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 .
Election/Restrictions
Applicant’s election without traverse of leucine, sucrose, a patient suffering from as the patient population, and hydrogel in the reply filed on 10/06/2023 is maintained. However, the election of species has been expanded to include glucose.
Priority
This application claims the benefit under 35 U.S.C. §119(e) of U.S. Provisional Patent Application Ser. No. 63/043,585, filed June 24, 2020.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 07/07/2026 has been considered by the examiner.
Claims status
Claims 2, 4, 11, 13, 20, 28, 61-62, 65-66, and 76-84 are pending. Claims 1, 3, 5-10, 12, 14-19, 21-27, 29-34, 37-60, 63-64, and 67-75 are canceled. Claims 4 and 65-66 remain withdrawn. Claims 2, 11, 13, 20, 28, 35, 61-62, and 76-84 are examined in accordance to the elected species. Acknowledgement is made of the receipt and entry of the amendment to the claims filed on July 07, 2026.
Action Summary
The rejection to claims 1, 2, 11, 13, 20, 28, 35-36, 39, 61, 62, 70, and 77 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph (lack of enablement), set forth in the prior office action, is withdrawn in view of the claim amendments. However, amended claims 2, 11, 13, 20, 28, 35, 61, 62, and 77-82 are rejected under 35 U.S.C. 102(a) for lack of enablement for the reasons set forth below.
Claims 1, 2, 11, 20, 28, 35-36, 39, 61, and 70 rejected under 35 U.S.C. 103 as being unpatentable over Smith et al (Diabetes. 2015 May; 64(5): 1555–1563.) in view of Takayama et al (Scientific Reports, volume 8, Article number: 8278 (2018)), Lund-Ricard et al (Int. J. Mol. Sci. 2020, 21, 2718), Kalogeropoulou et al (Metabolism Clinical and Experimental 57 (2008) 1747–1752), Pereira et al (Nutrients 2014, 6, 3981-4001, and Abrams et al. (NAS, Published online June 15, 2015, pages E3365–E3373), are withdrawn in light of the claim amendment.
Claims 1, 2, 11, 13 20, 28, 35-36, 39, 61, 62, 70, and 76 rejected under 35 U.S.C. 103 as being unpatentable over Smith et al (Diabetes. 2015 May; 64(5): 1555–1563.) in view of Takayama et al (Scientific Reports, volume 8, Article number: 8278 (2018)), Lund-Ricard et al (Int. J. Mol. Sci. 2020, 21, 2718), Kalogeropoulou et al (Metabolism Clinical and Experimental 57 (2008) 1747–1752), Pereira et al (Nutrients 2014, 6, 3981-4001) and Abrams et al. (NAS, Published online June 15, 2015, pages E3365–E3373), as applied to claims 1, 2, 11, 20, 28, 35-36, 39, 61, and 70, in further view of Huang et al (ACS Biomater. Sci. Eng. 2020, 6, 5, 2913–2928) Richarson et al (Trends in Ecology & Evolution, Volume 24, Issue 6, June 2009, Pages 312-322), Sanguesa et al (Int J Mol Sci. 2019 Mar 5;20(5):1117, are also withdrawn in light of the claim amendment.).
New Rejection necessitated by claim amendment
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 2, 11, 13, 20, 28, 35, 61, 62, and 77-82 are rejected and claim 11 is rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for certain embodiments within the scope of the claim 2, including regeneration of at least one arm in a jellyfish and demonstrated regeneration of a digit in a mousse under the condition exemplified in the specification using the specific exemplified amount of L-leucine as Leucine methyl ester hydrochloride, insulin, and/or glucose/sucrose, the specification does not reasonably provide enablement for full scope of the claim. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The Examiner acknowledges that the specification provides sufficient enabling disclosure for certain embodiments within the scope of claim 2, including regeneration of an arm in jellyfish and demonstrates regeneration of a digit in a mousse under conditions exemplified in the specification. The rejection is therefore not based upon an absence of any operative embodiment of the claimed invention. Rather, the rejection is based upon the failure of the specification, when considered together with the state of the art, to enable the full scope of claim 2 without undue experimentation, particularly with respect to inducing regeneration of a limb in a fruit fly and the claimed extension of the disclosed digit-regeneration methods to a rat.
Independent claim 2 is directed to a method for inducing regeneration of a limb in a subject in need thereof, comprising administering to the subject: a therapeutically effective amount of a first regenerative agent comprising leucine; and a therapeutically effective amount of a second regenerative agent comprising one or more of insulin, sucrose and glucose, wherein the subject is: (i) a mouse or rat and the limb is a digit; (ii) a fruit fly and the limb is a leg; or (iii) a jellyfish and the limb is an arm.
The factors to be considered in determining whether undue experimentation is required are summarized in re Wands 858 F.2d 731, 8 USPQ2nd 1400 (Fed. Cir, 1988). The court in Wands states: "Enablement is not precluded by the necessity for some experimentation such as routine screening. However, experimentation needed to practice the invention must not be undue experimentation. The key word is 'undue,' not 'experimentation.' " (Wands, 8 USPQ2d 1404). Clearly, enablement of a claimed invention cannot be predicated on the basis of quantity of experimentation required to make or use the invention. "Whether undue experimentation is needed is not a single, simple factual determination, but rather is a conclusion reached by weighing many factual considerations." (Wands, 8 USPQ2d 1404). The factors to be considered in determining whether undue experimentation is required include: (1) the breadth of the claims, (2) the nature of the invention, (3) the state of the prior art, (4) the relative skill of those in the art, (5) the predictability or unpredictability of the art, (6) the amount or direction or guidance presented in the specification, (7) the presence or absence of working examples, and (8) the quantity of experimentation necessary. These factors need not be considered separately where they overlap but rather are weighed together based upon the evidence as a whole. See MPEP2164.01(a), 2164.04, and 2164.08.
the nature of the invention and (2) state and predictability of the art
The claimed invention concerns chemically induced appendage regeneration in
biologically distinct animal systems. Although the specification identifies modulation of pathways including mTOR as associated with regeneration and provides certain successful working examples, the evidence of record demonstrates that induction of appendage regeneration, particularly adult Drosophila, is highly dependent upon experimental conditions and is not a result that predictability follows merely from administration of leucine together with insulin or a sugar.
