DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
The amendment of 11/24/2025 has been entered. Claims 1-12, 14-15, 18-19, 24-25, and 28-33 are currently pending in this US patent application and were examined on their merits.
Information Disclosure Statement
The information disclosure statements filed in this application on 02/12/2025, 04/30/2025, and 11/24/2025 have been received and considered.
Withdrawn Rejections
All rejections of claims 16-17 and 26-27 set forth in the previous Office action are withdrawn in light of the amendment of 11/24/2025, which canceled these claims.
The rejection of the claims under 35 U.S.C. 112(b) as being indefinite for recitation of the undefined term of degree “low KLK1 levels” as set forth in the previous Office action is withdrawn in light of the amendment of 11/24/2025, which defined the low KLK1 levels.
All rejections of the claims under 35 U.S.C. 102 and 35 U.S.C. 103 that did not include discussion of previous claim 2 are withdrawn in light of the amendment of 11/24/2025, which brought the limitations of previous claim 2 into claim 1.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1, 3, 14-15, and 18 remain rejected under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023).
Diamedica discloses a method of treating chronic kidney disease (CKD) in a patient in need thereof, comprising administering to the patient a pharmaceutical composition that comprises one or more tissue kallikrein (KLK1) polypeptides (“dosing patients with chronic kidney disease…a recombinant form of human tissue kallikrein-1”; see entire document, including page 1, 1st paragraph; page 3, 2nd paragraph), wherein the patient has low KLK1 levels (“…restore normal KLK1 protein levels in patients with CKD…patients with moderate to severe CKD may excrete abnormally low levels of KLK1”; page 1, 2nd and 4th paragraphs; cf. claims 1 and 14; the Examiner notes that, given the lack of any qualification on the degree of “African descent” in the claims and the knowledge that Homo sapiens originally evolved in Africa, any human, including all of the humans referenced in Diamedica, can be considered to be of “African descent” as recited in instant claim 14). The administered KLK1 protein is DM199 (page 1, 1st paragraph; cf. claim 18). In addition, Diamedica teaches that chronic kidney disease may be caused by focal segmental glomerulosclerosis (page 1, 3rd paragraph; cf. claim 15).
However, Diamedica does not teach that the CKD patients administered DM199 in their method had CKD that was caused by focal segmental glomerulosclerosis as recited in instant claim 15 or the specific levels of KLK1 in the urine of the patient as recited in instant claims 1 and 3.
Naicker teaches that urinary tissue kallikrein excretion was significantly decreased in patients with mild renal disease to 16.6 +/- 6.7 ng/ng protein to and more markedly to 1.8 +/- 0.7 ng TK/microg protein in patients with severe renal failure, which falls within the range of “less than about…40 ng/mL” recited in instant claims 1 and 3 (see entire document, including abstract; cf. claims 1 and 3).
While Diamedica does not teach that the CKD patients administered DM199 in their method had CKD that was caused by focal segmental glomerulosclerosis as recited in instant claim 15, it would have been obvious to one of ordinary skill in the art to examine the effects of DM199 in any CKD patient based on the teachings of Diamedica, including CKD patients with focal segmental glomerulosclerosis. One of ordinary skill in the art would have a reasonable expectation that including patients with CKD of any etiology, including patients whose CKD had arisen from focal segmental glomerulosclerosis as taught by Diamedica, in the DM199 study of Diamedica would successfully produce information regarding the effect of DM199 supplementation in patients with CKD.
While Diamedica does not teach that the CKD patients had urinary KLK1 levels within the levels recited in instant claims 1 and 3, it would have been obvious to one of ordinary skill in the art in light of Diamedica to observe the effects of DM199 on any patients with CKD, including the CKD patients with the urinary KLK1 levels taught by Naicker, and to observe the KLK1 levels in the patients’ urine, as taught by Naicker. One of ordinary skill in the art would have a reasonable expectation that measuring KLK1 levels in patient urine as taught by Naicker and then administering the DM199 of Diamedica to CKD patients with urinary KLK1 levels that fall within the ranges taught by Naicker would successfully produce information regarding the effect of DM199 supplementation in patients with CKD.
Therefore, claims 1, 3, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker and are rejected under 35 U.S.C. 103.
