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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 06/09/2026 has been entered.
Status of the Application
Claims 1, 11-13, 23, 25, and 31-38 are pending.
Receipt and consideration of Applicants' amended claim set and remarks/arguments filed on 06/09/2026 are acknowledged. Claims 1, 11, 23, and 31-34 remain withdrawn, as being drawn to an unelected invention or specie. Claims 1, 12, 23, 25, and 31-34 is amended and new claims 35-38 are added. Claims under consideration in the instant office action are claims 12-13, 25, and 35-38.
Applicants' arguments, filed 06/09/2026, 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 Rejections and/or objections not reiterated from previous office actions are hereby withdrawn.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 12-13, 25, and 35-38 are rejected under 35 U.S.C. 103 as being unpatentable over Taveras et al. (WO 03/080053, as disclosed in IDS) in view of Adcock (Molecular Mechanisms of Corticosteroid Resistance, Chest, 2008, 134(2), pp. 394-401) and Colella et al. (1,3-Dibromo-1,1-difluoro-2-propanone as a Useful Synthon for a Chemoselective Preparation of 4‑Bromodifluoromethyl Thiazoles, ACS Omega, 2018, 3, pp. 14841-14848).
Taveras et al. teaches methods of treating chemokine-mediated diseases, including asthma, comprising the administration of combinations comprising CXC-chemokine receptor antagonists with other classes of pharmaceutical compounds (see abstract). Taveras et al. teaches such combinations comprising a steroid such as dexamethasone (pg. 3, lines 4-20). Taveras et al. teaches “The CXC-chemokines include interleukin-8 (IL-8), neutrophil-activating protein-1 (NAP-1 ), neutrophil-activating protein-2 (NAP-2), GROa, GROj3, GROy, ENA-78, GCP-2, IP-10, MIG and PF4. CC chemokines include RANTES, MIP -1a, MIP-213, monocyte chemotactic protein-1 (MCP-1 ), MCP-2, MCP-3 and eotaxin. Individual members of the chemokine families are known to be bound by at least one chemokine receptor, with CXC-chemokines generally bound by members of the CXCR class of receptors, and CC-chemokines by members of the CCR class of receptors. For example, IL-8 is bound by the CXCR-1 and CXCR-2 receptors.” (pg. 1, lines 12-25). Taveras et al. teaches active compounds formulated in the form of a pharmaceutically acceptable salt, including sodium and calcium salts (claims 59-60).
Taveras et al. does not teach a method of treating corticosteroid-resistant asthma. Taveras et al. does not teach a combination comprising DF2755.
Adcock is drawn towards mechanisms of corticosteroid resistance, particularly in asthma patients (see abstract). Adcock teaches GC-resistant or corticosteroid-refractory (CSR) asthma is defined as < 15% improvement in baseline FEV, after a 14-day course of oral prednisolone (40 mg/d) in patients who demonstrate > 15% improvement in FEV, with salbutamol therapy.” (pg. 395, left column, second paragraph). Adcock teaches “the multiple mechanisms underlying CSR asthma may indicate the need for patient-specific treatment with novel therapies directed at abnormal signaling pathways to restore asthma control' (Table 1).” (pg. 399, left column, third paragraph). Adcock teaches that combination therapies may be effective for patients with CSR asthma (pg. 399, right column, first paragraph).
Colella is drawn towards the use of 1,3-dibromo-1,1-difluoro-2-propanone as a synthon for drug discovery (see abstract). Colella teaches “our recent efforts focused on (2S)-2-(4-{[4-(trifluoromethyl)-1,3-thiazol-2-yl]- amino}phenyl)propanoic acid (DF2755Y) (Scheme 1), a small molecule belonging to a novel allosteric dual CXCR1/CXCR2 inhibitor with a favorable oral pharmacokinetic profile. This molecule selectively inhibited neutrophil chemotaxis induced by CXCR1/2 ligands without affecting on CXCL8 binding to these receptors. The activation of CXCR1/2 has been implicated in the genesis of inflammatory and postoperative pain and progression of severe chronic diseases, including rheumatoid arthritis, chronic obstructive pulmonary disease, Alzheimer’s disease, melanoma, and several urological diseases.” (pg. 14841, Introduction).
It would have been obvious to one of ordinary skill in the art to treat corticosteroid-resistant asthma, as suggested by Adcock, and produce the instant invention.
One of ordinary skill in the art would have been motivated to do so since Taveras et al. teaches combinations comprising CXC-chemokine receptor antagonists with other classes of pharmaceutical compounds as effective for the treatment of asthma, and Adcock suggests the use of combination therapies for the treatment of CSR asthma, 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 further administer compound DF2755, as suggested by Colella et al., and produce the instant invention.
