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 .
Priority
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
Information Disclosure Statement
The information disclosure statement(s) (IDS) was/were submitted on 9/23/2022, 9/25/2024, and 6/16/2025, before the mailing of a first office action. The submissions are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Status
Claims 1-25, filed 9/7/2022, are pending. Claims 1-25 are under examination.
Claim Objections
Claim 24 is objected to because of the following informalities. Claim 24 recites “diarrheal diseases”, “intestinal insufficiency”, “intestinal failure”, “celiac disease”, “obesity”, “diabetes” more than once. One of these should be removed.
Claim 24 also has an extra comma between “arginine deficiency” and “obesity”. One comma should be removed.
Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 19 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 19, the manner in which claim 19 is written requires reference to the specification for complete understanding. MPEP 2173.05(s) states: “ Where possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table "is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim. Incorporation by reference is a necessity doctrine, not for applicant’s convenience." Ex parte Fressola, 27 USPQ2d 1608, 1609 (Bd. Pat. App. & Inter. 1993).”
Consequently, claim 19 is rejected.
Claim 24 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 24, the usage of examples after a category is a logical stand-in for the phrase "for example", which renders the claim indefinite because it is unclear whether the limitation(s) following the phrase are part of the claimed invention. See MPEP § 2173.05(d).
Specifically, the phrases: “, brush border enzyme deficiencies (congenital lactase deficiency, congenital sucrase-isomaltase deficiency, congenital maltase-glucoamylase- deficiency), defects of membrane carriers (glucose-galactose-malabsorption, fructose malabsorption, Fanconi-Bickel syndrome, Acrodermatitis enteropathica, Congenital chloride / sodium diarrhoea, Lysinuric protein intolerance, Primary biliary malabsorption , cystic fibrosis), enzyme deficiencies (hereditary pancreatitis, congenital pancreas lipase deficiency), lipid/lipoprotein metabolism defects (chylomicron retention disease, hypobetalipoproteinemia, abetalipoproteinemia), defects of enterocyte differentiation or cellular polarisation (Microvillous atrophy, Tufting enteropathy, Trichohepatoenteric syndrome, Familiar haemophagocytic lymphohistiocytosis type 5), defects of enteroendocrine cells (Congenital malabsorptive diarrhoea, anendocrinosis, protein-convertase 1/3 deficiency)” in claim 24 follow this structure.
Also, the phrase "mucosal damage (e.g. cancer treatment), " renders the claim indefinite because it is unclear whether the limitation(s) following the phrase are part of the claimed invention. See MPEP § 2173.05(d).
Consequently, claim 24 is rejected.
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 21, 22, 24, and 25 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.
Regarding claim 21, claim 21 recites the case a compound of formula I has GLP-1 and/or GLP-2 activity. This formula has several variable positions. The variable positions AA4 and AA8 for example encompass a huge range of non-glycine amino acids because the substitutions on the C1-6 are not limited in any way. Also, the residues LysR is recited as “an N-substituted Lysine residue” with no limitations on what that substitution may be. A formal calculation of this genus size is not practicable here, but is assuredly enormous.
In this case, the written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the inventor was in possession of the claimed genus. See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406. (MPEP § 2163 (II.A.3.a.ii.))
According to MPEP § 2163 (II.A.3.a.ii.), a "representative number of species" means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus. See AbbVie Deutschland GmbH & Co., KG v. Janssen Biotech, Inc., 759 F.3d 1285, 1300, 111 USPQ2d 1780, 1790 (Fed. Cir. 2014).
As described above, claim 1 and by extension, claim 21 recites an extremely large genus of compounds.
MPEP § 2163 (II.A.3.a.ii.) states that “for inventions in an unpredictable art, adequate written description of a genus which embraces widely variant species cannot be achieved by disclosing only one species within the genus. See, e.g., Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406. Instead, the disclosure must adequately reflect the structural diversity of the claimed genus, either through the disclosure of sufficient species that are ‘representative of the full variety or scope of the genus,’ or by the establishment of ‘a reasonable structure-function correlation.’”
