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 Election/Restrictions Applicant’s election without traverse of Group I, corresponding to 1-17 and 20-23, in the reply filed on January 20, 2026, is acknowledged. Applicant further elected the following species without traverse: anxiety , Rac1 , and the TRPC compound of claim 6 . Claims 1-6, 12-17, 20, and 22 are readable on the elected species. The elected species compound is free of the prior art. However, each examined claim has been rejected below . The examiner expanded his search to expedite prosecution to the compound clemizole HCl which is the last compound claimed in claim 7. While claim 7 remains withdrawn, Clemizole HCl does fall within the scope of instant claims 1 and 2, among others. Suggestions for Allowance : File a Terminal Disclaimer over the relevant Patents and Patent Applications; limit the claims to the compound formulas of claims 5 and/or 6; limit the conditions claimed to be those supported by the Specification, such as specific kidney diseases/conditions; recite only those biomarkers that are known to be related to the claimed subject population; and provide specific guidance as to how to identify a subject population to be treated and/or how to measure and use a biomarker level to adjust a dosage up or down based upon a result of that measurement as a real number or relative to a healthy control. Any Amendment must find support in the Specification. Status of the Claims Claims 1-18 and 20-23 are pending. Claims 7-11, 18, 21, and 23 are preliminarily withdrawn. Claims 1-6, 12-17, 20, and 22 are examined. Claim Rejections - 35 USC § 112 Claims 1-6, 12, 13, 20 and 22 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. The phrase “ predetermined threshold ” is not defined by the Specification and it can be mean anything. It is not clear what this threshold means. Further, the quotation marks in claim 4 are confusing. The --- is defined within quotation marks but there does not appear to be an instance of --- being used. Clarification is requested. Claim Rejections - 35 USC § 112 Claims 2-6, 12-17, 20, and 22 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Claim 2 depends from claim 1. Claim 1 requires administering a composition to a subject. Claim 2 only requires administering only if a subject is determined to have a urinary level (i.e., a condition is met) . This means that administering is not required of claim 2 while it is required of claim 1 . Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements. Claim Rejections - 35 USC § 112 (Scope of Enablement) 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. Claims 1-6, 12-17, 20, and 22 are rejected under 35 U.S.C. 112, first paragraph, because the specification, while being enabling for most of those compounds set forth in the instant Specification are not considered enabled for the breadth of compounds of Formulas (I) and (II) and all calcineurin inhibitors are not considered enabled for the combinations of Rac1 urinary levels being a usable biomarker for each of the claimed subjects . Further, “treating” is defined to include prevention of a condition . Additionally, treating a subject that has any form of cancer or kidney disease also does not appear to be enabled. The compounds of instant claims 5 and 6 are free of the prior art and are considered enabled. The use of those compounds to treat FSGS is established. The statistical significan ce of levels of Rac1 in the urine for those in Figure B is not entirely clear with the low sample size for FSGS, PKD, and Alport and the low level of Rac1 in Alport. The Examples in the Specification do not refer to cancer, anxiety, or depression . Further, the examples only refer to calcineurin inhibitors, cyclosporine A and tacrolimus in Example 16. The S pecification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to arrive at the invention commensurate in scope with these claims. Each compound within the Scope of Formula s (I) and (II) of claim 1 is not enabled. Further, the bre adth of treating and preventing all conditions claimed is not enabled. Further, a link between urinary biomarkers for each condition is not enabled. Rac1 is not established for Alport syndrome, e.g., which is an example of a kidney disease shown in Figure 13. The standard for determining whether the Specification meets the enablement requirement was cast in the Supreme Court decision of Mineral Separation v. Hyde , 242 U.S. 261 (1916) which postured the question: is the experimentation needed to practice the invention undue or unreasonable? As recognized by the court in In re Wands , 858 F.2d 731 (Fed. Cir. 1988), that is still the standard to be applied, determined by consideration of the Wands factors (MPEP 2164.01(A)); namely, nature of the invention, breadth of the claims, guidance of the specification, the existence of working examples, state of the