One of ordinary skill in the art would have been motivated to do so since Colella et al. teaches DF2755Y as an effective CXCR1/CXCR2 inhibitor, and Taveras et al. teaches combinations comprising chemokine antagonists and other pharmaceutical compounds for the treatment of asthma. Thus, one of ordinary skill in the art would have been motivated to do so since it is prima facie obvious to combine components known for the same purpose for their combined additive effects, with a reasonable expectation of success absent evidence of criticality of the particular formulation. Additionally, “[T]he idea of combining them flows logically from their having been individually taught in the prior art.” In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980).
Therefore, it would have been prima facie obvious to combine dexamethasone and DF2755 in composition cojointly to treat CSR asthma.
Regarding claim 20, when the composition recitations are met, the desired properties are met, as any component that materially affects the composition and its properties would have to be present in the claim to be commensurate in scope (i.e. claim 20). Additionally, when the composition is delivered in the same manner as claimed, the effects of the composition would be the same such as the therapeutic profile, as they are a direct result of the components of the composition and the mode of administration which are met by the art, whereby the resulting properties and effects would intrinsically be met. A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. In re Spada 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). See MPEP 2112.01.
Response to Arguments
Applicant argues that “Thomson indicates that corticosteroid-insensitive asthma represents a distinct disease endotype with disrupted glucocorticoid signaling and a shift toward non-eosinophilic, neutrophil-associated inflammation, which together contributes to a reduced clinical response to standard corticosteroid treatment in a significant proportion of patients. “ The Examiner respectfully disagrees since Taveras et al. is drawn towards CXC-chemokine antagonists, which include interleukin-8 (IL-8), “which is responsible for chemotaxis of neutrophil and T-cell subsets into the inflammatory site” (pg. 1, lines 12-30, pg. 2, lines 5-10). Such teachings would be consistent with Thomson, which teaches that corticosteroid-insensitive asthma is associated with neutrophilic inflammation (pg. 3, right column, 2nd paragraph). Additionally, Thomson teaches that current pharmacological treatments comprise “A step-up in the dose of corticosteroid as well as the addition of other therapies may benefit individuals with asthma that is associated with corticosteroid insensitivity.” (pg. 8, left column, 2nd paragraph; pg. 13, left column, 2nd paragraph), and that “Novel small molecule drugs and biologics agents have been developed as possible new treatments for asthma, including for patients with corticosteroid insensitivity.” (pg. 9, right column, 1st paragraph). Given these teachings, one of ordinary skill in the art would have been motivated to treat corticosteroid-insensitive asthma by administering CXC-chemokine antagonists with a corticosteroid since Thomson teaches combining a stepped up dose of a corticosteroid with other therapies (e.g. non-corticosteroid treatment) as the current response to corticosteroid insensitivity, the agents disclosed by Taveras et al. can inhibit the neutrophilic inflammation present in corticosteroid-insensitive asthma, and novel treatments for patients with asthma generally would include for patients with corticosteroid insensitivity as taught by Thomson.
Applicant also argues that “a skilled person would have understood that treatment responses observed in asthma generally could not be reliably extrapolated to corticosteroid-insensitive asthma. Rather, the altered inflammatory signaling associated with corticosteroid-insensitive asthma would have created significant uncertainty as to whether therapies effective in conventional asthma would also be effective in corticosteroid-insensitive asthma. Thus, a skilled person would not have had a reasonable expectation that a non-corticosteroid treatment known for conventional asthma would be effective in corticosteroid-insensitive asthma.” The Examiner respectfully disagrees since although there may be associated with different inflammatory mechanisms including neutrophilic inflammation as disclosed by Thomson (pg. 3, right column, 2nd paragraph), Thomson does teach that “Novel small molecule drugs and biologics agents have been developed as possible new treatments for asthma, including for patients with corticosteroid insensitivity.” (pg. 9, right column, 1st paragraph). Taveras et al. is drawn towards CXC-chemokine antagonists, which include interleukin-8 (IL-8), “which is responsible for chemotaxis of neutrophil and T-cell subsets into the inflammatory site” (pg. 1, lines 12-30, pg. 2, lines 5-10). One of ordinary skill in the art would thus have been motivated to treat corticosteroid-insensitive asthma by administering CXC-chemokine antagonists since such compounds can inhibit the neutrophilic inflammation present in corticosteroid-insensitive asthma.
Conclusion
Claims 12-13, 25, and 35-38 are rejected.
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
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