NON-FINAL REJECTION
Receipt is acknowledged of Applicants' Amendments and Remarks, filed Feb. 20, 2026.
Rejections and/or objections not reiterated from previous Office Actions are hereby withdrawn. The rejections and/or objections set forth below are either maintained or newly applied, and constitute the complete set presently applied to the instant claims.
STATUS OF THE CLAIMS
Claims 1 and 3-8 have been amended and incorporate no new matter.
No new claims have been added.
Claim 6 stands withdrawn as drawn to nonelected species.
Thus, claims 1-5 and 7-11 now represent all claims currently pending and under consideration.
INFORMATION DISCLOSURE STATEMENT
The information disclosure statement (IDS) submitted on Nov. 24, 2025 was filed after the mailing date of the non-final action on Nov. 21, 2025. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
MAINTAINED REJECTIONS
The following rejections are maintained from the previous Office Action dated Nov. 21, 2025, on the ground that the references cited therein continue to read on the limitations of the amended claims.
Claim Rejections - 35 USC § 103
Claims 1-5 and 7-11 stand rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Bae et al. (US 2015/0218125), in view of Cha et al. (Lab. Inv. (97) 419-431 (2017)) and Jeong et al. (PLOS ONE (13)1, 1-22 (2018)).
Bae et al. claim methods of preventing or treating kidney disease comprising administer-ing to a mammal a composition comprising 1-(pyridin-2-yl)-3-phenyl-4-propyl-1H-pyrazol-5-ol (a.k.a. APX-115), or the HCl salt thereof (claim 6; paras. [0009]-[0011]; Examples 1 and 2):
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which reads on formula 1 as recited by claims 1-4.
Bae et al. exemplify the oral administration of APX-115 to mice at a dose of 10
mg/kg/day for 12 weeks (para. [0137]), which implicitly discloses the administration of APX-115 together with a pharmaceutically acceptable carrier or excipient, as recited by claim 11.
The kidney diseases treated or prevented include diabetic kidney disease, hypertensive nephropathy, glomerulonephritis, pyelonephritis, interstitial nephritis, lupus nephritis, polycystic kidney disease, and renal failure (claims 2 and 4).
In particular, Bae et al. exemplify the nephroprotective effects of APX-115 in reducing glomerular size and glomerular mesangial expansion in diabetic kidney disease-induced animal models (Example 11).
Bae et al. differs from the claims in that the reference does not disclose administering APX-115 to reduce contrast-induced nephrotoxicity (a.k.a. contrast-induced nephropathy, CIN), or to treat or prevent contrast-induced acute kidney injury (CI-AKI), as recited by claim 1.
However, diabetic kidney disease (DKD) and contrast-induced nephrotoxicity were known to share an overlapping etiology.
For example, Cha et al. show that treating diabetic nephropathy in db/db mice by administering APX-115 decreases Nox1, Nox2, and Nox4 protein expression in the kidney, thereby reducing the production of ROS (reactive oxygen species) and thus oxidative stress; as well as significantly improving mesangial expansion (abstract).
Further, Cha et al. compare APX-115 to the dual Nox1/Nox4 inhibitor GKT-137831, having the structural formula,
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and conclude that pan-Nox inhibition by APX-115 may provide better renoprotection than GKT-137831 in diabetic nephropathy (p. 430, right col.).
Jeong et al. teach that contrast-induced acute kidney injury (CI-AKI) is a leading cause of acute kidney injury following radiographic procedures, due to oxidative stress in the kidney.
Specifically, Jeong et al. report that the contrast agent iohexol, as recited by claims 5, 7, and 8, causes increased Nox4 expression in HK-2 kidney cells, causing tubular apoptosis and necrosis (pp. 13-15), as recited by claim 9; and an increase in ROS (reactive oxygen species) and oxidative stress (Table 1), as recited by claim 10.
