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 .
DETAILED ACTION
Claims 1-18 and 20 are pending and are consideration in the instant office action.
Election/Restrictions
Applicant’s election without traverse of the following species in their response dated 12/01/2025 is acknowledged.
Specie 1: Compound: Degrader 2 of claim 20 with the following structure
Specie 2: Circulating peripheral blood mononuclear cells -Monocytes of claim 10
Specie 3: Inflammatory biomarker to be monitored- IL6 of claim 13
Upon further consideration, the election of specie requirement above is withdrawn and the restriction requirement dated 10/01/2025 is withdrawn. Claims under consideration are claims 1-18 and 20
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 07/18/2023, 08/24/2023 and 09/23/2025 complies with the provisions of 37 CFR 1.97, 1.98 and MPEP § 609. Accordingly, it has been placed in the application file and the information therein has been considered as to the merits. See attached copy of the PTO-1449.
Priority
This application is a national stage filing under U.S.C. @371 of PCT International Application PCT/US2021/037952, filed June 17, 2021, which claims the benefit of U.S. Provisional Application No. 63/040,047, filed June 17, 2020, U.S. Provisional Application No. 63/070,022, filed August 25, 2020, and U.S. Provisional Application No. 63/089,398, filed October 8, 2020.
Claim Rejections - 35 USC § 102
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)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale or otherwise available to the public before the effective filing date of the claimed invention.
(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.
Claims 1-2 and 8-18 are rejected under 35 U.S.C. 102 (a) (1) and under 35 U.S.C 102(a)(2) as being anticipated by Weiss (US 2021/0228562, priority date 12/17/2019 and 06/18/2020, referenced in IDS) as evidenced by Brunner et al (Scientific reports, 7:8707, 2017, pages 1-12)
The applied reference has a common assignee with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2). This rejection under 35 U.S.C. 102(a)(2) might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C. 102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B) if the same invention is not being claimed; or (3) a statement pursuant to 35 U.S.C.102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement.
Instant claims are drawn to a method of treating hidradenitis suppurativa patient and/or atopic dermatitis in a patient having an elevated level of an inflammatory biomarker, comprising administering to the patient a therapeutically effective amount of an IRAK4 degraders
Weiss discloses compounds and methods useful for the modulation of one or more interleukin-1 receptor-associated kinases (“IRAK”) via ubiquitination and/or degradation by compounds and also provides pharmaceutically acceptable compositions comprising compounds of the present invention and methods of using said compositions in the treatment IRAK4-mediated disorder, disease, or condition in a patient comprising administering to said patient, IRAK4 degraders of formula as recited in their claims 1-6 ([0002]claim 10, [0013]) wherein the IRK4 mediated disorder includes atopic dermatitis and hidradenitis suppurativa, [0325][0329] [0426-0427]. It is noted that Weiss does not disclose that the patient has elevated level of an inflammatory biomarker. However, these conditions are highly inflammatory in nature and is inherently characterized by elevated levels of inflammatory biomarkers. This is evidenced by Brunner et al. who discloses that Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, associated with allergic manifestations (e.g. asthma, food allergies, seasonal allergies and other inflammatory diseases, including
