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 .
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.
Response to Amendment
The amendment filed February 26, 2026 has been entered. Claims 1, 5-8, 11, and 13 have been amended and claims 16-28 have been added. Applicant’s amendments to the claims have overcome the claim objections, 112a rejections, 112b rejections and 102 rejections previously set forth in the Non-Final Office Action mailed November 26, 2025. As such, these rejections and objections are hereby withdrawn.
Applicant’s arguments filed November 26, 2025 were fully considered but they were not persuasive. Modified/New rejections necessitated by Applicant’s amendment are addressed below.
Claims 1-18 are pending in this application.
Priority
This application is a continuation of and claims priority to PCT International Patent Application No. PCT/US2022/011998 filed January 11, 2022, which is a nonprovisional of and claims priority to U.S. Provisional Patent Application Serial No. 63/136,160 filed January 11, 2021.
Modified/New Claim Rejections - 35 USC § 103
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.
Claims 1-4, 6-7, 9-10, 12-18 are rejected under 35 U.S.C. 103 as being unpatentable over Cho (J. Allergy Clin. Immunol., 2019, IDS filed September 12, 2023) in view of Smith (JAMA, 2015, IDS filed September 12, 2023), Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023) as evidenced by Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892).
Regarding claims 1-4, 6-7, 9-10, 12-18: Cho (J. Allergy Clin. Immunol., 2019) teaches the administration of soy isoflavones reduce asthma exacerbation (worsening symptoms) (i.e. responsiveness determined as recited by instant claim 13) in asthmatic patients with high PAI-1-producing genotypes, such as the 4G4G/4G5G genotype (abstract). Cho (J. Allergy Clin. Immunol., 2019) teaches soy isoflavones reduce plasma levels of PAI-1 (pg. 114, col. 2, para. 2). Cho (J. Allergy Clin. Immunol., 2019) teaches there is a correlation between asthma development and 4G5G polymorphism (pg. 110, col. 2, para. 3). Cho (J. Allergy Clin. Immunol., 2019) teaches blocking PAI-1 with a specific inhibitor or small interfering RNA reduces airway inflammation, tissue remodeling, and airway hyperresponsiveness (pg. 110, col. 1, para. 2, i.e. improving airway hyperreactivity). Cho (J. Allergy Clin. Immunol., 2019) teaches the method comprises administration of a soy isoflavone supplement twice daily for 6 months and includes ages 12 years or older (i.e. pediatric patients) (pg. 110, col. 2, para. 4, study design, pg. 111, table 1). According to Smith, which is the study described in Cho (J. Allergy Clin. Immunol., 2019), the supplement comprised 49 mg of solely soy isoflavones genistein, daidzein, and glycitein and was administered orally (pg. 3, last para). According to Emma, adults can range in weight from 54-91 kg (pg. 3, para. 5). This equates a dose range of approximately 0.91 mg/kg to 0.54 mg/kg. Emma discloses infants reach 12-14 kg by age two (pg. 2, paras. 6-7). This equates a dose range of approximately 4.08 mg/kg to 3.5 mg/kg. Thus this this dosage falls within the claimed dose ranges. The method includes PAI-1 genotyping for the 5G and 4G alleles (pg. 112, (cols. 1-2, bridging para.). Cho (J. Allergy Clin. Immunol., 2019) teaches the soy isoflavones comprise genistein (pg. 114, col. 2, para. 2). Cho (J. Allergy Clin. Immunol., 2019) teaches soy isoflavone treatment can reduce asthma exacerbations resulting from viral infections (pg. 115, col. 2, para. 1). Cho (J. Allergy Clin. Immunol., 2019) teaches the 4G4G/4G5G genotype is associated with an increased risk of eczema (pg. 115, col. 2, para. 2).
Cho (J. Allergy Clin. Immunol., 2019) does not explicitly teach wherein the method results in the prevention of asthma development in pediatric patients.
However, Cho (J. Allergy Clin. Immunol., 2001) teaches PA11 gene variations correlate with increased PAI-1 levels and that the 4G allele of the PAI1 gene may be associated with the development of asthma in children (abstract, pg. 213, col. 1, para. 3). Cho (J. Allergy Clin. Immunol., 2001) teaches increased synthesis of PAI-1 may predispose the development of asthma by contributing to airway remodeling associated with asthma (pg. 213, col. 2, para. 2). Cho (J. Allergy Clin. Immunol., 2001) suggests inhibitors of PAI-1 may inhibit the development of asthma (i.e. prevent) or reduce the chronic airway remodeling that occurs in the disease.
