DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application is being examined under the pre-AIA first to invent provisions.
Priority
Applicant’s claim to priority from PCT/EP2011/061847 filed 07/12/2011 and Foreign Application EP10169309.1 filed 07/12/2010 is hereby acknowledged.
Application Status
Amendments to claims filed 11/19/2025 are hereby acknowledged. Claims 1-4, 6, 8-9, 15, 19 and 21-24 are canceled. Claims 5, 13, and 16 are currently amended.
Accordingly, claims 5, 7, 10-14, 16-18, 20 and 25-27 are under examination in this office action.
Any objection or rejection not reiterated herein has been overcome by Applicant’s amendments and is therefore withdrawn.
Applicant’s amendments and arguments have been thoroughly reviewed, but are not persuasive to place the claims in condition for allowance for the reasons that follow.
The following rejections are maintained from previous Office Action dated 07/16/2025, but are modified as necessitated by Applicant’s amendments filed 11/19/2025:
Claim Rejections - 35 U.S.C. § 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 pre-AIA 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negated by the manner in which the invention was made.
U.S. Patent Application Publication No. 2004/0055023 further in view of Mas et al.
Claims 5, 10-14, 16-18 and 25-27 are rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over U.S. Patent Application Publication No. 2004/0055023 (see ‘Information Disclosure Statement’, filed on 27 September 2021; herein “USPGPUB023”), in view of Mas et al. (“Reversal of Type 1 Diabetes by Engineering a Glucose Sensor in Skeletal Muscle. 2006. Diabetes. Vol. 55, pages 1546-1553; see ‘Information Disclosure Statement’, filed on 27 September 2021; herein “MAS’’) and Cui (Cui, H. et al. “Long-term metabolic control of autoimmune diabetes in spontaneously diabetic nonobese diabetic mice by nonvascularized microencapsulated adult porcine islets”. Transplantation, Vol. 88, No. 2 (2009), pp: 160-169; referred herein as CUI; previously cited).
The instant claims are directed to a method of treating diabetes comprising the administration of a vector carrying and allowing the expression of a Gck gene and a vector carrying and allowing the expression of an insulin (Ins) gene.
USPGPUB023 discloses gene therapy compositions comprising vectors comprising glucokinase and insulin (Abstract).
Regarding claims 5, 13, and 16 , USPGPUB023 provides for gene therapy
compositions for the expression of an insulin gene and a glucokinase gene in vectors (i.e., first and second, claim 16) that permit the combined expression of the disclosed genes (i.e., glucokinase (Gck or GK) and insulin (Ins) in muscle cells and methods of treatment thereof (Abstract; ¶[0009]-[0014] and ¶[0018]-[0023]).
USPGPUB023 states that “This invention also relates to a vector or vectors of expression which permits the expression of said chimeric genes jointly in muscle cells. Said vectors can be a plasmid, a viral vector or a non-viral vector” (see Abstract, and [0009]). USPGPUB023 also teaches that “In the case of a viral vector, this can be a retroviral vector, an adenoviral vector, an adeno-associated vector, a Sindbis viral vector, lentiviral vector or a vector derived from the herpes virus.” (see [0010]). Therefore, the chimeric genes can be on a single vector as claimed by USPGPUB023 on page 5 (claims 2-6 and 11).
Further, USPGPUB023 provides for the expression of these genes with adeno associated viral vectors (Id. ¶ [0010], [0029] and claim 6 of USPGPUB023) (claim 13).
Regarding claim 18, USPGPUB023 provides for injections to the muscle (i.e., intramuscular) (Abstract; ¶ [0033]).
Regarding claim 5, USPGPUB023 fails to teach long term benefit and whether the subject requires immunosuppression. However, MAS teaches that “The significance of our results is that, since normalization of glycemia is achieved, secondary complication of type 1 diabetes will not develop. This is certain to improve the quality of life of diabetic patients. Furthermore, because this approach is based on engineering skeletal muscle, it has several advantages (tissue accessibility, no need for immunosuppression) over other approaches such as engineering the liver or transplanting insulin-producing B-cells (see page 1552, left column, “In summary” paragraph).
Regarding claims 14, 16 and 17, USPGPUB023 fails to specifically teach the utilization of adeno associated virus vector of serotype (AAV1). MAS resolves the resolves the deficiency of USPGPUB023, wherein MAS similarly describes the expression of “insulin gene” and “glucokinase gene” for diabetes gene therapy (Abstract). MAS also teaches double transgenic mice expressing both insulin and glucokinase in skeletal muscle obtained by crossing transgenic mice expressing human proinsulin containing genetically engineered furin endoprotease cleavage sites to produce mature insulin in skeletal muscle, with glucokinase-expressing transgenic mice (see page 1547, left column, “Research design and methods” section”).
