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 .
Status of the Claims
Claims 1-8 and 19-20 are pending.
Claim 1 is newly amended.
Claims 1-8 and 19-20 have been examined on their merits.
Withdrawn Objections & Rejections
The objections and rejections presented herein represent the full set of objections and rejections currently pending in the application. Any objections or rejections not specifically reiterated are hereby withdrawn.
The previous rejection of claims 1 and 3-7 under 35 U.S.C. 102(a)(1) as anticipated by Mahmoud et al. (Japanese Journal of Joint Disease, 2015, on IDS 06/21/2022, previously cited) as evidenced by Dezawa et al. (US 20120244129 A1, 2012, on IDS 06/21/2022, previously cited), Mahmoud et al. (Stem Cells International, 2017, on IDS 06/21/2022, hereafter “Mahmoud 2017”), and Mahmoud et al. (The Japanese Journal of Orthopaedic Association, 2016, on IDS 06/21/2022, hereafter “Mahmoud 2016”) or, in the alternative, under 35 U.S.C. 103 as obvious over Mahmoud et al. (Japanese Journal of Joint Disease, 2015, on IDS 06/21/2022, previously cited) in view of Dezawa et al. (US 20120244129 A1, 2012, on IDS 06/21/2022, previously cited) and Mahmoud et al. (The Japanese Journal of Orthopaedic Association, 2016, on IDS 06/21/2022, hereafter “Mahmoud 2016”) are withdrawn due to amendment of the claims.
The previous rejection of claims 2 and 19-20 under 35 U.S.C. 103 as obvious over Mahmoud et al. (Japanese Journal of Joint Disease, 2015, on IDS 06/21/2022, previously cited) in view of Dezawa et al. (US 20120244129 A1, 2012, on IDS 06/21/2022, previously cited) and Mahmoud et al. (The Japanese Journal of Orthopaedic Association, 2016, on IDS 06/21/2022, hereafter “Mahmoud 2016” are withdrawn due to amendment of the claims.
The previous rejection of claim 8 under 35 U.S.C. 103 as obvious over Mahmoud et al. (Japanese Journal of Joint Disease, 2015, on IDS 06/21/2022, previously cited) in view of Dezawa et al. (US 20120244129 A1, 2012, on IDS 06/21/2022, previously cited) and Mahmoud et al. (The Japanese Journal of Orthopaedic Association, 2016, on IDS 06/21/2022, hereafter “Mahmoud 2016”), as applied to claim 1, and further in view of Yoshida et al. (US 20150196600 A1, 2015, previously cited) is withdrawn due to amendment of the claim.
Claim Rejections - 35 USC § 102 or in the alternative 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 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.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1 and 3-7 are rejected under 35 U.S.C. 102(a)(1) as anticipated by Mahmoud et al. (Japanese Journal of Joint Disease, 2015, on IDS 06/21/2022, previously cited) as evidenced by Dezawa et al. (US 20120244129 A1, 2012, on IDS 06/21/2022, previously cited), Mahmoud et al. (Stem Cells International, 2017, on IDS 06/21/2022, hereafter “Mahmoud 2017”), and Mahmoud et al. (The Japanese Journal of Orthopaedic Association, 2016, on IDS 06/21/2022, hereafter “Mahmoud 2016”) or, in the alternative, under 35 U.S.C. 103 as obvious over Mahmoud et al. (Japanese Journal of Joint Disease, 2015, on IDS 06/21/2022, previously cited) in view of Dezawa et al. (US 20120244129 A1, 2012, on IDS 06/21/2022, previously cited) and Mahmoud et al. (The Japanese Journal of Orthopaedic Association, 2016, on IDS 06/21/2022, hereafter “Mahmoud 2016”).
In regards to claim 1, Mahmoud discloses that osteochondral defects were created in the patellar groove of rat knees, upon where Muse were injected, and that macroscopically, defect margins were easily identified and that histological scoring was better in Muse-treated groups than non-treated groups who exhibited defects replaced with fibrous tissue, and that in 70-90% of the Muse-treated groups new subchondral bone was formed (Abstract, p347).