Jeong et al. show that pretreatment with GKT-137831 in a CI-AKI mouse model reduced iohexol renotoxicity, suggesting Nox4 as a key source of reactive oxygen species responsible for CI-AKI, and providing a potential option for prevention of CI-AKI (abstract).
Thus, Nox4 inhibition was known to reduce ROS production and oxidative stress in both diabetic kidney disease (DKD) and in contrast-induced acute kidney injury (CI-AKI); and Cha et al. suggest that APX-115 provides better renoprotection in DKD than GKT-137831.
Therefore, it would have been predictable to one of ordinary skill in the art as of the effective filing date to administer APX-115 to reduce nephrotoxicity induced by a contrast agent, e.g., iohexol, with a reasonable expectation of success, because upregulated Nox4, causing increased ROS and oxidative stress, was known to be a significant mechanism of kidney injury in both DKD and CI-AKI; both APX-115 and GKT-137831 were known to inhibit Nox4; and APX-115 was taught to be a more effective renoprotectant in DKD than GKT-137831.
As recognized by MPEP §2143, combining prior art elements according to known methods to yield predictable results would motivate the skilled artisan to modify the references with a reasonable expectation of success. The rationale to support a conclusion of prima facie obviousness is that all the claimed elements were known in the prior art, and a skilled artisan could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results to one of ordinary skill in the art. See KSR Int'l Co. v. Teleflex Inc. (550 U.S. 398, 409).
Double Patenting
Claims 1-5 and 7-11 stand rejected on the ground of nonstatutory double patenting as being unpatentable over claims 4-5 of U.S. Patent No. 11,174,240 in view of Cha et al. (Lab. Inv. (97) 419-431 (2017)) and Jeong et al. (PLOS ONE (13)1, 1-22 (2018)).
Reference claims 4-5 recite methods for treatment of a disease mediated by reactive oxygen species (ROS) comprising administering an effective amount of crystalline 3-phenyl-4-propyl-1-(pyridin-2-yl)-1H-pyrazol-5-ol hydrochloride (a.k.a. APX-115 HCl) to a subject in need thereof, wherein the disease mediated by reactive oxygen species (ROS) is selected from, inter alia, diabetic nephropathy (a.k.a. diabetic kidney disease, DKD).
The compound recited by the reference claims reads on formula 1 as recited by examined claims 1-2, and is identical to the compound recited by examined claims 3-4.
It is implicit in administering an effective amount of APX-115 HCl to a subject in need thereof that the compound is administered together with a pharmaceutically acceptable carrier or excipient, as recited by examined claim 11.
The reference claims differ from the examined claims in that the reference claims do not disclose administering APX-115 to treat or prevent the specific contrast agent-induced kidney disease claimed, i.e., to reduce contrast-induced nephrotoxicity (a.k.a. contrast-induced nephropathy, CIN), or to treat or prevent contrast-induced acute kidney injury (CI-AKI), as recited by examined claim 1.
However, diabetic kidney disease (DKD) and contrast-induced acute kidney injury (CI-AKI) were known to share an overlapping etiology.
For example, Cha et al. show that treating diabetic nephropathy in db/db mice by administering APX-115 decreases Nox1, Nox2, and Nox4 protein expression in the kidney, thereby reducing the production of ROS (reactive oxygen species) and thus oxidative stress; as well as significantly improving mesangial expansion (abstract).
Further, Cha et al. compare APX-115 to the dual Nox1/Nox4 inhibitor GKT-137831, and conclude that pan-Nox inhibition by APX-115 may provide better renoprotection than GKT-137831 in diabetic nephropathy (p. 430, right col.).
Jeong et al. teach that contrast-induced acute kidney injury (CI-AKI) is a leading cause of acute kidney injury following radiographic procedures, due to oxidative stress in the kidney.
Specifically, Jeong et al. report that the contrast agent iohexol, as recited by examined claims 5, 7, and 8, causes increased Nox4 expression in HK-2 kidney cells, causing tubular apoptosis and necrosis (pp. 13-15), as recited by examined claim 9; and an increase in ROS (reactive oxygen species) and oxidative stress (Table 1), as recited by examined claim 10.
