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 .
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 10-30-2025 has been entered.
Applicant’s arguments and amendment filed on 10-30-2025 has been received and entered. Claims 2, 4-7, 9-10, 13, 16-19, 22-32, 36-38, 40, 42-43, 45-47 have been canceled. Claim 51 has been added. Claims 1, 3, 8, 11-12, 14-15, 20-21, 33-35, 39, 41, 44, 48-51 are pending and under consideration.
Priority
This application is a 371 of PCT/US2020/031093 filed on 05/01/2020 which claims priority from a US Provisional application 62/842,150 filed on 05/02/2019.
Maintained in modified form & New -Claim Rejections - 35 USC § 103 - necessitated by amendments
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
Claims 1, 3, 8, 11, 15, 33, 41, 44, 48, 49, 50, 51 are rejected under 35 U.S.C. 103 as being unpatentable over Jain et al (WO 2018/022108 A1, 01 February 2018) (Applicant own work) in view of Dekel et al (Pub. No.: US 2018/0346882 A1, Pub. Date: Dec. 6, 2018).
Claim interpretation:
The specification of the claimed invention teaches that congenital anomaly of the kidney and urinary tract (CAKUT) includes a family of diseases of various anatomic spectrum, including renal anomalies, and anomalies of the bladder and urethra. In embodiments, the term "CAKUT" refers to one congenital abnormality (e.g., when referring to a subject who has CAKUT) (Page 10, lines 15-20). In embodiments, the term CAKUT refers to more than one congenital abnormality (e.g., when referring to a subject who has CAKUT). Thus, CAKUT is interpreted as one or more congenital abnormality.
Regarding to claim 1, Jain et al teach methods of treating chronic kidney disease (CKD) patients with a therapeutic composition composed of bioactive renal cells formulated in a biomaterial that provides stabilization and/or improvement and/or regeneration of kidney function. The method comprises percutaneously injecting into the renal cortex of at least one kidney of a patient having chronic kidney disease a therapeutically effective amount of a composition comprising a bioactive renal cell population (BRC) (Page 2, lines 15-21). The BRC cells are derived from a native autologous or allogeneic kidney sample (Page 3, lines 31-32). In all embodiments, the patient's kidney function is improved as a result of the treatment (Page 3, line 4)
Jain et al does not specifically teach the phrase “congenital anomalies of the kidney and urinary tract”. However, Dekel et al cures the deficiency.
Dekel et al teach a method of generating a nephrospheroid is disclosed. The method comprises culturing human adult kidney cells in a culture medium under non-adherent conditions (Abstract). Cells of the present invention can be used to treat any form of acute or chronic kidney disease, diabetic nephropathy, renal disease associated with hypertension, hypertensive acute tubular injury ischemic, toxic), interstitial nephritis, congenital anomalies (Aplasia/dysplasia /obstructive uropathy /reflux nephropathy) ([0138], page 8 and claim 12, page 18).
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art before the effective filing date of the rejected claims to combine the teachings of prior art to modify the method of treatment of chronic kidney disease by using homologous selected renal cells (SRC) or bioactive renal cells (BRC) as taught by Jain et al to apply and treat chronic kidney disease from congenital anomalies of the kidney as taught by Dekel et al. Said modification amounting to combining prior art elements according to known methods to yield predictable results. One of ordinary skill in the art would have been motivated to do so because Dekel et al teach that the cell populations of the invention (or cells which have been differentiated therefrom) can be used to supplement or substitute for kidney cells that have been destroyed or have reduced function. Thus, they can be used to treat patients having poor or no kidney function. The cell populations of the invention or cells derived there from may be capable of performing the filtration and reabsorptive/secretive functions of the kidney ([0136], page 8), and the cells of can be used to treat any form of acute or chronic kidney disease ([0138], page 8). One of ordinary skill in the art would have had a reasonable expectation of success in doing so because both Jain et al and Dekel et al provided detailed instructions for treating chronic kidney disease by using kidney cells.