rheumatoid arthritis, inflammatory bowel disease8, and systemic lupus erythematosus (page 1, 1stpara). They further disclose that blood of severe AD patients showed significantly increased T-cell activation and increases in serum cytokines that correlated with clinical severity. These markers are largely associated with Th1 (IFN-γ, CXCL9, TNF-β, lymphotoxin-α), but also Th17 (CCL20) (page 6. Para 2) . They disclose large set of markers exclusively upregulated in AD included Th1 (CXCL10, CXCL11), Th2 (IL-13, CCL13, CCL17, CCL11, IL-10), Th17/Th22 (S100A12) and Th1/Th17/Th22 (IL-12/IL-23p40) associated products in serum of AD patients (page 6, para 2). They further disclose that AD, , was characterized by significant upregulation of several additional Th1 (CXCL10, CXCL11), Th2 (IL-13, CCL13, CCL17, CCL11, IL-10), Th17/Th22 (S100A12) and Th1/Th17/Th22 (IL-12/ IL-23p40) associated products, as well as a broad array of proteins involved in the development and activation of
T-cells (CD40L, IL-7, CCL25, IL2RB, IL15RA, CD6, RANKL, TNFRSF9/CD137) and dendritic cells/DC (CD40, FLT3 ligand) (Fig. 1d). Mediators involved in atherosclerosis (CX3CL1/fractalkine, CCL8, M-CSF, CXCL5, CCL4, HGF), tissue remodeling (MMP-12, MMP-1, MMP-10) and angiogenesis (VEGF-A) were also increased in AD. The growth factor TGF-α, the NF-κB-activator IKBKG/NEMO, molecules mediating chemotaxis of
T-cells/B-cells/eosinophils (CCL28) and neutrophils (CXCL5, CXCL6), as well as the soluble cytokine receptors IL-10RB and IL-18R1 were also higher in AD (page 2, Para 4). As such evidentiary documentation explicitly discloses that atopic dermatitis as a highly inflammatory disorder charectrized by the increase in several different biomarkers. As such the atopic dermatitis patients being treated by the IRAK4 degraders in Weiss would therefor inherently have increased levels of several inflammatory markers. It is noted that In re Best (195 USPQ 430) and In re Fitzgerald (205 USPQ 594) discuss the support of rejections wherein the prior art discloses subject matter which there is reason to believe inherently includes functions that are newly cited or is identical to a product instantly claimed. In such a situation the burden is shifted to the applicants to "prove that subject matter shown to be in the prior art does not possess characteristic relied on" (205 USPQ 594, second column, first full paragraph). It is also noted that, "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art's functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430,433 (CCPA 1977).
In accordance with MPEP §2131.01, it is proper to rely upon a secondary reference for a rejection under 35 U.S.C. 102, provided that the additional reference is relied upon to demonstrate that a characteristic or property not disclosed by the primary reference is, in fact, inherent.
Therefore the composition disclosed by Weiss fully anticipates instant claims 1-2 and 8-18.
Claims 1-2, 8-18 and 20 are rejected under 35 U.S.C. 102 (a) (1) and under 35 U.S.C 102(a)(2) as being anticipated by Mainolfi et al (WO 2020/113233, priority date 11/30/2018, referenced in IDS) as evidenced by Brunner et al (Scientific reports, 7:8707, 2017, pages 1-12)
The applied reference has a common assignee with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2). This rejection under 35 U.S.C. 102(a)(2) might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C. 102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B) if the same invention is not being claimed; or (3) a statement pursuant to 35 U.S.C.102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement.
Instant claims are as recited above and claim 20 is drawn to wherein the IRAK4 degraders are
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Mainolfi et al. discloses the instantly claimed compounds as IRAK4 degrader 2 shown below ( See compound I-561 (page 539, table 1) and its synthesis (example 48)
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They disclose that these compounds are effective as degraders of IRAK kinases [00715] and are useful in the treatment of atopic dermatitis [00723]. They disclose administration to the patient through oral, topical, ophthalmic method [00698].