Even when several species are disclosed, these are not necessarily representative of the entire genus. AbbVie Deutschland GMBH v. Janssen Biotech, 111 USPQ2d 1780, 1790 (Fed. Cir. 2014) (“The ’128 and ’485 patents, however, only describe species of structurally similar antibodies that were derived from Joe-9. Although the number of the described species appears high quantitatively, the described species are all of the similar type and do not qualitatively represent other types of antibodies encompassed by the genus.”). Thus, when there is substantial variation within the genus, as here, one must describe a sufficient variety of species to reflect the variation within the genus to provide a "representative number” of species. Since each genus recited in the instant claims is large, it would be very challenging to describe sufficient species to cover the structures of the entire genus.
In the instant case, Applicant reduces 23 compounds to practice. In these compounds, three different examples for AA4 and three different examples for the LysR are provided.
At the time the invention was made, the level of skill for preparing peptides with desired functional properties was high. However, even if a synthesis and selection procedure was, at the time of the invention, sufficient to enable the skilled artisan to identify peptides that yield polypeptides with the recited properties, the written description provision of 35 U.S.C § 112 is severable from its enablement provision. Ariad Pharm., Inc. v. Eli Lilly & Co., 598 F.3d 1336 (Fed. Cir. 2010); see also Centocor Ortho Biotech Inc. v. Abbott Labs., 97 USPQ2d 1870, 1876 (Fed. Cir. 2011) (“The fact that a fully-human antibody could be made does not suffice to show that the inventors of the '775 patent possessed such an antibody.”) Absent the conserved structure (length) provided by the provided species, the skilled artisan generally would not be able to visualize or otherwise predict, a priori, what polypeptide with a particular set of properties would look like structurally.
Applicant reduces 23 compounds to practice. In these compounds, three different examples for AA4 and three different examples for the LysR are provided. Therefore, the provided examples only represent a limited structural diversity.
Since only a limited number of species of polypeptides are taught within the claimed genus above, the instant claim above fails the written description requirement. A representative number of species has not been taught to describe this genus. Regarding the peptides, a single point mutation can change the biophysical properties of a peptide: “In summary, we have shown that the structural changes in the fibrillar state of the Aβ42 peptide that are observed to occur upon introduction of single point mutations can be accompanied by changes in the dominance of the microscopic processes by which these aggregates are themselves formed.” (Bolognesi et al. ACS Chem Bio 9:2 (2013) page 381 col. 2 para. 3) and “In summary, while ovispirin-1 and novispirin G-10 both had solution structures that were helical and amphipathic in the presence of TFE, a relatively simple change in their primary structure (a single glycine–isoleucine exchange) had profound effects on their respective toxicities for human erythrocytes and epithelial cells.” (Sawai et al. Protein Eng. 15:3 (2002) page 232 col. 1 para. 3).
Furthermore, many sequences allowed by the current scope of the claims, result in non-functional aggregates. Wang (Wang, et al. MAbs. Vol. 1. No. 3. Taylor & Francis, (2009)) discloses a variety of aggregation prone motifs that occur in commercial antibodies (Wang, page 262, Table 2). The scope of the claims currently may incorporate such motifs and result in non-functional aggregates.
Given this unpredictability of polypeptide design, the skilled artisan would not have been in possession of the substantial repertoire of peptide species encompassed by the claimed invention; one of skill in the art would conclude that applicant was not in possession of the structural attributes of a representative number of species possessed by the members of the genus of every polynucleotide molecule recited by claim 21. One of skill in the art would conclude that the specification fails to disclose a representative number of species to describe the claimed genus. Therefore, claim 21 is rejected.
Regarding claim 22, claim 21 is rejected as described above. Claim 22 further recites the case wherein the compound of claim 21 has greater GLP-2 activity than GLP-1 activity. This claim does not reduce the genus size and arguably recites an activity limitation more difficult to predict than just having GLP-1 activity in the first place.
Consequently, the specification fails to disclose a representative number of species to describe the claimed genus and claim 22 is rejected.
Regarding claim 24, claim 24 has the same genus size as claim 21, discussed above. Claim 24 has more specific treatment requirement listed and does not reduce the size of the claimed genus.
Consequently, the specification fails to disclose a representative number of species to describe the claimed genus and claim 24 is rejected.
Regarding claim 25, claim 25 has the same genus size as claim 21, discussed above. Claim 25 has an even more specific treatment requirement listed and does not reduce the size of the claimed genus.
Consequently, the specification fails to disclose a representative number of species to describe the claimed genus and claim 25 is rejected.