Regarding claim 14, MAS examines the ability of genetic manipulation of skeletal muscle to counteract diabetic hyperglycemia (Abstract; and paragraph bridging pages 1546 and 1547), wherein MAS utilizes adeno-associated viral vectors for the expression of the insulin gene and the glucokinase gene (p1547, right col, 2nd ¶; p1549, ¶ bridging left and right col to p1550, right col, 2nd ¶; FIGS. 1, 2, and 4). MAS provides for the utilization of adeno-associated viral 1 (AAV1) vectors as a new gene therapy approach to diabetes (Abstract; p1549, ¶ bridging left and right col to p1550, right col, 2nd ¶). MAS further provides for the advantageous effects of AAV1 vectors, wherein MAS states:
“To obtain long-term expression of Ins-GK genes, we next examined the use of AAV vectors to transduce skeletal muscle. It is now well established that the AAV1 serotype transduces murine skeletal muscle more efficiently than the more widely used AAV2, and it confers long-term gene expression (24—26). Thus, to obtain AAV1-GFP, AAV1-Ins, and AAV1-GK vectors, the cytomegalovirus (CMV)/GFP, CMV/human proinsulin, or CMV/glucokinase gene was introduced into an AAV2-based vector that was packaged into an AAV1 capsid. When mouse tibialis cranialis muscle was injected with a single dose of 1 X 10’° viral genomes of AAV-1-GFP, ~80% of fibers expressed GFP (Fig. 3A). In these mice, no GFP expression was detected in the liver (data not shown).” (p1549, ¶ bridging left and right col).
Regarding claim 16, MAS teaches a composition that is a mixture
of 2 different vectors, AAV1-Ins and AAV1-GK in equal amounts (50%-50%) in Figure 3 (p1549).
Regarding claim 17, MAS indicates the simultaneous expression of the insulin gene and the glucokinase gene by single injection results in a synergistic effect thereby normalizing glycemia for >4 months (Abstract; p1549, ¶ bridging left and right col; ¶ bridging p1550-1551; ¶ bridging p1551-1552; FIGS. 1, 2, 4).
In view of the teachings found in USPGPUB023 and MAS (as stated above), it would have been obvious to a person of ordinary skill in the art at the time the invention was made to have expressed the glucokinase gene and the insulin gene with adeno-associated virus vectors of the serotype AAV1 as disclosed in MAS because MAS teaches that AAV1 are more efficient and confer long-term gene expression (p1549, ¶ bridging left and right col). USPGPUB023 provides a person of ordinary sill in the art some teaching, suggestion, or motivation for vectors (i.e., first and second), or a vector that permit the combined expression of the disclosed genes (i.e., glucokinase (Gck) and insulin (Ins) in muscle cells (¶[0009]). Similarly, MAS provides a person of ordinary skill in the art some teaching, suggestion, or motivation for the simultaneous expression of the insulin gene and the glucokinase gene by single injection results in a synergistic effect thereby normalizing glycemia for >4 months (“[A]bstract”; p1549, ¶ bridging left and right col; ¶ bridging p1550-1551; ¶ bridging p1551-1552; FIGS. 1, 2, 4). Furthermore, USPGPUB023 and MAS are directed to expression of a glucokinase gene and an insulin gene with adenoviral associated vectors and, thus, are drawn to the same purpose and/or outcome.
Regarding claims 5, 10-12 and 25-27, USPGPUB023 teaches testing with insulin tolerance test 21 days after administration of the drug and glycaemia determined at regular intervals of time (¶ [0038]). MAS teaches that modification/optimization of the vector yielded a normalization of glycaemia for > 4 months (“[A]bstract) after a single injection of transgene comprising both insulin and GcK. However, the combination of USPGPUB023 and MAS does not teach subjects remaining normoglycemic for 200, 300, 400, 500, 600, 700 or 800 days after treatment with the gene therapy.
However, CUI teaches a long-term follow up after anti-diabetic treatment, using a different modality. One with reasonable skills in the art would search for the presence of long-term follow-up in the art, to assess the stability, the feasibility and the efficacy of using gene therapy with adeno-associated viral vectors, compared to more “traditional therapies” such as islet transplantation. CUI teaches reversion of hyperglycemia in diabetic NOD mice on days 158, 234, 270, 367 and 466 post-transplantation (see page 163, right column, and Figure 1). CUI also teaches that in larger mammals (human patients) the follow-up after anti-diabetic xenogeneic islet transplant therapy was 3 years and 9.5 years in other reports (page 167, right column, lines 5-19).