Jeong et al. show that pretreatment with GKT-137831 in a CI-AKI mouse model reduced iohexol renotoxicity, suggesting Nox4 as a key source of reactive oxygen species responsible for CI-AKI, and providing a potential option for prevention of CI-AKI (abstract).
Thus, Nox4 inhibition was known to reduce ROS production and oxidative stress in both diabetic kidney disease (DKD) and in contrast-induced acute kidney injury (CI-AKI); and Cha et al. suggest that APX-115 provides better renoprotection in DKD than GKT-137831.
Therefore, it would have been predictable to one of ordinary skill in the art as of the effective filing date to administer APX-115 to prevent CI-AKI or to reduce nephrotoxicity induced by a contrast agent, e.g., iohexol, with a reasonable expectation of success, because upregulated Nox4, causing increased ROS and oxidative stress, was known to be a significant mechanism of kidney injury in both DKD and CI-AKI; both APX-115 and GKT-137831 were known to inhibit Nox4; and APX-115 was taught to be a more effective renoprotectant in DKD than GKT-137831.
As recognized by MPEP §2143, combining prior art elements according to known methods to yield predictable results would motivate the skilled artisan to modify the references with a reasonable expectation of success. The rationale to support a conclusion of prima facie obviousness is that all the claimed elements were known in the prior art, and a skilled artisan could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results to one of ordinary skill in the art. See KSR Int'l Co. v. Teleflex Inc. (550 U.S. 398, 409).
RESPONSE TO ARGUMENTS
Applicant's arguments filed Feb. 20, 2026 have been fully considered but they are not persuasive.
With regard to the rejection under 35 U.S.C. 103 over Bae et al., Cha et al., and Jeong et al., Applicant argues that there are no teachings nor implementations that suggest the compounds disclosed in the cited references could also be applied to kidney injury induced by contrast medium (CI-AKI). The instant disclosure identifies ischemic injury and direct tubular cell injury as the main causes of contrast media-induced acute kidney injury (Remarks, p. 7).
Applicant argues that Bae, Cha, and Jeong do not teach administering APX-115 to treat or prevent CI-AKI or to reduce contrast-induced nephrotoxicity, as recited by claim 1.
In particular, Applicant contends argues that Cha's "better than GKT-137831" conclusion is made only in the DKD context and does not teach that broader NOX inhibition will translate to efficacy in CI-AKI (Remarks, p. 8). Similarly, Jeong's CI-AKI results are limited to GKT-137831; nor does Jeong teach that inhibiting additional NOX isoforms beyond Nox4 would be desirable (or at least not harmful) in the acute CI-AKI context (Remarks, pp. 8-9).
Applicant argues that an expectation of success depends on importing Cha's DKD-centric comparative statement into Jeong's CI-AKI setting, but the cited record provides no basis to predict that APX-115's DKD performance relative to GKT-137831 would translate to iohexol CI-AKI (Remarks, p. 9).
Next, Applicant argues that it is not obvious to a person skilled in the art to expect a similar pharmaceutical effect of an identical compound in different diseases. Due to the complexity of pharmacological actions and the inherent complexity of chemical compounds and their mechanisms of action, applying an identical compound to different diseases is quite difficult. Kidney injury induced by contrast media is undoubtedly different from kidney injury caused by other diseases. Therefore, even a person skilled in the art would not be able to establish the use of the present invention based on the disclosures in the asserted references (Remarks, p. 9).
To support these assertions, Applicant argues that Exhibit 1 and Exhibit 2 provide support for distinguishing diseases based on their pathogenesis (Remarks, pp. 9-10).
