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 Claims
Currently, claims 92, 95, 101, 104, 105, 107, 108, 110, 113, and 155-159 are pending in the instant application. All the amendments and arguments have been thoroughly reviewed but are deemed insufficient to place this application in condition for allowance. The following rejections are either newly applied, as necessitated by amendment, or are reiterated. They constitute the complete set being presently applied to the instant Application. Response to Applicant's arguments follow. This action is FINAL.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Any rejection not reiterated is hereby withdrawn in view of the amendments to the claims.
Claim Rejections - 35 USC § 103
Claims 92, 95, 97, 104, 105, and 110, are rejected under 35 U.S.C. 103 as being unpatentable over Hamzaoui (Hamzaoui et al; J Asthma. 2013 Oct; vol 50, pages 803-809; cited in the IDS dated 10/4/23) in view of Coyle (US 20100260770; cited in the IDS dated 10/4/23).
Hamzaoui teaches assessing the levels of sST2 and IL-33 in subjects with moderate as well as severe asthma (see page 2). Hamzaoui teaches that sST2 and IL-33 levels in induced sputum (IS) samples and serum were significantly higher in asthmatic children compared with healthy controls (see page 3, col 2) and that values of sST2 and IL-33 observed in IS were found to correlate with disease activity. Hamzaoui teaches that elevated IL-33 mRNA expression in IS was correlated with TNF-α mRNA levels and reflected the inflammatory process observed in the lung of young asthmatics (abstract).
Hamzaoui does not teach administering an IL-33 axis binding antagonist to a patient with levels of sST2 determined to be at or above a reference level, or assessing a treatment response of a patient treated with an IL-33 axis binding antagonist by determining the level of sST2 in a sample from the patient at a time point during the treatment. Coyle teaches that IL-33 activation induces various inflammatory mediators (para 0006, Fig. 2). Coyle teaches that expression of IL-33 in human asthmatic lung biopsies was increased (para 0027, Fig. 23) and that IL-33 specific binding polypeptides can be used to treat inflammatory disorders such as chronic inflammatory disorders including, among others, asthma, (para 0029, abstract). Therefore, it would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the invention to have administered asthma treatment as taught by Coyle to the patients taught by Hamzaoui for the obvious benefit of treating the patients for asthma, in view of the teachings of Hamzaoui and Coyle.
Claims 92, 95, 97, 104, 105 and 110 are rejected under 35 U.S.C. 103 as being unpatentable over Levy (US 20130157290) in view of Coyle.
Levy teaches a method comprising determining level of sST2 level, including protein level (para 0045) in a biological sample from a subject and comparing it to a control level (para 0008-0011). Levy teaches the biological sample includes whole blood, plasma, or serum (para 0051). Levy teaches that sST2 levels that are higher than that of a normal control is indicative of poor prognosis. Levy teaches that the method can also monitor the efficacy of treatment of a disease (para 0020), including asthma. Levy teaches the treatment includes administering an sST2 antagonist (para 0022). Levy does not teach administering an IL33 antibody for treatment, or assessing a treatment response of a patient treated with an IL-33 axis binding antagonist by determining the level of sST2 in a sample from the patient at a time point during the treatment. Coyle teaches that IL-33 activation induces various inflammatory mediators (para 0006, Fig. 2). Coyle teaches that expression of IL-33 in human asthmatic lung biopsies was increased (para 0027, Fig. 23) and that IL-33 specific binding polypeptides can be used to treat inflammatory disorders such as chronic inflammatory disorders including, among others, asthma, (para 0029, abstract). Therefore, it would have been prima facie obvious to one of ordinary skill in the art prior to the effective filing date of the invention to have administered asthma treatment as taught by Coyle to the patients taught by Levy for the obvious benefit of treating the patients for asthma, in view of the teachings of Levy and Coyle.