Claims 1-3, 14-15, and 18 are newly rejected as necessitated by amendment under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), and Bovee et al., Am. J. Physiol. Renal Physiol. 319: F729-F745 (2020).
As discussed above, claims 1, 3, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker. Diamedica also teaches that hypertension is one of the primary causes of CKD (page 1, paragraph 3). However, Diamedica and Naicker do not teach that the CKD patient has salt-sensitive hypertension as recited in instant claim 2.
Bovee teaches that CKD causes salt-sensitive hypertension that is often resistant to treatment and contributes to the progression of kidney injury and cardiovascular disease (see entire document, including page F729, abstract; cf. claim 2).
While Diamedica and Naicker not teach that the CKD patients administered DM199 in their method had salt-sensitive hypertension as recited in instant claim 2, it would have been obvious to one of ordinary skill in the art to examine the effects of DM199 in any CKD patient based on the teachings of Diamedica and Naicker, including CKD patients with salt-sensitive hypertension as taught by Bovee. One of ordinary skill in the art would have a reasonable expectation that including any CKD patients, including patients with salt-sensitive hypertension, in the DM199 study of Diamedica would successfully produce information regarding the effect of DM199 supplementation in patients with CKD.
Therefore, claims 1-3, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker and Bovee and are rejected under 35 U.S.C. 103.
Claims 1, 3-5, 14-15, and 18 are newly rejected as necessitated by amendment under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), and Slim et al., J. Am. Soc. Nephrol. 13: 968-976 (2002; cited as reference 448 on the IDS filed 12/27/2023).
As discussed above, claims 1, 3, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker. However, Diamedica and Naicker do not teach that the CKD patients with low urinary KLK1 levels (cf. page 1, 4th paragraph) have the R53H mutation recited in instant claims 4-5.
Slim teaches that an R53H mutation in exon 3 of the KLK1 gene was detected in Afro-Caribbean patients with hypertension and low urinary KLK1 levels (see entire document, including abstract and page 971, left column, paragraph 1; cf. claims 4-5).
While Diamedica and Naicker do not teach that the CKD patients with low urinary KLK1 levels have the R53H mutation recited in instant claims 4-5, it would have been obvious to one of ordinary skill in the art at the time of the invention to screen patients for this mutation because Slim teaches that the R53H mutation is found in subjects with low urinary KLK1 levels. One of ordinary skill in the art would have a reasonable expectation that determining whether the CKD patients with low urinary KLK1 levels who were administered DM199 in the method of Diamedica and Naicker have the particular mutation that is found in patients with low urinary KLK1 levels as taught by Slim would successfully provide information regarding whether DM199 is an effective treatment for CKD patients with the R53H mutation.
Therefore, claims 1, 3-5, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker and Slim and are rejected under 35 U.S.C. 103.
Claims 1, 3-4, 6, 14-15, and 18 are newly rejected as necessitated by amendment under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), and Yu et al., Kidney International 61: 1030-1039 (2002; cited on the IDS filed 12/27/2023).
As discussed above, claims 1, 3, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker. However, Diamedica and Naicker do not teach that the CKD patients with low urinary KLK1 levels (cf. page 1, 4th paragraph) have the 12G promoter allele status recited in instant claims 4 and 6.
Yu teaches that the 12G promoter allele for the KLK1 gene was detected in African American patients with end-stage renal disease and low urinary KLK1 levels (see entire document, including abstract; cf. claims 4 and 6; the Examiner notes that ESRD is a subset of CKD).
While Diamedica and Naicker do not teach that the CKD patients with low urinary KLK1 levels have the 12G promoter allele status recited in instant claims 4 and 6, it would have been obvious to one of ordinary skill in the art at the time of the invention to screen patients for this mutation because Yu teaches that the 12G promoter allele for the KLK1 gene is found in subjects with end-stage renal disease and low urinary KLK1 levels. One of ordinary skill in the art would have a reasonable expectation that determining whether the CKD patients with low urinary KLK1 levels who were administered DM199 in the method of Diamedica and Naicker have the particular 12G promoter allele that is found in patients with ESRD and low urinary KLK1 levels as taught by Yu would successfully provide information regarding whether DM199 is an effective treatment for CKD patients with the 12G promoter allele.