Regarding to claim 3, 11, and 15, Dekel et al teach congenital anomalies (Aplasia/dysplasia /obstructive uropathy /reflux nephropathy) ([0138], page 8 and claim 12, page 18).
Regarding to claim 8, Jain et al teach that at screening, patients enroll in clinical trial not previously injected with NKA with CKD defined as a glomerular filtration rate (GFR) of 20 – 50 mL/min/l.73m2 inclusive (Page 39, lines 28-29). Also, inclusion criteria for the study population of the clinical trial include microalbuminuria which is defined as urinary albumin-creatinine ratio (UACR) ≥ 30 mg/g or urine albumin excretion ≥ 30 mg/day on 24-hour urine collection (Page 40, lines 5-7).
Regarding to claim 33, Jain et al teach that in all embodiments, the formulations are suitable for administration to a subject in need of improved kidney function (Page 25, lines 31-32).
Regarding to claim 41, 44 Jain et al teach Figure 2 which depicts the estimated glomerular filtration rate pre- and post-NKA injection of the entire cohort showing improvement in eGFR
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Regarding to claim 48, Jain et al teach the dose of NKA for this study is 3 x 106 cells/g estimated kidney weight (g KWest) (Page 44, lines 24-25).
Regarding to claim 49-50, Jain et al teach that the bioactive renal cell population is obtained after exposure to hypoxic culture conditions. In another embodiment, the bioactive renal cell population is a selected renal cell (SRC) population obtained after density gradient separation of the expanded renal cells (Page 3, lines 13-17). In one embodiment, SRCs are obtained from the patient's renal cortical tissue via a kidney biopsy and selected by density gradient separation of the expanded renal cells (Page 6, lines 28-29).
Regarding to claim 51, Jain et al teach that “In another embodiment, the expanded heterogeneous mixtures of renal cells are cultured in hypoxic conditions to further enrich the composition of cells with regenerative capacity” (Page 11, lines 26-27), and “wherein the bioactive renal cell population is obtained after exposure to hypoxic culture conditions” (e.g., claim 23, page 57). Thus, wherein the bioactive renal cell population is hypoxia resistant.
Claims 12, 14 are rejected under 35 U.S.C. 103 as being unpatentable over Jain et al (WO 2018/022108 A1, 01 February 2018) in view of Dekel et al (Pub. No.: US 2018/0346882 A1, Pub. Date: Dec. 6, 2018) as applied to claims 1, 3, 8, 11, 15, 33, 41, 44, 48, 49, 50, 51 above, and further in view of Nicolaou et al (Nat. Rev. Nephrol. advance online publication 18 August 2015; doi:10.1038/nrneph.2015.140).
The teachings of Jain et al and Dekel et al are as described above and are incorporated herein in their entirety.
The above references do not specifically teach CAKUT correlated with a genetic factor or an environmental factor. However, Nicolaou et al cures the deficiency.
Regarding to claims 12, 14, Nicolaou et al teach genetic, environmental, and epigenetic factors involved in CAKUT (Title). Congenital anomalies of the kidney and urinary tract (CAKUT) refer to a spectrum of structural renal malformations and are the leading cause of end-stage renal disease in children, and the current knowledge regarding the genetic susceptibility underlying CAKUT and the approaches used to investigate the genetic basis of CAKUT and outlined the associated environmental risk factors and epigenetic influences on CAKUT and discuss the challenges and strategies used to fully address the involvement and interplay of these factors in the pathogenesis of the disease (Abstract).
