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 .
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 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.
Status of the Claims
Applicant’s election without traverse of Group II, drawn to a method of treating obesity or obesity related disorder comprising administering an FKBP-L polypeptide, a biologically active fragment of an FKBP-L polypeptide, a derivative of an FKBP-L polypeptide, or a derivative of a biologically active fragment of an FKBP-L polypeptide, or a nucleic acid sequence capable of being expressed in a subject to provide FKBP-L or a biologically active fragment or derivative thereof, claimed in claims 8-11 and 14-16 was previously acknowledged.
Election was made without traverse of the nucleic acid, SEQ ID NO: 30 (nucleic acid sequence) and diabetes (disorder).
A search of the prior art uncovered the elected and unelected species. Therefore, the species election was withdrawn.
In the reply filed 2/12/24, Applicants amended claims 8 and 14. Claims 9-11 and 15-16 were canceled. Claims 17-22 are newly added.
In the reply filed 9/30/24, Applicants amended claim 8.
In the reply filed 8/12/25, Applicants amended claim 8.
Claims 1-8, 12-14 and 17-22 are pending.
Claims 1-7 and 12-13 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected group, there being no allowable generic or linking claim.
Claims 8, 14 and 17-22 read on the elected Group II and are under consideration.
Claim Rejections - 35 USC § 103-Modified
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.
The rejection of claims 8, 14 and 17-20 are rejected under 35 U.S.C. 103 as being unpatentable over Robson et al. (US 2009/0192085) as evidenced by sis maintained.
Robson et al. teach FKBP-L polypeptides and nucleic acids for treatment of a disorder mediated by angiogenesis with a polynucleotide encoding an FKBP-L polypeptide [0010]. Robson et al. claims a method of inhibiting angiogenesis in a subject in need thereof, comprising a polynucleotide encoding an FKBP-L peptide (claim 34). In particular, Robson et al. teach treatment of diabetic retinopathy [0094, 0222,0226]. Robson et al. teach angiogenic damage is associated with diabetic retinopathy [0226] and claims treatment of a subject with an ocular disorder mediated by angiogenesis (claim 37) Robson et al. teach FKBP-L polynucleotides that encode FKBP-L peptides are shown in nucleotide sequences of SEQ ID NO: 30-39. Figure 2 ,discloses polypeptide sequences of full length FKBP-L and some of its deletion mutants and variant [0015]. Instant SEQ ID NO: 30 is identical to SEQ ID NO: 30 of Robson et al. Robson et al. teach the invention comprises vectors containing the isolated nucleic acid molecules of the invention, and comprise cells transfected with such vectors, such that an FKBP-L polypeptide is expressed [0107]. Therefore, Robson et al. teach the FKBP-L polypeptide encoded by the nucleic acid sequence of SEQ ID NO: 30, meeting the limitations of claims 8 (in part a).
Robson et al. does not teach an example of treatment of diabetic retinopathy. However, the teachings of Robson et al. are suggestive of the limitation.
In addition to the teachings above, Robson et al. teach treatment of wound healing including diabetic chronic ulcers [0220]. Robson et al. teach that methods of the invention can be used to treat diabetic retinopathy and diabetic neovascularization [0094, 0222, 0226].
Diabetic retinopathy is an eye condition that can cause vision loss and blindness in people who have diabetes. Please note that MPEP 2131.01 states: that an extra reference or evidence can be used to show an inherent characteristic of the thing taught by the primary reference. In the instant case, The NIH National Eye Institute is relied upon only to establish that diabetic retinopathy is an eye condition is people who are diabetic.
