Attorney Docket No.: 47702.0112WO1 USES OF ANTI-C3 ANTIBODIES CROSS-REFERENCE TO RELATED APPLICATIONS [0001] This applications claims the benefit of priority of U.S. Provisional Appl. Nos. 63/379,882 filed October 17, 2022, and 63/422,042 filed November 3, 2022, the content of both of which are incorporated by reference in their entirety herein. SEQUENCE LISTING [0002] The instant application contains a Sequence Listing which has been submitted electronically in XML format and is hereby incorporated by reference in its entirety. Said XML copy, created on September 21, 2023, is named 47702- 0112WO1_SL.xml and is 64,144 bytes in size. FIELD OF THE INVENTION [0003] The present disclosure generally relates to methods of treating geographic atrophy (GA), slowing down growth of total GA lesion area, preventing development of choroidal neovascularization (CNV), and/or reducing the development of (conversion to) CNV in an eye of a human subject having GA, the methods comprising administering to the human subject an antibody that specifically binds human complement component C3. BACKGROUND [0004] The complement cascade is primarily involved in the detection and removal of foreign pathogens such as bacteria. The complement system includes more than 30 cell- associated and circulating proteins (e.g., C1, C1q, C1r, C1s, C2, C3, C3a, C3b, C4, Factor B, Factor D, Factor H, Factor I). There are three main pathways that activate complement, the classical pathway (CP), the lectin pathway (MBL), and the alternative pathway (AP). Attorney Docket No.: 47702.0112WO1 [0005] The three complement pathways are initiated by different factors, each resulting in the cleavage of complement component C3. The classical complement pathway is activated when the C1 complex binds specific antigen-antibody complexes, often immunoglobulin M (IgM), IgG3, or IgG1. This induces a conformational change in the C1 complex, allowing it to cleave C4 and C2 to generate the C4bC2b complex. C4bC2b acts as the C3 convertase of the classical pathway. The lectin complement pathway is activated when mannose-binding lectin (MBL) binds mannose-containing polysaccharides on microorganisms, initiating the cleavage of C4 and C2 by the MBL- MBL-associated serine protease complex. As in the classical pathway, the C4bC2b complex forms the C3 convertase of the lectin pathway. The oldest evolutionary signaling pathway of the three, the alternative complement pathway acts both independently of, and as an amplification loop for, the classical and lectin pathways. The alternative complement pathway undergoes low-level self-activation through the slow, spontaneous hydrolysis of C3. Once hydrolyzed, C3(H ₂ O) binds complement Factor B, which is subsequently cleaved by complement Factor D into C3(H2O)Bb, forming the C3 convertase of the alternative complement pathway. These different pathways converge with the cleavage of complement component C3 into C3a and C3b. On host cells, endogenous factors shut down the complement cascade. On pathogens, the complement cascade continues with the cleavage of complement component C5, which triggers cell death via phagocytosis, inflammation, and ultimately membrane attack complex (MAC) activation. (Immunobiology: The Immune System in Health and Disease.5th edition; Chapter: The complement system and innate immunity; New York: Garland Science; 2001.) [0006] Although the complement system is traditionally considered part of the immune system, i.e., protection against foreign pathogens, complement activity also has a role in maintaining healthy tissue. For example, clearance of apoptotic cells is facilitated by the complement pathway. However, inappropriate or excessive complement activation is thought to be a cause or contributing factor to a number of diseases and disorders. Attorney Docket No.: 47702.0112WO1 [0007] Among the diseases that complement activation is thought to be involved in is aged-related macular degeneration (AMD). AMD is the main cause of vision loss among the elderly in developed countries and globally affects approximately 9% of the world’s population. There are two types of AMD, dry (approximately 85-90% of patients) and wet (approximately 10-15% of patients). Wet AMD occurs when abnormal blood vessels (known as choroidal neovascularization or CNV) grow under the retina and macula. These new blood vessels may bleed and leak fluid, causing the macula to bulge or lift up from its normally flat position, thus distorting or destroying central vision. Under these circumstances, vision loss may be rapid and severe. Dry AMD is characterized by formation of drusen under the retina. Geographic atrophy (GA) is the advanced (late) form of dry AMD. GA is characterized by the progressive loss of areas of the retinal pigment epithelium (RPE), loss of photoreceptors (rods and cones), loss of neuroretina, and loss of choriocapillaris. The loss of one or more of these cells and/or tissues results in permanent central vision loss. Although there has been some progress in the development of new therapeutics for wet AMD, particularly the use of VEGF inhibitors, until the recent approval of SYFOVRE™ there were no approved treatments for dry AMD and/or GA. Thus, new therapeutic agents, methods of using those agents, and for selecting patients, for treatment of AMD and/or GA are needed. BRIEF SUMMARY [0008] In one aspect, the invention provides a method for treating geographic atrophy (GA) in an eye of a human subject identified as having GA, the method comprising (a) identifying the human subject as having a total GA lesion area in the eye of about 4.0 mm ² - about 10.5 mm ² and (b) administering to the human subject, by intravitreal injection, a therapeutically effective dose of an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a heavy chain variable region (VH) comprising VH complementarity determining region (CDR)1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a light chain variable region (VL) comprising VL CDR1, VL CDR2, and VL CDR3 from Attorney Docket No.: 47702.0112WO1 the amino acid sequence set forth in SEQ ID NO:25. In some instances, the method involves treating GA in an eye of a human subject identified as having GA, the method comprising administering to the subject, by intravitreal injection, a therapeutically effective dose of an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, wherein the subject was previously identified as having a total GA