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 .
2. Applicant’s amendment on 05/03/2024 is acknowledged. Claims 1-13 and 17-23 are pending and under consideration.
3. Applicant’s IDS documents filed on 05/03/2024 and 09/25/2026 have been considered.
4. 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.
5. Claims 1-6, 9-13 and 17-23 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-19 of U.S. Patent No. 11,203,628 (PTO-892; Reference A).
Although the claims at issue are not identical, they are not patentably distinct from each other because claims 1-19 of US Patent are directed to a mutated CD200 protein, comprising an amino acid sequence with at least about 99% sequence identity to SEQ ID NO: 1, wherein said amino acid sequence additionally comprises at least one substitution mutation selected from K130Y and I131Y, and wherein the mutated CD200 protein is an agonist of the CD200 receptor of claim 1; which comprises one or more additional mutations selected from G1291, F128R, and N81K of claim 2; comprising the sequence of SEQ ID NO: 12 or SEQ ID NO: 13 of claim 3; a mutated CD200 protein extracellular domain, comprising: an amino acid sequence with at least about 99% sequence identity to SEQ ID NO: 2, wherein said amino acid sequence additionally comprises at least one substitution mutation selected from K130Y and I131Y, wherein residue positions 130 and 131 correspond to residue numbering of SEQ ID NO: 1, wherein the mutated CD200 protein extracellular domain binds the CD200 receptor, and wherein the mutated CD200 protein is an agonist of the CD200 receptor of claim 4; comprising the sequence of SEQ ID NO: 3 or SEQ ID NO: 4 of claim 5; a fusion protein, comprising: the mutated CD200 protein extracellular domain of claim 4 fused to a non-CD200 protein or peptide that does not bind a CD200 receptor, wherein an optional linker portion links the mutated CD200 protein extracellular domain and the non-CD200 protein or peptide of claim 6; wherein said linker portion is a peptide comprising between 1 and 15 amino acids of claim 7; wherein said non-CD200 protein or peptide is an antibody or fragment thereof of claim 8; wherein said non-CD200 protein or peptide is an Fc fragment of claim 9; comprising the sequence of SEQ ID NO: 6 or SEQ ID NO: 7 of claim 10; a polynucleotide encoding a protein of claim 1 of claim 11; a pharmaceutical composition comprising the protein of claim 1 of claim 12; a method for the treatment of autoimmune disease, comprising: providing the pharmaceutical composition of claim 14 of claim 13; a method for the treatment of autoimmune disease, comprising: providing the protein of claim 1 of claim 14; wherein said non-CD200 protein or peptide is an antibody or fragment thereof of claim 15; a polynucleotide encoding a protein of claim 4 of claim 16; a pharmaceutical composition comprising the protein of claim 3 of claim 17; a method for treatment of autoimmune disease, comprising providing the pharmaceutical composition of claim 18 and a method for the treatment of autoimmune disease, comprising: providing the protein of claim 4 of claim 19.
Instant SEQ ID NO:26 is 100% sequence identical to reference SEQ ID NO:2
Instant SEQ ID NO:26 is 99.5% sequence identical to reference SEQ ID NOs:4 and 7.
Instant SEQ ID NO:27 is 99.7% sequence identical to reference SEQ ID NO:13.
Instant SEQ ID NO:27 is 99.5% sequence identical to reference SEQ ID NO:12.
Instant SEQ ID NOs 1-22 are encompassed by the reference fusion proteins with the recited reference amino acid changes.
The reference teachings anticipate the claimed invention.
