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 .
Response to Amendment
The amendment filed April 30, 2026 has been entered. Claims 1, 4, 15, 21, 23, 31, 43, have been amended, and claims 2-3, 5-6, 8-10, 14, 18-19, 22, 24-26, 28, 30, 32-41, 44-47, and 50-90 have been cancelled. Applicants amendment to the drawings filed April 30, 2026 have been entered and overcome the objections previously set forth in the Non-Final Office Action mailed February 4, 2026. As such, these objections are hereby withdrawn.
Applicant’s arguments filed October 9, 2025 were fully considered but they were not persuasive. Modified/New rejections necessitated by Applicant’s amendment and response to arguments are addressed below.
Claims 1, 4, 7, 11-13, 15-17, 20-21, 23, 27, 29, 31, 42-43, 48-49, and 91-93 are pending in this application.
Priority
The instant application is a 371 of PCT/US2020/037207, filed on 6/11/2020, which claims domestic benefit to provisional application 62/860,180, filed on 06/11/2019, 62/875,915 filed on 07/18/2019, 62/882,981 filed on 08/05/2019, and 62/883,025 filed on 08/05/2019.
Information Disclosure Statement
The information disclosure statements (IDS) filed April 30, 2026 complies with the provisions of 37 CFR 1.97, 1.98 and MPEP § 609. Accordingly, the information disclosure statements have been considered by the Examiner.
New Claim Rejections - 35 USC § 112 (d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 21 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 21 recites inter alia, “wherein the subject is at least 30 years of age.”. However, claim 21 depends from claim 20 which species a human subject, and ultimately from claim 1, which is directed to a subject with “geriatric skeletal muscle”, which one of ordinary skill in the art would recognize as a human subject that is at least 30 years old. Thus, claim 21 fails to further limit a claim of which it depends.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Modified/New 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.
Claims 1, 4, 7, 11-12, 15-17, 20-21, 23, 27, 29, 31, 42, 48-49, and 91-93 are rejected under 35 U.S.C. 103 as being unpatentable over Blau et al. (WO 2017/152044 A1; cited in previous action) in view of Larsson et al. (Physiol Rev. 2018; cited in previous action) and Shavlakadze (Biogerontology, 2010, cited on PTO-892).
Regarding claims 1, 4, 7, 11-12, 15-17, 20-21, 23, 29, 31, 42, 48-49, 91, and 93, Blau teaches that aging leads to loss of muscle mass, strength, and function in skeletal muscles [0003]. Blau recognizes that the elderly are a known subject population that suffer from such skeletal wasting [0129]. Blau teaches that the muscle atrophy can be caused by normal aging, such as sarcopenia [0087], and teaches a method for treating muscle atrophy [0093]. This method comprises administering a compound that attenuates PGE2 catabolism (claim 44) by inactivating or blocking 15-hydroxyprostaglandin dehydrogenase (15-PGDH) (claim 46). Blau teaches that the enzymatic activity of 15-PGDH is to degrade PGE2 and is blocked by a 15-PDGH inhibitor such as SW033291 (page 37, lines 9-11, and Fig. 2C). The muscle would therefore experience an increase in PGE2 levels after treatment with a 15-PDGH inhibitor
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Blau teaches that administering a compound inactivating or blocking 15-PGDH enhances muscle function and increases the population of muscle cells (claims 32 and 27). Increasing PGE2 reduces cell death [0133]. This compound may be a small molecule such as SW033291 (Fig. 2C, and examples in [0204] [0238]), neutralizing peptide, biological product, or neutralizing antibody (claim 32 and [0031]).The compound may be administered once or twice daily [0111] to a human subject [0043]. Blau further indicates that the cells of the muscle being treated may be muscle cells other than muscle stem cells, such as myocytes (claim 29 and 30), and that the method is expected to affect smooth muscle cells (claim 47 and [0075]).
Blau does not teach that the muscle is geriatric muscle that has an accumulation of senescent cells, does not teach the biomarkers of the aged subject, and does not teach the administration of senolytic agents.