As evidenced by Dezawa (who is noted is both an author of Mahmoud and an instant Inventor), Muse cells are SSEA-3 positive pluripotent stem cells isolated from mesenchymal body tissue (Abstract, claims 1 14); are positive for CD105 (claim 2); have low or no telomerase activity (claim 6); have the ability to differentiate into the three germ layers (claim 7); do not exhibit tumorigenic proliferation (claim 8); and have self-renewal capability (claim 9).
Thus, the Muse cells are disclosed by Mahmoud are the same as the claimed SSEA-3 positive pluripotent stem cells.
In regards to use of the method for assessing a repair effect of SSEA-3 positive pluripotent stem cells, in support for these limitations, Applicant points to paragraph [0044] and Table 3-2 (Remarks 05/19/2025, p4). It is noted that the term “assess” does not appear in paragraph and Table 3-2 (nor does it appear anywhere in the specification). However, paragraph [0044] and Table 3-2 refers to evaluation of histological samples, which a person of ordinary skill in the art would have realized is synonymous with assessing, and therefore there is implicit disclosure of this feature (see MPEP 2144.01).
As above, Mahmoud discloses identifying the effects of Muse treatment on defect margins, by histological scoring, on osteochondral defect sites, which as identified by Applicant, reads on “assessing a repair effect” of SSEA-3 positive pluripotent stem cells.
While Mahmoud is silent on assessing integration of articular cartilage specifically, it is noted that the method steps of Mahmoud are identical to the invention as claimed.
Additionally, Mahmoud explicitly discloses the effects of Muse cells on “osteochondral repair” (Abstract, p347). As defined in the specification “Damage extending to cartilage and subchondral bone is referred to as osteochondral damage” (paragraph [0045]). Therefore, the method of Mahmoud for osteochondral repair indicates the likelihood of repair to both bone and cartilage.
Furthermore, as evidenced by Dezawa, it is known in the art that Muse cells can differentiate into both osteoblasts or chondrocytes (paragraph [0164]), and can differentiate into cartilage specifically (paragraph [0071]; Fig. 23-3).
Additionally, as evidenced by the post-filing art of Mahmoud 2017, when conducting the same experiment (creating osteochondral defects in the patellar groove of rats and injecting the same number of Muse cells) resulted in repair at the cartilage defect site (Abstract, p1).
Moreover, as further evidenced by the prior art of Mahmoud 2016, sites of osteochondral damage treated with Muse cells exhibited repair of both bone and cartilage (3-7-EW-2). Thus, it was known in the art before the effective filing date that Muse cells could simultaneously repair both bone and cartilage at sites of osteochondral damage.
Therefore, since not only does Mahmoud teach methods for osteochondral repair that are the same as the instant claims, but also because, as evidenced by Dezawa, it was known in the art that Muse cells differentiate into chondrocytes and cartilage, because, as evidenced by Mahmoud 2017 above, in another identical experiment, cartilage repair was observed, and because as evidenced by Mahmoud 2016 it was known in the art before the effective filing date that Muse cells simultaneously repair bone and cartilage at sites of osteochondral damage, it would be expected not only that the method of Mahmoud would repair articular cartilage, but that the assessment of the margins of osteochondral damage would also refer to the assessment articular damage as well.
However, even if the method of Mahmoud did not, it would still have been prima facie obvious to assess the integration of repair tissue with the surrounding articular cartilage because, as taught by Mahmoud 2016, sites of osteochondral damage include damage both subchondral bone and articular cartilage (3-7-EW-2), and a person of ordinary skill in the art would want to analyze the totality of damages tissues.
