DETAILED ACTION
This Office action supersedes the non-final rejection dated 2/13/2026. The action corrects the finality paragraph in the previous action and resets the period for reply.
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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 12/23/2025 has been entered.
Applicant’s amendments to the claims dated 12/23/2025 are acknowledged. Claims 1-30 are cancelled. Claims 31-55 are newly added and subject to prosecution.
The cancellation of claims 1-30 results in the cancellation of all previously pending claims. New independent claims 31, 54, and 55 are broadly directed to methods of administering a recombinant rAAV to a kidney of a subject, wherein the method comprises, at least,
blocking a renal artery of the kidney such that flow of blood is substantially or completely stopped; and
administering a solution of the rAAV into the renal pelvis of the kidney (via retrograde administration through the ureter), wherein the solution comprises about 0.13 to about 0.33 mL/kg of the subject.
New independent claims 31, 54, and 55 newly require wherein a renal artery is blocked, which encompasses a non-required alternate embodiment of previously pending claims. Initially, the Examiner notes no previously pending independent claims required blocking any renal blood vessel(s). The method of previously pending independent claim 1 could be performed with, or without, blocking a renal blood vessel, as defined by dependent claims 12 and 13. Previously pending claim 12 (dependent upon claim 1) required blocking “a renal blood vessel of the kidney, selected from the group consisting of a renal artery, a renal vein, and a combination thereof.” Blocking “a renal artery” was only one option of renal blood vessels and not technically required. Previously pending claim 13 (also dependent upon claim 1) recites “wherein a renal blood vessel selected from the group consisting of a renal artery, a renal vein, and a combination thereof is not blocked during performance of the method.” Thus, the requirement wherein the method comprising blocking “a renal artery” in each of new claims 31, 54, and 55 encompass a narrower scope than any previously pending claim.
Declaration of Dr. Moullier
A declaration under 37 CFR 1.132 was submitted on 2/6/2026 by Dr. Philippe Moullier, a named inventor of the instant application. The declaration asserts unexpected results in the form of increased kidney transduction in proximal tubule cells by retro-ureteral administration of rAAV with renal artery occlusion.
When considering evidence of non-obviousness, “the applicant should establish a nexus between the rebuttal evidence and the claimed invention, i.e., objective evidence of non-obviousness must be attributable to the claimed invention. Additionally, the evidence must be reasonably commensurate in scope with the claimed invention. See MPEP 2145. Any differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. See MPEP 716.02. Further, the burden is on Applicant to establish that the evidence provided are unexpected and significant. The evidence relied upon should establish "that the differences in results are in fact unexpected and unobvious and of both statistical and practical significance." See MPEP 716.02(b).
For an assertion of unexpected results to overcome a finding of obviousness, the scope of the claims and the experimental conditions used to achieve any unexpected results must be fully commensurate. See MPEP 716.02(d). The independent claims of the instant application are broader in terms of subject; degree, method, and duration of renal artery stoppage; rAAV capsid serotype, transgene, and promoter; solution volume; viral genome number; and intrarenal pressure, and insufficient data are provided for one of ordinary skill in the art to be able to readily extrapolate the results shown in the declaration to every permutation of the method of administration encompassed by the instant claims.
The Examiner notes that Dr. Moullier does not actually articulate how anything within the declaration is relevant to the pending claims. However, the Examiner has tried to consider the declaration to the extent any evidence appears to be encompassed within the scope of the pending claims.
The data of the declaration is not the data disclosed within the pending specification. Sections 5-6 of the declaration provides methodologies of administering an AAV virus to pigs via the retro-ureteral route. Example 1 administers viruses without renal artery occlusion to two pigs; example 2 is a control and administers a solution without virus and without rental artery occlusion to a single pig; and example 3 administers viruses with a 15 minute renal artery occlusion prior to administration of the viruses to four pigs. The three examples administer viruses of a single capsid (AAV2G9), at a single dosage and volume range.
The declaration describes the viral transduction data from examples 1-3, as shown in fig. 1B, 1A, and 1C, respectively. Example 1, viral transduction without renal arterial occlusion showed that 5% of kidney cells were transduced; example 2 (the control) showed no viral transduction; and example 3, viral transduction with a 15 minute renal arterial occlusion showed “estimated 30% or more of kidney cells transduced.”
Sections 7-8 of the declaration provide methodologies of administering an AAV virus to pigs via the retro-ureteral route, wherein the time of renal artery occlusion is a 10 min occlusion period or a 15 min occlusion period. The total number of pigs treated is not disclosed, but the methodologies administer the viruses of a single capsid (AAV2G9), at a single dosage and volume that were exemplified in examples 1 and 3 above.