lesion area in the eye of about 4.0 mm ² - about 10.5 mm ² . [0009] In another aspect, the invention provides a method for reducing the growth rate of total GA lesion area in an eye of a human subject identified as having GA, the method comprising (a) identifying the human subject as having a total GA lesion area in the eye of about 4.0 mm ² - about 10.5 mm ² and (b) administering to the human subject, by intravitreal injection, a therapeutically effective dose of an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a heavy chain variable region (VH) comprising VH complementarity determining region (CDR)1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a light chain variable region (VL) comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. In some instances, the method involves reducing the growth rate of total GA lesion area in an eye of a human subject identified as having GA, the method comprising administering to the subject, by intravitreal injection, a therapeutically effective dose of an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, wherein the subject was previously identified as having a total GA lesion area in the eye of about 4.0 mm ² - about 10.5 mm ² . Attorney Docket No.: 47702.0112WO1 [0010] In another aspect, the invention provides a method for reducing the loss of visual acuity in an eye of a human subject identified as having GA, the method comprising (a) identifying the human subject as having a total GA lesion area in the eye of about 4.0 mm ² - about 10.5 mm ² and (b) administering to the human subject, by intravitreal injection, a therapeutically effected dose of an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a heavy chain variable region (VH) comprising VH complementarity determining region (CDR)1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a light chain variable region (VL) comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. In some instances, the method involves reducing the growth rate of total GA lesion area in an eye of a human subject identified as having GA, the method comprising administering to the subject, by intravitreal injection, a therapeutically effective dose of an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, wherein the subject was previously identified as having a total GA lesion area in the eye of about 4.0 mm ² - about 10.5 mm ² . [0011] In another aspect, the invention provides a method for preventing development of choroidal neovascularization in an eye of a human subject identified as having GA, the method comprising administering to the human subject, by intravitreal injection, a therapeutically effective dose of an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a heavy chain variable region (VH) comprising VH complementarity determining region (CDR)1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a light chain variable region (VL) comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. In some embodiments, the subject is identified as having a total GA lesion area in the eye of less than about 4.0 mm ² , about Attorney Docket No.: 47702.0112WO1 4.0 mm ² – about 10.5 mm ² , greater than about 10.5 mm ² , or less than about 9.6 mm ² (e.g., less than about 9.4 mm ² , 9.5 mm ² , 9.6 mm ² , 9.7 mm ² , or 9.8 mm ² ). [0012] In another aspect, the invention provides a method for reducing the development of choroidal neovascularization in an eye of a human subject identified as having GA, the method comprising administering to the human subject, by intravitreal injection, a therapeutically effective dose of an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a heavy chain variable region (VH) comprising VH complementarity determining region (CDR)1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a light chain variable region (VL) comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. In some embodiments, the subject is identified as having a total GA lesion area in the eye of less than about 4.0 mm ² , about 4.0 mm ² – about 10.5 mm ² , greater than about 10.5 mm ² ,or less than about 9.6 mm ² (e.g., less than about 9.4 mm ² , 9.5 mm ² , 9.6 mm ² , 9.7 mm ² , or 9.8 mm ² ). [0013] In some embodiments of any of the foregoing aspects, the dose of the antibody is about 5mg, about 10 mg, about 15 mg, about 20 mg, about 25 mg, about 30 mg or more. In one particular embodiment, the dose of the antibody is 15 mg. [0014] In some embodiments of any of the foregoing aspects, the interval between successive doses/administrations of the antibody is about every 4 weeks, about every 8 weeks, about every 12 weeks, or about every 16 weeks. In some particular embodiments, the interval is every four weeks or every eight weeks. It is understood that, in practice, nominal variations around the target interval may occur based on practical matters such as subject compliance, scheduling, and other practical issues. [0015] In some embodiments of any of the foregoing aspects, the subject is treated for at least about 24 weeks, at least about 52 weeks, at least about 76 weeks, at least about 104 weeks, or even for the lifetime of the patient. [0016] In some embodiments of any of the foregoing aspects, the GA is secondary to age-related macular degeneration (AMD). Optionally, the human subject has a single Attorney Docket No.: 47702.0112WO1 focal GA lesion in the eye prior to administering the anti-C3 antibody. Optionally, the human subject has multifocal GA lesions in the eye being prior to administering the anti- C3 antibody to the eye, from which at least one lesion area is at least 1.25 mm ² . [0017] In some embodiments of any of the foregoing aspects, the human subject has Best Corrected Visual Acuity (BCVA) score of at least 34 early treatment diabetic retinopathy study (ETDRS) letters (20/200 or better Snellen equivalent) in the eye prior to administering the anti-C3 antibody (i.e., at the initiation of therapy). [0018] In some embodiments of any of the foregoing aspects, the human subject has a GA lesion in fovea in the eye prior to administering the anti-C3 antibody. [0019] In some embodiments of any of the foregoing aspects, the human subject does not have a GA lesion in fovea in the eye prior to administering the anti-C3 antibody. [0020] In some embodiments of any of the foregoing aspects, the human subject has no current or prior choroidal neovascularization in the eye prior to administering the anti- C3 antibody. [0021] In some embodiments of any of