Furthermore, because as taught by Dezawa, MSC fractions (including Muse cells) have the ability to differentiate not only into bone but cartilage as well (paragraph [0005, 0071]; Fig. 23-3), and as discussed above, can differentiate into chondrocytes specifically (paragraph [0164]); because Mahmoud 2016 teaches that Muse cells simultaneously repair bone and cartilage at sites of osteochondral damage; and because Mahmoud teaches that sites of osteochondral damaged can be assed for repair by Muse cells, it could have been done with predictable results and a reasonable expectation of success.
In regards to claim 3, as either evidenced by or in the alternative taught by Dezawa SSEA-3 positive pluripotent stem cells (Muse cells) are CD117-negative and CD146-negative (claim 3).
In regards to claim 4, as either evidenced by or in the alternative taught by Dezawa SSEA-3 positive pluripotent stem cells (Muse cells) are CD117-negative, CD146-negative, NG2- negative, CD34-negative, vWF-negative and CD271-negative (claim 4).
In regards to claim 5, as either evidenced by or in the alternative taught by Dezawa SSEA-3 positive pluripotent stem cells (Muse cells) are CD34-negative, CD117-negative, CD146- negative, CD271-negative, NG2-negative, vWF-negative, Sox10-negative, Snail-negative, Slug-negative, Tyrpl-negative and Dct-negative (claim 5).
In regards to claims 6, as above, Mahmoud discloses that at sites of osteochondral damage, histological scoring was significantly better in Muse-treated groups than non-treated groups who exhibited defects replaced with fibrous tissue, and that in 70-90% of the Muse-treated groups new subchondral bone was formed (Abstract, p347). Therefore, a person of ordinary skill in the art would recognize that these cells would accumulate at these sites.
In regards to claim 7, as discussed above, as either evidenced by or in the alternative taught by Dezawa SSEA-3 positive pluripotent stem cells (Muse cells) can differentiate into chondrocytes (paragraph [0164]).
Therefore, the method of Mahmoud either anticipates or the combined method of Mahmoud, Dezawa, and Mahmoud 2016 renders obvious the invention as claimed.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
The statutory basis under 35 USC 103 and the factual inquiries for establishing a background for determining obviousness under 35 USC 103 are discussed above.
Claims 2 and 19-20 are rejected under 35 U.S.C. 103 as obvious over Mahmoud et al. (Japanese Journal of Joint Disease, 2015, on IDS 06/21/2022, previously cited) in view of Dezawa et al. (US 20120244129 A1, 2012, on IDS 06/21/2022, previously cited) and Mahmoud et al. (The Japanese Journal of Orthopaedic Association, 2016, on IDS 06/21/2022, hereafter “Mahmoud 2016”).
The rejection of claim 1 is discussed above.
In regards to claims 2 and 19-20, Mahmoud does not explicitly teach that the SSEA-3 positive pluripotent stem cells (Muse cells) can be concentrated by an external stress stimulation.
However, Dezawa teaches that Muse cells can be enriched (concentrated) by subjecting mesenchymal to external stress or trauma including the protease trypsin (paragraphs, [0115, 0118-0119]). A person of ordinary skill in the art would have been motivated to concentrate Muse cells because Dezawa teaches that “cell fractions containing many Muse cells” can be obtained this way (paragraph 0129]). Furthermore, because Dezawa teaches methods for concentrating Muse cells including with the protease trypsin (paragraphs, [0115, 0118-0119]), it could have been done with predictable results and a reasonable expectation of success so as to increase the number of Muse cells for the method of Mahmoud.
Therefore, the combined teachings of Mahmoud and Dezawa render the invention unpatentable as claimed.
Claims 8 is rejected under 35 U.S.C. 103 as obvious over Mahmoud et al. (Japanese Journal of Joint Disease, 2015, on IDS 06/21/2022, previously cited) in view of Dezawa et al. (US 20120244129 A1, 2012, on IDS 06/21/2022, previously cited) and Mahmoud et al. (The Japanese Journal of Orthopaedic Association, 2016, on IDS 06/21/2022, hereafter “Mahmoud 2016”), as applied to claim 1, and further in view of Yoshida et al. (US 20150196600 A1, 2015, previously cited 02/12/2024).