art, predictability of the art and the amount of experimentation necessary. All of the Wands factors have been considered, with the most relevant factors discussed below Nature of the Invention : As stated in MPEP 2164.05(a), “[t]he initial inquiry” for determining whether the Specification is enabling “is into the nature of the invention, i.e., the subject matter to which the claimed invention pertains.” In the instant case, the claimed invention pertains to compounds of Formula ( I ) or (II) , which are alleged by the Specification to inhibit TRPC5 , thereby treating and preventing all forms of kidney disease, cancer, anxiety, and depression . The invention include administration of a vast group of compounds, for treating and preventing a vast group of conditions. The invention is considered extremely broad. The State of the Prior Art and the Relative Skill of those in the Art : As stated in MPEP 2164.05(a), “[t]he state of the prior art is what one skilled in the art would have known, at the time the application was filed, about the subject matter to which the claimed invention pertains” and, as stated in MPEP 2164.05(b), “[t]he relative skill of those in the art refers to the skill of those in the art in relation to the subject matter to which the claimed invention pertains at the time the application was filed.” As discussed above, the instantly claimed invention pertains to compounds of Formula s (I ) and (II) , which are alleged by the Specification to modulate TRPC5 to treat and prevent associated-conditions including all forms of cancer . At the time the instant application was filed, it would have been known by those of ordinary skill in the art that - compounds, in the vast majority of cases, demonstrate a remarkably high correlation between their structure, specificity and ability to produce a pharmacological effect. At the same time, it would have also been generally assumed that two compounds with similar chemical properties would exhibit similar biological effects. Thus, given a series of compounds that are shown to exert an activity of interest (or given a target of interest), the ordinarily skilled artisan would have expected that a limited genus of related compounds (e.g., compounds exhibiting near equal molecular shapes and volumes, approximately the same distribution of electrons, and similar physical properties such as hydrophobicity) would interact with the given target to elicit a related biological response. Accordingly, at the time the invention was made, the relative skill of those in the art tasked with identifying compounds exerting an activity of interest would have been high, as the ordinarily skilled artisan would have had, at minimum, a Ph.D. and experience with screening techniques including computer assisted virtual screening techniques such as ligand-based and structure-based design methods. Deciding which technique to use would have been determined by the skilled artisan’s knowledge regarding the compound and target of interest. Ligand based drug design relies on knowledge of a compound or compounds of interest (i.e., ligands) to derive new compounds that will, in theory, similarly interact with the target of interest to elicit the activity of interest. Conversely, structure based drug design relies on knowledge of the three dimensional structure of the target of interest (i.e., receptor, ion channel, or enzyme) to derive new compounds that will, in theory, interact with the target of interest to elicit the activity of interest. In either case, the compounds derived from these techniques (applied alone or in combination) are then subjected to in vitro testing for validation. The Level of Predictability in the Art : Once a compound has been identified by ligand based and/or structure based drug design methods as potentially binding to the target molecule, it must be evaluated. However, as discussed by Anderson (Chem and Biol 10:787-797, 2003), “it is important to consider that the ranking assigned by the scoring function is not always indicative of a true binding constant, since the model of the target:ligand interaction is inherently an approximation. Usually, several molecules which scored well during the docking run are evaluated in further tests since even the top scoring molecule could fail in vitro assays… Finally, leads are brought into the wet lab for biochemical evaluation” (Page 794, Column 1). By that point, as noted by Thiel (Nature Biotechnol 2:513-519, 2004), “libraries are small and hit rates are on the order of one in ten” (Page 517, Column 2). This low level of predictability is not surprising considering that even minor structural changes can, and frequently will, drastically alter or eradicate a parent compound’s ability to modulate the activity of a specific receptor or enzyme. Indeed, modifying even a single atom in a compound can dramatically change the compound’s