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
The present application claims priority to the following applications: 63/183,358, 63/316,617, and PCT/US2022/027280, with effective filing dates of 3 May 2021, 3 March 2022, and 2 May 2022.
Claim Status
This Office Action is in response to Applicant’s Response to Restriction filed, 10 March 2026.
Applicant’s election of Group I (claims 1-3, 5-13, 15-16, 18-20, and 22-24) and species of Compound 17 (
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) in the reply filed on 10 March 2026 is acknowledged. Because Applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Claims 2, 7-8, 13, 15, 18, 20, and 22 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Claim 2 specifies wherein Q is
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, which does not read on the elected species. Claim 7 specifies that the linker is an alkyl chain, which does not read on the elected species. Claim 8 specifies that the linker is an alkyl chain, which does not read on the elected species. Claim 13 specifies that the degron is a cereblon (CRBN) ligand, which does not read on the elected species. Claim 15 specifies that that structure is represented by any one of structure I-13 to I-52, which does not read on the elected species. Claim 18 specifies that Z is
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, which does not read on the elected species. Claim 20 specifies that the degron is an IAP degron, which does not read on the elected species. Claim 22 specifies that that structure is represented by any one of structure I-113 to I-162, which does not read on the elected species.
Claims 25-27 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected group (Group II), there being no allowable generic or linking claim.
Election was made without traverse in the reply filed on 10 March 2026.
Claims 1, 3, 5-6, 9-12, 16, 19, and 23-24 are pending.
Information Disclosure Statement
The Information Disclosure Statement filed on 25 October 2023 and 31 March 2026 and the references cited therein have been considered, unless indicated otherwise.
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.
1. Claim 16 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.
Claim 16 recites the degron binds VHL and is represented by any one of structures (D2-a) to (D2-f). However, the structures specified in claim 16 are named as (D1-a) – (D1-f). Further, claim 13 specifies CRBN structures for (D1-a) – (D1-c). Accordingly, claim 16 is unclear.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
2. Claim(s) 1, 3, 5-6, 9-12, 16, 19, and 23-24 are rejected under 35 U.S.C. 103 as being unpatentable over Hebach (U.S. Patent No. 9,056,843, issued 16 June 2015, see IDS filed 25 Oct 2023) in view of Cromm (J. Am. Chem. Soc.¸ 2018, 140(49), 17019-17026) and Crews (U.S. Patent PreGrant Publication 2020/0038513, published 6 Feb 2020) as evidenced by Zagidullin (Explor. Target Antitumor Ther., 2020, 1, 381-390), Wikipedia (“Cereblon,” Wikipedia, 26 Oct 2019, <web.archive.org/web/20191026111915/https://en.wikipedia.org/wiki/Cereblon>, accessed 13 Apr 2026), and Krieger (ChemMedChem, 2023, 18(e202200615), 1-11).
Hebach teaches trifluromethyl-oxadizaole derivatives as inhibitors of HDAC4 for treating Huntington’s disease, which is a neurodegenerative disease (abstract; column 1, lines 12-15 and 21-23). Hebach specifically teaches the compound,
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, which is the protein of interest (POI) ligand of Compound 17 (Example 132, column 104).
Regarding claim 1, Hebach fails to teach a heterobifunctional degrader.
Cromm teaches heterobifunctional degraders that induced protein degradation via small molecule inhibitors that failed in initial clinical trials (abstract; page 17019, column 1, paragraph 1; page 17019, column 2, paragraph 1; page 17020, Figure 1). Cromm specifically teaches the compound,
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(PROTAC-3; page 17020, Figure 1), which utilizes VHL and a flexible PEG linker to best enable formation of the ternary complex as evidenced by Zagidullin. Zagidullin teaches that PEG linkers are soluble and flexible and that PEG linkers stabilize the ternary complex by cooperative binding (page 383, paragraph 3). Further, Cromm teaches utilizing VHL and cereblon (CRBN) E3 ligase ligands, which have been extensively used in the degrader landscape (page 17019, column 2, paragraph 2). While both VHL and CRBN are popular E3 ligase ligands, a significant drawback to utilization of CRBN is the associated teratogenic effect as evidenced by Wikipedia (page 1, paragraph 2).