Taken together, it would have been prima facie obvious to apply the method of Cho (J. Allergy Clin. Immunol., 2019) to prevent the development of asthma in pediatric patients as suggested by Cho (J. Allergy Clin. Immunol., 2001). A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success in that Cho (J. Allergy Clin. Immunol., 2001) suggests increased PAI-1 synthesis predisposes the development of asthma, and Cho (J. Allergy Clin. Immunol., 2019) establishes that soy isoflavones (within soy) are capable of reducing asthmatic exacerbation and PAI-1 plasma levels in asthmatic patients. A person of ordinary skill would recognize the preventative potential in administering soy isoflavones to decrease plasma PAI-1 levels, thereby reducing the risk or preventing the development of asthma in patients with these genotypes.
Claim 6 is rejected under 35 U.S.C. 103 as being unpatentable over Cho (J. Allergy Clin. Immunol., 2019, IDS filed September 12, 2023), Smith (JAMA, 2015, IDS filed September 12, 2023), Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023), and Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892) as applied to claims 1-4, 7, 9-10, 12-18 above, in view of Cho (PLoS ONE, 2016, IDS filed September 12, 2023).
Regarding claim 6: As discussed above, the prior art renders obvious the method of claim 1. Cho (J. Allergy Clin. Immunol., 2019) teaches the administration of soy isoflavones reduce asthma exacerbation (worsening symptoms) (i.e. responsiveness determined as recited by instant claim 13) in asthmatic patients with high PAI-1-producing genotypes, such as the 4G4G/4G5G genotype (abstract). Cho (J. Allergy Clin. Immunol., 2019) teaches soy isoflavones reduce plasma levels of PAI-1 (pg. 114, col. 2, para. 2). Cho (J. Allergy Clin. Immunol., 2019) teaches soy isoflavone treatment can reduce asthma exacerbations resulting from viral infections (pg. 115, col. 2, para. 1). Cho (J. Allergy Clin. Immunol., 2019) teaches the method comprises administration of a soy isoflavone supplement twice daily for 6 months and includes ages 12 years or older (i.e. pediatric patients) (pg. 110, col. 2, para. 4, study design, pg. 111, table 1). Cho (J. Allergy Clin. Immunol., 2001) teaches PA11 gene variations correlate with increased PAI-1 levels and that the 4G allele of the PAI1 gene may be associated with the development of asthma in children (abstract, pg. 213, col. 1, para. 3).
The prior art relied upon does not teach wherein the method can be applied to a pediatric patient that is up to 24 months of age (i.e. 2 years old).
However, Cho (PLoS ONE, 2016) teaches plasminogen activator inhibitor-1 (PAl-1) is induced in airways by virus and may mediate asthmatic airway remodeling and a method of evaluating genetic variants and early life lower respiratory infections jointly affect asthma risk (abstract). Cho (PLoS ONE, 2016) teaches PAl-1 genetic variants that increase PAI-1 production, together with early life lower respiratory infection, was associated with asthma diagnosis, asthma exacerbations, and asthma severity (pg. 11, last para.). Cho (PLoS ONE, 2016) suggests PAI-1 variants may serve as a biomarker of risk, providing impetus for clinical trials in the primary prevention of asthma, and interventions affecting airway responses at time of early life in these at risk individuals will decrease the chances of developing asthma (pg. 11, last para.). Cho (PLoS ONE, 2016) teaches that viruses resulting in symptomatic illnesses in the first year of life (i.e. infant), including RSV, increase risk of asthma by age 7 (pg. 11, para. 2). Cho (PLoS ONE, 2016) suggests increased production of airway PAI-1 as a result of viral insult may affect lung development in infants an cause structural airway changes that lead to lower lung function in subjects with asthma (pg. 11, para. 1).