overall structure and - even though complementarity in one portion of the compound might be improved by the chemical revision - the overall binding or activity might be severely compromised. Thi s is certainly true in the case. The Amount of Direction Provided by the Inventor / Existence of Working Examples : The amount of direction provided by the Applicant is considered to be determined by the Specification and the working examples. In the instant case, the Specification discloses approximately 16 examples of compounds shown in claim 7. The claims include thousands of different compounds . Further, the Specification provides a total of 17 examples and in those examples the subjects/assays show treatment of acute kidney injury, hypertensive rats, an Alport disease knockout mouse (i.e., a rare kidney disease) , a model of diabetic nephropathy, kidney disease, DN, FSGS, PKD, and Alport Syndrome. Further, there is no t one single example of preventi ng of any condition , and there is no t one example directed towards depression, anxiety, or any form of cancer . Scope or Breadth of the Claims : As stated in MPEP 2164.01(c), “when a compound or composition claim is not limited by a recited use, any enabled use that would reasonably correlate with the entire scope of that claim is sufficient to preclude a rejection for nonenablement based on how to use” (emphasis added). Thus, as stated in MPEP 2164.08, “[t]he focus of the examination inquiry is whether everything within the scope of the claim is enabled” (emphasis added). Indeed, the Federal Circuit has repeatedly held that “the specification must teach those skilled in the art how to make and use the full scope of the claimed invention without ‘undue experimentation’.” In re Wright , 999 F.2d 1557 (Fed. Cir. 1993) (emphasis added). At the same time, however, it is also recognized that not everything necessary to practice the invention need be disclosed. Nor is it necessary that an Applicant test all the embodiments of his invention. In re Angstadt , 537 F.2d 498 (CCPA 1976) (emphasis added). In fact, as stated by the court in In re Buchner , 929 F.2d 660 (Fed. Cir. 1991), a patent need not teach, and preferably omits, what is well known in the art. Accordingly, for purposes of enablement, the relevant concern is whether the scope of enablement provided to one skilled in the art by the disclosure is commensurate in scope with the protection sought by the claims. Thus, while “a patent application is entitled to claim his invention generically” it is necessary that “he provide a disclosure sufficient to enable one skilled in the art to carry out the invention commensurate with the scope of his claims". Amgen, In c . , v. Chugai Pharmaceutical Co., Ltd . (Fed. Cir. 1991). As noted by the court in In re Fisher , 427 F.2d 833 (CCPA 1970), the scope of enablement must bear a “reasonable correlation” to the scope of the claims. See also Ak Steel Corp. v. Sollac , 344 F.3d 1234 (Fed. Cir. 2003) and In re Moore , 439 F.2d 1232 (CCPA 1971). As stated in MPEP 2164.08, resolution of this concern requires two stages of inquiry: “[t]he first is to determine how broad the claim is with respect to the disclosure. The entire claim must be considered. The second inquiry is to determine if one skilled in the art is enabled to make and use the entire scope of the claim without undue experimentation”. As to the first inquiry, as discussed above, the claims are drawn to compounds of Formula (I ) or (II) , which are alleged by the Specification to inhibit TRPC5 and prevent and treat cancer, kidney disease, depression, and anxiety. Yet, as discussed above, the instant Specification discloses approximately 17 similarly structured compound s pecies encompassed by Formula (I ) - yet such structural deviations pale in comparison to the drastic breadth of the claimed compounds. Similarly, treatment is shown in a for hypertension and kidney diseases, without any form of prevention or showing relating to any form of cancer, e.g. There is also no established link among the claimed biomarkers to all of the conditions claimed. According to Dagon et al. , Urinary Rac1, a Novel Predictive Biomarker, Is Elevated in FSGS and Diabetic Nephropathy Patients and Reduced by TRPC5 Inhibition with GFB-887 in a Rat FSGS Model PO1965 ,” J Am Soc Nephrol 31: 2020, while urinary Rac1 concentrations were elevated in FSGS and DN, they were not elevated in Alport patients. Alport syndrome is characterized by kidney disease. Thus, not all kidney diseases, let alone anxiety, and all forms of cancer are necessarily able to rely upon urinary Rac1 levels as a threshold biomarker for determining treatment. Further, Golden et al. , “ Epigenetic regulation of RAC1 induces synaptic remodeling in stress disorders and depression ,” Nature Medicine Volume 19, Number 3, March 2013 , teaches: Golden teaches that there is a sustained