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 .
Claim Status
Claims 1-9 are rejected.
No claims are allowable.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 12/10/2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement has been considered by the examiner.
Maintained 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.
Claims 1-9 are rejected under 35 U.S.C. 103 as being unpatentable over Matic, (Stability Of Bovine Milk Exosomes And Their Effect On Proliferation Of Raw 264.7 Cells, May 2019) (hereinafter Matic) in view of Panich et al., (Ultraviolet Radiation-Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging, April 11, 2016) (hereinafter Panich).
Matic discloses exosomes isolated from commercially available fat-free milk (Great Value brand) by differential centrifugation. Milk was centrifuged at 13,000 x g at 4 °C for 30 min in 250 mL centrifuge bottles. The whey was collected, transferred into polycarbonate 26.3 mL Beckman centrifuge tubes, and centrifuged at 100,000 x g at 4 °C for 60 min. The final supernatant was collected, transferred to 26.3 mL centrifuge tubes and centrifuged at 135,000 x g at 4 °C for 90 min. The supernatant was discarded, and the pellet was washed with PBS twice. The exosome pellet was collected and resuspended in PBS. Isolated exosomes were sterile filtered through 0.22 µm filters and the protein concentration was adjusted to 6 mg/mL (pages 31-32, 2.3.2 Isolation of exosomes). Matic teaches that reactive oxygen species are generated under oxidative stress and that exosome treatment significantly reduced the ROS production when compared to untreated cells. There was no significant difference in ROS production between the cell treated with 100 µg/mL and 200 µg/mL exosomes (i.e., an effective amount) (page 72, 3.4.3 Bovine milk exosomes reduced production of ROS in RAW 264.7 cell under hypoxic conditions). The application of milk exosomes as a potential functional food ingredient (i.e., functional health food) depends on the ability of exosomes to survive human digestion and to reach intestines and circulation in an intact form (page 40, 2.4.3 Bovine milk exosomes resist pepsin-pancreatin hydrolysis). It was found that exosomes are resistant to simulated digestive conditions (page 42, first paragraph).
Matic differs from the instant claims insofar as not teaching a method of inhibiting UV-induced oxidative damage of cells, comprising treating the cells with an effective amount for inhibiting UV-induced oxidative damage.
However, Panich teaches that ultraviolet radiation (UVR) is a major cause of stem cell DNA damage and can contribute to depletion of stem cells (ESCs and mesenchymal stem cells) leading to photoinduced skin aging (Abstract). UV-A-induced ROS (reactive oxygen species) is responsible for ESCs DNA damage. Accumulated oxidative damage to biomolecules in the cells, caused by repetitive exposure to environmental insults, in particular UVR, may compromise their self-renewal capacity and promote loss of ESC numbers, resulting in premature aging (page 6, 6. UV-Induced Oxidative Stress: A Major Assault on Skin and a Potential Preventive and Therapeutic Target for Antioxidants in Skin Photoaging). Production of the DNA toxic ROS from UV-A leads to damage of dermal fibroblasts, resulting in skin aging (page 5, Figure 1). Exposure of human skin fibroblasts, an important cellular component of skin microenvironment, to UVR produced ROS has been shown to result in oxidative stress and high level of ROS was also reported to induce skin fibroblasts to secrete high levels of matrix metalloproteinases (MMPs), which caused extensive ECM remodeling in dermal layers. However, due to the transient nature of ROS, it is possible to ameliorate its effect and protect the skin from premature aging. Pharmacologically, ROS has been considered as a potential target for photoaging prevention and therapies (page 7, fourth and fifth paragraphs).
As discussed above, Matic teaches that an effective amount of bovine milk exosome treatment, wherein the exosomes are not drug carriers, significantly reduced the ROS production in cells. Accordingly, it would have been prima facie obvious to one of ordinary skill in the art to have used an effective amount of bovine milk exosomes in a method of inhibiting UV-induced oxidative damage of cells because UVR produced ROS has been shown to result in oxidative damage of cells, as taught by Panich. Thus, a significant reduction in ROS production in cells would result in inhibited UV-induced oxidative damage of cells.
Regarding claims 3-7, as discussed above, Matic discloses bovine derived exosomes prepared by substantially the same process as instantly claimed. Even though product-by- process claims are limited by and defined by the process, determination of patentability is based on the product itself. The patentability of a product does not depend on its method of production. If the product in the product-by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process, In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985), see MPEP 2113. The final product disclosed in the instant application holds no patentably distinct structural differences from the final product disclosed by Matic.
