IP Library › Granted Patent US 12,735,473
Granted Patent B2
US 12,735,473 · App. 18/032,084 · Granted Sep 15, 2026

Method of treating a blood disorder associated with C1q-mediated activation of the classical complement pathway by administering an anti-C1q antibody

Inventors: Ted Yednock (Forest Knolls, CA); Sethu Sankaranarayanan (Fremont, CA)
Assignee: Annexon, Inc.
C07K16/18A61P7/06A61K2039/54A61K2039/545
View Patent ↗
Loading inventors, assignments & file history…
Monitor This Case
Get email alerts when status or documents change.
Order Certified Copies
Most orders are placed with the USPTO same day — all within 24 business hours.
Order via The Patent Place →
Pre-filled with this patent's details
Quick Facts
Patent No.
US 12,735,473
App. No.
18/032,084
Granted
Sep 15, 2026
Kind
B2
Abstract

The present disclosure relates generally to methods of preventing, reducing risk of developing, or treating a blood disorder (e.g., cold agglutinin hemolytic anemia (cold agglutinin disease), cold antibody hemolytic anemia, ABO incompatible acute hemolytic reactions, warm agglutinin hemolytic anemia, warm antibody hemolytic anemia, warm antibody autoimmune hemolytic anemia (WAIHA)), autoimmune hemolytic anemia (AIHA), autoimmune thrombocytopenia, paroxysmal cold hemoglobinuria (PCH), antiphospholipid syndrome (APS), Evans syndrome, red blood cell alloimmunization, Felty's syndrome, neonatal alloimmune thrombocytopenia, heparin-induced thrombocytopenia (HIT), heparin-induced thrombocytopenia and thrombosis (HITT), thrombotic thrombocytopenic purpura (TTP), immune thrombocytopenic purpura (ITP), thrombocytopenia, thrombosis, vasculitis, lupus nephritis, systemic lupus erythematosus (SLE), glomerulonephritis, anti-phospholipid antibody syndrome (APS), an infection, or a drug-induced hematologic disorder), comprising administering to a subject an inhibitor of the complement pathway.

Claims (24)

1 . A method of treating a blood disorder associated with C1q-mediated activation of the classical complement pathway in a subject in need thereof, comprising administering to the subject a Cle inhibitor an anti-C1q antibody, wherein the anti-C1q antibody is a full-length antibody or antigen-binding fragment thereof comprising a light chain variable domain comprising an HVR-L1 having the amino acid sequence of SEQ ID NO: 5, an HVR-L2 having the amino acid sequence of SEQ ID NO: 6, and an HVR-L3 having the amino acid sequence of SEQ ID NO: 7; and a heavy chain variable domain comprising an HVR-H1 having the amino acid sequence of SEQ ID NO: 9, an HVR-H2 having the amino acid sequence of SEQ ID NO: 10, and an HVR-H3 having the amino acid sequence of SEQ ID NO: 11; and wherein:

(i) the full-length antibody is administered to the subject by intravenous injection or infusion once a week, once every other week, or once a month at a dose between 10 mg/kg and 150 mg/kg, or at a dose between 75 mg/kg and 100 mg/kg;

(ii) the full-length antibody is administered to the subject by subcutaneous or intramuscular injection at a dose between 1 mg/kg and 10 mg/kg, or at a dose between 3 mg/kg and 5 mg/kg; or

(iii) the antigen-binding fragment is administered to the subject by intravenous injection or infusion, by intramuscular injection, or by subcutaneous injection at a dose between 0.1 mg/kg and 50 mg/kg, or at a dose between 0.3 mg/kg and 10 mg/kg.

2 . The method of claim 1 , wherein the anti-C1q antibody or antigen-binding fragment thereof is a monoclonal antibody, a polyclonal antibody, a recombinant antibody, a humanized antibody, a human antibody, a chimeric antibody, a monovalent antibody, a multispecific antibody, or antibody derivative thereof.

3 . The method of claim 2 , wherein the anti-C1q antibody is an antigen-binding fragment and the antigen-binding fragment is a Fab fragment, a Fab′ fragment, a F(ab′)2 fragment, a Fv fragment, a diabody, or a single-chain variable fragment.

