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 .
Claim Status
1. The amendment filed 01/29/2025 has been entered. Claims 1 – 17 remain pending and are under consideration.
Priority
2. This application is a Continuation of PCT International Application No. PCT/IB2021/000794 filed on November 17, 2021, which claims priority under 35 U.S.C. § 119 to U.S. Provisional Patent Application No. 63/115,242 filed on November 18, 2020.
Information Disclosure Statement
3. The information disclosure statements (IDS) submitted on 12/23/2025 are acknowledged. The submissions are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
Withdrawn Specification Objection
4. The objection to the specification for improper trade name or marker usage is withdrawn in view of Applicant’s amendment to the specification.
Withdrawn Claim Objections
5. The objection to claim 8 is withdrawn in view of Applicant’s amendment to the claim.
Withdrawn Claim Rejections
6. The rejections of claims 1 – 3 and 13 – 16 under 35 U.S.C. 102(a)(1) is withdrawn in view of Applicant’s amendment to claim 1 requiring the target cells be specialized cells.
Claim Interpretation
7. For the purpose of applying prior art, “specialized cells” in claims 1, 4, and 17 is interpreted as fully differentiated cells based on Applicant’s specification at para. 00142.
8. For the purpose of applying prior art, “obtained from induced pluripotent stem cells (iPSCs)” of claims 1, 4, and 17 is interpreted as a product-by-process limitation (see MPEP 2113) and does not add structure to the recited “target cells” that are “specialized cells”.
9. For the purpose of applying prior art, “the amount of the secretome administered to the culture of target cells is determined based on the amount of secreting cells that produced the secretome” of claim 1, 4, and 17 is interpreted as the amount of secreting cells that produced the secretome, the protein content of the secretome, the RNA content of the secretome, the exosome amount of the secretome, or the number of particles in the secretome based on Applicant’s specification at para. 00197.
10. For the purpose of applying prior art, “optionally” in claim 4 is interpreted as the claim does not require “culturing said target cells in the presence of the secretome”.
Objections/Rejections Necessitated by Amendment
Claim Objections
11. Claim 1 is objected to because of the following informalities: in line 7, “the amount of the secretome” lacks antecedent basis but does not rise to rejection under 35 U.S.C. 112(b) because it is clear that “the amount” refers to the secretome. Appropriate correction is required.
12. Claim 1 is objected to because of the following informalities: in line 8, “the amount of the secreting cells that produces the secretome” lacks antecedent basis but does not rise to rejection under 35 U.S.C. 112(b) because it is clear that “the amount” refers to the cells that produced the secretome. Appropriate correction is required.
13. Claim 4 is objected to because of the following informalities: in line 7, “the amount of the secretome” lacks antecedent basis but does not rise to rejection under 35 U.S.C. 112(b) because it is clear that “the amount” refers to the secretome. Appropriate correction is required.
14. Claim 4 is objected to because of the following informalities: in line 8, “the amount of the secreting cells that produces the secretome” lacks antecedent basis but does not rise to rejection under 35 U.S.C. 112(b) because it is clear that “the amount” refers to the cells that produced the secretome. Appropriate correction is required.
15. Claim 17 is objected to because of the following informalities: in line 7, "the secretome" lacks antecedent basis but does not rise to rejection under 35 U.S.C. 112(b) because it is clear that “the secretome” refers to a secretome as recited prior to amending the claim. Appropriate correction is required.
16. Claim 17 is objected to because of the following informalities: in line 8, “the amount of the secretome” lacks antecedent basis but does not rise to rejection under 35 U.S.C. 112(b) because it is clear that “the amount” refers to the secretome. Appropriate correction is required.
17. Claim 17 is objected to because of the following informalities: in line 9, “the amount of the secreting cells that produces the secretome” lacks antecedent basis but does not rise to rejection under 35 U.S.C. 112(b) because it is clear that “the amount” refers to the cells that produced the secretome. Appropriate correction is required.
