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 Applicant’s election with traverse of species: 1) contact dermatitis; 2) a n antibody variable region comprising a V H comprising three CDRs of a V H comprising an amino acid sequence set forth in SEQ ID NO: 6 and a V L comprising three CDRs of a V L comprising an amino acid sequence set forth in SEQ ID NO: 18 ; 3) a combination of clauses a), b), and c) in the reply filed on February 18, 2026 is acknowledged. Applicant’s traverse the election of species requirement on the basis that the Office has not shown that a serious burden exists to examine all of the alleged species together. Regarding Applicant’s arguments about search and examination burden, the instant application is a National Stage application filed under 35 U.S.C. §371 and the restriction of the various groups is determined with respect to unity of invention as covered in Chapter 1800 of the MPEP. See MPEP 801. Burden of search is not the criteria for proper restriction under 37 C.F.R. 1.475, PCT article 17(3) (a), and 37 C.F.R 1.476 (c). Thus, Applicant’s arguments are not found persuasive. Nevertheless, after reconsideration, the election of species requirement set forth in the previous office action of 12/19/2025 is hereby withdrawn . All species encompassed by the pending claims would be under consideration. In view of the withdrawal of the restriction requirement, applicant(s) are advised that if any claim presented in a divisional application is anticipated by, or includes all the limitations of, a claim that is allowable in the present application, such claim may be subject to provisional statutory and/or nonstatutory double patenting rejections over the claims of the instant application. Once the restriction requirement is withdrawn, the provisions of 35 U.S.C. 121 are no longer applicable. See In re Ziegler , 443 F.2d 1211, 1215, 170 USPQ 129, 131-32 (CCPA 1971). See also MPEP § 804.01. Claims 1-15, 18 and 19 are pending and under consideration. Priority It is acknowledged that t his application is a 371 of International Application No. PCT/AU2021/051442, filed on December 3, 2021, which claims priority of Australian Patent Application No. 2020904494, filed on December 4, 2020, and Australian Patent Application No. 2021901818, filed on June 17, 2021. Certified copies of foreign priority applications have been received as required by 37 CFR 1.55. The priority date has been established as December 4, 2020. Information Disclosure Statement The Information Disclosure Statement filed on 05/30/2023 ha s been considered and entered by examiner . Sequence Interpretation The Office interprets claims comprising SEQ ID NOs: in the following manner: "comprising a sequence set forth in SEQ ID NO: XX " requires only a 2mer of SEQ ID NO: XX , "comprising the sequence of SEQ ID NO: XX " requires the full-length sequence with 100% identity to SEQ ID NO: XX with any N-/C-terminal additions or any 5'/3' additions . “ compris e residues in the region of xxxx of SEQ ID NO: XX” requires any two residues within the recited region. Claim Rejections - 35 USC § 112 The following is a quotation of 35 U.S.C. 112(b): (b ) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention. The following is a quotation of 35 U.S.C. 112 (pre-AIA), second paragraph: The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the appl icant regards as his invention. Claim 15 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention. Claim 15 recites “domain 1 of a CD131” and “domain 4 of another CD131”, which render the claim indefinite. The domain 1 and domain 4 is not clearly defined by the specification or in the art. One of ordinary skill in the art would not be reasonably apprised of the scope of the invention. It is not clear which amino acids of CD131 constitute “domain 1” or “domain 4” of CD131. Claim Rejections - 35 USC § 112 The following is a quotation of 35 U.S.C. 112(d): (d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers. The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph: Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers. Claim 1 2 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Claim 1 2 depends from claim 1 1 , which is directed to a protein comprising a Fv. Claim 1 2 , subpart (viii) is directed to the protein of claim 1 1 comprising a Fv, and this property of claim 1 2 (viii) does not limit the scope of the protein of claim 1 1 . It is noted that since the embodiments of claim 1 2 are given in the alternative, this rejection is deemed appropriate. Applicant may cancel the claim, amend the claim to place the claim in proper dependent form, rewrite the claim in independent form, or present a sufficient showing that the dependent claim complies with the statutory requirements. Claim Rejections - 35 USC § 112 The following is a quotation of the first paragraph of 35 U.S.C. 112(a): (a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention. The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112: The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention. Claim s 1-15, 18 and 19 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. This is a WRITTEN DESCRIPTION rejection . The claims are drawn to a method for treating an inflammatory skin condition in a subject, the method comprising administering a compound that binds to CD131 and neutralizes signaling by granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL) 5 