Regarding claim 8, it would have been obvious to treat human dermal fibroblasts (i.e., cells) with an effective amount of bovine milk exosomes isolated since DNA toxic ROS from UV-A results in oxidative stress damage of human dermal fibroblasts as taught by Panich, and as discussed above, an effective amount of the exosomes of Matic significantly reduced the ROS production in cells.
Response to Arguments
Applicant argues that the reported results of Matic are unreliable because Matic acknowledges that its results were controversial and not consistent with current literature which included reports of experiments that achieved opposite results, i.e., where hypoxic conditions were found to increase ROS.
Applicant’s arguments have been fully considered but are not found to be persuasive. Matic discloses on the bottom of page 72 that in their study, hypoxia caused a significant 4- fold ROS reduction in untreated cells when compared to the untreated cell under normoxic conditions and it is still controversial whether hypoxic conditions increase ROS production, making their findings not consistent with current literature. Thus, the controversial results of the study of Matic are in regards to whether or not hypoxic conditions increase ROS production. The results discussed above indicating that the exosome treatment significantly reduced the ROS production when compared to untreated cells in hypoxic conditions are not indicated as controversial by Matic.
Applicant argues that a person of ordinary skill would have understood that Matic's observed reductions in ROS could reflect effects of oxygen deprivation itself and that no difference in effect was seen between treatment with 100 µg/ml or 200 µg/ml exosomes.
Applicant’s arguments have been fully considered but are not found to be persuasive. As discussed above, Matic teaches that exosome treatment significantly reduced the ROS production when compared to untreated cells in hypoxic conditions. Therefore, an effect of decreased ROS production is seen with exosome treatment. The disclosure that no difference in effect was seen between treatment with 100 µg/ml or 200 µg/ml exosomes means that the effect seen at an amount of 100 µg/ml exosomes was significantly the same as the effect seen with an amount of 200 µg/ml exosomes. Thus one of ordinary skill in the art would conclude that the same level of decrease in ROS production would be noted whether the dose of exosomes was 100 µg/ml or 200 µg/ml, which does not contradict the conclusion that an effect of decreased ROS production is seen with exosome treatment.
Further, Matic discloses that they noted a decrease in ROS when the cells were exposed to hypoxia which may be due to exposing the cells to hypoxia for a longer period of time where no more available oxygen was present to produce ROS. The reduction in ROS generation may be explained by possible transformation or elimination of ROS over a prolonged period under hypoxia when reoxygenation was not present (page 73, bottom paragraph). This disclosure is further discussing the controversial results above regarding to whether or not hypoxic conditions increase ROS production. As discussed above, Matic teaches that exosome treatment significantly reduced the ROS production when compared to untreated cells in hypoxic conditions. Thus, regardless of whether or not hypoxic conditions decrease ROS production, it was shown by Matic that when cells were treated with exosomes, a significant reduction in ROS production was observed versus when cells were not treated with exosomes. Thus, it can be concluded that if a reduction in ROS production was noted, some amount of ROS must have been present in order to be measured. Since treatment with exosomes was compared to treatment without exosomes, under the same conditions, resulting in a significant decrease in ROS production when cells were treated with exosomes, one of ordinary skill in the art would have reasonably concluded that exosome treatment reduces ROS production.
Applicant argues that if Matic's bovine milk exosomes played a role in suppressing ROS generation, one of ordinary skill in the art would have expected treatment with bovine milk exosomes to inhibit expression of HIF-la but the bovine milk exosomes did not affect the expression of HIF-la at all.
Applicant’s arguments have been fully considered but are not found to be persuasive. Applicant has not provided any objective evidence supporting Applicant’s assertion that in suppressing ROS one must also inhibit expression of HIF-la. Therefore, since Applicant’s argument is merely speculative, Applicant’s argument is unpersuasive.
Applicant argues that UV-induced oxidative damage is mechanistically distinct from hypoxia-induced oxidative stress, therefore because bovine milk exosome treatment did not alter HIF-la expression a person of ordinary skill would not reasonably expect bovine milk exosomes to mitigate the entirely different UV-induced oxidative damage pathway involved in the methods of the present claims.
Applicant’s arguments have been fully considered but are not found to be persuasive. As discussed above, Applicant has not provided any objective evidence supporting Applicant’s assertion that in suppressing ROS one must also inhibit expression of HIF-la. Therefore, since Applicant’s argument is merely speculative, Applicant’s argument is unpersuasive.