reduction in Rac1 expression after chronic social defeat stress and depression-related behavior . Overexpression of Rac1 after chronic social defeat stress reverses depression-related behaviors. See Abstract. Models of social stress are useful for underlying mood or anxiety-related disorders as well. See p338, 1 st full par. The model captures depression, PTSD, and social anxiety too. Chronic stress is concluded to induce long-term transcriptional downregulation of Rac1. Ho p kins Corey (WO2019/051197) teaches: A majority of FSGS yield a functional consequence of excess Rac1 signaling in podocytes. See par.’s 2 and 3. As such, Golden and Hopkins Corey provides differing and nuanced insight into the overexpression and/or downregulation of Rac1 in claimed conditions at least with respect to when such levels are assessed. Such timing is not requir ed. As such, the claim is extremely broad with respect to the disclosure. The second inquiry is discussed in detail below. Amount of Experimentation Necessary : In view of all of the foregoing, at the time the invention was made, it would have required undue experimentation to practice the entire scope of the invention as claimed. As discussed above, the claims are drawn to compounds of Formula ( I ) and (II) , which are alleged by the Specification to inhibit TRPC5 and prevent and treat kidney diseases, cancers, depression, and anxiety . Since identifying any compound which is capable of modulating the activity of a specific receptor, ion channel, or enzyme is extremely complex, the nature of the instant invention considered to be one of extreme complexity. Although the relative skill of those in the art to which the invention pertains is high, the state of the art and unpredictability within the art is such that even the most talented artisan (armed with screening techniques including computer assisted virtual screening techniques such as ligand-based and structure-based design methods) could not reasonably predict which of the structural changes and embodiments of compounds encompassed by Formula ( I ) or (II) would exert the alleged activity based on the limited disclosure shown in the Specification with regard to efficacy . Although the skilled artisan would have known that certain chemical modifications to the disclosed compounds may predictably provide structurally related compounds having similarly activity, the skilled artisan would have also known that even minor structural changes can, and frequently will, drastically alter or eradicate a parent compound’s ability to modulate the activity of a specific receptor or enzyme. Thus, in order to identify usable c ompounds of Formula (I ) or (II) , the skilled artisan (at minimum) would have to carry out ligand based drug design methods using the similarly structured 17 disclosed compounds as a starting point and, assuming the structure of the target receptor was known, combine the findings with data derived from structure based drug design methods to arrive at a small library of “lead” compounds believed to possess the activity of interest. The skilled artisan would then synthesize lead compounds that are within Formula (I) or (II) for in vitro testing. At this point, however, even "the top scoring molecule could fail in vitro assays” (Page 794, Column 1) and “hit rates are on the order of one in ten” (Page 517, Column 2). Given the unpredictability of the claimed compounds , as evidenced by Table 3 of the instant Specification , it is highly unpredictable whether any compound within the sub genus of compounds of Formula ( I ) or (II) identified by rational drug design based on the instant disclosure would, in fact, be usable. Whether t he other compounds of Formula ( I ) or (II) (i.e., those not identified by rational drug design based on the instant disclosure) would be usable is even less predictable. As such, the only way to ascertain which of the conditions among the many that can be treated with specific claimed compounds would require undue experimentation. This merely arrives at usable compounds to test for prevention and treatment of all forms of cancers, kidney disease, anxiety and depression. That is, the only way one skilled in the art is enabled to use the entire scope of the claim based on the instant disclosure entails undue experimentation. To overcome this rejection , Applicant should narrow the scope of the claims such that they bear a reasonable correlation with the disclosure. Claim Rejections - 35 USC § 103 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. Claim s 1, 2, 20, and 22 are rejected under 35 U.S.C. 103 as being unpatentable over Chong et al. , (US2011/0319417) , in view of Golden et al. , “ Epigenetic regulation of RAC1 induces synaptic remodeling in stress disorders and depression ,” Nature Medicine Volume 19, Number 3, March 2013 and in view of Robins et al. , “Rac1 activation in