Therefore, claims 1, 4, 6, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker and Yu and are rejected under 35 U.S.C. 103.
Claims 1, 3-4, 7, 14-15, and 18 are newly rejected as necessitated by amendment under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), and Reidy et al., Curr. Opin. Pediatrics 30(2): 252-259 (2018; cited on the IDS filed 12/27/2023).
As discussed above, claims 1, 3, 14-15, and 18 are rendered obvious by Diamedica and Naicker. However, Diamedica and Naicker do not teach that the CKD patients have the APOL1 gene mutations recited in instant claims 4 and 7.
Reidy teaches that three single nucleotide polymorphisms in APOL1 in the G1 and G2 haplotypes result in a high risk of progression to end-stage renal disease (see entire document, including page 2, paragraph 1; cf. claims 4 and 7; the Examiner notes that ESRD is a subset of CKD).
While Diamedica and Naicker do not teach that the CKD patients have the APOL1 gene mutations recited in instant claims 4 and 7, it would have been obvious to one of ordinary skill in the art at the time of the invention to screen patients for these mutations because Reidy teaches that particular mutations in APOL1 in the G1 and G2 haplotypes result in a high risk of progression to end-stage renal disease. One of ordinary skill in the art would have a reasonable expectation that determining whether the CKD patients who were administered DM199 in the method of Diamedica and Naicker have the particular APOL1 mutations in the G1 and G2 haplotypes that result in a high risk of progression to end-stage renal disease as taught by Reidy would successfully provide information regarding whether DM199 is an effective treatment for CKD patients with those particular APOL1 mutations.
Therefore, claims 1, 3-4, 7, 14-15, and 18 are rendered obvious by Diamedica in view of Reidy and are rejected under 35 U.S.C. 103.
Claims 1, 3-4, 8, 14-15, and 18 are newly rejected as necessitated by amendment under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), and Pratt, J. Am. Soc. Nephrol. 16: 3154-3159 (2005; cited on the IDS filed 12/27/2023).
As discussed above, claims 1, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker. However, Diamedica and Naicker do not teach that the CKD patients have the T594M mutation in ENaC recited in instant claims 4 and 8.
Pratt teaches that the T594M variant in the C-terminus of beta-ENaC is associated with hypertension (see entire document, including page 3154, right column, paragraph 2; cf. claims 4 and 8; the Examiner notes that Diamedica teaches that hypertension contributes to the progression of CKD in page 1, paragraph 4).
While Diamedica and Naicker do not teach that the CKD patients have the T594M mutation recited in instant claims 4 and 8, it would have been obvious to one of ordinary skill in the art at the time of the invention to screen patients for this mutation because Pratt teaches that the T594M variant in beta-ENaC is associated with an increased risk of hypertension and because Diamedica teaches that hypertension is associated with the progression of CKD. One of ordinary skill in the art would have a reasonable expectation that determining whether the CKD patients who were administered DM199 in the method of Diamedica and Naicker have the particular beta-ENaC mutation that results in an increased risk of hypertension as taught by Pratt would successfully provide information regarding whether DM199 is an effective treatment for CKD patients with that particular beta-ENaC variant.
Therefore, claims 1, 3-4, 8, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker and Pratt and are rejected under 35 U.S.C. 103.
Claims 1, 3-4, 9-10, 14-15, and 18 are newly rejected as necessitated by amendment under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), and Zhang et al., Hypertension Res. 33: 478-484 (2010; cited on the IDS filed 12/27/2023).
As discussed above, claims 1, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker. However, Diamedica and Naicker do not teach that the CKD patients have the mutations in CYP11B1 and CYP11B2 recited in instant claims 4 and 9-10.
Zhang teaches that particular polymorphisms in the CYP11B1 and CYP11B2 genes are associated with the development of hyperaldosteronism, which is a common form of hypertension (see entire document, including abstract and page 3478, left column, paragraph 1; cf. claims 4 and 9-10; the Examiner notes that Diamedica teaches that hypertension contributes to the progression of CKD in page 1, paragraph 4).
