DETAILED ACTION
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 .
Election/Restrictions
Applicant’s election of Group I in the reply filed on 2/9/2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Applicant’s elected species are in the following.
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Claim Status
Claims 1-2, 25, 29, and 35-50 are pending.
Claims 3-24, 26-28, and 30-34 are cancelled.
Claims 1-2, 25, 29, and 35-50 have been examined.
Priority
This application is a CON of PCT/US2021/053239 10/01/2021
PCT/US2021/053239 has PRO 63/163,655 03/19/2021
PCT/US2021/053239 has PRO 63/156,870 03/04/2021
PCT/US2021/053239 has PRO 63/111,337 11/09/2020
PCT/US2021/053239 has PRO 63/111,460 11/09/2020
PCT/US2021/053239 has PRO 63/111,476 11/09/2020
PCT/US2021/053239 has PRO 63/086,858 10/02/2020
PCT/US2021/053239 has PRO 63/086,894 10/02/2020
PCT/US2021/053239 has PRO 63/086,860 10/02/2020
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 1/26/2024, 5/30/2025, 6/16/2025, and 2/9/2026 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement has been considered by the examiner.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1, 29, and 37-39 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Seehra et al. (WO 2018/089706 A2, cited in IDS) and evidenced by Suarez-Mendez et al. (Biomedicine & Pharmacotherapy 105 (2018) 956–961).
Claim 1 is drawn to a method of treating a subject having a disease or condition comprising administration of a therapeutically effective amount of a polypeptide comprising SEQ ID NO: 69; wherein, the disease can be treated with erythropoietin (EPO) or an erythropoiesis-stimulating agent.
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Seehra et al. teach a method of administering a chimeric polypeptide comprising an extracellular ActRlla variant fused to an Fc domain monomer or moiety to treat weakness and atrophy of muscles and metabolic diseases of Type-1 and Type-2 diabetes (Abstract). Seehra et al. show extracellular ActRlla variant of SEQ ID NO; 69 as follows (p27) with 100% identity to the elected species.
Seehra et al. teach the extracellular ActRlla variant (SEQ ID NO: 69) fused to the N-terminus of hFc through a GGG linker (p43, Example 1-(4)). Seehra et al. teach the effective dosage of the chimeric protein ranging from 0.01 to 500 mg/kg (p39, para 2). Suarez-Mendez et al. is cited as evidence to show diabetes can be treated by erythropoietin (EPO) with the facts of (a) Erythropoietin (EPO) as a cardio-protector and neuroprotective agent in treating diabetic neuropathy (p957, Sec, 2.2; p958, Fig 1, legend) and (b) Diabetic patients (types 1 and 2), with or without anemia, present low EPO plasmatic levels (p959, col 1, Sec 3.1. Erythropoietin and diabetic neuropathy).
With respect to claim 29, Suarez-Mendez et al. is cited as evidence to show diabetic patients (types 1 and 2), with or without anemia, present low EPO plasmatic levels (p959, col 1, Sec 3.1. Erythropoietin and diabetic neuropathy).
With respect to claim 37-39, Seehra et al. teach the chimeric polypeptide comprising extracellular ActRlla variant (SEQ ID NO: 69) fused to the N-terminus of hFc through a GGG linker (p43, Example 1-(4)).
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1, 25, and 37-41 are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Seehra et al. (WO 2019/217715 A1, cited in IDS) and evidenced by Suarez-Mendez et al. (Biomedicine & Pharmacotherapy 105 (2018) 956–961).
Claim 1 is drawn to a method of treating a subject having a disease or condition comprising administration of a therapeutically effective amount of a polypeptide comprising SEQ ID NO: 69; wherein, the disease can be treated with erythropoietin (EPO) or an erythropoiesis-stimulating agent.