In regards to claim 8, Mahmoud teaches that Muse cells were administered to rats at a concentration of 5 x 104 cells (Abstract). While Mahmoud is silent as to the mass of these rats, as evidenced by Paronis, adult Winstar rats have a mean body weight of 238.22 ± 34.9 g (Abstract, p188), which comports with what is well-known in the art that lab rats typically have a weight range of about 200 to 300 g (with males being heavier than females). When normalized to a cells/kg per individual rat, this corresponds to a concentration of about 1.6 to 2.5 x 105 cells/kg per individual, which overlaps with the range as in claim 8. Therefore, the method of Mahmoud with a Winstar rat makes obvious this concentration.
Furthermore, Yoshida teaches that Muse cells can be suitably adjusted in consideration of the gender, age, and body weight of the subject, disease state and state in which the cells are used so as to obtain the desired effect (paragraph [0070]). In particular, Yoshida teaches that superior effects can be expected to be obtained by administering 1.7 x 105 to 2.5 x 105 cells per kg per individual based on body weight (paragraph [0070]), which overlaps with the range of 1.6 to 2.5 x 105 cells per individual based on body weight, as in claim 8. Therefore, a person of ordinary skill in the art would have been motivated to administer Muse cells based on the body weight of an individual to provide individualized treatment based on their unique physiological needs. Furthermore, because Yoshida teaches that the number of Muse cells can be adjusted based on patient need, and teaches administering a specific dose of 1.7 x 105 to 2.5 x 105 cells per kg per individual based on body weight (paragraph [0070]), which overlaps with the range of 1.6 to 2.5 x 105 cells per individual based on body weight, it could have been done with predictable results and a reasonable expectation of success.
Therefore, the combined teachings of Mahmoud, Dezawa, and Yoshida renders obvious the invention as claimed.
Response to Arguments
Applicant argues that Mahmoud, of which the Office only references the Abstract, is silent and thus does not disclose the method, as amended, nor does it disclose assessing the integration of repair tissue with the surrounding articular cartilage (Remarks, p4).
Continuing, Applicant argues that a person of ordinary skill in the art would not have inferred that assessing the repair effect could be achieved by assessing integration of repair tissue with the surrounding articular cartilage (Remarks, p4).
Furthermore, Applicant argues that a person of ordinary skill in the art would not have inferred that assessing the repair effect could be achieved by assessing integration of repair tissue with the surrounding articular cartilage (Remarks, p4).
Specifically, Applicant argues, by repairing articular cartilage simultaneously in addition to subchondral bone, the integration of the repaired tissue and the surrounding articular cartilage can be significantly evaluated and observed, that such an evaluation is not taught or suggested in any of the cited references, and that Mahmoud is silent as to this dual therapeutic effect (Remarks, p5).
Applicant's arguments filed 05/19/2025 have been fully considered but they are not persuasive.
In regards to the use of the method for assessing or the step of assessing articular cartilage, as discussed above, in regards to use of the method for assessing a repair effect of SSEA-3 positive pluripotent stem cells, in support for these limitations, Applicant points to paragraph [0044] and Table 3-2 (Remarks 05/19/2025, p4). It is noted that the term “assess” does not appear in paragraph and Table 3-2 (nor does it appear anywhere in the specification). However, paragraph [0044] and Table 3-2 refers to evaluation of histological samples, which a person of ordinary skill in the art would have realized is synonymous with assessing, and therefore there is implicit disclosure of this feature (see MPEP 2144.01).
As above, Mahmoud discloses identifying the effects of Muse treatment on defect margins, by histological scoring, on osteochondral defect sites, which as identified by Applicant, reads on “assessing a repair effect” of SSEA-3 positive pluripotent stem cells.
While Mahmoud is silent on assessing integration of articular cartilage specifically, it is noted that the method of Mahmoud is identical to the invention as claimed.