Taken together it would have been prima facie obvious to apply the method rendered obvious over Cho (J. Allergy Clin. Immunol., 2019) and Cho (J. Allergy Clin. Immunol., 2019) to the prevention of asthma development in infants as suggested by Cho (PLoS ONE, 2016). A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as infants with RSV are a known subject population at risk of developing asthma, and the art establishes RSV in the first year of life increases the risk of said patient in acquiring asthma by way of increased PAI-1 production, and as discussed previously, administration of soy isoflavones is a viable option to reduce plasma PAI-1, thereby reducing the risk or preventing the development of asthma.
Claims 5 and 11 are rejected under 35 U.S.C. 103 as being unpatentable over Cho (J. Allergy Clin. Immunol., 2019, IDS filed September 12, 2023), Smith (JAMA, 2015, IDS filed September 12, 2023), Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023), Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892)and Cho (PLoS ONE, 2016, IDS filed September 12, 2023) as applied to claims 1-4, 6-7, 9-10, 12-18 above, in view of Lopes (Bioscience Reports, 2020, cited in previous action).
Regarding claims 5 and 11: As discussed above, the prior art renders obvious the method of claim 1. Cho (J. Allergy Clin. Immunol., 2019) teaches soy isoflavone treatment can reduce asthma exacerbations resulting from viral infections (pg. 115, col. 2, para. 1). Cho (J. Allergy Clin. Immunol., 2019) teaches PAI-1 production is further increased by viral infection or other asthma triggers in patients who already have high PAI-1 production in the airways by virtue of their genetic mutation and soy isoflavones can alleviate this tipping point by reducing PAI-1 production in those with high baseline levels (pg. 116, col. 1, para. 2). Cho (PLoS ONE, 2016) teaches that viruses resulting in symptomatic illnesses in the first year of life (i.e. infant), including RSV, increase risk of asthma by age 7 (pg. 11, para. 2). Cho (PLoS ONE, 2016) suggests increased production of airway PAI-1 as a result of viral insult may affect lung development in infants an cause structural airway changes that lead to lower lung function in subjects with asthma (pg. 11, para. 1).
They do not teach application of the method during winter and fall.
However, Lopes teaches it is known in the art that exposure to RSV serves as a primer for the development of asthma or exacerbating asthma (pg. 2, para. 1). Lopes teaches that RSV is more prevalent in the rainy season (pg. 1, abstract). Lopes teaches that in countries of temperate zones, upper respiratory tract infections are more frequent in autumn and spring, rising during winter, following weather changes (pg. 2, para. 2).
Taken together, it would have been prima facie obvious to a person of ordinary skill to apply the method of Cho (J. Allergy Clin. Immunol., 2019), Cho (J. Allergy Clin. Immunol., 2019), and Cho (PLoS ONE, 2016) to patients at risk of developing asthma during a viral season, such as fall or winter as taught by Lopes. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success in order to preempt the increased risk of RSV infection associated with viral seasons that is known to increase the risk of asthma development; the administration would thus decrease the PAI-1 levels and prevent the development of asthma in the patient upon infection with RSV.
Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Cho (J. Allergy Clin. Immunol., 2019, IDS filed September 12, 2023), Smith (JAMA, 2015, IDS filed September 12, 2023), Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023), and Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892) as applied to claims 1-4, 7, 9-10, 12-18 above, in view of Thomsen (European Clinical Respiratory Journal, 2015, cited in previous action).
Regarding claim 8: As discussed above the prior art render obvious the method of claim 7.
They do not teach wherein the patient has a high risk of developing asthma due to uni- or biparental asthma.
However, Thomsen teaches that children of asthmatic parents are at increased risk of asthma (abstract).
Taken together, it would have been prima facie obvious to a person of ordinary skill in the art to apply the method to children with parents who have asthma. A person of ordinary skill would have had the motivation to do so with a reasonable expectation of success as this subject population is known, are in need in treatment/prevention, and have a higher risk of developing asthma, in order to effectively reduce the risk or prevent the development of asthma in the child.
