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 of SW033291 as the elected 15-PDGH inhibitor species and brain as the elected non-skeletal muscle tissue or non-skeletal muscle organ in the reply filed on 09/19/2025 is acknowledged and maintained. However, a search for the amended age-dysregulated cytokine signaling identifies liver, colon, and lung as the non-skeletal muscle organ or tissue. Therefore, the election of non-skeletal muscle or organ has been expanded to colon, bone marrow, and liver.
Priority
This application claims priority to the international stage Application No. U S. Provisional Patent Application No. PCT/US2021/037068, filed Jun 11, 2021, which claims priority to U S. Provisional Patent No. 63/03 7,852, filed June 11, 2020.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 03/24/2026 has been considered by the examiner.
Status of Claims
Acknowledgement is made of the receipt and entry of the amendment to the claims filed on March 24, 2026. Claims 1, 2, 6, 11, 13-17, 53, 55, 60, 63-65, 67, 69-70, and 72 are pending. Claims 3-5, 7-9, 12, 18-52, 54, 56-59, 61, 62, 66, 68, 71, and 73 are canceled. Claims 14 and 15 are withdrawn. Claims 1, 2, 6, 11, 13, 16-17, 53, 55, 60, 63-65, 67, 69-70, and 72 are examined in accordance to the elected species.
Action Summary
Claims 1, 2, 6, 11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72 rejected under 35 U.S.C. 102(a)(1) as being anticipated by Markowitz et al (WO2018/017582 A1) as evidenced by Swenson et al (Translational Medicine of Aging, Volume 3, 2019, Pages 17-25), are maintained, but modified and revisited in light of the claim amendment.
Claim 64 rejected under 35 U.S.C. 103 as being unpatentable over Markowitz et al (WO2018/017582 A1) and Swenson et al (Translational Medicine of Aging, Volume 3, 2019, Pages 17-25) as applied to Claims 1, 2, 6, 11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72 in view of Richardson et al (Experimental Gerontology 55 (2014) 80–91), is maintained.
It is noted the prior Office Action inadvertently omitted claim 10 from the rejection header under 35 U.S.C. 102. However, claim 10 was substantively addressed within the body of the rejection. The omission is therefore considered a typographical/clerical error. Claim 10 is now included in the rejection set forth below.
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1, 2, 6, 10, 11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Markowitz et al (WO2018/017582 A1) as evidenced by Swenson et al (Translational Medicine of Aging, Volume 3, 2019, Pages 17-25).
Markowitz teaches a method of promoting neuroprotection or treating neurological disease/disease includes but not limited to Alzheimer's disease, dementias related to Alzheimer's disease, Parkinson's, Lewy diffuse body diseases, senile dementia, Huntington's disease, Gilles de Ia Tourette's syndrome, multiple sclerosis, amyotrophic lateral sclerosis, hereditary motor and sensory neuropathy, diabetic neuropathy, progressive supranuclear palsy, epilepsy, or, traumatic brain injury, or Jakob-Creutzfeldt disease, the method comprising administering to a subject in need thereof, a therapeutically effective amount of a 15-PGDH inhibitor, wherein the subject has or is at risk of axonal degeneration, neuronal cell death, and/or glia cell damage after injury. (See claims 1, 2, 8, and 13.) Markowitz teaches the 15-PGDH inhibitor inhibits the enzymatic activity of recombinant 15-PGDH at an IC50 of less than 1uM, or preferably at an IC50 of less than 250 nM, or more preferably at an IC50 of less than 50 nM, or more preferably at an IC50 of less than 10 nM, or more preferably at an IC50 of less than 5 nM at a recombinant 15-PGDH concentration of about 5 nM to about 10 nM. (See claim 22.)
Markowitz also teaches the 15-PGDH inhibitor is SW033291
PNG
media_image1.png
195
233
media_image1.png
Greyscale
and is administered by a single intraperitoneal (IP) injection. (See paragraph [00177] and Figures.) The administration is daily or twice daily. (See paragraph [00165].) The single IP injection reads on single dose administration. Markowitz teaches the admiration is through various routes including oral. (See paragraph [00162.) Oral administration reads on systemic administration. Moreover, Markowitz teaches the subject is an adult or a newborn human. (See paragraph [0059].) SW033291 is a small molecule. Markowitz teaches compounds that inhibit, reduce, and/or antagonize short-chain dehydrogenase activity, such as 15-PGDH inhibitors, can be used to increase PGE2 levels in the nervous system (e.g., brain) of a mammal. PGE2 elevates cyclic AMP via binding to EP2 and EP4 receptors, which are highly expressed in the cerebral cortex, hippocampus, and striatum. (See paragraph [0005].)
