DETAILED ACTION
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 1/5/2026 has been entered.
Claim Status
As of the Final Office Action mailed 09/08/2025, claims 1 and 4-9 were pending and claims 8-9 were withdrawn for being drawn to non-elected inventions.
In Applicant's Response filed on 11/24/2025, claims 1 and 4 were amended and claim 6-7 were cancelled.
As such, claims 1, 4-5, and 8-9 are pending and claims 1 and 4-5 have been examined herein.
Withdrawn Objections/Rejections
The objections and rejections presented herein represent the full set of objections and rejections currently pending in this application. Any objections or rejections not specifically reiterated are hereby withdrawn.
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 1 and 4-5 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.
The term “enhanced ability” in claim 1 and 4 is a relative term which renders the claim indefinite. The term “enhanced” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. The specification does not define what it means for the mesenchymal stem cell to have “enhanced ability” to inhibit fat accumulation or increase in adipose tissue. Thus, the claims are indefinite. Claim 5 is included in this rejection for being dependent on indefinite claim 4.
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 4-5 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 a pharmaceutical composition for alleviating or inhibiting the progress of fat accumulation dysfunction in thyroid-associated ophthalmopathy, does not reasonably provide enablement for (i) preventing diseases associated with abnormal adipogenesis or abnormal fat metabolic dysfunction, or (ii) treating other diseases associated with abnormal adipogenesis or abnormal fat metabolic dysfunction. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
While determining whether a specification is enabling, one considered 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 requirement, 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 at 737, 8 USPQ2d 1400, 1404 (Fed. Cir.1988)).
Furthermore, the USPTO does not have laboratory facilities to test if an invention with 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, therefore, skepticism raised in the enablement rejection are those raised in the art by artisans of expertise.
Nature of the invention:
A pharmaceutical composition for preventing or treating a disease associated with abnormal adipogenesis or abnormal fat metabolic dysfunction, the pharmaceutical composition comprising a genetically engineered placenta- derived mesenchymal stem cell overexpressing phosphatase of regenerating liver-1 (PRL-1) compared to a non-genetically engineered parent cell, wherein the genetically engineered placenta-derived mesenchymal stem cell has enhanced ability to inhibit fat accumulation or adipose tissue increase compared to a non- genetically engineered parent cell, and wherein the enhanced ability comprises reduced expression levels of adipogenesis- related genes selected from the group consisting of Adipsin, Adiponectin, PPARy, Leptin, LPL, and FABP4 compared to the non-genetically engineered parent cell.
The state of the prior art:
The state of the prior art for preventing diseases associated with abnormal adipogenesis or abnormal fat metabolic dysfunction was unpredictable before the effective filing date of the claimed invention. The state of the prior art for treating diseases associated with abnormal adipogenesis or abnormal fat metabolic dysfunction was unpredictable before the effective filing date of the claimed invention.
The breadth of the claims:
The claims encompass PRL-1 overexpressing placental mesenchymal stem cells to prevent or treat any diseases associated with abnormal adipogenesis or abnormal fat metabolic dysfunction. The specification (para 33) defines treatment as “refers to or includes alleviating, inhibiting the progress of, or preventing a disease, a disorder, or a disease condition, or one or more symptoms thereof.” The claims embrace a large genus of “diseases” such as pituitary tumors, Bardet-Biedl syndrome, diabetes, polycystic ovarian syndrome, hypothyroidism, hypertension, thyroid associated ophthalmopathy, prolactinoma, GERD, IBS, estrogen deficiency, Cushing’s syndrome, fatty liver disease, etc.
The level of skill in the art:
The level of skill is high that requires a researcher with a PhD degree.
The working examples and guidance provided:
The specification discloses working examples in which mesenchymal stem cells were prepared to increase expression of PRL-1 (working example 1). Example 3 describes co-culturing PRL-1 overexpressing placental derived mesenchymal stem cells with orbital fibroblasts from normal subjects or subjects with thyroid-associated ophthalmopathy. After 10 days, fat accumulation in fibroblast of the TAO patients was significantly reduced (see also fig. 11 of the disclosure).
The specification fails to provide any working examples in which diseases of abnormal fat accumulation are prevented utilizing the instantly claimed cell. The specification fails to provide any working examples in which diseases of abnormal fat accumulation (other than TAO) are treated using the instantly claimed cells.
