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 .
Foreign Priority
The present application claims priority to the application, EP 21305196.4, with effective filing date of 17 February 2021.
Claim Status
This Office Action is in response to Applicant’s Amendment filed, 14 August 2023, wherein the Applicant amended claims 1-7 and added claims 8 and 9.
Claims 1-9 are pending.
Information Disclosure Statement
The Information Disclosure Statements filed on 14 August 2023 and 7 November 2024 and the references cited therein have been considered, unless indicated otherwise.
Claim Rejections - 35 USC § 112
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.
1. Claims 1 and 4-6 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 claims contain 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.
Claims 1, 5, and 6 specify the generic term "a cancer.” However, the specification details methods of treating only pancreatic cancer via the claimed invention with Panc02 and KPC cell lines (murine pancreatic cancer cell lines; see the specification, page 21, lines 15-36). Thus, the specification does not describe the claimed subject matter that would reasonably convey to one of skill in the art a method of treating all types of cancer via use of a STING activator and SERCA2 inhibitor.
Similarly, claim 4 specifies “a colon cancer, a colorectal cancer, a melanoma, a bone cancer, a breast cancer, a thyroid cancer, a prostate cancer, an ovarian cancer, a lung cancer, a pancreatic cancer, a glioma, a cervical cancer, an endometrial cancer, a head and neck cancer, a liver cancer, a bladder cancer, a renal cancer, a skin cancer, a stomach cancer, a testis cancer, an urothelial cancer or an adrenocortical carcinoma, leukemia and lymphoma.” However, the specification only describes use of the claimed invention on murine pancreatic cell lines, Panc02 and KPC (see the specification, page 21, lines 15-36). Thus, the specification does not describe the claimed subject matter that would reasonably convey to one of skill in the art a method of treating a colon cancer, a colorectal cancer, a melanoma, a bone cancer, a breast cancer, a thyroid cancer, a prostate cancer, an ovarian cancer, a lung cancer, a glioma, a cervical cancer, an endometrial cancer, a head and neck cancer, a liver cancer, a bladder cancer, a renal cancer, a skin cancer, a stomach cancer, a testis cancer, an urothelial cancer or an adrenocortical carcinoma, leukemia and lymphoma via use of a STING activator and SERCA2 inhibitor.
2. Claims 1 and 4-6 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 method of treating breast cancer, bladder cancer, prostate cancer, pancreatic cancer, colorectal cancer, melanoma, leukemia, and lymphoma with a SERCA2 inhibitor and a STING activator in, does not reasonably provide enablement for a) , specifically colon cancer, a bone cancer, a thyroid cancer, an ovarian cancer, a lung cancer, a glioma, a cervical cancer, an endometrial cancer, a head and neck cancer, a liver cancer, a renal cancer, a skin cancer, a stomach cancer, a testis cancer, an urothelial cancer, and an adrenocortical carcinoma. 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.
The criteria for enablement set out in the In re Wands, MPEP 2164.01(a), considers the following factors:
Breadth of the Claims
The instant claims are directed to a method of treating or preventing a cancer via administration of at least one inhibitor of SERCA2 and at least one activator of STING. Thus, encompassing all cancers and prevention thereof.
As such, the breadth of the claims is great.
Level of Skill in the Art
The level of skill in the art is a clinician or an artisan with a PhD.
State of the Prior Art
Genovese (Cell Calcium, 2020, 92(102308), 1-18, see IDS filed 14 August 2023) specifies how proteins involved in mitophagy modulation are dysregulated in cancer patients, but they can act as tumor suppressors or promoters depending on the cancer subtype and context (page 2, column 1, paragraph 3). Genovese further specifies “[m]ost of the main proteins that take part in the mitophagic process have been shown to be dysregulated in cancer cells derived from patients, but whether they behave as tumor promoters or suppressors seems to be high cancer subtype-related” (page 6, column 2, paragraph 1). Genovese further teaches methods of treating breast cancer, bladder cancer, and prostate cancer with a SERCA2 inhibitor as well as colorectal cancer, pancreatic cancer, and melanoma with a STING agonist (page 11, column 2, paragraph 3; page 8, column 2, paragraph 3).
