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
The amendment filed July 1, 2026 in response to the Office Action of April 2, 2026 is acknowledged and has been entered.
Claims 1, 4, 6, and 19 have been amended.
Claims 2, 3, 7-15, and 18 been cancelled.
Claims 1, 4-6, and 19 are currently under consideration as drawn to the elected invention.
In view of claim 15 cancellation, the 112(b) rejection set forth in the previous Office Action of April 2, 2026 is hereby withdrawn.
In view of claim 12 cancellation, the 112(d) rejection set forth in the previous Office Action of April 2, 2026 is hereby withdrawn.
In view of claim 1 amendment and Application’s arguments, the 112(a) rejection set forth in the previous Office Action of April 2, 2026 is hereby withdrawn.
MAINTAINED/MODIFIED REJECTION
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.
Claims 1, 4-6, and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Owczarek (Owczarek et al., US 2019/0062438 A1, Publication Date: 02/28/2019, of record) in view of Dudeck (Dudeck et al., Immunity, 34, 973-984, Publication Date: 06/24/2011, of record), as evidenced by Fernandez (Fernandez et al., Merck Manual, downloaded from: Overview of Allergic and Atopic Disorders - Allergy and Immunology - Merck Manual Professional Edition; Publication Date: Aug. 2024, of record).
Owczarek teaches that the pleiotropic cytokines interleukin (IL)-3 (IL-3), IL-5 and granulocyte-macrophage colony stimulating factor (GM-CSF) play critical and overlapping roles in the differentiation and function of myeloid cells. They contribute significantly to the development and progression of inflammatory pathologies ([0004]).
Owczarek teaches that each of IL-3, IL-5 and GM-CSF all signal through a multimeric receptor comprising CD131 ([0005]).
Owczarek teaches antibodies that bind to CD131 and neutralize signaling by IL-3, IL-5 and GM-CSF ([0008]), such as 9A2-VR24.29 ([0806], Fig. 12, Table 1, [1262], [1263]).
Owczarek teaches that the antibodies bind to CD131 within a region designated “Site 2” and also found that certain residues within site 2 which are important for binding IL-3, IL-5 and GM-CSF ([0008]).
Owczarek teaches that neutralizing signaling of IL-3, IL-5 and GM-CSF is an effective manner of reducing survival of eosinophils ([0010]);
Owczarek teaches that antibody 9A2 inhibits signaling IL-3, IL-5 and GM-CSF ([1262], [1263]).
Owczarek teaches that the antibodies can be used to treat conditions caused or exacerbated by signaling through CD131 including inflammatory condition or allergic condition ([1143], [1144]). In one example, the condition is an allergic condition, for example exfoliative dermatitis ([1147], [1156]), or other skin condition psoriasis ([1160]).
Owczarek teaches dosages and timing of administration for these antibodies to a subject in need ([1179] to [1189]).
Owczarek teaches 9A2-VR24.29 comprises VL of SEQ ID NO: 5 and VH of SEQ ID NO: 64 (Table 1), which are identical to SEQ ID NO: 18 and SEQ ID NO: 6 of the instant specification, respectively (alignment shown below).
US-15-779-252-5
Query Match 100.0%; Score 555; Length 112;
Best Local Similarity 100.0%;
Matches 108; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIQMTQSPSSVSASVGDRVTITCRASQGISSWLAWYQQKPGKAPKLLIYAASSLQSGVPS 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIQMTQSPSSVSASVGDRVTITCRASQGISSWLAWYQQKPGKAPKLLIYAASSLQSGVPS 60
Qy 61 RFSGSGSGTDFTLTISSLQPEDFATYYCQQANSFPITFGQGTRLEIKR 108
||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 RFSGSGSGTDFTLTISSLQPEDFATYYCQQANSFPITFGQGTRLEIKR 108
US-15-779-252-64
Query Match 100.0%; Score 631; Length 117;
Best Local Similarity 100.0%;
Matches 117; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 EVQLLESGGGLVQPGGSLRLSCAASGFTFPWYRVHWVRQAPGKGLEWVSSIRSSGGFPYY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 EVQLLESGGGLVQPGGSLRLSCAASGFTFPWYRVHWVRQAPGKGLEWVSSIRSSGGFPYY 60
Qy 61 NYKVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARFYDSFFDIWGQGTMVTVSS 117
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 NYKVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARFYDSFFDIWGQGTMVTVSS 117
Thus, 9A2-VR24.29 reads on the antibody of instant claims 1 and 19.