It is noted that Mainolfi et al. does not disclose that the patient has elevated level of an inflammatory biomarker. However, these conditions are highly inflammatory in nature and is inherently characterized by elevated levels of inflammatory biomarkers. This is evidenced by Brunner et al. who discloses that Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, associated with allergic manifestations (e.g. asthma, food allergies, seasonal allergies and other inflammatory diseases, including rheumatoid arthritis, inflammatory bowel disease8, and systemic lupus erythematosus (page 1, 1stpara). They further disclose that blood of severe AD patients showed significantly increased T-cell activation and increases in serum cytokines that correlated with clinical severity. These markers are largely associated with Th1 (IFN-γ, CXCL9, TNF-β, lymphotoxin-α), but also Th17 (CCL20) (page 6. Para 2) . They disclose large set of markers exclusively upregulated in AD included Th1 (CXCL10, CXCL11), Th2 (IL-13, CCL13, CCL17, CCL11, IL-10), Th17/Th22 (S100A12) and Th1/Th17/Th22 (IL-12/IL-23p40) associated products in serum of AD patients (page 6, para 2). They further disclose that AD, , was characterized by significant upregulation of several additional Th1 (CXCL10, CXCL11), Th2 (IL-13, CCL13, CCL17, CCL11, IL-10), Th17/Th22 (S100A12) and Th1/Th17/Th22 (IL-12/ IL-23p40) associated products, as well as a broad array of proteins involved in the development and activation of
T-cells (CD40L, IL-7, CCL25, IL2RB, IL15RA, CD6, RANKL, TNFRSF9/CD137) and dendritic cells/DC (CD40, FLT3 ligand) (Fig. 1d). Mediators involved in atherosclerosis (CX3CL1/fractalkine, CCL8, M-CSF, CXCL5, CCL4, HGF), tissue remodeling (MMP-12, MMP-1, MMP-10) and angiogenesis (VEGF-A) were also increased in AD. The growth factor TGF-α, the NF-κB-activator IKBKG/NEMO, molecules mediating chemotaxis of
T-cells/B-cells/eosinophils (CCL28) and neutrophils (CXCL5, CXCL6), as well as the soluble cytokine receptors IL-10RB and IL-18R1 were also higher in AD (page 2, Para 4). As such evidentiary documentation explicitly discloses that atopic dermatitis as a highly inflammatory disorder characterized by the increase in several different biomarkers. As such the atopic dermatitis patients being treated by the IRAK4 degraders in Mainolfi et al. would therefor inherently have increased levels of several inflammatory markers. It is noted that In re Best (195 USPQ 430) and In re Fitzgerald (205 USPQ 594) discuss the support of rejections wherein the prior art discloses subject matter which there is reason to believe inherently includes functions that are newly cited or is identical to a product instantly claimed. In such a situation the burden is shifted to the applicants to "prove that subject matter shown to be in the prior art does not possess characteristic relied on" (205 USPQ 594, second column, first full paragraph). It is also noted that, "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art's functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430,433 (CCPA 1977).
In accordance with MPEP §2131.01, it is proper to rely upon a secondary reference for a rejection under 35 U.S.C. 102, provided that the additional reference is relied upon to demonstrate that a characteristic or property not disclosed by the primary reference is, in fact, inherent.
Therefore the method disclosed by Mainolfi et al. fully anticipates instant claims 1-3, 8-18 and 20.
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 set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied 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.
Claims 3-7 are rejected under 35 U.S.C. 103(a) as being unpatentable over by Weiss (US 2021/0228562, priority date 12/17/2019 and 06/18/2020) as evidenced by Brunner et al (Scientific reports, 7:8707, 2017, pages 1-12) as applied to claims 1-3 and 8-18, in view of Thijs et al. (J. Clin. Med 2015, 4, pages 479-487),
Claims 3-7 are drawn to a method of treating hidradenitis suppurativa patient and/or atopic dermatitis in a patient, comprising administering to a patient a therapeutically effective amount of an IRAK4 degrader, measuring an inflammatory biomarker level in a sample of a patient after a treatment with an IRAK4 degrader, selecting a patient having a reduced level of an inflammatory biomarker after a treatment with an IRAK4 degrader, and administering to the patient a therapeutically effective amount of an IRAK4 degrader.
The teachings of Weiss and Brunner et al recited above in the 102 rejection is reiterated below.