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Seehra et al. teach the use of an extracellular ActRIIA variant fused to an Fe domain monomer to treat diseases and conditions involving low red blood cell levels (Abstract). Seehra et al. teach an extracellular ActRIIA variant is SEQ ID NO: 69 (p19, line 5; p27) with 100% identity to the elected species of SEQ ID NO: 69 shown above. Seehra et al. teach the Fc domain is IgG1 (p31, line 32). Seehra et al. further teach the use of a flexible linker GGG (p35, line 7) to link SEQ ID NO: 69 and IgG1 (Fc domain) together. Seehra et al. teach compositions and methods described herein can also be used to treat subjects that do not respond well to erythropoietin (EPO) or that are susceptible to adverse effects of EPO, e.g., hypertension, headaches, vascular thrombosis, influenza-like syndrome, obstruction of shunts, and myocardial infarction, (p46, line 36-38; claim 21), reading on the disease can be treated with erythropoietin (EPO) or an erythropoiesis-stimulating agent in claim 1.
With respect to claim 25, Seehra et al. teach the fusion protein is administered to subject having or at risk of developing anemia or blood loss associated disease or condition (p7. line 12-16). Seehra et al. teach the treated anemia or blood loss associated conditions comprising diabetes, surgery, trauma, hematopoietic stem cell transplantation, graft versus host disease, and others (p7, line 21-26). To prevent the risk of developing anemia and/or blood loss resulting from surgery, one of ordinary skill in the art would at once envisage to administer the fusion protein to increase red blood cells prior to surgery to minimize the risk of developing anemia and reduce loss of red blood cells during surgery.
With respect to claims 37-39, Seehra et al. teach the use of a flexible linker GGG to link SEQ ID NO: 69 and IgG1 (Fc domain) together (p35, line 7).
With respect to claims 40-41, Seehra et al. teach the monomer Fc domain is IgG1 (p31, line 32).
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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.
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.
1. Claims 1, 29, 37-42, and 49 are rejected under 35 U.S.C. 103 as being unpatentable over Seehra et al. (WO 2018/089706 A2, cited in IDS) and evidenced by Suarez-Mendez et al. as applied to claims 1, 29, 37-39 and further in view of Hui (WO 2007/018619 A2).
Seehra et al. teach the chimeric polypeptide the extracellular ActRlla variant (SEQ ID NO: 69) fused to the N-terminus of hFc through a GGG linker (p43, Example 1-(4)).
Seehra et al. and evidenced by Suarez-Mendez et al. dis not specify polypeptide sequence of hFc.
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Similarly, Hui teaches a fusion protein containing Fc fragment of an immunoglobulin preferred to be IgG containing SEQ ID NO: 3 (p5, para 4) with 100% identity to the instant SEQ ID NO: 155 shown as follows, reading on claims 40-42. Hui shows the use of 3xGly linker (GGG linker) for conjugate a bioactive peptide to the IgG Fc (p29, Example 5).
With respect to claim 49, Seehra et al. show extracellular ActRlla variant of SEQ ID NO;
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69 as follows (p27) with 100% identity to the elected species. Seehra’s SEQ ID NO: 69 linked to Hui’s IgG1 Fc domain with a GGG linker generates a chimeric polypeptide with 100% homology to the instant SEQ ID NO: 156.
One of ordinary skill in the art before the effective filing date of this invention would have found it obvious to combine Seehra et al. and evidenced by Suarez-Mendez et al. with Hui’s IgG1 Fc polypeptide because (a) Seehra et al. teach a fusion protein comprising an extracellular ActRlla variant (SEQ ID NO: 69) linked to an Fc domain via a GGG linker and (b) Hui teaches SEQ ID NO: 3 as the use of a preferred IgG Fc fragment containing SEQ ID NO: 3 (p5, para 4) for conjugation to a functional domain via a linker. The combination would have reasonable expectation of success because both Seehra et al. and Hui teach a fusion protein comprising a functional domain linked to a Fc domain via a linker.
2. Claims 1-2, 29, and 36-50 are rejected under 35 U.S.C. 103 as being unpatentable over Seehra et al. in view of Hui and evidenced by Suarez-Mendez et al. as applied to claims 1, 29, 37-42, 49 and further in view of Dussiot et al. (Nat Med. 2014 April ; 20(4): 398–407, cited in IDS) and Carrancio et al. (British Journal of Haematology, 2014, 165, 870–882).
Claim 2 is drawn to a method of increasing erythropoietin levels or erythropoietin receptor levels in a subject in need thereof, comprising administering to the subject a therapeutically effective amount of a polypeptide comprising an extracellular activin receptor type Ila (ActRIIa) variant, wherein the variant comprises the sequence of SEO ID NO: 69.