podocytes induces the spectrum of nephrotic syndrome,” Kidney International (2017) 92, 349–364 . Chong teaches methods of treating pain and anxiety by modulating TRPC5 by inhibiting TRPC5-medited ion flux. See par. 3. TRPC5 can be used to treat and prevent anxiety, including OCD, GAD, and others. See par. 102. Prior art claims 1 and 2 are directed to a method of administering a TRPC5 antagonist to treat a subject with anxiety. Pharmaceutically acceptable carriers and excipients can be used with the active agent. See par.’s 126-128, e.g. Golden teaches that there is a sustained reduction in Rac1 expression after chronic social defeat stress and depression-related behavior . Overexpression of Rac1 after chronic social defeat stress reverses depression-related behaviors. See Abstract. Models of social stress are useful for underlying mood or anxiety-related disorders as well. See p338, 1 st full par. The model captures depression, PTSD, and social anxiety too. Chronic stress is concluded to induce long-term transcriptional downregulation of Rac1 . Robins teaches that in familial protein uric diseases in humans, Rac1 activations plays an important role. Prolonged Rac1 activation causes podocyte shedding. See p352, 5 th par. The urinary loss of podocytes was confirmed. Further, podocyte loss causes the development of histological changes that resemble FSGS in humans. See p353, 1 st par. Severity of proteinuria correlates with degree of expression of the Rac1 transgene . Rac1 activation caused a spectrum of phenotypes including MCD to FSGS. In the current study, the shedding of transgene expressing podocytes into the urine was clearly observed after 1 month. See p360, 2 nd full par. It would have been prima facie obvious to a person having ordinary skill in the art prior to the filing of the instant application to arrive at the claimed methods in view of the cited prior art. One would be motivated to do so because TRPC5 inhibitors are taught to treat anxiety. Further, the relationship of Rac1 levels after chronic social defeat stress, which is a model for anxiety as well as mood and other disorders is recognized and understood. Even further, the ability to measure levels of Rac1 in the urine of a subject wa s described bv Robins. As such, when a subject has an anxiety disorder, the corresponding degree of expression of Rac1 would be expected, which includes an initial overexpression which can ultimately yield a transcriptional downregulation of Rac1 in chronic stress . In any event, when a subject has a severe or other form of anxiety, e.g., it would be obvious to administer an agent known to treat the same. In a chronic stress environment, an elevated level would be expected and measurable in the urine of a subject. As such, there is a reasonable and predictable expectation of success in arriving at the claimed method in view of the cited prior art. Claim s 1, 2, 12-17, 20, and 22 are rejected under 35 U.S.C. 103 as being unpatentable over Greka et al . , (US20110135574), in view of Richter et al. , “ Clemizole Hydrochloride Is a Novel and Potent Inhibitor of Transient Receptor Potential Channel TRPC5 ,” Mol Pharmacol 86:514–521, November 2014 , in view of Ho p kins Corey (WO2019/051197) (filed September 7, 2018) , in view of Robins et al. , “Rac1 activation in podocytes induces the spectrum of nephrotic syndrome,” Kidney International (2017) 92, 349–364 . Greka teaches treating kidney disease s by administering a TRPC5 inhibitor. See prior art claim 1. Richter teaches Clemizole HCl is a potent TRPC5 inhibitor. See Abstract. Pharmacological inhibition of TRPC5 is a promising target for protecting the glomerular filter barrier in kidney injury. See p514, 1 st full par. Clemizole is shown below: Hopkins Corey teaches TRPC5 inhibitors protect podocytes and/or treat kidney disease. See Abstract. A majority of FSGS yield a functional consequence of excess Rac1 signaling in podocytes. See par.’s 2 and 3. Robins teaches that in familial protein uric diseases in humans, Rac1 activations plays an important role. Prolonged Rac1 activation causes podocyte shedding. See p352, 5 th par. The urinary loss of podocytes was confirmed. Further, podocyte loss causes the development of histological changes that resemble FSGS in humans. See p353, 1 st par. Severity of proteinuria correlates with degree of expression of the Rac1 transgene. Rac1 activation caused a spectrum of phenotypes including MCD to FSGS. In the current study, the shedding of transgene expressing podocytes into the urine was clearly observed after 1 month . See p360, 2 nd full par It would appear that a subject with excessively high levels of Rac1 would identify a subject with kidney disease including FSGS, among others. Such identification would be present in expressing podocytes in the urine and severe proteinuria as a correlate to Rac1. TRPC5 inhibitors are known to protect