The unpredictable nature of the art:
The claims read on preventing or treating a broad genus of diseases associated with abnormal fat accumulation/abnormal adipogenesis with PRL-1 overexpressing placental-derived mesenchymal stem cells. This was unpredictable at the time of filing.
Preventing diseases associated with abnormal adipogenesis/abnormal fat metabolic dysfunction with PRL-1 overexpressing placental mesenchymal stem cells:
Placental mesenchymal stem cells are not an “end-all, be all” treatment for fat accumulation related diseases. Disease treatment varies widely depending on the specific condition. No example exists for the efficacy of a single product against all disorders of fat accumulation/abnormal adipogenesis. Diseases associated with abnormal adipogenesis or abnormal fat accumulation cannot be prevented.
The American Thyroid Association (retrieved from the Internet 4/2/2026 from https://www.thyroid.org/thyroid-eye-disease/) states that thyroid eye disease (TAO/Grave’s Ophthalmopathy) is an autoimmune disease affecting those with autoimmune thyroid disease. It states that More research on TED is needed to better understand why some people get it and others do not. However, research has identified some factors that can make it more likely for TED to develop or get worse: exposure to cigarette smoke, even secondhand smoke, having abnormal thyroid hormone levels (high or low) can make your eye disease worse, and treatment of your overactive thyroid with radioactive iodine (RAI), especially in people who also smoke and/ or people who already have TED.
Treating diseases associated with abnormal adipogenesis/abnormal fat metabolic dysfunction:
Post-dated Cleveland Clinic ( last updated 1/28/2026; retrieved from the internet 4/2/2026 from https://my.clevelandclinic.org/health/diseases/5497-cushing-syndrome) states that Cushing’s syndrome is a rare hormonal condition that occurs when the body has too much cortisol. The most common causes of Cushing syndrome are taking corticosteroid medications or developing a tumor on your pituitary or adrenal glands. Treatment for Cushing’s focuses on lowering cortisol levels.
Wong (Advances in Experimental Medicine and Biology. Epub 29 June 2018 vol 1061. p. 149-157) discusses current prevention and treatment options for NAFLD (title). The reference states that healthy lifestyle is the cornerstone for the prevention and management of NAFLD and should be recommended to every patient at risk or having established NAFLD (abstract). Lifestyle management is currently the only acceptable method to prevent NAFLD/NASH. Body weight and metabolic parameters are closely associated with NAFLD in epidemiological studies. Lifestyle management is also the cornerstone for the management of NAFLD/NASH (Lifestyle changes, para 1). The degree of weight reduction is pivotal to the control of NAFLD/NASH. In a randomized controlled trial testing a 1-year lifestyle modification program versus usual care in 154 community NAFLD subjects, 97% of those who lost more than 10% of the baseline body weight had complete resolution of NAFLD as determined by proton-magnetic resonance spectroscopy and transient elastography, compared with 13% who lost <3% of the baseline body weight and 41–60% of those losing 3–10% (Fig. 12.1). In another prospective cohort study of 293 NAFLD patients from Cuba using paired liver biopsy, resolution of NASH was achieved in a substantial proportion of patients who lost more than 7% of the baseline body weight, whereas fibrosis regression was only apparent in those having ≥10% weight reduction. The optimal diet for the prevention and treatment of NAFLD/NASH has not been well defined (Lifestyle, para 2). Low-carbohydrate, low-fat, low-glycemic-index and Mediterranean diets have all been shown to improve NAFLD in small studies of relatively short duration of follow-up. The main challenge to lifestyle modification is long-term maintenance of weight loss, which is possible but only achieved by few (Pharmacological treatment para 1). Therefore, pharmacological treatment is still needed in some patients with confirmed NASH. Agents include vitamin E, pioglitazone, liraglutide, obeticholic acid. Other interventions include bariatric surgery
The art shows that the level of predictability for one of ordinary skill in the art for using placental mesenchymal stem cells over-expressing PRL-1 alone as a treatment modality or preventative for diseases associated with abnormal adipogenesis/abnormal fat metabolic dysfunction is low.