the foregoing aspects, the human subject has banded or diffuse junctional hyperautofluorescence in the eye prior to administering the anti-C3 antibody. [0022] In some embodiments of any of the foregoing aspects, the human subject has low luminance deficit (LLD) score of at least 30 ETDRS letters in the eye prior to administering the anti-C3 antibody. [0023] In some embodiments of any of the foregoing aspects, the human subject has LLD score of at least 10 ETDRS letters in the eye prior to administering the anti-C3 antibody. [0024] In another aspect, the disclosure features a method treating geographic atrophy secondary to age-related macular degeneration in a human subject in need thereof. The method comprises administering to the human subject by intravitreal injection a dose of 15 mg of an anti-C3 antibody once every 4 weeks or once every 8 Attorney Docket No.: 47702.0112WO1 weeks. In some instances the dose is administered in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [0025] In yet another aspect, the disclosure provides a method of stabilizing or reducing GA lesion size or lesion growth in a human subject in need thereof. The method comprises administering to the human subject by intravitreal injection a dose of 15 mg of an anti-C3 antibody once every 4 weeks or once every 8 weeks. In some instances the dose is administered in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [0026] In a further aspect, the disclosure relates to a method for treating geographic atrophy (GA) in a human subject; a method for reducing the growth rate of total GA lesion area in an eye of a human subject; a method for reducing the loss of visual acuity in an eye of a human subject; a method for reducing the development of choroidal neovascularization in an eye of a human subject; or a method for preventing development of, choroidal neovascularization (CNV) in an eye of a human subject. The method comprises administering to the human subject by intravitreal injection a dose of 15 mg of an anti-C3 antibody once every 4 weeks or once every 8 weeks. In some instances the dose is administered in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [0027] In some instances, in the above aspects, the human subject has a total GA lesion area in the eye of about 4.0 mm ² to about 10.5 mm ² . In certain instances, the human subject shows reduced (relative to baseline) or an absence of choroidal neovascularization. In some instances, the human subject does not have intraocular inflammation, optionally wherein the intraocular inflammation is vitritis, vitreal cells, iridocyclitis, anterior chamber cells, uveitis, iritis, or anterior chamber flare. In certain instances, the human subject does not have an ocular or periocular infection. [0028] In some instances, the above methods further comprise monitoring for one or more conditions selected from the group consisting of endopthalmitis, retinal detachment, neovascular AMD, intraocular inflammation, and increased intraocular pressure, Attorney Docket No.: 47702.0112WO1 optionally wherein if any of these conditions are present treatment is halted until resolution of the condition. In some cases, if the human subject shows signs of neovascular AMD, the method further involves administering to the human subject a therapeutically effective amount of a VEGF inhibitor. The VEGF inhibitor can be an anti-VEGF antibody. In some cases, the anti-VEGF antibody is ranibizumab, bevacizumab, brolucizumab, or faricimab. In some cases, the VEGF inhibitor is aflibercept or conbercept. In some instances, the anti-VEGF antibody or a VEGF inhibitor is intravitreally administered to the human subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, or 12 times a year to the human subject. [0029] In some instances, the above methods involve further administering to the human subject by intravitreal injection a therapeutically effective amount of any one or more of pegcetacoplan, aflibercept, conbercept, ranibizumab, or bevacizumab, brolucizumab, and faricimab. In some cases, the therapeutically effective amount is about 15 mg once every 25 to 60 days. In other cases, the therapeutically effective amount is about 7.5 mg once every 25 to 60 days. In certain other cases, the therapeutically effective amount is about 15 mg once every 50 to 120 days. [0030] In some embodiments of any of the foregoing aspects, the anti-C3 antibody comprises: a heavy chain variable region (VH) comprising VH complementarity determining region (CDR)1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a light chain variable region (VL) comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. [0031] In some cases, the VH CDR1 comprises the amino acid sequence set forth in SEQ ID NO:121, the VH CDR2 comprises the amino acid sequence set forth in SEQ ID NO:14, the VH CDR3 comprises the amino acid sequence set forth in SEQ ID NO:9, the VL CDR1 comprises the amino acid sequence set forth in SEQ ID NO:10, the VL CDR2 comprises the amino acid sequence set forth in SEQ ID NO:11, and the VL CDR3 comprises the amino acid sequence set forth in SEQ ID NO:12. [0032] In some embodiments of any of the foregoing aspects: Attorney Docket No.: 47702.0112WO1 (a) the VH comprises a sequence that is at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID NO:21; (b) the VL comprises a sequence that is at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID NO:25; (c) the VH comprises a sequence that is at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID NO:21 and the VL comprises a sequence that is at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID NO:25; (d) the VH comprises the amino acid sequence set forth in SEQ ID NO:21; or (e) the VL comprises the amino acid sequence set forth in SEQ ID NO: 25. [0033] In some embodiments of any of the foregoing aspects, the VH comprises the amino acid sequence set forth in SEQ ID NO:21 and the VL comprises the amino acid sequence set forth in SEQ ID NO:25. [0034] In some embodiments of any of the foregoing aspects, the antibody comprises a heavy chain and a light chain, wherein: (a) the heavy chain comprises a sequence that is at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID NO:29; (b) the light chain comprises a sequence that is at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID NO:31; (c) the heavy chain comprises a sequence that is at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID NO:29 and the light