6. Claims 1-13 and 17-23 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-26 of copending Application No. 18/863,133(reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because claims 1-26 are directed to a fusion protein comprising:(i) a mutated CD200 portion comprising mutations at amino acid residue positions 130 and 131, wherein said mutations are K130Y and 1131Y; and(ii) a non-CD200 portion, wherein said non-CD200 portion is an IgG4 Fc fragment and comprises an S228P mutation according to the EU numbering system and deletion of the first 5 amino acids of the hinge, wherein Glycine 232 of the mutated CD200 portion is directly fused to the non-CD200 IgG4 Fc fragment at amino acid 6 according to the IMGT numbering system of claim 1; wherein the fusion protein comprises the amino acid sequence of SEQ ID NO: 1 of claim 2; wherein the fusion protein consists of the amino acid sequence of SEQ ID NO: 1 of claim 3; wherein the mutated CD200 portion comprises an N terminal signal sequence representing the first 30 amino acids of the CD200 portion of claim 4; wherein the N-terminal signal sequence is a human IgG chain signal peptide of claim 5; wherein the N-terminal signal sequence comprises the amino acid sequence of SEQ ID NO; 3 of claim 6; wherein the fusion protein comprises the amino acid sequence of SEQ ID NO: 2 of claim 7; wherein the N-terminal signal sequence is cleaved prior to secretion from a cell of claim 8; which is a modulator of the CD200 receptor of claim 9; which is an agonist of the CD200 receptor of claim 10; wherein the fusion protein inhibits cytokine secretion of claim 11; wherein the cytokine is IL-6 of claim 12; wherein the cytokine is IL-8 of claim 13; wherein the cytokine is TNFa of claim 14; wherein the fusion protein inhibits ERK activation to a greater extent than wild-type CD200-Fc fusion protein of claim 15; a polynucleotide encoding the fusion protein of claim 16; a composition comprising the fusion protein and a pharmaceutically acceptable carrier of claim 17; a method of treating a subject having an autoimmune disease, an allergic disease, a neurodegenerative disorder, neuropathic pain, an inflammatory disorder, Th2- induced airway inflammation, or diabetic neuropathy, comprising administering to the subject the fusion protein of claim 18; wherein the is the subject has rheumatoid arthritis, asthma, or atopic dermatitis of claim 19; wherein the subject has an autoimmune disease affecting a neuromuscular system, vascular system, eye, skin, digestive tract, lung, kidney, liver, peripheral or central nervous system, bone, cartilage or joints of claim 20; wherein the subject has acute disseminated encephalomyelitis (ADEM); acute necrotizing haemorrhagic leukoencephalitis; Addison's disease; agammaglobulinemia; alopecia areata; amyloidosis; ankylosing spondylitis; anti- GBM/anti-TBM nephritis; antiphospholipid syndrome (APS); asthma, atopic dermatitis; Autoimmune angioedema; autoimmune aplastic anemia; autoimmune dysautonomia; autoimmune hepatitis; autoimmune hyperlipidemia; autoimmune immunodeficiency; autoimmune inner ear disease (AIED); autoimmune myocarditis; autoimmune oophoritis; autoimmune pancreatitis; autoimmune retinopathy; autoimmune thrombocytopenic purpura (ATP); autoimmune thyroid disease; autoimmune urticarial; axonal & neuronal neuropathies; Balo disease; Behcet's disease; bullous pemphigoid and related autoimmune blistering diseases; cardiomyopathy; Castleman disease; celiac disease (such as refractory celiac disease type II); Chagas disease; chronic idiopathic urticaria; chronic inflammatory demyelinating polyneuropathy (CIDP); chronic recurrent multifocal ostomyelitis (CRMO); chronic spontaneous urticaria; Churg-Strauss syndrome; cicatricial pemphigoid/benign mucosal pemphigoid; Crohn's disease; Cogans syndrome; cold agglutinin disease; congenital heart block; Coxsackie myocarditis; CREST disease; essential mixed cryoglobulinemia; demyelinating neuropathies; dermatitis