It would have been obvious to one with ordinary skills in the art before the invention was made to have modified the protocol used in USPGPUB023 modified by MAS’s composition comprising a transgene, AAV1-Ins-GcK, optimized for stability, and extend the follow-up time periods to 200, 300, 400, 500, 600, 700 or 800 days after treatment, as taught by CUI. One with ordinary skill in the art would have been motivated to test the stability of the transgenes comprising insulin and glucokinase genes, and also compare to other therapies’ durability and effectiveness with a reasonable expectation of success.
In KSR Int 'l v. Teleflex, the Supreme Court, indicated that “[T]he principles underlying [earlier] cases are instructive when the question is whether a patent claiming the combination of elements of prior art is obvious. 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”. KSR Int'l v. Teleflex lnc., 127 S. Ct. 1727, 1740 (2007).
Therefore, regarding claims 5, 10-18 and 25-27, applying the KSR standard of obviousness to USPGPUB023, MAS and CUI, it is concluded that the combination of the references represents a combination of known elements which yield the predictable result. At the time of invention, a practitioner could have combined the teachings of USPGPUB023, MAS and CUI as detailed above. At the time the invention was made, one with ordinary skills in the art would have expressed the glucokinase gene and the insulin gene with adeno-associated virus vectors of the serotype AAV1 as disclosed in MAS because MAS teaches that AAV1 are more efficient and confer long-term gene expression. It would have been obvious to have substituted the constructs used in USPGBUP023 with one optimized construct, based on constructs used in MAS for more efficiency and longevity. One with ordinary skills in the art, motivated in the treatment of diabetes and prevention of long term complications, could have modified the time schedule for testing for longevity and efficacy of the transgenes according to a time schedule taught by CUI, from 158 to 466 days post administration of therapy, and on larger mammals, up to 3 to 9 years. As a result, the predictable result of obtaining a method of treating diabetes as claimed would be achieved. Such a combination is merely a "predictable use of prior art elements according to their established functions." KSR Int’l 7, 127 S. Ct. at 1740.
Therefore, regarding claims 5, 10-18 and 25-27, the combination of USPGPUB023, MAS and CUI renders all elements of the claims obvious and unpatentable.
Claim 7 is rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over U.S. Patent Application Publication No. 2004/0055023 (see ‘Information Disclosure Statement’, filed on 27 September 2021; herein “USPGPUB023”) in view of Mas et al. (“Reversal of Type 1 Diabetes by Engineering a Glucose Sensor in Skeletal Muscle. 2006. Diabetes. Vol. 55, p1546-1553; see ‘Information Disclosure Statement’, filed on 27 September 2021; herein “MAS’’) and Cui (Cui, H. et al. “Long-term metabolic control of autoimmune diabetes in spontaneously diabetic nonobese diabetic mice by nonvascularized microencapsulated adult porcine islets”. Transplantation, Vol. 88, No. 2 (2009), pp: 160-169; referred herein as CUI; previously cited) as applied to claim 5 above, and in further view of Harlan (Harlan, D.M. “Gene-altered islets for transplant: giant leap or small step?”. Endocrinology, Vol. 145, no. 2(2004), pp: 463-466; referred herein as HARLAN; previously cited).
Regarding claim 7, the combination of USPGPUB023, MAS and CUI renders the elements of claim 5 obvious. USPGPUB023 and MAS are silent on “Brittle diabetes” and its treatment.
However, CUI teaches that a viable therapy for Brittle diabetics is pancreas transplantation (see p160, left column, lines 3-4). CUI teaches a method of encapsulating islets for xenogeneic transplantation with long-term success treating autoimmune diabetes, i.e. type 1 diabetes (see title and summary).
CUI also teaches however that in transplantation modality, major immunosuppression is required, leading to serious side-effects (see p160, left column, lines 3-5). There is therefore a recognition in the field, that Brittle diabetes ( a severe form of type 1 diabetes/autoimmune diabetes, not responsive to insulin alone) needs better and advanced therapeutic modalities. CUI teaches that microencapsulated islet transplantation does not require immunosuppression (see title).