With respect to the term “individual or subject,” the instant specification discloses the subject is less than 30 years of age. The subject is greater than 30 years of age. (See paragraph [0009].) The instant specification also discloses that the terms "aged tissue" and "aged organ" as used herein refer to any tissue or organ (e.g., non-skeletal muscle tissue or non-skeletal muscle organ) that exhibits one or more characteristics of a tissue or organ affected by an age-related condition, an age-related disease or disorder, and/or by the natural aging processes due to the passage of time. (See paragraph [0031].) Therefore, while Markowtiz does not necessarily teach rejuvenating a function of an aged non-skeletal muscle tissue or aged non-skeletal muscle organ which is the elected brain and limitations that further limit the function as recited in the dependent claims 13, in claim 17 (b), and in claim 55 said limitations simply express the intended outcome of the method step positively recited. Said limitations would naturally flow from the fact that the method step of the prior art is the same as the claimed method step.
With respect to the limitation directed to age-dysregulated cytokine signaling, Swenson teaches aging is associated with altered systemic cytokine signaling including altered circulating cytokine levels and chronic low-grade inflammation (“inflammaging”). (See Abstract and left column of page 17; second paragraph of the left column of page 21.) Swenson further teaches aging tissues accumulate senescent cells and exhibit tissue dysfunction. (See Abstract.) Therefore, the age/adult subjects treated by Markowitz inherently possess age/dysregulated cytokine signaling as presently claimed. Furthermore, Applicant’s own specification (paragraph [0246]) does not define “age-dysregulated cytokine signaling” as a narrowly limited pathological subpopulation distinct from ordinary aging. Rather, paragraph [0246] expressly teaches that aging itself is associated with altered inflammation, altered circulating cytokine levels, and dysregulated cytokine signaling pathways. The specification further associates such age-dysregulated cytokine signaling with cellular senescence, frailty, and age-related tissue dysfunction. One of ordinary skill in the art would understand the claimed “individual with age-dysregulated cytokine signaling” to encompass aged subject exhibiting age-associated cytokine dysregulation as taught by the prior art.
With regard to the limitations of claims directed to rejuvenation, increased PGE2 levels, modulation of serum cytokines, and restoration toward youthful levels, Markowitz expressly teaches that administration of 15-PGDH inhibitor in this case SW033291 increases tissue PGE2 levels and promote regeneration and repair in multiple tissues and organs. (See Figure 8(A-B) and claims 9, 11.) Markowitz teaches the subject is an adult or a newborn human. (See paragraph [0059].) Swenson teaches aging is associated with chronic inflammatory signaling, altered cytokine profiles, senescence-associated secretory phenotypes (SASP), and elevated inflammatory cytokines including Il-1β, IL-6, and TNF-α that contribute to age-associated tissue dysfunction. Accordingly, administration of the same 15-PGDH inhibitor taught by Markowitz to the same aged tissue and inflammatory environment taught by Swenson would inherently result in modulation of age-associated cytokine signaling and amelioration of age-related tissue dysfunction, corresponding to the claimed rejuvenation and cytokine modulation limitations.
With regard to the following limitations: “the administering results in …. after the administering the brain exhibits results …” and “the administering results in: increased adaptive and/or innate immune response in the individual relative to prior to the administering, decreased severity of infection in the individual relative to prior to the administering, decreased production of auto-antibodies relative to prior to the administering”; these limitations simply express the intended outcome of the method step positively recited. Said limitations would naturally flow from the fact that the method step of the prior art is the same as the claimed method step.
Acknowledgement is made of the receipt and entry of Applicant’s remarks/arguments filed on March 24, 2026.