herpetiformis; dermatomyositis; Devic's disease (neuromyelitis optica); discoid lupus; Dressler's syndrome; endometriosis; eosinophilic esophagitis; eosinophilic fasciitis; erythema nodosum; experimental allergic encephalomyelitis; Evans syndrome; fibrosing alveolitis; giant cell arteritis (temporal arteritis); giant cell myocarditis; glomerulonephritis; Goodpasture's syndrome; granulomatosis with polyangiitis (GPA) (Wegener's granulomatosis); graft-versus- host disease (GvHD); Graves' disease; Guillain-Barre syndrome; Hashimoto's encephalitis; Hashimoto's thyroiditis; hemolytic anemia; Henoch-Schonlein purpura; herpes gestationis; hypogammaglobulinemia; idiopathic thrombocytopenic purpura (ITP); IgA nephropathy; IgG4- related sclerosing disease; immunoregulatory lipoproteins; inclusion body myositis; inflammatory bowel disorder (IBD); inflammatory skin disease; interstitial cystitis; juvenile arthritis; juvenile diabetes (type 1 diabetes); juvenile myositis; Kawasaki syndrome; Lambert- Eaton syndrome; leukocytoclastic vasculitis; lichen planus; lichen sclerosus; ligneous conjunctivitis; linear IgA disease (LAD); lupus (SLE); lyme disease, chronic; macrophage activation syndrome (MAS); mastocytosis; Meniere's disease; microscopic polyangiitis; mixed connective tissue disease (MCTD); Mooren's ulcer; Mucha-Habermann disease; multiple sclerosis; myasthenia gravis; myositis; narcolepsy; neuromyelitis optica (Devic's); neutropenia; ocular cicatricial pemphigoid; optic neuritis; palindromic rheumatism; PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus); paraneoplastic cerebellar degeneration; paroxysmal nocturnal hemoglobinuria (PNH); Parry Romberg syndrome; Parsonnage-Turner syndrome; pars planitis (peripheral uveitis); pemphigus; peripheral neuropathy; perivenous encephalomyelitis; pernicious anemia; POEMS syndrome; polyarteritis nodosa; type I, II, & III autoimmune polyglandular syndromes; polymyalgia rheumatic; polymyositis; postmyocardial infarction syndrome; postpericardiotomy syndrome; progesterone dermatitis; primary biliary cirrhosis; primary sclerosing cholangitis; psoriasis; psoriatic arthritis; idiopathic pulmonary fibrosis; pyoderma gangrenosum; pure red cell aplasia; Raynauds phenomenon; reactive arthritis; reflex sympathetic dystrophy; Reiter's syndrome; relapsing polychondritis; restless legs syndrome; retroperitoneal fibrosis; rheumatic fever; rheumatoid arthritis; sarcoidosis; Schmidt syndrome; scleritis; scleroderma; Sjogren's syndrome; sperm & testicular autoimmunity; stiff person syndrome; subacute bacterial endocarditis (SBE); Susac's syndroms; sympathetic ophthalmia; Takayasu's arteritis; temporal arteritis/giant cell arteritis; thrombocytopenic purpura (TTP); Tolosa-Hunt syndrome; transverse myelitis; type 1 diabetes; ulcerative colitis; undifferentiated connective tissue disease (UCTD); uveitis; vasculitis; vesiculobullous dermatosis; or vitiligo of claim 21; wherein the fusion protein is administered as the sole therapeutic agent of claim 22; wherein the fusion protein is administered in combination with one of more other pharmaceutical agents indicated for treatment of an autoimmune disease, an allergic disease, a neurodegenerative disorder, neuropathic pain, an inflammatory disorder, Th2-induced airway inflammation, or diabetic neuropathy of claim 23; wherein the fusion protein is administered in combination with one or more immunosuppressive agents or adjuvants in immunosuppression therapy of claim 24; wherein the fusion protein is administered in combination with azathioprine, a methotrexate, a cyclosporine, a monoclonal antibody, a corticosteroid, or a combination thereof of claim 25; and
wherein the monoclonal antibody is basiliximab, daclizumab, or muromonab of claim 26.
Reference SEQ ID NOs 1 and 2 comprise 90% identical sequences to SEQ ID NOs 26 and 27.
Instant SEQ ID NOs 1-22 are encompassed by the reference fusion proteins with the recited reference amino acid changes.