Sustar et al. (BioRxiv, October 27, 2022), previously cited attempted to reproduce the reported dietary-induced leg regeneration in adult Drosophila and reported that, after amputation more than 1,000 fruit-fly tibiae and administering supplemented diets, no instances of leg regeneration were observed. Sustar et al. further reported that recent paper by Abrams et al. (2021) claimed that a simple dietary supplement is sufficient to induce appendage regeneration in jellyfish, flies, and mice. This would be remarkable, if true, because it was previously thought that flies and mice lack the capacity for regeneration after injury. We therefore sought to replicate their provocative results. (See Abstract.) Sustar et al. additionally, reported that an absence of neurons, muscles or other living cells in amputated tibiae and concluded that their results failed to provide evidence of leg regeneration under the conditions tested. (See page 2.)
Applicant has submitted Li et al. (eLife 2023;12: e85370) in the remarks/response of 07/07/2026 in response to Sustar et al. Li et al. attributes the different experimental outcomes to multiple differences between the protocols and identifies factors including amputation method, age of the flies, treatment concentration, anesthesia protocol, housing density, and regeneration assessment as parameters capable of altering the regenerative outcome. (See page 1.) Li et al. further identifies differences in the concentration of amino acids and insulin employed by Sustar et al. relative to the protocol relied upon by Applicant. (See page 3.)
Thus, although Li et al. provides explanation to why Sustar et al. may not have reproduced Applicant’s reported results, Li et al. does not establish that the claimed regenerative response is broadly predictable. Rather, the evidence demonstrates whether adult fruit-fly leg regeneration occurs depends upon the selection and control multiple experimental parameters and that materially different outcomes can result when those parameters are varied.
The state of the prior art further supports the unpredictability of the claimed fruit fly embodiment. Amaya et al. (eLife 2016;5: e21583) published before the filing date of the instant application, discusses appendage regeneration in orthopods and expressly states that although Drosophila melanogaster had long been employed as a model organism for development and genetic studies, “fruit flies cannot regenerate their limbs.” Amaya contrasts Drosophila with the crustacean Parhyale hawaiensis, which possesses appendage-regenerative capability. (See page 1.) Thus, at the time of Applicant’s invention, the art did not regard adult fruit-fly limb regeneration as an ordinary or predictable biological response.
This evidence does not establish that the particular regeneration reported by Applicant is impossible. Rather, it demonstrates that inducing such regeneration represented a departure from the ordinarily expected regenerative capacity of Drosophila and therefore required sufficient guidance to permit the skilled artisan to reproducibly achieve the claimed result without undue experimentation. This conclusion is further supported by Sustar’s subsequent inability to reproduce the reported regenerative response and by Li’s explanation that successful regeneration depends upon multiple experimental parameters, including treatment concentrations and other protocol conditions.
the breadth of the claims and (4) the guidance provided
Claim 2 does not limit the method to the particular concentrations, treatment
conditions, animal ages, amputation procedures, housing conditions, or other experimental parameters identified by Li et al. as effective whether a regenerative response is obtained. Instead, claim 2 broadly requires administration of a “therapeutically effective amount” of the first and second regenerative agents.
The Examiner recognizes that an amount that is not therapeutically effective does not satisfy the express language. Nevertheless, the functional recitation of a “therapeutically effective amount” does not itself provide the skilled artisan with the information necessary to identify the claimed regenerative result. Where the evidence demonstrates that successful regeneration depends upon multiple interacting experimental parameters, determining which concentrations and condition constitute therapeutically effective conditions throughout the claimed scope requires empirical determination.
The specification provides useful guidance and working examples for certain embodiments. However, the evidence does not establish a generally appliable relationship from which a skilled artisan could reasonably predict operative conditions across the entire presently claimed scope without substantial experimentation.
Mousse and Rats embodiments
The Examiner further acknowledges that the specification provides working examples of mousse digit regeneration, including regeneration following particular amputation procedures and administration conditions, including 500 nM for the insulin and 100 µM for the L-leucine where the L-leucine is L-leucine methyl ester hydrochloride. Accordingly, the rejection is not based upon a finding that mouse digit regeneration is itself wholly non-enabled.
Claim 2, however, encompasses alternatively a rat having a digit subjected to the claimed method. Applicant asserts that the disclosed mouse methods would have readily applicable to rats because rats are mammals having substantially similar physiology to mice. That assertion has been considered but does not establish, on the present record, that the particular appendage-regeneration response demonstrated in mouse digits would predictably occur in rats using the breadth of treatment conditions encompassed by claim 2.
That is particular significant in view of the evidence demonstrating that the claimed regenerative response can depend upon biological and experimental parameters and that changes in such parameters can determine whether regeneration occurs. The specification does not provide a rat working example or sufficient rat-specific guidance establishing that the disclosed mouse protocol may be transformed to rat digit regeneration without determining operative condition through additional experimentation.
(5) The quantity of experimentation and (6) Conclusion
The issue is not that some experimentation would be required. Rather, considering the nature of appendage-regeneration, the demonstrated sensitivity of the regenerative response to multiple experimental parameters, the conflicting reproduction results concerning adult fruit-fly limb regeneration, the breadth of the functionally defined “therapeutically effective amount,” and the absence of sufficient guidance establishing predictable application throughout the claimed fruit-fly and rat embodiments, the experimentation necessary to identify operative conditions throughout the full scope of claim 2 would have been undue.
Accordingly, the pre-filing sate of the art reflected by Amaya, together with the conflicting reproduction results and Li’s identification of multiple outcome-determinative experimental variables, weighs strongly against predictability and in favor of a finding that the experimenting necessary to identify operative conditions across the scope of the claimed fruit-fly embodiment would have been undue.