HARLAN teaches that Brittle diabetes being a more severe case of Diabetes, advanced modality of treatment such as islet transplantation improves glycemia control, but the blood glucose control is not normal for most patients, and certainly not commensurate with that typically is achieved after solid organ transplantation (see p464, left column, lines 43-48). HARLAN also teaches that investigators have long tried to develop new therapies, involving isolation of islet for transplantation, since whole pancreata from cadaveric donors are rare (p463, left column, “[I]slet transplantation (whether administered as part of a whole pancreas or as isolated cell clusters)” section, and right column, last ¶).
HARLAN teaches that a mix of modalities such as gene therapy-altered islets might be the solution to restoring euglycemia and overcoming the major limitation of the limited islet supply. HARLAN teaches that using an adenoviral vector to transduce cell ex vivo may help avoid toxicity and provide additional support to the therapy (see p465, right column, lines 19-25).
Therefore, it would have been obvious to one of ordinary skill in the art at the time the invention was made to combine the teachings of USPGPUB023 and MAS of providing a system using an optimized adeno-associated viral vector, AAV1-Ins-GK, optimized for stability, with the teachings of HARLAN of combining modalities using genetically-modified islet cells as gene therapy. One with ordinary skills in the art motivated in treating a more severe type of diabetes by providing a system that enhances blood glucose control over a longer term while avoiding immunologic toxicity of transplantation, and overcoming the limitation imposed by islet supply for transplantation, could have used the system of USPGPUB023 modified by MAS and modified the islets with the optimized AAV1-ins-GK transgenes, and delivered an effective dose of gene therapy according to the protocol using microencapsulated islets as taught by CUI. Given the stability of the transgenes taught by MAS, and given the efficiency and the longevity of the encapsulated islet transplantation method taught by CUI, one with ordinary skills in the art could have performed this modification with a reasonable expectation of success and arrived at a method of treating brittle diabetes.
Claim 20 is rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over U.S. Patent Application Publication No. 2004/0055023 (see ‘Information Disclosure Statement’, filed on 27 September 2021; herein “USPGPUB023”) in view of Mas et al. (“Reversal of Type 1 Diabetes by Engineering a Glucose Sensor in Skeletal Muscle. 2006. Diabetes. Vol. 55, p1546-1553; see ‘Information Disclosure Statement’, filed on 27 September 2021; herein “MAS’’) and Cui (Cui, H. et al. “Long-term metabolic control of autoimmune diabetes in spontaneously diabetic nonobese diabetic mice by nonvascularized microencapsulated adult porcine islets”. Transplantation, Vol. 88, No. 2 (2009), pp: 160-169; referred herein as CUI; previously cited) as applied to claims 5 and 18 above, and in further view of Dressman, D. (AAV-Mediated Gene Transfer to Models of Muscular Dystrophy: Insights into Assembly of Multi-Subunit Membrane Proteins. 2001. University of Pittsburgh, Graduate Faculty of the School of Medicine, Department of Biochemistry and Molecular Genetics in partial fulfillment of the requirements for the degree of Doctor of Philosophy. 183 pages; see ‘Information Disclosure Statement’, filed on 27 September 2021; herein “DRESSMAN’’).
The combination of USPGPUB023, MAS and CUI is herein applied from the ‘Claim Rejections — 35 U.S.C. § 103’ above. While the combination of USPGPUB023, MAS and CUI does teach and suggest the expression of “insulin gene” and “glucokinase gene” in a single adeno-associated viral vector (AAV) for gene therapy along with providing for a single injection to the muscle (see MAS at ¶ bridging p1550-1551; ¶ bridging p1551-1552; FIG. 4), none of the references specifically teaches the limitations found in claim 20. DRESSMAN resolves the deficiencies of USPGPUB023, MAS and CUI, wherein DRESSMAN describes adeno-associated viral vector (AAV) mediated gene therapy delivery methods and a multi-needle injection manifold for gene therapy delivery to different regions of the muscle (pi-iv).
DRESSMAN describes the successful administration of a single dose of an adeno-associated viral vector (AAV) mediated gene therapy (p20, 1st and 2nd full ¶; ¶ bridging p24-25; p39, 1st ¶; p52, 2nd ¶ to p53, 1st ¶; ¶ bridging p61-62 to p61, 1st ¶; Figures 8 and 10). DRESSMAN teaches that one hurdle facing AAV-mediated gene therapy is the delivery method, therefore, an injection manifold which can be used to safely, accurately and reproducibly/consistently deliver the genes in the same region of muscle was needed and was developed (page iv, second ¶).