Further, as discussed above, Matic teaches that an effective amount of bovine milk exosome treatment significantly reduced the ROS production in cells and Panich teaches that UVR produced ROS has been shown to result in oxidative damage of cells. Thus, a significant reduction in ROS production in cells would result in inhibited UV-induced oxidative damage of cells. Applicant has not shown where treatment with bovine milk exosomes would not significantly reduce the UVR produced ROS production in cells. Therefore, since Applicant’s argument is merely speculative, Applicant’s argument is unpersuasive.
Maintained 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.
Claims 1-9 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 14-15 and 21-39 of co-pending Application No. 17/780391 in view of Matic, (Stability Of Bovine Milk Exosomes And Their Effect On Proliferation Of Raw 264.7 Cells, May 2019) (hereinafter Matic) further in view of Panich et al., (Ultraviolet Radiation-Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging, April 11, 2016) (hereinafter Panich).
Co-pending application claims 14, 26, and 33 teach a method comprising applying a therapeutically effective amount of exosomes isolated from milk or goat milk to the skin of the subject but do not teach a method of inhibiting UV-induced oxidative damage of cells, comprising treating the cells with an effective amount for inhibiting UV-induced oxidative damage, as recited in instant claim 1.
However, Matic teaches that reactive oxygen species are generated under oxidative stress and that exosome treatment significantly reduced the ROS production when compared to untreated cells. There was no significant difference in ROS production between the cell treated with 100 µg/mL and 200 µg/mL exosomes (i.e., an effective amount) (page 72, 3.4.3 Bovine milk exosomes reduced production of ROS in RAW 264.7 cell under hypoxic conditions). Panich teaches that ultraviolet radiation (UVR) is a major cause of stem cell DNA damage and can contribute to depletion of stem cells (ESCs and mesenchymal stem cells) and damage of stem cell niche, eventually leading to photoinduced skin aging (Abstract). Exposure of human skin fibroblasts, an important cellular component of skin microenvironment, to UVR produced ROS has been shown to result in oxidative stress and high level of ROS was also reported to induce skin fibroblasts to secrete high levels of matrix metalloproteinases (MMPs), which caused extensive ECM remodeling in dermal layers. However, due to the transient nature of ROS, it is possible to ameliorate its effect and protect the skin from premature aging. Pharmacologically, ROS has been considered as a potential target for photoaging prevention and therapies (page 7, fourth and fifth paragraphs).
Regarding claims 1 and 2, it would be obvious to one of ordinary skill in the art to utilize exosomes derived from bovine milk for the intended use of inhibiting UV-induced oxidative damage of cells, comprising treating the cells with an effective amount for inhibiting UV-induced oxidative damage, with a reasonable expectation of success because bovine milk exosomes reduce production of ROS and UVR produced ROS has been shown to result in oxidative damage, as taught by Matic and Panich.
Claims 3-9 of the instant application are dependent on claim 1. Regarding claims 3-7, as discussed above, Matic, Panich, and the co-pending make obvious milk-derived exosome used for inhibiting UV-induced oxidative damage of cells. Even though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. The patentability of a product does not depend on its method of production. If the product in the product -by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process, In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985), see MPEP 2113. The final product disclosed in the instant application holds no patentably distinct structural differences from the final product taught above.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1-9 are provisionally rejected on the ground of nonstatutory double
patenting as being unpatentable over claims 1-6 and 9 of co-pending
Application No. 18/133,886 in view of Matic, (Stability Of Bovine Milk Exosomes And Their Effect On Proliferation Of Raw 264.7 Cells, May 2019) (hereinafter Matic) further in view of Panich et al., (Ultraviolet Radiation-Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging, April 11, 2016) (hereinafter Panich).
Co-pending application claim 1 teaches a method comprising applying a therapeutically effective amount of exosomes isolated from milk or goat milk to the skin of the subject but do not teach a method of inhibiting UV-induced oxidative damage of cells, comprising treating the cells with an effective amount for inhibiting UV-induced oxidative damage, as recited in instant claim 1.
However, Matic teaches that reactive oxygen species are generated under oxidative stress and that exosome treatment significantly reduced the ROS production when compared to untreated cells. There was no significant difference in ROS production between the cell treated with 100 µg/mL and 200 µg/mL exosomes (i.e., an effective amount) (page 72, 3.4.3 Bovine milk exosomes reduced production of ROS in RAW 264.7 cell under hypoxic conditions). Panich teaches that ultraviolet radiation (UVR) is a major cause of stem cell DNA damage and can contribute to depletion of stem cells (ESCs and mesenchymal stem cells) and damage of stem cell niche, eventually leading to photoinduced skin aging (Abstract). Exposure of human skin fibroblasts, an important cellular component of skin microenvironment, to UVR produced ROS has been shown to result in oxidative stress and high level of ROS was also reported to induce skin fibroblasts to secrete high levels of matrix metalloproteinases (MMPs), which caused extensive ECM remodeling in dermal layers. However, due to the transient nature of ROS, it is possible to ameliorate its effect and protect the skin from premature aging. Pharmacologically, ROS has been considered as a potential target for photoaging prevention and therapies (page 7, fourth and fifth paragraphs).