Therefore, when the Wands factors are considered as a whole, the disclosure does not enable a person of ordinary skill in the art to practice the full scope of the claim without undue experimentation. The dependent claims are rejected for the same reasons to the extent that they do not remove the foregoing non-enabled subject matter.
Acknowledgement is made of the receipt and entry of Applicant’s remarks/response filed on July 07, 2026.
Applicant’s arguments have been fully considered but are not persuasive to establish enablement commensurate in scope with the presently claimed subject matter.
Applicant correctly notes that claim 2 has been substantially narrowed and identifies examples demonstrating regeneration in mice and fruit flies. The Examiner has considered these examples and, as discussed above, acknowledges that the specification provides enabling disclosure for particular demonstrated embodiments, including mouse digit regeneration and jellyfish arm regeneration. The present rejection therefore does not rest upon the absence of working examples.
Applicant further relies upon Li et al. to explain the failure of Sustar et al. to reproduce the reported fruit-fly regenerative response. This evidence has been considered. However, Li et al. does not establish that the claimed fruit-fly regenerative response is predictable throughout the scope of claim 2. Rather, Li et al. identifies multiple differences between the protocols-including treatment concentration, amputation method, animal age, anesthesia, housing density, and regeneration assessment-as parameters capable of materially affective whether a regenerative response is observed.
Accordingly, Li et al.’s explanation of the negative Sustar results does not remove the enablement concern. Instead, the evidence demonstrates that successful fruit-fly appendage regeneration depends upon the selection and control of multiple experimental parameters. Claim 2 does not recite these parameters but instead functionally requires therapeutically effective amounts of the regenerative agents.
The Examiner acknowledges that an ineffective amount does not fall within the express “therapeutically effective amount” limitation. However, this functional limitation does not itself teach the skilled artisan which amounts and conditions will successful induce the claimed regeneration. The relevant question is whether the specification and knowledge in the art provide sufficient guidance for identifying operative conditions throughout the claimed scope without undue experimentation. In view of the conflicting experimental results and Li et al.’s identification of multiple outcome-determinative parameters, the evidence does not establish such predictability for the full scope presently claimed.
Applicant’s argument that the mouse protocol would readily extend to rats because rats and mice possess substantially similar physiology has likewise been considered. The specification demonstrates mouse embodiments but does not demonstrate rat digit regeneration or otherwise establish that the particular regenerative response at issue, predictably transfers from mouse to rat. General physiological similarity between the species does not, without further evidence, resolve the concern presented by a regenerative phenomenon shown by the evidence to be sensitive to biological and experimental conditions.
Therefore, although the amendments materially narrow the claims and overcome portions of the enablement deficiencies identified in the prior office action, the presently claimed subject matter continues to encompass fruit-fly leg regeneration and rat digit regeneration without disclosure sufficient to enable those portions of the claim without undue experimentation. Accordingly, the enablement rejection set forth above is maintained against the presently identified claims.
New Rejection necessitated by claim amendment
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.
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 non-obviousness.
Claims 2, 11, 20, 28, 35, and 61 are rejected under 35 U.S.C. 103 as being unpatentable over Lund-Ricard et al. (Int. J. Mol. Sci. 2020, 21, 2718) in view of Takayama et al. (Scientific Reports, volume 8, Article number: 8278 (2018)) and Smith et al. (Diabetes. 2015 May; 64(5): 1555–1563.).
Lund-Ricard teaches that many vertebrates are capable of appendage regeneration and specifically, that in mammals, regeneration in which the structure of lost tissue is recapitulated occurs at the distal tip of the digit. Lund-Ricard further teaches that in mice the digit-regeneration process includes wound closure, blastema formation, cell proliferation and differentiation. (See page 3, second paragraph.) Lund-Ricard also teaches that mTOR signaling is important in controlling appendage regeneration. Following appendage amputation, mTOR signaling is active in wound epidermal cells; osteoblasts, and the proliferative region of the blastema; inhibition of mTORC1 suppresses blastema formation, and mTORC1 is required for cell proliferation and survival during regenerative outgrowth. Lund-Ricard teaches that growth-factor-mediated activation of mTOR can alter the regenerative response and that mTOR activity is necessary for cell proliferation, survival, differentiation, and growth during appendage regeneration. (See third paragraph of page 3.) Lund-Ricard additionally taches that leucine stimulation is associated with mTOR signaling and that supplementation with amino acids such as leucine has been successfully tested in rats and mice to ameliorate regenerative processes. (See page 4, fourth paragraph.)
Lund-Ricard, however, does not expressly teach administering therapeutically effective amounts of leucine, including L-Leucine and glucose as the claimed first and second regenerative agents for inducing mammalian digit regeneration.
Takayama teaches leucine and glutamine treatment in an appendage-regeneration model and teaches that leucine/glutamine signaling through mTORC1 promotes cell proliferation and participates in position-dependent Zebrafish fin regeneration. (See Abstract.) Thus, Takayama provides evidence that leucine-mediated mTORC1 activation is useful in an appendage-regeneration process. Takayama expressly teaches the use of L-leucine in its appendage-regeneration experiment, including treatment of amputated zebrafish fins with L-leucine in combination with L-glutamine. (See Materials and Methods Section of page 11.)
Smith teaches that glucose and leucine stimulate mTOR phosphorylation and reports that insulin-glucose infusion and leucine-containing treatment increase muscle mTOR phosphorylation. (See page 1561, left column.)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to administer therapeutically effective amounts of leucine and glucose to a mouse having an injured distal digit in order to induce or promote the known regenerative response of the mammalian distal digit. One would have been motivated to do so because Lund-Ricard teaches that mammalian distal digit possesses regenerative capacity and identifies mTOR as an important regulator of appendage regeneration; Takayama teaches that leucine-mediated mTORC1 signaling participates in appendage regeneration, and Smith teaches that leucine and glucose stimulate the mTOR pathway.