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art before the effective filing date of the rejected claims to combine the teachings of prior art to modify the teachings of Jain et al and Dekel et al to treat kidney diseases and combine with teachings of Nicolaou et al to apply for patients with congenital anomalies of the kidney and urinary tract. One of ordinary skill in the art would have been motivated to do so because Nicolaou et al ’s teachings can be used to improve genetic diagnosis in CAKUT, prognostic counselling, personalized disease management and clinical practice (Page 2, left column, 1st para.). One of ordinary skill in the art would have had a reasonable expectation of success in doing so because Nicolaou et al describe the current knowledge regarding the genetic susceptibility underlying CAKUT and outline the associated environmental risk factors and epigenetic influences on CAKUT.
Claims 20-21 are rejected under 35 U.S.C. 103 as being unpatentable over Jain et al (WO 2018/022108 A1, 01 February 2018) in view of Dekel et al (Pub. No.: US 2018/0346882 A1, Pub. Date: Dec. 6, 2018) as applied to claims 1, 3, 8, 11, 15, 33, 41, 44, 48, 49, 50, 51 above, and further in view of Basu et al (Pub. No.: US 2015/0246073 A1, Pub. Date: Sep. 3, 2015).
The teachings of Jain et al and Dekel et al are as described above and are incorporated herein in their entirety. The above references do not specifically teach AQP2, hyaluronic acid synthase-2 (HAS-2). However, Basu et al cure the deficiency.
Regarding to claim 20, Basu et al teach presence of viable cells and SRC function was demonstrated by metabolism of PrestoBlue and production of VEGF and KIM-1. SRC actively secrete proteins that can be detected through analysis of conditioned medium. Cell function is assessed by the ability of cells to metabolize PrestoBlue and secrete VEGF (Vascular Endothelial Growth Factor) and KIM-1 (Kidney Injury Molecule-1) ([0343] – [0344], page 37). Basu et al teach TABLE 12.4 marker selected for phenotypic analysis of SRC (see below) ([0336], page 37) (For the claimed: wherein greater than 18% of cells of the bioactive renal cell population express GGT-1, and wherein greater than 80% of cells of the bioactive renal cell population express the CK, wherein the CK is CK18).
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Regarding to claim 21, Basu et al teach in another embodiment, the second cell population is enriched for renal tubular cells and contains collecting duct epithelial cells. In other embodiments, the renal tubular cells are characterized by the expression of one or more tubular cell markers that may include, without limitation, megalin, cubilin, hyaluronic acid synthase 2 (HAS2) ([0138], page 14-15). In one embodiment, the admixture contains HAS-2-expressing cells capable of producing and/or stimulating the production of high-molecular weight species of hyaluronic acid (HA) both in vitro and in vivo. In all embodiments, the first and second cell populations may be derived from kidney tissue or cultured kidney cells ([0090], page 9).
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art before the effective filing date of the rejected claims to combine the teachings of prior art to modify the teachings of Jain et al and Dekel et al to treat kidney diseases and combine with teachings of Basu et al for enriching heterogeneous mammalian renal cell populations characterized by biomarkers. One of ordinary skill in the art would have been motivated to do so because Basu et al teach that their populations of kidney cells can be used for the treatment of kidney disease, i.e., providing stabilization and/or improvement and/or regeneration of kidney function ([0075], page 7-8). One of ordinary skill in the art would have had a reasonable expectation of success in doing so because Basu et al provide detailed instructions with the identity of cellular marker for enrichment of renal tubular cells, and methods for treating kidney disease.
Claims 34-35, 39 are rejected under 35 U.S.C. 103 as being unpatentable over Jain et al (WO 2018/022108 A1, 01 February 2018) in view of Dekel et al (Pub. No.: US 2018/0346882 A1, Pub. Date: Dec. 6 , 2018) as applied to claims 1, 3, 8, 11, 15, 33, 41, 44, 48, 49, 50, 51 above, and further in view of Kidney International Supplements (Kidney International Supplements (2013) 3, 19–62; doi:10.1038/kisup.2012.64, January 2013).