Cromm teaches that CRBN-recruiting analogs are less effective than VHL-recruiting analogs (page 17020, column 2, paragraph 1). Additionally, Cromm teaches that while some previous small molecules were proven effective in preclinical studies, clinical success had yet to be observed and the leading Fak inhibitor (defactinib) failed its initial clinical trial targeting malignant pleural mesothelioma stem cells (page 17019, column 1, paragraph 1; page 17019, column 2, paragraph 1). Cromm teaches that heterobifunctional degraders exhibit better selectivity: defactinib binds to 100 kinases, while PROTAC-3 binds to 20 kinases (page 17021, column 1, paragraph 1). Further, Cromm teaches that PROTAC-3 outperforms the clinical candidate (defactinib) with respect to Fak activation (autophosphorylation) and inhibition of downstream signaling (including Fak’s kinase-independent signaling) (page 17023, column 1, paragraphs 2-3; page 17023, column 2, paragraph 1). Thus, Cromm teaches that degraders are able to target an increasing range of kinases and therapeutic areas (i.e. resistance mechanisms and protein targets that were inaccessible) and thus drug the undruggable (page 17023, column 2, paragraph 2). Additionally, Cromm teaches the VHL ligand having the same stereochemical assignments as the VHL ligand in Compound 17: 1) the t-butyl is (S); 2) the alcohol of the hydroxyproline is (R); and (3) the amide is (S) (page 17020, Figure 1). However, the VHL ligand taught by Cromm is missing the methyl at the benzylic position of the VHL ligand as shown in Compound 17.
Crews teaches heterobifunctional degraders comprising defactinib, PEG linkers, and VHL for targeting FAK (abstract). Crews specifies that protein-protein interactions are notoriously difficult to target using small molecules ([0004]). Crews further teaches that E3 ubiquitin ligases confer substrate specificity for ubiquitination and therefore are more attractive therapeutic targets than general proteasome inhibitors due to specificity for certain protein substrates ([0004]). Crews teaches that non-specific effects at treating FAK-mediated diseases and disorders and inability to target and modulate FAK remain as obstacles to the development of effective treatments and that small-molecule therapeutic agents that target FAK and leverage VHL’s substrate specificity would be very useful ([0012]). Crews specifically teaches the VHL ligand,
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, wherein the methyl of the ligand has the stereochemical assignment of (S) (page 111). Crews further details other VHL ligands possessing a methyl at the benzylic position, and all the VHL ligands having 1) a methyl at the benzylic position and 2) specified stereochemistry then have the methyl at the wedge position and the hydrogen at the hash position (i.e. producing a stereochemical assignment of (S) (page 69, [0664]; page 98; page 111; page 120; page 122-125), as evidenced by Krieger. Krieger teaches that the (R) enantiomer is known to be significantly less active (Table 2, page 3; page 2, column 2, paragraph 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 modify the POI ligand of Hebach to incorporate the PEG linker and VHL ligand of Cromm and Crews to arrive Compound 17:
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(a compound of Formula (I)). One of ordinary skill in the art would have been motivated to make such a selection, with a reasonable expectation of success, because:
-Hebach teaches trifluromethyl-oxadizaole derivatives as inhibitors of HDAC4 for treating Huntington’s disease, which is a neurodegenerative disease,
-Hebach teaches the compound,
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, which is the protein of interest (POI) ligand of Compound 17,
-Cromm teaches heterobifunctional degraders that induced protein degradation via small molecule inhibitors that failed in initial clinical trials,
-Cromm teaches the compound,
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(PROTAC-3), which utilizes VHL and a flexible PEG linker to best enable formation of the ternary complex as evidenced by Zagidullin. Zagidullin teaches that PEG linkers are soluble and flexible and that PEG linkers stabilize the ternary complex by cooperative binding,
-Cromm teaches utilizing VHL and cereblon (CRBN) E3 ligase ligands, which have been extensively used in the degrader landscape. While both VHL and CRBN are popular E3 ligase ligands, a significant drawback to utilization of CRBN is the associated teratogenic effect as evidenced by Wikipedia,
-Cromm teaches that CRBN-recruiting analogs are less effective than VHL-recruiting analogs,
-Cromm teaches that while some previous small molecules were proven effective in preclinical studies, clinical success had yet to be observed and the leading Fak inhibitor (defactinib) failed its initial clinical trial targeting malignant pleural mesothelioma stem cells,
-Cromm teaches that heterobifunctional degraders exhibit better selectivity: defactinib binds to 100 kinases, while PROTAC-3 binds to 20 kinases,
-Cromm teaches that PROTAC-3 outperforms the clinical candidate (defactinib) with respect to Fak activation (autophosphorylation) and inhibition of downstream signaling (including Fak’s kinase-independent signaling),
-Cromm teaches that degraders are able to target an increasing range of kinases and therapeutic areas (i.e. resistance mechanisms and protein targets that were inaccessible) and thus drug the undruggable,
-Cromm teaches that the VHL ligand having the same stereochemical assignments as the VHL ligand in Compound 17: 1) the t-butyl is (S); 2) the alcohol of the hydroxyproline is (R); and (3) the amide is (S),
-Crews teaches heterobifunctional degraders comprising defactinib, PEG linkers, and VHL for targeting FAK,
-Crews teaches that that protein-protein interactions are notoriously difficult to target using small molecules,
-Crews teaches that that E3 ubiquitin ligases confer substrate specificity for ubiquitination and therefore are more attractive therapeutic targets than general proteasome inhibitors due to specificity for certain protein substrates,
-Crews teaches that non-specific effects at treating FAK-mediated diseases and disorders and inability to target and modulate FAK remain as obstacles to the development of effective treatments and that small-molecule therapeutic agents that target FAK and leverage VHL’s substrate specificity would be very useful,
-Crews teaches the VHL ligand,
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, wherein the methyl of the ligand has the stereochemical assignment of (S) and
-Crews teaches other VHL ligands possessing a methyl at the benzylic position, and all the VHL ligands having 1) a methyl at the benzylic position and 2) specified stereochemistry have the methyl at the wedge position and the hydrogen at the hash position (i.e. producing a stereochemical assignment of (S), as evidenced by Krieger. Krieger teaches that the (R) enantiomer is known in the art to be significantly less active (Table 2, page 3; page 2, column 2, paragraph 1).