The extremely broad scope of the claims and lack of guidance in the specification exacerbates a highly unpredictable art. While the results presented in the art do not necessarily preclude Applicant’s hypothesis, they certainly fail to support it in its totality that PRL-1 overexpressing PMSCs can prevent or treat any diseases associated with abnormal adipogenesis/abnormal fat metabolic dysfunction on its own. Applicants do not provide the details of how one of ordinary skill would reasonably administer the cells to a person and assess the effect of the administered cells on any disease associated with abnormal adipogenesis/abnormal fat metabolic dysfunction (other than co-culture with fibroblast from TAO patients) nor is there a reduction to practice the full scope of the instant method. Consequently, the prior and post-filling art, when combined with the lack of any disclosed direct experimental test of Applicant’s hypothesis, shows that one of ordinary skill would have no basis to reasonably predict or conclude that PRL-1 overexpressing PMSCs would result in tangible effects as instantly claimed. Though not controlling, the lack of working examples is, nevertheless, a factor to be considered in a case involving both physiological activity and an underdeveloped art. When a patent applicant chooses to forego exemplification and bases utility on broad terminology and general allegations, they run the risk that unless one of ordinary skill in the art would accept the allegations as obviously valid and correct, the PTO may, properly, ask for evidence to substantiate them. Ex parte Sudilosky, 21 USPQ2d 1702, 1705 (BPAI 1991); In re Novak, 134 USPA 335 (CCPA 1962); In re Fouche, 169 USPQ 429 (CCPA 1971).
It has been established by legal decision that a patent is not a hunting license. It is not a reward for the search, but compensation for its successful conclusion. Tossing out the germ of an idea does not constitute an enabling disclosure. While every aspect of a generic claim need not have been carried out by an inventor or exemplified in the specification, reasonable detail must be provided in order to enable one of ordinary skill to understand and carry out the invention. It is true that a specification need not disclose what is well known in the art. However, that general, oft-repeated statement is merely a rule of supplementation, not a substitute for a basic enabling disclosure. It means that the omission of minor details does not cause a specification to fail to meet the enablement requirement under 35 U.S.C. 112(a) or 35 U.S.C. 112, first paragraph.
Absent specific guidance, one skilled in the art before the effective filing date of the claimed invention would not know how to practice the claimed invention and would require undue experimentation to practice over the full scope of the invention claimed.
The amount of experimentation necessary:
The specification only describes reduction of fat accumulation in fibroblasts from patients with TAO using the instantly claimed cells. It is not enabling for using the instantly claimed cells as a preventative or treatment protocol of all diseases associated with abnormal adipogenesis/abnormal fat metabolic dysfunction. The specification leaves it entirely up to one of ordinary skill to determine which diseases could be treated, which population or subpopulations of “patients in need” would be able to be treated, what administration route would be appropriate given a variety of factors and unpredictable nature of effective delivery, effective dosages for the wide ranges of diseases to be treated in the disease populations, etc. One of ordinary skill in the art could not reasonably take the working examples and readily or immediately apply the resulting data in the working examples to the prevention or treatment of diseases abnormal adipogenesis/abnormal fat metabolic dysfunction as broadly embraced by the claims.
For the reasons set forth above, one skilled in the art before the effective filing date of the claimed invention would not be able to make and/or use the invention as claimed. This is particularly true given the nature of the invention, the state of the prior art, the breadth of the claims, the amount of experimentation necessary, the level of skill which is high, the working examples provided and scarcity of guidance in the specification, and the unpredictable nature of the art.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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 and 4-5 is/are rejected under 35 U.S.C. 103 as being unpatentable over Meise et al (US 2006/0135419 A1, 3 Dec 2003; Ref. 1 of US Patent Documents in IDS filed 5 Oct 2022; previously cited) in view of Ichim et al (US 20120269774 A1, 20 Sept 2007; Published 25 Oct 2012; previously cited) and Brandebourg et al (Prolactin upregulates its receptors and inhibits lipolysis and leptin release in male rat adipose tissue. Biochem Biophys Res Commun. 2007 Jun 1;357(2):408-13). Please note that this rejection is necessitated by amendment due to Applicant’s amendments to instant claim 1 and 4.
