DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claims 1-10 are cancelled.
Claims 11-24 are pending and examined on the merits.
Notice Re: Prior Art Available Under Both Pre-AIA and AIA
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.
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.
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 11-24 are rejected under 35 U.S.C. 103 as being unpatentable over Sethi (JASN. June 2019. 30: 1123-1136. Listed on IDS filed 4/4/24) in view of Beck (The New England Journal of Medicine. 2009. 361(1): 11-21) and Aaltonen (Nephrol. Dial. Transplant. 2011. 26: 2871-2877).
Sethi studied 224 cases of biopsy-proven PLA2R-negative membranous nephropathy (MN) and 102 controls which include 47 cases of PLA2R-associated MN in pilot and discovery cohorts (Methods section of abstract). In particular, kidney biopsy samples from patients (directed to a mammal that is a human, meeting limitation of instant claims 12 and 19) were studied (page 1124, left column, second and third paragraphs). Mass spectrometry was used for identifying proteins in the biopsy specimens (page 1124, paragraph bridging left and right columns). It was found that all control and PLA2R-associated MN cases were negative for exostosin 1 (EXT1) and exostosin 2 (EXT2) (page 1125, right column, first paragraph). Additionally, immunohistochemical (IHC) staining for EXT1 and EXT2 was performed on kidney biopsy specimens (page 1124, right column, second paragraph). Of 224 cases of PLA2R-negative MN which underwent the IHC staining, 198 (88.4%) cases were negative for EXT1 and EXT2 (paragraph bridging pages 1126 and 1127). Further regarding the finding of the IHC staining, all 95 control cases were negative for both EXT1 and EXT2, which include PLA2R-associated MN cases (page 1127, first paragraph). In determining that at least the PLA2R-associated MN cases and 198 PLA2R-negative MN cases were negative for EXT1 and EXT2, then Sethi discloses determining that kidney tissue from a mammal having membranous nephropathy does not express a polypeptide, wherein said polypeptide is an EXT1 polypeptide or an EXT2 polypeptide. Thus, Sethi meets limitations of step (a) of instant claim 11, and the limitation of instant claim 18 of a mammal identified as having kidney tissue that does not express a polypeptide, wherein said polypeptide is an EXT1 polypeptide or an EXT2 polypeptide.
Sethi differs from the claimed invention in that Sethi does not disclose that, in a patient having a biopsy sample negative for EXT1 and EXT2, the membranous nephropathy is membranous nephropathy likely to progress to end stage kidney disease, nor does Sethi disclose treating said patient. Sethi further differs from instant claim 11 (and its dependent claims) in that Sethi does not expressly disclose administering an immunosuppressant to the patient to reduce the rate of progression to end stage kidney disease. Sethi further differs from instant claim 18 (and its dependent claims) in that Sethi does not expressly disclose administering an immunosuppressant to the patient (directed to a mammal identified as having kidney tissue that does not express an EXT1 polypeptide or an EXT2 polypeptide, as claimed).
Beck discloses that a majority of patients with idiopathic membranous nephropathy have antibodies against a conformation-dependent epitope in PLA2R (Conclusions section of Abstract). The findings of Beck’s study suggest that PLA2R is a major target antigen in patients with idiopathic membranous nephropathy (page 20, right column, last paragraph).
Aaltonen discloses that one-third of idiopathic membranous nephropathy patients have persistent heavy proteinuria and they are at risk of eventually progressing to end-stage renal disease (ESRD) (page 2871, right column, first paragraph). Aaltonen discusses immunomodulating treatment, teaching that cyclosporine alone or combined with low-dose steroids is effective in inducing remission in idiopathic membranous nephropathy (page 2875, right column, second-to-last paragraph). It is concluded that the clinical course of idiopathic membranous nephropathy can be affected by immunomodulating treatment, and it is recommended providing that treatment to patients that are presumed to be at risk of developing progressive renal insufficiency (page 2875, right column, last paragraph).
Before the effective filing date of the claimed invention, it would have been obvious that the PLA2R-associated MN cases of Sethi have idiopathic membranous nephropathy based on the teachings in Beck regarding the association between PLA2R and idiopathic membranous nephropathy. For the PLA2R-associated MN cases found negative for EXT1 and EXT2 in Sethi, it would have been obvious to the person of ordinary skill in the art that at least some of the cases have an idiopathic membranous nephropathy that is likely to progress to end stage kidney disease. One of ordinary skill in the art would have expected this based on the teaching in Aaltonen that one-third of idiopathic membranous nephropathy patients are at risk of eventually progressing to end-stage renal disease. Moreover, before the effective filing date of the claimed invention, it would have been obvious to the person of ordinary skill in the art to administer an immunomodulating agent, such as cyclosporine (directed to an ‘immunosuppressant’; see page 8, lines 16-20 of the instant specification), to the EXT1/EXT2-negative PLA2R-associated MN patients. One of ordinary skill in the art would have been motivated to do this because it is a recognized treatment for idiopathic membranous nephropathy, and such treatment is effective inducing remission in idiopathic membranous nephropathy and affects the clinical course of the disease, as indicated in Aaltonen. In affecting the clinical course of the disease, then the immunomodulating agent (directed to an ‘immunosuppressant’) reduces the rate of progression to end stage kidney disease.
Therefore, Sethi in view of Beck and Aaltonen renders obvious instant claims 11-15, 17-22, and 24.
Regarding instant claims 16 and 23, Sethi discloses that laser capture microdissection was also performed for protein identification by mass spectrometry in their study (page 1124, paragraph bridging left and right columns). Thus, the references also render obvious instant claims 16 and 23.
Conclusion
No claims are allowed.
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Sef
/SUSAN E. FERNANDEZ/Examiner, Art Unit 1651