Additionally, Mahmoud explicitly discloses the effects of Muse cells on “osteochondral repair” (Abstract, p347). As defined in the specification “Damage extending to cartilage and subchondral bone is referred to as osteochondral damage” (paragraph [0045]).
Furthermore, as evidenced by Dezawa, it is known in the art that Muse cells can differentiate into both osteoblasts or chondrocytes (paragraph [0164]), and can differentiate into cartilage specifically (paragraph [0071]; Fig. 23-3).
Additionally, as evidenced by the post-filing art of Mahmoud 2017, when conducting the same experiment (creating osteochondral defects in the patellar groove of rats and injecting the same number of Muse cells) resulted in repair at the cartilage defect site (Abstract, p1).
Moreover, as further evidenced by the prior art of Mahmoud 2016, sites of osteochondral damage treated with Muse cells exhibited repair of both bone and cartilage (3-7-EW-2). Thus, it was known in the art before the effective filing date that Muse cells could simultaneously repair both bone and cartilage at sites of osteochondral damage.
Therefore, since not only does Mahmoud teach methods for osteochondral repair that are the same as the instant claims, but also because, as evidenced by Dezawa, it was known in the art that Muse cells differentiate into chondrocytes and cartilage, because, as evidenced by Mahmoud 2017 above, in another identical experiment, cartilage repair was observed, and because as evidenced by Mahmoud 2016 it was known in the art before the effective filing date that Muse cells simultaneously repair bone and cartilage at sites of osteochondral damage, it would be expected not only that the method of Mahmoud would repair articular cartilage, but that the assessment of the margins of osteochondral damage would also refer to the assessment articular damage as well.
Furthermore, even if Mahmoud did not, as discussed above, it would still have been prima facie obvious to assess the integration of repair tissue with the surrounding articular cartilage in addition to subchondral bone at sites of osteochondral damage because, as taught by Mahmoud 2016, sites of osteochondral damage include damage both subchondral bone and articular cartilage (3-7-EW-2).
Furthermore, because as taught by Dezawa, MSC fractions (including Muse cells) have the ability to differentiate not only into bone but cartilage as well (paragraph [0005, 0071]; Fig. 23-3), and as discussed above, can differentiate into chondrocytes specifically (paragraph [0164]); because Mahmoud 2016 teaches that Muse cells simultaneously repair bone and cartilage at sites of osteochondral damage; and because Mahmoud teaches that sites of osteochondral damaged can be assed for repair by Muse cells, it could have been done with predictable results and a reasonable expectation of success.
In regards to a dual therapeutic effect, it is noted that the claims as newly amended are drawn to a method of “assessing” not providing a dual therapeutic effect, and the claims do not necessarily imply that a dual therapeutic effect necessarily occurs.
Thus, in response to applicant's argument that the references fail to show certain features of the invention, it is noted that the features upon which applicant relies (i.e., a dual therapeutic effect) are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993).
In regards to the evidentiary references, in regards to Dezawa, Applicant argues that merely because Muse cells can differentiate into both osteoblasts or chondrocytes does not necessarily mean that it does so in vivo (Remarks, p5).
Applicant's arguments filed 05/19/2025 have been fully considered but they are not persuasive.
While it could be true that merely because Muse cells can differentiate into both osteoblasts or chondrocytes does not necessarily mean that it does so in vivo, as discussed above, as evidenced by the post-filing art of Mahmoud 2017, conducting the same experiment (creating osteochondral defects in the patellar groove of rats and injecting the same number of Muse cells) resulted in repair at the cartilage defect site (Abstract, p1). Thus, this appears to be a natural outcome of practicing the method of Mahmoud.
Moreover, as further evidenced by the prior art of Mahmoud 2016, as discussed above, sites of osteochondral damage treated with Muse cells exhibited repair of both bone and cartilage (3-7-EW-2).
Therefore, as discussed above, it would be expected that the method of Mahmoud would repair articular cartilage in addition to subchondral bone at sites of osteochondral damage.