Larsson teaches that cellular senescence refers to the essentially irreversible growth arrest that occurs when cells experience potentially oncogenic insults or damage, including inflammatory or metabolic stress (paragraph bridging pages 479-480). Larsson teaches that it is well known in the prior art that aged muscle has an accumulation of senescent cells – of which p16Ink4a is an indicator (479, paragraph 6). Larsson teaches muscle satellite cells are sensitive to systemic soluble factors in serum, inflammation, and local growth factors, which all change during aging with an impact on satellite cell function, resulting in an aging-related impairment or delay in the repair and regeneration process in response to a damaging insult to skeletal muscle (463, paragraph 2). Aged muscle also has an increased expression level of atrogenes (atrophy genes) – the two most important of which are atrogin1/Mafbx and MuRF1 (466, paragraph 2). Larsson teaches that senescence of cells is expected to contribute to local and systemic tissue dysfunction including physical dysfunction of muscles in, for example, grip strength and 400-meter walk speed (paragraph bridging pages 479-480). Eliminating senescent cells enhances health span and blunts aging-related declines in activity as well as sarcopenia (paragraph 1, page 480), and Larsson suggests that targeting senescent cells may be a therapeutic option for aging related loss of muscle function (paragraph 3, page 480). Larsson teaches that senolytic agents, such as Bcl-2 family inhibitors (480, paragraph 3), specifically eliminate senescent cells and may be a therapeutic option for aging related loss of muscle function. Additionally, Shavlakadze teaches significant sarcopenia occurs from 50 to 80 years of age (363, introduction). Shavlakadze establishes that geriatric models, albeit delayed, are capable of regenerating skeletal muscle through myogenesis (abstract). Shavlakadze teaches that myogenic (stem) cells retain a good capacity for myogenesis in geriatric skeletal muscles (pg. 374, para. 1).
It would have been prima facie obvious before the effective filing date of the invention to apply the method of Blau to patients with the age-related muscle loss, such as the elderly (i.e. geriatric), which necessarily have cellular senescence as taught by Larsson and are known to have sarcopenia and can regenerate muscle tissue as taught by Shavlakadze. Larsson teaches that aged muscle has an accumulation of senescent cells that contributes to tissue dysfunction and sarcopenia, and Blau teaches a method for treating patients experiencing age-related muscle atrophy. Thus one of ordinary skill in the art would have a reasonable expectation that the geriatric patients can be treated by the method of Blau that necessarily have an accumulation of senescent cells because Blau teaches a method for treating patients experiencing age-related muscle atrophy and Larsson suggests that patients experience age-related muscle atrophy have an accumulation of senescent cells and Shavlakadze establishes that geriatric subjects are capable of regenerating skeletal muscle through myogenesis. Although Blau does not specifically state the impact of the method on senescent cells relative to muscle not having a an accumulation of senescent cells, given that Blau teaches administration to the treatment of age-related muscle atrophy, this effect flows naturally as a result of practicing the method. The reason or motivation to modify the reference may often suggest what the inventor has done, but for a different purpose or to solve a different problem. It is not necessary that the prior art suggest the combination to achieve the same advantage or result discovered by applicant (See MPEP 2144 (IV)).
Regarding claim 27, Blau demonstrates that delivery of PGE2 increases myofiber cross-sectional area ([0137] and Fig 8A-8B).
Blau does not expressly teach that administering a compound that inactivates or blocks 15-PGDH will increase myofiber cross sectional area.
However, in order to show that delivery of PGE2 stimulates muscle regeneration, Blau demonstrates that delivery of PGE2 increases myofiber cross-sectional area ([0137] and Fig 8A-8B). Thus, Blau teaches that an increase of myofiber cross-sectional area is an indicator of successful muscle regeneration. Furthermore, Blau teaches that 15-PGDH degrades PGE2 ([0005], Fig. 2C), and indicates that both 15-PGDH inhibitors and PGE2 have the same purpose of increasing PGE2 levels and regenerating muscle cells. Because Blau teaches that administering a 15-PGDH inhibitor causes regeneration of muscle cells, and that regeneration of muscle cells allows an increase in myofiber cross-sectional area, it would be prima facie obvious to person of ordinary skill in the art before the effective filing date of the invention that muscle regeneration with 15-PGDH inhibitors provides reasonable expectation of success for increasing myofiber cross-sectional area.