Regarding claim 6, as evidenced by paragraph [0243] of the instant publication US 2023/0406943 A1, 9A2-VR24.29 is also referred to as CSL311, which is used in the Examples of the instant application. Thus, the antibody would have the same properties and functionalities of CSL311, including reducing swelling at the site of inflammation, reducing CD8+ T cells, neutrophils, eosinophils and mast cells at the inflammation site ([0378] and [0379] of the instant publication US 2023/0406943 A1).
In addition, the limitations a) to e) recited by claim 6 are merely intended results of the method steps positively recited. The court noted (quoting Minton v. Nat'/ Ass'n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) that a "'whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited."' Id. Therefore, the limitations a) to e) of claim 6 are given no weight.
Owczarek teaches the method of treating inflammatory condition or allergic condition including skin condition exfoliative dermatitis with 9A2-VR24.29 which bind to CD131 and neutralizes signaling by GM-CSF, IL-3 and IL-5, as set forth above. However, Owczarek does not teach treating a type IV hypersensitivity skin condition, such as allergic contact dermatitis.
Owczarek further teaches that myeloid cells include neutrophils, basophils, plasmacytoid dendritic cells (pDCs), mast cells and CD34+ BM cells ([1276]). 9A2-VR24.29 inhibits activation and survival of myeloid cells stimulated with IL-3, GM-CSF and IL-5 ([1276]-[1279]).
Owczarek further teaches that IL-3 can regulate mast cell generation and functions and is a strong activator of mast cells. 9A2-VR24.29 can inhibit this effect of IL-3 on mast cells (Fig. 16 and [1278]); and CD34+ human BM cell formation ([1279] and Fig. 16).
Owczarek further teaches that in vivo administration of 9A2-VR24.29 can reduce the number of mast cells (Fig. 22 and [1289]).
Dudeck teaches: a prominent feature of sensitizing environmental compounds that cause allergic contact dermatitis is the rapid induction of an innate inflammatory response that seems to provide danger signals for efficient T cell priming (§ Summary). It’s noted that allergic contact dermatitis is an example of type IV hypersensitivity reaction, as evidenced by paragraph [0224] of the instant publication.
Dudeck teaches that mast cell deficiency resulted in impaired emigration of skin DCs to the lymph node and contact hypersensitivity was dramatically reduced in the absence of mast cell (§ Summary).
Dudeck teaches that mast cell are essential promoters of contact hypersensitivity (§ Summary). Selective mast cell deficiency results in an almost complete abrogation of the allergic T cell response (Results – Reduced CHS responses in MC-deficient Mice). Contact allergens induce a mast cell-dependent immediate response of the skin vasculature (the bridging paragraph of pages 975-976). Mast cells promote DC migration and hypertrophy of lymph nodes draining contact allergen-treated skin (page 979, col. 1).
It would have prima facie been obvious to one of ordinarily skilled in the art before the time the invention was filed to combine the teachings of Owczarek and Dudeck and to apply the method of Owaczarek for treating allergic contact dermatitis. One of ordinary skill in the art would have had a reasonable expectation that 9A2-VR24.29 would be effective for allergic contact dermatitis because: 1) 9A2-VR24.29 can be used to treat allergic and inflammatory skin condition; 2) 9A2-VR24.29 can 9A2-VR24.29 can inhibit this effect of IL-3 on mast cells and reduce mast cells in vitro and in vivo as taught by Owczarek; 3) mast cells are essential for hypersensitivity reaction in allergic contact dermatitis as taught by Dudeck. The motivation would have been to extend the application of the antibody and to develop a new treatment for type IV hypersensitivity skin condition.