Modified/New Nonstatutory 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, 4, 7, 9, 12-13, and 15-18 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the claims of copending Application No. 18/814,657 (US 2024/0415802, cited in previous action) in view of Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023) as evidenced by Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892). Although the claims at issue are not identical, they are not patentably distinct from each other because:
Regarding claims 1-2, 4, 7, 9, 12-13, and 15-18: The copending claims teach a method for decreasing plasminogen activator inhibitor I (PAI-1) levels in a patient having a disease characterized by increased plasminogen activator inhibitor 1 (PAI-1) comprising administering genistein (i.e. a soy isoflavone according to instant claim 2)(claim 1). The copending claims teach wherein the disease is asthma (claim 6). The copending claims teach performing genotype analysis of the PAI-1 gene in the patient (claim 2). The copending claims teach wherein the composition is administered if the patient has a 4G allele of the PAI-1 gene (claim 3). The copending claims teach wherein the patient has 4G/5G polymorphism (claim 7). The copending claims teach the amount is administered from 500mg/day to about 1500mg/day (i.e. per day, claim 5). The copending claims teach wherein the amount of genistein is at least 32 mg (claim 14). According to Emma, adults can range in weight from 54-91 kg (pg. 3, para. 5). This equates a dose range of approximately 0.59 mg/kg to 0.35 mg/kg. Emma discloses infants reach 12-14 kg by age two (pg. 2, paras. 6-7). This equates a dose range of approximately 2.67 mg/kg to 2.28 mg/kg. Thus this this dosage falls within the claimed dose ranges.
The copending claims do not explicitly teach wherein the method results in the prevention of asthma development in pediatric patients.
However, Cho (J. Allergy Clin. Immunol., 2001) teaches PA11 gene variations correlate with increased PAI-1 levels and that the 4G allele of the PAI1 gene may be associated with the development of asthma in children (abstract, pg. 213, col. 1, para. 3). Cho (J. Allergy Clin. Immunol., 2001) teaches increased synthesis of PAI-1 may predispose the development of asthma by contributing to airway remodeling associated with asthma (pg. 213, col. 2, para. 2). Cho (J. Allergy Clin. Immunol., 2001) suggests inhibitors of PAI-1 may inhibit the development of asthma (i.e. prevent) or reduce the chronic airway remodeling that occurs in the disease (pg. 213, col. 2, para. 2).
Taken together, it would have been prima facie obvious to a person of ordinary skill in the art to apply the method of the copending claims to the prevention of asthma development in children. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as Cho (J. Allergy Clin. Immunol., 2001) suggests increased PAI-1 synthesis predisposes the development of asthma, and copending claims teach that genistein (a soy isoflavone) is capable of reducing PAI-1 plasma levels in asthmatic patients. A person of ordinary skill would recognize the preventative potential in administering soy isoflavones to decrease plasma PAI-1 levels, thereby reducing the risk or preventing the development of asthma in patients with these genotypes.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 3, 10, and 14 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the claims of copending Application No. 18/814,657 (US 2024/0415802, cited in previous action), Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023) and Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892) as applied to claims 1-2, 4, 7, 9, 12-13, and 15-18 above in view of Cho (J. Allergy Clin. Immunol., 2019, IDS filed September 12, 2023) and Smith (JAMA, 2015, IDS filed September 12, 2023). Although the claims at issue are not identical, they are not patentably distinct from each other because:
Regarding claims 3, 10, and 14: As discussed above, the copending claims and prior art renders obvious the method of claims 1, 7, and 13.
They do not explicitly teach oral administration of the soy isoflavone.
However, Cho (J. Allergy Clin. Immunol., 2019) teaches the administration of soy isoflavones reduce asthma exacerbation (worsening symptoms) (i.e. responsiveness determined as recited by instant claim 13) in asthmatic patients with high PAI-1-producing genotypes, such as the 4G4G/4G5G genotype (abstract). According to Smith, which is the study described in Cho (J. Allergy Clin. Immunol., 2019), the supplement comprised solely soy isoflavones genistein, daidzein, and glycitein and was administered orally (pg. 2034, col. 1, last para).
Taken together, it would have been prima facie obvious to a person of ordinary skill in the art to modify the method of the copending by administering the composition orally. A person of ordinary skill in the art would have the motivation to do so with a reasonable expectation of success as administering compositions comprising soy isoflavones, such as genistein, orally is a routine practice in the art of treating asthmatic conditions.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim 6 is provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the claims of copending Application No. 18/814,657 (US 2024/0415802, cited in previous action), Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023), and Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892) as applied to claims 1-2, 4, 7, 9, 12-13, and 15-18 above in view of Cho (PLoS ONE, 2016, IDS filed September 12, 2023). Although the claims at issue are not identical, they are not patentably distinct from each other because:
Regarding claims 6: As discussed above, the copending claims and prior art renders obvious the method of claim 1, wherein a pediatric patient is to be treated.