The declaration at section 7, pages 4-5 describes the viral transduction data from the 10 min or 15 min occlusion period on the quantity of transduced PCT cells, as shown in fig. 2A and 2B, respectively. A 10 min renal arterial occlusion showed an average of 1-5% of PCT cells transduced and a maximum of 35% of PCT cells transduced; a 15 min renal arterial occlusion showed an average of 8-25% of PCT cells transduced and a maximum of 60% of PCT cells transduced.
The only discussion of unexpected results is in section 8 of the declaration, in a single sentence:
“Fig. 1A-1C and Fig. 2A-2B thus demonstrate that renal artery occlusion during retro-ureteral administration to the kidney unexpectedly increases rAAV kidney transduction.”
The declaration discloses that the renal occlusion prior to the viral administration confines the administered viruses to the pelvic cavity for the duration of the occlusion period (See section 5, page 2). In other words, Dr. Moullier asserts that it is unexpected that increasing the duration of exposure of tissue to a virus, already known to have tropism to that tissue, results in increasing the total number of tissue cells transduced by the virus. The idea that increasing the length of exposure of administered AAV viruses within the renal pelvic cavity to improve viral transduction was known at the time of filing. For example, Rubin et al. discuss prior art methodologies of improved AAV delivery and transduction of the kidney, including retrograde ureteral injection, and multiple instances where “use of clips on the renal artery, renal vein and ureter to enhance the time for which the AAV in the injection fluid had physical exposure to cells in the kidney” (See page 384, col. 1, 1). Thus, it does not appear that that renal artery occlusion during retro-ureteral administration to the kidney unexpectedly increases rAAV kidney transduction, as asserted by Dr. Moullier.
Status of Prior Rejections/Response to Arguments
RE: Rejection of claims 1-5, 8-10, and 12-30 under 35 U.S.C. 103 over Holzmeister et al. (WO 2022175546 A1) in view of Kruse et al. (WO 2022204535 A1):
The cancellation of claims 1-5, 8-10, and 12-30 renders the rejection thereto moot.
RE: Rejection of claims 1-30 under 35 U.S.C. 103 over Holzmeister et al. (WO 2022175546 A1) in view of Kruse et al. (WO 2022204535 A1), further in view of Shen et al. (Journal of Biological Chemistry, 2013):
The cancellation of claims 1-30 renders the rejection thereto moot.
New Rejections
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claim 31- 55 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 enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
New independent claims 31, 54, and 55 are broadly directed to methods of administering a recombinant rAAV to a kidney of a subject, wherein the method comprises, at least,
blocking a renal artery of the kidney such that flow of blood is substantially or completely stopped; and
administering a solution of the rAAV into the renal pelvis of the kidney (via retrograde administration through the ureter), wherein the solution comprises about 0.13 to about 0.33 mL/kg of the subject;
wherein the subject is a pig, non-human primate or a human; and
wherein the methodology results in at least 25% transduction of proximal tubules or 25% transduction of nephrons in the kidney.
The factors to be considered in determining whether undue experimentation is required are summarized in In re Wands, 858 F.2d 731, 737, 8 U.S.P.Q.2d 1400, 1404 (Fed. Cir. 1988) (a) the breadth of the claims; (b) the nature of the invention; (c) the state of the prior art; (d) the level of one of ordinary skill; (e) the level of predictability in the art; (f) the amount of direction provided by the inventor; (g) the existence of working examples; and (h) the quantity of experimentation needed to make or use the invention based on the content of the disclosure. While all of these factors are considered, a sufficient number are discussed below so as to create a prima facie case.
The breadth of the claims; the nature of the invention:
The claims are directed to large genera of methods of administering rAAV via a retrograde ureteral route, wherein a renal artery is blocked, wherein the virus is administered to a pig, a non-human primate or a human in a volume adjusted for the weight of the subject treated, wherein the renal artery may be blocked for 15 minutes, and wherein the methodologies predictably result in at least transduction of 25% of the proximal tubule cells or 25% of nephrons in the kidney. The claims are broad, with no specific AAV serotype, dosage, or intrarenal pressure required.