chain comprises a Attorney Docket No.: 47702.0112WO1 sequence that is at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the amino acid sequence set forth in SEQ ID NO:31; (d) the heavy chain comprises the amino acid sequence set forth in SEQ ID NO:29; or (e) the light chain comprises the amino acid sequence set forth in SEQ ID NO:31. [0035] In some embodiments of any of the foregoing aspects, the antibody comprises a heavy chain and a light chain, wherein the heavy chain comprises the amino acid sequence set forth in SEQ ID NO:29 and the light chain comprises the amino acid sequence set forth in SEQ ID NO:31. [0036] In some embodiments of any of the foregoing aspects, the antibody comprises a heavy chain and a light chain, wherein the heavy chain consists of the amino acid sequence set forth in SEQ ID NO:29 and the light chain consists of the amino acid sequence set forth in SEQ ID NO:31. [0037] In some embodiments of any of the foregoing aspects, the antibody is formulated as a sterile pharmaceutical composition comprising the antibody and a pharmaceutically acceptable carrier. [0038] In some embodiments of any of the foregoing aspects, the antibody is administered at a dose and interval that does not cause an increase in intraocular inflammation and/or does not cause an increase in intraocular pressure that is measurable for more than 48 hours. [0039] In another aspect, the disclosure features a pharmaceutical formulation comprising an anti-C3 antibody at a concentration of 75 mg/mL to 175 mg/mL; L- histidine at a concentration of 10 mM to 30 mM; sucrose at a concentration of 5% to 10%; and polysorbate 20 (PS20) at a concentration of 0.01% to 0.05%. The pharmaceutical formulation has a pH of 5.0 to 6.0. Attorney Docket No.: 47702.0112WO1 [0040] In some cases, the pharmaceutical formulation comprises the anti-C3 antibody at a concentration of 150 mg/mL; L-histidine at a concentration of 20 mM; sucrose at a concentration of 8.2%; and PS20 at a concentration 0.02%. The pharmaceutical composition has a pH of 5.5 [0041] In some cases, the anti-C3 antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. [0042] In some cases, the VH CDR1 comprises the amino acid sequence set forth in SEQ ID NO:121, the VH CDR2 comprises the amino acid sequence set forth in SEQ ID NO:14, the VH CDR3 comprises the amino acid sequence set forth in SEQ ID NO:9, the VL CDR1 comprises the amino acid sequence set forth in SEQ ID NO:10, the VL CDR2 comprises the amino acid sequence set forth in SEQ ID NO:11, and the VL CDR3 comprises the amino acid sequence set forth in SEQ ID NO:12. [0043] In some cases, the VH comprises a sequence that is at least 80% identical to the amino acid sequence set forth in SEQ ID NO:21; the VL comprises a sequence that is at least 80% identical to the amino acid sequence set forth in SEQ ID NO:25; the VH comprises a sequence that is at least 80% identical to the amino acid sequence set forth in SEQ ID NO:21 and the VL has at least 80% identical to the amino acid sequence set forth in SEQ ID NO:25; the VH comprises the amino acid sequence set forth in SEQ ID NO:21; or the VL comprises the amino acid sequence set forth in SEQ ID NO: 25. [0044] In some cases, the VH comprises the amino acid sequence set forth in SEQ ID NO:21 and the VL comprises the amino acid sequence set forth in SEQ ID NO:25. [0045] In some cases, the anti-C3 antibody comprises a heavy chain and a light chain, wherein: (a) the heavy chain comprises a sequence that is at least 80% identical to the amino acid sequence set forth in SEQ ID NO:29; (b) the light chain comprises a sequence that is at least 80% identical to the amino acid sequence set forth in SEQ ID NO:31;(c) the heavy chain comprises a sequence that is at least 80% identical to the amino acid Attorney Docket No.: 47702.0112WO1 sequence set forth in SEQ ID NO:29 and the light chain comprises a sequence that is at least 80% identical to the amino acid sequence set forth in SEQ ID NO:31;(d) the heavy chain comprises the amino acid sequence set forth in SEQ ID NO:29; or (e) the light chain comprises the amino acid sequence set forth in SEQ ID NO:31. [0046] In some cases, the anti-C3 antibody comprises a heavy chain and a light chain, wherein the heavy chain comprises the amino acid sequence set forth in SEQ ID NO:29 and the light chain comprises the amino acid sequence set forth in SEQ ID NO:31. [0047] In certain cases, the anti-C3 antibody comprises a heavy chain and a light chain, wherein the heavy chain consists of the amino acid sequence set forth in SEQ ID NO:29 and the light chain consists of the amino acid sequence set forth in SEQ ID NO:31. [0048] In some instances, the pharmaceutical formulation is administered with a second agent useful for treating GA or any adverse effects resulting from treatment with the pharmaceutical formulation. In some cases, the second agent is any one or more of pegcetacoplan, aflibercept, conbercept, ranibizumab, or bevacizumab, brolucizumab, and faricimab. [0049] In another aspect, the disclosure provides a method of treating geographic atrophy secondary to age-related macular degeneration in a human subject in need thereof. The method comprises administering the pharmaceutical formulation described herein to the human subject by intravitreal injection. In some cases, the pharmaceutical formulation is intravitreally administered at a dose of 15 mg once every 4 weeks or once every 8 weeks. In some cases, the pharmaceutical formulation is administered in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [0050] In another aspect, the disclosure features a method of stabilizing or reducing GA lesion size or lesion growth in a human subject in need thereof. The method comprising administering the pharmaceutical formulation described herein to the human subject by intravitreal injection. In some cases, the pharmaceutical formulation is intravitreally administered at a dose of 15 mg once every 4 weeks or once every 8 weeks. Attorney Docket No.: 47702.0112WO1 In some cases, the pharmaceutical formulation is administered in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [0051] In some instances, the human subject has a total GA lesion area in the eye of about 4.0 mm ² to about 10.5 mm ² . [0052] In some instances, the above methods involve administering the pharmaceutical formulation with a second agent that is useful for treating GA or for treating any adverse effects resulting