Regarding claim 92, Blau does not expressly address that the method results in maintenance of muscle tissue homeostasis. However, Blau teaches that the method provides treatment to a subject experiencing muscle atrophy [0093]. Thus, Blau discloses a method comprising administering a 15-PGDH inhibitor such that a currently healthy subject will experience an increase in cell survival or a decrease in protein degradation such that muscle atrophy is prevented, which indicates that the homeostasis of the muscle tissue is maintained.
Claim 13 is rejected under 35 U.S.C. 103 as being unpatentable over Blau et al. (WO 2017/152044 A1; cited in previous action) in view of Larsson et al. (Physiol Rev. 2018; cited in previous action) and Shavlakadze (Biogerontology, 2010, cited on PTO-892) as applied to claims 1, 4, 7, 11-12, 15-17, 20-21, 23, 27, 29, 31, 42, 48-49, and 91-93 above, further in view of Prattichizzo et al. (Aging, 2016; cited in previous action).
Regarding claim 13: The combined teachings of Blau in view of Larsson are as discussed above. Blau discloses a method for regenerating muscle cells in a subject having muscle atrophy through administering a compound that inactivates or blocks 15-PGDH to enhance muscle function or to increase the population of muscle cells (claims 32 and 27). Larsson teaches that it is well known in the prior art that aged skeletal muscle displays the p16(Ink4a) biomarker indicating an accumulation of senescent cells (479, paragraph 6).
The combined teachings of Blau, Larsson, and Shavlakadze do not teach that the senescent cells are macrophages.
Prattichizzo teaches that aging is characterized by a failure to maintain tissue homeostasis, and that the accumulation of senescent cells is a causal agent in this process (page 3159, paragraph 1). Furthermore, macrophages play a key role in the aging process (page 3159, paragraph 3). Macrophages with a senescence-like phenotype are characterized by an increased expression of p16(Ink4a) (page 3159, paragraph 2). It would have been prima facie obvious before the effective filing date of the claimed invention that the patients treated by the method of Blau have an accumulation of senescent cells, as suggested by Larsson, and that some of these senescent cells are macrophages, as suggested by Prattichizzo. This would have been prima facie obvious for one of ordinary skill in the art because Blau teaches a method for treating patients with age-related muscle atrophy, and Larsson teaches that the presence of senescent cells, which are known to have an increased expression of p16(Ink4a), is observed in patients with sarcopenia. Finally, Prattichizzo teaches that senescent macrophages are known to exhibit increased levels of p16Ink4a and are present in patients with an aging related failure to maintain tissue homeostasis. Thus one of ordinary skill in the art would have a reasonable expectation that the population of patients treated by the method of Blau overlaps with the population of patients having senescent macrophages taught by Prattichizzo.
Claim 43 is rejected under 35 U.S.C. 103 as being unpatentable over Blau et al. (WO 2017/152044 A1; cited in previous action) in view of Larsson et al. (Physiol Rev. 2018; cited in previous action) and Shavlakadze (Biogerontology, 2010, cited on PTO-892), as applied to claims 1, 4, 7, 11-12, 15-17, 20-21, 23, 27, 29, 31, 42, 48-49, and 91-93, further in view of Puchert et al. (Cellular Signaling, 2016; cited in previous action) and Zhang et al. (Science, 2015; cited in previous action).
Regarding claim 43: The combined teachings of Blau in view of Larsson are as discussed above. Furthermore, Blau discloses a method for regenerating muscle cells in a subject having muscle atrophy through administering a compound that inactivates or blocks 15-PGDH to enhance muscle function or to increase the population of muscle cells (claims 32 and 27).