One of ordinary skill in the art would have had a reasonable expectation of successfully inducing or promoting regeneration because the proposed modification does not require creating regenerative capacity in tissue for which no regenerative response was known. Rather, Lund-Ricard expressly teaches that the mammalian digital tip possesses the capacity to regenerate lost tissue and identifies mTOR signaling as important to the regerative response. The skilled artisan therefore would reasonably have expected administration of agents known to stimulate the implicated mTOR pathway to promote that known regenerative response.
Regarding claim 11, Takayama expressly teaches leucine, including L-leucine and L-glutamine as the amino acids used in the mTOR-associated regenerative pathway. Accordingly, selection of L-leucine and L-glutamine as the first regenerative agents would have been obvious. Although the claims do not require L-glutamine, the “comprising” language for the first regenerative agent does not exclude other agents including L-glutamine.
Regarding claim 20, Lund-Ricard’s mammalian digit-regeneration teaching concerns regeneration following amputation or injury. A mammalian subject having an amputated portion of a digit is a subject having an acute injury to the limb. Accordingly, the modified method satisfies the additional limitation of claim 20.
Regarding claim 28, Lund-Ricard teaches mammal regeneration in which the structure of the lost digit tissue is recapitulated and describes the mouse process as involving wound closure, blastema formation, proliferation, and differentiation. (See page 3, second paragraph.) The resulting regeneration therefore represents therefore represents patterned regeneration rather than merely nonspecific would healing. It would have been reasonably expected that promoting this known regenerative process would produce the patterned regeneration recited in claim 28.
Regarding claim 35, Lund-Ricard teaches that control of when and for how long an mTOR-targeting agent is active is a valuable parameter of treatment design and further teaches the importance of understanding the “regenerative window” because treatment must occur in a regeneration-competent environment. (See first paragraph of “Conclusion” section of page 16.) Accordingly, it would have been obvious to initiate administration of one or both regenerative agents within a therapeutically effective time window corresponding to the regeneration-competent period following injury, with a reasonable expectation of promoting regeneration. Thus, at least alternative (iii) of claim 35 would have been obvious.
Regarding claim 61, Smith directly evaluates whether Leucine-mediated mTOR activation impairs insulin-mediated glucose disposal. Simth teaches that leucine ingestion increased mTOR signaling but, unlike whey protein, did not impair insulin-mediated glucose disposal. (See first paragraph of the left column of page 1560.) Smith’s experimental protocol administered insulin and dextrose during hyperinsulinemic-euglycemic claim while leucine was ingested. (See right column of page 1556.). Thus, Smith provides direct experimental evidence that leucine can be administered under insulin/glucose conditions while activating mTOR without inducing the insulin-resistant response measured by impaired insulin-mediated glucose disposal. Accordingly, one of ordinary skill would have had reason to employ treatment conditions known to provide the desired mTOR activation without inducing insulin resistance and would reasonably have expected the modified method to possess the physiological result recited in claim 61.
Claim 13 is rejected under 35 U.S.C. 103 as being unpatentable over Lund-Ricard et al. (Int. J. Mol. Sci. 2020, 21, 2718) in view of Takayama et al. (Scientific Reports, volume 8, Article number: 8278 (2018)) and Smith et al. (Diabetes. 2015 May; 64(5): 1555–1563.) as applied to claims 2, 11, 20, 28, 35, and 61 above.
The teachings of Lund-Ricard et al., Takayama et al., and Smith et al. have been discussed above.
However, Lund-Ricard et al., Takayama et al., and Smith et al. collectively do not expressly teach administering leucine, a sugar, and insulin for inducing regeneration in a digit of a mouse.
Simth teaches simultaneous administration of human insulin, dextrose, and leucine and demonstrates increased mTOR signaling under such conditions. (See page 1556.). Lund-Ricard further teaches that insulin-like growth-factor signaling activates mTORC1 during appendage regeneration and that such growth-factor-mediated mTOR activation contributes to wound covering, blastema formulation, and regerative outgrowth. (See third paragraph of page 3.)
It would therefore have been obvious to employ insulin as the second regenerative agent in the modified method because insulin-mediated signaling was known to activate the same mTOR-associated pathway implicated in regenerative processes. One of ordinary skill would have reasonably expected insulin-mediated stimulation of the pathway to promote the known regenerative response of the mammalian distal digit.
Claim 62 is rejected under 35 U.S.C. 103 as being unpatentable over Lund-Ricard et al. (Int. J. Mol. Sci. 2020, 21, 2718) in view of Takayama et al. (Scientific Reports, volume 8, Article number: 8278 (2018)) and Smith et al. (Diabetes. 2015 May; 64(5): 1555–1563.) as applied to claims 2, 11, 20, 28, 35, and 61 above, in further view of Huang et al (ACS Biomater. Sci. Eng. 2020, 6, 5, 2913–2928)
The teachings of Lund-Ricard et al., Takayama et al., and Smith et al. have been discussed above.
The combination of Lund-Ricard et al., Takayama et al., and Smith et al. does not expressly teach contacting the subject with the scaffold required by claim 62.
Huang teaches a regenerative scaffold comprising a leucine-zipper-based self-assembling hydrogel having function-specific motifs for tissue regeneration and capable of tethering regenerative growth factors, including BMP-2 and providing controlled release of such growth factors with regenerative activity in vivo. (See Abstract.) The Office Action’s Huang mapping specifically identifies hydrogel scaffold carrying BMP-2 and other regenerative growth factors.
Claim 77 is rejected under 35 U.S.C. 103 as being unpatentable over Lund-Ricard et al. (Int. J. Mol. Sci. 2020, 21, 2718) in view of Takayama et al. (Scientific Reports, volume 8, Article number: 8278 (2018)) and Smith et al. (Diabetes. 2015 May; 64(5): 1555–1563.) as applied to claims 2, 11, 20, 28, 35, and 61 above, in further view of Sanguesa et al (Int J Mol Sci. 2019 Mar 5;20(5):1117).
The teachings of Lund-Ricard et al., Takayama et al., and Smith et al. have been discussed above.