to the subject . Paragraph [0191] of the instant publication US 2023/0406943 A1 states: “A "compound", as contemplated by the present disclosure, can take any of a variety of forms including natural compounds, chemical small molecule compounds or biological compounds or macromolecules. Exemplary compounds include an antibody or a protein comprising an antigen binding fragment of an antibody, a nucleic acid, a polypeptide, a peptide, and a small molecule”. These compounds vary significantly, have different structures and physical/chemical properties, and function through different mechanisms. However, t he specification teaches only one antibody: CSL311 which has the required functionality/property to be used in the claimed method. No other types of compounds that binds to CD131 and neutralizes signaling by GM-CSM and IL-5 have been disclosed. No other antibodies (comprising different CDRs from CSL311) that binds to CD131 and neutralizes signaling by GM-CSM and IL-5 have been disclosed. Thus, the specification lacks written description support for the broadly claimed compounds that bind to CD131 and neutralizes signaling by GM-CSF and IL-5. Vas-Gath, Inc. v" Mahurkar , 19 USPQ2d 1111, makes clear that "to satisfy the written description requirement, an applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention, and that the invention, in that context, is whatever is now claimed". The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics . i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus. See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406. However, in view of the above, the specification does not provide adequate written description of claimed compounds . Specifically, Applicant fails to disclose any compounds that bind to CD131 and neutralizes signaling by GM-CSF and IL-5, besides a specific antibody (CSL311) (see Examples 1-3) , and therefore does not represent the substantial variety covered by the genus of compound s encompassed by the claims. The Specification does not provide support and disclosure for all imaginable compounds having said property or effect and there is no general knowledge of this kind available to the person skilled in the art. In addition, the claims identify the compounds (including antibody or antigen binding site) by function only, where the function is to: binding to CD131 and neutralizing signaling by GM-CSF and IL-5 (claim s 1 , 9 ) ; or GM-CSF, IL-5 and IL- 3 (claim 7 ); treating inflammatory skin condition, including a contact dermatitis or atopic dermatitis (claims 3-5); reduc ing swelling at the site of inflammation , and/or reduc ing mast cell infiltration at the site of inflammation , and/or reduc ing neutrophil infiltration at the site of inflammation , and/or reduc ing CD8+ T cell infiltration at the site of inflammation ; and/or reduc ing eosinophil infiltration at the site of inflammation (claim 6 ) ; inhibiting GM-CSF-induced proliferation of TF-1 cells with an IC50 of at least 100 nM ; and/or inhibiting IL-5-induced proliferation of TF-1 cells with an IC50 of at least 100 nM ; and/or inhibiting IL-3-induced proliferation of TF-1 cells with an IC50 of at least 100 nM (claim 8); K D for a polypeptide comprising s sequence set forth in SEQ ID NO: 5 is about 10 nM or less (claim 10); competing with 9A2-VR24.29 (claim 13); binding to an epitope within Site 2 or CD131, and/or binding to an epitope formed upon dimerization of two CD131 polypeptides; and/or binding to residues within domain 1 of a CD131 polypeptide and residues within domain 4 of another CD131 polypeptide and/or binding to specific residues (claims 15 and 1 8 ) . The specification and prior art have not established the relationship between the claimed functions and the structure of the compound . One of ordinary skilled in the art would not be able to readily recognize/visualize an antibody with required properties. Taken together, applicant has not provided sufficient evidence to show that the inventors possess a genus of compounds binding to CD131 and neutralizing signaling by GM-CSF and IL-5 which can be used in the claimed method. In addition, by the time the invention was made, it is well established in the art that the formation of an intact antigen-binding site in an antibody usually required the association of the complete heavy and light chain variable regions of a given antibody, each of which consists of three "complementarity determining regions" ("CDRs") which provide the majority of the contact residues for the binding of the antibody to its target epitope. Even a single point mutation in HCDR1 region could lead to antibody lose its binding activity (Ni et al., The Protein Journal, 43, pp. 683-696, July 2024, see Abstract). Wong (Wong et al., MABS, 2021, Vol. 13, No. 1, e1873478, Publication Year: 2021) teaches that sequence-distant antibodies can target the same epitope (Abstract). Thus, one ordinary skill in the art would not be able to visualize other antibody or antigen binding site thereof encompassed by the claims (including single domain antibody of claim 13) , which binds to CD131 and neutralizing signaling by GM-CSF and IL-5 and can be used to treat inflammatory skin condition, based on only one antibody CSL311. Claim 19 recites sequences of the CD131 binding protein: “ (a) an antibody variable region comprising a V H comprising three CDRs of a V H comprising an amino acid sequence set forth in SEQ ID NO: 6 