The combined teachings of Blau, Larsson, and Shavlakadze do not teach that expression of one or more atrogenes is decreased.
However, Zhang teaches that administration of the 15-PGDH inhibitor SW033291 induced a greater than fourfold increase in expression of CXCL12 in CD45– cells through its function of increasing PEG2 levels (page 3, paragraph 2 and fig. 2D). Furthermore, Puchert teaches that CXCL12 promotes the growth of myotubes and inhibit expression of the atrogene MuRF-1 (page 1210, paragraph 4).
Thus, wherein the method rendered obvious over Blau and Larsson teaches the administration of SW033291, the result of decreasing atrogen expression necessarily results from practicing the method given that SW033291induces CXCL12 expression which in turn inhibits atrogen MURF-1.
Response to Arguments
Applicant’s arguments filed April 30, 2026 with respect to claims have been fully considered but they are not persuasive.
On page 11 of Applicant’s response, Applicant argues the newly amended claims which specify geriatric skeletal muscle overcome the rejections previously set forth because prior art does not teach administering to geriatric muscle or reducing muscle loss due to aging in the geriatric skeletal muscle (para. 3).
However, Applicant’s arguments with respect to the phrase “geriatric” differing from the prior art is found not-persuasive, because the phrase is not clearly differentiated between the phrase “aged” in the instant specification. The instant specification does not clearly define the phrase, and mentions the phrase a single time when referring to figure 1C (pg. 71, line 32). Figure 1C itself uses the phrase “aged” in the figure and does not use the term “geriatric”. The declaration of Blau filed October 9, 2025 states that mice aged 20-24 months are considered old, while mice from around 28-32 months are considered geriatric according to Sousa-victor (pg. 3, section 8). The instant specification separates mice by ages into three categories, young (2-4 months), middle aged (18-20 months) and aged (>24 months) (pg. 98, para. 0258). The instant specification also refers to mice that are 20 months old to be considered “aged” (pg. 72, para. 0203). According to The Jackson Laboratory (The Jackson Laboratory , Blog post, 2017, IDS filed April 30, 2026) mice ranging from 18-24 months of age correlate with humans ranging from 56-69 years of age and are considered “old” while greater than 24 months can be considered “very old” (pg. 1, para. 6). Thus, the instant specification does not clearly differentiate the term geriatric from aged, old, very old, and is more akin to an approximation that overlaps with other terms of the art. Wherein the art establishes treatment of aging populations that suffer from sarcopenia, geriatric populations are necessarily encompassed as discussed in the 103 rejections above. As discussed above, Blau teaches treatment of elderly populations. Thus, the arguments pertaining towards there being a difference between aged muscle and geriatric muscle are not persuasive on these grounds.
On page 11 of Applicant’s response, Applicant argues that there is a difference in regenerative capacity of skeletal muscle stem cells in geriatric skeletal muscle versus non-geriatric skeletal muscle wherein geriatric muscle stem cells switch reversible quiescence into senescence (last para.). On pages 11-12 of Applicant’s response, Applicant argues that upon injury, the pre-senescent skeletal muscle stem cells in geriatric skeletal muscle undergo entry into a full senescent state resulting in a loss of regenerative and self-renewal capacity (bridging para.). Applicant points to the declaration of Blau, filed October 9, 2025, which states that the skeletal muscle stem cells of mice at 18-20 months of age are reversibly quiescent and have the capacity to be activated and to regenerate skeletal muscle, while in mice greater than 24 months (i.e. geriatric mice) cells have switched to a pre-senescent/senescent state and have a diminished capacity to be activated to regenerate muscle (applicants arguments, pg. 12, para. 2). Applicant argues the mechanism described in Blau teaches the treatment of aged muscle cells that are dysregulated due to increased 15-PGDH levels and can be treated with a 15PGDH inhibitor leading to increased muscle stem cell regeneration (applicant’s arguments, pg. 12, para. 3). Applicant argues that the mechanism of Blau (the cited reference) is dependent on skeletal muscle stem cells that are in the reversible quiescent state, and not the pre-senescent/senescent state as in the instant application (pg. 12, para. 3). Applicant argues in the art would not find the method of Blau to be applicable to geriatric muscle that has switched the pre-senescent/senescent state (pg. 12, para. 3).