Applicant contends that Exhibit 1 (Fioretto et al., SGLT2 Inhibitors and the Diabetic Kidney (2016)) shows that SGLT2 inhibitors are effective in treating kidney injury caused
by diabetes by reducing glomerular hyperfiltration in diabetic patients, and demonstrates that SGLT2 inhibitors can mitigate the adverse effects of diabetes on the kidneys (Remarks, p. 10).
Applicant contends that Exhibit 2 (Wang et al., Unveiling the Mysteries of Contrast-Induced Acute Kidney Injury: New Horizons in Pathogenesis and Prevention (2024)) teaches that SGLT2 inhibitors are identified as one of the main risk factors for contrast media-induced kidney injury. This contradiction arises due to the complexity of pharmacological actions and the inherent complexity of chemical compounds and their mechanisms of action. Although the consequence of both pathogeneses may result in kidney injury, the differences in their underlying causes lead to distinct treatment mechanisms (Remarks, pp. 10-11).
Applicant contends that the efficacy of SGLT2 inhibitors is primarily due to the disease's association with diabetes, yet are also considered a major risk factor for contrast media-
induced kidney injury. Thus, CI-AKI follows a different pathogenesis than that of diabetes-related kidney injury, and are fundamentally different diseases, requiring distinct treatment approaches (Remarks, p. 11).
Applicant contends that a skilled artisan cannot be certain that APX-115 treats kidney injury independently of its association with diabetes; and would not expect that a compound effective for treating diabetic kidney injury would exhibit the same effectiveness for treating contrast media-induced kidney injury, due to the inherent complexity of pharmacological actions and the potential for varied drug responses across different diseases (Remarks, pp. 11-12).
Thus, Applicant argues that the cited references do not establish a reasonable expectation that administering APX-115 prior to and/or simultaneously with contrast medium administration, would succeed in CI-AKI. Bae and Cha evaluate APX-115 in DKD/chronic contexts, which do not predict efficacy in CI-AKI's acute mechanism and therapeutic window. Jeong's CI-AKI disclosure pertains to a different inhibitor and does not teach that APX-115 would predictably provide the same benefit. The rejection therefore lacks the required reasonable-expectation-of-success showing and instead relies on hindsight (Remarks, p. 12).
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
In addition, the test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981).
As discussed above, Bae et al. disclose and claim methods of administering the claimed compound, APX-115, to treat or prevent both diabetic and non-diabetic kidney diseases, including hypertensive nephropathy, glomerulonephritis, pyelonephritis, interstitial nephritis, lupus nephritis, polycystic kidney disease, and renal failure (claim 4). Thus, a skilled artisan would have had a reasonable expectation that the claimed compound would be effective for treating a broad range of kidney diseases, regardless of its mechanism or etiology.
As recognized by MPEP §2123, a reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill the art, including alternative or non-preferred embodiments. Merck & Co. v. Biocraft Laboratories, 874 F.2d 804, 10 USPQ2d 1843 (Fed. Cir.), cert. denied, 493 U.S. 975 (1989).
Applicant cites Fioretto et al. ("SGLT2 Inhibitors and the Diabetic Kidney" (2016)) as Exhibit 1, to support the argument that some drugs known to treat diabetic kidney disease also exacerbate CI-AKI. However, this knowledge would have no bearing on a skilled artisan's expectations with regard to the claimed compounds, which are not SGLT2 inhibitors.
Applicant also cites Wang et al. ("Unveiling the Mysteries of CI-AKI: New Horizons in Pathogenesis and Prevention" (2024)) as Exhibit 2. However, because Wang et al. was published in 2024, it could not have informed the knowledge or expectations of a skilled artisan as of the effective filing date (Apr. 8, 2020), and thus has no probative value.
In addition, rejections under 35 U.S.C. 103 must be supported by a reasonable expectation of success – not a guaranteed or certain expectation of success. As recognized by MPEP § 2143.02(I), conclusive proof of efficacy is not required to show a reasonable expectation of success. OSI Pharm., LLC v. Apotex Inc., 939 F.3d 1375, 1385, 2019 USPQ2d 379681 (Fed. Cir. 2019); the expectation of success need only be reasonable, not absolute. Pfizer, Inc. v. Apotex, Inc., 480 F.3d 1348, 1364, 1367–68 (Fed. Cir. 2007).
