearic hinderance, in this case low stearic hinderance. Additionally, Example 38 describes enzyme digestions to single nucleosides for LC-MS/MS analysis and draws conclusions of LC-MS/MS data which “corroborated” findings from the dot blot analysis, however states repeatedly “data not shown”. Without data which is significantly more sensitive, such as LC-MS/MS data, it is not clear that BRG1, and more specifically, its helicase domain, is capable of performing demethylation. Rather, all data provided aligns best with the art recognized function of BRG1 as a recruiter of demethylases. This further supports that without direct guidance, the method remains unpredictable.
Therefore, this method is found to be unpredictable with regards to BRG1 functioning as a demethylase, and unpredictable as to the method encompassing providing a demethylase to cardiomyocytes.
(5) The relative skill of those in the art:
The relative skill of those in the art is high.
(6) The amount of direction or guidance presented
The specification details examples 1-46. Example 1 details obtaining mice. Example 2 details cell maintenance and transfection protocols. Example 3 details m6A dot blot assays. Example 4 details 2D-TLC assays. Example 5 details m6A-RNA immunoprecipitation. Example 6 details real time quantitative PCR. Example 7 details detection of m6A sites and m6A motif analysis. Example 8 details RNA immunoprecipitation. Example 9 details a western blot analysis. Example 10 details m6A individual-nucleotide resolution cross-linking and immunoprecipitation. Example 11 details MazF digestion and pPCR assay. Example 12 details an ATPase assay. Example 13 details mRNA stability assay. Example 14 details a 4-thiouracil (4tU) pulse and uracil chase assay. Example 15 details 3-Deazaadenosine treatment. Example 16 details histology and BrdU staining. Example 17 details cardiac troponin T and phosphor-histone H3 co-staining. Example 18 details m6A immunostaining. Example 19 details protein expression and purification. Example 20 details a biochemical assay of m6A demethylation activity in vitro. Example 21 details a nucleosome assembly assay. Example 22 details liquid chromatography tandem mass spectrometry protocol. Example 23 details RNA electrophoretic mobility shift assay and Kd calculation for Biotin-labeled RNA control. Example 24 details a BRG1 R973Q inducible point mutation mouse line. Example 25 details yeast genetics and RNA m6A analysis. Example 26 details statistical analysis protocols. Example 27 details transcriptional activity of BRG1 on BMP10 promoter by reporter assays and states that “[p]revious studies revealed that the SWI/SNF-like chromatin remodeler BRG1 maintains BMP10 mRNA levels in embryonic hearts to promote cardiomyocyte proliferation”. Example 28 details the assessment of whether BRG1 acts as a m6A demethylase through a BRG1 knockout model in which it was found that knockdown of BRG1 which occurs at day 8.5-9.5 of embryonic development results in an increase in m6A methylation, but most importantly “such m6A changes occurred in the absence of protein changes of m6A reader (YTHDF2), methyltransferases (METTL3 and 14), or demethylases (FTO, ALKBH5)(data not shown)”. Example 29 details experimentation confirming the predominant m6A site of action on BMP10 mRNA. Example 30 details experimentation confirming that embryonic hearts which lack BRG1 contained enhanced m6A methylation. Example 31 details modifications of m6A that control RNA stability. Example 32 details identification of a specific BMP10 m6A site in which the specification concludes “these observations suggest a primary function of BRG1 in m6A but not m6Am demethylation”. Example 33 details the effect of m6A demethylation of BMP10 stability by BRG1. Example 34 details the interaction between BRG1 and YTHDF2 in controlling BMP10 mRNA stability in cardiomyocytes. Example 35 details in vivo fetal cardiomyocyte proliferation. Example 36 details testing the general role of BRG1 in cells beyond cardiomyocytes. Example 37 details testing the helicase domain of BRG1 for its importance in erasing m6A marks. Example 38 details the testing of BRG1, the helicase of BRG1, and the individual subunits of BRG1 helicase, for ability to remove m6A marks. Example 39 details experimentation demonstrating the biochemical requirement of R/R and H/D motifs for BRG1. Example 40 details testing mutated versions of BRG1 in vivo. Example 41 details testing of missense mutations found in human cancers. Example 42 details experimentation in yeast. Example 43 details a yeast chromatin remodeler which acts similarly to BRG1. Example 44 details yeast haploid strains for m6A demethylation testing. Example 45 details RNA m6A modification as a new function of BRG1. Example 46 details the m6A action of SWI/SNF chromatin remodelers in yeast RNA.
(7) the presence or absence of working examples:
Based on the art recognized abilities of BRG1, it appears that the specification does not provide any working examples of providing a demethylase to a cardiomyocyte. The examples heavily rely on dot blot analysis and 2D-TLC to demonstrate the alleged demethylase activities of BRG1, which have been addressed above.
(8) The quantity of experimentation necessary:
Considering the state of the art as discussed above and the high unpredictability and the lack of guidance provided in the specification, one of ordinary skill in the art would be burdened with undue experimentation to use the claimed invention within the broad scope as instantly claimed.
It is the examiner’s position that one skilled in the art could not practice the invention
commensurate in the breadth of the claims without undue experimentation. Therefore, claims 1-2, and 5-8 are rejected under 35 U.S.C. 112, first paragraph, for a lack of enablement.