Claim 21, 22, 24, and 25 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for example compounds 1-23 for the treatment of, promoting intestinal recovery and nutritional status of patients with malabsorption disorders, intestinal failure, intestinal insufficiency, diarrheal diseases, chronic inflammatory bowel disorders, improve mucosal barrier function, ameliorate gut inflammation, inflammatory disorders, celiac disease, congenital and acquired digestion and malabsorption syndromes, conditions caused by mucosal damage (e.g. cancer treatment), hyperglycemia during enteral and parenteral nutrition therapy in patients with intestinal failure, insufficiency or malabsorption disorders, gastrointestinal injury, acid- induced intestinal injury, arginine deficiency, , obesity, chemotherapy- induced enteritis, diabetes, obesity, fat malabsorption, steatorrhea, , food allergies, gastric ulcers, gastrointestinal barrier disorders, Parkinson's disease, sepsis, bacterial peritonitis, inflammatory bowel disease, bowel trauma, bowel ischemia, mesenteric ischemia, short bowel syndrome, malnutrition, necrotizing enterocolitis, necrotizing pancreatitis, neonatal feeding intolerance, NSAID-induced gastrointestinal damage, nutritional insufficiency, total parenteral nutrition damage to gastrointestinal tract, neonatal nutritional insufficiency, radiation-induced enteritis, radiation-induced injury to the intestines, mucositis, pouchitis, ischemia, non-alcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), insulin resistance, hyperglycemia, insulin resistance, glucose intolerance, brush border enzyme deficiencies (congenital lactase deficiency, congenital sucrase-isomaltase deficiency, congenital maltase-glucoamylase- deficiency), defects of membrane carriers (glucose-galactose-malabsorption, fructose malabsorption, Fanconi-Bickel syndrome, Acrodermatitis enteropathica, Congenital chloride / sodium diarrhoea, Lysinuric protein intolerance, Primary biliary malabsorption , cystic fibrosis), enzyme deficiencies (hereditary pancreatitis, congenital pancreas lipase deficiency), lipid/lipoprotein metabolism defects (chylomicron retention disease, hypobetalipoproteinemia, abetalipoproteinemia), defects of enterocyte differentiation or cellular polarisation (Microvillous atrophy, Tufting enteropathy, Trichohepatoenteric syndrome, Familiar haemophagocytic lymphohistiocytosis type 5), defects of enteroendocrine cells (Congenital malabsorptive diarrhoea, anendocrinosis, protein-convertase 1/3 deficiency) or congenital diarrheal diseases., does not reasonably provide enablement for every possible compound of formula (1) for all possible gastrointestinal and metabolic diseases, all possible chronic diarrhoeal diseases, all possible autoimmune diseases, all possible chemotherapy-associated tissue damage. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
In order to determine compliance with the enablement requirement of 35 U.S.C. 112(a), the Federal Circuit developed a framework of factors in In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988), referred to as the Wands factors to assess whether any necessary experimentation required by the specification is "reasonable" or is "undue." Consistent with Amgen Inc. et al. v. Sanofi et al., 598 U.S. 594, 2023 USPQ2d 602 (2023), the Wands factors continue to provide a framework for assessing enablement in a utility application or patent, regardless of technology area. Guidelines for Assessing Enablement in Utility Applications and Patents in View of the Supreme Court Decision in Amgen Inc. et al. v. Sanofi et al., 89 FR 1563 (January 10, 2024). These factors include, but are not limited to:
The breadth of the claims;
Claim 1 and therefore claims 21, 22, 24, and 25 have a very broad range of claimed compounds. Furthermore, the disorder categories of all possible gastrointestinal and metabolic diseases, all possible chronic diarrhoeal diseases, all possible autoimmune diseases, all possible chemotherapy-associated tissue damage are all very broad as well.
The nature of the invention;
The invention is a compound of formula (I), which according to claim 21 possesses GLP-1 and/or GLP-2 activity.