from treatment with the pharmaceutical formulation. In some cases, the second agent is any one or more of pegcetacoplan, aflibercept, conbercept, ranibizumab, or bevacizumab, brolucizumab, and faricimab. [0053] In yet another aspect, the disclosure relates to a delivery device (e.g., a syringe or a pump) comprising a sterile preparation of the pharmaceutical formulation described herein adapted for intravitreal administration of the anti-C3 antibody at a fixed dose of 15 mg. In some cases, the delivery devices comprises the pharmaceutical formulation in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [0054] Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs. Although methods and materials similar or equivalent to those described herein can be used in the practice or testing of the present invention, the exemplary methods and materials are described below. All publications, patent applications, patents, and other references mentioned herein are incorporated by reference in their entirety. In case of conflict, the present application, including definitions, will control. The materials, methods, and examples are illustrative only and not intended to be limiting. [0055] Other features and advantages of the invention will be apparent from the following detailed description and from the claims. Attorney Docket No.: 47702.0112WO1 BRIEF DESCRIPTION OF THE FIGURES [0056] FIGS.1A-1C are a series of line graphs demonstrating the effect of anti-C3 therapy on the growth rate of GA lesions. FIG.1A shows the GA lesion growth rate in sham (bottom most line relative to x-axis), Q4W (topmost line from x-axis), and Q8W (middle line) subjects having a total GA lesion area of <4 mm ² at the initiation of treatment. FIG.1B shows the GA lesion growth rate in sham (top most line at week 24), Q4W (lowest line at week 24), and Q8W (middle line at week 24) subjects having a total GA lesion area of >10.5 mm ² at the initiation of treatment. FIG.1C shows the GA lesion growth rate in sham (top most line at week 52), Q4W (lowest line at week 52), and Q8W (middle line at week 52) subjects having a total GA lesion area of 4 – 10.5 mm ² at the initiation of treatment. [0057] FIGS.2A-2B are a series of line graphs demonstrating the effect of anti-C3 therapy on the GA lesion growth rate using a post-hoc analysis excluding the quartile of patients having the largest lesions (>9.64 mm ² ) at the initiation of therapy. FIG.2A shows the results of the MMRM analysis of the lower three quartiles. FIG.2B shows the results of a slope analysis. [0058] FIGS.3A-3C are a series of line graphs demonstrating the effect of anti-C3 therapy on the growth rate of GA lesions using a post-hoc analysis of regraded FAF images. FIG.3A shows the results of the MMRM analysis of the entire dataset of included patients. FIG.3B shows the results of the MMRM analysis of the middle two quartiles of patients based on initial lesion size. FIG.3C shows the results of a slope analysis on those middle two quartiles. DETAILED DESCRIPTION [0059] The present disclosure is based on the discovery that anti-C3 therapy, and the IVT administration of an anti-C3 antibody (e.g., Hz38G10(G56A)), slows the growth rate of GA lesions secondary to AMD, reduces the incidence of CNV. The anti-C3 therapy Attorney Docket No.: 47702.0112WO1 was found to be particularly effective in subjects having a moderate GA lesion area of 4 – 10.5 mm ² at the initiation of therapy. Anti-C3 Antibodies [0060] Amino acid (aa) sequences for human C3 (UniProtKB No. P01024), cynomolgus monkey (“cyno”) (NCBI Ref No. XP_005587776.1), and rat C3 (UniProtKB No. P01026) are provided herein as SEQ ID NO:1, SEQ ID NO:32, and SEQ ID NO:37, respectively. As used herein, reference to amino acid positions of C3 refer to the numbering of amino acid sequences including the signal sequence. [0061] Provided herein are antibodies that specifically bind human complement component C3 (SEQ ID NO:2) (also referred to herein as “anti-C3 antibodies”). [0062] In some instances, the anti-C3 antibody is Hz38G10(G56A). Hz38G10(G56A) is a humanized, IgG1 monoclonal antibody having a molecular weight of approximately 150 kDa. The VH and VL of Hz38G10(G56A) are set forth in SEQ ID NO: 21 and SEQ ID NO:25, respectively. The heavy chain and light chain of Hz38G10(G56A) are set forth in SEQ ID NO:29 and SEQ ID NO:31, respectively. Hz38G10(G56A) binds to human C3 with a KD of approximately 340 pM. [0063] In some instances, the anti-C3 antibody comprises the VH CDR1, the VH CDR2, the VH CDR3, the VL CDR1, the VL CDR2, and the VL CDR3 of Hz38G10(G56A). In some instances, the anti-C3 antibody comprises a VH comprising the VH CDR1, the VH CDR2, and the VH CDR3 of Hz38G10(G56A) and a VL comprising the VL CDR1, the VL CDR2, and the VL CDR3 of Hz38G10(G56A). In some instances, the anti-C3 antibody comprises the VH and the VL of Hz38G10(G56A). In some instances, the anti-C3 antibody comprises the heavy chain and the light chain of Hz38G10(G56A). [0064] In some instances, the anti-C3 antibody comprises a VH and a VL, wherein the VH comprises a VH CDR1, a VH CDR2, and a VH CDR3 based on any one of the CDR definitions set forth in Table 1, and wherein the VL comprises a VL CDR1, a VL CDR2, and a VL CDR3 based on any one of the CDR definitions set forth in Table 1. Attorney Docket No.: 47702.0112WO1 [0065] In some instances, the anti-C3 antibody comprises a VH comprising a VH CDR1, a VH CDR2, and a VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising a VL CDR1, a VL CDR2, and a VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. [0066] CDRs are defined by a variety of methods/systems by those skilled in the art. These systems and/or definitions have been developed and refined over a number of years and include Kabat, Chothia, IMGT, AbM, and Contact. The Kabat definition is based on sequence variability and generally is the most commonly used. The Chothia definition is based on the location of the structural loop regions. The IMGT system is based on sequence variability and location within the structure of the variable domain. The AbM definition is a compromise between Kabat and Chothia. The Contact definition is based on analyses of the available antibody crystal structures. An Exemplary system is a combination of Kabat and Chothia. Software programs (e.g., abYsis (www.bioinf.org.uk/abysis/sequence_input/key_annotation/key_ annotation.cgi)) are available and known to those of skill