Seehra et al. in view of Hui and evidenced by Suarez-Mendez et al. teach administration a chimeric polypeptide comprising the extracellular ActRlla variant (SEQ ID NO: 69) - (GGG linker) - IgG1 Fc domain (SEQ ID NO: 3) to treat diabetic patients with low EPO plasmatic levels (a disease or condition capable of being treated with erythropoietin or an erythropoiesis-stimulating agent) as applied to claims 1, 29, 37-42, and 49 above.
Seehra et al. in view of Hui and evidenced by Suarez-Mendez et al. do not specify the chimeric polypeptide capable of increasing erythropoietin levels or erythropoietin receptor levels in a subject in need.
Dussiot et al. teach an activin receptor IIA ligand trap (receptor IIA ligand-binding fusion protein) able to correct ineffective erythropoiesis in β-thalassemia (Title). Dussiot et al. teach a ligand trap that consists of the extra-cellular domain of ActRIIA linked to the human IgG1 Fc domain able to increase hematocrit and hemoglobin levels (p2, last para) and reverse ineffective erythropoiesis in thalassemic mice (p3, para 1). Similarly, Carrancio et al. teach an activin receptor IIA ligand trap promotes erythropoiesis resulting in a rapid induction of red blood cells and haemoglobin (Title). Carrancio et al. show an activin receptor IIA ligand trap/antagonist able to increases red blood cell parameters in wild type mice with faster kinetics than erythropoietin (p873, Fig 1, legend). Carrancio et al. show an activin receptor IIA ligand trap/antagonist able to
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increase plasma EPO level and increase EPO expression in kidney shown as follows (p876, Fig 3C and 3D; p877, legend of Fig 3). Because both Dussiot et al. and Carrancio et al. teach the beneficial use of an activin receptor IIA ligand-binding protein to treat a subject in need resulting increase plasma EPO level and EPO expression in kidney, in particular for the patients not responding to EPO as taught by Carrancio et al. (p870, col 2), one of ordinary skill in the art would have been taught (A) a treated diabetic patients (types 1 and 2), with or without anemia, with low EPO plasmatic levels (See Seehra et al. p959, col 1, Sec 3.1. Erythropoietin and diabetic neuropathy) would receive additional benefit to increase plasma EPO level and EPO expression in kidney and (B) administration of Seehra’s chimeric polypeptide to treat patients not responding to EPO, reading on the instant claim 2.
The specification shows SEQ ID NO: 69 fusion to Fc domain would be sufficient to increase EPO level in the blood of mice (p109, example 1) and in kidney (p110, Example 2), consistent with Dussiot et al. and Carrancio et al. It is further noted that Seehra’s chimeric polypeptide comprising the extracellular ActRlla variant (SEQ ID NO: 69) - (GGG linker) - IgG1 Fc domain (SEQ ID NO: 3) is identical the instant SEQ ID NO: 156; thus, the same compound administered at the same dosage range (0.01 to 500 mg/kg disclosed in example 2 at page p110 in SPEC) must have the same therapeutic effect and properties as claimed. Where the claimed and prior art products are identical or substantially identical in structure or composition, or are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established. In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977). See MPEP 2112.01(I).
One of ordinary skill in the art before the effective filing date of this invention would have found it obvious combine (i) Seehra et al. in view of Hui and evidenced by Suarez-Mendez et al. with (ii) Dussiot et al. in view of Carrancio et al. because (a) Seehra et al. in view of Hui and evidenced by Suarez-Mendez et al. teach administration the chimeric protein of extracellular ActRlla variant (SEQ ID NO: 69) - (GGG linker) - IgG1 Fc domain (SEQ ID NO: 3) to treat diabetic patients with low EPO plasmatic levels and (b) both Dussiot et al. and Carrancio et al. teach the beneficial use of an activin receptor IIA ligand-binding protein to treat a subject in need resulting increase plasma EPO level and EPO expression in kidney, in particular for the patients not responding to EPO as taught by Carrancio et al. (p870, col 2). The combination would have reasonable expectation of success because administration of extracellular ActRlla variant (SEQ ID NO: 69) - (GGG linker) - IgG1 Fc domain (SEQ ID NO: 3) to treat diabetic patients with low EPO plasmatic levels is expected to increase plasma EPO level and EPO expression in kidney in the treated patients as suggested by Carrancio et al. (p876, Fig 3C and 3D; p877, legend of Fig 3).