It would have been obvious to a person of ordinary skill in the art before the effective filing date of the invention to treat diabetic retinopathy with the nucleic acid and FKBP-L peptides of Robson et al. (SEQ ID NO: 2, 10, 30) because Robson et al. teach treatment of disorders mediated by angiogenesis with FKBP-L nucleic acids and FKBP-L polypeptides and diabetic retinopathy is a condition mediated by angiogenesis. There is a reasonable expectation of success given that Robson et al. teach methods of making and using the nucleic acids of SEQ ID NO: 30 and the FKBP-L polypeptides. Importantly, administering the same nucleic acid or polypeptide of Robson et al. would necessarily have all of the activities and properties of the composition of claim 8. The MPEP § 2112 states: “Once a reference teaching product appearing to be substantially identical is made the basis of a rejection, and the Examiner presents evidence or reasoning tending to show inherency, the burden shifts to the Applicant to show an unobvious difference ‘[t]he PTO can require an Applicant to prove that the prior art products do not necessarily or inherently possess the characteristics of his [or her] claimed product. Whether the rejection is based on inherency’ under 35 U.S.C. 102, on prima facie obviousness’ under 35 U.S.C. 103, jointly or alternatively, the burden of proof is the same…[footnote omitted].” The burden of proof is similar to that required with respect to product-by-process claims. In re Fitzqerald, 619 F.2d 67, 70, 205 USPQ 594, 596 (CCPA 1980) (quoting In re Best, 562 F.2d 1252, 1255, 195 USPQ 430,433- 34 (CCPA 1977)).” In other words, Robson et al. teach administering the same composition (FKBP-L nucleic acid or polypeptide ) to the same patient population (a subject that has diabetes and is suffering from diabetic retinopathy), therefore the same results would necessarily occur. Moreover, MPEP 2112.01 states: “Products of identical chemical composition cannot have mutually exclusive properties.” In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present.
With respect to claim 14, Robson et al. teach nucleic acids, including RNA [0060,0175].
With respect to claims 17-20, Robson et al. teach nucleic acids, including DNA and RNA [0060,0175]. Robson et al. teach a wide variety of host cells may be used for expression of the nucleic acids [0177]. Robson et al. teach FKBP-L fragments of SEQ ID NO: 10 (which identical to instantly claimed SEQ ID NO: 10), SEQ ID NO: 14 (which is identical to instantly claimed SEQ ID NO: 40), meeting the limitations of claims 17-20.
Response to Arguments
Applicant's arguments filed 8/12/25 have been fully considered but they are not persuasive. Applicants argue that the Examiner’s extrapolation of Robson to encompass all diabetic conditions is misplaced. Applicants argue that they identified a role for FKBPL in insulin resistance and subsequence beta-cell failure through a mechanism that is distinct from FKBPL’s established role in angiogenesis. Applicants point to p. 3 and 4 (specification) where Applicants determined that angiogenesis is not the driver of FKBPL mediated protection against obesity and other insulin resistant condition, such as type 2 diabetes. Applicants argue that the primary pathophysiology of diabetic retinopathy differs from angiogenesis-related processes like diabetic retinopathy. Applicants argue that insulin resistance in type 2 diabetes arises from impaired insulin signaling in skeletal muscle, liver and adipose tissue driven by chronic caloric excess and lipid accumulation (Accili et al. Ref attached). Applicants argue that diabetic retinopathy stems from hyperglycemia drive VEGF activation and microvascular damage. Applicants state that the condition is strongly associated with chronic hyperglycemia and while insulin resistance exacerbates retinal inflammation, it is not the primary driver of retinopathy (Zheng et al. Ref attached). Applicants argue that the instant application highlights that the method by which FKBPL works by targeting defects in the IRS-1 signaling pathways. Ex. 5 in conjunction with Fig. 7 discloses that FKBPL’s therapeutic peptide ALM201 can reduce secreted leptin, TIMP and IL-8 in cells. Ex. 6 discloses FKBPL can reduce the pro-inflammatory response in adipose tissue. Ex. 3 demonstrates that targeting such pathways results in improved glucose tolerance. Applicants argue that it is clear from the instant application that the FKBPL polypeptide and nucleic acid treats the glucose intolerance associated with diabetes and Robson provides no indication that FKBP-L could be used to treat diabetes by targeting such pathways. Applicants also argues that the patient population is same. Applicants argue that not all diabetic patients have diabetic retinopathy. Applicants argue only a third of diabetic patients are considered to have diabetic retinopathy (Lee et al. Ref attached). Applicants argue that even if Robson disclosed a subset of diabetic patients (who have diabetic retinopathy), the document provides no teaching that diabetic patients without diabetic retinopathy would also benefit from treatment with an FKBPL polypeptide or nucleic acid. Applicants argue that the examples of Robson are limited to angiogenesis and a skilled artisan would have no way of knowing that FKBPL would be suitable for all patients with diabetes (those without diabetic retinopathy). Applicants argue that Robson teaches away from using FKBPL for treatment of diabetes because the primary pathophysiology behind the two conditions is entirely different. Applicant argue PHOSITA would not be motivated to by Robson to treat diabetes and have a reasonable expectation of success.