The amount of direction provided by the inventor; the existence of working examples:
The specification provides little guidance for the successful practice over the breath of the now pending claims. Generic disclosures relating to the treated subject being to a pig, a non-human primate or a human, the AAV capsids that can be used, the transgenes that can be encoded on the AAV vectors, and effective dosages that can be infused are disclosed (See ¶0008-0012, 0016-0020, 0024, 0026-0027, 0042-0059, 0076-0079, 0082, 0144-0154, 0158, 0190-0191, 0201-0204, 0215-0224, 0228-0263, 0272-0286, and 0370). It is noted that these are generic disclosures relating to the claimed limitations. Generic disclosures wherein the administration of the AAV results in at least transduction of 25% of the proximal tubule cells or 25% of nephrons in the kidney are found through the previously cited sections and additionally in sections reciting ranges of transduction or transduction efficiencies that may be a result of administration (See ¶0014 and 0161-0168).
Claims 31, 54, and 55 require “wherein the method results in the transduction of at least about 25% of proximal tubules in the kidney with the rAAV”, “to thereby transduce at least about 25% of proximal tubules in the kidney”, and “to thereby transduce at least about 25% of nephrons in the kidney”, respectively.
However, the specification discloses that transduction of a nephron or a proximal tubule encompasses one or more cells within a nephron, or one or more cells within a proximal tubule. The specification also discloses that the transduction efficiency can be the transduction of a percent of nephrons or proximal tubules of the kidney (See ¶0159) or the transduction efficiency normalized to AAV9 transduction efficiency See ¶0155 and 0794):
[0158] As used herein, the terms "transducing a nephron" or "transducing nephrons" interchangeably refer to transducing at least one cell of a nephron, the at least one cell being: a glomerulus cell (including cells of Bowman's capsule); a proximal tubule (also referred to as a proximal convoluted tubule) cell; a cell of the loop of Henle (including descending and/or ascending limbs, and thick and/or thin regions thereof); a distal tubule (also referred to as a distal convoluted tubule) cell; a collecting duct cell; or a combination thereof. Similarly, the terms "transducing a nephron 'component"' or "transducing nephron 'components"' interchangeably refer to transducing at least one cell of a nephron component, the nephron component being: a glomerulus (including Bowman's capsule); a proximal tubule (also referred to as a proximal convoluted tubule); the loop of Henle (including descending and/or ascending limbs, and thick and/or thin regions thereof); a distal tubule (also referred to as a distal convoluted tubule); or a collecting duct.
[0159] The terms "nephron transduction efficiency" and "nephron component transduction efficiency" refer to a number of transduced nephrons or nephron components relative to the total number of nephrons or total number of nephron components in a kidney, respectively. Accordingly, a nephron transduction efficiency of 10% means that 10% of the total number of nephrons in the kidney are transduced. For example, in a hypothetical kidney having exactly 1 million (1,000,000) nephrons, a nephron transduction efficiency of 10% means that 100,000 of the 1,000,000 nephrons are transduced.
[0160] Because a transduced nephron component can have more than one cell that is transduced, this aspect can be discussed in terms of a "cellular transduction efficiency." For example, a single nephron can have a nephron cellular transduction efficiency of 30%, which means that 30% of the total number cells making up that single nephron are transduced. Similarly, a single proximal tubule may have a proximal tubule cellular transduction efficiency of 30%, which means 30% of the total number cells in that single proximal tubule are transduced. It is understood that even though 30% of the total number cells in the proximal tubule are transduced, this aspect does not preclude transduction of other components of the same nephron. For example, a cell can have a proximal tubule cellular transduction efficiency of 30% along with specified or unspecified cellular efficiency relating to cells of the loop of Henle (ascending and/or descending limbs, and thick and/or thin regions thereof), cells of the distal tubule, and/or cells of the corresponding collecting duct.
[0161] Accordingly, in some aspects, the current technology provides for both a nephron transduction efficiency and a cellular transduction efficiency. As an example, the term "a proximal tubule transduction efficiency of at least 20% and a proximal tubule cellular transduction efficiency of at least 30%" means that at least 20% of the of the total number of proximal tubules in a kidney are transduced and at least 30% of the proximal tubule cells in each of the transduced proximal tubules are transduced, or to put it another way, at least 30% of the proximal tubule cells in at least 20% of the total number proximal tubules in the kidney are transduced.
[0162] Descriptions herein, for example, of transduction of a percentage of nephrons in a kidney may refer to a nephron transduction efficiency, a nephron component transduction efficiency, and/or a cellular transduction efficiency.
[0155] As used here, a "high efficiency" means a level of transduction, e.g., a nephron transduction efficiency or nephron component transduction efficiency, that results in detectable and/or measurable levels of rAAV in cells of the kidney. In various embodiments, a high efficiency corresponds to a nephron transduction efficiency or nephron component transduction efficiency of at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, or at least 50%, or more. In some embodiments, a high efficiency corresponds to an efficiency index (as defined herein; see e.g., Formula I) that is greater than 1, e.g., having efficiency higher than what is achieved by administering rAAV comprising an AAV9 capsid.