Tang (Cancer Res. 2016, 75(8), 2137-2152, see IDS filed 7 November 2024) teaches methods of treating cancer via STING agonist. They found that STING agonists are cytotoxic to B-cell leukemia, lymphoma, and multiple myeloma (page 2144, column 2, paragraph 2). Additionally, they discovered that STING agonists did not induce apoptosis in B16 (melanoma), Hepa 1-6 (hepatoma) and LL/2 (Lewis lung cancer) but ultimately lead to production of type I interfons, which stimulate the immune system and restores health (page 2137, column 1, paragraph 1; page 2147, column 1, paragraph 4; page 2149, column 2, paragraph 3).
Thus, while the prior art teaches methods of treating breast cancer, bladder cancer, prostate cancer, pancreatic cancer, colorectal cancer, melanoma, leukemia, and lymphoma with a SERCA2 inhibitor or a STING agonist, these methods are taught for the treatment of specific cancers. The prior art is silent regarding a method for treating colon cancer, a bone cancer, a thyroid cancer, an ovarian cancer, a lung cancer, a glioma, a cervical cancer, an endometrial cancer, a head and neck cancer, a liver cancer, a renal cancer, a skin cancer, a stomach cancer, a testis cancer, an urothelial cancer, and an adrenocortical carcinoma. Additionally, the prior art is silent regarding a method of preventing cancer.
Predictability in the Art
Regarding the translation of pancreatic cancer murine models (such as KPC) to clinical trials, Lee (Current Protocols in Pharmacology, 2016, 14.39.1-14.39.20, 1-20) teaches that the KPC mouse model reproduces many of the key features of the immune microenvironment observed in human pancreatic ductal adenocarcinoma (PDAC), is the most extensively studied genetic model of PDAC, and reproduces clinical responses observed in PDAC patients (page 3, paragraph 1).
As such, Lee teaches that treating pancreatic cancer cells in a mouse model is predictable to humans.
Genovese comments on the controversial nature of the prior art in that evidence shows that most of the proteins involved in mitophagy modulation are dysregulated in cancer patients, but they can act as tumor suppressor or promoters depending on the cancer subtype and context (page 2, column 1, paragraph 3). Additionally, Genovese details that the literature is still conflicting on the nature of Ca2+ signaling in diverse pathological settings, such as cancer, and that there is a lack of clarity about the specific role of mitochondria in boosting or inhibiting cancer progression (page 2, column 1, paragraphs 5 and 8).
Regarding treating cancer with a SERCA2 inhibitor, Genovese only teaches methods of treating breast cancer, bladder cancer, and prostate cancer. Regarding treating cancer via STING agonist, Genovese teaches methods of treating colorectal cancer, pancreatic cancer, and melanoma, amongst other methods of treating cancer via small molecule (page 11, column 2, paragraph 3; page 8, column 2, paragraph 3; Table 1, page 10).
However, Genovese further elaborates that targeting mitophagy as an anticancer therapeutic option and the reaction of healthy cells to mitophagy modulator remain unclear and needs further investigation (pages 12, column 1, paragraph 7; column 2, paragraph 1).
As such, Genovese teaches that treating cancer is unpredictable, much less preventing cancer.
Working Examples
While the instant specification teaches that specific species of SERCA2 inhibitors and STING activators treat pancreatic cancer, the instant specification does not teach the combination of SERCA2 inhibitor and STING activator can treat a colon cancer, a colorectal cancer, a melanoma, a bone cancer, a breast cancer, a thyroid cancer, a prostate cancer, an ovarian cancer, a lung cancer, a glioma, a cervical cancer, an endometrial cancer, a head and neck cancer, a liver cancer, a bladder cancer, a renal cancer, a skin cancer, a stomach cancer, a testis cancer, an urothelial cancer or an adrenocortical carcinoma, leukemia and lymphoma. Further, the instant specification only exemplifies two STING agonists (DMXAA and ADU-S100) and two SERCA2 inhibitors (CPA and thapsigargin) (page 15, lines 18-19; page 16, lines 19-20; page 18, lines 19-22; page 21, lines 15-36) in two murine pancreatic cancer cell lines: Panc02 and KPC.