This arguments and references discussed above were considered but are not persuasive because administering the same nucleic acid or polypeptide of Robson et al. would necessarily have all of the activities and properties of the composition of claim 8. Please see MPEP § 2112. Robson et al. teach administering the same composition (FKBP-L nucleic acid or polypeptide ) to the same patient population (a subject that has diabetes and is suffering from diabetic retinopathy), therefore the same results would necessarily occur. Moreover, MPEP 2112.01 states: “Products of identical chemical composition cannot have mutually exclusive properties.” In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. With respect to Applicants arguments that the Applicants have identified a role for FKBPL in insulin resistance through a specific mechanism (refs were provided in the response to arguments, p. 6-55), the MPEP 2112 states: "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In the instant case, the property is inherently present in the prior art and administering it to a subject with diabetes that has diabetic retinopathy would necessarily have the claimed function. The argument that the patient population is distinct because not all diabetic patients have diabetic retinopathy is not persuasive because diabetic retinopathy is a complication of diabetes and occurs in subjects that have diabetes. Therefore, a subject that has diabetic retinopathy is necessarily a subject that is diabetic. The arguments that Robson teaches away from using FKBPL to treat diabetes is not persuasive because Robson does not criticize, discredit or otherwise discourage the solution claimed (see MPEP 2145). In fact, Robson is suggestive of FKBPL protein or nucleic administration to subjects that have diabetic retinopathy.
For the reasons presented above, the rejection is maintained.
The rejection of claims 8, 14 and 17-22 under 35 U.S.C. 103 as being unpatentable over Robson et al. (US 2009/0192085, cited on IDS) as evidenced by NIH National Eye Institute in view of McCarthy et al. (WO2014/087023, cited on IDS) is maintained.
The teachings of Robson et al. are presented above in detail. The reference does not teach the composition further comprises the delivery peptide, RALA. However, the teachings of McCarthy et al. cure this deficiency.
McCarthy et al. teach amphipathic peptides for delivery of small molecules, in particular therapeutic agents that include nucleic acids or other small molecules (Abstract; Introduction p. 1, 1st para.). McCarthy et al. teach the amphipathic peptide of RALA (Table 1, p. 3). McCarthy et al. teach that it is understood that the amphipathic cell penetrating peptide complexes to nucleic acids or other agents to form a nanoparticle which penetrates a cell (p. 4, lines 18-23). McCarthy et al. provides examples of RALA peptide for complexed with nucleic acids for delivery to a cell (Fig. 2-9).
With respect to claims 21 and 22, it would have been obvious to a person of ordinary skill in the art before the effective filing date of the invention to complex the FKBP-L nucleic acid to the RALA peptide of McCarthy et al. for delivery to a cell. A person of ordinary skill in the art would be motivated to include the RALA peptide because McCarthy et al. teach that RALA complexes to nucleic acids and forms a nanoparticle which penetrates a cell. Therefore, a skilled artisan would be motivated to include RADA with the nucleic acid of Robson et al. to deliver the nucleic acid for treatment diabetic retinopathy. There is a reasonable expectation of success given that McCarthy et al. teaches RALA nucleic acid complexes are delivered to cells.
Response to Arguments
Applicant's arguments filed 8/12/25 have been fully considered but they are not persuasive. Applicants argue McCarthy does not cure the deficiencies of Robson.
This argument is not persuasive for the reasons presented above.
Conclusion
No claims are allowed.
THIS ACTION IS MADE FINAL. 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.
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/TARA L MARTINEZ/Examiner, Art Unit 1654