Claim interpretation:
The claimed invention teaches that the improved kidney function is demonstrated by reduction in total serum creatinine or the rate of increase in serum creatine (sCr) (Page 20, lines 5-6). As shown in Figure 2, a comparison of sCR after REACT treatment (gray line) versus sCr before REACT treatment (black-line) showed that the cohort experienced a reduction in the rate of increase for sCr post-REACT treatment (Page 107, lines 13-16).
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Thus, improving renal function can be interpreted as reduction in the rate of increase for serum creatine (sCr).
The teachings of Jain et al and Dekel et al are as described above and are incorporated herein in their entirety. The above references do not specifically teach ACR greater than 300 mg/g or ACR less than 30 mg/g. However, the Kidney International Supplements cure the deficiency.
Regarding claim 34, Jain et al teach FIG. 6 which depicts serum creatinine pre- and post-NKA injection of the entire cohort showing improved renal function with reduction in the rate of increase for serum creatine (sCr) (which is identical to the Figure 2 of claimed invention, see above).
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It should be noted that the estimated glomerular filtration rate (eGFR) which is another indicator for improved kidney function in the claimed invention in Figure 1 is identical to eGFR in figure 2 as taught by Jain et al.
Jain et al also teaches the patient with CKD exhibits microalbuminuria defined by a urinary albumin-creatinine ratio (UACR) ≥ 30 mg/g (Page 3, lines 1-2). Additionally, the Kidney International Supplements teaches that the normal urine ACR in young adults is <10 mg/g (<1 mg/mmol) and urine ACR 30-300 mg/g (3–30 mg/mmol; category A2) generally corresponds to “microalbuminuria” referred to as “moderately increased”, and urine ACR >300 mg/g (>30 mg/mmol; category A3) generally corresponds to “macroalbuminuria” termed “severely increased”. Thus, it would have been obvious for a person of ordinary skill in the art to use ACR <10 mg/g as a standard for assessing of improvement renal function from patient with “microalbuminuria” or “macroalbuminuria”.
Regarding claim 35, the Kidney International Supplements teaches the use of urine ACR <10 mg/g that can be used as standard for assessing improvement renal function, and Jain et al teach the level of serum creatine from a cohort of patient showing improvement with reduction in the rate of increase for serum creatine (sCr) in Figure 6 (see above), in some patients the level of serum creatine improved significantly (reduction in the rate of increase for serum creatine (sCr) more than 50%) (For example, patient 1 and 2 in Figure 7 as taught by Jain et al, see below). Since the method and renal cell population used in the claimed invention and the teachings of Jain et al are identical (applicant own work), it would have been obvious to expect similar results, and a person of ordinary skill in the art would be able to optimize and combine prior art elements according to known methods as taught by Jain et al and the Kidney International Supplements that would yield predictable results of level of urine ACR <10 mg/g which is a reduction of more than 50% relative to patients with microalbuminuria or macroalbuminuria in which the urine ACR is 30-300 mg/g or ACR is >300 mg/g as taught by the Kidney International Supplements.
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Regarding claim 39, as showing in the above Figure 6, patient 1 and 2 in Figure 7, Jain et al teach improved renal function with reduction in the rate of increase for serum creatine within 100 days (within 3-6 months).
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art before the effective filing date of the rejected claims to combine the teachings of prior art to modify the teachings of Jain et al and Dekel et al to treat kidney diseases and combine with teachings of Kidney International Supplements to use the criteria of Kidney damage with normal urine ACR, moderately increased ACR, or severely increased ACR. One of ordinary skill in the art would have been motivated to do so because with specific criteria of Kidney damage as taught by Kidney International Supplements, it would improve accuracy of assessing recovery of patient with kidney diseases. One of ordinary skill in the art would have had a reasonable expectation of success in doing so because Kidney International Supplements provides detailed criteria for CKD with rationale and evidence for the development of CDK.
Response to Arguments
Applicant's arguments filed 10-30-2025 have been fully considered but they are not persuasive.