Thus, it is not possible to determine all the types of cancer that the combination of a STING activator and SERCA2 inhibitor can treat, much less prevent.
Quantity of Experimentation
The amount of experimentation required to determine which STING activator, which SERCA2 inhibitor, and which cancer, in what amounts, what order, would be astronomical. A skilled artisan would be required to start with proof-of-concept and proceed through all levels of lead identification and optimization, which is invention and not development; this is undue amount of experimentation.
As such, while the specification is enabling for a method of treating breast cancer, bladder cancer, prostate cancer, pancreatic cancer, colorectal cancer, melanoma, leukemia, and lymphoma with a SERCA2 inhibitor and a STING activator, it does not reasonably provide enablement for a method of treating all cancer or preventing any and all cancer. Further, the specification does not reasonably provide enablement for treating colon cancer, a bone cancer, a thyroid cancer, an ovarian cancer, a lung cancer, a glioma, a cervical cancer, an endometrial cancer, a head and neck cancer, a liver cancer, a renal cancer, a skin cancer, a stomach cancer, a testis cancer, an urothelial cancer, and an adrenocortical carcinoma.
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.
3. Claims 2-4 and 7-9 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.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c).
In the present instance, claim 2 recites the broad recitation “the inhibitor of SERCA2 is a compound that reversibly or irreversibly binds to SERCA2 and decreases its activity,” and the claim also recites “preferably the inhibitor is non-competitive, preferably the inhibitor is specific of SERCA2, preferably it is a small molecule,” which is the narrower statement of the range/limitation.
In the present instance, claim 3 recites the broad recitation “the inhibitor of SERCA2 is thapsigargin or thapsigargin derivatives (such as Mipsagargin or JQ-FT), cyclopiazonic acid, artemisinin, CAD204520, Casearin J, Curcumin, CXL017, DBHQ or sHA 14-1,” and the claim also recites “preferably the inhibitor of SERCA2 is thapsigargin or cyclopiazonic acid,” which is the narrower statement of the range/limitation.
In the present instance, claim 4 recites the broad recitation “the cancer is solid or non-solid,” and the claim also recites “preferably selected from a colon cancer, a colorectal cancer, a melanoma, a bone cancer, a breast cancer, a thyroid cancer, a prostate cancer, an ovarian cancer, a lung cancer, a pancreatic cancer, a glioma, a cervical cancer, an endometrial cancer, a head and neck cancer, a liver cancer, a bladder cancer, a renal cancer, a skin cancer, a stomach cancer, a testis cancer, an urothelial cancer or an adrenocortical carcinoma, leukemia and lymphoma,” which is the narrower statement of the range/limitation.
In the present instance, claim 7 recites the broad limitation “the activator of STING is chosen from DMXAA, ADU-S100, amidobenzimidazole-based STING agonists, G10, ulevostinag, 3-Amino-bicyclo[3.2.1]octan-8-ol and EK7766,” and the claim also recites “preferably chosen from DMXAA, ADU-S100, amidobenzimidazole-based STING agonists and G10,” which is the narrower statement of the range/limitation.
Similarly, in the present instance, claim 8 recites the broad limitation “the activator of STING is chosen from DMXAA, ADU-S100, amidobenzimidazole-based STING agonists, G10, ulevostinag, 3-Amino-bicyclo[3.2.1]octan-8-ol and EK7766,” and the claims also recites “preferably chosen from DMXAA, ADU- S100, amidobenzimidazole-based STING agonists and G10,” which is the narrower statement of the range/limitation.
Similarly, in the present instance, claim 9 recites the broad limitation “the activator of STING is chosen from DMXAA, ADU-S100, amidobenzimidazole-based STING agonists, G10, ulevostinag, 3-Amino-bicyclo[3.2.1]octan-8-ol and EK7766,” and the claim also recites “preferably chosen from DMXAA, ADU- S100, amidobenzimidazole-based STING agonists and G10,” which is the narrower statement of the range/limitation.