Example 1 discloses clamping a renal artery and then administering a library of different AAV capsids encoding a reporter transgene via retrograde infusion to a rat. Administered solutions ranged from 260 µl/kg to 300 µl/kg with dosages from 1 x 1013 to 2 x 1013. The renal arteries were declamped between 15 to 45 minutes after infusion. Paragraph 0791 states, “FIG. 1 shows histological sections of an exposed, i.e., treated, left kidney and unexposed right kidney following the retrograde ureter administration of the rAAV library to the left kidney. The top panel shows YFP expression (stained brown) in the library exposed left kidney and the bottom panel shows no detectable YFP expression in the unexposed right kidney. These results demonstrate that the exposed kidney was heavily transduced by the rAAV library, with about 30% of the nephrons being transduced.” However, the 30% transduction of nephrons appears to be a single example from one of the AAV in the library, and the AAV used is not disclosed.
The working examples from the library allege that multiple AAVs from the virus library can be used in the invention, based on their efficiency normalized to AAV9 (See ¶0794-0795 and table 3). That is, the transduction efficiency of a AAV capsid for a nephron can be normalized to the AAV9 transduction efficiency:
[0794] FIG. 4 is a bar graph showing the efficiency index of library rAAVs normalized to AAV9 in the kidney medulla (e.g., substantially comprising loops of Henle and collecting ducts) or kidney cortex ( e.g., substantially comprising glomeruli, proximal tubules, and distal tubules). The efficiency index of each tested rAAV normalized to AAV9 was calculated as follows in Formula I: (cDNA reads [%]/input [%])/(cDNAAAV9 reads [%]/inputAAV9 [%]). FIG. 5 is a dot plot showing the efficiency index of selected rAAVs from FIG. 4 normalized to AAV9 in the kidney medulla or kidney cortex. Table 3 provides values for each of the capsids shown in FIG. 5. Relative to AAV9, AAV2g9 exhibits about 3500-fold higher combined efficiency, AAV2.5 exhibits over 800-fold higher combined efficiency, AAVDJ exhibits over 200-fold higher combined efficiency, and AAV2 exhibits over 100-fold higher combined efficiency.
Regardless of the fact that the data is generated in rats, it is not clear how the data from this section shows at least 25% percent nephrons in the cell are transduced or how 25% of the proximal tubules are transduced.
Example 2, using pigs, comprises clamping a renal artery and then administering AAV2G9 encoding a reporter transgene via retrograde infusion to the pigs. Administered solutions were injected at 0.24 mL/kg with a total dosage of 1.41 x 1013 viral genomes. The renal arteries were declamped 15 min after infusion. Paragraph [0796] states, “As a result, about 30% or more of the nephrons in the kidneys can be transduced with no significant immune response detected in the kidneys.” It is not clear where support for this statement can be found within the example, fig. 6A-6X, or table 4-7, or whether support is from a hard count or how the transduction efficiency was calculated.
Example 3, using non-human primates, comprises clamping a renal artery and then administering AAV2G9 encoding a reporter transgene via retrograde ureteral infusion to the primates. Solutions of 0.2083 mL/kg with a total dosage of 5.75 x 1013 were administered. The renal artery was declamped 15 min after infusion. The method quantifies transduced PCT cells against total PCT cells in the animals and shows transduction of 28-84% of the PCT (See table 11). The method also quantifies transduced DCT cells against total DCT cells in the animals and shows transduction of 21-27% of the DCT (See table 12).
Example 4 is a prophetic example of administering an AAV vector to humans and generates no data.
Example 5 comprises clamping a renal artery in a pig having immunity to the virus and then administering AAV2G9 capsids encoding a reporter transgene via retrograde ureteral infusion. A solution of 0.25 mL/kg with a total dosage of 1.00 x 1014 was administered. The renal artery was declamped 15 min after infusion. Paragraph 0825 states that the method “resulted in robust transduction in the injected kidney”. It does not appear that any quantification of transduced cells is actually reported or whether such transduction meets the claimed 25% transduction requirements.
Thus, the specification generates a limited number of pigs and non-human primates encompassed by the pending claims, wherein all the animals are administered the same AAV2G9 virus. Of these animals, the results of some of the exemplified animals are not clearly showing the required percentage transduced PCTs or nephrons, as required by the claims. The data exemplified in example 1 occurred in rats. In addition, the complexity of the specification’s teaching regarding “transducing” and “transduction efficiency” and their calculations add to undermine the data in the working examples.