Response to Arguments
For the rejection under 35 U.S.C. 103, Applicant argues:
Owczarek does not teach or suggest the use of CSL311 (9A2-VR24.29) for the treatment of type IV hypersensitivity skin conditions, nor does it provide a basis for a reasonable expectation that such treatment would reduce or eliminate inflammation associated with those conditions. While Owczarek discloses 9A2-VR24.29 and its ability to inhibit signaling through the CD131 receptor, the focus of that disclosure is on general modulation of cytokine-driven immune responses. Importantly, Owczarek does not identify type IV hypersensitivity skin conditions, such as allergic contact dermatitis, as a target indication, nor does it provide any data or rationale linking CD131 inhibition by 9A2-VR24.29 to the treatment of such conditions.
Further, although Owczarek reports that 9A2-VR24.29 can affect myeloid cell activation and influence mast cell biology, these teachings do not provide a reasonable expectation of success in the context of type IV hypersensitivity. For example, the effects of 9A2-VR24.29 described in Owczarek do not establish that modulation of CD131 signaling would translate into a meaningful therapeutic effect in reducing or eliminating inflammation in type IV hypersensitivity skin conditions.
Dudeck does not cure these deficiencies. At most, Dudeck indicates that mast cells may contribute to aspects of the inflammatory response observed in allergic contact dermatitis. However, this general observation does not provide a specific teaching or suggestion that targeting CD131 signalling generally, or administering 9A2-VR24.29 in particular, would be effective in treating such conditions. Nor does it provide a predictive mechanistic link that would give the skilled person a reasonable expectation
that inhibition of mast cell-associated pathways would be sufficient to address the complex pathology of type IV hypersensitivity. The Office's position therefore relies on an impermissible hindsight reconstruction of the present invention, rather than any clear teaching or suggestion in the cited prior art.
Applicant’s arguments have been fully considered but they are only partially persuasive. In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
As set forth above, Owczarek clearly teaches the method of treating inflammatory condition or allergic skin condition with 9A2-VR24.29 which bind to CD131 and neutralizes signaling by GM-CSF, IL-3 and IL-5. Owczarek further teaches that 9A2-VR24.29 can inhibit this effect of IL-3 on mast cells (Fig. 16 and [1278]) and in vivo administration of 9A2-VR24.29 can reduce the number of mast cells (Fig. 22 and [1289]). Dudeck explicitly teaches that mast cells are essential promoters of contact hypersensitivity (§ Summary). Selective mast cell deficiency results in an almost complete abrogation of the allergic T cell response (Results – Reduced CHS responses in MC-deficient Mice). Contact allergens induce a mast cell-dependent immediate response of the skin vasculature (the bridging paragraph of pages 975-976). Mast cells promote DC migration and hypertrophy of lymph nodes draining contact allergen-treated skin (page 979, col. 1). Thus, Dudeck provides experimental evidence that mast cells are critical for developing allergic contact dermatitis. Combining teachings of Owczarek and Dudeck, one of ordinary skill in the art would have a reasonable expectation that 9A2-VR24.29 would be effective for treating allergic contact dermatitis.
Furthermore, in the field of biological technology, no invention has absolute certainty of success before experimental tests. Thus, only a reasonable expectation of success (not absolute) would have motivated an artisan to use 9A2-VR24.29 for treating allergic contact dermatitis. Given the teachings from references, an ordinary skilled in the art would have would have had a reasonable expectation of success in producing the claimed invention.
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 conflicting claims 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); 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 nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) 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 www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
U.S. Patent No. 10,894,834
Claims 1, 4-6, and 19 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-5 of U.S. Patent No. 10,894,834 B2 (hereinafter Pat. 834, Appl. No. 15/779,252, of record) in view of Owczarek (Owczarek et al., US 2019/0062438 A1, Publication Date: 02/28/2019, of record) and Dudeck (Dudeck et al., Immunity, 34, 973-984, Publication Date: 06/24/2011, of record), as evidenced by Fernandez (Fernandez et al., Merck Manual, downloaded from: Overview of Allergic and Atopic Disorders - Allergy and Immunology - Merck Manual Professional Edition; Publication Date: Aug. 2024, of record).
It is noted that Owczarek et al., US 2019/0062438 A1, corresponds to the same (Application No. 15/779,252) as Pat. 834, thus, they share the same disclosure.