Maintained Claim Rejections
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.
18. Claim(s) 1, 8, 10, and 12 – 16 remain rejected under 35 U.S.C. 102(a)(1) as being anticipated by Barile (Barile, Lucio, et al. Cardiovascular research 114.7 (2018): 992-1005; previously cited), hereinafter Barile. Although maintained, note that the rejection is updated in light of the amendments to the claims.
Claim 1 is drawn to A method for analyzing an activity of a secretome, said method comprising:
(a) contacting a culture of target cells with a pre-treatment medium, culturing said
target cells in said pre-treatment medium under at least one stress-inducing condition, wherein
the target cells are specialized cells obtained from induced pluripotent stem cells (iPSCs);
(b) administering the secretome to the culture of target cells, culturing said target cells in the presence of the secretome, wherein the amount of the secretome administered to the culture of target cells is determined based on the amount of secreting cells that produced the secretome; and
(c) measuring at least one property of the cultured target cells one or more times during
the culturing of step (b).
Regarding claim 1, Barile teaches culturing HL-1 cardiomyocytes (CMs) (“the target cells are specialized cells”) in Claycomb medium and in the presence of staurosporine (step (a)) (page 993, right col. para. 3; Expanded Methods, page 2, last para.). Barile teaches exosomes (“secretome”) were added to the culture and twelve hours later (step (b)), cell viability and cell apoptosis was measured (step (c)) (page 993, right col. para. 3; Expanded Methods, page 2, last para; page 3, para. 1). Barile teaches pooled samples of exosomes (from n=4 patients each; 106 particles/cm2) were added to the culture of CMs (“the amount of the secretome”) (page 996, right col.; Expanded Methods page 2, last para.; Figure 2). Barile teaches the presence of proteins in the exosomes in Figure 1B by Western blotting and flow cytometry in Figure 1C (page 995, right col.).
Regarding claim 8, Barile teaches culturing in the presence of staurosporine to induce cell death (page 993, right col. para. 3; Expanded Methods, page 2, last para.).
Regarding claim 10, Barile teaches staurosporine induces apoptosis (page 993, right col. para. 3; Expanded Methods, page 2, last para.).
Regarding claim 12, Barile teaches staurosporine (page 993, right col. para. 3; Expanded Methods, page 2, last para.).
Regarding claim 13 and 14, Barile teaches measuring cell viability (page 993, right col. para. 3; Expanded Methods, page 2, last para; page 3, para. 1).
Regarding claim 15, Barile teaches exosomes are isolated from cardiac progenitor cells (CPCs), bone marrow mesenchymal stem/progenitor cells (BMCs), and dermal fibroblasts (“multipotent progenitor cells” and “end-stage differentiated cells”) (page 993, para. 2).
Regarding claim 16, Barile teaches the CPC and BMC exosomes are sEVs because the particle size is 100 – 200 nm (Figure 1; page 995, right col.).
Therefore, Barile anticipates claims 1, 8, 10, and 12 – 16.
19. Claim(s) 4 – 7 and 9 remain rejected under 35 U.S.C. 102(a)(1) as being anticipated by Gartz (Gartz, Melanie, et al. Scientific reports 8.1 (2018): 16519; previously cited), hereinafter Gartz. Although maintained, note that the rejection is updated in light of the amendments to the claims.
Claim 4 is drawn to a method for analyzing an activity of a secretome, said method comprising:
(a) contacting a culture of target cells with a pre-treatment medium, and-culturing said
target cells in said pre-treatment medium, wherein the target cells are specialized cells obtained
from induced pluripotent stem cells (iPSCs);
(b) administering the secretome to the culture of target cells, optionally culturing said target cells in the presence of the secretome, wherein the amount of the secretome administered to the culture of target cells is determined based on the amount of secreting cells that produced the secretome;
(c) culturing the target cells under at least one stress-inducing condition; and
(d) measuring at least one property of the cultured target cells one or more times during
the culturing of step (c).