As such, an artisan having ordinary skill in the art would have been motivated to substitute
one known element for another to predictably arrive at a compound of Formula (I):
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.
Regarding claim 3, Hebach teaches the compound
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, wherein Q is
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(Example 132, column 104).
Regarding claim 5, Hebach teaches the compound
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, wherein Q1 is ethyl (Example 132, column 104).
Regarding claim 6, Hebach teaches the compound
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(Example 132, column 104). Cromm teaches the compound,
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(PROTAC-3), which utilizes VHL and a flexible PEG linker to best enable formation of the ternary complex (page 17020, Figure 1). Further, Crews specifically teaches the VHL ligand,
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, wherein the methyl of the ligand has the stereochemical assignment of (S) (page 111). Accordingly, the combination of Hebach, Cromm, and Crews teaches the compound,
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, which falls into structure (I-2). Thus, the combination of Hebach, Cromm, and Crews teaches claim 6.
Regarding claim 9, Cromm teaches the compound,
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(PROTAC-3), which utilizes a PEG linker (page 17020, Figure 1).
Regarding claim 10, Cromm teaches the compound,
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(PROTAC-3), which utilizes a PEG linker that comprises 2 PEG units (page 17020, Figure 1).
Regarding claim 11, Cromm teaches the linker,
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(page 17020, Figure 1).
Regarding claim 12, Hebach teaches the compound
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(Example 132, column 104). Cromm teaches the compound,
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(PROTAC-3), which utilizes VHL and a flexible PEG linker to best enable formation of the ternary complex (page 17020, Figure 1). Further, Crews specifically teaches the VHL ligand,
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, wherein the methyl of the ligand has the stereochemical assignment of (S) (page 111). Accordingly, the combination of Hebach, Cromm, and Crews teaches the compound,
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, which falls into structure (I-12). Thus, the combination of Hebach, Cromm, and Crews teaches claim 12.
Regarding claim 16, Cromm teaches the compound,
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(PROTAC-3), which utilizes VHL ligand, (D1-a) (page 17020, Figure 1).
Regarding claim 19, Hebach teaches the compound
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(Example 132, column 104). Cromm teaches the compound,
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(PROTAC-3), which utilizes VHL and a flexible PEG linker to best enable formation of the ternary complex (page 17020, Figure 1). Further, Crews specifically teaches the VHL ligand,
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, wherein the methyl of the ligand has the stereochemical assignment of (S) (page 111). Accordingly, the combination of Hebach, Cromm, and Crews teaches the compound,
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, which falls into structure (I-107). Thus, the combination of Hebach, Cromm, and Crews teaches claim 19.
Regarding claim 23, Hebach teaches the compound
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(Example 132, column 104). Cromm teaches the compound,
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(PROTAC-3), which utilizes VHL and a flexible PEG linker to best enable formation of the ternary complex (page 17020, Figure 1). Further, Crews specifically teaches the VHL ligand,
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, wherein the methyl of the ligand has the stereochemical assignment of (S) (page 111). Accordingly, the combination of Hebach, Cromm, and Crews teaches the compound,
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, which is Compound 17. Thus, the combination of Hebach, Cromm, and Crews teaches claim 23.
Regarding claim 24, Hebach teaches compositions of HDAC4 inhibitors (column 35, lines 32-48). Further, Crews teaches compositions of heterobifunctional degraders ([0028]; [0065]).