Weiss discloses compounds and methods useful for the modulation of one or more interleukin-1 receptor-associated kinases (“IRAK”) via ubiquitination and/or degradation by compounds and also provides pharmaceutically acceptable compositions comprising compounds of the present invention and methods of using said compositions in the treatment IRAK4-mediated disorder, disease, or condition in a patient comprising administering to said patient, IRAK4 degraders of formula as recited in their claims 1-6 ([0002]claim 10, [0013]) wherein the IRK4 mediated disorder includes atopic dermatitis and hidradenitis suppurativa, [0325][0329] [0426-0427]. It is noted that Weiss does not disclose that the patient has elevated level of an inflammatory biomarker. However, these conditions are highly inflammatory in nature and is inherently characterized by elevated levels of inflammatory biomarkers. This is evidenced by Brunner et al. who discloses that Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, associated with allergic manifestations (e.g. asthma, food allergies, seasonal allergies and other inflammatory diseases, including
rheumatoid arthritis, inflammatory bowel disease8, and systemic lupus erythematosus (page 1, 1stpara). They further disclose that blood of severe AD patients showed significantly increased T-cell activation and increases in serum cytokines that correlated with clinical severity. These markers are largely associated with Th1 (IFN-γ, CXCL9, TNF-β, lymphotoxin-α), but also Th17 (CCL20) (page 6. Para 2) . They disclose large set of markers exclusively upregulated in AD included Th1 (CXCL10, CXCL11), Th2 (IL-13, CCL13, CCL17, CCL11, IL-10), Th17/Th22 (S100A12) and Th1/Th17/Th22 (IL-12/IL-23p40) associated products in serum of AD patients (page 6, para 2). They further disclose that AD, , was characterized by significant upregulation of several additional Th1 (CXCL10, CXCL11), Th2 (IL-13, CCL13, CCL17, CCL11, IL-10), Th17/Th22 (S100A12) and Th1/Th17/Th22 (IL-12/ IL-23p40) associated products, as well as a broad array of proteins involved in the development and activation of
T-cells (CD40L, IL-7, CCL25, IL2RB, IL15RA, CD6, RANKL, TNFRSF9/CD137) and dendritic cells/DC (CD40, FLT3 ligand) (Fig. 1d). Mediators involved in atherosclerosis (CX3CL1/fractalkine, CCL8, M-CSF, CXCL5, CCL4, HGF), tissue remodeling (MMP-12, MMP-1, MMP-10) and angiogenesis (VEGF-A) were also increased in AD. The growth factor TGF-α, the NF-κB-activator IKBKG/NEMO, molecules mediating chemotaxis of
T-cells/B-cells/eosinophils (CCL28) and neutrophils (CXCL5, CXCL6), as well as the soluble cytokine receptors IL-10RB and IL-18R1 were also higher in AD (page 2, Para 4). As such evidentiary documentation explicitly discloses that atopic dermatitis as a highly inflammatory disorder characterized by the increase in several different biomarkers. As such the atopic dermatitis patients being treated by the IRAK4 degraders in Weiss would therefor inherently have increased levels of several inflammatory markers. It is noted that In re Best (195 USPQ 430) and In re Fitzgerald (205 USPQ 594) discuss the support of rejections wherein the prior art discloses subject matter which there is reason to believe inherently includes functions that are newly cited or is identical to a product instantly claimed. In such a situation the burden is shifted to the applicants to "prove that subject matter shown to be in the prior art does not possess characteristic relied on" (205 USPQ 594, second column, first full paragraph). It is also noted that, "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art's functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430,433 (CCPA 1977).
Weiss does not disclose measuring inflammatory biomarkers in samples of patients with hidradenitis suppurativa patient and/or atopic dermatitis treated with their inventive IRAK 4 degraders, and further selecting a patient having reduced level of an inflammatory biomarker and further administering another dosage of the IRAK4 degrader to the same patient.
However, Thijs et al. discloses that frequently reported serum biomarkers for disease severity in AD include eosinophilic cationic protein (ECP) [11], IL-2R [12], and thymus and activation-regulated chemokine (TARC/CCL17) (page 481. Section 2.2). They teach that while blood is the commonly used fluid for biomarker measurements, dried blood spots and saliva are potential alternatives (page 482, section 3). They conclude that the application of biomarkers in AD offers great opportunities, both in daily clinical practice as well as for research purposes and offer reliable and objective outcome measures. They further teach that the heterogeneous character of the disease and lack of clinical stratifiers makes AD highly suitable for a biomarker based stratification. A panel of biomarkers can assess multiple molecular entities, and will be more suitable for assessing disease severity in AD compared to an individual biomarker. Biomarker stratification will identify subgroups of patients that will respond to treatment and enable tailoring of drugs to the biological signature of individual patients, accelerating the translation of new medicine from bench to bedside and can revolutionize AD therapy. They conclude that the use of biomarkers will enhance the efficacy of AD treatment by facilitating the individualization of therapy targeting the patient’s specific biological signature and also by providing tools for predicting and monitoring of therapeutic response( page 484 , section 4).