The state of the prior art;
Drucker (Drucker, Daniel J. Cell metabolism 27.4: 740-756. (2018)) discloses the fundamental mechanism of GLP-1 agonists and the fact that aspects of GLP-1 activity are not completely understood: “The actions of GLP-1 to potentiate glucose-dependent insulin secretion and inhibit glucagon secretion in islet cells while minimizing hypoglycemia supported the development of multiple structurally distinct GLP-1R agonists for the treatment of T2D (Drucker et al., 2017; Drucker and Nauck, 2006; Ussher and Drucker, 2014). The physiological importance of endogenous GLP-1 is illustrated by studies employing the GLP-1R antagonist exendin(9–39), which increased glycemic excursion following oral glucose ingestion in human subjects (Edwards et al., 1999). Complementary studies demonstrated impairment of glucose tolerance and defective glucose-stimulated insulin secretion in Glp1r−/− mice (Scrocchi et al., 1996). Remarkably, the insulinotropic properties of GLP-1 are preserved in human subjects with T2D who fail to respond to sulfonylurea therapy (Nauck et al., 1998). The mechanisms through which GLP-1R signaling rapidly restores glucose sensitivity to failing diabetic human β cells are incompletely understood and likely involve crosstalk between membrane ion channels, cyclic AMP (cAMP)-dependent signaling, and intracellular glucose metabolism.” (Drucker et al., page 741, col. 1, para. 3).
Baldassano et al. (Baldassano, et al. Regulatory peptides 194: 6-10. (2014)) discloses the general effect of GLP-2 agonists: “GLP-2 protects the ENS during mucosal inflammation. Usually, during intestinal inflammation there is a decrease in the numbers of submucosal and myenteric neurons and changes to enteric glial cells within the enteric ganglia. These acute changes in neuronal cell numbers are accompanied by changes in specific neuronal activity, including the integrated motor and secretory functions of the intestine [44]. GLP-2 in this state is able to enhance survival of the enteric neurons in culture and to counteract mast cell induced neuronal cell death [45]. Moreover, in a culture of submucosal plexus neurons, GLP-2 is able to influence the profile of expression of the enteric neurons [46]. This suggests that GLP-2-induced neuroprotection of enteric neurons is mediated by direct stimulation of neuronal GLP-2R. However, experimental evidence has led to the proposal that GLP-2 effects could involve different indirect mediators and diverse signalling pathways.” (Baldassano et al., page 7, col. 2, para. 4).
Consoli et al. (Consoli, et al. Expert opinion on drug safety 14.2: 207-218. (2015)) discloses that GLP-1 agonists can actually cause diarrheal symptoms rather than treating them: “Treatment with GLP-1 Rx agonists might also cause diarrhea,and this seems to occur in ~ 10 -- 20% of patients [30] . Themechanisms underlying this adverse effect are unclear, but, as opposite to nausea and vomiting, diarrhea seems to occur more frequently with the long-acting GLP-1 Rx agonists than with the short-acting compounds [37] . Also, a subgroup analysis of the Sun et al. meta-analysis aimed at exploring the impact of exenatide b.i.d. (twice a day), Exenatide LAR and liraglutide on GI adverse events in type 2 diabetic patients revealed that with prolongation of treatment (26 weeks) the risk of vomiting sharply decreased, while no corresponding trend was observed for diarrhea.” (Consoli et al., page 209, col. 1, para. 5).
The level of one of ordinary skill;
A person of ordinary skill in the art typically would possess at least a Master’s level education and frequently a Ph.D.
The level of predictability in the art;
Regarding the peptides, a single point mutation can change the biophysical properties of a peptide: “In summary, we have shown that the structural changes in the fibrillar state of the Aβ42 peptide that are observed to occur upon introduction of single point mutations can be accompanied by changes in the dominance of the microscopic processes by which these aggregates are themselves formed.” (Bolognesi et al. ACS Chem Bio 9:2 (2013) page 381 col. 2 para. 3) and “In summary, while ovispirin-1 and novispirin G-10 both had solution structures that were helical and amphipathic in the presence of TFE, a relatively simple change in their primary structure (a single glycine–isoleucine exchange) had profound effects on their respective toxicities for human erythrocytes and epithelial cells.” (Sawai et al. Protein Eng. 15:3 (2002) page 232 col. 1 para. 3).
Furthermore, many sequences allowed by the current scope of the claims, result in non-functional aggregates. Wang (Wang, et al. MAbs. Vol. 1. No. 3. Taylor & Francis, (2009)) discloses a variety of aggregation prone motifs that occur in commercial antibodies (Wang, page 262, Table 2). The scope of the claims currently may incorporate such motifs and result in non-functional aggregates.
(F) The amount of direction provided by the inventor and the existence of working examples and the quantity of experimentation needed to make or use the invention based on the content of the disclosure.
Applicant discloses 23 examples with limited structural diversity compared to the claimed genera as described above. However, it would require undue experimentation to both to test all the structures claimed by claim 21 for the required activity and to test all active compounds against the open-ended ended disease categories recited by claim 24.