However, as discussed above, Blau generally teaches that the method is applicable to treating muscle atrophy that can be caused by normal aging, such as sarcopenia [0087], and teaches a method for treating muscle atrophy [0093]. Through the disclosure of Blau, a person of ordinary skill would recognize its applicability directed towards the treatment of the elderly [0129]. The reason or motivation to modify the reference may often suggest what the inventor has done, but for a different purpose or to solve a different problem. It is not necessary that the prior art suggest the combination to achieve the same advantage or result discovered by applicant (See MPEP 2144 (IV)). Additionally see newly cited Shavlakadze that establishes that geriatric models, albeit delayed, are capable of regenerating skeletal muscle through myogenesis (abstract). Shavlakadze teaches that myogenic (stem) cells retain a good capacity for myogenesis in geriatric skeletal muscles (pg. 374, para. 1). Thus a person of ordinary skill in the art would have recognized the applicability of the method of Blau to geriatric models.
On pages 12-13 of Applicant’s response, applicant argues Larson fails to teach treatment of geriatric skeletal muscle and merely teaches that aged muscle has an accumulation of senescent calls (bridging para.).
However, as discussed above, Shavlakadze teaches that myogenic (stem) cells retain a good capacity for myogenesis in geriatric skeletal muscles (pg. 374, para. 1). Thus a person of ordinary skill in the art would have recognized the applicability of the method of Blau to geriatric models.
On page 13 of Applicant’s response, Applicant argues that a person of ordinary skill would not have had a reasonable expectation of success in administering a 15-PGDH inhibitor to reduce muscle loss in geriatric muscle because geriatric skeletal muscle stem cells are irreversibly senescent and are incapable of regenerating (last para.). On pages 13-14 of Applicant’s response, Applicant points to the Blau declaration which states that it is known in the art exhibit a reduced ability to regenerate muscle and also that geriatric mice (around 28-32 months of age) were still capable of regenerating muscle but markedly diminished (bridging para.).
However, see response to arguments above wherein the phrase geriatric is not specifically defined. Additionally the declaration reinforces Shaylakadze discussed above that establishes geriatric mice are capable of regenerating muscle albeit after a delay.
On page 14 of Applicant’s response, Applicant argues that Blau (cited reference) teaches aged muscle cells were dysregulated due to increased 15-PGDH levels and could be treated with PGE2 or a 15-PGDH inhibitor, leading to an increase in muscle stem cell regeneration (para. 2). Thus the method of Blau relies on quiescent skeletal muscle stem cells that are capable of being activated and regenerating muscle (para. 2). Applicant repeats the argument that geriatric skeletal muscle stem cells are irreversibly senescent and have lost the ability to be activated and self renew.
However, this conflicts with newly cited Shavlakadze that establishes that geriatric models, albeit delayed, are capable of regenerating skeletal muscle through myogenesis (abstract).
On pages 15-16 of Applicant’s response, Applicant argues the Office relies on impermissible hindsight because geriatric skeletal muscles were known to be incapable of regenerating muscle. Applicant argues that a decrease in PGE2, 15-PGDH activity was dramatically increased in geriatric muscle tissue which led to the unexpected discovery that the source of increased 15-PGDH levels in geriatric skeletal muscle is senescent macrophage cells accumulated in the muscle. A person of ordinary skill in the art would have recognized that 15-PGDH inhibition to reduce loss of muscle function would not have relied on activation or regeneration of muscle stem cells.
However, as discussed above, newly cited Shavlakadze that establishes that geriatric models, albeit delayed, are capable of regenerating skeletal muscle through myogenesis (abstract). Additionally Blau recognizes the general trend that gaining increases 15-PGDH activity that renders PGE2 inactive (pg. 35, para. 0129). Thus a person of ordinary skill in the art would recognize the applicability to geriatric models which would also have increased 15-PGDH levels generally.
