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 .
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
This action is in response to the papers filed on March 25, 2026.
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 03/25/2026 has been entered.
Claims 1-19 are currently pending in the application.
Claims 16-19 have been newly added, claims 1, 2, and 5 have been amended and no claims have been canceled.
Therefore, claims 1-19 are examined on the merits.
Priority
The present application is a continuation of US Application 15/610,540 (US Patent No. 11,273,208) filed May 31, 2017, which is a continuation application filed under 35 U.S.C. §111(a) claiming the benefit under 35 U.S.C. §§120 and 365(c) of International Application No. PCT/US2015/063118, filed December 1, 2015, which additionally claims the benefit of U.S. Provisional Application No. 62/086,026, filed December 1, 2014.
Thus, the earliest possible priority for the instant application is December 01, 2014.
Maintained objections/ Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 112 (a)
Claims 1-15 remain and new claims 16-19 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 for improving the ejection fraction in the heart of a patient, wherein the patient suffers acute myocardial infarction, comprising administering conditioned media of 2 million cells or 2 million cells expressing CAMKKI via intracardiac injection, wherein said cells comprise a recombinant vector comprising a nucleic acid encoding a constitutively active human calcium/calmodulin-dependent protein kinase kinase 1 (CAMKKl) protein comprising a CAMKK1 1-413 truncation as set forth in SEQ ID NO: 4.
does not reasonably provide enablement for
a method of treatment of any ischemic or inflammatory condition in any organ or tissue via any route of administering the claimed modified cells or vectors at any dosage. The claims are not enabling for a genus of nucleic acids encoding constitutively active human calcium/calmodulin-dependent protein kinase kinase 1 (CAMKKl) protein and constitutively active equivalents able to overexpress the CAMKKl protein.
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.
This rejection has been modified as necessitated by Applicant’s arguments and amendments filed March 25, 2026
While determining whether a specification is enabling, one considers 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 requirements, 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 731, 737, 8 USPQ2ds 1400, 1404 (Fed. Cir. 1988)). Furthermore, USPTO does not have laboratory facilities to test if an invention will 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. And thus, skepticism raised in the enablement rejections are those raised in the art by artisans of expertise.
The Breadth of the Claims and The Nature of the Invention
Claim 1 recites a method of treating an ischemic or inflammatory condition in an organ or tissue of a patient, comprising administering to the patient: (a) a vector comprising a nucleic acid encoding human constitutively active calcium/calmodulin-dependent protein kinase kinase 1 (CAMKK1); or (b) cells comprising the vector or conditioned media from a culture of the cells”
This claim is broad as it encompasses a method of treatment of any ischemic or inflammatory condition in any organ or tissue via any route of administering the claimed modified cells (which are not specified as MSCs so they additionally are broad for any cell) at any dosage to achieve the result of treating any ischemic condition. The claims encompass a genus of nucleic acids encoding constitutively active human calcium/calmodulin-dependent protein kinase kinase 1 (CAMKKl) protein able to overexpress the CAMKKl protein.
Claim 2 recites “heart, myocardium, liver, kidney, brain, spine, lungs, small intestine, large intestine, arteries, joints, cartilage, skin, or any combination thereof” which is an extremely broad group of organs with different barriers to delivery.
Claim 7 recites “wherein the ischemic or inflammatory condition is acute myocardial infarction, heart failure, peripheral artery disease, stroke, liver disease, ischemic kidney disease, multiple sclerosis, traumatic brain injury, spinal cord injury, graft versus host disease (GVHD), diabetes, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis, an injury from a solid organ transplant, an orthopedic injury, a cartilage disorder, a wound, or any combination thereof” which is a broad group of conditions.
The State of the Prior Art, The Level of One of Ordinary Skill and The Level of Predictability in the Art
As stated in the MPEP, the physiological art is recognized as unpredictable. (MPEP 2164.03.)