The combination of Lund-Ricard et al., Takayama et al., and Smith et al. does not expressly teach the second regenerative agent comprising sucrose.
Sanguesa teaches that activation of mTORC1 by nutrients including amino acids and simple sugar. Sucrose is a simple sugar. (See Last paragraph of page 1 bridging first paragraph of page 2.)
In view of the teaching that simple sugars activate the same mTORC1 pathway implicated in the regenerative process, it would have been obvious to select sucrose as an alternative second regenerative agent for use with leucine. One of ordinary skill would have reasonably expected sucrose, as a member of the taught class of simple sugars, to provide nutritional modulation of the mTOR-associated pathway and therefore to be suitable for use with leucine in promoting the regerative response.
Claims 78-80 are rejected under 35 U.S.C. 103 as being unpatentable over Lund-Ricard et al. (Int. J. Mol. Sci. 2020, 21, 2718) in view of Takayama et al. (Scientific Reports, volume 8, Article number: 8278 (2018)) and Smith et al. (Diabetes. 2015 May; 64(5): 1555–1563.) as applied to claims 2, 11, 20, 28, 35, and 61 above, in further view of Dolan et al. (Stem Cells Translational Medicine 2018;7:262–270) and Dawson et al. (Regeneration.2017;4:140–150.) Dawson is submitted with the IDS filed on September 27, 2021.
The teachings of Lund-Ricard et al., Takayama et al., and Smith et al. have been discussed above.
The combination of Lund-Ricard et al., Takayama et al., and Smith et al. does not expressly teach the mouse subject comprising a loss of at least 30% of a distal phalange of the digit (claim 78) where the loss is at least 60% of the distal phalange (claim 79), and where the loss is not more than a portion of a middle phalange of the digit.
Dolan teaches that endogenous mouse digit regeneration is dependent upon the level of amputation. Dolan teaches a naturally regeneration-competent distal P3 amputation removing approximately 15-20% of P3 and separately identifies a 70% P3 amputation as nonregenerative proximal amputation. (See part I of page 263 bridging page 264.)
Dolan nevertheless teaches that regeneration-incompetent digit wounds possess latent regenerative potential capable of being activated through targeted regenerative treatment. (See page 267.) Thus, the natural boundary between regenerative and nonregenerative digit injuries was known to represent an absolute inability of the digit to respond to regenerative stimulation.
Dawson reinforces this teaching. Dawson explains that mammalian regeneration is normally restricted to portions of distal P3 and that amputations proximal to the P3 nail matrix ordinarily result in truncation and scar formation. (See page 140.) Nevertheless, Dawson experimentally demonstrates that exogenous BMP-2 induces regeneration of an ordinary regeneration-incompetent adult mouse P2 amputation and expressly identifies a temporal “regeneration window” during which the injured tissue is responsive to regenerative stimulation. (See Abstract.)
Thus, Dolan and Dawson teach that increasingly proximal digit injuries that fail to regenerate spontaneously nevertheless retain regenerative potential capable of therapeutic activation.
For claim 78 that requires a mouse or a rat, sucrose or glucose as the secondary regenerative agent, and loss of at least 30% of a distal phalange, it would have been obvious to apply the regerative-promoting treatment to the modified Lund-Ricard method to a mouse having a P3 injury extending beyond the naturally regenerative distal region, including an injury involving at least 30% of P3, Doan expressly teaches therapeutic approaches directed toward extending regenerative potential beyond the natural distal digit boundary. One of ordinary skill would therefore have been motivated to apply the mTOR-modulating regenerative treatment to such a digit injury and would have reasonably expected a regenerative response because the art teaches that more proximal wounds retain latent regenerative potential susceptible to therapeutic activation.
With respect to claim 79, claim 79 expressly requires loss of at least 60% of the distal phalange. Dolan expressly teaches a 70% P3 amputation as a proximal nonregenerative digit injury. Because 70% falls within the recited range of “at least 60%,” Dolan directly teaches an injury within the numerical scope of claim 798. Although Dolan’s 70% P3 injury does not ordinarily regenerate spontaneously, Dolan teaches that nonregenerative digit wounds retain latent regenerative potential capable of therapeutic activation. Dawson further demonstrates that an even more proximal, ordinarily regeneration-incompetent P2 amputation can be induced to regenerate by targeted regenerative treatment. Accordingly, one of ordinary skill would have been motivated to administer the regeneration-promoting treatment of the modified method to the 70% P3 injury taught by Dolan and would have reasonably expected a regenerative response because the art demonstrates that regenerative failure at proximal digit levels can be overcome by appropriate regenerative stimulation.
With respect to claim 80, claim 80 further requires that the loss be no more than a portion of a middle phalanx of the digit.
Dawson expressly uses adult mouse P2 (middle-phalanx) amputation as a model for therapeutically induced regeneration and teaches that exogenous BMP-2 stimulates regeneration of the amputated P2 bone. Dawson further teaches that the response depends upon administration during a regeneration-permissive window.
It would have been obvious to apply the regeneration-promoting treatment to the modified method to a mouse having digit loss extending into P2 because Dawson establishes that even such a normally nonregenerative proximal digit injury can respond successfully to regenerative stimulation. Dawson is relied upon for its teaching that P2 injury is susceptible to therapeutically induced regeneration, and not for a proposition that BMP-2 and leucine are equivalent agents. The reason for selecting the claimed leucine/second-agent treatment is supplied by Lund-Ricard, Takayama, and Smith.
Claims 83 and 84 are rejected under 35 U.S.C. 103 as being unpatentable over Lund-Ricard et al. (Int. J. Mol. Sci. 2020, 21, 2718) in view of Takayama et al. (Scientific Reports, volume 8, Article number: 8278 (2018)) and Smith et al. (Diabetes. 2015 May; 64(5): 1555–1563.) as applied to claims 2, 11, 20, 28, 35, and 61 above, in further view of Abrams et al. (NAS, Published online June 15, 2015, pages E3365–E3373)).
The teachings of Lund-Ricard et al., Takayama et al., and Smith et al. have been discussed above.