and a V L comprising three CDRs of a V L comprising an amino acid sequence set forth in SEQ ID NO: 18; and/or (b) a VH comprising an amino acid sequence set forth in SEQ ID NO: 6 and a VL comprising a n amino acid sequence set forth in SEQ ID NO: 18; and/or (c) a heavy chain comprising an amino acid sequence set forth in SEQ ID NO: 14 and a light chain comprising an amino acid sequence set forth in SEQ ID NO: 15 ” . As such by the recitation of “ an amino acid sequence set forth in ” that is underlined above, the components of the specific protein encompass components that comprise partial sequences of recited SEQ ID NOs (i.e., “ an amino acid sequence set forth in” rather than “ the amino acid sequence of” a recited SEQ ID NO). As set forth above, a function antibody requires a complete set of HCDRs 1-3 and LCDRs 1-3 , but claim 19 encompasses proteins which do not have the complete set of HCDRs: 1-3 and LCDRs: 1-3. Although Applicants may argue that it is possible to screen for compounds (including antibodies ) with claimed properties/functions , the court found in (Rochester v. Searle, 358 F.3d 916, Fed Cir., 2004) that screening assays are not sufficient to provide adequate written description for an invention because they are merely a wish or plan for obtaining the claimed chemical invention. "As we held in Lilly, "[a]n adequate written description of a DNA ... 'requires a precise definition, such as by structure, formula, chemical name, or physical properties,' not a mere wish or plan for obtaining the claimed chemical invention." 119 F.3d at 1566 (quoting Fiers , 984 F.2d at 1171 ). For reasons stated above, that requirement applies just as well to non-DNA (or RNA) chemical inventions." Knowledge of screening methods provides no information about the structure of any future antibodies or antibody fragments yet to be discovered that may function as claimed. Taken together, the instant specification has not provided a sufficient description showing the necessary functional characteristics coupled with a known or disclosed correlation between functions and the structure . Thus, the specification is not sufficient to show the applicant was in possession of the genus of compounds broadly encompassed for the claimed method . Claims 1-15, 18 and 19 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, because the specification, while being enabling for : a method for reducing or eliminating an inflammatory skin condition in a subject, the method comprising administering a compound that binds to CD131 and neutralizes signaling by granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL) 5 to the subject , wherein the compound is CSL311 ; does not reasonably provide enablement for : a method for treating an inflammatory skin condition in a subject, the method comprising administering a compound that binds to CD131 and neutralizes signaling by granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL) 5 to the subject . The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims. This is a SCOPE of ENABLEMENT rejection . To be enabling, the specification must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation. In re Wright , 999 F.2d 1557, 1561 (Fed. Cir.,1993). Explaining what is meant by "undue experimentation," the Federal Circuit has stated that: The test is not merely quantitative, since a considerable amount of experimentation is permissible, if it is merely routine, or if the specification in question provides a reasonable amount of guidance with respect to the direction in which experimentation should proceed to enable the determination of how to practice a desired embodiment of the claimed invention. PPG v. Guardian, 75 F.3d 1558, 1564 (Fed. Cir. 1996). The factors that may be considered in determining whether a disclosure would require undue experimentation are set forth by In re Wands , 8 USPQ2d 1400 (CAFC 1988) at 1404 wherein, citing Ex parte Forman , 230 USPQ 546 (Bd. Apls. 1986) at 547, the court recited eight factors to consider when assessing whether or not a disclosure would require undue experimentation. These factors are: 1) the quantity of experimentation necessary, 2) the amount of direction or guidance provided, 3) the presence or absence of working examples, 4) the nature of the invention 5) the state of the art, 6) the relative skill of those in the art, 7) the predictability of the art and 8) the breadth of the claims. These factors are always applied against the background understanding that scope of enablement varies inversely with the degree of unpredictability involved. In re Fisher , 57 CCPA 1099, 1108,427 F.2d 833, 839, 166 USPQ 18, 24 (1970). Keeping that in mind, the Wands factors are relevant to the instant fact situation for the following reasons: The claims are drawn to a method for treating an inflammatory skin condition in a subject, the method comprising administering a compound that binds to CD131 and neutralizes signaling by granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL) 5 to the subject . Based on paragraph [0191] of the instant publication US 2023/0406943 A1: the term “treating” would encompass preventing a condition . Thus, the claims encompass methods of preventing a inflammatory skin condition by administering a broad genus of compounds that bind to CD131 and neutralizes signaling by granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL) 5 to the subject. As set forth above, the