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 .
Application Status
The Amendment filed on 03/03/2026 in response to the Non-Final Rejection of 9/11/2025 is acknowledged and has been entered. Claims 1-2, 5-6, 8-9, 11-14, 17-18, 20, 24 and 26 are currently pending and under consideration.
Rejections Withdrawn in view of Applicants Amendment
The rejection of Claim(s) 1-4, 8, 14-16, 20 and 22 under 35 U.S.C. 102a(1) as being anticipated by Umetsu et al. (US2015/0297593A1, 2015-10-22) is withdrawn in view of Applicants amendments.
The rejection of Claim(s) 13 and 26 under 35 U.S.C. 103 as being unpatentable over Umetsu et al. (US2015/0297593A1, 2015-10-22), as applied to claims 1-4, 8, 14-16, 20 and 22 above, in view of Abrams et al. (CMAJ 2020 May 19; 192:E551) is withdrawn in view of Applicants amendments.
The rejection of Claim(s) 5-6, 9, 11-12, 17-18 and 24 under 35 U.S.C. 103 as being unpatentable over Umetsu et al. (US2015/0297593A1, 2015-10-22) in view of Abrams et al. (CMAJ 2020 May 19; 192:E551), as applied to claims 1-4, 8, 13-16, 20, 22 and 26 above, in further view of Farag et al. (DOI 10.26434/chemrxiv.12003930.v4, 2020-05-14) is withdrawn in view of Applicants amendments.
New Rejections Necessitated by Amendment
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)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claim(s) 1, 13-14 and 26 is/are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Fuchs, Ephraim (US20230172941A1, 2023-06-08, cited in previous action as pertinent art, but not relied upon).
Fuchs teach a method of treating SARS coronavirus infection in a subject in need thereof comprising administering to the subject an effective amount of a tyrosine kinase inhibitor to the subject thereby treating the SARS infection (claim 3 of Fuchs). With regards to the SARS coronavirus infection, Fuchs teach that the SARS coronavirus infection is SARS-CoV-2 (claim 4 of Fuchs). With regards to the tyrosine kinase inhibitor, Fuchs teach that the tyrosine kinase inhibitor is ibrutinib (claim 5 of Fuchs). Specifically, Fuchs teaches that the present invention is based on the hypothesis that ibrutinib, a small molecule tyrosine kinase inhibition that is approved to treat B cell malignancies, will improve the outcome of subjects exposed to or infected with SARS-CoV-2 by inhibiting virus-induced inflammation and by enhancing clearance of the virus (paragraph 0017). While the prior art does not specifically teach forming a target cell/agent complex, the claimed limitation does not appear to result in a patentable difference since both the claims and prior art administer the same agent, ibrutinib, to the same patient population, a subject having coronavirus. Applicants are reminded that the office does not have the facilities or resources to determine whether such target cell/agent complex forms. The burden is on Applicant to identify that such a complex does not form by following the teachings of the prior art.
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.
Claim(s) 2, 5-6, 17-18, 20 and 24 is/are rejected under 35 U.S.C. 103 as being unpatentable over Fuchs, Ephraim (US20230172941A1, 2023-06-08, cited in previous action as pertinent art, but not relied upon), as applied above to claims 1, 13-14 and 26, in view of Hur et al. (Experimental and Molecular Medicine 2007; 39(3), 367-375).
Fuchs teach a method of treating SARS coronavirus infection in a subject in need thereof comprising administering to the subject an effective amount of a tyrosine kinase inhibitor to the subject thereby treating the SARS infection (claim 3 of Fuchs). With regards to the SARS coronavirus infection, Fuchs teach that the SARS coronavirus infection is SARS-CoV-2 (claim 4 of Fuchs). With regards to the tyrosine kinase inhibitor, Fuchs teach that the tyrosine kinase inhibitor is ibrutinib, wherein ibrutinib is administered to the subject between 100 mg/day to 1000 mg/day (claim 5 and 8 of Fuchs). Specifically, Fuchs teaches that the present invention is based on the hypothesis that ibrutinib, a small molecule tyrosine kinase inhibition that is approved to treat B cell malignancies, will improve the outcome of subjects exposed to or infected with SARS-CoV-2 by inhibiting virus-induced inflammation and by enhancing clearance of the virus (paragraph 0017). Moreover, Fuchs teach that there is evidence that SARS from coronavirus results from inappropriate differentiation of virus-specific CD4+T cells into the type 2 (Th2) subset, leading to inadequate activation of virus-specific, CD8+ cytotoxic T cells (paragraph 0008). Lastly, Fuchs teach that ibrutinib can be combined with another biologically active agent (paragraph 0063).