Applicant argues that Markovitz and Swenson do not disclose rejuvenating a function of a non-skeletal muscle tissue or non-skeletal muscle organ in an individual with age-dysregulated cytokine signaling by inhibiting 15-PGDH. Applicant further argues that the instant specification demonstrates age-dysregulated cytokine signaling using aged mice (>24 months), whereas Markowitz uses younger mice (12-14 weeks old) alleged not affected by senescence or age-dysregulated cytokine signaling.
In response, Applicant’s argument is not persuasive. Specifically, Markowitz expressly teaches administration of 15-PGDH inhibitor including SW033291 to promote neuroprotection, neural survival, axonal protection, and recovery of nervous system tissue following injury and neurodegenerative conditions. Markowitz further teaches treatment of neurological disorders including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, ALS, and traumatic brain injury. Accordingly, Markowitz teaches functional improvement and recovery of the elected non-skeletal muscle organ, namely brain tissue. Applicant’s own specification broadly characterizes “rejuvenation” as improvement, restoration, reversal, slowing or amelioration of age-related functional decline in non-skeletal muscle tissues and organs. (See spec. at paragraph [0020].) Thus, Markowitz’s disclosed improvement and recovery of nervous system tissue function falls within the scope of the presently claimed rejuvenation. Swenson teaches aging is associated with chronic inflammatory signaling, altered cytokine signaling, senescence-associated inflammatory phenotype, and tissue dysfunction. Swenson further teaches senescent cells accumulate with aging and produce inflammatory cytokines and signaling factors that negatively effect tissue function. Moreover, Applicant’s own specification broadly characterizes such signaling as altered inflammatory and cytokine signaling associated with aging generally. (See Spec.at paragraph [0246].) Accordingly, the prior art teaches the same biological signaling environment and therapeutic modulation thereof as presently claimed.
Applicant argues that mice disclosed in Markowitz are past development but not yet altered by senescence and therefore, one of ordinary skill in the art would conclude such tissues are not affected by senescent cells nor have aged-dysregulated cytokines signaling.
In response, Applicant’s argument is not persuasive. Again, Markowitz expressly teaches the subject or individual may be an adult subject. (See paragraph [00559].) Further, Applicant has not established that Markowitz expressly limit all disclosed animals to the alleged 12–14-week age range asserted by Applicant. The cited C57BL/7 strain designation of Markowitz identifies the mouse strain and does not itself define the biological age of the animals. Moreover, the presently pending claims do not require geriatric subjects, advanced senescence, a minimum biological age, or a particular threshold degree of cytokine dysregulation. Rather, the claims broadly recite “an individual with age-dysregulated cytokine signaling.” Applicant’s own specification broadly characterizes such signaling as altered inflammatory and cytokine signaling associated with aging generally. (See Spec.at paragraph [0246].) Applicant therefore improperly attempts to import limitations from exemplary embodiments using older mice into the present claims. The exemplary aged mouse models disclosed in the specification does not represent the only subjects encompassed by the claims.
Applicant argues that Swenson merely teaches accumulation of senescent cells in the CNS with increasing age but does not teach the specific mice in Markowitz would possess senescent cells or age-dysregulated cytokine signaling.
In response, Applicant’s argument is not persuasive. The rejection does not rely on Swenson teaching the exact mice of Markowitz were expressly identified as senescent. Rather, Swenson is cited as evidentiary support demonstrating that aging and tissue dysfunction are associated with inflammatory cytokine dysregulation and senescence-associated inflammatory signaling. Swenson expressly teaches senescent cells acquire a pro-inflammatory secretory phenotype comprising cytokines and inflammatory signaling factors that negatively impact neighboring tissue function. Swenson additionally teaches aging is associated with elevated inflammatory cytokines, including IL-1β, IL-6, and TNF-α and prolong inflammatory signaling contributing to tissue dysfunction. Anticipation by inherency does not require explicit disclosure, express recognition, or contemporaneous appreciation of the inherent characteristic in the prior art reference. MPEP 2112. Accordingly, the prior art subjects taught by Markowitz inherently possess the same age-associated inflammatory and cytokines signaling environment evidenced by Swenson.
Applicant argues Markowitz is directed merely to neuroprotection and neuronal survival rather than rejuvenation of aged tissues exhibiting aged-dysregulated cytokine signaling.