The reference teachings anticipate the claimed invention.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
7. Claims 1-13 and 17-23 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-26 of copending Application No. 18/863,179 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because claims 1-26 are directed to a fusion protein comprising:(i) a mutated CD200 portion comprising mutations at amino acid residue positions 130 and 131, wherein said mutations are K130Y and 1131Y; and(ii) a non-CD200 portion, wherein said non-CD200 portion is an IgG4 Fc fragment and comprises an S228P mutation according to the EU numbering system and deletion of the first 5 amino acids of the hinge, wherein Glycine 232 of the mutated CD200 portion is directly fused to the non-CD200 IgG4 Fc fragment at amino acid 6 according to the IMGT numbering system of claim 1; wherein the fusion protein comprises the amino acid sequence of SEQ ID NO: 1 of claim 2; wherein the fusion protein consists of the amino acid sequence of SEQ ID NO: 1 of claim 3; wherein the mutated CD200 portion comprises an N terminal signal sequence representing the first 30 amino acids of the CD200 portion of claim 4; wherein the N-terminal signal sequence is a human IgG chain signal peptide of claim 5; wherein the N-terminal signal sequence comprises the amino acid sequence of SEQ ID NO; 3 of claim 6; wherein the fusion protein comprises the amino acid sequence of SEQ ID NO: 2 of claim 7; wherein the N-terminal signal sequence is cleaved prior to secretion from a cell of claim 8; which is a modulator of the CD200 receptor of claim 9; which is an agonist of the CD200 receptor of claim 10; wherein the fusion protein inhibits cytokine secretion of claim 11; wherein the cytokine is IL-6 of claim 12; wherein the cytokine is IL-8 of claim 13; wherein the cytokine is TNFa of claim 14; wherein the fusion protein inhibits ERK activation to a greater extent than wild-type CD200-Fc fusion protein of claim 15; a polynucleotide encoding the fusion protein of claim 16; a composition comprising the fusion protein and a pharmaceutically acceptable carrier of claim 17; a method of treating a subject having an autoimmune disease, an allergic disease, a neurodegenerative disorder, neuropathic pain, an inflammatory disorder, Th2- induced airway inflammation, or diabetic neuropathy, comprising administering to the subject the fusion protein or a polynucleotide encoding the fusion protein of claim 18; wherein the subject has hay fever, allergic rhinitis, allergic contact dermatitis, seasonal allergies, anaphylaxis, food allergies, asthma, or atopic dermatitis of claim 19; wherein the subject has an autoimmune disease affecting a neuromuscular system, vascular system, eye, skin, digestive tract, lung, kidney, liver, peripheral or central nervous system, bone, cartilage or joints of claim 20; wherein the subject has acute disseminated encephalomyelitis (ADEM); acute necrotizing haemorrhagic leukoencephalitis; Addison's disease; agammaglobulinemia; alopecia areata; amyloidosis; ankylosing spondylitis; anti- GBM/anti-TBM nephritis; antiphospholipid syndrome (APS); asthma, atopic dermatitis; Autoimmune angioedema; autoimmune aplastic anemia; autoimmune dysautonomia; autoimmune hepatitis; autoimmune hyperlipidemia; autoimmune immunodeficiency; autoimmune inner ear disease (AIED); autoimmune myocarditis; autoimmune oophoritis; autoimmune pancreatitis; autoimmune retinopathy; autoimmune thrombocytopenic purpura (ATP); autoimmune thyroid disease; autoimmune urticarial; axonal & neuronal neuropathies; Balo disease; Behcet's disease; bullous pemphigoid and related autoimmune blistering diseases; cardiomyopathy; Castleman disease; celiac disease (such as refractory celiac disease type II); Chagas disease; chronic idiopathic urticaria; chronic inflammatory demyelinating polyneuropathy (CIDP); chronic recurrent multifocal ostomyelitis (CRMO); chronic spontaneous urticaria; Churg-Strauss syndrome; cicatricial pemphigoid/benign mucosal pemphigoid; Crohn's disease; Cogans syndrome; cold agglutinin disease; congenital heart block; Coxsackie myocarditis; CREST disease; essential mixed cryoglobulinemia; demyelinating neuropathies; dermatitis herpetiformis; dermatomyositis; Devic's disease (neuromyelitis optica); discoid lupus; Dressler's syndrome; endometriosis; eosinophilic esophagitis; eosinophilic fasciitis; erythema nodosum; experimental allergic encephalomyelitis; Evans syndrome; fibrosing alveolitis; giant cell arteritis (temporal arteritis); giant cell myocarditis; glomerulonephritis; Goodpasture's syndrome; granulomatosis with polyangiitis (GPA) (Wegener's granulomatosis); graft-versus- host disease (GvHD); Graves' disease; Guillain-Barre syndrome; Hashimoto's encephalitis; Hashimoto's thyroiditis; hemolytic anemia; Henoch-Schonlein purpura; herpes gestationis; hypogammaglobulinemia; idiopathic thrombocytopenic purpura (ITP); IgA nephropathy; IgG4- related sclerosing disease; immunoregulatory lipoproteins; inclusion