Fuchs does not specifically teach that the additional agent is Gefitinib. Nor does the Fuchs teach the amounts of the kinase inhibitors or Gefitinib as claimed.
Hur et al. teach the effects of gefitinib on ovalbumin (OVA)-induced, allergic inflammation in airway epithelia of mice, wherein OVA-sensitized mice were pretreated with gefitinib at two different doses (12.5 and 50 mg/kg) and then challenged with OVA (Abstract). In particular, Hur et al. teach that gefitinib can effectively reduce allergic inflammation by decreasing OVA-induced Th2 cytokine production (IL-13 and IL-4), eosinophil recruitment, mucin production and AHR in a murine asthma model, wherein the finding suggest inhibition of the EGFR cascade may have therapeutic potential in the treatment of asthma (Page 374, 1st column, last paragraph).
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the method taught by Fuchs to include gefitinib as the additional therapeutic agent in view of the teachings of Hur et al.. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
- Hur et al. teach that gefitinib can effectively reduce allergic inflammation by decreasing OVA-induced Th2 cytokine production (IL-13 and IL-4), eosinophil recruitment, mucin production and AHR in a murine asthma model, wherein the finding suggest inhibition of the EGFR cascade may have therapeutic potential in the treatment of asthma
Moreover, It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to optimize the amounts of the agents in view of the teachings of the combination of Fuchs and Hur et al.. One of ordinary skill in the art would have been motivated to make such an optimization, with a reasonable expectation of success, because:
- Fuchs teaches treating SARS-coronavirus with ibrutinib, wherein ibrutinib is administered to the subject between 100 mg/day to 1000 mg/day; and
- Hur et al. teach the effects of gefitinib on ovalbumin (OVA)-induced, allergic inflammation in airway epithelia of mice, wherein OVA-sensitized mice were pretreated with gefitinib at two different doses (12.5 and 50 mg/kg) and then challenged with OVA.
Additionally, differences in concentration or temperature will not support the patentability of subject matter encompassed by the prior art unless there is evidence indicating such concentration or temperature is critical. "[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)
Claim(s) 2, 8-9, 20 and 24 is/are rejected under 35 U.S.C. 103 as being unpatentable over Fuchs, Ephraim (US20230172941A1, 2023-06-08, cited in previous action as pertinent art, but not relied upon), as applied above to claims 1, 13-14 and 26, in view of Umetsu et al. (US2015/0297593A1, 2015-10-22, cited in the prior office action).
Fuchs teach a method of treating SARS coronavirus infection in a subject in need thereof comprising administering to the subject an effective amount of a tyrosine kinase inhibitor to the subject thereby treating the SARS infection (claim 3 of Fuchs). With regards to the SARS coronavirus infection, Fuchs teach that the SARS coronavirus infection is SARS-CoV-2 (claim 4 of Fuchs). With regards to the tyrosine kinase inhibitor, Fuchs teach that the tyrosine kinase inhibitor is ibrutinib, wherein ibrutinib is administered to the subject between 100 mg/day to 1000 mg/day (claim 5 and 8 of Fuchs). Specifically, Fuchs teaches that the present invention is based on the hypothesis that ibrutinib, a small molecule tyrosine kinase inhibition that is approved to treat B cell malignancies, will improve the outcome of subjects exposed to or infected with SARS-CoV-2 by inhibiting virus-induced inflammation and by enhancing clearance of the virus (paragraph 0017). Moreover, Fuchs teach that there is evidence that SARS from coronavirus results from inappropriate differentiation of virus-specific CD4+T cells into the type 2 (Th2) subset, leading to inadequate activation of virus-specific, CD8+ cytotoxic T cells (paragraph 0008). Lastly, Fuchs teach that ibrutinib can be combined with another biologically active agent (paragraph 0063).