Considering the mode of administration, the specification simply requires administration of the cell or cell condition media to the subject by any means. The specification only provides prophetic means of administration:
“The protein, vector, cells, or conditioned media can be administered systemically, directly into the ischemic or inflamed tissue or about the periphery of the ischemic or inflamed tissue. Suitable techniques for systemic administration include enteral administration or parenteral administration (injection, infusion, or implantation). The protein, vector, cells, or conditioned media can be administered, for example, orally, epidurally, intracerebrally, intracerebroventricularly, intraarterially, intraarticularly, intracardially, intramuscularly, intralesionally, intraperitoneally, intrathecally, intravenously, subcutaneously, or any combination thereof” (para. 0044)
The art has demonstrated through numerous publications, delivery of nucleic acid vectors in vivo is highly unpredictable for successful human therapy.
At issue in general are organ barriers, failure to persist, side-effects in other organs, T-cell responses, virus neutralizing antibodies, humoral immunity, normal tropism of the vector to other organs and more. The challenge is to maintain the efficiency of delivery and expression while minimizing any pathogenicity of the virus from which the vector was derived. The inability to develop an adequate means of overcoming obstacles such as humoral; responses and refractory cells limits the successful means by which the nucleic acid can be administered.
The Existence of Working Examples and The Amount of Direction Provided by the Inventor
‘
The examples can be found in the Figure descriptions in para. 0009-15, 56-57. These examples provided in the specification are directed towards increasing injection/ cardiac function, in a heart of a mouse model of acute myocardial infarction. The examples do not give guidance on which vector is utilized to modify CAMKK1 as claimed.
In paragraph 0009, Figure 1A-G provide “exemplary vector maps for use in the disclosed methods” but do not provide enough disclosure to indicate reduction to practice.
In paragraph 0010, cardiac function (ejection fraction) is shown when the media is treated with TGF beta, “Akt” which is not disclosed in the specification and Dab2 siRNA. None of these are the claimed CAMKK1 vector MSCs.
The only guidance for CAMKK1 link is an “exemplary analysis of CAMKKI expression in cells with decreased DAB2 expression (siRNADab2) compared to controls (control or CDNADAb2)) (para. 0012), however this still does not show a reduction to practice of the genus of nucleic acids encoding the CAMKK1 proteins of the claims.
Figure 5A-C does not describe CAMKK1 MSCs of the present claim set merely MSCs or MSCs conditioned to modify CAMKK1 not utilizing the vector claimed: injection of 2 million MSC or the concentrated condition media from 2 million MSC into the infarct border zone. “In the absence of CAMKK1, however, there is no significant increase in cardiac function in response to the injection of MSC or MSC conditioned media (FIG.5A).” “The area of collagen deposition and vascular density in response to MSC and MSC conditioned media injections was quantified. An increase in collagen deposition (FIG. 5B) and a blunting in the increase in vascular density (FIG. 5C) was observed in response to MSC transfected with CAMKKl:siRNA compared to control MSC. (para. 0056)
Additionally, only intracardiac injection of cells is described para. 0057.
FIG. 6 represents exemplary results from treatment of rats following LAD
ligation with a plasmid encoding CAMKK1, however which CAMKK1 is not described.
FIG. 7 illustrates the effects of CAMKKI (DNA) over-expression on Ejection Fraction in rodent model of AMI, however it is only disclosed animals were injected with 0.5 mg of CAMKK1 plasmid or saline in 5 divided 50-100 pl injections. Paragraphs [0031] and [0059] discloses increase in the level of CAMKK1 in heart can be achieved by administering a constitutively active CAMKK1. The constitutively active CAMKK1 can comprise a CAMKK1 having 1-413 amino acids in length as set forth in SEQ ID NO:4.
As paragraph 0056 states “CAMKK1 has not previously been demonstrated to be involved in inducing or enhancing endogenous regenerative pathway.”