Claim 1 of Pat. 834 teaches: a CD131-binding protein comprising an antigen binding domain of an antibody, wherein the antigen binding domain binds to or specifically binds to CD131 and neutralizes signaling by interleukin (IL) 3, IL-5 and granulocyte-macrophage colony stimulating factor (GM-CSF), and wherein the antigen binding domain comprises: (i) a VH comprising CDRs 1, 2 and 3 of the sequence set forth in SEQ ID NO: 64 and a VL comprising CDRs 1, 2 and 3 of the sequence set forth in SEQ ID NO: 5; or (ii) a VH comprising the sequence set forth in SEQ ID NO: 64 and a VL comprising the sequence set forth in SEQ ID NO: 5. Owczarek teaches 9A2-VR24.29 comprises VL of SEQ ID NO: 5 and VH of SEQ ID NO: 64 (Table 1), which are identical to SEQ ID NO: 18 and SEQ ID NO: 6 of the instant specification, respectively as set forth above. Thus, 9A2-VR24.29 is a species of claim 1 of Pat. 834.
Claim 2 of Pat. 834 teaches: The CD131-binding protein of claim 1, which has one or more of the following activities: (i) reduces or inhibits activation of isolated human neutrophils by GM-CSF as determined by reducing or inhibiting GM-CSF-induced increase in neutrophil cell size; (ii) reduces or inhibits IL-3-induced IL-8 secretion by human basophils; (iii) reduces IL-3-mediated survival or plasmacytoid dendritic cells (pDCs); (iv) reduces activation of human peripheral blood eosinophils by IL-5 as determined by assessing change in forward scatter assessed by flow cytometry; (v) reduces survival of human peripheral blood eosinophils in the presence of IL-5 and/or GM-CSF and/or IL-3; (vi) reduces IL-3-induced tumor necrosis factor (TNF) a release from human mast cells; (vii) reduces IL-3-induced IL-13 release from human mast cells; (viii) reduces potentiation of IgE-mediated IL-8 release from human mast cells by IL-3 and/or IL-5 and/or GM-CSF; or (ix) reduces formation of colony forming units granulocytes-macrophages (CFU-GM) by CD34+ human bone marrow cells cultured in the presence of stem cell factor (SCF), GM-CSF, IL-3 and IL-5.
Claim 3 of Pat. 834 teaches: The CD131-binding protein of claim 1, wherein if the VH and VL are in a single polypeptide chain, the protein is: (i) a single chain Fv fragment (scFv); (ii) a dimeric scFv (di-scFv); (iii) one of (i) or (ii) linked to a constant region of an antibody, Fc or a heavy chain constant domain (CH) 2 and/or CH3; or (iv) one of (i) or (ii) linked to a protein that binds to an immune effector cell, or if the VH and VL are in separate polypeptide chains the protein is: (i) a diabody; (ii) a triabody; (iii) a tetrabody; (iv) a Fab; (v) a F(ab′)2; (vi) a Fv; (vii) one of (i) to (vi) linked to a constant region of an antibody, Fc or a heavy chain constant domain (CH) 2 and/or CH3; (viii) one of (i) to (vi) linked to a protein that binds to an immune effector cell; or (ix) an antibody.
Taken together, the claims of Pat. 834 teach a CD131-binding protein comprising an antigen binding domain of an antibody, wherein the antigen binding domain binds to or specifically binds to CD131 and neutralizes signaling by interleukin (IL) 3, IL-5 and granulocyte-macrophage colony stimulating factor (GM-CSF). Thus, the claims of Pat. 834 teach the compounds of the instant claims. However, the claims of Pat. 834 do not teach the method of treating a type IV hypersensitivity skin condition as instantly claimed.