Fuchs does not specifically teach an additional agent is Imatinib. Nor does the Fuchs reach the amounts of the kinase inhibitors or imatinib as claimed.
Umetsu et al. teach a method of treating respiratory pathology, airway inflammation, airway hyperreactivity (AHR) or acute asthma in a subject comprising administering an effective amount of a c-kinase inhibitor (c-Kit), wherein the subject has a viral infection (claims 1 and 5 of the PG Pub). With regards to the viral infection, the PG Pub teaches that the viral infection is of a virus that causes asthma symptoms such as coronavirus (claims 10-11 of the PG Pub). With regards to the c-kinase inhibitors, the publication teaches that c-kinase inhibitors include, but are not limited to, Midostaurin, Imatinib, Axitinib and Sunitinib (paragraph 0296). Moreover, the publication teaches that the method includes administering a c-kinase inhibitor in combination with an additional therapeutic agent including, but not limited to, an additional anti-asthma medication (paragraph 0303). Lastly, Umetsu et al. teach that in vivo treatment with imatinib directly inhibits the proliferation, expansion and cytokine production (IL-13 and IL-5) of lung nuocytes during influenza infection (Examples 3 and 4)
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the method taught by Fuchs to include imatinib as the additional therapeutic agent in view of the teachings of Umetsu et al. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
- Umetsu et al. teach a method of treating respiratory pathology, airway inflammation, airway hyperreactivity (AHR) or acute asthma in a subject comprising administering an effective amount of imatinib, wherein the subject has a viral infection such as coronavirus.
Moreover, It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to optimize the amounts of the agents in view of the teachings of the combination of Fuchs and Umetsu et al. One of ordinary skill in the art would have been motivated to make such an optimization, with a reasonable expectation of success, because:
- Fuchs teaches treating SARS-coronavirus with ibrutinib, wherein ibrutinib is administered to the subject between 100 mg/day to 1000 mg/day; and
- Umetsu et al. teach that the dose ranges from 0.01 mg to 250 mg or alternatively, 50 nM to 1mM, wherein determination of an effective amount is well within the capability of those skilled in the art and generally, an effective amount is determined by first administering a low dose and then incrementally increasing the administered dose until the desired effect.
Additionally, differences in concentration or temperature will not support the patentability of subject matter encompassed by the prior art unless there is evidence indicating such concentration or temperature is critical. "[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)
Claim(s) 1-2, 5-6, 8-9, 11-12, 14, 17-18, 20 and 24 is/are rejected under 35 U.S.C. 103 as being unpatentable over Umetsu et al. (US2015/0297593A1, 2015-10-22, cited in the previous office action) in view of Hur et al. (Experimental and Molecular Medicine 2007; 39(3), 367-375).
Umetsu et al. teach a method of treating respiratory pathology, airway inflammation, airway hyperreactivity (AHR) or acute asthma in a subject comprising administering an effective amount of a c-kinase inhibitor (c-Kit), wherein the subject has a viral infection (claims 1 and 5 of the PG Pub). With regards to the viral infection, the PG Pub teaches that the viral infection is of a virus that causes asthma symptoms such as coronavirus (claims 10-11 of the PG Pub). With regards to the c-kinase inhibitors, the publication teaches that c-kinase inhibitors include, but are not limited to, Midostaurin, Imatinib, Axitinib and Sunitinib (paragraph 0296). Moreover, the publication teaches that the method includes administering a c-kinase inhibitor in combination with an additional therapeutic agent including, but not limited to, an additional anti-asthma medication (paragraph 0303). Lastly, Umetsu et al. teach that in vivo treatment with imatinib directly inhibits the proliferation, expansion and cytokine production (IL-13 and IL-5) of lung nuocytes during influenza infection (Examples 3 and 4)
Umetsu et al. does not specifically teach that the additional agent is Gefitinib. Nor does the combination reach the amounts of the kinase inhibitors or Gefitinib as claimed.