Regarding claim 4, Gartz teaches culturing cardiomyocytes (“target cells are specialized cells”) with U0126 (step (a)), adding exosomes (step (b)), culturing cells under stress (step (c)), and measuring cell viability (step (d)) (page 12, para. 8; Supplemental Figure 7; page 5, para. 2 – 3). Gartz teaches the cardiomyocytes were differentiated from iPSCs (page 2, para. 3; page 10, last para.). Gartz teaches a dose of 5 µl containing approximately 2.25 x 107 exosomes was used (“the amount of the secretome”) (page 3, para. 2).
Regarding claim 5, Gartz teaches the cardiomyocytes are cultured with exosomes before inducing stress because Gartz teaches U0126 abolished the protective effects of exosomes on stress-induced cell death (page 5, para. 2; Figure 7f).
Regarding claim 6, Gartz teaches removing the exosomes before inducing stress because Gartz teaches the exosomes were added to the cardiomyocytes before stress induction after stress the cells are recovered in a different medium (page 12, para. 8).
Regarding claim 7, Gartz teaches culturing the cardiomyocytes with exosomes and H2O2 together (page 12, para. 8).
Regarding claim 9, Gartz teaches the cellular stress agent is H2O2 (“apoptosis-inducing agent) (page 12, para. 8).
Therefore, Gartz anticipates claims 4 – 6 and 9.
20. Claim(s) 17 remains rejected under 35 U.S.C. 102(a)(1) as being anticipated by Barile (Barile, Lucio, et al. Cardiovascular research 114.7 (2018): 992-1005; previously cited), hereinafter Barile. Although maintained, note that the rejection is updated in light of the amendments to the claims.
Claim 17 is drawn to method for analyzing an activity of a small molecule therapeutic, said method comprising:
(a) contacting a culture of target cells with a pre-treatment medium, culturing said target cells in said pre-treatment medium in the presence of the small molecule or a chemotherapy agent, wherein the target cells are specialized cells obtained from induced pluripotent stem cells (iPSCs);
(b) administering the secretome to the culture of target cells, culturing said target cells in the presence of the secretome, wherein the amount of the secretome administered to the culture of target cells is determined based on the amount of secreting cells that produced the secretome; and
(c) measuring at least one property of the cultured cells one or more times during the
culturing of step (b).
Barile teaches culturing HL-1 cardiomyocytes (CMs) (“target cells are specialized cells”) in Claycomb medium and in the presence of staurosporine (step (a)) (page 993, right col. para. 3; Expanded Methods, page 2, last para.). Barile teaches exosomes (“secretome”) were added to the culture and twelve hours later (step (b)), cell viability and cell apoptosis was measured (step (c)) (page 993, right col. para. 3; Expanded Methods, page 2, last para; page 3, para. 1). Barile teaches pooled samples of exosomes (from n-4 patients each; 106 particles/cm2) were added to the culture of CMs (“the amount of the secretome”) (page 996, right col.; Expanded Methods page 2, last para.; Figure 2). Barile teaches the presence of proteins in the exosomes in Figure 1B by Western blotting and flow cytometry in Figure 1C (page 995, right col.).
Therefore, Barile anticipates claim 17.
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.
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.
21. Claim(s) 4 – 7, 9, and 11 remain rejected under 35 U.S.C. 103 as being unpatentable over Gartz (Gartz, Melanie, et al. Scientific reports 8.1 (2018): 16519; previously cited), hereinafter Gartz in view of Barile (Barile, Lucio, et al. Cardiovascular research 114.7 (2018): 992-1005; previously cited), hereinafter Barile in view of Li (Li, Xin, et al. Cell Death & Disease 10.10 (2019): 691; previously cited), which is cited on the IDS filed 08/21/2023.
Gartz anticipates claims 4 – 7 and 9 as set forth above.