The Quantity of Any Necessary Experimentation to Make or Use the Invention
Thus, the quantity of necessary experimentation to make or use the invention as claimed, based upon what is known in the art and what has been disclosed in the specification, will create an undue burden for a person of ordinary skill in the art to demonstrate that the broadly claimed genus of any cells comprising a vector comprising the claimed truncated CAMKK1 or mutants which may be administered by the broadly encompassed administration routes at a broad dosage so as to necessarily and predictably achieve a real-world, clinically meaningful therapeutic result of treating any disease associated with ischemia or inflammation.
It is generally recognized in the art that biological compounds often react unpredictably under different circumstances (Nationwide Chem. Corp. v. Wright, 458 F. supp. 828, 839, 192 USPQ95, 105(M.D. Fla. 1976); Affd 584 F.2d 714, 200 USPQ257 (5th Cir. 1978); In re Fischer, 427 F.2d 833, 839, 166 USPQ 10, 24(CCPA 1970)). The relative skill of the artisan and the unpredictability of the pharmaceutical art are very high. Where the physiological activity of a chemical or biological compound is considered to be an unpredictable art (Note that in cases involving physiological activity such as the instant case, "the scope of enablement obviously varies inversely with the degree of unpredictability of the factors involved" (See In re Fischer, 427 F.2d 833, 839, 166 USPQ 10, 24(CCPA 1970))), the skilled artisan would have not known how to extrapolate the results provided in the instant specification to utilize the appropriate vector, appropriate cell, effective dosage, and effective administration rout to achieve the claimed result.
In conclusion, the specification fails to provide any guidance as to how an artisan would have dealt with the art-recognized limitations of the claimed method commensurate with the scope of the claimed invention, therefore limiting the scope of the claims is proper.
Dependent claims are included in the basis of the rejection because they do not correct the primary deficiencies of the independent claim(s).
In response to Applicant’s arguments and amendments regarding the 112a rejection previously set forth,
Applicant’s arguments and amendments have been considered, however they are not persuasive.
Applicant argues that the specification provides adequate guidance for administration, constructs and experimental evidence for the overexpression of the claimed vector, cells, and conditioned culture medium thereof. Moreover, Applicant argues that regardless of the injured tissue location, and regardless of the injection site, and that the specification demonstrates that exosomes are localize to the injured tissue.
Examiner disagrees. Applicant has not pointed out where the specification has taught that any injection site would result in localization of the exosomes to injured tissue. As discussed above, the only injection site showing a reduction to practice where exosomes are “localized” to the injured tissue is a myocardial infarction rodent model where the CAMKK1 is administered directly into the infarct boarder zone. This does not support the breadth of the claims wherein something could be administered for example, orally, and still localize to the heart.
Applicant stated that the CAMKK1 overexpression results in more exosomes being released into the conditioned media which mediates therapeutic activity.
The Examiner once again reiterates that while this is demonstrated in the specification, the specification only discloses exosomes with this overexpression in a model of AMI and direct injection of a particular dosage (i.e. 2 million cells in conditioned media). This does not enable the full scope of what is claimed in claim 1.
Applicant reiterates their arguments that their success with the AMI model is only exemplary which validates the anti-ischemic and inflammatory effect of administration of the claimed composition and one of ordinary skill in the art would reasonably know how to apply the treatment to other types of in vivo ischemia related disorders. Applicant cites Weibo Wang and Nakamura to support the entire breadth of claim 1 is known in the art due to known mechanisms of exosome trafficking.
Examiner disagrees. As previously set forth, Applicant does not reasonably enable for any disorder or disease which has an ischemic condition. To apply a treatment for AMI which utilizes only intracardial injection to another inflammatory condition would suggest that a treatment for something such as arthritis would be effective by intracardial administration. Applicant does not reasonably enable any condition and any administration route at any dosage to arrive at the treatment of the vast genus of any ischemic or inflammatory condition or disorder.