claims encompass a broad genus of compounds such as an antibody or a protein comprising an antigen binding fragment of an antibody, a nucleic acid, a polypeptide, a peptide, and a small molecule. These compounds vary significantly, have different structures and physical/chemical properties, and function through different mechanisms. However, the specification teaches only one antibody: CSL311 which has the required functionality/property to be used in the claimed method. No other types of compounds that binds to CD131 and neutralizes signaling by GM-CSM and IL-5 have been disclosed. No other antibodies (comprising different CDRs from CSL311) that binds to CD131 and neutralizes signaling by GM-CSM and IL-5 have been disclosed. Even only considering antibodies or proteins comprising antigen-binding site, by the time the invention was made, it is well established in the art that the formation of an intact antigen-binding site in an antibody usually required the association of the complete heavy and light chain variable regions of a given antibody, each of which consists of three "complementarity determining regions" ("CDRs") which provide the majority of the contact residues for the binding of the antibody to its target epitope. Even a single point mutation in HCDR1 region could lead to antibody lose its binding activity (Ni et al., The Protein Journal, 43, pp. 683-696, July 2024, see Abstract). Wong (Wong et al., MABS, 2021, Vol. 13, No. 1, e1873478, Publication Year: 2021) teaches that sequence-distant antibodies can target the same epitope (Abstract). Thus, one ordinary skill in the art would not be able to predict which antibody or antigen binding site thereof encompassed by the claims can be used to treat inflammatory skin condition, based on only one antibody CSL311. The working example of the specification and prior art teach one antibody: CSL311 which can bind CD131 and neutralize signaling by GM-CSF and IL-5 and shows therapeutic activity to atopic dermatitis and contact dermatitis (Examples 1-3). However, working examples do not support the scope of the claims which encompass preventing inflammatory skin condition and/or the broadly claimed compounds. The factors outlined in In Re Wands' mentioned above apply here, and in particular as per the MPEP 2164.01 (a): "A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation. In re Wright 999 F.2d 1557, 1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993)." It is very clear that one could not make/use this very broad invention that has no working examples in this unpredictable art without undue experimentation. Genetech Inc vs Nova Nordisk 42 USPQ 2d 1001 "A patent is not a hunting license. It is not a reward for search but compensation for its successful conclusion and patent protection is granted in return for an enabling disclosure of an invention, not for vague intimations of general ideas that may or may not be workable .” Given the numerous unspecified compounds encompassed by claim 1, the lack of specific guidance and the insufficient working example s , undue experimentation would be required of one of skilled in the art to produce the invention commensurate with the scope of the method as claimed. 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 1, 2, 4, 6-15, 18, 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), 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). 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 the antibodies can be used to treat conditions caused or exacerbated by signaling through CD131 ([1143]). In one example, the condition is an allergic condition, for example atopic dermatitis, 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]). Taken together, although Owczarek teaches every components of instant claim 1, Owczarek does not teach all the components in a single embodiment. It would have prima facie been obvious to one of ordinarily skilled in the art at the time the invention was filed to relate the all the teachings of Owczarek and to develop the claimed method e.g. treating atopic dermatitis with 9A2-VR24.29, with a reasonable expectation of success, because Owczarek teaches that condition such as atopic dermatitis is a condition caused or exacerbated by signaling through CD131 and 9A2-VR24.29 is suitable for treating such conditions as taught by Owczarek . The motivation would have been to develop a new treatment for atopic dermatitis. Regarding claim 2, as evidenced by Fernandez, atopic dermatitis is a Type I hypersensitive reaction (§ Type I hypersensitivity reactions). Thus, Owczarek teaches treating atopic dermatitis would read on the instant claim 2. 