Lund-Ricard teaches mTOR as an important regulator of regenerative processes regulator and teaches that growth-factor-mediated mTOR activation participates in wound response, blastema formation, cell proliferation, differentiation, and regenerative outgrowth. Lund-Ricard further discusses the involvement of mTOR signaling in regenerative processes extending across animal systems.
Smith teaches insulin-glucose administration and demonstrates activation of mTOR signaling under insulin/glucose conditions.
The combination of Lund-Ricard et al., Takayama et al., and Smith et al. does not expressly teach the subject is a jellyfish comprising a loss of at least a full arm (claim 83), wherein the loss is no more than three arms (claim 84).
Abrams teaches newly strobilated Aurelia aurita ephyrae having eight arms and subjects these ephyrae to arm-amputation injuries. Abrams expressly describes post-amputation ephyrae having five, six, and seven arms, corresponding to loss of three, tow, and one full arm, respectively. (See figures 1 and 2.) Accordingly, Abrams teaches the jellyfish ephyra and full-arm-loss limitations recited in claims 83-084. Abrams teaches that untreated amputated ephyrae restore radial symmetry by recognizing their remaining arms rather than by regenerating the missing arms. Indeed, Abrams expressly states that the ephyrae do not regenerate the lost parts. (See Abstract.) The Examiner therefore does not rely upon Abrams as teaching regeneration of the amputated arm. Rather, Abrams is relied upon for the claimed ephyra/arm-amputation model. Lund-Ricard and Smith provide the reason to employ mTOR-promoting regenerative signaling, including insulin-mediated signaling, in an effort to induce regenerative response following that known appendage injury.
It would have been obvious to one of ordinary skill seeking to promote regenerative following the known ephyra arm-amputation injury of Abrams to administer insulin as an mTOR-promoting regenerative agent. One of ordinary skill in the art would have had a reasonable expectation of promoting a regenerative response because the art identified mTOR signaling as an important regulator of regenerative processes and identified insulin/growth-factor signaling as a means of activating that pathway.
Regarding claim 84, Abrams’ disclosure of an ephyra having seven remaining arms after amputations corresponds to loss of one full arm and therefore falls within the recited “no more than three arms.” Abrams additionally teaches post-amputation ephyrae having five, and six arms corresponding to loss of three and two arms.
Claim 76 is rejected under 35 U.S.C. 103 as being unpatentable over Lund-Ricard et al. (Int. J. Mol. Sci. 2020, 21, 2718) in view of Takayama et al. (Scientific Reports, volume 8, Article number: 8278 (2018)) and Smith et al. (Diabetes. 2015 May; 64(5): 1555–1563.) as applied to claims 2, 11, 20, 28, 35, and 61 above, in further view of Abrams et al. (NAS, published online June 15, 2015, pages E3365–E3373)) as applied to claims 83 and 84.
The combination of Lund-Ricard et al., Takayama et al., Smith et al., and Abrams does not expressly teach the jellyfish is in a hypoxic condition.
Abrams teaches that Aurelia jellyfish are adapted to and can thrive in oxygen-poor waters. (See page E335, left column.) Thus, Abrams establishes that oxygen-poor/hypoxic conditions constitute an environmental condition tolerated by the claimed jellyfish.
It would therefore have been obvious to practice the otherwise obvious regenerative method in an Aurelia Jellyfish under hypoxic conditions because the art expressly teaches that the organism survives and thrives under such conditions. Claims 76 does not require that hypoxia causes or enhances regeneration, but merely that the jellyfish be in a hypoxic condition. Accordingly, one of ordinary skill would reasonably to practice the otherwise obvious regenerative method in a jellyfish under such a known, tolerated environmental condition.
Applicants’ argument
Acknowledgement is made of the receipt and entry of Applicant’s remarks/response filed on July 07, 2026.
Applicant’s arguments filed on July 07, 2026, in response to the prior art rejection have been fully considered but are not persuasive to overcome the rejections as presently formulated. The rejection has been reconsidered and modified in view of the amended claims and Applicant’s arguments. In particular, Lund-Ricard, rather than Smith, is relied upon as the principal reference for the mouse/rat digit-regeneration embodiment of claim 2, and additional references are applied only when necessary to address the limitations of the respective dependent claims.
Applicant argues that Smith is directed to hyperinsulinemic-euglycemic clamp study in human subjects concerning glucose disposal and insulin resistance, rather than limb regeneration, and therefore does not provide a proper basis for extrapolating leucine/glucose treatment to appendage regeneration. This argument does not address the rejection as presently formulated. The Examiner agrees that Smith, standing alone, does not teach mammalian digit regeneration and does not rely upon Smith for that teaching. Rather, Lund-Ricard expressly teaches that, in mammals, regeneration in which the structure of lost tissue is recapitulated occurs at the distal tip of the digit and further teaches that the mouse digit-regeneration process includes wound closure, blastema formation, cell proliferation, and differentiation. Lund-Ricard additionally identifies mTOR as an important regulator of appendage regeneration. (See Page 3.) Takayama provides the further teaching that leucine-mediated mTORC1 signaling participates in an appendage-regeneration process, while Smith is relied upon more narrowly for its teaching concerning leucine/glucose modulation of mTOR signaling. Smith expressly states that studies in cultured rat muscle demonstrate that both glucose and leucine stimulate mTOR phosphorylation and further reports increased mTOR phosphorylation under insulin/glucose and leucine-containing conditions.
Accordingly, the rejection is not based upon an assumption that the metabolic effects observed by Smith in humans would, by themselves, predict limb regeneration. Instead, the references are relied upon for what they could collectively have taught one of ordinary skill: (1) the mammalian distal digit is regeneration competent; (2) mTOR signaling is important to appendage regeneration; (3) leucine-mediated mTOR signaling participates in appendage regeneration; and (4) leucine and glucose are known modulators of the implicated mTOR pathway. The skilled artisan would therefore expect to employ the known mTOR-modulating agents to promote the regenerative response already known to occur in the mammalian distal digit.