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
3. Claim 1, 3, 5-6, 9-12, 16, 19, and 23-24 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 and 13-15 of copending Application No. 17/774,002 (reference application) in view of Hebach (U.S. Patent No. 9,056,843, issued 16 June 2015, see IDS filed 25 Oct 2023). Although the claims at issue are not identical, they are not patentably distinct from each other.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
U.S. Application No. 17/774,002 claims a compound
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, and claim 13 specifically teaches the compound,
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(Compound 14). Claim 14 specifies a composition of claim 1. Claim 15 specifies treating a disease or disorder characterized or mediated by aberrant activity of HDAC3.
Regarding claim 1, ‘002 fails to teach the HDAC4 inhibitor,
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.
Hebach teaches trifluromethyl-oxadizaole derivatives as inhibitors of HDAC4 for treating Huntington’s disease, which is a neurodegenerative disease (abstract; column 1, lines 12-15 and 21-23). Hebach specifically teaches the compound,
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, which is the protein of interest (POI) ligand of Compound 17 (Example 132, column 104).
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 modify the POI ligand of Hebach to incorporate the PEG linker and VHL ligand of ‘002 to arrive Compound 17:
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(a compound of Formula (I)). One of ordinary skill in the art would have been motivated to make such a selection, with a reasonable expectation of success, because:
-‘002 teaches selective HDAC3 degraders for treating Huntington’s disease,
-‘002 teaches the compound,
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(Compound 13),
-Hebach teaches trifluromethyl-oxadizaole derivatives as Class IIa-selective HDAC4 inhibitors for treating Huntington’s disease, which is a neurodegenerative disease,
-Hebach teaches that class IIa inhibitors do not target histones, like Class I HDAC inhibitors (column 2, lines 33-40),
-Hebach teaches that it is advantageous to develop Class IIa-selective HDAC4 inhibitors for treating Huntington’s disease (column 2, liens 40-44), and
-Hebach teaches the compound,
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, which is the protein of interest (POI) ligand of Compound 17.
As such, an artisan having ordinary skill in the art would have been motivated to substitute
one known element for another to predictably arrive at a compound of Formula (I):
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.
Regarding claim 3, Hebach teaches the compound
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, wherein Q is
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(Example 132, column 104).
Regarding claim 5, Hebach teaches the compound
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, wherein Q1 is ethyl (Example 132, column 104).
Regarding claim 6, Hebach teaches the compound
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(Example 132, column 104). ‘002 teaches the compound,
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(Compound 14; claim 13). Accordingly, the combination of Hebach and ‘002 teaches the compound,
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, which falls into structure (I-2). Thus, the combination of Hebach and ‘002 teaches claim 6.
Regarding claim 9, ‘002 teaches the compound,
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(Compound 14; claim 13), which utilizes a PEG linker.
Regarding claim 10, ‘002 teaches the compound,
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(Compound 14; claim 13), which utilizes a PEG linker that comprises 2 PEG units.
Regarding claim 11, ‘002 teaches the linker,
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(Compound 14, claim 13).
Regarding claim 12, Hebach teaches the compound
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(Example 132, column 104). ‘002 teaches the compound,
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(Compound 14; claim 13). Accordingly, the combination of Hebach and ‘002 teaches the compound,
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, which falls into structure (I-12). Thus, the combination of Hebach and ‘002 teaches claim 12.
Regarding claim 16, ‘002 teaches the compound,
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(Compound 14; claim 13), which utilizes VHL ligand, (D1-a) (page 17020, Figure 1).
Regarding claim 19, Hebach teaches the compound
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(Example 132, column 104). ‘002 teaches the compound,
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(Compound 14; claim 13). Accordingly, the combination of Hebach and ‘002 teaches the compound,
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, which falls into structure (I-107). Thus, the combination of Hebach and ‘002 teaches claim 19.
Regarding claim 23, Hebach teaches the compound
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(Example 132, column 104). ‘002 teaches the compound,
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(Compound 14; claim 13). Accordingly, the combination of Hebach and ‘002 teaches the compound,
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, which is Compound 17. Thus, the combination of Hebach and ‘002 teaches claim 23.
Regarding claim 24, Hebach teaches compositions of HDAC4 inhibitors (column 35, lines 32-48). Further, ‘002 teaches compositions of heterobifunctional degraders (claim 14 of ‘002).
Conclusion
No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Madeline M Dekarske whose telephone number is (571)272-1789. The examiner can normally be reached Monday - Thursday 10am - 4pm.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James Alstrum-Acevedo can be reached at 571-272-5548. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/MADELINE M. DEKARSKE/Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
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