Owczarek and Dudeck’s teachings are described above. For example, Owczarek teaches that CD131 antibodies (such as 9A2-VR24.29) can be used to treat conditions caused or exacerbated by signaling through CD131. In one example, the condition is an allergic skin condition, for example, exfoliative dermatitis. Owczarek teaches dosages and timing of administration for these antibodies to a subject in need. Owczarek further teaches that myeloid cells include neutrophils, basophils, plasmacytoid dendritic cells (pDCs), mast cells and CD34+ BM cells. 9A2-VR24.29 inhibits activation and survival of myeloid cells stimulated with IL-3, GM-CSF and IL-5. Dudeck teaches that mast cell are essential promoters of contact hypersensitivity. Selective mast cell deficiency results in an almost complete abrogation of the allergic T cell response.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to combine the teachings of the claims of Pat. 834, Owczarek and Dudeck and to apply the method of Owaczarek for treating allergic contact dermatitis. One of ordinary skill in the art would have had a reasonable expectation that 9A2-VR24.29 would be effective for allergic contact dermatitis because: 1) 9A2-VR24.29 can be used to treat allergic and inflammatory skin condition; 2) 9A2-VR24.29 can 9A2-VR24.29 can inhibit this effect of IL-3 on mast cells and reduce mast cells in vitro and in vivo as taught by Owczarek; 3) mast cells are essential for hypersensitivity reaction in allergic contact dermatitis as taught by Dudeck. The motivation would have been to extend the application of the antibody and to develop a new treatment for type IV hypersensitivity skin condition.
U.S. Patent No. 11,840,573
Claims 1, 4-6, and 19 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 11,840,573 B2 (hereinafter Pat. 573, Appl. No. 16/953,499, of record) in view of Owczarek (Owczarek et al., US 2019/0062438 A1, Publication Date: 02/28/2019, of record) and Dudeck (Dudeck et al., Immunity, 34, 973-984, Publication Date: 06/24/2011, of record), as evidenced by Fernandez (Fernandez et al., Merck Manual, downloaded from: Overview of Allergic and Atopic Disorders - Allergy and Immunology - Merck Manual Professional Edition; Publication Date: Aug. 2024, of record).
It is noted that Pat. 573 correspond to application Appl. No. 16/953,499 which is a continuation of Appl. No. 15/779,252. Thus, Owczarek (US 2019/0062438 A1, corresponding to Appl. No. 15/779,252) and Pat. 573, share the same disclosure.
Claim 11 of Pat. 573 teaches, a CD131-binding protein comprising an antigen binding domain of an antibody, wherein the antigen binding domain binds to or specifically binds to CD131 and neutralizes signaling by interleukin (IL) 3, IL-5 and granulocyte-macrophage colony stimulating factor (GM-CSF), and wherein the antigen binding domain comprises: … (cxvii) a VH comprising CDRs 1, 2 and 3 of the sequence set forth in SEQ ID NO: 64 and a VL comprising CDRs 1, 2 and 3 of the sequence set forth in SEQ ID NO: 5;....
As set forth above, Owczarek teaches 9A2-VR24.29 comprises VL of SEQ ID NO: 5 and VH of SEQ ID NO: 64 (Table 1), which are identical to SEQ ID NO: 18 and SEQ ID NO: 6 of the instant specification, respectively as set forth above. Thus, 9A2-VR24.29 is a species of claim 1 of Pat. 573.
Claim 12 of Pat. 573 teaches: the CD131-binding protein of claim 11, wherein the Ko of the CD131-binding protein comprises a polypeptide comprising the sequence set forth in SEQ ID NO: 194 is about 100 nM or less, when the polypeptide is immobilized on a solid surface and the Ko is determined by surface plasmon resonance.
Claim 13 of Pat. 573 teaches: the CD131-binding protein of claim 11, which has one or more of the following activities: (i) reduces or inhibits activation of isolated human neutrophils by GM-CSF as determined by reducing or inhibiting GM-CSF-induced increase in neutrophil cell size; (ii) reduces or inhibits IL-3-induced IL-8 secretion by human basophils; (iii) reduces or prevents IL-3-mediated survival or plasmacytoid dendritic cells (pDCs); (iv) reduces or prevents activation of human peripheral blood eosinophils by IL-5 as determined by assessing change in forward scatter assessed by flow cytometry; (v) reduces or prevents survival of human peripheral blood eosinophils in the presence of IL-5 and/or GM-CSF and/or IL-3; (vi) reduces or prevents IL-3-induced tumor necrosis factor (TNF) a release from human mast cells; (vii) reduces or prevents IL-3-induced IL-13 release from human mast cells; (viii) reduces or prevents potentiation of IgE-mediated IL-8 release from human mast cells by IL-3 and/or IL-5 and/or GM-CSF; or (ix) reduces or prevents formation of colony forming units-granulocytes-macrophages (CFU-GM) by CD34+ human bone marrow cells cultured in the presence of stem cell factor (SCF), GM-CSF, IL-3 and IL-5.