1. Applicants argue and asserts that one of ordinary skill in the art would have no reasonable expectation of success in using an autologous bioactive renal cell population for treatment of CKD from CAKUT based on the teachings of Jain and Dekel.
The Examples of Jain relate to actual treatment of chronic kidney disease associated with diabetes ("diabetic kidney disease" or "DKD")….. DKD is different from CKD from CAKUT. As such, one of skill in the art would not have had a reasonable expectation that a treatment for DKD as disclosed in Jain could be applied to and actually treat CKD from CAKUT. The speculation in Dekel that a different therapeutic composition can be used to treat kidney disease from a congenital abnormality does nothing to provide reasonable expectations that a DKD treatment as taught by Jain could effectively treat CKD from CAKUT.
If anything, Dekel' s asserted disclosure related to treating chronic kidney disease from "congenital anomalies" by using kidney cells is merely an invitation to pursue a general area of research without more and accordingly does not establish a primafacie case of obviousness (Remarks, page 7-8).
Response to Arguments:
In response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In this case: Jain et al (applicant own work) teach exact the same cell populations and route of administration as the claimed invention for any Chronic kidney disease (CKD) with contemplation for a congenital anomaly/birth defect:
Jain et al teach methods of treating chronic kidney disease (CKD) patients with a therapeutic composition composed of bioactive renal cells formulated in a biomaterial that provides stabilization and/or improvement and/or regeneration of kidney function. The method comprises percutaneously injecting into the renal cortex of at least one kidney of a patient having chronic kidney disease a therapeutically effective amount of a composition comprising a bioactive renal cell population (BRC) (Page 2, lines 15-21). The BRC cells are derived from a native autologous or allogeneic kidney sample (Page 3, lines 31-32). In all embodiments, the patient's kidney function is improved as a result of the treatment (Page 3, line 4).
Dekel et al teach a method comprises culturing human adult kidney cells in a culture medium under non-adherent conditions (Abstract) and “Cells of the present invention can be used to treat any form of acute or chronic kidney disease, diabetic nephropathy, renal disease associated with hypertension, hypertensive acute tubular injury ischemic, toxic), interstitial nephritis, congenital anomalies (Aplasia/dysplasia /obstructive uropathy /reflux nephropathy)” ([0138], page 8 and claim 12, page 18). Additionally, since Jain et al teach isolating and culturing bioactive renal cell “the bioactive renal cell population is obtained from isolation and expansion of renal cells from kidney tissue under culturing conditions that enrich for cells capable of kidney regeneration” (Page 3, lines 13-14), one of ordinary skill in the art would have been motivated to combine teachings of Jain et al with Dekel et al’ teachings to use isolated and cultured renal cells to treat any form of acute or chronic kidney disease such as congenital anomalies because Dekel et al teach that the cell populations of the invention (or cells which have been differentiated therefrom) can be used to supplement or substitute for kidney cells that have been destroyed or have reduced function. Thus, they can be used to treat patients having poor or no kidney function. The cell populations of the invention or cells derived there from may be capable of performing the filtration and reabsorptive/secretive functions of the kidney ([0136], page 8), and the cells of can be used to treat any form of acute or chronic kidney disease ([0138], page 8). One of ordinary skill in the art would have had a reasonable expectation of success in doing so because both Jain et al and Dekel et al provided detailed instructions for treating chronic kidney disease by using kidney cells.