As such it would have been prima facia obvious to a person of ordinary skill in the art to arrive at the instant claims motivated and guided by the combined teachings of Weiss and Thijs et al. to arrive at the instant claims. Treatment of Atopic dermatitis with IRAK4 inhibitors is already well known in the art as taught by Weiss , Use of biomarkers in atopic dermatitis for objective determination of the disease , severity , confirmation of clinical diagnosis and ot predict response to treatment was also very well know in the art at the time of this application as taught by Thijs et al. As such an ordinarily skilled artisan would be motivated from to utilize the biomarker analysis to determine the efficacy of any type of treatment of atopic dermatitis which includes treatment with IRAK4 inhibitors taught by Weiss, absence of evidence to the contrary. It would be obvious to an ordinarily skilled artisan to determine the biomarker levels after treatment to access the efficacy of the drugs and if the elevated markers are reduced, indicating the efficacy of the treatment, it would be obvious to further treat the patient with the same agent which has just shown efficacy with a reasonable expectation of success, absence of evidence to the contrary.
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 claims at issue 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); and 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 a nonstatutory double patenting ground provided the reference application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The USPTO internet Web site contains terminal disclaimer forms which may be used. Please visit http://www.uspto.gov/forms/. The filing date of the application will determine what form 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 http://www.uspto.gov/patents/process/file/efs/guidance/eTD-info-I.jsp.
Claims 1-18 and 20 are provisionally rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 19-21 and 27-29 of copending Application No. 18/955,054 (‘054)
Instant claims are drawn to a method of treating hidradenitis suppurativa patient and/or atopic dermatitis in a patient having an elevated level of an inflammatory biomarker, comprising administering to the patient a therapeutically effective amount of an IRAK4 degrader.
‘054 claims are drawn to a method for treating an autoimmune/autoinflammatory disease or a hematological malignancy in a patient, comprising administering to the patient a therapeutically effective amount of the spray-dried formulation of any one of claims 1-7, or the a unit dosage form of any one of claims 8-18 comprising a spray-dried formulation, the spray-dried formulation comprising Compound A or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable polymer;wherein Compound A is 5-((1R,4R)-2-oxa-5-azabicyclo[2.2.1]heptan-5-yl)-N-(3- (difluoromethyl)-1-((1r,4R)-4-((4-((3-(1-(2,6-dioxopiperidin-3 -yl)-3-methyl-2-oxo-2,3 -dihydro-1H- benzofd]imidazol-4-yl)prop-2-yn- 1 -yl)oxy)piperidin- 1 -yl)methyl)cyclohexyl)-1H-pyrazol-4- yl)pyrazolo[1,5-a]pyrimidine-3-carboxamide; and wherein the unit dosage form is a tablet of about 208 mg, comprising: a tablet core of about 200 mg, comprising intragranularly: about 25 mg Compound A free base, about 75 mg hydroxypropylmethylcellulose acetate succinate MG grade (HPMCAS-M), about 15 mg mannitol, about 15 mg microcrystalline cellulose, about 40 mg hydroxypropyl-beta-cyclodextrin, about 19.34 mg croscarmellose sodium, about 2 mg stearyl fumarate sodium, and about 2 mg colloidal silicon dioxide; and extragranularly: about 4.66 mg croscarmellose sodium, about 1 mg stearyl fumarate sodium, and about 1 mg colloidal silicon dioxide (Claim 19) wherein the autoimmune condition is selected from atopic dermatitis (AD) and hidradenitis suppurativa (HS) (claim 21)
While the claims are not identical, they are obvious over each other since the compound A claimed in ‘054 is the same as the degrader 2 recited in instant claim 20 and the condition being treated is the same in the both sets of claims. With regards to the tablet formulation recited in claim 19 of ‘054, Developing compositions and formulating it in tablet form with the well known excipients known in the art would be obvious to a person of ordinary skill in the art and.
Given the teachings ‘054, a person of ordinary skill in the art would have been motivated select the degrader 2, which is an IRK4 inhibitor for treatment of hidradenitis suppurative or atopic dermatitis. With regards to the limitation in the instant claim 1 wherein the patient has an elevated level of inflammatory markers, any patient with autoimmune or inflammatory diseases will inherently have high levels of inflammatory biomarkers, absence of evidence to the contrary.
This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
Conclusion
Claims 1-18 and 20 are rejected. No claims are allowed
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SAVITHA RAO whose telephone number is (571)270-5315. The examiner can normally be reached on Mon-Fri 7 am to 4 pm..
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Dierdre (Renee) Claytor can be reached on (571) 272-8394. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/SAVITHA M RAO/Primary Examiner, Art Unit 1691