They do not teach wherein the pediatric patient that is up to 24 months of age (i.e. 2 years old).
However, Cho (PLoS ONE, 2016) teaches plasminogen activator inhibitor-1 (PAl-1) is induced in airways by virus and may mediate asthmatic airway remodeling and a method of evaluating genetic variants and early life lower respiratory infections jointly affect asthma risk (abstract). Cho (PLoS ONE, 2016) teaches PAl-1 genetic variants that increase PAI-1 production, together with early life lower respiratory infection, was associated with asthma diagnosis, asthma exacerbations, and asthma severity (pg. 11, last para.). Cho (PLoS ONE, 2016) suggests PAI-1 variants may serve as a biomarker of risk, providing impetus for clinical trials in the primary prevention of asthma, and interventions affecting airway responses at time of early life in these at risk individuals will decrease the chances of developing asthma (pg. 11, last para.). Cho (PLoS ONE, 2016) teaches that viruses resulting in symptomatic illnesses in the first year of life (i.e. infant), including RSV, increase risk of asthma by age 7 (pg. 11, para. 2). Cho (PLoS ONE, 2016) suggests increased production of airway PAI-1 as a result of viral insult may affect lung development in infants an cause structural airway changes that lead to lower lung function in subjects with asthma (pg. 11, para. 1).
Taken together it would have been prima facie obvious to apply the method to the prevention of asthma development in infants in the first year of life as suggested by Cho (PLoS ONE, 2016). A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success as infants with RSV are a known subject population at risk of developing asthma, and the art establishes RSV in the first year of life increases the risk of said patient in acquiring asthma by way of increased PAI-1 production, and as discussed previously, administration of soy isoflavones is a viable option to reduce plasma PAI-1, thereby reducing the risk or preventing the development of asthma.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 5 and 11 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the claims of copending Application No. 18/814,657 (US 2024/0415802, cited in previous action), Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023), Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892), and Cho (PLoS ONE, 2016, IDS filed September 12, 2023) as applied to claims 1-2, 4, 6-7, 9, 12-13, and 15-18 above in view of Lopes (Bioscience Reports, cited in previous action). Although the claims at issue are not identical, they are not patentably distinct from each other because:
Regarding claims 5 and 11: As discussed above, the copending claims and prior art renders obvious the method of claims 1 and 7.
They do not teach application of the method during a viral season.
Lopes teaches it is known in the art that exposure to RSV serves as a primer for the development of asthma or exacerbating asthma (pg. 2, para. 1). Lopes teaches that RSV is more prevalent in the rainy season (pg. 1, abstract). Lopes teaches that in countries of temperate zones, upper respiratory tract infections are more frequent in autumn and spring, rising during winter, following weather changes (pg. 2, para. 2).
Taken together, it would have been prima facie obvious to a person of ordinary skill to apply the method to patients at risk of developing asthma during a viral season, such as fall or winter as taught by Lopes. A person of ordinary skill in the art would have had the motivation to do so with a reasonable expectation of success in order to preempt the increased risk of RSV infection associated with viral seasons that is known to increase the risk of asthma development; the administration would thus decrease the PAI-1 levels and prevent the development of asthma in the patient upon infection with RSV.
Claim 8 is provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the claims of copending Application No. 18/814,657 (US 2024/0415802, cited in previous action) and Cho (J. Allergy Clin. Immunol., 2001, IDS filed September 12, 2023) and Emma (Snuggy Mom, average weight chart, web, 2026, cited on PTO-892) as applied to claims 1-2, 4, 7, 9, 12-13, and 15-18 above in view of Thomsen (European Clinical Respiratory Journal, 2015, cited in previous action). Although the claims at issue are not identical, they are not patentably distinct from each other because:
Regarding claim 8: As discussed above the copending claims and prior art render obvious the method of claim 7.
They do not teach wherein the patient has a high risk of developing asthma due to uni- or biparental asthma.
However, Thomsen teaches that children of asthmatic parents are at increased risk of asthma (abstract).