body myositis; inflammatory bowel disorder (IBD); inflammatory skin disease; interstitial cystitis; juvenile arthritis; juvenile diabetes (type 1 diabetes); juvenile myositis; Kawasaki syndrome; Lambert- Eaton syndrome; leukocytoclastic vasculitis; lichen planus; lichen sclerosus; ligneous conjunctivitis; linear IgA disease (LAD); lupus (SLE); lyme disease, chronic; macrophage activation syndrome (MAS); mastocytosis; Meniere's disease; microscopic polyangiitis; mixed connective tissue disease (MCTD); Mooren's ulcer; Mucha-Habermann disease; multiple sclerosis; myasthenia gravis; myositis; narcolepsy; neuromyelitis optica (Devic's); neutropenia; ocular cicatricial pemphigoid; optic neuritis; palindromic rheumatism; PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus); paraneoplastic cerebellar degeneration; paroxysmal nocturnal hemoglobinuria (PNH); Parry Romberg syndrome; Parsonnage-Turner syndrome; pars planitis (peripheral uveitis); pemphigus; peripheral neuropathy; perivenous encephalomyelitis; pernicious anemia; POEMS syndrome; polyarteritis nodosa; type I, II, & III autoimmune polyglandular syndromes; polymyalgia rheumatic; polymyositis; postmyocardial infarction syndrome; postpericardiotomy syndrome; progesterone dermatitis; primary biliary cirrhosis; primary sclerosing cholangitis; psoriasis; psoriatic arthritis; idiopathic pulmonary fibrosis; pyoderma gangrenosum; pure red cell aplasia; Raynauds phenomenon; reactive arthritis; reflex sympathetic dystrophy; Reiter's syndrome; relapsing polychondritis; restless legs syndrome; retroperitoneal fibrosis; rheumatic fever; rheumatoid arthritis; sarcoidosis; Schmidt syndrome; scleritis; scleroderma; Sjogren's syndrome; sperm & testicular autoimmunity; stiff person syndrome; subacute bacterial endocarditis (SBE); Susac's syndroms; sympathetic ophthalmia; Takayasu's arteritis; temporal arteritis/giant cell arteritis; thrombocytopenic purpura (TTP); Tolosa-Hunt syndrome; transverse myelitis; type 1 diabetes; ulcerative colitis; undifferentiated connective tissue disease (UCTD); uveitis; vasculitis; vesiculobullous dermatosis; or vitiligo of claim 21; wherein the fusion protein is administered as the sole therapeutic agent of claim 22; wherein the fusion protein is administered in combination with one of more other pharmaceutical agents indicated for treatment of an autoimmune disease, an allergic disease, a neurodegenerative disorder, neuropathic pain, an inflammatory disorder, Th2-induced airway inflammation, or diabetic neuropathy of claim 23; wherein the fusion protein is administered in combination with one or more immunosuppressive agents or adjuvants in immunosuppression therapy of claim 24; wherein the fusion protein is administered in combination with azathioprine, a methotrexate, a cyclosporine, a monoclonal antibody, a corticosteroid, or a combination thereof of claim 25; and
wherein the monoclonal antibody is basiliximab, daclizumab, or muromonab of claim 26.
Reference SEQ ID NOs 1 and 2 comprise 90% identical sequences to SEQ ID NOs 26 and 27.
Instant SEQ ID NOs 1-22 are encompassed by the reference fusion proteins with the recited reference amino acid changes.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
8. 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.
9. Claims 1-8, 10-13 and 17-23 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: SEQ ID Nos 1-22 and 26-27 with the recited mutations, compositions thereof, methods of administering the compositions and nucleic acids encoding SEQ ID Nos 1-22 and 26-27 with the recited mutations, does not reasonably provide enablement for: the recitations of claims 1-8, 10-13 and 17-23 which may have many undisclosed mutations.
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 the claims. The specification disclosure does not enable one skilled in the art to practice the invention without an undue amount of experimentation.
Factors to be considered in determining whether undue experimentation is required to practice the claimed invention are summarized In re Wands (858 F2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)). The factors most relevant to this rejection are the scope of the claim, the amount of direction or guidance provided, the lack of sufficient working examples, the unpredictability in the art and the amount of experimentation required to enable one of skill in the art to practice the claimed invention.
The art of Hatherly et al. (PTO-892; Reference U) teaches that CD200 binds to CD200R for function and that numerous single point mutations in CD200 prevent binding of CD200 to CD200R. (In particular Figure 5, whole document). As such, the specification is not enabled for the genus of CD200 proteins comprising any number of additional amino acid changes other than K130Y and I131Y. Changing additional amino acids within the protein other than the amino acid changes that have been exemplified in the specification in SEQ ID NOs 3-4, 6-7 and 12-13 will have unpredictable effects.
