Notice of Pre-AIA or AIA Status The present application is being examined under the pre-AIA first to invent provisions. Claims 1-15 are pending and under examination. 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. Claims 1-15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-33 of U.S. Patent No. 10683367 (hereinafter the ‘367) in view of U.S. Patent No. 11008404 (hereinafter the ‘404) (both cited herewith) . Representative claim 1 of the ‘367 is drawn to “An isolated monoclonal antibody, or antigen binding fragment thereof, that binds human MASP-2, wherein the antibody comprises: a) a heavy chain variable region comprising: the amino acid sequence set forth in SEQ ID NO:20, or a variant thereof comprising an amino acid sequence having at least 95% identity to the amino acid sequence set forth in set forth in SEQ ID NO: 20, wherein the following residues of the variant are unchanged: residue 31 is an R, residue 32 is a G, residue 33 is a K, residue 34 is an M, residue 35 is a G, residue 36 is a V, residue 37 is an S, residue 50 is an L, residue 51 is an A, residue 52 is an H, residue 53 is an I, residue 54 is an F, residue 55 is an S, residue 56 is an S, residue 57 is a D, residue 58 is an E, residue 59 is a K, residue 60 is an S, residue 61 is a Y, residue 62 is an R, residue 63 is a T, residue 64 is an S, residue 65 is an L, residue 66 is a K, residue 67 is an S, residue 95 is a Y, residue 96 is a Y, residue 97 is a C, reside 98 is an A, residue 99 is an R, residue 100 is an I, residue 101 is an R, residue 102 is an R or A, residue 103 is a G, residue 104 is a G, residue 105 is an I, residue 106 is a D and residue 107 is a Y; and b) a light chain variable region comprising the amino acid sequence set forth in SEQ ID NO:24 or a variant thereof comprising an amino acid sequence having at least 95% identify to the amino acid sequence set forth in set forth in SEQ ID NO: 24 wherein the following residues of the variant are unchanged: residue 23 is an S, residue 24 is a G, residue 25 is an E or D, residue 26 is a K, residue 27 is an L, residue 28 is a G, residue 29 is a D, residue 30 is a K, residue 31 is a Y or F, residue 32 is an A, residue 33 is a Y, residue 49 is a Q, residue 50 is a D, residue 51 is a K or N, residue 52 is a Q or K, residue 53 is an R, residue 54 is a P, residue 55 is an S, residue 56 is a G, residue 88 is a Q, residue 89 is an A, residue 90 is a W, residue 91 is a D, residue 92 is an S, residue 93 is an S, residue 94 is a T, residue 95 is an A, residue 96 is a V and residue 97 is an F, wherein the antibody or variant thereof inhibits MASP-2 dependent complement activation.” Moreover, reference claims 2-15 of the ‘367, which are depe n dent on reference claim 1 of the ‘367, recit e the features of instant claims 2-15 , including for example that the reference antibody (i) binds an epitope in the CCP1 domain of MASP-2, (ii) inhibits C3b deposition, and (iii) does not substantially inhibit the classical pathway. However, the reference claims are not drawn to “ a method of treating a mammalian subject at risk for developing …ischemia reperfusion injury comprising administering…” the antibody of the reference claims to said subject. Representative claim 1 of the ‘404 is drawn to “[a] method of treating a subject suffering from, or at risk for developing, an ischemia/reperfusion injury resulting from an acute myocardial infarction comprising administering to said subject a therapeutically effective dosage of a monoclonal antibody or antigen-binding fragment thereof specifically recognizing and binding an epitope within the C-terminal part of MASP-2 consisting of the CCP1, CCP2 and serine protease domains (amino acid residues 293 to 686 of SEQ ID NO:1), wherein the monoclonal antibody, or antigen-binding fragment thereof, is capable of inhibiting MASP-2 catalyzed C4 deposition.” Moreover, reference claims 2-15 of the ‘404, which are dependent on reference claim 1 of the ‘404, recite the features of instant claims 2-15 , including for example that in practicing the reference method of treatment with the reference antibody, said antibody (i) binds an epitope in the CCP1 domain of MASP-2, (ii) inhibits C3b deposition, and (iii) does not substantially inhibit the classical pathway. Given the reference claims of the ‘367 and the ‘404 set forth above, it would have been obvious to one of ordinary skill in the art that the antibody of reference claims ‘367, said ‘367 antibody being one that (i) binds an epitope in the CCP1 domain of MASP-2, (ii) inhibits C3b deposition, and (iii) does not substantially inhibit the classical pathway, will, like the antibody use d in the reference method s of treatment of the ‘404 which shares each of these same properties (i)-(iii), also be an antibody that “ is capable of inhibiting MASP-2 catalyzed C4 deposition.” Indeed, it was well understood by one of ordinary skill in the art as of the earliest filing date associated with the instant application that two antibodies which bind the same epitope (the CCP1 domain of MASP-2), and that share the same functional properties (inhibit C3b deposition without substantially inhibiting the classical pathway), will obviously share the ability to inhibit MASP-2 catalyzed C4 deposition, which is the initiating step of the lectin complement pathway and lies upstream of C3b deposition. Based on the above reasoning it would have been prima facie obvious to one of ordinary skill in the art to use the antibody of reference claims ‘367 in the method of treating a subject suffering from, or at risk for developing, an ischemia/reperfusion injury resulting from an acute myocardial infarction as set forth in the reference claims of the ‘404. In view of the reference teachings it was apparent that one of ordinary skill in the art would have had a reasonable expectation of success in arriving at the claimed invention. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made. Claims 1-15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-33 of U.S. Patent No. 10683367 (hereinafter the ‘367) in view of U.S. Patent No. 11225526 (hereinafter the ‘526) (both cited herewith) . Representative claim 1 of the ‘367 is drawn to “An isolated monoclonal antibody, or antigen binding fragment thereof, that binds human MASP-2, wherein the antibody comprises: a) a heavy chain variable region comprising: the amino acid sequence set forth in SEQ ID NO:20, or a variant thereof comprising an amino acid sequence having at least 95% identity to the amino acid sequence set forth in set forth in SEQ ID NO: 20, wherein the following residues of the variant are unchanged: residue 31 is an R, residue 32 is a G, residue 33 is a K, residue 34 is an M, residue 35 is a G, residue 36 is a V, residue 37 is an S, residue 50 is an L, residue 51 is an A, residue 52 is an H, residue 53 is an I, residue 54 is an F, residue 55 is an S, residue 56 is an S, residue 57 is a D, residue 58 is an E, residue 59 is a K, residue 60 is an S, residue 61 is a Y, residue 62 is an R, residue 63 is a T, residue 64 is an S, residue 65 is an L, residue 66 is a K, residue 67 is an S, residue 95 is a Y, residue 96 is a Y, residue 97 is a C, reside 98 is an A, residue 99 is an R, residue 100 is an I, residue 101 is an R, residue 102 is an R or A, residue 103 is a G, residue 104 is a G, residue 105 is an I, residue 106 is a D and residue 107 is a Y; and b) a light chain variable region comprising the amino acid sequence set forth in SEQ ID NO:24 or a variant thereof comprising an amino acid sequence having at least 95% identify to the amino acid sequence set forth in set forth in SEQ ID NO: 24 wherein the following residues of the variant are unchanged: residue 23 is an S, residue 24 is a G, residue 25 is an E or D, residue 26 is a K, residue 27 is an L, residue 28 is a G, residue 29 is a D, residue 30 is a K, residue 31 is a Y or F, residue 32 is an A, residue 33 is a Y, residue 49 is a Q, residue 50 is a D, residue 51 is a K or N, residue 52 is a Q or K, residue 53 is an R, residue 54 is a P, residue 55 is an S, residue 56 is a G, residue 88 is a Q, residue 89 is an A, residue 90 is a W, residue 91 is a D, residue 92 is an S, residue 93 is an S, residue 94 is a T, residue 95 is an A, residue 96 is a V and residue 97 is an F, wherein the antibody or variant thereof inhibits MASP-2 dependent complement activation.” Moreover, reference claims 2-15 of the ‘367, which are dependent on reference claim 1 of the ‘367, recite the features of instant claims 2-15, including for example that the reference antibody (i) binds an epitope in the CCP1 domain of MASP-2, (ii) inhibits C3b deposition, and (iii) does not substantially inhibit the classical pathway. However, the reference claims are not drawn to “a method of treating a mammalian subject at risk for developing …ischemia reperfusion injury comprising administering…” the antibody of the reference claims to said subject. Representative claim 1 of the ‘526 is drawn to “[a] method of treating a subject suffering from, or at risk for developing, an ischemia/reperfusion injury resulting from a percutaneous transluminal coronary angioplasty or resulting from coronary artery bypass grafting or resulting from brain ischemia comprising administering to said subject a therapeutically effective dosage of a monoclonal antibody or antigen-binding fragment thereof specifically recognizing and binding an epitope within the C-terminal part of MASP-2 consisting of the CCP1, CCP2 and serine protease domains (amino acid residues 293 to 686 of SEQ ID NO:1), wherein the monoclonal antibody, or antigen-binding fragment thereof, is capable of inhibiting MASP-2 catalyzed C4 deposition.” Moreover, reference claims 2-5 of the ‘526, which are dependent on reference claim 1 of the ‘526, recites certain feature of instant claims 6 and 7. Given the reference claims of the ‘367 and the ‘ 526 set forth above, it would have been obvious to one of ordinary skill in the art that the antibody of reference claims ‘367, said ‘367 antibody being one that (i) binds an epitope in the CCP1 domain of MASP-2, (ii) inhibits C3b deposition, and (iii) does not substantially inhibit the classical pathway, will, like the antibody used in the reference method of treatment of the ‘ 526 which binds “an epitope within the C-terminal part of MASP-2 consisting of the CCP1, CCP2 and serine protease domains (amino acid residues 293 to 686 of SEQ ID NO:1),” will also be an antibody that “is capable of inhibiting MASP-2 catalyzed C4 deposition.” Indeed, it was well understood by one of ordinary skill in the art as of the earliest filing date associated with the instant application that antibodies which bind “an epitope in the CCP1 domain of MASP-2” / antibodies which bind “an epitope within the C-terminal part of MASP-2 consisting of the CCP1, CCP2 and serine protease domains (amino acid residues 293 to 686 of SEQ ID NO:1),” will each obviously share the ability to inhibit MASP-2 catalyzed C4 deposition, which is the initiating step of the lectin complement pathway and lies upstream of C3b deposition. Based on the above reasoning it would have been prima facie obvious to one of ordinary skill in the art to use the antibody of reference claims ‘367 in the method of treating a subject suffering from, or at risk for developing, an ischemia/reperfusion injury resulting from a percutaneous transluminal coronary angioplasty or resulting from coronary artery bypass grafting or resulting from brain ischemia as set forth in the reference claims of the ‘ 526 . In view of the reference teachings it was apparent that one of ordinary skill in the art would have had a reasonable expectation of success in arriving at the claimed invention. Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made. No claims are allowed. 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