Regarding claims 1 and 2, it would be obvious to one of ordinary skill in the art to utilize exosomes derived from bovine milk for the intended use of inhibiting UV-induced oxidative damage of cells, comprising treating the cells with an effective amount for inhibiting UV-induced oxidative damage, with a reasonable expectation of success because bovine milk exosomes reduce production of ROS and UVR produced ROS has been shown to result in oxidative damage, as taught by Matic and Panich.
Claims 3-9 of the instant application are dependent on claim 1. Regarding claims 3-7, as discussed above, Matic, Panich, and the co-pending make obvious milk-derived exosome used for inhibiting UV-induced oxidative damage of cells. Even though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. The patentability of a product does not depend on its method of production. If the product in the product -by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process, In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985), see MPEP 2113. The final product disclosed in the instant application holds no patentably distinct structural differences from the final product taught above.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1-7 are provisionally rejected on the ground of nonstatutory double
patenting as being unpatentable over claims 1-7 of co-pending
Application No. 18/133,901 in view of Matic, (Stability Of Bovine Milk Exosomes And Their Effect On Proliferation Of Raw 264.7 Cells, May 2019) (hereinafter Matic) further in view of Panich et al., (Ultraviolet Radiation-Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging, April 11, 2016) (hereinafter Panich).
Co-pending application claim 1 teaches a method comprising applying a therapeutically effective amount of exosomes isolated from milk or goat milk to the subject but do not teach a method of inhibiting UV-induced oxidative damage of cells, comprising treating the cells with an effective amount for inhibiting UV-induced oxidative damage, as recited in instant claim 1.
However, Matic teaches that reactive oxygen species are generated under oxidative stress and that exosome treatment significantly reduced the ROS production when compared to untreated cells. There was no significant difference in ROS production between the cell treated with 100 µg/mL and 200 µg/mL exosomes (i.e., an effective amount) (page 72, 3.4.3 Bovine milk exosomes reduced production of ROS in RAW 264.7 cell under hypoxic conditions). Panich teaches that ultraviolet radiation (UVR) is a major cause of stem cell DNA damage and can contribute to depletion of stem cells (ESCs and mesenchymal stem cells) and damage of stem cell niche, eventually leading to photoinduced skin aging (Abstract). Exposure of human skin fibroblasts, an important cellular component of skin microenvironment, to UVR produced ROS has been shown to result in oxidative stress and high level of ROS was also reported to induce skin fibroblasts to secrete high levels of matrix metalloproteinases (MMPs), which caused extensive ECM remodeling in dermal layers. However, due to the transient nature of ROS, it is possible to ameliorate its effect and protect the skin from premature aging. Pharmacologically, ROS has been considered as a potential target for photoaging prevention and therapies (page 7, fourth and fifth paragraphs).
Regarding claims 1 and 2, it would be obvious to one of ordinary skill in the art to utilize exosomes derived from bovine milk for the intended use of inhibiting UV-induced oxidative damage of cells, comprising treating the cells with an effective amount for inhibiting UV-induced oxidative damage, with a reasonable expectation of success because bovine milk exosomes reduce production of ROS and UVR produced ROS has been shown to result in oxidative damage, as taught by Matic and Panich.
Claims 3-9 of the instant application are dependent on claim 1. Regarding claims 3-7, as discussed above, Matic, Panich, and the co-pending make obvious milk-derived exosome used for inhibiting UV-induced oxidative damage of cells. Even though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. The patentability of a product does not depend on its method of production. If the product in the product -by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process, In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985), see MPEP 2113. The final product disclosed in the instant application holds no patentably distinct structural differences from the final product taught above.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Arguments
Applicant argues that all OTDP rejections should be withdrawn in view of Applicant’s arguments regarding Matic and Panich.
Applicant’s arguments have been fully considered but are not found to be persuasive. The Examiner submits that Applicant’s argument with regards to Matic and Panich is addressed above and is unpersuasive. Therefore, these rejections are maintained.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Samantha J Knight whose telephone number is (571)270-3760. The examiner can normally be reached Monday - Friday 8:30 am to 5:00 pm ET.
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/S.J.K./ Examiner, Art Unit 1614
/TRACY LIU/ Primary Examiner, Art Unit 1614