The art of Li et al. (PTO-892; Reference V) teaches that most if not all of CD200’s immunological function relates to its capacity to engage and signal through its receptor because CD200 itself lacks an intracellular signaling motif (In particular, page 14, whole document). As such, the contribution of CD200 to autoimmune disease and the treatment thereof is due to the interaction of CD200 with its receptor. Li et al. also teaches that very little is known about the role of CD200 in autoimmune disease (In particular, whole document). Therefore, given the fact that variants of SEQ ID NO:1 will have unpredictable binding to its receptor and the fact that the binding of CD200 to its receptor is required for immunological functions, attempting to make and use a genus of CD200 variants, including modulators of the CD200 receptor and agonist of the CD200 receptor, for use in treatment of autoimmune disease is unpredictable.
The combination of an unpredictable genus of CD200 variants with any “non-CD200 portion” only confounds the ability of the genus of compositions to be made and used commensurate in scope with the specification. A non-CD200 protein coding portion may itself have any number of functions including functions which would promote autoimmune disease or which would reduce the effectiveness of the CD200 portion. Making and using a genus of fusion proteins comprising CD200 is unpredictable.
Since no in vivo studies were used as model system to treat any autoimmune disorder it is not clear that reliance on the in vitro data accurately reflects the relative animal efficacy of the claimed therapeutic strategy. The specification does not adequately teach how to effectively treat any disorders or reach any therapeutic endpoint in animals by administrating the recited proteins and compositions thereof, much less any disorder as encompassed by the instant claims. The specification does not teach how to extrapolate data obtained from the in vitro studies to the development of effective in vivo animal therapeutic treatment, commensurate in scope with the claimed invention.
Although, the specification describes in vitro experiments, there is no correlation on this record between the in vitro studies and treating autoimmune disease in currently available form for humans or animals. It is not enough to rely on in vitro studies where, as here, a person having ordinary skill in the art has no basis for perceiving those studies as constituting recognized screening procedures with clear relevance to efficacy in humans or animals (emphasis added). Ex parte Maas, 9 USPQ2d 1746
In view of the absence of a specific and detailed description in Applicant's specification of how to effectively use the genus of proteins, fusion proteins and compositions claimed, absence of working examples providing evidence which is reasonably predictive that the genus of claimed agents are effective for in vivo use for treatment of disease, and the lack of predictability in the art at the time the invention was made, an undue amount of experimentation would be required to practice the claimed vaccine compositions with a reasonable expectation of success.
Substantiating evidence may be in the form of animal tests, which constitute recognizedscreening procedures with clear relevance to efficacy in humans. See Ex parte Krepelka, 231USPQ 746 (Board of Patent Appeals and Interferences 1986) and cases cited therein. Ex parteMaas, 9 USPQ2d 1746.
Reasonable correlation must exist between the scope of the claims and scope of the enablement set forth. In view on the quantity of experimentation necessary the limited working examples, the nature of the invention, the state of the prior art, the unpredictability of the art and the breadth of the claims, it would take undue trials and errors to practice the claimed invention.
10. Claims 1-8, 10-13 and 17-23 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.
Applicant is in possession of: SEQ ID Nos 1-22 and 26-27 with the recited mutations, compositions thereof, methods of administering the compositions and nucleic acids encoding SEQ ID Nos 1-22 and 26-27 with the recited mutations.
Applicant is not in possession of: the recitations of claims 1-8, 10-13 and 17-23 which may have many undisclosed mutations.
Applicant has disclosed only SEQ ID Nos 1-22 and 26-27 with the recited mutations. Therefore, the skilled artisan cannot envision all the contemplated CD200 possibilities recited in the instant claims. Consequently, conception cannot be achieved until a representative description of the structural and functional properties of the claimed invention has occurred, regardless of the complexity or simplicity of the method.
The specification has not adequately described the genus of CD200 polypeptides recited in the claims.
The specification has not adequately demonstrated the correlation between the structure of the variants having substitutions, deletions and additions and the functions of being able to modulators of the CD200 receptor, which are agonists of the CD200 receptor and which can treat the genus of recited diseases. As discussed supra and as evidenced by the examples in the specification the function binding to CD200R is not predictable based upon its structure.