Meise teaches a recombinant host cell exhibiting a modified expression of the PRL-1 homologous peptide and the cell is a human cell (see claim 20 and 21 of Meise) (“a genetically engineered . . . cell secreting PRL-1” as in instant claim 1 in-part). The PRL-1 homologous peptide is a nucleic acid that contributes to the regulation of energy homeostasis within an expression vector (see claim 2, 5, and 7 of Meise) (“wherein the PRL-1 is cloned into an expression vector . . . and transferred to the . . . cell and expressed therein” as in instant claim 1 in-part). It is capable of treating and alleviating metabolic diseases or dysfunctions such as obesity (i.e., disease of excessive fat accumulation), diabetes, hypertension, and dyslipidemia (see claim 13 of Meise). The reference also teaches that the nucleic acid molecule results in the overexpression of PRL-1 and that it can be mixed with a pharmaceutically acceptable carrier (see claims 32 and 34 of Meise). This reads on “a pharmaceutical composition comprising a genetically engineered placenta-derived mesenchymal stem cell secreting PRL-1” as in instant claim 4 in-part, “wherein the disease associated with abnormal adipogenesis or abnormal fat metabolic dysfunction is selected from the group consisting of obesity, diabetes, dyslipidemia, and metabolic diseases, hypertension” as in instant claim 5 and “wherein the . . . stem cell inhibits fat accumulation” as in instant claim 1 in-part and instant claim 6. Finally, the reference teaches that the expression vector can also contain a selection agent or marker gene that confers antibiotic resistance such as the neomycin, hygromycin or puromycin resistance genes (para 50) (“wherein the genetically engineered . . . stem cell is selected by antibiotic treatment for the selection marker” as in instant claim 1 in-part).
Meise differs from the instantly claimed invention in that it does not teach that the recombinant host cell is a placenta-derived mesenchymal stem cell (related to instant claim 1 in-part, 4 in-part, and 7).
Ichim teaches a method of allogeneic stem cell therapy comprising, matching a patient with a stem cell source, manipulating the stem cell source and administering the stem cell source (see claim 1 of Ichim). The reference teaches that the cells can undergo ex vivo manipulation that consists of exposing the cells to agents such as proteins, small molecules, and nucleic acids (para 90). The reference also teaches that the stem cells can be used to treat an inflammatory disease such as obesity, metabolic disturbances associated with obesity, (see claim 7 of Ichim) and can be mesenchymal stem cells derived from placental tissue (see claim 10 and para 43 of Ichim) (“placenta-derived mesenchymal stem cell” as in instant claim 1 in-part, 4 in-part and 7). Selection of cells to be used in the practice of the invention can be performed based on a number of relevant factors to the clinical utilization, including patient characteristics, and availability of the cells for administration (para 35). This shows that mesenchymal stem cells, such as those derived from the placenta, can be manipulated and used to treat obesity and metabolic diseases.
Therefore, it would have been obvious prior to the effective filing date of the instantly claimed invention to engineer a stem cell to express PRL-1 as taught by Meise, wherein the stem cell is a placental mesenchymal stem cell as taught by Ichim, to arrive at the instantly claimed invention. As Ichim teaches that placental mesenchymal stem cells can be used to treat obesity, one of ordinary skill would have been motivated to simply substitute one known element [stem cell of Meise] for another [placental MSC of Ichim] to obtain the predictable result of having a cell overexpressing PRL-1 that can alleviate diseases of fat accumulation as taught by the prior art.
Both references differ from the instantly claimed invention in that they do not teach that “the enhanced ability comprises reduced expression levels of adipogenesis- related genes selected from the group consisting of Adipsin, Adiponectin, PPARy, Leptin, LPL, and FABP4 compared to the non-genetically engineered parent cell” (related to instant claim 1 in-part, 4 in-part).
Brandebourg teaches Prolactin (PRL) is recognized as a metabolic regulator during lactation (see abstract). Brandebourg teaches the examination of the expression and regulation of PRL isoforms in male rat adipose tissue, b) compare the effects of PRL on lipolysis in adipose explants and mature adipocytes from male and female rats, and c) determine whether PRL affects the release of leptin and adiponectin (see pg. 2, para 3), and specifically teaches that PRL is capable of inhibiting lipolysis and suppresses leptin release in epididymal adipose explants and adipocytes (see pgs. 3-4; see also Fig. 5).