Applicant’s argument in light of Nakamura is taken from a paper which is focused on skeletal muscle regeneration. Applicant has not pointed to the support within this document for their argument. In Nakamura, exosomes from MSCs are injected locally to a rodent model of muscle injury. This does not provide enablement for the full scope of the claims, but rather supports what has been said previously. Nakamura injects exosomes directly into the muscle of the leg at a particular dosage and the present application injects exosomes directly into the muscle of the heart at a particular dosage. This does not provide support or guidance for other administration routes to treat muscle.
Applicant’s argument in light of Weibo Wang is to support renal treatment of inflammation through exosomes whether local or systemically. However, Applicant has not cited where Weibo Wang states this is the case. Weibo Wang states that the route to the kidneys remains “heavily reliant on intravenous administration (p. 15, last paragraph). The paper goes on to say that active homing to various sites is based on a modification with targeting peptides. This is not found in Applicant’s specification or results. Therefore, the paper would indicate a systemic delivery is appropriate for renal diseases but not necessarily all other disorders or all other administration routes claimed in the scope of the claims. In looking at Table 1 of Weibo Wang, there is only systemic administration present through various veins, some of which are close in proximity to the targeted kidneys, thus an artisan would not expect such administration routes as oral or topical and others to have the same effect with a reasonable expectation of success in the same manner as the systematic administration without undue experimentation.
While Examiner can agree that it is known in the art for exosomes having therapeutic effect, it does not enable that any conditioned treated by exosomes would be enabled for the particular dosage as well as administration route. For instance, it is known in the art as shown in Zhang et al. (2025, Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Volume 1880, Issue 3, 189300) that the cellular origin of exosomes “significantly impacts their organotropism, with multiple studies demonstrating the role of parent cell lines in directing exosome delivery to the brain” (p. 5, last paragraph). In some studies it is shown that neural stem cell (NSC)-derived exosomes exhibited superior brain-targeting capabilities compared to mesenchymal stem cell (MSC)-derived exosomes in a mouse model” (p. 5. Last paragraph). Another study “demonstrated that blood cell-derived exosomes could cross the BBB through transferrin-transferrin receptor interactions, enabling dopamine-loaded blood exosomes to serve as an effective delivery system for treatment” (p. 6, 1st pargraph). Therefore, it is known in the art that there is a level of unpredictability when administering exosomes from different cell origins for different diseases at any dosage which would cause undue experimentation.
Double Patenting
Claim 1-15 remain rejected and claims 16-19 are newly rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 11,273,208 (Patent ‘208).
This rejection has been modified as necessitated by Applicant’s arguments and amendments filed 07/30/2025.
Although the claims at issue are not identical, they are not patentably distinct from each other because:
Regarding claim 1, Patent ‘208 recites “a method of preventing fibrosis or increasing vascular density in an organ or tissue of a patient, the method comprising administering to the patient:
(a) cells comprising:
a vector comprising a nucleic acid encoding human calcium/calmodulin-dependent protein kinase kinase 1 (CAMKK1) selected from the group of: the protein of SEQ ID NO: 4, the T108A mutant CAMKK1, the S459A mutant CAMKK1, or the T108A/S459A mutant CAMKK1, wherein T108 corresponds to position 108 of SEQ ID NO: 2 and S459 corresponds to position 458 of SEQ ID NO: 2, to said organ or tissue, and optionally wherein the vector is a plasmid or a viral vector; or
(b) conditioned media from a culture of the cells of (a) that have been modified to have an increase of the level of human CAMKK1 protein to said organ or tissue, thereby preventing fibrosis or increasing vascular density in the organ or tissue of the patient” and expressing elevated CAMKK1 (Claim 1, 3). This CAMKK1 protein is a constitutively active protein.
This claim is nearly identical to the instant claims except for the preamble. The method of treating an ischemic of inflammatory condition has the same result from the same method steps as Patent ‘208’s prevention of fibrosis and increase in vascular density. Therefore, the independent claims are not patentably distinct.
Regarding claim 2, Patent ‘208 recites “the method of claim 1, wherein said organ or tissue is heart, myocardium, liver, kidney, brain, spine, lungs, small intestine, large intestine, arteries, joints, cartilage, skin, or any combination thereof” (Claim 2). This is identical to the instant claim.