In response, Applicant’s argument is not persuasive. Applicant’s elected species is directed to brain tissue and nervous system function. Markowitz expressly teaches administration of 15-PGDH inhibitor for promoting neuroprotection, neuronal survival, axonal protection, and nervous system tissue recovery. Markowitz further teaches treatment of neurological and neurodegeneration disorder affecting brain tissue. Accordingly, Markowitz teaches functional improvement and recovery of the elected non-skeletal muscle organ. Further, the claims do not require a particular minimum age, advanced senescence phenotype, or severe inflammatory dysfunction. Rather, the claims broadly recite “an individual with age-dysregulated cytokine signaling.” As discussed supra, Applicant’s own specification broadly characterizes age-dysregulated cytokine signaling as altered inflammatory and cytokine signaling associated with aging generally. (Spec. at paragraph [0246].) Thus, Applicant improperly attempts to narrow the claims to the specific aged-mouse embodiments disclosed in the specification, limitations which are not recited in the presently pending claims.
Claims 1, 2, 6, 10-11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Zhang et al (Science 348, aaa2340(2015).)
Zhang teaches inhibition of the prostaglandin degrading enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH) potentiates tissue regeneration in multiple organs and tissues. Zhang teaches administration of the small molecule 15-PGDH inhibitor SW033291 to increase prostaglandin PGE2 levels and promote regeneration and repair of multiple tissues including bone marrow, colon, liver, and lung among other tissues. (. (See Abstract; p. 3.) Zhang teaches a method comprising administering a 15-PGDH inhibitor to an individual in an amount effective to inhibit 15-PGDH enzymatic activity. Zhang specifically teaches the small molecule inhibitor SW033291 inhibits 15-PGDH activity and increases endogenous PGE2 signaling. (See pp. 2-4 under Results Section.) Zhang further teaches systemic administration of S033291, including intraperitoneal administration. (See pp.6; first paragraph.)
With respect to the claimed “individual with age-dysregulated cytokine signaling,” Applicant’s own specification broadly characterizes such signaling as altered inflammatory and cytokine signaling associated with aging generally. (Spec. at paragraph [0246].) Zhang teaches administration of SW033291 promotes tissue repair, tissue recovery, and restoration of tissue function through modulation of prostaglandin signaling pathway associated with inflammatory signaling and tissue regeneration. Zhang additionally teaches enhanced recovery and regeneration of multiple tissues following administration of SW033291. (See Abstract and pp.9.) Accordingly, Zhang teaches administration of a 15-PGDH inhibitor to subjects exhibiting age-associated tissue dysfunction and inflammatory signaling environment corresponding to the presently claimed age-dysregulated cytokine signaling limitation.
Zhang further teaches regeneration and recovery of multiple non-skeletal muscle tissues and organs including colon tissue, liver tissue, bone marrow, epithelial tissue, and blood-related tissues following the administration of SW033291. (See Abstract; pp 4-9). Accordingly, Zhang teaches rejuvenation and functional improvement of non-skeletal muscle tissues and organs as presently claimed.
With respect to claims 2, 6, 10, 11, and 67 directed to rejuvenation, increased PGE2 levels, modulation of cytokine-associated signaling, and restoration toward youthful tissue function, Zhang expressly teaches administration of SW033291 increases endogenous PGE2 signaling and promotes tissue regeneration, tissue recovery, and restoration of tissue function. Zhang also teaches enhanced tissue recovery, and amelioration of tissue dysfunction following administration of SW033291. (See Abstract; pp. 3; and pp. 9.) Such teachings correspond to the presently claimed rejuvenation and PGE2-associated limitations.
With respect to claims 13 and 17, Zhang teaches regeneration and repair of multiple tissues and organs including epithelial tissue, blood-related tissue, colon tissue, liver tissue, and additional organs. To the extent claim 17 further recites improved or enhanced tissue functions following administration, such limitations merely express the natural result of administering the same regenerative 15-PGDH inhibitor taught by Zhang to the same tissues taught by Zhang.
With respect to claim 16, Zhang teaches tissue recovery, tissue regeneration, and improved tissue repair associated with administration of SW033291 and increased PGE2 signaling. Such teachings correspond to the claimed improvement of tissue function and inflammatory-associated dysfunction.
With respect to claim 53, Zhang teaches administration of SW033291 to subjects exhibiting tissue dysfunction, inflammatory signaling, and regenerative deficiencies associates with aging, which constitute biomarkers associated with aging.