The claims are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
4. Claims 1-9 are rejected under 35 U.S.C. 102(a)(1) and 102(a)(2) as being anticipated by Wang (U.S. Patent Publication No. US 2021/008190, published 14 Jan 2021, see IDS filed 7 Nov 2024), as evidenced by Merriam-Webster (“Inhibitor,” Merriam-Webster.com Dictionary, Merriam-Webster, https://www.merriam-webster.com/dictionary/inhibitor, accessed 13 Nov 2025).
Wang teaches formulations and methods of treating cancer via utilizing a STING agonist (abstract) and an inhibitor of SERCA2.
Wang specifically teaches injecting both curcumin and ADU-S100 into a Her2 positive tumor (a solid tumor) (page 12, [0105]).
Regarding claim 1, Wang teaches a formulation comprising: a) at least one inhibitor of SERCA2 (curcumin; defined as a SERCA2 inhibitor by claim 3) and b) at least one activator of STING (ADU-S100), which is injected into a solid tumor (page 12, [0105]). Because the products (curcumin and ADU-S100) exist as a formulation that is injected, they are administered simultaneously (page 12, [0105]).
Regarding claim 2, Wang teaches the use of curcumin, which claim 3 defines as an inhibitor of SERCA2 (page 12, [0105]). Further, Merriam-Webster defines an inhibitor as a compound that reduces or suppresses the activity of another substance (such as an enzyme). Thus, Wang teaches a small molecule that reversibly or irreversibly binds to SERCA2 and decreases it activity a SERCA2 inhibitor (page 12, [0105]).
Regarding claim 3, Wang teaches the inhibitor of SERCA2 is curcumin (page 12, [0105]).
Regarding claim 4, Wang teaches the cancer is solid (page 12, [0105]). Wang additionally teaches the cancer is melanoma (page 21, [0184]).
Regarding claim 5, Wang teaches a formulation comprising administering an inhibitor of SERCA2 (curcumin) in combination with at least one activator of STING (ADU-S100), which is injected into a solid tumor (page 12, [0105]). Because the products (curcumin and ADU-S100) exist as a formulation that is injected, they are administered simultaneously (page 12, [0105]).
Regarding claim 6, Wang teaches a formulation comprising administering an inhibitor of SERCA2 (curcumin) in a subject treated by a STING activator (ADU-S100) via injecting the formulation into the Her2 positive tumor of a patient every 10 days for a total of 3 times (page 12, [0105]).
Regarding claim 7, Wang teaches the activator of STING is ADU-S100 (page 12, [0105]).
Regarding claim 8, Wang teaches the activator of STING is ADU-S100 (page 12, [0105]).
Regarding claim 9. Wang teaches the activator of STING is ADU-S100 (page 12, [0105]).
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.
5. Claims 1-9 are rejected under 35 U.S.C. 103 as being unpatentable over Wang (U.S. Patent Publication No. 2021/008190, published 14 Jan 2021) in view of Genovese, et al. (Cell Calcium, 2020, 92 (102308), 1-18).
Wang (U.S. Patent Publication No. 2021/008190) is applied as discussed in the 35 U.S.C. 102 rejection above.
The Examiner notes the relevant teachings with respect to claims 1-9 are set forth above and are incorporated herein by reference.
Additional relevant teachings are set forth below.
Wang teaches formulations and methods of treating cancer via utilizing a STING agonist and a SERCA2 inhibitor (abstract; page 12, [0105]).
Wang specifically teaches injecting both curcumin and ADU-S100 into a Her2 positive tumor (a solid tumor) (page 12, [0105]).
Wang further teaches a formulation comprising: a) at least one inhibitor of SERCA2 (curcumin; defined as a SERCA2 inhibitor by claim 3) and b) at least one activator of STING (ADU-S100), which is injected into a solid tumor (page 12, [0105]). Because the products (curcumin and ADU-S100) exist as a formulation that is injected, they are administered simultaneously (page 12, [0105]).