Regarding claim 3, Patent ‘208 recites “wherein the organ or tissue is heart or myocardium” (Claim 10). This is identical to the instant claim.
Regarding claim 4, Patent ‘208 recites “optionally wherein optionally wherein the vector is a plasmid or a viral vector” (Claim 1) which encompasses the limitation of a viral vector.
Regarding claim 5, Patent ‘208 recites “wherein the cells or conditioned media are administered systemically, directly into said organ or tissue, or about the periphery of said organ or tissue, wherein said organ or tissue is inflamed or damaged” (Claim 4). This is identical to the instant claim.
Regarding claim 6, Patent ‘208 recites “the method of claim 1, wherein the cells are mesenchymal stem cells” (Claim 5). This is identical to the instant claim.
Regarding claim 7, Patent ‘208 recites “wherein the heart or myocardium is associated with a condition of heart failure or stroke, wherein the heart failure is with or without ejection fraction” (Claim 11). This encompasses the limitation of “stroke” and “heart failure” in line 2.
Regarding claim 8, Patent ‘208 recites “further comprising administering one or more additional regenerative therapies” (Claim 6). This is identical to the instant claim.
Regarding claim 9, Patent ‘208 recites “wherein the one or more regenerative therapies comprise administering mesenchymal stem cells derived from bone marrow, adipose tissue, placental tissue, umbilical cord, Wharton's Jelly, menstrual blood, stem cells, M2 macrophages, monocytes, or any combination thereof“ (Claim 7). This encompasses the present claims.
Regarding claim 10, Patent ‘208 recites “wherein the stem cells are neural progenitor cells, endothelial progenitor cells, organ specific endogenous stem cells, or any combination thereof” (Claim 8). This is identical to the instant claim.
Regarding claim 11, Patent ‘208 recites “wherein the organ specific endogenous stem cells are cardiac ckit+ cells” (Claim 9). This is identical to the instant claim.
Regarding claims 12-19, Patent ‘208 recites the description of these substitutions within the SEQ ID’s in claim 1.
Therefore claims 1-19 of the instant application are rejected on the ground of nonstatutory double patenting.
In response to Applicant’s arguments and amendments regarding the double patenting previously set forth,
Applicant’s request to hold the rejection in abeyance is denied and the rejection is maintained.
Applicant further notes that the arguments for ‘208 have not been substantiated to show an obvious variation of the claims such that a skilled artisan would readily expect the compositions to treat inflammatory conditions from compositions treating fibrosis.
Examiner states that ischemic or inflammatory conditions can comprise fibrotic tissue. Ischemic injury and acute myocardial infarction demonstrate fibrosis. In the present application’s disclosure it states “prolonged inflammation can cause tissue destruction, fibrosis or necrosis” (para. 0005). Moreover paragraph 0061 discusses the treatment and its myocardial fibrosis. The same steps are claimed in claim 1 and claim 28 of Patent ‘208 and do not specify a disorder or disease or a route of administration, therefore the two overlap in subject matter.
New grounds objections/ Rejections in response to Applicants’ arguments or amendments
Objections to the Specification
The disclosure is objected to because of the following informalities:
Paragraphs 0031-0032 and subsequent disclosures of SEQ ID NO: 6, 8, and 10 do not describe the SEQ ID NOs as disclosed in the sequence listing or claimed. The terminology for T108A is known in the art as a Threonine to Alanine substitution. However, SEQ ID NO: 6 demonstrates an aspartic acid substitution at position 108. No paragraph within the specification discloses wherein aspartic acid is substituted.No sequence IDs are provided for alanine substitutions, moreover not at T108 in SEQ ID NO: 6.
Furthermore, S459A mutants are known in the art as an alanine to serine substitution at amino acid 459, however the SEQ ID NO: 8 and 10, there is an aspartic acid substitution at amino acid 458 when compared to the reference sequence SEQ ID NO: 2. A substitution of amino acid 458 is not disclosed in the entirety of the specification.