4 . The method of claim 1 , wherein the anti-C1q antibody or antigen-binding fragment thereof comprises a light chain variable domain comprising an amino acid sequence with at least about 95% sequence identity to the amino acid sequence selected from any one of SEQ ID NO: 4 and 35-38.

5 . The method of claim 4 , wherein the light chain variable domain an amino acid sequence selected from any one of SEQ ID NO: 4 and 35-38.

6 . The method of claim 1 , wherein the anti-C1q antibody or antigen-binding fragment thereof comprises a heavy chain variable domain comprising an amino acid sequence with at least about 95% sequence identity to the amino acid sequence selected from any one of SEQ ID NO: 8 and 31-34.

7 . The method of claim 6 , wherein the heavy chain variable domain comprises an amino acid sequence selected from any one of SEQ ID NO: 8 and 31-34.

8 . The method of claim 1 , wherein the anti-C1q antibody is an antibody antigen-binding fragment comprising a heavy chain Fab fragment of SEQ ID NO: 39 and a light chain Fab fragment of SEQ ID NO: 40.

9 . The method of claim 1 , wherein the full-length antibody is administered by subcutaneous or intramuscular injection daily, once every other day, once a week, once every other week, or once a month.

10 . The method of claim 1 , wherein the antigen-binding fragment is administered daily, once every other day, once a week, once every other week, or once a month.

11 . The method of claim 10 , wherein the antigen-binding fragment is administered at an initial predose that is higher than the daily, once every other day, once a week, once every other week, or once a month dose.

12 . The method of claim 11 , wherein the initial predose is between 3 mg/kg and 50 mg/kg or between 3 mg/kg and 20 mg/kg.

13 . The method of claim 1 , wherein the blood disorder is cold agglutinin hemolytic anemia (cold agglutinin disease), cold antibody hemolytic anemia, ABO-incompatible acute hemolytic reactions, warm agglutinin hemolytic anemia, warm antibody hemolytic anemia, warm autoimmune hemolytic anemia (WAIHA), autoimmune hemolytic anemia (AIHA), autoimmune thrombocytopenia, paroxysmal cold hemoglobinuria (PCH), antiphospholipid syndrome (APS), Evan's syndrome, neonatal alloimmune thrombocytopenia, red blood cell alloimmunization, Felty's syndrome, antibody-mediated thrombocytopenia, heparin-induced thrombocytopenia (HIT), heparin-induced thrombocytopenia and thrombosis (HITT), thrombotic thrombocytopenia purpura (TTP), immune thrombocytopenia purpura (ITP), thrombocytopenia, thrombosis, vasculitis, lupus nephritis, systemic lupus erythematosus (SLE), glomerulonephritis, anti-phospholipid antibody syndrome (APS), an infection, or a drug-induced hematologic disorder.

14 . The method of claim 1 , wherein the antigen-binding fragment is rapidly cleared, thereby sparing C1q activity outside a subject's blood space.

15 . The method of claim 1 , wherein the anti-C1q antibody or antigen-binding fragment thereof selectively inhibits C1q within a subject's blood space, thereby sparing C1q activity outside the subject's blood space.

16 . The method of claim 14 , wherein the blood space is confined within a blood vessel.

17 . The method of claim 16 , wherein the blood vessel is an artery, an arteriole, a capillary, a venule, or a vein.

18 . The method of claim 14 , wherein the blood space comprises serum, platelets, endothelial cells, blood cells, or hematopoietic cells.

19 . The method of claim 14 , wherein inhibiting C1q within the subject's blood space reduces tissue damage in a highly vascularized tissue.

20 . The method of claim 19 , wherein the highly vascularized tissue is kidney, alveoli, capillary bed, or glomerulus.

21 . The method of claim 1 , wherein the blood disorder is autoimmune thrombocytopenia, cold agglutinin hemolytic anemia (cold agglutinin disease), paroxysmal cold hemoglobinuria (PCH), warm autoimmune hemolytic anemia (WAIHA), or heparin-induced thrombocytopenia (HIT).