With respect to claim 36, Suarez-Mendez et al. is cited as evidence to show diabetic patients (types 1 and 2), with or without anemia, present low EPO plasmatic levels (p959, col 1, Sec 3.1. Erythropoietin and diabetic neuropathy).
With respect to claim 43-45, Seehra et al. teach the chimeric polypeptide comprising extracellular ActRlla variant (SEQ ID NO: 69) fused to the N-terminus of hFc through a GGG linker (p43, Example 1-(4)).
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With respect to claims 46-48, Hui teaches a fusion protein containing Fc fragment of an immunoglobulin preferred to be IgG containing SEQ ID NO: 3 (p5, para 4) with 100% identity to the instant SEQ ID NO: 155 shown as follows.
With respect to claim 50, Seehra et al. show extracellular ActRlla variant of SEQ ID NO; 69 as follows (p27) with 100% identity to the elected species. Seehra’s SEQ ID NO: 69 linked to Hui’s IgG1 Fc domain with a GGG linker generates a chimeric polypeptide with 100% homology to the instant SEQ Id NO: 156.
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3. Claims 1-2, 25, 29, and 35-50 are rejected under 35 U.S.C. 103 as being unpatentable over Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 and further in view of Bennett et al. (Surgery (Oxford). Volume 37, Issue 8, 2019, Pages 424-430).
Claims 25 and 35 are drawn to a condition of administering the polypeptide to a subject.
Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach administration of a chimeric polypeptide to treat a patient with low serum erythropoietin and capable of promoting erythropoiesis resulting in a rapid induction of red blood cells and haemoglobin as well as increase of plasma EPO level and EPO expression in kidney.
Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. do not specify administration of the activin receptor IIA ligand binding polypeptide to a person in need prior to surgery.
Bennett et al. teach both red blood cell (RBC) transfusion and anaemia or low haematocrit increase morbidity and mortality associated with surgery. Where bleeding is anticipated anaemia should be treated medically to avoid (RBC) transfusion which will increase the risk to the patient (Abstract). Bennett et al. teach acute anaemia during surgery and operating on patients who require transfusion during surgery will expose them to increased risk. Allowing them to become anaemic before transfusing is an additive risk (p425, col 2, Acute anaemia during surgery). Because surgery causes bleeding and loss of red blood cell but red blood cell transfusion further expose patients to increases risk, one of ordinary skill in the art would have found it obvious to beneficially administer the activin receptor IIA ligand binding polypeptide taught by the combined references to a person prior to surgery to promote endogenous erythropoiesis resulting in a rapid induction of red blood cells and haemoglobin without red blood transfusion to reduce ischaemic risk and anaemia, reading on claims 25 and 35. Furthermore, it is known that stem cell transplantation and tissue/organ transplantation also require a surgery procedure.
One of ordinary skill in the art before the effective filing date of this invention would have found it obvious to combine (a) Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. and (b) Bennett’s teaching surgery because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach administration of a chimeric polypeptide to treat a patient with low serum erythropoietin and capable of promoting erythropoiesis resulting in a rapid induction of red blood cells and haemoglobin as well as increase of plasma EPO level and EPO expression in kidney (Carrancio et al. Title; p876, Fig 3C and 3D; p877, legend of Fig 3) and (b) Bennett et al. teach both red blood cell (RBC) transfusion and anaemia or low haematocrit increase morbidity and mortality associated with surgery (Abstract) and acute anaemia during surgery and operating on patients who require transfusion during surgery will expose them to increased risk. Allowing them to become anaemic before transfusing is an additive risk (p425, col 2, Acute anaemia during surgery). The combination would have reasonable expectation of success because Seehra’s extracellular ActRlla variant of SEQ ID NO; 69 fusion to Hui’s Fc domain via a GGG linker is expected to promoting endogenous erythropoiesis resulting in a rapid induction of red blood cells and haemoglobin as well as increase of plasma EPO level and EPO expression in kidney without red blood cell infusion (See Carrancio et al. Title; p876, Fig 3C and 3D; p877, legend of Fig 3).
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.