Claim 101 is rejected under 35 U.S.C. 103 as being unpatentable over Hamzaoui in view of Coyle as applied to claims 92, 95, 97, 104, 105, and 110 above, and further in view of Matsumoto (Allerg Int.; vol 63, pages 153-160. Epub 2014 Apr 25; cited in the IDS dated 10/4/23).
The teachings of Hamzaoui and Coyle are set forth above. Hamzaoui and Coyle do not teach further determining the level of periostin in a sample from the patient besides determining the level of sST2. Matsumoto teaches the use of periostin as a marker of pulmonary function decline and refractory Th2/eosinophilic inflammation in patients with asthma receiving long-term ICS treatment; and that serum periostin could be a companion diagnostic for targeted therapy against refractory Th2/eosinophilic inflammation (abstract, for example). Therefore, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to measure the levels of sST2 and periostin in a patient such as an asthmatic patient following the teachings of Hamzaoui and Matsumoto. The person of ordinary skill in the art would have been motivated to do so for better diagnosis and guided/targeted therapy. There would have been a reasonable expectation of success because Hamzaoui has demonstrated the significantly higher sST2 and IL-33 levels in IS and serum samples of asthmatic patients, which correlate with disease activity; and Matsumoto teaches the use of periostin as a marker of pulmonary function and inflammation in patients with asthma.
Claim 113 is rejected under 35 U.S.C. 103 as being unpatentable over Hamzaoui in view of Coyle as applied to claims 92, 95, 97, 104, 105, and 110 above, and further in view of Cairns (Pulmonary Pharmacology and Therapeutics, vol 18, pages 55-66, 2005; cited in the IDS dated 10/4/23).
The teachings of Hamzaoui and Coyle are set forth above. Hamzaoui and Coyle do not teach treatment with an IL-33 antagonist in combination with a tryptase-beta binding antagonist. Cairns teaches that a tryptase inhibitor could limit airway remodeling, a component of disease not addressed by current therapies including leukotriene antagonists; that tryptase has an acute dependence on its catalytic activity, providing a firm rationale that inhibitors directed at the enzymatic activity of tryptase will have some therapeutic benefit in asthma (page 57, 2nd column, 2nd paragraph); and that studies with the tryptase inhibitor from Axys, APC 366 (tryptase beta inhibitor) in the sheep and pig antigen models confirmed a role for mast cell tryptase beta in mediating airway hyperresponsiveness, which has advanced into human clinical trials for asthma (page 58, 2nd column, 2nd paragraph; and page 59, 1st column, 1st and 2nd paragraphs). Therefore, it would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to treat an asthma patient with an IL-33 specific binding polypeptide in combination with a tryptase beta inhibitor; and to measure the level of sST2 in a sample from said patient at a time point during the treatment following the teachings of Hamzaoui, Coyle, and Cairns. The person of ordinary skill in the art would have been motivated to do so in order to evaluate or assess the effectiveness of the treatment and to make better determination for the future therapy; and reasonably would have expected success because Hamzaoui has demonstrated that the significantly higher sST2 and IL-33 levels in IS and serum samples of asthmatic patients correlate with disease activity.
Response to Arguments
The response traverses the rejections and asserts that the claims have been amended to recite “and likely to respond to treatment”. This argument has been thoroughly reviewed but was not found persuasive because this recitation is an intended use limitation and does not distinguish the claims from the prior art because this recitation does not distinguish the active steps required by the claims from that which is recited in the prior art. The rejections are maintained.
Conclusion
Claims 155-159 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to examiner Jehanne Sitton whose telephone number is (571) 272-0752. The examiner is a hoteling examiner and can normally be reached Mondays-Fridays from 8:00 AM to 2:00 PM Eastern Time Zone.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner's supervisor, Winston Shen, can be reached on (571) 272-3157. The fax phone number for organization where this application or proceeding is assigned is (571) 273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/JEHANNE S SITTON/Primary Examiner, Art Unit 1682
Prosecution Insights