While Diamedica and Naicker do not teach that the CKD patients have the mutations in CYP11B1 and CYP11B2 recited in instant claims 4 and 9-10, it would have been obvious to one of ordinary skill in the art at the time of the invention to screen patients for these mutations because Zhang teaches that particular polymorphisms in the CYP11B1 and CYP11B2 genes are associated with the development of hyperaldosteronism, which is a common form of hypertension, and because Diamedica teaches that hypertension is associated with the progression of CKD. One of ordinary skill in the art would have a reasonable expectation that determining whether the CKD patients who were administered DM199 in the method of Diamedica and Naicker have the particular mutations in CYP11B1 and CYP11B2 that result in an increased risk of hypertension as taught by Zhang would successfully provide information regarding whether DM199 is an effective treatment for CKD patients with those particular CYP11B1 and CYP11B2 variants.
Therefore, claims 1, 3-4, 9-10, 14-15, and 18 are rendered obvious by Diamedica in view of Zhang and are rejected under 35 U.S.C. 103.
Claims 1, 3-4, 11, 14-15, and 18 are newly rejected as necessitated by amendment under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), and Simon et al., Nat. Genet. 13: 183-188 (1996; cited on the IDS filed 12/27/2023).
As discussed above, claims 1, 3, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker. However, Diamedica and Naicker not teach that the CKD patients have the SLC12A1 gene mutations recited in instant claims 4 and 11.
Simon teaches that Bartter’s syndrome, an inherited disorder that often progresses to renal failure, is linked to mutations in the NKCC2 gene, which is also called SLC12A1 (see entire document, including abstract; page 183, right column, paragraph 1, to page 184, left column, paragraph 1; page 184, right column, paragraph 1; cf. claims 4 and 11; the Examiner notes that renal failure is a subset of CKD).
While Diamedica and Naicker do not teach that the CKD patients have a mutation in the SLC12A1 gene as recited in instant claims 4 and 11, it would have been obvious to one of ordinary skill in the art at the time of the invention to screen patients for mutations in this gene because Simon teaches that mutations in SLC12A1 are linked to Bartter’s syndrome, a disorder that often progresses to renal failure. One of ordinary skill in the art would have a reasonable expectation that determining whether the CKD patients who were administered DM199 in the method of Diamedica and Naicker have the particular SLC12A1 mutations that result in a disorder that progresses to renal failure as taught by Simon would successfully provide information regarding whether DM199 is an effective treatment for CKD patients with mutations in SLC12A1.
Therefore, claims 1, 3-4, 11, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker and Simon and are rejected under 35 U.S.C. 103.
Claims 1, 3-4, 12, 14-15, and 18 are rejected under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), Coniglio et al., JACC: Heart Failure 10(2): 129-138 (February 2022; cited on the IDS filed 12/27/2023), and Gillmore et al., Eur. Heart J. 39: 2799-2806 (2018).
As discussed above, claims 1, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker. However, Diamedica and Naicker do not teach that the CKD patients have the V142I mutation in transthyretin recited in instant claims 4 and 12.
Coniglio teaches that the V142I variant in transthyretin causes cardiac amyloidosis (see entire document, including abstract; cf. claims 4 and 12).
Gillmore teaches that cardiac amyloidosis resulting from mutations in transthyretin is associated with CKD (see entire document, including page 2800, left column, paragraph 3; page 2800, right column, paragraph 4; page 2801, Table 1; please note that every ATTR amyloidosis patient in the study had CKD, as discussed in Table 1).
While Diamedica and Naicker do not teach that the CKD patients have the V142I mutation in the transthyretin gene as recited in instant claims 4 and 12, it would have been obvious to one of ordinary skill in the art at the time of the invention to screen patients for mutations in this gene because Coniglio teaches that the V142I mutation in transthyretin causes cardiac amyloidosis, a disorder that Gillmore teaches results in CKD. One of ordinary skill in the art would have a reasonable expectation that determining whether the CKD patients who were administered DM199 in the method of Diamedica and Naicker have the particular TTR mutations that result CKD as taught by Coniglio and Gillmore would successfully provide information regarding whether DM199 is an effective treatment for CKD patients with the V142I mutation in TTR.
Therefore, claims 1, 3-4, 12, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker, Coniglio, and Gillmore and are rejected under 35 U.S.C. 103.