In regards to Mahmoud 2017, Applicant argues that this reference was published after the effective filing date and therefore cannot be used as prior art (Remarks, p5).
Applicant argues that even if Mahmoud 2017 is used merely to show inherency of the claims, Mahmoud 2017 concluded that the repaired tissue had “a mostly smooth homogenous surface,” which does not indicate that two separate types of tissue were repaired, since two different tissues would not be expected to form a single homogenous surface of only one color. Mahmoud 2017 at Abstract
Applicant's arguments filed 05/19/2025 have been fully considered but they are not persuasive.
Mahmoud 2017 is not used as prior art, but to provide evidence that when an identical method to that of Mahmoud is performed (creating osteochondral defects in the patellar groove of rats and injecting the same number of Muse cells) resulted in repair at the cartilage defect site (Abstract, p1).
In regards to evidentiary references (see MPEP 2124), references cited to show a universal fact need not be available as prior art before applicant’s filing date. In re Wilson, 311 F.2d 266, 135 USPQ 442 (CCPA 1962). Such facts include the characteristics and properties of a material or a scientific truism. Some specific examples in which later publications showing factual evidence can be cited include situations where the facts shown in the reference are evidence. In re Corneil, 347 F.2d 563, 568, 145 USPQ 702, 705 (CCPA 1965). Furthermore, MPEP 2112.01(II) recites that "products of identical chemical composition cannot have mutually exclusive properties. A chemical composition and its properties are inseparable."
Moreover, there is no requirement that a person of ordinary skill in the art would have recognized the inherent or natural disclosure at the time of filing of the invention, but only that the subject matter is in fact inherent or natural property in the prior art reference. As stated above, the Examiner has provided extrinsic evidence that makes clear that the missing descriptive matter is necessarily present in the cells described in the prior art reference, and that it would be so recognized by persons of ordinary skill.
Finally, since the Patent Office does not have the facilities for examining and comparing Applicants' cells with the cells of the prior art reference, the burden is upon Applicants to show a distinction between the material structural and functional characteristics of the claimed cells and the cells of the prior art. See In re Best, 562 F.2d 1252, 195 USPQ 430 (CCPA 1977) and In re Fitzgerald et al., 205 USPQ 594.
In regards to Applicant’s argument that Mahmoud 2017 evidences that the repaired tissue had “a mostly smooth homogenous surface which does not indicate that two separate types of tissue were repaired, since two different tissues would not be expected to form a single homogenous surface of only one color”, by the identical method of Mahmoud, Mahmoud 2017 explicitly evidences that there was in fact neocartilage formation at sites of osteochondral damage (Table 2, p2).
Applicant argues that Mahmoud 2016 cannot be characterized as “the same method” as claimed, let alone be used to support a finding that it necessarily teaches the same effects, such as to support an inherency conclusion (Remarks, p6).
Applicant's arguments filed 05/19/2025 have been fully considered but they are not persuasive.
As discussed above, as discussed above, evidenced by Mahmoud, sites of osteochondral damage treated with Muse cells exhibited repair of both bone and cartilage (3-7-EW-2). Thus, it was known in the art before the effective filing date that Muse cells could simultaneously repair both bone and cartilage at sites of osteochondral damage.
Applicant argues that because Mahmoud, Dezawa, and Mahmoud 2016 do not teach independent claim 1, claims 2 and 19-20 are patentable (Remarks, p6).
Applicant's arguments filed 05/19/2025 have been fully considered but they are not persuasive.
As discussed above, the method of Mahmoud either anticipates or the combined method of Mahmoud, Dezawa, and Mahmoud 2016 renders obvious claim 1 as amended.
Furthermore, claims 2 and 19-20 are prima facie obvious as discussed above.
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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/JOSEPH PAUL MIANO/Examiner, Art Unit 1631
/ARTHUR S LEONARD/Examiner, Art Unit 1631