With respect to claim 55, Applicant’s own specification characterizes aging-associated tissue dysfunction as associated with cellular senescence and inflammatory signaling. (Spec at paragraph [0246].) Zhang teaches administration of SW033291 to aged or damaged tissues exhibiting regenerative decline and impaired tissue function. Accordingly, the tissues treating according to Zhang inherently possess age-associated cellular senescence relative to younger healthy tissue.
With respect to claim 60, Zhang expressly teaches SW033291 is a small molecule inhibitor of 15-PGDH. (See pp. 2-4.)
With respect to claim 63, Zhang expressly teaches administration to mammalian subject including human subjects. (See p. 2.)
With respect to claim 65, Zhang expressly teaches SW033291 inhibits enzymatic activity of 15-PGDH. (See pp. 2-4.)
With respect to claim 69-70, Zhang teaches systemic administration including intraperitoneal administration. (See pp. 5-8.)
With respect to claim 72, Zhang teaches repeated daily administration regiments (see pp. 6-7), which reads on periodic administration.
Therefore, Zhang anticipates claims 1, 2, 6, 10-11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72.
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 nonobviousness.
Claim 64 is rejected under 35 U.S.C. 103 as being unpatentable over Markowitz et al (WO2018/017582 A1) and Swenson et al (Translational Medicine of Aging, Volume 3, 2019, Pages 17-25) as applied to Claims 1, 2, 6, 11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72 in view of Richardson et al (Experimental Gerontology 55 (2014) 80–91).
The collective teachings of Markowitz and Swenson have been discussed supra.
Markowitz and Swenson collectively do not teach the human subject is at least 30 years.
Richardson teaches many physiological functions show a decline from 30 years of age. (See left column first paragraph of section 4.3.)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to modify the method taught by Markowitz by including an adult subject of at least 30 years old to give Applicant’s claimed invention. One would have been motivated to do so, because Richardson teaches many physiological functions show a decline from 30 years of age. (See left column first paragraph of section 4.3.) One would reasonably expect an adult of at least 30 years of age to benefit from the method of Markowitz with success.
Applicant argues that claim 64 is not obvious over Markowitz and Swenson in view of Richardson because Richardson allegedly does not cure the asserted deficiencies of Markowitz and Swenson regarding amended claim 1.
In response, Applicant’s argument is not persuasive. As discussed supra, the Examiner maintains that Markowitz as evidenced by Swenson teaches or at least renders obvious the limitation of amended claim 1, including administration of a 15-PGDH inhibitor to an adult individual exhibiting age-associated inflammatory and cytokine signaling associated aging. Richardson additionally teaches many physiological functions decline beginning around 30 years of age. Accordingly, Richardson evidences that adult subjects at or above 30 years of age experience age-associated physiological decline and therefore would have been obvious candidates for the regenerative and neuroprotective methods taught by Markowitz. Applicant does not separately contest Richardson’s teachings, the Examiner articulated rational for combination, or the reasonable expectation of success. Nor does Applicant identify any teaching away, criticality, unexpected results, or other objective evidence of nonobviousness associated with the related age limitation. Further, claim 64 merely recites “wherein the individual is at least 30 years of age.” Selection of an adult subject experiencing age-associated physiological decline constitutes nothing more than the predictable use of prior art methods according to their established functions.
Claim 64 is rejected under 35 U.S.C. 103 as being unpatentable over Zhang et al (Science 348, aaa2340(2015) as applied to claims 1, 2, 6, 10-11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72 in view of Richardson et al (Experimental Gerontology 55 (2014) 80–91).
As discussed supra, Zhang teaches administration of the 15-PGDH inhibitor SW033291 to promote tissue regeneration, tissue repair, increased PGE2 signaling, and restoration of tissue function in mammals. Zhang further teaches systemic administration of SW033291 to improve regenerative capacity and tissue recovery in multiple tissues and organs.
Zhang, however, does not expressly teach the individual is at least 30 years of age.