Jain et al teach treating any chronic kidney disease (CKD) with contemplation for a congenital anomaly/birth defect: “The primary objective of the study was to assess the safety and optimal injection of NKA injected at one site in a recipient kidney as measured by procedure and/or product related adverse events (AEs) through 12 months post-injection.” (Page 32, lines 15-17), and “An adverse event is classified as a "Serious Adverse Events" (SAE) if it meets the following criteria: …… results in a congenital anomaly/birth defect in a neonate/infant born to a mother exposed to the investigational product” (Page 11, lines 3-9) (Note: Jain et al teach the term ''Neo-Kidney Augment (NKA)" refers to a bioactive cell formulation (page 9, line3))
Applicant attempts to engage selective reading teachings of Jain et al to state that “one of skill in the art would not have had a reasonable expectation that a treatment for DKD as disclosed in Jain could be applied to and actually treat CKD from CAKUT” is not persuasive because applicants do not provide evidences for congenital anomalies of the kidney and urinary tract (CAKUT) is not a form of chronic kidney disease (CKD). There is no teachings/suggestions from to limit chronic kidney disease (CKD) to only "diabetic kidney disease" or "DKD" or the method of Jain et al is only applicable to one type of chronic kidney disease.
2. Applicants argue that As illustrated in the table below, the pathophysiology and patterns of nephron loss are quite different between DKD patients and CKD from CAKUT patients….
Subjects having CKD from CAKUT as recited in claim 1 have structural, e.g., anatomical, malformations in their kidney and/or urinary tract. See Applicant' specification at page 10, lines 15-17: "Congenital anomalies of the kidney and urinary tract (CAKUT) includes a family of diseases of various anatomic spectrum, including renal anomalies, and anomalies of the bladder and urethra." (emphasis added). Also see Exhibit 1
…….
It should also be noted Applicant' specification discloses actual treatment of a patient having CKD from CAKUT, e.g., a posterior urethral valve. See specification at page 140, line 26 to page 141, line 13. In particular, as shown in Figure 8, injection of the patient with REACT improved, i.e., increased, the patient's renal function as measured by eGFR. Furthermore, the patient's improved kidney function was observed via a decrease in the patient's Albumin-toCreatinine Ratio (ACR) (see, Figure 9).
By contrast, subjects having CKD from a metabolic syndrome, such as diabetic CKD, do not have structural, or anatomical, malformations in their kidney and/or urinary tract, e.g., arenot subjects having CKD from CAKUT Subjects having CKD from a metabolic syndrome, such as diabetic CKD, have CKD resulting from iniurv, caused by the metabolic syndrome, to their kidney. See Exhibit 2
……
In addition, treatments for CKD from CAKUT leading up to renal replacement therapy (RRT) tend to differ from those for CKD ftom metabolic disease. See Exhibit 3 at Tables 3 and 4, which discloses that treatment of vesicoureteral reflux (VUR), the most common childhood urinary tract abnormality, includes continuous antibiotic prophylaxis (CAP) or corrective surgery. See also Exhibit 4, which discloses that two other conditions associated with CAKUT, e.g., vesicoureteral reflux (VUR) and posterior urethral valves (PUV), are also managed by CAP or corrective surgery. Exhibit 4 at page 14, last paragraph states: "Management options for VUR (Remarks, pages 9-11)
Response to Arguments:
In response to applicant's argument pertaining to Jain et al and Dekel et al, it appears that Applicant is arguing that the cited references do not expressly suggest the claimed invention. However, it is well established in case law that a reference must be considered not only for what it expressly teaches, but also for what it fairly suggests. In re Burkel, 201 USPQ 67 (CCPA 1979). Furthermore, in the determination of obviousness, the state of the art as well as the level of skill of those in the art are important factors to be considered. The teaching of the cited references must be viewed in light of these factors. The references Jain et al and Dekel et al are cited to show a method for the treatment of chronic kidney disease, the method comprising percutaneously injecting into the renal cortex of at least one kidney of a patient having said chronic kidney disease a therapeutically effective amount of a composition comprising a bioactive renal cell population (BRC) (see claim 1, page 56 of Jain et al), and Dekel et al teach culturing human adult kidney cells in a culture medium (Abstract) and “Cells of the present invention can be used to treat any form of acute or chronic kidney disease, …… congenital anomalies (Aplasia/dysplasia /obstructive uropathy /reflux nephropathy)” ([0138], page 8 and claim 12, page 18 of Dekel et al). Thus, one of ordinary skill in the art would have been motivated to combine teachings of Jain et al with Dekel et al’ teachings to use isolated and cultured renal cells to treat any form of acute or chronic kidney disease such as congenital anomalies because Dekel et al teach that the cell populations of the invention (or cells which have been differentiated therefrom) can be used to supplement or substitute for kidney cells that have been destroyed or have reduced function ([0136], page 8 of Dekel et al), and the cells of can be used to treat any form of acute or chronic kidney disease ([0138], page 8 of Dekel et al).