Regarding claim 11, Gartz teaches staurosporine induces apoptosis in cardiomyocytes (page 13, para. 1; Supplemental Figure 6) but does not evaluate the protective effects of exosomes on cardiomyocytes treated with staurosporine. Gartz teaches exosomes from cardiomyocytes decrease stress-injury by decreasing cell death and this protection was dependent on the presence of exosomal surface proteins and activation of ERK1/2 and p38 MAPK signaling (Abstract). Gartz teaches identifying the exosomal surface protein involved in initiating the cardioprotective effects may provide a novel target for the treatment of dystrophin-deficient cardiomyopathy (page 9, para. 1). Gartz teaches cardiomyopathy is the leading cause of death for patients with Duchenne muscular dystrophy (DMD), which is due to dystrophin deficiency resulting from mutations in the DMD gene (page 1, para. 1). Gartz teaches both wild type cardiomyocyte-derived and DMD cardiomyocyte-derived exosomes protect DMD-cardiomyocytes against H2O2-induced stress (page 5, para. 5 – 6). Gartz teaches understanding how endogenous exosomes are changing the phenotype of the dystrophin-deficient cardiomyocyte will give greater understanding of the mechanisms of dystrophin-deficient cardiomyopathy (page 2, para. 2).
Barile teaches culturing HL-1 cardiomyocytes (CMs) in Claycomb medium and in the presence of staurosporine (page 993, right col. para. 3; Expanded Methods, page 2, last para.). Barile teaches exosomes were added to the culture and twelve hours later, and cell viability and cell apoptosis was measured (page 993, right col. para. 3; Expanded Methods, page 2, last para; page 3, para. 1). Barile teaches culturing in the presence of staurosporine to induce apoptosis (page 993, right col. para. 3; Expanded Methods, page 2, last para.). Barile teaches exosomes isolated from cardiac progenitor cells are cardioprotective and the surface of these exosomes have the protein PAPP-A that releases IGF-1, which is a key cardioprotective factor (page 993, left col. para. 3; page 998, right col. para. 2; page 999, right col.; page 1000, left col.). Barile teaches exosomal PAPP-A is cardioprotective in vitro and in vivo where knockdown of PAPP-A prevents in vitro anti-apoptotic activity of the exosomes and prevents an increase in LVEF in vivo (page 1000, right col. para. 2; Figure 7 – 8).
It would have been obvious prior to the effective filing date of the invention as claimed for the person of ordinary skill in the art to combine the teachings of Gartz regarding a method of analyzing the cardiac cell protective activity of exosomes with H2O2 with the teachings of Barile regarding a method of analyzing the cardiac cell protective activity of exosomes with staurosporine to arrive at the claimed method where the apoptosis-inducing agent is staurosporine. One would have been motivated to combine the teachings of Gartz and Barile in a method to analyze the activity of surface exosomal proteins on protecting cardiac cells from apoptosis as Gartz teaches identifying the exosomal surface protein involved in initiating the cardioprotective effects may provide a novel target for the treatment of dystrophin-deficient cardiomyopathy and cardiomyopathy is the leading cause of death for patients with Duchenne muscular dystrophy. One would have a reasonable expectation of success in combining the teachings as Gartz and Barile teach exosomes derived from cardiac cells protect cardiac cells from apoptosis and Gartz teaches this is due in part to the presence of a surface protein on the exosomes and Barile teaches PAPP-A is a surface protein on exosomes that is responsible for the protective effect of the exosomes.
Rejections Necessitated by Amendment
22. Claim(s) 1 – 3, 8, 10, and 13 – 16 is/are rejected under 35 U.S.C. 103 as being unpatentable over Li (Li, Xin, et al. Cell Death & Disease 10.10 (2019): 691; previously cited), which is cited on the IDS filed 08/21/2023 in view of Sharma (Sharma, Arun, et al. Circulation research 115.6 (2014): 556-566.), hereinafter Sharma.