Claim 14 of Pat. 573 teaches: the CD131-binding protein of claim 11, wherein if the VH and VL are in a single polypeptide chain, the protein is: a single chain Fv fragment (scFv); (ii) a dimeric scFv (di-scFv); (iii) one of (i) or (ii) linked to a constant region of an antibody, Fc or a heavy chain constant domain (CH) 2 and/or CH3; or (iv) one of (i) or (ii) linked to a protein that binds to an immune effector cell, or if the VH and VL are in separate polypeptide chains the protein is: (i) a diabody; (ii) a triabody; (iii) a tetrabody; (iv) a Fab; (v) a F(ab′)2; (vi) a Fv; (vii) one of (i) to (vi) linked to a constant region of an antibody, Fc or a heavy chain constant domain (CH) 2 and/or CH3; (viii) one of (i) to (vi) linked to a protein that binds to an immune effector cell; or (ix) an antibody.
Taken together, the claims of Pat. 573 teach a CD131-binding protein comprising an antigen binding domain of an antibody, wherein the antigen binding domain binds to or specifically binds to CD131 and neutralizes signaling by interleukin (IL)-3, IL-5 and granulocyte-macrophage colony stimulating factor (GM-CSF). Thus, the claims of Pat. 573 teach the compounds of the instant claims. However, the claims of Pat. 573 do not teach the method of treating inflammatory skin condition as instantly claimed.
Owczarek and Dudeck’s teachings are described above. For example, Owczarek teaches that CD131 antibodies (such as 9A2-VR24.29) can be used to treat conditions caused or exacerbated by signaling through CD131. In one example, the condition is an allergic condition, for example atopic dermatitis, exfoliative dermatitis. Owczarek teaches dosages and timing of administration for these antibodies to a subject in need. Owczarek further teaches that myeloid cells include neutrophils, basophils, plasmacytoid dendritic cells (pDCs), mast cells and CD34+ BM cells. 9A2-VR24.29 inhibits activation and survival of myeloid cells stimulated with IL-3, GM-CSF and IL-5. Dudeck teaches that mast cell are essential promoters of contact hypersensitivity. Selective mast cell deficiency results in an almost complete abrogation of the allergic T cell response.
It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to combine the teachings of the claims of Pat. 834, Owczarek and Dudeck and to apply the method of Owaczarek for treating allergic contact dermatitis. One of ordinary skill in the art would have had a reasonable expectation that 9A2-VR24.29 would be effective for allergic contact dermatitis because: 1) 9A2-VR24.29 can be used to treat allergic and inflammatory skin condition; 2) 9A2-VR24.29 can 9A2-VR24.29 can inhibit this effect of IL-3 on mast cells and reduce mast cells in vitro and in vivo as taught by Owczarek; 3) mast cells are essential for hypersensitivity reaction in allergic contact dermatitis as taught by Dudeck. The motivation would have been to extend the application of the antibody and to develop a new treatment for type IV hypersensitivity skin condition.
Response to Arguments
For the Double Patenting rejections, Applicant argues:
As explained above, nothing in Owczarek, Dudeck, or Fernandez cures this deficiency. For example, Owczarek does not teach or suggest the use of CSL311 (9A2-VR24.29) for the treatment of type IV hypersensitivity skin conditions, nor does it provide a basis for a reasonable expectation that treatment with an antibody comprising the six CDRs of CSL311 would reduce or eliminate inflammation associated with type IV hypersensitivity skin conditions, as claimed. And neither Dudeck nor Fernandez teach use of an antibody comprising the six CDRs of CSL311 at all, much less suggest its efficacy for reducing or eliminating an inflammatory skin condition, as claimed.
Applicant is reiterating the arguments set forth above. Thus, for the reasons set forth above the rejection is maintained.
Conclusion
No claims are allowed.
THIS ACTION IS MADE FINAL. 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 CHENG LU whose telephone number is (571)272-0334. The examiner can normally be reached Monday-Friday 8-5.
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, Samira Jean-Louis can be reached at (571)270-3503. The fax phone number for the 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.
/CHENG LU/Examiner, Art Unit 1642
/SAMIRA J JEAN-LOUIS/Supervisory Patent Examiner, Art Unit 1642
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