As explained above, there is nowhere in the teachings of Jain et al to specify that their method for the treatment of chronic kidney disease can only applicable to diabetic kidney disease. This interpretation of Jain et al is applicants’ opinion while Jain et al teach method for the treatment of any chronic kidney disease (see claim 1, page 56 of Jain et al) . Also, the use of isolated and cultured human adult kidney cells for treating chronic kidney disease congenital anomalies have been taught in the art (See teaching of Dekel et al as described above). Therefore, Applicants’ opinion that Jain et al only teach chronic kidney disease caused by diabetes is not persuasive. Additionally, while applicants argue for the differences of DKD and CAKUT, applicants have not provided evidence for the method of Jain et al which is included identical method step (administration routes-percutaneously injecting) with the same cell type (bioactive renal cell population) for the same category of chronic kidney disease would not work for congenital anomalies of the kidney and urinary tract (CAKUT) in view of Dekel et al. The differences between kidney diseases of the same category chronic kidney disease cannot be evidenced for the cited method being unsuccessful because the method steps and material of the treatment method are the same as the claimed method. Furthermore, the use of isolated and cultured renal cells to treat any form of acute or chronic kidney disease such as congenital anomalies have been taught in Dekel et al: “Cells of the present invention can be used to treat any form of acute or chronic kidney disease, …… congenital anomalies (Aplasia/dysplasia /obstructive uropathy /reflux nephropathy)” ([0138], page 8 and claim 12, page 18 of Dekel et al). Since both Jain et al and Dekel et al are successful in treating chronic kidney disease, a person of ordinary skill in the art would have had reasonable expectation of success. As per MPEP 716.01(c) (II), Arguments presented by the applicant cannot take the place of evidence in the record. In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965) and In re De Blauwe, 736 F.2d 699, 705, 222 USPQ 191, 196 (Fed. Cir. 1984). Examples of statements which are not evidence and which must be supported by an appropriate affidavit or declaration include statements regarding unexpected results, commercial success, solution of a long-felt need, inoperability of the prior art, invention before the date of the reference, and allegations that the author(s) of the prior art derived the disclosed subject matter from the inventor or at least one joint inventor.
3. Applicants argue that the present claims are not directed to a composition but rather are directed to a method. While it may be the case that discovery of a new property of an old composition fails to render the composition patentably new, it is settled law that the new use of an old composition may be patentable. New and nonobvious uses of previously known compositions are patentable when the use is based on unknown properties of the composition. See, MPEP § 2112.02(11), citing In re Hack, 245 F.2d 246,248, (CCPA 1957). In the present case, the claims are directed to a method of treating CKD from CAKUT where the application illustrates such an effective use when the cited prior art provides no reasonable expectation of success. Accordingly, Applicant's new claimed use/method is patentable (Remarks, page 13).
Response to Arguments:
As described above, the claims are directed to a method that include the same method step as the claimed invention (administration routes-percutaneously injecting) with the same cell type as the claimed invention (bioactive renal cell population) for the same category of chronic kidney disease as the claimed invention. Thus, it is expected to have the same results with a reasonable expectation of success. In absence of any unexpected or superior results, it would be routine to use the cited method of the references above to treat any chronic kidney disease.
Conclusion
No claim is allowed.
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/KHOA NHAT TRAN/Examiner, Art Unit 1632
/PETER PARAS JR/Supervisory Patent Examiner, Art Unit 1632