Claims 2, 6, and 8 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 2 recites the limitation of an “amino acid sequence having at least 95% sequence identity to a sequence selected from the group consisting of SEQ ID NO: 3, SEQ ID NO: 4, and SEQ ID NO: 5”. The specification describes the nucleic acid sequence of SEQ ID NOs: 3-5 but not a sequence which is 95% identical to SEQ ID NOs: 3-5 (pg. 2, lines 1-15). Claim 6 recites the limitation of a “nucleic acid sequence having at least 95% identity to SEQ ID NO 10”. The specification describes the nucleic acid sequence of SEQ ID NO: 10 but not a sequence which is 95% identical to SEQ ID NO: 10 (pg. 2, lines 1-15). Claim 8 recites limitations requiring at least 95% sequence identity to at least one of SEQ ID NOs: 3-5 and in addition to 95% sequence identity to SEQ ID NO: 10”. The specification describes the nucleic acid sequence of SEQ ID NOs: 3-5 and SEQ ID NO: 10 but not a sequence which is 95% identical to SEQ ID NOs: 3-5 and SEQ ID NO: 10 (pg. 2, lines 1-15).
The concept of any amino acid sequence encoding components of BRG1 having greater than 95% identity to SEQ ID NOs: 3-5, as recited in claims 2 and 8, lacks written description other than the sequences that are 100% identical to SEQ ID NOs: 3-5. The art at the time and since the time of filling taught sequences encoding components of BRG1 that are 100% identical to SEQ ID NOs: 3, 4, and 5 (See A_Geneseq search results for SEQ ID NOs: 3-5). The specification does not correlate SEQ ID NOs: 3-5 to any other amino acids having at least 95% identity that still encode a protein with the same structural and functional characteristics of SEQ ID NOs: 3-5. The specification and the art at the time of filing do not teach variants of SEQ ID NO: 3-5 that encoded components of BRG1 and had at least 95% identity with SEQ ID NOs: 3-5. The specification and the art at the time of filing do not teach variants of SEQ ID NOs: 3-5 encoding mutants of the components of BRG1 that had at least 95% identity with SEQ ID NOs: 3-5. Accordingly, the concept lacks written description other than SEQ ID NOs: 3-5. It cannot be readily envisioned which 5% can be altered and still retain structure and function.
The concept of any M2+M3 site of region 2 of the BMP10 mRNA having greater than 95% identity to SEQ ID NO: 10, as recited in claims 6 and 8, lacks written description other than the nucleic acid sequence having 100% sequence identity of SEQ ID NO: 10. The art at the time and since the time of filing taught multiple nucleic acids that are at least 100% identical to SEQ ID NO: 10 (see N_Genseq search results). The specification does not correlate SEQ ID NO: 10 to any other nucleic acids having up to 5% sequence variation that still possess the same structural and functional characteristics of SEQ ID NO: 10. The specification and the art at the time of filing do not teach variants of the BMP10 mRNA that had at least 95% identity with SEQ ID NO: 10. The specification and the art at the time of filing do not teach mutants of human Ascl1 that had at least 95% identity with SEQ ID NO: 10. Accordingly, the concept lacks written description other than SEQ ID NO: 10.
There is no evidence on the record of a relationship between the structures of the amino acid sequences coding for BRG1 and the amino acid sequence set forth by SEQ ID NOs: 3-5 or the BMP10 mRNA and the nucleic acid sequence set forth by SEQ ID NO: 10 that would provide any reliable information about the structure of the protein or DNA molecules within the genus of variants. The claimed invention as a whole is not adequately described if the claims require essential or critical elements that are not adequately described in the specification and that is not conventional in the art as of applicants effective filing date. Possession may be shown by actual reduction to practice, clear depiction of the invention in a detailed drawing, or by describing the invention with sufficient relevant identifying characteristics such that a person skilled in the art would recognize that the inventor had possession of the claimed invention. Pfaff v. Wells Electronics, Inc., 48 USPQ2d 1641,1646 (1998).
With the exception of the sequence referred to above, the skilled artisan cannot envision the detailed chemical structure of the encompassed polynucleotides or polypeptides, and therefore conception is not achieved until reduction to practice has occurred regardless of the complexity or simplicity of the method of isolation. The skilled artisan cannot envision the detailed chemical structure of the encompassed nucleic acid and amino acid molecules and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it. The nucleic acid itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016.
One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483. In Fiddes, claims directed to mammalian FGF' s were found to be unpatentable due to lack of written description for that broad class. The specification provided only the bovine sequence.
In view of the above considerations one of skill in the art would not recognize that applicant was in possession of the necessary common features or attributes possessed by any member of the genus of BRG1 or the BMP10 mRNA or the corresponding variants and portions encompassed by the claims. Therefore, only the components of BRG1 encoded by SEQ ID NOs: 3-5 and the BMP10 mRNA encompassed by SEQ ID NO: 10, but not the full breadth of the claims meet the written description provision of 35 U.S.C. §112, first paragraph. University of California v. Eli Lilly and Co., 43 USPQ2d 1398, 1404, 1405 held that “to fulfill the written description requirement, a patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude “the inventor invented 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 2, 6, and 8 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.
Claims 2 and 8 require the limitations of the demethylase comprising an amino acid selected from the SEQ ID NOs: 3-5. SEQ ID NOs: 3-5 encode for a portion or component of the BRG1 protein, which is not known to be a demethylase, additionally, the disclosure does not support that BRG1 is a protein which acts as a demethylase. Appropriate clarification is required.
Claim 6 recites the phrase “wherein site M2+M3 comprises the nucleic acid having at least 95% sequence identity to SEQ ID NO 10”, which is indefinite. It is unclear what “the nucleic acid sequence” refers to because there can be more than one sequence having at least 95% identity to SEQ ID NO: 10. Appropriate clarification is required.
Conclusion
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CONSTANTINA E STAVROU whose telephone number is (571)272-9899. The examiner can normally be reached M-F 8:00-5:00.
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CONSTANTINA E. STAVROU
Examiner
Art Unit 1632
/PETER PARAS JR/Supervisory Patent Examiner, Art Unit 1632