Richardson teaches many physiological functions begin to decline beginning around 30 years of age. Richardson further teaches aging-associated physiological decline affects tissue function, regenerative capacity, inflammatory signaling, and organ performance. (See Section 4.3, left column, first paragraph.)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to administer the regenerative 15-PGDH inhibitor treatment taught by Zhang to an individual at least 30 years of age because Richardson teaches such individual experiences age-associated physiological decline and therefore would reasonably benefit from regenerative and tissue restorative therapies. One would have a reasonable expectation of success because Zhang teaches SW033291 enhances tissue regeneration and tissue recovery through increased endogenous PGE2 signaling.
Double Patenting rejections necessitated by filing the IDS filed on 03/24/2026
Double Patenting
The nonstatutory 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 nonstatutory 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 nonstatutory 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 nonstatutory 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 1, 2, 6, 10-11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 7, 11-13, 15-17, 20-21, 23, 27, 29, and 31 of copending Application No. 17/616,966 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other.
The copending claims teach methods of administering a 15-PGDH inhibitor to aging or senescent-cell-associated tissues to rejuvenate tissue function, modulate inflammatory/cytokine signaling, and ameliorate age-associated dysfunction.
The instant claims differ from the copending claims in that the copending claims are directed more specifically to geriatric skeletal muscle, muscle-related biomarkers, muscle strength/endurance, and related functional characteristics. However, such limitations are considered to be obvious variation of the claims of the instant claims because skeletal muscle represent an obvious tissue target for treatment of aging-associated dysfunction and senescence-related tissue degeneration using the same 15-PGDH inhibitory mechanism.
Further, the recited increases in muscle mass, strength, endurance, PGE2 levels, and restoration toward non-geriatric function merely represent expected or inherent therapeutic results arising from administration of the same 15-PGDH inhibitor to aging tissue.
Accordingly, the copending claims are not patentably distinct from the instant claims because bot sets of claims are directed to the same inventive concept of treating or rejuvenating age-associated tissue dysfunction through inhibition of 15-PGDH.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1, 2, 6, 10-11, 13, 16-17, 53, 55, 60, 63, 65, 67, 69-70, and 72 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 31-44 and 47-50 of copending Application No. 18/615,080 and over claims 1-18 of copending Application No. 19/386,538 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other.
The copending claims are directed to methods of regenerating muscle in a subject having muscle damage, muscle injury or muscle atrophy through administration of a 15-PGDH inhibitor in an amount effective to inhibit 15-PGDH and activate muscle stem cells, thereby regenerating muscle in the subject. The copending claims further teach enhancement of muscle repair, muscle function, muscle strength, and muscle mass, as well as administration to human subjects through various administration routes.
The instant claims differ from the claims in that the instant claims are directed more specifically to geriatric skeletal muscle age-dysregulated cytokine signaling, rejuvenating a function of a non-skeletal muscle tissue or organ. However, such limitations are considered to be obvious variation of the claims of the instant claims because skeletal muscle represent an obvious tissue target for treatment of aging-associated dysfunction and senescence-related tissue degeneration using the same 15-PGDH inhibitory mechanism.
The claimed limitations are not considered patentably distinct from the claims of the copending application because both applications are directed to the same inventive concept of improving or regenerating skeletal muscle function through inhibition of 15-PGDH activity. Specifically, the recited age-dysregulated cytokine signaling, senescent-cell accumulation, inflammatory signaling, altered PGE2 signaling, and biomarkers of aging merely characterize biological conditions associated with aging-related muscle dysfunction and degeneration that would have been obvious properties or conditions of the muscle damage, muscle injury, and muscle atrophy treated in the copending application. Further, muscle regeneration, muscle repair, increased muscle strength, increased muscle mass, and restoration toward youthful or non-geriatric muscle function represent overlapping and expected therapeutic outcomes arising from the administration of the same PDGH inhibitory treatment recited in the copending claims.
Accordingly, the copending claims are not patentably distinct from the instant claims because both sets of claims are directed to the same inventive concept of treating or rejuvenating age-associated tissue dysfunction through inhibition of 15-PGDH.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Claims 1, 2, 6, 11, 13, 16-17, 53, 55, 60, 63-65, 67, 69-70, and 72 are not 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JEAN P CORNET whose telephone number is (571)270-7669. The examiner can normally be reached Monday-Thursday from 7.00am-5.30pm.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Amy L Clark can be reached at 571-272-1310. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/JEAN P CORNET/Primary Examiner, Art Unit 1628
Prosecution Insights