Regarding claim 20, DRESSMAN describes a multi-needle injection manifold to consistently deliver gene therapy viruses to muscle (p114, 1st ¶; p117, 1st ¶; p121, 1st ¶; Figure 27).
In view of the teachings found in USPGPUB023, MAS, CUI and DRESSMAN (as stated above), it would have been obvious to a person of ordinary skill in the art at the time the invention was made to have administered the adeno-associated virus vector of serotype (AAV1) comprising the insulin gene and the glucokinase gene formed from the teachings and suggestions of USPGPUB023 and MAS in a single dose with a single multi-needle injection as described in DRESSMAN. One with ordinary skills in the art, aware of variations in multiple injections and the hurdle of delivering the transgene consistently, motivated in injecting the transgene in multiple muscle cells simultaneously, would consider DRESSMAN’s teachings and modify the injection manifold accordingly, for single dose administration of the optimized adeno-associated viral vector (AAV) mediated gene therapy with the described multi-needle injection manifold (Id.). Furthermore, USPGPUB023, MAS, and DRESSMAN are directed to gene transfer methodologies with adeno associated viral vectors and, thus, are drawn to the same purpose and/or outcome.
Accordingly, USPGPUB023 further in view of MAS, CUI and DRESSMAN renders the instant claim unpatentable.
Response to Arguments
Applicant’s arguments filed 10/16/2025 and 11/19/2025 with respect to claims 5, 7, 10-14, 16-18, 20, and 25-27 have been fully considered but they are not persuasive.
Regarding the Remarks filed 10/16/2025, on p5-9, Applicant argues that amending the claims to add “the subject does not receive life-long immunosuppression” renders the claims non-obvious and suggests that the rejections are rendered moot as a result.
In response to applicant's arguments against the references individually, one cannot show non-obviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
The combination of USPGPUB023, MAS and CUI clearly renders all the elements of claim 5 obvious. USPGPUB023 clearly claims that the chimeric genes can be on a single vector on page 5 (claims 2-6 and 11). MAS summarizes their invention by stating the long-term advantage of muscle engineering compared to other methods necessitating immunosuppression (see page 1552, left column). CUI teaches the long-term correction of diabetes without immunosuppression (see page 162, right column, “Results” section).
Therefore, the rejections are maintained.
Double Patenting
The non-statutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A non-statutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on non-statutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a non-statutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 5, 13-14, 17, 20, and 26-27 are rejected on the ground of non-statutory double patenting as being unpatentable over claims 1-4, 7-11 of U.S. Patent No. 11,001,857 (US App. No. 14/951,810). Although the claims at issue are not identical, they are not patentably distinct from each other because:
Regarding claim 5, Claims 1, 8, 9 and 11 of USPat. ‘857 recite a single vector comprising the Ins gene and the Gck gene operatively linked.
Regarding claims 13-14, claims 3 and 4, and 9 of USPat.’ 857 recite a method of treatment of diabetes wherein the vector is an adeno-associated virus (AAV) and serotype 1, AAV1.
Regarding claims 17 and 20, claim 2 of USPat.’857 recites a single multi-needle injection.
Regarding claims 26-27, claims 7,10 and 11 of USPat. ‘857 recite a method of treating diabetes whereby fasting plasma glucose levels in the subjects are normalized for at least two years following administration of the single dose of gene therapy.
Therefore, the claims are not deemed to be patentably distinct.
Response to Arguments
Applicant's arguments filed 11/19/2025 have been fully considered but they are not persuasive.
Applicant traverses the NSDP rejection and provide arguments stating that
“Claims 1-4 and 7-11 of US '857 do not recite or predict all of the features of the currently claimed method, i.e., a method of treating diabetes, wherein the subject remains normoglycemic for 200 days after treatment and wherein the subject does not receive life-long immunosuppression. In particular, claims 1-4 and 7-11 of US '857 are silent regarding the subject remaining normoglycemic for 200 days after treatment and the subject not receiving life-long immunosuppression. For at least these reasons, claims 1-4 and 7-11 of US '857 would not render the pending claims obvious. “
In response, the argument is found not to be persuasive, since the method
recited in instant application comprises the same steps and compositions claimed in US’857. In instant application, Applicant merely claimed results, e.g., “wherein the subject remains normoglycemic for 200 days after treatment”, previously not shown from the already patented method. Therefore, there being no distinguishable method step nor structures in the compositions used, the rejections are maintained.
Conclusion
No claim is allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
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/A.D./Examiner, Art Unit 1636
/NANCY J LEITH/Primary Examiner, Art Unit 1636