The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claims 1-9 are canceled. Claims 10-18 are pending and under consideration.
Priority: This application is a 371 of PCT/JP2021/042463, filed November 18, 2021, which claims benefit of foreign applications JP 2021-145795, filed September 7, 2021, and JP-2020-192844, filed November 19, 2020. Copies of the foreign priority documents have been received in the instant application on May 19, 2023 and are not in the English language.
Specification
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code: see at least paragraph 0021 (of the application publication). Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
Claim Rejections - 35 USC § 103
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 10-12, 14-18 are rejected under 35 U.S.C. 103 as being unpatentable over Park et al. (2003 Experimental and Molecular Medicine 35(6): 494-500; IDS 10.04.23). Park et al. disclose adenoviral mediated hepatocyte growth factor (HGF) gene attenuates hyperglycemia and beta cell destruction in overt diabetic mice (at least p. 494). Park et al. disclose constructing a recombinant adenoviral vector encoding human HGF (hHGF) (Ad.hHGF) and administering the recombinant vector expressing hHGF to a diabetic mammal at dose 1 x 1011 particles of Ad.hHGF (at least p. 495). Park et al. disclose the recombinant adenoviral vector comprises hHGF cDNA under the control of CMV immediate early enhancer/promoter (at least p. 495). Park et al. disclose Ad.hHGF attenuates hyperglycemia and increases expression of insulin in diabetic mice (at least p. 497-498). Park et al. disclose that the in vivo results suggest that adenoviral mediated hHGF gene therapy has beneficial effect on glucose in advanced diabetic phase and may serve as a therapeutic application for clinically overt diabetic patients (at least p. 499). Therefore, Park et al. disclose administering a viral vector encoding the same therapeutic product (HGF) recited to a mammal for treating the same condition recited and at a dose that is similar to the recited dose.
“[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation.” In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). MPEP 2144.05.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to arrive at the claimed method for treating a mammal with diabetes, comprising administering a recombinant adenoviral vector expressing HGF to the mammal, wherein the vector is administered at the recited dose of 1010-1012 virus particles (vp)/kg body weight, and comprises a nucleic acid encoding HGF downstream of a promoter with transcriptional activity capable of affording a therapeutically effective blood HGF level at said dose (instant claims 10-11) because the prior art discloses a method for treating the same condition recited in a mammal and comprising administering the same product to the mammal. It would have been further obvious to one of ordinary skill to arrive at the recited dose of 1010-1012 virus particles (vp)/kg body weight by routine optimization because it is similar to the dose disclosed in the prior art Park et al. One of ordinary skill would have a reasonable expectation of success because the prior art discloses that adenoviral mediated hHGF gene therapy has beneficial effect on glucose and attenuating hyperglycemia in a diabetic mammal.
Regarding instant claim 12, Park et al. disclose the concentrations of glucose were monitored for 21 days after Ad.hHGF infection (at least p. 497-498). As noted above, “[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation.” In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). Therefore, it would have been obvious to one of ordinary skill to arrive at the recited dosing regimen of a single dose or multiple doses at an interval of at least 60 days, by routine optimization.
Regarding instant 14, Park et al. disclose that the Ad.hHGF gene therapy into diabetic mice pay prevent the further destruction and present as a beneficial remedy for type I diabetic patients (at least p. 494). Therefore, it would be obvious to one of ordinary skill that the diabetes is a type I diabetes.
Regarding instant claim 15, as noted above, Park et al. disclose that the Ad.hHGF gene therapy into diabetic mice pay prevent the further destruction and present as a beneficial remedy for type I diabetic patients (at least p. 494). Therefore, it would be obvious to one of ordinary skill that the Ad.hHGF gene therapy can be administered to a human patient.
Regarding instant claims 16-18, Park et al. disclose the Ad.hHGF particles were intravenously injected into a tail vein (at least p. 495). Therefore, it would be obvious to one of ordinary skill that the viral vector can be administered intravenously via a peripheral vein.
Claims 10-12, 13, 14-18 are rejected under 35 U.S.C. 103 as being unpatentable over Park et al. (2003 Experimental and Molecular Medicine 35(6): 494-500; IDS 10.04.23) in view of Panakanti (Therapeutic Gene Delivery to Human Pancreatic Islets for Treatment of Diabetes and the Effect of TFO on Liver Fibrosis Induced by Bile Duct Ligation (2010) Theses and Dissertations (ETD). Paper 206. (121 pages)). The teachings of Park et al. over at least instant claims 10-12, 14-18 are noted above.
Regarding instant claim 13, Panakanti also discloses utilizing adenoviral vectors encoding proteins, including HGF, for treatment of diabetes (abstract). Panakanti discloses that sustained gene expression is difficult to achieve; however, some promoters have been reported to confer sustained gene expression from plasmid DNA in vivo; these promoters include β-actin, elongation factor 1-α (EF1-α), or ubiquitin (p. 7). Panakanti discloses that the activity of these promoters is usually lower than that of viral promoters, but can be increased by addition of viral or cellular enhancer components (p. 7). Panakanti discloses CMV early enhancer/chicken β actin (CAG) is a promoter of this kind; it consists of CMV enhancer and first intron of chicken (or human skeletal) β-actin (p. 7). Panakanti discloses that it shows activity similar to CMV promoter and shows greater activity in viral vectors (p. 7). Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to incorporate the CAG promoter of Panakanti for the CMV promoter in the Ad.hHGF administered to a diabetic mammal of Park et al. noted above. The motivation to do so is given by the prior art, which disclose CAG is a promoter having similar activity to CMV promoter and shows greater activity in viral vectors. One of ordinary skill would have a reasonable expectation of success because promoters for adenoviral vectors encoding therapeutic proteins were known and available in the prior art.
No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Marsha Tsay whose telephone number is (571)272-2938. The examiner can normally be reached M-F.
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/Marsha Tsay/Primary Examiner, Art Unit 1656