Applicant further argues that Takayama concerns Zebrafish fin regeneration rather than mouse or rat digit regeneration.
In response, this argument is not persuasive because Takayama is not relied upon as teaching the claimed mammalian subject or digit. Lund-Ricard supplies those teachings. Takayama is relied upon for the more limited but pertinent proposition that treatment involving leucine can modulate mTORC1 in an appendage-regeneration context. A reference need not individually disclosure every limitation of the claimed invention where the rejection is based upon the combined teachings of the references.
Applicant also relies upon Lund-Ricard’s statement that, in mammals, regeneration is which lost tissue is recapitulated “appears to be limited to the distal tip of the digit.” Rather than teaching away from broad claim 2, that disclosure supports the rejection of claim 2 because the claim merely requires a mouse or rat in which “the limb is a digit” and does not require that the injury extend proximately beyond the regeneration-competent distal regions. Thus, the naturally regenerative distal digit expressly taught Lund-Ricard falls within the scope of claim 2.
Applicant additionally notes Lund-Richard’s teaching that mTORC1 is necessary for myofiber growth but not myogenesis.
In response, this rejection does not equate muscle regeneration or myogenesis with the claimed digit regeneration. Lund-Ricard separately and expressly discusses appendage regeneration, including blastema formation, proliferation, survival, differentiation, and regenerative outgrowth, and states that mTOR signaling is important in controlling that process. The cited statement concerning myogenesis relates to a different regeneration context and does not negate Lund-Ricard’s express teachings regarding the role of mTOR in appendage regeneration.
Applicant further argues that Pereira merely concerns recovery of tibialis anterior muscle in rats and therefore does not establish regeneration of a mammalian digit.
In response, this argument is moot with respect to the presently formulated principal rejection because Pereira is no longer necessary to establish the limitations of claim 2. The mammalian digit-regeneration teaching is supplied directly by Lund-Ricard.
Applicant argues that successful regeneration of a mouse digit would not have been reasonably predicted because the prior art recognized that mammalian regeneration was limited to the distal digit tip and because Sustar subsequently characterized the reported regeneration results as remarkable and expressed skepticism concerning appendage regeneration.
In response, this argument does not overcome claim 2. The rejection of claim 2 does not require a reasonable expectation of regenerating an ordinarily nonregenerative proximal digit injury. Lund-Ricard expressly establishes that the distal mammalian digit is regeneration competent. Thus, for claim 2, the skilled artisan is not being asked to create an unknown regenerative capacity, but rather to promote a regenerative process already known to occur within the scope of the claim. The Examiner has nevertheless considered the evidence concerning the natural regenerative boundary when applying the prior art to the more specific newly added claims 78-80. Those claims are not rejected merely on the basis that the naturally regenerative distal tip would predict regeneration at every more proximal amputation level. Dolan expressly distinguishes naturally regenerative distal P3 amputations from proximal nonregenerative amputations and teaches that the mouse digit constitutes a model for exploring the regenerative potential of nonregenerative amputations. Dolan explains that distal P3 amputation removes approximately 15-20% of P3 and regenerates, while the reference proceeds to discuss approaches for stimulating regeneration where it does not ordinarily occur. Moreover, Dolan expressly identifies a 70% P3 amputation as a nonregenerative proximal injury. Because 70% falls within the “at least 60%” limitation of claim 79, the injury severity recited in claim 79 was itself known. More importantly, Dolan and Dawson teach that the endogenous regenerative boundary is not an absolute biological barrier to induced regeneration. Dawson expressly describes P2 as a model for testing approaches that enhance regeneration and demonstrates that exogenous BMP-2 can induce regeneration of an ordinarily nonregenerative middle-phalanx amputation.
Thus, with respect to claims 78-80, the rejection does not reason that a proximal injury would spontaneously regenerate. Rather, the art teaches the opposite-such injuries ordinarily do not regenerate-and the art expressly demonstrates that a regeneration-promoting intervention can activate regenerative potential beyond the natural boundary. Accordingly, the prior art provides both a reason to apply a regeneration-promoting treatment to such injuries and a reasonable expectation that appropriately stimulated proximal digit tissue can mount a regenerative response.
Applicant reliance upon expression of disbelief therefore does not establish non-obviousness of the presently rejected mouse claims. Expressions of skepticism are relevant evidence and have been considered. However, obviousness determination must be based upon the evidence as a whole. Here, Dolan and Dawson provide affirmative pre-filing evidence that regeneration-incompetent mammalian digit injuries retain therapeutically accessible regenerative potential. The act that spontaneous regeneration at a particular amputation level was regarded as unexpected does not establish that therapeutically induced regeneration at that level would have lacked a reasonable expectation of success where the prior art expressly taught strategies for inducing regeneration beyond the endogenous boundary.
The Examiner also notes that Sustar’s skepticism was directed substantially to the reported broad appendage-regeneration phenomenon, particularly the Drosophila work. Claims 81-82, which specifically select the fruit-fly embodiment, are not rejected under 103 in the present action. Thus, no position is taken in the 103 rejection that a skilled artisan would have had a reasonable expectation of successfully inducing the fruit-leg regeneration recited in claims 81-82.
To the extent Applicant maintains that the cited references fail to teach the administration schedule of claim 35, the argument is not persuasive in view of the presently applied teaching of Lund-Ricard. Claim 35 is written in the alternative, and only one alternative needs to be established. Alternative (iii) requires initiation of one or both regenerative agents within a therapeutically effective time window. Lund-Ricard expressly teaches that controlling when and how long a drug affecting mTOR is active represents a valuable treatment-design parameter and emphasizes the importance of the “regeneration window,” because treatment must occur in a regenerative-competent environment. This teaching directly provides a reason for initiating regenerative treatment within a therapeutically effective time-period following injury. Accordingly, the rejection no longer relies upon the prior “patient compliance” rationale.