Hur et al. teach the effects of gefitinib on ovalbumin (OVA)-induced, allergic inflammation in airway epithelia of mice, wherein OVA-sensitized mice were pretreated with gefitinib at two different doses (12.5 and 50 mg/kg) and then challenged with OVA (Abstract). In particular, Hur et al. teach that gefitinib can effectively reduce allergic inflammation by decreasing OVA-induced Th2 cytokine production (IL-13 and IL-4), eosinophil recruitment, mucin production and AHR in a murine asthma model, wherein the finding suggest inhibition of the EGFR cascade may have therapeutic potential in the treatment of asthma (Page 374, 1st column, last paragraph).
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the method taught by Umetsu et al. to include gefitinib as the additional therapeutic agent in view of the teachings of Hur et al.. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
- Hur et al. teach that gefitinib can effectively reduce allergic inflammation by decreasing OVA-induced Th2 cytokine production (IL-13 and IL-4), eosinophil recruitment, mucin production and AHR in a murine asthma model, wherein the finding suggest inhibition of the EGFR cascade may have therapeutic potential in the treatment of asthma
Moreover, It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to optimize the amounts of the agents in view of the teachings of the combination of Umetsu et al. and Hur et al.. One of ordinary skill in the art would have been motivated to make such an optimization, with a reasonable expectation of success, because:
- Umetsu et al. teach that the dose ranges from 0.01 mg to 250 mg or alternatively, 50 nM to 1mM, wherein determination of an effective amount is well within the capability of those skilled in the art and generally, an effective amount is determined by first administering a low dose and then incrementally increasing the administered dose until the desired effect; and
- Hur et al. teach the effects of gefitinib on ovalbumin (OVA)-induced, allergic inflammation in airway epithelia of mice, wherein OVA-sensitized mice were pretreated with gefitinib at two different doses (12.5 and 50 mg/kg) and then challenged with OVA.
Additionally, differences in concentration or temperature will not support the patentability of subject matter encompassed by the prior art unless there is evidence indicating such concentration or temperature is critical. "[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)
While the prior art does not specifically teach forming a target cell/agent complex, the claimed limitation does not appear to result in a patentable difference since both the claims and prior art administer the same agent, a c-Kit kinase inhibitor or gefitinib, to the same patient population, a subject having coronavirus. Applicants are reminded that the office does not have the facilities or resources to determine whether such target cell/agent complex forms. The burden is on Applicant to identify that such a complex does not form by following the teachings of the prior art.
Claim(s) 13 and is/are rejected under 35 U.S.C. 103 as being unpatentable over Umetsu et al. (US2015/0297593A1, 2015-10-22, cited in the previous office action) in view of Hur et al. (Experimental and Molecular Medicine 2007; 39(3), 367-375), as applied to claims 1-2, 5-6, 8-9, 11-12, 14, 17-18, 20 and 24 above, in view of Abrams et al. (CMAJ 2020 May 19; 192:E551, cited in the previous office action).
As described above and incorporated herein, the combination of Umetsu et al. and Hur et al. teach a method of treating respiratory pathology, airway inflammation, airway hyperreactivity (AHR) or acute asthma in a subject comprising administering a combination of an effective amount of a c-kinase inhibitor (c-Kit), such as imatinib, and gefitinib, wherein the subject has a viral infection that causes asthma symptoms such as coronavirus.
The combination of Umetsu et al. and Hur et al. do not specifically teach that the coronavirus is SARS-CoV-2.
Abrams et al. teach that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) triggers asthma exacerbations, wherein the most common presenting symptoms of COVID-19, dry cough and shortness of breath, are also common with acute exacerbation of asthma (1 and 2).
It would have been prima facie obvious to one of ordinary skill in the art, prior to the effective filing date of the instantly claimed invention, to modify the method taught by the combination to include a patient suffering from SARS-CoV-2 in view of the teachings of Abrams et al.. One of ordinary skill in the art would have been motivated to make such a modification, with a reasonable expectation of success, because:
-Abrams et al. teaches that SARS-CoV-2 causes asthma symptoms such as dry cough and shortness of breath.
Conclusion
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 BRANDON J FETTEROLF whose telephone number is (571)272-2919. The examiner can normally be reached M-F 6AM-4PM.
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/BRANDON J FETTEROLF/Primary Examiner, Art Unit 1626