podocytes and treat kidney disease. As such, clemizole as a known potent inhibitor of TRPC5 and as explicitly taught to treat kidney disease would be administered to this same subject population. In view of the known relationship of urine expressing podocytes and relationship to Rac1 levels being excessively high as an identifier of the same, it would be obvious to determine a level of Rac1 that is normal and when such level is tested in a subject that is suspected of having FSGF, e.g., understand that an excessively high level of Rac1 would confirm the same. If such subject has FSGS in view of excessively high Rac1, it would be obvious to treat that subject with clemizole or another TRPC5 inhibitor because they are known to treat these same conditions and protect podocytes and treat kidney disease. If a subject is shown to have extremely high levels of Rac1 in urinary podocytes, it would appear to be inclusive of those subjects with levels above 75% and 90% compared to a control. An excessively high level would also appear to include levels above 100 pg/mL, e.g. Absent a showing of a criticality associated with a claimed level, an excess of Rac1 would appear to be taught and would not exclude the highest levels tested. As such, there is a reasonable and predictable expectation of success in arriving at the claimed method in view of the cited prior art. 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 . Claim s 1-6, 12-17, 20, and 22 are rejected on the ground of nonstatutory double patenting a s being unpatentable over claims 1-20 of U.S. Patent No. 11,046,690 , in view of Ho p kins Corey (WO2019/051197) (filed September 7, 2018), in view of Robins et al. , “Rac1 activation in podocytes induces the spectrum of nephrotic syndrome,” Kidney International (2017) 92, 349–364 , as applied above . Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ‘690 patent are directed to method of treating kidney disease with the claimed compounds. Claim s 1-6, 12-17, 20, and 22 are rejected on the ground of nonstatutory double patenting a s being unpatentable over claims 1-4 of U.S. Patent No. 10,654,850 , in view of Ho p kins Corey (WO2019/051197) (filed September 7, 2018), and in view of Robins et al. , “Rac1 activation in podocytes induces the spectrum of nephrotic syndrome,” Kidney International (2017) 92, 349–364 , as applied above . Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ‘850 patent are directed to claimed compounds. Further, the use of the claimed compounds are for treating kidney diseases in a subject in need thereof. Claim 1-6, 12-17, 20, and 22 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 7, and 17 of copending Application No. 16/575,161 , in view of Ho p kins Corey (WO2019/051197) (filed September 7, 2018), and in view of Robins et al. , “Rac1 activation in podocytes induces the spectrum of nephrotic syndrome,” Kidney International (2017) 92, 349–364 , as applied above . . Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ‘161 application are directed to claimed compounds. Further, the use of the claimed compounds are for treating kidney disease, anxiety, depression, and others in a subject in need thereof. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. Claim s 1-6, 12-17, 20, and 22 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 13, and 16-29 of copending Application No. 1 7/360,303 , in view of Ho p kins Corey (WO2019/051197) (filed September 7, 2018), and in view of Robins et al. , “Rac1 activation in podocytes induces the spectrum of nephrotic syndrome,” Kidney International (2017) 92, 349–364 , as applied above . Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the ‘303 application are directed to method of treating kidney disease, anxiety, depression, and others in a subject in need thereof. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. As such, no claim is allowed. Conclusion Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT JARED D BARSKY whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-2795 . The examiner can normally be reached on FILLIN "Work schedule?" \* MERGEFORMAT 9-5 M-F . If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Amy Clark can be reached on 571-272-1310. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of an application may be obtained from the Patent Application Information Retrieval (PAIR) system. Status information for published applications may be obtained from either Private PAIR or Public PAIR. Status information for unpublished applications is available through Private PAIR only. For more information about the PAIR system, see http://pair-direct.uspto.gov. Should you have questions on access to the Private PAIR system, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative or access to the automated information system, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /JARED BARSKY/ Primary Examiner, Art Unit 1628