Taken together, it would have been prima facie obvious to a person of ordinary skill in the art to apply the method to children with parents who have asthma. A person of ordinary skill would have had the motivation to do so with a reasonable expectation of success as this subject population is known, are in need in treatment/prevention, and have a higher risk of developing asthma, in order to effectively reduce the risk or prevent the development of asthma in the child.
Response to Arguments
Applicant’s arguments filed February 26, 2026 with respect to the claims have been fully considered but they are not persuasive.
On page 11 of Applicant’s response, Applicant argues Applicant argues that the combination of Cho 2019 with Smith and Cho 2001 fails to teach administration to a patient not previously diagnosed with asthma and administration of at least isoflavone preventing development of asthma by at least improving airway hyperreactivity in the patient (para. 2). Cho 2001 explicitly states that asthma was defined using a previously validated questionnaire together with a physician diagnosis of asthma (para. 2). Applicant argues that Cho 2019 and Smith teach that the method did not result in improved lung function or clinical outcomes in the entire population (para. 2).
However, while the subject population examined in Cho 2001 have a diagnosis of asthma, disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments (See MPEP 2123 (II)). Cho (J. Allergy Clin. Immunol., 2001) suggests inhibitors of PAI-1 may inhibit the development of asthma (i.e. prevent) or reduce the chronic airway remodeling that occurs in the disease(pg. 213, col. 2, para. 2). Cho (J. Allergy Clin. Immunol., 2001) teaches increased synthesis of PAI-1 may predispose the development of asthma by contributing to airway remodeling associated with asthma (pg. 213, col. 2, para. 2). Cho (J. Allergy Clin. Immunol., 2019) teaches the administration of soy isoflavones reduce asthma exacerbation (worsening symptoms) (i.e. responsiveness determined as recited by instant claim 13) in asthmatic patients with high PAI-1-producing genotypes, such as the 4G4G/4G5G genotype (abstract). Cho (J. Allergy Clin. Immunol., 2019) teaches soy isoflavones reduce plasma levels of PAI-1 (pg. 114, col. 2, para. 2). Wherein the art establishes soy isoflavones can reduce PAI-1, and suggests PAI-1 inhibition is a viable pathway to inhibit the development of asthma, a person of ordinary skill in the art would have had the requisite motivation to do use the composition to prevent the development of asthma with a reasonable expectation of success as these patients are predisposed to developing asthma as a result of having the claimed genotype. Additionally, Cho (J. Allergy Clin. Immunol., 2019) teaches blocking PAI-1 with a specific inhibitor or small interfering RNA reduces airway inflammation, tissue remodeling, and airway hyperresponsiveness (pg. 110, col. 1, para. 2, i.e. improving airway hyperreactivity). Thus applying the method for this purpose, would necessarily have the effect of improving airway hyperreactivity, absent evidence to the contrary.
On page 12 of Applicant’s response, Applicant argues the population studied in Cho 2016 were latinos from age 8-21, which does not portray teaching administration to infants as claimed in claim 6 (para. 3).
However, while the subject population examined in Cho 2016 have a diagnosis of asthma and were between the ages of 8-21, disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments (See MPEP 2123 (II)). Cho (PLoS ONE, 2016) determined that RSV infection early in life contributed to the development of asthma in these subjects. Cho (PLoS ONE, 2016) teaches that viruses resulting in symptomatic illnesses in the first year of life (i.e. infant), including RSV, increase risk of asthma by age 7 (pg. 11, para. 2). Cho (PLoS ONE, 2016) suggests increased production of airway PAI-1 as a result of viral insult may affect lung development in infants an cause structural airway changes that lead to lower lung function in subjects with asthma (pg. 11, para. 1). Thus, wherein the art establishes soy isoflavones can reduce PAI-1, suggests PAI-1 inhibition is a viable pathway to inhibit the development of asthma, and viral insult in infants results in an increase in PAI-1, a person of ordinary skill in the art would have had the requisite motivation to target this subject population early in life so with a reasonable expectation of success to prevent the development of asthma.
On page 13 of Applicant’s response, Applicant argues Lopes does not cure the deficiencies 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 § 103 and double patenting rejections are maintained for reason of record and foregoing discussion.
Conclusion
No claims are allowed in this action.
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.
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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