Claims 1-2, 29, and 36-50 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 9-10 of U.S. Patent No. 11,013,785 B2 (the ‘785 patent) in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. (cited above).
Claim 1 and 9 of the ‘785 patent disclosed an extracellular activin receptor type IIa (ActRIIa) variant of SEQ ID NO: 69 with 100% identity to the instant SEQ ID NO: 69.
Claim 10 of the ‘785 patent disclosed SEQ ID NO: 69 fusion to an Fc domain by a linker.
Claims 1 and 9-10 of the ‘785 patent do not specify the Fc domain as an IgG1 or the use of the fusion protein to treat a disease or condition.
The relevancy of Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 not repeated here.
Because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach the beneficial fusion of SEQ ID NO: 69 taught by the ‘785 patent to an IgG1 Fc domain via a GGG linker to treat a patient with low serum erythropoietin, one of ordinary skill in the art would have found it obvious to combine claims 1 and 9-10 of the ‘785 patent with Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Thus, claims 1-2, 29, and 36-50 are obvious to claims 1 and 9-10 of the ‘785 patent in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Claims 1-2, 29, and 36-50 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 5-8 of U.S. Patent No. 11,090,361 B2 (the ‘361 patent) in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. (cited above).
Claim 1 and 8 the ‘361 patent disclosed an extracellular activin receptor type IIa variant polypeptide of SEQ ID NO: 69 fusion to an Fc domain.
Claim 5-7 the ‘361 patent disclosed SEQ ID NO: 69 linked to Fc domain via a GGG linker.
Claims 1 and 5-8 of the ‘361 patent do not specify administration of the fusion protein to treat a disease or condition.
The relevancy of Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 not repeated here.
Because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach the beneficial fusion of SEQ ID NO: 69 taught by the ‘361 patent to an IgG1 Fc domain via a GGG linker to treat a patient with low serum erythropoietin, one of ordinary skill in the art would have found it obvious to combine claims 1 and 5-8 of the ‘361 patent with Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Thus, claims 1-2, 29, and 36-50 are obvious to claims 1 and 5-8 of the ‘361 patent in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Claims 1-2, 29, and 36-50 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4 and 9-10 of U.S. Patent No. 11,484,573 B2 (the ‘573 patent) in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. (cited above).
Claims 1 and 4 the ‘573 patent disclosed an extracellular activin receptor type IIa variant polypeptide of SEQ ID NO: 69.
Claims 9-10 the ‘573 patent disclosed SEQ ID NO: 69 linked to a Fc domain by way of a linker.
Claims 1, 4 and 9-10 of the ‘573 patent do not teach administration of the fusion protein to treat a patient with low serum erythropoietin.
The relevancy of Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 not repeated here.
Because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach the beneficial fusion of SEQ ID NO: 69 taught by the ‘573 patent to an IgG1 Fc domain via a GGG linker to treat a patient with low serum erythropoietin, one of ordinary skill in the art would have found it obvious to combine claims 1, 4 and 9-10 of the ‘573 patent with Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Thus, claims 1-2, 29, and 36-50 are obvious to claims 1, 4 and 9-10 of the ‘573 patent in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Claims 1-2, 29, and 36-50 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 3-5 of U.S. Patent No. 12,350,313 B2 (the ‘313 patent) in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. (cited above).
Claims 1 and 4-5 of the ‘313 patent disclosed a fusion protein comprising SEQ ID NO: 69 and Fc domain monomer.
Claim 3 of the ‘313 patent disclosed SEQ ID NO: 69 linked to Fc domain via a linker.
Claims 1 and 3-5 of the ‘313 patent do not teach administration of the fusion protein to treat a patient with low serum erythropoietin.
The relevancy of Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 not repeated here.
Because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach the beneficial fusion of SEQ ID NO: 69 taught by the ‘313 patent to an IgG1 Fc domain via a GGG linker to treat a patient with low serum erythropoietin, one of ordinary skill in the art would have found it obvious to combine claims 1 and 3-5 of the ‘313 patent with Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Thus, claims 1-2, 29, and 36-50 are obvious to claims 1 and 3-5 of the ‘313 patent in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Claims 1-2, 29, and 36-50 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 5 and 7-9 of U.S. Patent No. 12,364,737 B2 (the ‘737 patent) in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. (cited above).