Assignments (1)
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 5, 2023
From: YEDNOCK, TED; SANKARANARAYANAN, SETHU
To: ANNEXON, INC.
Reel/Frame 064149/0277 →
Continuity (2)
Provisional Application 63093029 · Oct 16, 2020
Related Publication 20230391858A1 · Dec 7, 2023
References Cited (36)
US 10227398B2 · Rosenthal · 2019 [cited by examiner]
US 20160145336A1 · Francis et al. · 2016 [cited by applicant]
US 20160159890A1 · Rosenthal et al. · 2016 [cited by applicant]
US 20160326231A1 · Hu et al. · 2016 [cited by applicant]
US 20160355574A1 · Rosenthal et al. · 2016 [cited by applicant]
US 20170152309A1 · Yednock et al. · 2017 [cited by applicant]
US 20240109957A1 · Yednock et al. · 2024 [cited by applicant]
CN 103596576A · 2014 [cited by applicant]
WO WO2009077483A1 · 2009 [cited by applicant]
WO WO2013082563A1 · 2013 [cited by applicant]
WO WO2013192240A2 · 2013 [cited by applicant]
WO WO2015006504A1 · 2015 [cited by applicant]
WO WO2016073685A1 · 2016 [cited by applicant]
WO WO2017091719A1 · 2017 [cited by applicant]
WO WO2021076991A1 · 2021 [cited by applicant]
WO WO2022081997A1 · 2022 [cited by applicant]
CognitiveVitality.org (Alzheimer's Drug Discovery Foundation). “Anti-C1q” (Apr. 1, 2019). pp. 1-16. [cited by examiner]
Synapse by patsnap. “What are C1q inhibitors and how do theywork?” (Jun. 21, 2024). 3 pages. [cited by examiner]
Phuan P-W, et al. (Jun. 2013) Acta Neuropathol. 125(6):829-840. (doi:10.1007/s00401-013-1128-3). [cited by examiner]
Gertz MA, et al. (Dec. 2, 2016) Blood. 128(22):1265. (http://doi.org/10.1182/blood.V128.22.1265.1265). [cited by examiner]
Wat et al., “Molecular actions of heparin and their implications in preventing pre-eclampsia.” Journal of Thrombosis and Haemostasis 16 (2018): 1510-1522. [cited by applicant]
Dunkelberger et al., “Complement and its role in innate and adaptive immune responses.” Cell Research 20 (2010): 34-50. [cited by applicant]
Hom et al., “Complement Inhibitors for Treatment of Geographic Atrophy and Advanced Non-exudative AMD.” Retinal Physician 16 (2019): 28-31. [cited by applicant]
Pickering et al., “Canonical and noncanonical functions of complement in systemic lupus erythematosus.” European Journal of Immunology 54 (2024): 2350918. [cited by applicant]
Schulz et al., “C1q as a target molecule to treat human disease: What do mouse studies teach us?. ” Frontiers in Immunology 13 (2022): 958273. [cited by applicant]
Walport, “Complement and systemic lupus erythematosus.” Arthritis Research & Therapy 4.Suppl 3 (2002): S279. [cited by applicant]
Broome et al. “Safety and efficacy of classical complement pathway inhibition with sutimlimab in chronic immune thrombocytopenia.” Blood Advances 7.6 (2023): 987996. [cited by applicant]
De Boer et al., “C1-inhibitor treatment in patients with severe complement mediated autoimmune hemolytic anemia,” Blood Advances 7.13 (2023): 3128-3139. [cited by applicant]
Extended European Search Report for EP Application No. 20877082.6 dated Apr. 28, 2023. [cited by applicant]
International Search Report and Written Opinion for International Application No. PCT/US20/56121 mailed Feb. 2, 2021. [cited by applicant]
Janeway et al., “The Complement System and Innate Immunity,” Immunobiology: The Immune System in Health and Disease (2001): 15 pages. [cited by applicant]
Janeway et al., “The Interaction of the Antibody Molecule with Specific Antigen,” Immunobiology: The Immune System in Health and Disease (2001): 5 pages. [cited by applicant]
Mehta et al., “Hemophilia,” StatPearls, Jun. 5, 2023. [cited by applicant]
Nayak et al., “Complement and noncomplement activating functions of Clq: a prototypical innate immune molecule.” Innate Immunity 18.2 (2012): 350-363. [cited by applicant]
Extended European Search Report for EP Application No. 21881186.7 dated Feb. 24, 2025. [cited by applicant]
International Search Report and Written Opinion for International Application No. PCT/US2021/055216 mailed Jan. 12, 2022. [cited by applicant]