Applicant discloses the GLP-1 and GLP-2 activity for the 23 examples, but does not provide data that would sufficiently enable open-ended disease categories.
Regarding claim 21, claim 21 depends upon claim 1. Claim 1 encompasses an enormous number compounds. The activity of any one of these claimed compounds is unpredictable, especially for the variable positions with tremendous diversity for the side chains or open-ended modification or substitutions. It would require undue experimentation for a person of ordinary skill in the art to determine if all the claimed compounds possess the required activity.
Consequently, the specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with this claims and claim 21 is rejected.
Regarding claim 22, claim 21 is rejected as described above. Claim 22 specifies an even more specific activity. Possessing more GLP-2 activity than GLP-1 activity requires even more experimentation than determining whether a given compound just possess GLP-1 or GLP-2 activity. It would require undue experimentation for a person of ordinary skill in the art to determine if all the claimed compounds possess the required activity.
Consequently, the specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with this claim and claim 22 is rejected.
Regarding claim 24, claim 24 is dependent upon claim 1 and further recites a Markush group of conditions to be treated by compound (1). Claim 24 requires the compound testing of claim 21 to determine activity and further requires experimentation to determine efficacy against the open-ended groups of all possible gastrointestinal and metabolic diseases, all possible chronic diarrhoeal diseases, all possible autoimmune diseases, all possible chemotherapy-associated tissue damage. As Consoli describes above, sometimes GLP-1 agonists are a cause of diarrhoea and therefore require even more experimentation for diarrhoeal diseases. Also, metabolic diseases not related to insulin or the GI tract would require undue experimentation to determine efficacy. Applicant provides data for intestinal mass and glucose tolerance but this information is not informative against all claimed disease states.
Consequently, the specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with this claim and claim 24 is rejected.
Regarding claim 25, claim 24 is rejected above. Claim 25 narrows down the disease state to be treated to Tufting enteropathy. The relationship of this disease to GLP-1/GLP-2 activity would be a known by a person of ordinary skill in the art. However, claim 25 still possess the same compound scope problem discussed above for claim 21. It would require undue experimentation for a person of ordinary skill in the art to determine if all the claimed compounds possess the required activity.
Consequently, the specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with this claims and claim 25 is rejected.
Allowable Subject Matter
Claims 1-18, 20 and 23 are free of the prior art.
The following is a statement of reasons for the indication of allowable subject matter: Alagarsamy et al. US 8,580,918, published 11/12/2013, discloses SEQ ID NO: 55, HGDGSFSDENledFTILDLLAARDFINWLIQTKITD, aligned against Applicant Example 2 below for illustrative purposes:
Query Match 87.9%; Score 131; Length 33;
Best Local Similarity 90.0%;
Matches 27; Conservative 1; Mismatches 2; Indels 0; Gaps 0;
Qy 2 GSFSDEXFTILDLKAAKDFINWLIQTKITD 31
||||||| ||||| ||:|||||||||||||
Db 4 GSFSDEXXTILDLLAARDFINWLIQTKITD 33
Alagarsamy matches Formula (I) to the greatest extent in the case wherein
W is Gly Ser
AA2 is Phe
X is Ser Asp Glu Nle DPhe Thr
AA3 is Ile
Y is Leu Asp
AA4 is Leu
AA5 is Ala
Z is Asp Phe Ile Asn Trp Leu Ile Gln Thr
AA7 is Lys
AA8 is Ile
AA9 is Asp
However, Alagarsamy has Leu in place of LysR, R in the place of AA6, and the N-terminal residues HGD do not match the N-terminal requirements of Q and AA1 in the instant application. Furthermore, Alagarsamy SEQ ID NO: 55 discloses two extra amino acids and this violates the formula as well. No teaching, suggestion, or motivation to make these modifications as a group is present in the prior art.
Conclusion
Claims 1-18, 20, and 23 are allowable.
Claim 24 is objected to.
Claims 19, 21, 22, 24, and 25 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to David Paul Bowles whose telephone number is (571)272-0919. The examiner can normally be reached Monday-Friday 8:30-5:00.
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/DAVID PAUL BOWLES/ Examiner, Art Unit 1654
/LIANKO G GARYU/ Supervisory Patent Examiner, Art Unit 1654