Claims 1 and 7-8 of the ‘737 patent disclosed a polypeptide comprising SEQ ID NO: 69.
Claim 5 of the ‘737 patent disclosed the polypeptide further comprising an Fc domain monomer.
Claim 9 of the ‘737 patent disclosed SEQ ID NO: 69fusion to the Fc domain via a linker.
Claims 1, 5 and 7-9 of the ‘737 patent do not teach administration of the fusion protein to treat a patient with low serum erythropoietin.
The relevancy of Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 not repeated here.
Because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach the beneficial fusion of SEQ ID NO: 69 taught by the ‘737 patent to an IgG1 Fc domain via a GGG linker to treat a patient with low serum erythropoietin, one of ordinary skill in the art would have found it obvious to combine claims 1, 5 and 7-9 of the ‘737 patent with Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Thus, claims 1-2, 29, and 36-50 are obvious to claims 1, 5 and 7-9 of the ‘737 patent in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Claims 1-2, 29, and 36-50 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, and 8-10 of copending Application No. 19/244,381 (the ‘381 application 6/20/2025) in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Claims 1 and 4 of the ‘381 application disclosed a polypeptide comprising SEQ ID NO: 69.
Claims 8-9 of the ‘381 application disclosed SEQ ID NO: 69 fusion to a human IgG1 Fc domain via a linker.
Claim 10 of the ‘381 application disclosed the linker as GGG of other glycine linkers.
Claims 1, 4, and 8-10 of the ‘381 application do not teach administration of the fusion protein to treat a patient with low serum erythropoietin.
The relevancy of Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 not repeated here.
Because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach the beneficial fusion of SEQ ID NO: 69 taught by the ‘381 application to an IgG1 Fc domain via a GGG linker to treat a patient with low serum erythropoietin, one of ordinary skill in the art would have found it obvious to combine claims 1, 4, and 8-10 of the ‘381 application with Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Thus, claims 1-2, 29, and 36-50 are obvious to claims 1, 4, and 8-10 of the ‘381 application in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
This is a provisional nonstatutory double patenting rejection.
Claims 1-2, 29, and 36-50 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 147-148 of copending Application No. 19/229,468 (the ‘468 application 11/6/2025) in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Claim 147 disclosed a polypeptide comprising SEQ ID NO: 69 linked to Fc domain via a GGG linker.
Claim 148 disclosed Fc domain is a human IgG1 Fc domain.
Claims 147-148 of the ‘468 application do not teach administration of the fusion protein to treat a patient with low serum erythropoietin.
The relevancy of Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 not repeated here.
Because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach the beneficial fusion of SEQ ID NO: 69 taught by the ‘468 application to an IgG1 Fc domain via a GGG linker to treat a patient with low serum erythropoietin, one of ordinary skill in the art would have found it obvious to combine claims 147-148 of the ‘468 application with Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Thus, claims 1-2, 29, and 36-50 are obvious to claims 147-148 of the ‘468 application in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
This is a provisional nonstatutory double patenting rejection.
Claims 1-2, 29, and 36-50 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 7 and 146-148 of copending Application No. 17/945,324 (the ‘324 application 2/10/2026) in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Claim 7 of the ‘324 application disclosed a polypeptide comprising SEQ ID NO: 69.
Claim 146-148 of the ‘324 application disclosed SEQ ID NO: 69 fusion to an Fc domain via a GGG linker.
Claims 7 and 146-148 of the ‘324 application do not teach administration of the fusion protein to treat a patient with low serum erythropoietin.
The relevancy of Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. as applied to claims 1-2, 29, and 36-50 not repeated here.
Because Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al. teach the beneficial fusion of SEQ ID NO: 69 taught by the ‘324 application to an IgG1 Fc domain via a GGG linker to treat a patient with low serum erythropoietin, one of ordinary skill in the art would have found it obvious to combine claims 147-148 of the ‘324 application with Seehra et al. in view of Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
Thus, claims 1-2, 29, and 36-50 are obvious to claims 147-148 of the ‘324 application in view of Seehra et al. Hui, Dussiot et al., Carrancio et al. and evidenced by Suarez-Mendez et al.
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claim is allowed.
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/J.L/Examiner, Art Unit 1658
15-March-2026
/LI N KOMATSU/ Primary Examiner, Art Unit 1658