in the art for analysis of antibody sequences and determination of CDRs. The specific CDR sequences defined herein are generally based on a combination of Kabat and Chothia definitions (Exemplary system). However, it will be understood that reference to a VH CDR or CDRs and/or a VL CDR or CDRs of a specific antibody will encompass all CDR definitions as known to those of skill in the art. [0067] In some instances, the anti-C3 antibody comprises a VH comprising a VH CDR1 comprising the amino acid sequence set forth in SEQ ID NO:7, a VH CDR2 comprising the amino acid sequence set forth in SEQ ID NO:14, and a VH CDR3 comprising the amino acid sequence set forth in SEQ ID NO:9; and (ii) a VL comprising a VL CDR1 comprising the amino acid sequence set forth in SEQ ID NO:10, a VL CDR2 comprising the amino acid sequence set forth in SEQ ID NO:11, and a VL CDR3 comprising the amino acid sequence set forth in SEQ ID NO:12. [0068] In some instances, the anti-C3 antibody comprises a VH comprising a VH CDR1 comprising the amino acid sequence set forth in SEQ ID NO:120, a VH CDR2 comprising the amino acid sequence set forth in SEQ ID NO:131, and a VH CDR3 Attorney Docket No.: 47702.0112WO1 comprising the amino acid sequence set forth in SEQ ID NO:9; and (ii) a VL comprising a VL CDR1 comprising the amino acid sequence set forth in SEQ ID NO:10, a VL CDR2 comprising the amino acid sequence set forth in SEQ ID NO:11, and a VL CDR3 comprising the amino acid sequence set forth in SEQ ID NO:12. [0069] In some instances, the anti-C3 antibody comprises a VH comprising a VH CDR1 comprising the amino acid sequence set forth in SEQ ID NO:7, a VH CDR2 comprising the amino acid sequence set forth in SEQ ID NO:132, and a VH CDR3 comprising the amino acid sequence set forth in SEQ ID NO:9; and (ii) a VL comprising a VL CDR1 comprising the amino acid sequence set forth in SEQ ID NO:10, a VL CDR2 comprising the amino acid sequence set forth in SEQ ID NO:11, and a VL CDR3 comprising the amino acid sequence set forth in SEQ ID NO:12. [0070] In some instances, the anti-C3 antibody comprises a VH comprising a VH CDR1 comprising the amino acid sequence set forth in SEQ ID NO:121, a VH CDR2 comprising the amino acid sequence set forth in SEQ ID NO:14, and a VH CDR3 comprising the amino acid sequence set forth in SEQ ID NO:9; and (ii) a VL comprising a VL CDR1 comprising the amino acid sequence set forth in SEQ ID NO:10, a VL CDR2 comprising the amino acid sequence set forth in SEQ ID NO:11, and a VL CDR3 comprising the amino acid sequence set forth in SEQ ID NO:12. [0071] In some instances, the anti-C3 antibody comprises a VH comprising a VH CDR1 comprising the amino acid sequence set forth in SEQ ID NO:122, a VH CDR2 comprising the amino acid sequence set forth in SEQ ID NO:133, and a VH CDR3 comprising the amino acid sequence set forth in SEQ ID NO:126; and (ii) a VL comprising a VL CDR1 comprising the amino acid sequence set forth in SEQ ID NO:127, a VL CDR2 comprising the amino acid sequence set forth in SEQ ID NO:128, and a VL CDR3 comprising the amino acid sequence set forth in SEQ ID NO:129. [0072] In some instances, the VH comprises a sequence that is at least 80%, at least 90%, at least 95%, or at least 97% sequence identical to the amino acid sequence set forth in SEQ ID NO:21. Attorney Docket No.: 47702.0112WO1 [0073] In some instances, the VL comprises a sequence that is at least 80%, at least 90%, at least 95%, or at least 97% sequence identical to the amino acid sequence set forth in SEQ ID NO:25. [0074] In some instances, the VH comprises a sequence that is at least 80%, at least 90%, at least 95%, or at least 97% sequence identical to the amino acid sequence set forth in SEQ ID NO:21 and the VL comprises a sequence that is at least 80%, at least 90%, at least 95%, or at least 97% sequence identical to the amino acid sequence set forth in SEQ ID NO:25. [0075] In some instances, the anti-C3 antibody comprises a VH comprising the amino acid sequence set forth in SEQ ID NO:21. In some instances, the anti-C3 antibody comprises a VH consisting of the amino acid sequence set forth in SEQ ID NO:21. [0076] In some instances, the anti-C3 antibody comprises a VL comprising the amino acid sequence set forth in SEQ ID NO:25. In some instances, the anti-C3 antibody comprises a VL consisting of the amino acid sequence set forth in SEQ ID NO:25. [0077] In some instances, the anti-C3 antibody comprises a VH comprising the amino acid sequence set forth in SEQ ID NO:21 and a VL comprising the amino acid sequence set forth in SEQ ID NO:25. [0078] In some instances, the anti-C3 antibody comprises a VH consisting of the amino acid sequence set forth in SEQ ID NO:21 and a VL consisting of the amino acid sequence set forth in SEQ ID NO:25. [0079] In some instances, the anti-C3 antibody comprises a heavy chain and a light chain, wherein the heavy chain comprises a sequence that is at least 80%, at least 90%, at least 95%, or at least 97% sequence identical to the amino acid sequence set forth in SEQ ID NO:29. [0080] In some instances, the anti-C3 antibody comprises a heavy chain and a light chain, wherein the light chain comprises a sequence that is at least 80%, at least 90%, at Attorney Docket No.: 47702.0112WO1 least 95%, or at least 97% sequence identical to the amino acid sequence set forth in SEQ ID NO:31. [0081] In some instances, the anti-C3 antibody comprises a heavy chain and a light chain, wherein the heavy chain has at least 80%, at least 90%, at least 95%, or at least 97% sequence identical to the amino acid sequence set forth in SEQ ID NO:29 and the light chain has at least 80%, at least 90%, at least 95%, or at least 97% sequence identical to the amino acid sequence set forth in SEQ ID NO:31. [0082] In some instances, the anti-C3 antibody comprises a heavy chain comprising the amino acid sequence set forth in SEQ ID NO:29. In some instances, the anti-C3 antibody comprises a heavy chain consisting of the amino acid sequence set forth in SEQ ID NO:29. [0083] In some instances, the anti-C3 antibody comprises a light chain comprising the amino acid sequence set forth in SEQ ID NO:31. In some instances, the anti-C3 antibody comprises a light chain consisting of the amino acid sequence set forth in SEQ ID NO:31. [0084] In some instances, the anti-C3 antibody comprises a heavy chain comprising the amino acid sequence set forth in SEQ ID NO:29 and a light chain comprising the amino acid sequence set forth in SEQ ID NO:31. [0085] In some instances, the anti-C3 antibody comprises a heavy chain consisting of the amino acid sequence set forth in SEQ ID NO:29 and a light chain consisting of the amino acid sequence set forth in SEQ ID NO:31.