It is acknowledged that the pathogenesis of both diabetic kidney disease and CI-AKI are each thought to involve multiple mechanisms. The overlapping mechanisms in both diabetic kidney disease (DKD) and contrast-induced nephropathy (CIN) were well known in the art.
For example, Gorin et al. (cited on PTO-892) teach that NADPH oxidases of the Nox family are a major source of reactive oxygen species in the diabetic kidney (abstract). Ample in vivo and in vitro experimental evidence supports a role for the Nox family of NADPH oxidases, particularly Nox4, in the pathogenesis and pathophysiology of diabetic nephropathy (DN). Orally administrable small-molecule inhibitors from the pyrazolo pyridine chemical series, particularly GKT-136901 and GKT-137831, effectively attenuate the pathological changes observed in renal complications of diabetes. Although the mechanisms by which these compounds inhibit Nox4 and Nox1 remain unclear, they may act as competitive inhibitors because their structures resemble that of NADPH (p. 137, right col.).
As shown below, APX-115 is structurally similar to GKT-136901 and GKT-137831, and thus may also act as a competitive inhibitor of NADPH:
APX-115
(claimed compound)
GKT-137831
GKT-136901
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Further, Heyman et al. (cited on PTO-892) teach that renal hypoxia, combined with the generation of reactive oxygen species, plays a central role in the pathogenesis of CIN, and the diabetic kidney is particularly susceptible to intensified hypoxic and oxidative stress following the administration of contrast media (abstract). Heyman et al. detail the overlapping mechanisms in both DKD and contrast-induced kidney injury, and depict this overlap in Fig. 1:
Heyman et al. teach that diabetes and the administration of iodinated radiocontrast agents are both associated with marked alterations of renal physiology, including changes in GFR and renal hemodynamics, enhanced tubular transport activity and oxygen expenditure and intensification of medullary hypoxia, and ROS generation (p. 6, left col.).
Thus, it was known in the art that diabetic kidney disease shares multiple mechanisms of pathogenesis with contrast-induced kidney injury; that Nox4 plays a key role in both DKD and CI-AKI; and that structurally similar Nox inhibitors were effective in treating DKD.
The nexus between the cited references are the common mechanisms shared by DKD and CI-AKI – increased intrarenal oxidative stress, caused by activation of NADPH oxidases – which is reduced by administration of a Nox inhibitor, with Cha et al. explicitly suggesting that the pan-Nox inhibitor APX-115 may provide better protection than the dual Nox1/Nox4 inhibitor GKT-137831 in diabetic nephropathy. On this basis, one of ordinary skill in the art would have had a reasonable expectation that a Nox4 inhibitor effective to treat diabetic kidney disease would also be effective to treat contrast-induced kidney injury.
Third, Applicant contends that the present invention clearly demonstrates unexpected technical effects. Applicant argues that, while the cited references describe certain effects, they are insufficient to arrive at, predict, or expect the superior effects demonstrated by the claimed method, as shown in Figs. 3-8 of the present application, specifically:
1) The albumin level reduction achieved is nearly one-third of that in the non-treated
group, showing a significant difference from the effect observed in Cha.
2) The MCP-1 reduction in the present invention is more pronounced than in Cha.
3) The ROS reduction, confirmed by DHE staining, is close to one-fourth of the non-
treated group, whereas Cha only achieved a reduction to one-third.
4) The F4/80 marker exhibits a significantly stronger effect in the present invention
compared to Bae.
Applicant asserts that these findings could not could not have been predicted from the cited references; demonstrate that the pharmaceutical effects of the same compound can vary depending on the underlying pathological mechanisms; and show that the same compound cannot simply be applied to another target condition based solely on a few overlapping pharmaceutical effects (Remarks, pp. 13-14).