Regarding claims 1 – 3, Li teaches culturing cardiac progenitor cells (CPCs) (“target cells” of claim 1) and infecting the cells with coxsackievirus B3 (CVB3) (step (a) of claim 1) and after 1 hour of infection cells were washed and replenished with fresh media (claim 2) (page 3, right col. para. 2; page 6, right col. para. 2). Li teaches adding 200 ng/mL of CPC-derived exosomes (“the amount of the secretome” of claim 1) at 1 hour after CVB3 infection (step (b) of claim 1 and claim 3) (page 6, left col. para. 2). Li teaches measuring apoptosis 24 and 48 hours post infection and the exosomes inhibited CVB3-induced apoptosis (step (c) of claim 1) (page 6, left col. para. 1; page 3, left col. para. 3). Li teaches characterization of the exosomes including proteins expressed by the exosomes in Figure 1 (page 4, right col. para. 4). Li does not teach the “target cells are specialized cells” of claim 1, which is interpreted as fully differentiated cells.
Regarding claim 8, Li teaches coxsackievirus B3 (page 3, right col. para. 2).
Regarding claim 10, Li teaches CVB3 is an apoptosis-inducing agent (Abstract; page 6, left col. para. 1).
Regarding claim 13 and 14, Li teaches measuring cell apoptosis (“cell viability”) (page 3, left col. para. 3; page 6, right col. para. 2; Figure 5A).
Regarding claim 15, Li teaches the exosomes are isolated from CPCs (“multipotent progenitor cells”) (page 1, right col. para. 2; page 2, right col. para. 1 – 2).
Regarding claim 16, Li teaches the exosomes are sEV because they are 30 – 100 mm in diameter (page 4, right col. last para.).
Li does not teach the “target cells are specialized cells” of claim 1, which is interpreted as fully differentiated cells. Li teaches the CPCs were generated from the hearts of 2-month-old rats (page 2, right col. para. 1). However, Li teaches viral myocarditis is potentially fatal and lacking a specific treatment (Abstract; page 2, left col. para. 4; page 11, left col. para. 3). Li teaches viral myocarditis (VMC) is a common cause of dilated cardiomyopathy and sudden death and therefore finding effective therapies for VMC is still a big challenge (page 1, left col.). Li teaches CVB is a common enterovirus that can cause myocarditis (page 2, left col. para. 3). Li teaches the dysregulation of the apoptotic pathway is an important pathological process of CVB3-induced VMC and the CPC-derived exosomes could alleviate the apoptosis induced by CVB3 by inhibiting the virus replication (page 11, right col. para. 2; page 15, left col. para. 2).
Sharma teaches a method of infecting human iPSC-derived cardiomyocytes (hiPSC-CMs) with CVB3 as a model for testing potential antiviral compounds (Abstract; page 557, right col. para. 3 – 4; Figure 1; page 559, right col. para. 2; Figure 2; page 560, left col. para. 1). Sharma teaches the viability of hiPSC-CMs decreased with CVB3 infection (page 560, left col. para. 2 and right col. para. 1; Figure 3).
Sharma teaches the hiPSC-CMs infected with CVB3 could be used to determine the antiviral effect of compounds on cell viability, metabolic activity, and cell morphology (page 560, right col. para. 2; Table; page 561, left col. para. 2 and right col.; Figure 5 and 6; page 562).
