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 Application
Claims 1-2 and 4-18 are pending.
Receipt and consideration of Applicants' amended claim set and remarks/arguments filed on 11/12/2025 are acknowledged. Claims 1, 4, and 8-16 are amended. Claims under consideration in the instant office action are claims 1-2 and 4-18.
Applicants' arguments, filed 11/12/2025, have been fully considered but they are not deemed to be persuasive. Rejections and/or objections not reiterated from previous office actions are hereby withdrawn. The following rejections and/or objections are either reiterated or newly applied. They constitute the complete set presently being applied to the instant application.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1-2 and 4-18 are rejected under 35 U.S.C. 103 as being unpatentable over Oda et al. (Chemokine profiles of interstitial pneumonia in patients with dermatomyositis: a case control study, Scientific Reports, 2017, 7(1635), pp. 1-10) in view of Miyazaki et al. (Higher serum CCL17 may be a promising predictor of acute exacerbations in chronic hypersensitivity pneumonitis, Respiratory Research, 2013, 14:57, pp. 1-11) and Flaherty et al. (Prognostic Implications of Physiologic and Radiographic Changes in Idiopathic Interstitial Pneumonia, American Journal of Respiratory and Critical Care Medicine, 2003, 168(5), pp. 543-548).
Oda et al. is drawn towards chemokine profiles of interstitial pneumonia (see abstract). Oda et al. teaches “Richards et al. reported that serum CXCL9 and CXCL10 levels were higher in patients with IP with anti-Jo-1 antibody than in those with idiopathic pulmonary fibrosis. Gono et al. reported that the serum CXCL10 level related to the disease activity of PM/DM-IP. In our study, serum CXCL10 and CXCL11 levels at 2 weeks after treatment initiation were significantly higher in the death group and the change ratio of serum CXCL10 and CXCL11 levels were higher in the death group. This suggests that serum CXCL10 and CXCL11 levels could be possible markers for prognosis during the treatment course.” (pg. 8, second paragraph).
Oda et al. does not teach wherein the measurement result of the biomarker indicates a high risk of a decrease in the respiratory function of the patient when the measured value of CCL17 is higher than a corresponding predetermined threshold. Oda et al. does not teach wherein the risk of a decrease in the respiratory function is a risk of a decrease in vital capacity 6 months after collection of the biological sample.
Miyazaki et al. is drawn towards serum CCL17 levels as a predictor acute exacerbations (“AE”) in chronic hypersensitivity pneumonitis (see abstract). Miyazaki et al. teaches that “AE was significantly more frequent in the higher-CCL17 group than in the lower CCL17 group (Figure 1C, log-rank test, p = 0.0006).” (pp. 4-5, bridging paragraph). Miyazaki et al. teaches that “Increased concentrations of CCL17 are initially found in the BAL fluid of IPF patients, which suggests that CCL17 is involved in the pathogenesis of IPF via the recruitment of Th2 cells. Regarding chronic HP, we showed that elevated levels of CCL17 may contribute to the development of UIP histological patterns. Increased serum CCL17 levels at baseline were predictive of AE in chronic HP in the present study.” (pp. 7-8, bridging paragraph). As a consequence it would follow that a lower serum CCL17 level would indicate a lower incidence of acute exacerbations regarding claim 13.
Flaherty et al. is drawn towards the use of physiologic and radiographic parameters to predict survival for patients with interstitial pneumonia (see abstract). Flaherty et al. teaches “Changes in PFT and HRCT scores were determined by estimating percent change for absolute value of HRCT and PFT measurements over a 6-month period. Measurements over a 6-month period related to the biopsy time were used to fit a linear regression for each patient. The fitted line from the linear regression was then used to estimate a6-month measurement, which, together with the baseline measurement, allowed the calculation of percent change…The levels of more than 10% increase, be-tween 10% decrease and 10% increase, and more than 10% decrease were used to study percent changes of the PFT and HRCT scores.” (pg. 543, right column, paragraphs 4-5). Flaherty et al. teaches “In a multivariate Cox proportional hazards model controlling for histopathologic diagnosis, gender, smoking history, baseline forced vital capacity, and 6-month change in forced vital capacity, a decrease in forced vital capacity remained an independent risk factor for mortality (decrease > 10%; hazard ratio 2.47; 95% confidence interval 1.29, 4.73; p = 0.006).” (see abstract). Flaherty et al. teaches treatment regimens including prednisone alone, prednisone with azathioprine or cyclophosphamide, zileuton, and azathioprine alone (see Table 1).
It would have been obvious to one of ordinary skill in the art to obtain information on a risk of a decrease in a respiratory function of a patient with interstitial pneumonia wherein the measurement result of the biomarker indicates a high risk of a decrease in the respiratory function of the patient when the measured value of CCL17 is higher than a corresponding predetermined threshold, as suggested by Miyazaki et al., and produce the instant invention.
One of ordinary skill in the art would have been motivated to do so since Miyazaki et al. teaches that elevated levels of CCL17 may contribute to the development of usual interstitial pneumonia histological patterns and acute exacerbations, with a reasonable expectation of success absent evidence of criticality of the particular steps.
It would have been obvious to one of ordinary skill in the art to obtain information on a risk of a decrease in a respiratory function of a patient with interstitial pneumonia wherein the risk of a decrease in the respiratory function is a risk of a decrease in vital capacity 6 months after collection of the biological sample, as suggested by Flaherty et al., and produce the instant invention.
One of ordinary skill in the art would have been motivated to do so since such sampling provides “additional prognostic information to baseline features for patients with idiopathic interstitial pneumonia” (see abstract) as taught by Flaherty et al., with a reasonable expectation of success absent evidence of criticality of the particular steps.
With regards to the limitation claimed in instant claim 4, which claims “wherein the risk of a decrease in vital capacity is a risk that the vital capacity 6 months after the collection of the biological sample is decreased by 5% or more from the vital capacity”, Flaherty et al. does not specifically teach the exact percentage decrease claimed in instant claim 4. However, Flaherty et al. does teach a percentage decrease of at least 10% (see abstract), and it would be within the skill of an ordinary artisan to be able to modify the parameter threshold in order to obtain the desired modelling of the risk factor. It is noted that "[W]here the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation." In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955).
Response to Arguments
Applicant argues that “Oda, when directly addressing the prognostic value of chemokines in their own study, presents findings for CCL17 that are directly contradictory to the presently claimed method and finds no significant association of CXCL9 with prognosis. The teachings of Oda would, in fact, actively discourage one of ordinary skill in the art from using higher CCL17 as a predictor of respiratory function decline.” The Examiner respectfully disagrees since although CCL17 exhibited higher levels of serum CCL117 levels in the survival group than the death group, such a higher level may be attributed to the patient population of interstitial pneumonia patients that have dermatomyositis given the teachings of Miyazaki et al. Miyazaki et al. teaches that elevated levels of CCL17 may contribute to the development of usual interstitial pneumonia histological patterns and acute exacerbations (pp. 7-8, bridging paragraph). One of ordinary skill in the art would thus have been motivated to use serum CCL17 levels to indicate a high risk of a decrease in the respiratory function of the patient as taught by Miyazaki et al.
Conclusion
Claims 1-2 and 4-18 are rejected.
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 ANDREW P LEE whose telephone number is (571)270-1016. The examiner can normally be reached Monday-Friday 9am-5pm.
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/ANDREW P LEE/Examiner, Art Unit 1691
/RENEE CLAYTOR/Supervisory Patent Examiner, Art Unit 1691