On page 2 of the declaration of Blau, filed October 9, 2025, Blau points to Sousa-Victor which discloses that it is known in the art that geriatric skeletal muscle stem cells are incapable of maintaining their normal quiescent state in muscle homeostatic conditions, and this irreversibility affects their intrinsic regenerative and self-renewal capacities (last para.). On page 3 of the declaration, Blau states that this phenomenon was shown to occur in geriatric cells with sarcopenia (para. 1). Blau argues that based on the teachings of Blau and Larsson, a person of ordinary skill would not have recognized that Blau disclosed age-related loss of muscle mass having cellular senescence (pg. 3, paras. 2-3). Blau argues that the mice were 18-20 months of age, and a person of ordinary skill would have recognized that the muscle stem cells in Blau were quiescent and capable of being activated (pg. 3, para. 3). On page 4 of the declaration, Blau argues that the mice used in the instant application were of geriatric age (i.e. greater than 24 months), which had skeletal muscle stem cells in an irreversibly senescent state, which would not have been recognized to be treatable by the method of Blau (para. 2). Blau points to Palla which teaches there is a distinction between studying young muscle and aged muscle (para. 2). On pages 4-5 of the declaration of Blau, Blau argues that the instant application demonstrates the unexpected result that 15-PGDH inhibition could reduce muscle function loss in geriatric muscle (having an accumulation of senescent cells), via inhibiting the increased 15-PGDH levels in geriatric skeletal muscle resulting from senescent macrophage cells accumulated in the muscle (bridging para). On page 5 of the declaration, Blau concludes that a person of ordinary skill would not have expected that 15-PGDH inhibition can reduce muscle function loss in a muscle having an accumulation of senescent cells (para. 2). In summation the declaration of Blau argues that because Blau (cited reference) is specifically directed towards the treatment of aged (not geriatric) mice, a person would not have had a reasonable expectation of success in a treatment directed towards subjects with an accumulation of senescent cells (i.e. geriatric patients), and would not have recognized the feature of senescence at that time.
However, the argument of the Examiner is not that a person of ordinary skill would have recognized the relevant feature of the cells being in a senescent state, rather that based upon the teaching of Blau (i.e. suggesting treating elderly patients) this would naturally flow as a result of practicing the method. There is no disclosure in Blau that teaches away from treating elderly patients, rather toward. While Blau suggests the compounds can trigger proliferation in muscle cells that are quiescent [0075], Blau does not teach the compounds would be ineffective in irreversibly senescent cells, wherein such cells naturally have elevated PGDH levels. It is not necessary that the prior art suggest the combination to achieve the same advantage or result discovered by applicant (See MPEP 2144 (IV)). In other words, wherein it would have been obvious to treat a subject population that necessarily have an accumulation of senescent cells, the effect of reducing loss of muscle function flows naturally as a result of practicing the method. Furthermore, while Sousa Victor teaches geriatric satellite cells switch to presenescent/senescent cells leading to impaired stem-cell self renewal, this does not lead to complete impairment of myogenesis. Blau (cited reference) recognizes that during aging, the proportion of functional MuSCs markedly decreases, hindering muscle regeneration (pg. 35, para. 0129), but not the complete lack thereof. As discussed above, newly cited Shavlakadze that establishes that geriatric models, albeit delayed, are capable of regenerating skeletal muscle through myogenesis (abstract).
On the remaining paragraphs of pages 16-17 Applicant argues that the remaining rejections are overcome due to the arguments described above.
See response to arguments above.
Applicant’s reply is considered to be a bona fide attempt at a response and is being accepted as a complete response. The 35 USC § 112(d) and 103 rejections are maintained for reason of record and foregoing discussion.
Conclusion
No claims are 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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/S.L.G./Examiner, Art Unit 1693
/ANDREA OLSON/Primary Examiner, Art Unit 1693
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