Attorney Docket No.: 47702.0112WO1 Table 1: Hz38G10(G56A) CDR, VH, VL, Heavy Chain, and Light Chain Sequences Exemplary Chothia AbM Kabat Contact GYTFTDFYMD GYTFTDF GYTFTDFYMD DFYMD TDFYMD 2) N 3) 6) 7) Y 8) 9) I D I A K D T G D Y N Attorney Docket No.: 47702.0112WO1 [0086] In certain instances, the anti-C3 antibody is an antibody described in International Patent Application Publication No. WO 2019/195136, which is incorporated by reference herein in its entirety. In certain instances, the anti-C3 antibody is an antibody described in International Patent Application Publication No. WO 2021/159946, which is incorporated by reference herein in its entirety. In certain instances, the anti-C3 antibody is an antibody described in International Patent Application Publication No. WO 2023/118312, which is incorporated by reference herein in its entirety. In certain instances, the anti-C3 antibody is an antibody described in International Patent Application Publication No. WO 2004/031240, which is incorporated by reference herein in its entirety. [0087] In some instances, the anti-C3 antibody comprises a human IgG1 heavy chain constant region. In some instances, the anti-C3 antibody comprises a human IgG2 heavy chain constant region. In some instances, the anti-C3 antibody comprises a human IgG4 heavy chain constant region. [0088] In some instances, the anti-C3 antibody comprises a human kappa light chain constant region. In some instances, the anti- C3 antibody comprises a human lambda light chain constant region. [0089] In some instances, the anti-C3 antibody comprises a human IgG1 heavy chain constant region and a human kappa light chain constant region. [0090] In some instances, the anti-C3 antibody comprises a human IgG1 heavy chain constant region and a human lambda light chain constant region. [0091] In some instances, the anti-C3 antibody is a monoclonal antibody. [0092] The anti-C3 antibodies described herein can be produced by any suitable method known in the art. Such methods range from direct protein synthesis methods to constructing a DNA sequence encoding polypeptide sequences and expressing those sequences in a suitable host. See, e.g., International Patent Application Publication No. Attorney Docket No.: 47702.0112WO1 WO 2019/195136, which is incorporated by reference herein in its entirety, for a description of various methods for producing antibodies. [0093] The anti-C3 antibody described herein may be formulated for use as or in a pharmaceutical composition. The pharmaceutical composition may be used in the methods and uses described herein. In some instances, the pharmaceutical composition comprises an anti-C3 antibody described herein and a pharmaceutically acceptable carrier. In some instances, the pharmaceutical composition is formulated for administration to a human subject via intravitreal injection. The pharmaceutical compositions may be sterile. In some instances, the pharmaceutical composition comprises an anti-C3 antibody and a pharmaceutically acceptable carrier, wherein the anti-C3 antibody comprises a VH comprising a VH CDR1, a VH CDR2, and a VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21 and a VL comprising a VL CDR1, a VL CDR2, and a VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. In some instances, the pharmaceutical composition comprises an anti-C3 antibody and a pharmaceutically acceptable carrier, wherein the anti-C3 antibody comprises a VH comprising a VH CDR1 comprising the amino acid sequence set forth in SEQ ID NO:121, a VH CDR2 comprising the amino acid sequence set forth in SEQ ID NO:14, and a VH CDR3 comprising the amino acid sequence set forth in SEQ ID NO:9, and a VL comprising a VL CDR1 comprising the amino acid sequence set forth in SEQ ID NO:10, a VL CDR2 comprising the amino acid sequence set forth in SEQ ID NO:11, and a VL CDR3 comprising the amino acid sequence set forth in SEQ ID NO:12. In some instances, the pharmaceutical composition comprises an anti-C3 antibody and a pharmaceutically acceptable carrier, wherein the anti-C3 antibody comprises a VH comprising the amino acid sequence set forth in SEQ ID NO:21 and a VL comprising the amino acid sequence set forth in SEQ ID NO:25. In some instances, the pharmaceutical composition comprises an anti-C3 antibody and a pharmaceutically acceptable carrier, wherein the anti-C3 antibody comprises a heavy chain comprising the amino acid sequence set forth in SEQ ID NO:29 and a light chain comprising the amino acid sequence set forth in SEQ ID NO:31. In some instances, the pharmaceutical composition Attorney Docket No.: 47702.0112WO1 comprises an anti-C3 antibody and a pharmaceutically acceptable carrier, wherein the anti-C3 antibody comprises a heavy chain consisting of the amino acid sequence set forth in SEQ ID NO:29 and a light chain consisting of the amino acid sequence set forth in SEQ ID NO:31. Uses and Methods of Treatment [0094] Provided herein is a method of treating GA in an eye of a human subject in need thereof, the method comprising administering to the human subject an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, wherein the administering is via intravitreal injection of the eye. In some instances, the dose and interval are 5 mg, 10 mg, 15 mg, 20 mg, 25 mg, or 30 mg, administered once every 4 weeks, 8 weeks, 10 weeks, 12 week, or 16 weeks, and the human subject has only extrafoveal GA lesions (i.e., does not have GA lesions in the fovea) or has both foveal and extrafoveal GA lesions at the initiation of therapy. In some instances, the duration of therapy is at least 26 weeks, 52, weeks, 78 weeks, 104 weeks, 130 weeks, 156 weeks, or for the lifetime of the patient. In some instances, the antibody is administered at a dose and an interval that does not cause adverse events in the human subject. In some instances, the criteria for GA comprises an area of pallor in the fundus with visibility of the underlying choroidal blood vessels and sharply defined borders, occupying (1) a diameter > 175 µm; (2) a diameter > 250 µm; or (3) a diameter of at least 433 µm. Currently, there is no consensus on the minimum diameter for the diagnosis of