Therefore, it would have been obvious prior to the effective filing date of the instantly claimed invention to engineer a stem cell to express PRL-1 as taught by Meise and Ichim, and reduce leptin expression and release as taught by Brandebourg to arrive at the instantly claimed invention. As Brandebourg teaches that that PRL is capable of inhibits lipolysis and suppresses leptin release in epididymal adipose explants and adipocytes, one of ordinary skill would have been motivated to use PRL-1 to advantageously reduce leptin with a reasonable expectation of successfully reducing fat accumulation, which flows from the combined teachings of the cited references.
Response to Arguments
Applicant’s arguments have been fully considered but are not persuasive.
On p. 5 Applicant argues that Meise discloses increased triglyceride levels in cells overexpressing PRL-1, which Applicant argues that is a demonstration of promoting fat accumulation and a teaching away of the instant invention. In response, the examiner notes that Applicant has not provided any empirical evidence to substantiate their argument that increased tryiglyceride levels in response to PRL-1 expression promotes fat accumulation. Second, increased or decreased levels of triglyceride levels are not commensurate in scope with the instant claims. Rather, the claims require that the increase in PRL-1 expression reduce gene expression of adipogenesis related cells. Moreover, newly cited reference Brandebourg teaches that PRL is capable of inhibiting lipolysis and suppresses leptin release in epididymal adipose explants and adipocytes (i.e., reduces leptin as instantly claimed). Thus, Applicant’s argument is not persuasive.
On p. 6-7 of Remarks, Applicant argues that Ichim “merely lists obesity” among other metabolic disorders and provides no experimental data or working examples related to fat accumulation or adipose tissue reduction. Applicant further argues that the enhanced ability as instantly claimed is a concrete effect produced by PRL-1 overexpression and it would not have been expected based on the disclosures of the prior art. Applicant argues that examples 1-4 of the specification demonstrate that the instantly claimed cells reduced fat accumulation in fibroblasts from thyroid-associated ophthalmopathy patients compared to non-genetically engineered cells. Applicant argues that these results are directly contrary to increased fat accumulation purportedly predicted by Meise et al.
In response, the examiner disagrees. Regarding Applicant’s assertions about the Meise reference, the examiner reminds applicant that arguments presented by applicant cannot take the place of evidence in the record. See In re De Blauwe, 736 F.2d 699, 705, 222 USPQ 191, 196 (Fed. Cir. 1984); In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965); In re Geisler, 116 F.3d 1465, 43 USPQ2d 1362 (Fed. Cir. 1997) (see MPEP 2145).
“A greater than expected result is an evidentiary factor pertinent to the legal conclusion of obviousness ... of the claims at issue." In re Corkill, 771 F.2d 1496, 226 USPQ 1005 (Fed. Cir. 1985). However, a greater than additive effect is not necessarily sufficient to overcome a prima facie case of obviousness because such an effect can either be expected or unexpected. Applicants must further show that the results were greater than those which would have been expected from the prior art to an unobvious extent, and that the results are of a significant, practical advantage. Ex parte The NutraSweet Co., 19 USPQ2d 1586 (Bd. Pat. App. & Inter. 1991) (see MPEP § 716.02(a)). Moreover, as per MPEP § 716.02, any differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). The examiner directs applicant to at least para 27 of the Meise reference which states that PRL-1 homologous polypeptides (either cells expressing PRL-1 or other means) can be used to treat metabolic diseases or dysfunctions including obesity, diabetes mellitus, hypertension, etc. (i.e., diseases with abnormal adipogenesis/metabolic dysfunction). Applicant’s assertions related to the unexpected result instant claimed cell was already known in the prior art before the effective filing date of the instantly claimed invention. Finally, the Ichim reference was cited to render prima facie obvious the use of mesenchymal stem cells as claimed. Moreover, patents are relevant as prior art for all they contain (see MPEP 2123). "The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain." In re Heck, 699 F.2d 1331, 1332-33, 216 USPQ 1038, 1039 (Fed. Cir. 1983) (quoting In re Lemelson, 397 F.2d 1006, 1009, 158 USPQ 275, 277 (CCPA 1968)). Thus, Applicant’s arguments are not persuasive.
Conclusion
No claim is allowed.
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/G.R./Examiner, Art Unit 1632
/PETER PARAS JR/Supervisory Patent Examiner, Art Unit 1632