Regarding claim 2, Wang teaches the use of curcumin, which claim 3 defines as an inhibitor of SERCA2 (page 12, [0105]). Further, Merriam-Webster defines an inhibitor as a compound that reduces or suppresses the activity of another substance (such as an enzyme). Thus, Wang teaches a small molecule that reversibly or irreversibly binds to SERCA2 and decreases it activity a SERCA2 inhibitor (page 12, [0105]).
However, Wang fails to teach that the inhibitor is non-competitive and the inhibitor is specific of SERCA2.
Genovese teaches methods of treating specific types of cancer via SERCA2 inhibitor or STING agonist.
Genovese specifically teaches a selective inhibitor (thapsigargin) that is non-competitive and specific to SERCA2 (page 11, column 2, paragraph 3). While Genovese does not explicitly teach that thapsigargin is a non-competitive inhibitor of SERCA2, this is an inherent property of thapsigargin, as evidenced by Davidson (J. Biol. Chem., 1995 270(20), 11731-11734). Davidson specifies that thapsigargin binds in the stalk region in a non-competitive manner and not at the catalytic site (page 11732, column 2, paragraph 1). This non-competitive binding is present in Genovese as described by Davidson, because Davidson teaches the mechanism of action for thapsigargin acting upon SERCA2 (abstract; page 11732, column 2, paragraph 1), and Genovese teaches that thapsigargin is a selective inhibitor of SERCA2 (page 11, column 2, paragraph 3). See MPEP 2163.07(a). Thus, Genovese teaches a non-competitive inhibitor that is specific to SERCA2 (thapsigargin; page 11, column 2, paragraph 3; page 10, Table 1).
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention to select the SERCA2 inhibitor (thapsigargin) of Genovese to develop a method of treating breast cancer, bladder cancer, prostate cancer, pancreatic cancer, colorectal cancer, melanoma, leukemia, or lymphoma via the combination of a STING activator and a SERCA2 inhibitor, to arrive at instant claim 2. One of ordinary skill in the art would have been motivated to make such a selection, with a reasonable expectation of success, because:
-Wang teaches formulations and methods of treating cancer via utilizing a STING agonist in combination with a SERCA2 inhibitor,
-Wang teaches that STING plays an important role in innate immunity and discloses methods to treat a tumor cell and cancer in addition to boosting immunity against a tumor cell,
-Genovese teaches cancer is the second leading cause of death worldwide and that a hallmark of cancer is reprogramming of metabolic needs and energy metabolism, in which mitochondria play a crucial role,
-Genovese teaches that mitochondria represent central hubs for the regulation of Ca2+ flux in cells and influence the decision between cell life and death, particularly for cancer cell fate,
-Genovese teaches that Ca2+ is fundamental for mitochondrial health, function, and metabolism, and that sufficient impairments in Ca2+ homeostasis have detrimental effects on ATP production and cell viability, and
-Genovese teaches therapies centered on mitochondrial-dependent signaling pathways are under increasing investigation since they provide intriguing and successful strategies for cancer and other disease treatment as well as the latest findings in mitochondria-oriented cancer therapy.
As such, an artisan having ordinary skill in the art would have been motivated to make such a selection, to predictably arrive at a method of treating breast cancer, bladder cancer, prostate cancer, pancreatic cancer, colorectal cancer, melanoma, leukemia, or lymphoma with a STING activator and a SERCA2 inhibitor.
Regarding claim 3, Genovese teaches that the SERCA2 inhibitor is thapsigargin (page 11, column 2, paragraph 3; page 10, Table 1).
Regarding claim 4, Genovese teaches that the cancer is breast cancer, bladder cancer, prostate cancer, colorectal cancer, pancreatic cancer, or melanoma (page 8, column 2, paragraph 3; page 11, column 2, paragraph 3).
Regarding claim 7, Genovese teaches that the STING activator is DMXAA (page 10, Table 1; page 12, column 2, paragraph 2).
Regarding claim 8, Genovese teaches that the STING activator is DMXAA (page 10, Table 1; page 12, column 2, paragraph 2).
Regarding claim 9, Genovese teaches that the STING activator is DMXAA (page 10, Table 1; page 12, column 2, paragraph 2).
Conclusion
No claim is allowed.
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/MADELINE M. DEKARSKE/Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622