The claims encompass variants. The specification has not adequately described the genus of compositions comprising variants for use in treatment of autoimmune disease. The specification has only described compositions comprising SEQ ID Nos 1-22 and 26-27 with the recited mutations and methods of administration using the compositions; therefore, the skilled artisan cannot envision all the contemplated composition possibilities recited in the instant claims. Consequently, conception cannot be achieved until a representative description of the structural and functional properties of the claimed invention has occurred, regardless of the complexity or simplicity of the method. Adequate written description requires more than a mere statement that it is part of the invention. See Fiers v. Revel, 25 USPQ2d 1601, 1606 (CAFC1993). The Guidelines for the Examination of Patent Application Under the 35 U.S.C.112, ¶1”Written Description” Requirement make clear that the written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species 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 genus (Federal Register, Vol. 66, No. 4, pages 1099-1111, Friday January 5, 20001, see especially page 1106 3rd column).
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, makes clear that “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. The invention is, for purposes of the written description inquiry, whatever is now claimed.” (See page 1117.) The specification does not “clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed.” (See Vas-Cath at page 1116.). Consequently, Applicant was not in possession of the instant claimed invention. See University of California v. Eli Lilly and Co. 43 USPQ2d 1398.
11. 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.
12. 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.
13. Claims 1-6, 9-13 and 17-23 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by WO 2017/194941 (IDS filed on 05/03/2024; Reference 1).
WO 2017/194941 teaches to a mutated CD200 protein, comprising an amino acid sequence with at least about 99% sequence identity to SEQ ID NO: 1, wherein said amino acid sequence additionally comprises at least one substitution mutation selected from K130Y and I131Y, and wherein the mutated CD200 protein is an agonist of the CD200 receptor;
which comprises one or more additional mutations selected from G1291, F128R, and N81K;
comprising the sequence of SEQ ID NO: 12 or SEQ ID NO: 13;
a mutated CD200 protein extracellular domain, comprising: an amino acid sequence with at least about 99% sequence identity to SEQ ID NO: 2, wherein said amino acid sequence additionally comprises at least one substitution mutation selected from K130Y and I131Y, wherein residue positions 130 and 131 correspond to residue numbering of SEQ ID NO: 1, wherein the mutated CD200 protein extracellular domain binds the CD200 receptor, and wherein the mutated CD200 protein is an agonist of the CD200 receptor;
comprising the sequence of SEQ ID NO: 3 or SEQ ID NO: 4;
a fusion protein, comprising: the mutated CD200 protein extracellular domain fused to a non-CD200 protein or peptide that does not bind a CD200 receptor, wherein an optional linker portion links the mutated CD200 protein extracellular domain and the non-CD200 protein or peptide;
wherein said linker portion is a peptide comprising between 1 and 15 amino acids; wherein said non-CD200 protein or peptide is an antibody or fragment thereof;
wherein said non-CD200 protein or peptide is an Fc fragment;
comprising the sequence of SEQ ID NO: 6 or SEQ ID NO: 7;
wherein said non-CD200 protein or peptide is an antibody or fragment thereof of claim 15;
a polynucleotide encoding the protein;
a pharmaceutical composition comprising the protein;
a method for the treatment of autoimmune disease, comprising: providing the pharmaceutical composition;
a method for the treatment of autoimmune disease, comprising: providing the protein
(In particular, claims, whole document).
Instant SEQ ID NO:26 is 100% sequence identical to reference SEQ ID NO:2
Instant SEQ ID NO:26 is 99.5% sequence identical to reference SEQ ID NOs:4 and 7.
Instant SEQ ID NO:27 is 99.7% sequence identical to reference SEQ ID NO:13.
Instant SEQ ID NO:27 is 99.5% sequence identical to reference SEQ ID NO:12.
Instant SEQ ID NOs 1-22 are encompassed by the reference fusion proteins with the recited reference amino acid changes.
The reference teachings anticipate the claimed invention.
14. No claim is allowed.
15. Any inquiry concerning this communication or earlier communications from the examiner should be directed to NORA MAUREEN ROONEY whose telephone number is (571)272-9937. The examiner can normally be reached on M-F from 8:00am to 4:30pm.
If attempts to reach the examiner by telephone are unsuccessful, the examiner' s supervisor, Misook Yu, can be reached at telephone number (571) 272-0839. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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September 27, 2026
/Nora M Rooney/
Primary Examiner, Art Unit 1641