Applicant’s argument concerning insulin resistance have also been considered. Smith acknowledges prior reports associating branched-amino acids and leucine with impaired insulin sensitivity under certain experimental conditions. However, Smith’s own experimental results directly distinguish leucine from the insulin desensitizing response caused by whey protein. Smith reports that leucine ingestion increased muscle mTOR signaling but did not impar insulin-mediated glucose disposal; whole-body glucose disposal was essentially identical between the leucine and corresponding control studies, and leucine did not reduce insulin-stimulated leg glucose uptake. (See right column of page 1556.). Smith expressly concludes that whey protein, but not leucine impaired glucose disposal notwithstanding leucine-mediated mTOR activation. Accordingly, the rejection does not rest on merely upon an unsupported assertion that absence of insulin resistance necessarily inheres in every leucine-containing method. Smith provides direct evidence that treatment conditions involving leucine, insulin, and glucose can activate mTOR without producing the impaired insulin-mediated glucose disposal used by Smith to evaluate insulin resistance. Thus, one of ordinary skill would have had reason to select such conditions with a reasonable expectation of success of obtaining the result recited in claim 61
Kalogeropoulou, although no longer cited in the rejection, supports the metabolic compatibility of leucine and glucose by teaching that leucine administered with glucose synergistically increase insulin secretion while attenuating the glucose response, This evidence further undermines the proposition that administration of leucine with the claimed second regenerative agent necessarily produces insulin-resistant condition.
Applicant argues that Abrams does not teach regeneration of an amputated jellyfish arm because Abrams expressly reports recovery of radial symmetry through recognition of existing structures without regenerating the lost arm.
In response, the Examiner agrees with Applicant as to that characterization of Abrams. Abrams expressly states that injured ephyrae do not regenerate the missing arms but instead reorganize the remaining structures to restore symmetry. However, the present rejection does not rely upon Abrams as teaching regeneration of the missing arm. Abrams is relied upon for different limitations. It teaches that Aurelia ephyra arm-amputation model and expressly provides ephyrae having one, two, or three full arms removed. Accordingly, Abrams teaches the “jellyfish ephyra,” “loss at least a full arm,” and “no more than three arms” limitations of claims 83 and 84. The modification to promote a regenerative response is instead based upon the art teaching mTOR signaling as a pro-regenerative pathway and insulin/growth-factor signaling as a means of stimulating that pathway. Thus, Applicant’s observation that Abrams’ untreated ephyrae symmetrize rather than regenerate does not identify a missing injury limitation; rather, it identifies the known starting condition that provides the reason to attempt a pro-regenerative modification.
Applicant additionally relies upon Sustar’s expression of disbelief concerning Jellyfish regeneration.
In response, this evidence has been considered but does not overcome the rejection. Unlike the fruit-fly embodiment addressed under 112(a), the prior art recognizes substantial regenerative capacity among cnidarians and identifies mTOR as participating in regenerative processes. The rejection therefore does not depend upon Abrams itself demonstrating the ultimate regenerative result, it relies upon Abrams for the known ephyra injury model and upon mTOR/insulin teachings for the modification intended to promote regeneration.
Applicant’s argument that the references do not establish regeneration under hypoxia is not persuasive because claim 76 does not require that hypoxia causes or enhances regeneration. It merely requires that the jellyfish subject be in hypoxic condition. Abrams teaches that Aurelia is capable of thriving in oxygen-poor waters. Thus, once the underlying jellyfish regenerative treatment is rendered obvious, practicing the method in an environmental condition known to be tolerated by the organism represents an obvious selection of a known suitable environment.
Applicant argues that Huang merely concerns a hydrogel scaffold for regenerative medicine applications and does not cure the alleged deficiencies of the preceding references.
In response, this argument is not persuasive because Huang is not relied upon to cure the deficiency concerning the basic digit-regeneration method. The combination of Lund-Ricard, Takayama, and Smith is relied upon for that method. Huang is relied upon only for the additional scaffold limitation of claim 62. Huang teaches a regenerative hydrogel scaffold capable of presenting growth factors including BMP-2 for tissue regeneration. Accordingly, Huang provides the additional teaching for which it is cited and needs not independently tech the remainder of the method already supplied by the underlying combination.
Applicant’s argument concerning the absence of an express teaching of the claimed sucrose-containing regenerative combination, have also been considered. The rejection does not require a reference expressly demonstrating that precise combination mammalian digit. Sanguesa teaches mTORC1 activation by nutrients including amino acids, and simple sugars. In view of the established regenerative/mTOR rationale of the underlying combination, selection of sucrose, a conventional simple sugar, represents selection of a known member of the taught class for the function attributed to that class. Accordingly, the references collectively provide a reason for selecting sucrose as the second regenerative agent with reasonable expectation that it would perform the mTOR-associated nutritional function relied upon in the combination.
Overall Conclusion
Appliant’s arguments largely address the prior rejection as though Smith alone-or each secondary reference individually-must teach the complete claimed regenerative method. That is not the basis of the present rejections. The references are considered for their combined teachings, and the rejection has been reformulated in light of the claim amends so that the principal reference begins with the claimed regenerative biological context rather than with an unrelated metabolic treatment.
For the mouse/rat digit embodiments, Lund-Ricar supplies the known mammalian mTOR regeneration relationship; Takayama supplies the leucine/mTORC1 appendage-regeneration teaching and Smith supplies the pertinent leucine/glucose/insulin mTOR teachings. Dolan and Dawson further establish, for claims 78-80, that the endogenous distal digit boundary can be therapeutically overcome and that even normally nonregenerative proximal digit injuries retain inducible regenerative potential. For the jellyfish claims, Abrams supplies the specific ephryrae and arm-amputation conditions, while the mTOR/insulin art supplies the regenerative modification.
Accordingly, Applicant’s arguments do not overcome the rejection under 35 U.S.C. 103, and the rejections are maintained as formulated.
Conclusion
Claims 2, 11, 13, 20, 28, 35, 61-62, and 76-84 are not allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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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/JEAN P CORNET/ Primary Examiner, Art Unit 1628
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