In other words, the amino acid descriptions correlating to the specific SEQ ID NOs do not match any of the SEQ ID NOs submitted. The specification and sequence listing currently have the following issues in need of correction:
SEQ ID NO: 6 shows an aspartic acid substitution at T108 of SEQ ID NO: 2. This is not described in paragraph 0031 or anywhere in the specification.
SEQ ID NO: 8 shows an aspartic acid substitution at T458 of SEQ ID NO: 2. This is not described in paragraph 0031 or anywhere in the specification.
There are no alanine substitutions as paragraph 0031 describes in the SEQ ID NOs when compared to the native sequence SEQ ID NO: 2.
No sequences have been provided that show alanine substitutions at any position.
No sequences have been provided which show any substitutions at position 459.
Appropriate correction is required.
Nucleotide and/or Amino Acid Sequence Disclosures
Specific deficiency - This application contains sequence disclosures in accordance with the definitions for nucleotide and/or amino acid sequences set forth in 37 CFR 1.821(a)(1) and (a)(2). However, this application fails to comply with the requirements of 37 CFR 1.821 - 1.825.
The sequence disclosures are located throughout the application particularly at paragraph 0031 which discloses sequences such as “T108A” and “S459A” which are not present in the sequence listing. As described above, the descriptions of the SEQ ID NOs in paragraph 0031 which are disclosed as corresponding to the substitution does not match the submitted sequence. For example:
SEQ ID NO: 6, paragraph 0031 discloses is a T108A mutant. The aspartic acid is highlighted in the 108 position.
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SEQ ID NO: 8, paragraph 0031 discloses is a S459A mutant, however as seen in SEQ ID NO: 2 below position 459 is naturally a Phenylalanine (Phe/F).
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The mutation reflected in SEQ ID NO: 8 is highlighted in the 458 position where serine is substituted for aspartic acid. The instant specification states “the S459A mutant” of SEQ ID NO: 2 (para. 0031) where Ser (S) is substituted to Ala (A) demonstrated in SEQ ID NO: 8. Residue 458 is a Serine (Ser/S). However, there is no sequence provided for a Ser (S) to Ala (A) substitution at either 458 or 459.
If accepting S459 means residue 458, SEQ ID NO: 8 shows said amino acid is substituted from Ser to an Asp (D).
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SEQ ID NO: 10 is the combination of the two mutations, T108/S459A and exhibits both issues described above regarding SEQ ID NO: 6 and 8.
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If the invention involves Aspartic acid substitutions, it should be reflected in the specification.
If the invention involves Alanine substitutions, a SEQ ID NO exhibiting the claimed sequence is required.
Required response – Applicant must provide:
A "Sequence Listing" part of the disclosure, as described above in item 1); as well as
An amendment specifically directing entry of the "Sequence Listing" part of the disclosure into the application in accordance with 1.825(b)(2);
A statement that the "Sequence Listing" includes no new matter in accordance with 1.825(b)(5); and
A statement that indicates support for the amendment in the application, as filed, as required by 37 CFR 1.825(b)(4).
If the "Sequence Listing" part of the disclosure is submitted according to item 1) a) or b) above, Applicant must also provide:
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required incorporation-by-reference paragraph, consisting of:
A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
A copy of the amended specification without markings (clean version); and
A statement that the substitute specification contains no new matter;
If the "Sequence Listing" part of the disclosure is submitted according to item 1) b), c), or d) above, Applicant must also provide:
A replacement CRF in accordance with 1.825(b)(6); and
Statement according to item 2) a) or b) above.
Claim Objections
Claim 1 is objected to because of the following informalities:
Claim 1 recites “from a culture of the cells of” in line 5. The second “of” is a typographical and grammatical error.
Appropriate correction is required.
Conclusion
No claims allowed.
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/ALEXANDRA F CONNORS/Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634
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