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 USPQ 2d 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. Regarding claim 7, Owczarek teaches that antibody 9A2 inhibits signaling IL-3, IL-5 and GM-CSF ([1262], [1263]). Regarding claim 8, Owczarek teaches that 9A2 is an antagonist of GM-CSF and IL-5 activity with an IC50 of 456 nM (GM-CSF) in the TF-1 cell proliferation assay (Fig. 6B; [1264]; and Table 3). Regarding claim 9, given Broadest Reasonable Interpretation (BRI), antibody 9A2-VR24.29 is a protein comprising an antigen binding site that binds to CD131. Regarding claim 10, it is noted that SEQ ID NO:5 of instant application represents the amino acid sequence of soluble Homo sapiens CD131. Owczarek teaches that 9A2-VR24.29 has a KD of 0.1 nM to soluble human CD131 (shCD131) using surface plasmon resonance ([0804]), the antigen is immobilized on solid surface ([1089], [1232]). Regarding claims 11, 9A2-VR24.29 comprises a variable domain which reads on Fv. Regarding claims 12, 9A2-VR24.29 is an antibody. Regarding claim 13, Owczarek teaches in some examples, the CD131 binding protein is or comprises a single-domain antibody ([0998]) Regarding claims 14, 9A2-VR24.29 would competitively inhibit the binding of antibody 9A2-VR24.29. Regarding claims 15 and 18, Owczarek teaches 9A2-VR24.29 binds to an epitope within Site 2 of CD131 ([1281] and [1282]). Owczarek teaches the antigen binding domain binds to an epitope formed upon dimerization of two CD131 polypeptides. For example, the antigen binding domain binds to residues within domain 1 of a CD131 polypeptide and residues within domain 4 of another CD131 polypeptide ([0019], claim 1). Figure 20 of Owczarek teaches that domain 1 comprises residues in the region of 101-107 of CD131, domain 4 comprises residues in the region 364-367 of CD131 ([0814]). Regarding claim 19, 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 Claim s 3 and 5 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) as applied to claims 1, 2, 4, 6-15, 18, and 19 above, and further in view of Dudeck ( Dudeck et al., Immunity, 34, 973-984, Publication Date: 06/24/2011). It’s noted that allergic contact dermatitis is a n example of type IV hypersensitivity reaction, as evidenced by paragraph [0224] of the instant publication. Owczarek teaches the method of instant claim 1: treating a skin condition such as atopic dermatitis with 9A2-VR24.29 which bind to CD131 and neutralizes signaling by GM-CSF 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]). D udeck 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). 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 vascula ture (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 at 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 mast cells are essential for hypersensitivity reaction in allergic contact dermatitis as taught by Dudeck , and 9A2-VR24.29 can effectively inhibit mast cells both in vitro and in vivo as taught by Owaczarek . The motivation would have been to extend the application of the antibody. 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 1-15, 18 and 19 are rejected on the ground of nonstatutory double patenting a s being unpatentable over claims 1-5 of U.S. Patent No. 10,894,834 B2 (hereinafter Pat. 834 , Appl. No. 15/779,252 ) in view of Owczarek ( Owczarek et al., US 2019/0062438 A1, Publication Date: 02/28/2019) and Dudeck ( Dudeck et al., Immunity, 34, 973-984, Publication Date: 06/24/2011), 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). 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 V H comprising CDRs 1, 2 and 3 of the sequence set forth in SEQ ID NO: 64 and a V L comprising CDRs 1, 2 and 3 of the sequence set forth in SEQ ID NO: 5; or (ii) a V H comprising the sequence set forth in SEQ ID NO: 64 and a V L 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 V H and V L 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 (C H ) 2 and/or C H 3; or (iv) one of ( i ) or (ii) linked to a protein that binds to an immune effector cell, or if the V H and V L 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 (C H ) 2 and/or C H 3; (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 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 all the teachings of the claims of Pat. 834, Owczarek and to develop the claimed method e.g. treating atopic dermatitis with 9A2-VR24.29, with a reasonable expectation of success, because Owczarek teaches that condition such as atopic dermatitis is a condition caused or exacerbated by signaling through CD131 and 9A2-VR24.29 is suitable for treating such conditions as taught by Owczarek . The motivation would have been to develop a new treatment for atopic dermatitis. Regarding claims 3 and 5, i t 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 mast cells are essential for hypersensitivity reaction in allergic contact dermatitis as taught by Dudeck , and 9A2-VR24.29 can effectively inhibit mast cells both in vitro and in vivo as taught by Owaczarek . The motivation would have been to extend the application of the antibody. U.S. Patent No. 1 1,840,573 Claims 1-15, 18 and 19 are rejected on the ground of nonstatutory double patenting a s being unpatentable over claims 1-20 of U.S. Patent No. 11,840,573 B2 (hereinafter Pat. 573, Appl. No. 16/953,499) in view of Owczarek ( Owczarek et al., US 2019/0062438 A1, Publication Date: 02/28/2019) and Dudeck ( Dudeck et al., Immunity, 34, 973-984, Publication Date: 06/24/2011), 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). 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 1 1 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 V H comprising CDRs 1, 2 and 3 of the sequence set forth in SEQ ID NO: 64 and a V L 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: t he 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: th e CD131-binding protein of claim 11, wherein if the V H and V L 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 (C H ) 2 and/or C H 3; or (iv) one of ( i ) or (ii) linked to a protein that binds to an immune effector cell, or if the V H and V L 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 (C H ) 2 and/or C H 3; (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 r