As recognized by MPEP §716.02, where Applicant alleges unexpected results, 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. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986) (differences in sedative and anticholinergic effects between prior art and claimed antidepressants were not unexpected).
To overcome a rejection under 35 U.S.C. § 103, evidence of unexpected results must be commensurate with the scope of the claims. As recognized by MPEP §716.02(d),
Whether the unexpected results are the result of unexpectedly improved results or a property not taught by the prior art, the “objective evidence of non-obviousness must be commensurate in scope with the claims which the evidence is offered to support.” In other words, the showing of unexpected results must be reviewed to see if the results occur over the entire claimed range. In re Clemens, 622 F.2d 1029, 1036, 206 USPQ 289, 296 (CCPA 1980).
This is addressed by the new rejection set forth infra.
With regard to the double patenting rejection, Applicant asserts that the reference claims in combination with Cha and Bae do not suggest administering the compound of Formula I prior to and/or concurrently with contrast medium administration to attain the recited effects, and are thus patentably distinct from the examined claims (Remarks, p. 14).
As discussed above, the cited references would have led a skilled artisan to reasonably expect that pretreatment with APX-115 would reduce nephrotoxicity induced by a contrast agent, e.g., iohexol, because upregulated Nox4, causing increased ROS and oxidative stress, was known to be a significant mechanism of kidney injury in both DKD and CI-AKI; both APX-115 and GKT-137831 were known to inhibit Nox4; and APX-115 was taught to be a more effective renoprotectant in DKD than GKT-137831.
For the foregoing reasons, the rejections of claims 1-5 and 7-11 under 35 U.S.C. §103 and on the ground of obviousness-type double patenting are maintained.
NEW REJECTIONS
Claim Rejections - 35 U.S.C. § 112(b) – Indefiniteness
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 1-5 and 7-11 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 pre-AIA the applicant regards as the invention.
As recognized by MPEP § 2173.05(c)(III), the common phrase "an effective amount" may or may not be indefinite. The proper test is whether or not one skilled in the art could determine specific values for the amount based on the disclosure. See In re Mattison, 509 F.2d 563, 184 USPQ 484 (CCPA 1975).
Here, independent claim 1 is drawn to a method of protecting a kidney by reducing contrast media-induced nephrotoxicity in a mammal or for preventing or treating contrast media-induced acute kidney injury in a mammal, comprising administering an effective amount of a compound of following Formula 1 or a pharmaceutically acceptable salt thereof to the mammal:
However, the specification fails to define or quantify the "effective amount" of a compound of formula (I) that achieves the claimed results; nor does it provide any objective criteria, dose ranges, blood-level targets, minimum efficacy thresholds, or other boundaries that would allow a skilled artisan to determine what amounts fall within or outside the claim scope.
Only a single example is disclosed, in which Compound 1 was orally administered to 6-week-old male mice at a dose of 60 mg/kg daily for 5 days before administration of contrast media (pp. 21-25). The specification provides no accompanying dose-response data or other guidance, which is insufficient to clearly define the metes and bounds of the dosage range that constitutes an "effective amount."
Because the specification fails to define or quantify an "effective amount" of a compound of formula (I), one of ordinary skill in the art would be unable to clearly determine the specific amount(s) of the compound to administer to achieve the claimed effects. Accordingly, the term "effective amount" renders the metes and bounds of the claims indefinite.
CONCLUSION
Claims 1-5 and 7-11 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SARA E. TOWNSLEY whose telephone number is 571-270-7672. The examiner can normally be reached on Mon-Fri from 10:00 am to 6:00 pm (EST). If attempts to reach the examiner by telephone are unsuccessful, the examiner's supervisor, Jeff S. Lundgren, can be reached at 571-272-5541. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/SARA E. TOWNSLEY/Examiner, Art Unit 1629
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