Claims 1, 3, 14-15, 18-19, 24-25, and 28-33 are newly rejected as necessitated by amendment under 35 U.S.C. 103 as being unpatentable over DiaMedica Therapeutics, “DiaMedica Therapeutics Doses First Patient in Phase 1b Clinical Study of DM199 in Patients with Chronic Kidney Disease,” February 2019 (cited as reference 244 on the IDS filed 12/27/2023; hereafter ‘Diamedica’), in view of Naicker et al., Immunopharmacology 44: 183-192 (1999; cited on the IDS filed 12/27/2023), and international patent application publication WO 2018/165551 filed by Pauls et al., published 09/13/2018 (cited on the IDS filed 12/27/2023).
As discussed above, claims 1, 3, 14-15, and 18 are rendered obvious by Diamedica in view of Naicker. However, Diamedica and Naicker do not teach the specific dosage forms recited in instant claims 19, 24-25, and 28-33.
Pauls teaches KLK1 polypeptides and methods of use thereof (see entire document, including page 1, lines 17-20). Claims 1-30 of Pauls recite all of the limitations of the KLK1 polypeptide dosage form recited in instant claims 19, 24-25, and 28-33 and that the KLK1 polypeptide can be administered for the treatment of CKD (Pauls claim 30; cf. instant claims 1, 19, 24-25, and 28-33).
While Diamedica and Naicker do not teach that KLK1 dosage forms other than DM199 are administered to patients for the treatment of CKD, it would have been obvious to one of ordinary skill in the art to do so because Pauls teaches that the KLK1 polypeptide dosage forms of instant claims 19, 24-25, and 28-33 may be administered for the treatment of CKD. One of ordinary skill in the art would have a reasonable expectation that administering the dosage forms of Pauls in the method of Diamedica and Naicker would successfully result in the amelioration of at least one symptom of CKD in the patients.
Therefore, claims 1, 3, 14-15, 18-19, 24-25, and 28-33 are rendered obvious by Diamedica in view of Naicker and Pauls and are rejected under 35 U.S.C. 103.
The Supreme Court has acknowledged:
When a work is available in one field of endeavor, design incentives and other market forces can prompt variations of it, either in the same field or a different one. If a person of ordinary skill can implement a predictable variation…103 likely bars its patentability…if a technique has been used to improve one device, and a person of ordinary skill in the art would recognize that it would improve similar devices in the same way, using the technique is obvious unless its actual application is beyond that person’s skill. A court must ask whether the improvement is more than the predictable use of prior-art elements according to their established functions……the combination of familiar elements according to known methods is likely to be obvious when it does no more than yield predictable results (see KSR International Co. v. Teleflex Inc., 82 USPQ2d 1385 U.S. 2007) (emphasis added).
From the teachings of the references, it is apparent that one of ordinary skill in the art would have had a reasonable expectation of success in producing the claimed invention. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
Response to Arguments
Applicant has traversed the above rejection of the claims under 35 U.S.C. 103 as being unpatentable over Diamedica in view of Naicker. Applicant states that the cited references provide no tangible basis to select urinary KLK1 levels of less than 40 ng/mL as a specific threshold for treating a CKD patient with KLK1. Applicant states that Applicant has unexpectedly identified urinary KLK1 levels of 39.4 ng/mL as representing the 50th percentile (remarks, pages 9-10). This argument has been fully considered but has not been found persuasive.
The Examiner notes that the instant claims make no recitation about the selection of a specific threshold of any sort. Rather, the instant claims are drawn to administering KLK1 to a patient with urinary KLK1 levels less than 40 ng/mL. As discussed above, urinary levels of KLK1 below 40 ng/mL are known in CKD patients, and so it would be expected by one of ordinary skill in the art that CKD patients can have urinary KLK1 levels below 40 ng/mL. Also, it is obvious to treat any CKD patient, including those with urinary levels of KLK1 below 40 ng/mL, with KLK1. Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993).
Therefore, the Examiner has maintained the rejections presented above.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Erin M. Bowers, whose telephone number is (571)272-2897. The examiner can normally be reached Monday-Friday, 7:30-5:00.
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/Erin M. Bowers/Primary Examiner, Art Unit 1653
03/20/2026