The art was unpredictable:
Rubin et al. teach that gene therapy for the kidney has not advanced as far as gene therapy for other organs. Rubin et al. disclose that therapeutic efficacy is hindered by the complex architecture of the organ and the many different cell types within the organ (See page 376, col. 1, full ¶1-2 and col. 2, ¶1-3 and page 377, col. 1, ¶1-2 and col. 2, ¶1). Delivery of vectors intravenously is reduced compared to other organs because the kidney is a natural filter, excluding molecules based on size, and thus has required alternative routes of delivery (page 377, col. 1, full ¶1-2 and col. 2, ¶1-3 and page 378, col. 1, ¶1-2 and col. 2, ¶1). Use of AAV to deliver transgenes to kidneys is impeded by reduced or inconsistent transduction of kidney cells in vivo (page 382, col. 2, full ¶3 and page 383, col. 1, ¶1). Rubin et al. recognize that improvements in AAV transduction includes engineering capsids with improved tropism for kidney cells and different modes of AAV delivery in vivo, such as retrograde ureteral injection. Such improvements have shown increased transduction of kidney cells or specific cell types, but increased transduction is still relatively reduced compared to the numbers of total cells, if quantified, and many results of “increased” transduction are qualitative, and not quantitative, and/or fail to distinguish between transduced cell types (See page 384, col. 1, ¶1).
Konkalmatt et al. disclose methods of administering rAAV encoding luciferase, GFP, or DRD2 to a mouse kidney in vivo via a retrograde ureteral route (See page 10, ¶3 and fig. 1). The method comprises placing a microvenous clip on the renal artery of the target kidney and then administering a solution comprising the rAAV into the kidney through the ureter (See page 10, ¶3). Following injection of the rAAV, the arterial microvenous clips were maintained for 15 min (See page 10, ¶3). Konkalmatt et al. disclose that the methodology results in increased kidney-specific transduction, as determined by luminescence, fluorescence, and AAV copy number (See fig. 1). However, Konkalmatt et al. do not disclose a quantified amount of transduced cells, PCTs, or nephrons.
Peek et al. also acknowledge the challenges of using AAV for gene delivery to the kidney. Peek et al. teach that the different types of cells within the kidney have been shown to have specific viral receptors, implying that subcellular localization of the receptor(s) or kidney architecture may contribute to a lack of kidney transduction (See page 9, ¶1). Peek et al. also acknowledge inconsistencies in transduction capabilities of the same serotype among researchers and that methods of detecting viral transduction may not be accurate (See page 11, ¶1-2).
Thus, the art recognized that transduction of the kidney with AAV is generally considered low. Even when methods to improve transduction are exemplified, the art does not consistently determine quantified transduction data, and the methodologies used to detect and quantify AAV transduction in cells may not be accurate.
The quantity of experimentation needed to make or use the invention based on the content of the disclosure:
The skilled artisan would be required to perform undue levels of experimentation in order to practice the claimed invention. The instant specification does not exemplify working examples across the scope claimed to show how modifications to any of the claimed parameters/steps would still be able to arrive at the claimed transduced cell percentages. The instant specification also does not provide guidance on how to reasonably predict what changes or variations of the claimed virus capsid, dosage, subject, etc., can be made that would still predictably result in the claimed transduced cell percentages. Every alteration would require generating an animal according the claimed steps and then determining how to define and quantify a percentage of transduced nephrons and PCT cells based on the specification’s definitions of a transduced cell and transduction efficiency.
Conclusion
When all of the Wands factors are considered together, they establish a prima facie case that the specification is not enabling for the claims. The lack of guidance in the specification relating to how modification the few working examples—which all appear to use the same vector, similar dose ranges, etc.—would predictably result in the claimed transduction percentages, combined with the unpredictable nature of the art, provides additional weight to the lack of enablement in consideration of the Wands factors as a whole. Thus, one of ordinary skill in the art would not have had a reasonable expectation of success in making or using the claimed invention. Claims 32-53 are included in the rejection because they depend from a rejected claim.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 31-53 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.
Claim 31 recites the limitation “at a sufficient volume of about 0.13 mL/kg to about 0.33 mL/kg”. It is unclear in what respect the volume must be “sufficient”. Dependent claims 32-53 are included in the rejection.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JENNIFER S SPENCE, whose telephone number is 571-272-8590. The examiner can normally be reached M-F 8:30-5:30.
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/J.S.S./Examiner, Art Unit 1633 /CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633