Sharma teaches VMC is a disease for which there remains no effective antiviral treatment and there is a shortage of treatments for combating CVB3-induced myocarditis (page 563, left col. para. 3; page 564, left col. para. 2). Sharma teaches there is significant interest in finding safe and effective antiviral compounds for treating CVB3-induced myocarditis (page 564, left col. para. 2). Sharma teaches that hiPSC-CMs are more representative structurally and physiologically of the cardiac cell populations damaged during CVB3-induced myocarditis (page 564, left col. para. 2). Sharma teaches testing novel therapeutics on hiPSC-CMs allows for the assessment of potential cardiotoxicities and drug-induced arrhythmias, which are leading causes of drug withdrawal from the pharmaceutical market (page 564, left col. para. 2). Sharma teaches although the tested compounds were successful in reducing and delaying viral proliferation, a single-digit number of viral particles may be sufficient to propagate CVB3 infection on an entire well of hiPSC-CMs (page 564, right col. para. 1). Sharma teaches the hiPSC-CMs system could be used in a high-throughput manner to screen for novel, noncardiotoxic, antiviral therapeutics (page 557, left col. para. 2; page 564, right col. para. 1). Sharma teaches the hiPSC-CMs are ideal cells for studying the mechanisms of coxsackievirus-induced VMC because they are nonimmortalized human cardiomyocytes that express relevant ion channels and sarcomeric proteins found in adult human cardiomyocytes (page 557, left col. para. 2).
It would have been obvious prior to the effective filing date of the invention as claimed for the person of ordinary skill in the art to substitute the CPCs of Li with the hiPSC-CMs of Sharma to arrive at the claimed method where the target cells are adult human cardiomyocytes. One would have been motivated to make such a substitution as Sharma teaches the hiPSC-CMs are ideal cells for studying the mechanisms of coxsackievirus-induced VMC because they are nonimmortalized human cardiomyocytes that express relevant ion channels and sarcomeric proteins found in adult human cardiomyocytes and that hiPSC-CMs are more representative structurally and physiologically of the cardiac cell populations damaged during CVB3-induced myocarditis and testing novel therapeutics on hiPSC-CMs allows for the assessment of potential cardiotoxicities and drug-induced arrhythmias, which are leading causes of drug withdrawal from the pharmaceutical market. One would have a reasonable expectation of success in carrying out the substitution as Sharma teaches the hiPSC-CMs could be infected with CVB3 and the infected cells could be used to test the potential of antiviral compounds to reduce CVB3 replication by measuring cell viability, metabolic activity, and cell morphology.
Applicant Arguments/ Response to Arguments
23. Applicant Argues: On page 10, para. 2, Applicant asserts that Barile, Li, and Gartz do not disclose or suggest that the amount of secretome is determined based on the amount of secreting cells that produced the secretome.
Response to Argument: This is not found persuasive because the limitation of the amount of secretome is interpreted as the amount of secreting cells that produced the secretome, the protein content of the secretome, the RNA content of the secretome, the exosome amount of the secretome, or the number of particles in the secretome based on Applicant’s specification at para. 00197. Barile, Li, and Gartz each teach a specific amount of exosomes as set forth in the revised anticipation rejections and new rejection set forth above.
Applicant Argues: On page 11, Applicant asserts that Barile, Li, and Gartz are not concerned with the reliability of an assay for determining the activity of a secretome in general or of a small molecule by administering a secretome to cells. Applicant asserts that those skilled in the art would not expect that the reliability of assays for measuring secretome activity can be improved by changing the type of target cell and determining the amount of secretome based on the amount of secretory cells that produced the secretome and there is no motivation to adopt the newly claimed limitations.
Response to Argument: This is not found persuasive because each of Barile, Li, and Gartz teach treating target cells with a specific amount of exosomes to determine their effect on apoptosis. Barile teaches in Figure 2 and 7 the reproducibility of the effect of a specific amount of exosomes on inhibiting small molecule-induced cardiomyocyte death. Li teaches in Figure 2 and 5 the reproducibility of the effect of a specific amount of exosomes on inhibiting viral-induced apoptosis. Gartz teaches in Figure 4, 5, 7, and 8 the reproducibility of the effect of a specific amount of exosomes on inhibiting small molecule-induced apoptosis. Further, claims 1 and 17 are anticipated by Barile and claim 4 is anticipated by Gartz and therefore no motivation or reasonable expectation of success is stated.
Conclusion
No claims 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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/Z.M.B./Examiner, Art Unit 1632
/MARCIA S NOBLE/Primary Examiner, Art Unit 1632