GA. [0095] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of less than about 4 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of less than about 4 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion Attorney Docket No.: 47702.0112WO1 area of between about 4 mm ² and 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of between about 4 mm ² and 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of greater than about 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of greater than about 10.5 mm ² at the initiation of therapy. [0096] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject does not have CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject does not have CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has banded or diffuse junctional hyperautofluorescence in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has banded or diffuse junctional hyperautofluorescence in the eye at the initiation of therapy. [0097] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a low luminance deficit (LLD) score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a LLD score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, Attorney Docket No.: 47702.0112WO1 and the human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. [0098] In some instances of any of the foregoing methods, the adverse event not caused by the intravitreal injection is an increase (e.g., a measurable increase) in intraocular pressure (IOP), an increase in IOP that last longer than 24 hours, 48 hours, or 72 hours after injection, an increase (e.g., a measurable increase) in intraocular inflammation, CNV conversion or the development of neovascular AMD, the likelihood of CNV conversion, or ischemic neuropathy. [0099] There are a number of imaging modalities used by medical practitioners skilled in the art, including but not limited to, color fundus photography (CFP), fundus autofluorescence (FAF), optical coherence tomography (OCT), fluorescein angiography (FA), and indocyanine green angiography (ICGA). Imaging modalities allow for the direct measurement and quantification of GA lesion area. [00100] In some instances, treating comprises a therapeutic measure that aims to cure, slow down, lessen symptoms of, and/or halt progression of a pathologic condition or disorder. In some instances, treating comprises reducing the growth rate of the total GA lesion size (e.g., relative to an untreated subject), stopping the growth/increase in the size existing GA lesions, slowing or preventing the development of CNV in a subject that is not diagnosed as having CNV at the initiation of therapy, and/or slowing the progression of CNV in a subject diagnosed as having CNV at the initiation of therapy. [00101] Also provided herein is a method of reducing the growth rate of the total GA lesion area in an eye of a human subject in need thereof, the method comprising administering to the human subject an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, wherein the administering is via intravitreal injection of the eye. In some instances, the dose and interval are 15 mg and Attorney Docket No.: 47702.0112WO1 once every 4 weeks, respectively, and the human subject does not have GA lesions in the fovea. In some instances, the dose and interval are 5 mg, 10 mg, 15 mg, 20 mg, 25 mg, or 30 mg, administered once every 4 weeks, 8 weeks, 10 weeks, 12 week, or 16 weeks, and the human subject has only extrafoveal GA lesions (i.e., does not have GA lesions in the fovea) or has both foveal and extrafoveal GA lesions at the initiation of therapy. In some instances, the duration of therapy is at least 26 weeks, 52, weeks, 78 weeks, 104 weeks, 130 weeks, 156 weeks, or for the lifetime of the patient. In some instances, the antibody is administered at a dose and an interval that does not cause adverse events in the human subject. [00102] In humans, an exemplary mean rate of progression of GA area is 1.5 to 2.2 mm ² /year, with a range of 0.53 to 4.0 mm ² /year. In some instances, the method of reducing total GA lesion area reduces the rate of progression of the total GA lesion area to less than 4.0 mm ² /year, less than 3.75 mm ² /year, less than 3.5 mm ² /year, less than 3.25 mm ² /year, less than 3 mm ² /year, less than 2.75 mm ² /year, less than 2.5 mm ² /year, less than 2.25 mm ² /year, less than 2 mm ² /year mm ² /year, less than 1.9 mm ² /year, less than 1.8 mm ² /year, less than 1.7 mm ² /year, less than 1.6 mm ² /year, less than 1.5 mm ² /year, less than 1.4 mm ² /year, less than 1.3 mm ² /year, less than 1.2 mm ² /year, less than 1.1 mm ² /year, less than 1.0 mm ² /year, less than 0.9 mm ² /year, less than 0.8 mm ² /year, less than 0.7 mm ² /year, less than 0.6 mm ² /year, less than 0.5 mm ² /year, less than 0.4 mm ² /year, or less than 0.3 mm ² /year. In some instances, the method of reducing total GA lesion area reduces the rate of progression of the total GA lesion area to 0.3 to 4 mm ² /year, 0.3 to 3.5 mm ² /year, 0.3 to 3.0 mm ² /year, 0.3 to 2.5 mm ² /year, 0.3 to 2 mm ² /year, 0.3 to 1.5 mm ² /year, 0.3 to 1 mm ² /year, 0.5 to 3.0 mm ² /year, 0.5 to 2.5 mm ² /year, 0.5 to 2 mm ² /year, 0.5 to 1.75 mm ² /year, 0.5 to 1.5 mm ² /year, 0.5 to 1.25 mm ² /year, 0.5 to 1 mm ² /year, 1 to 1.5 mm ² /year, or 1 to 2 mm ² /year. [00103] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of less than about 4 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of less than Attorney Docket No.: 47702.0112WO1 about 4 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of between about 4 mm ² and 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of between about 4 mm ² and 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of greater than about 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of greater than about 10.5 mm ² at the initiation of therapy. [00104] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject does not have CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject does not have CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has banded or diffuse junctional hyperautofluorescence in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has banded or diffuse junctional hyperautofluorescence in the eye at the initiation of therapy. [00105] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a low luminance deficit (LLD) score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a LLD score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the Attorney Docket No.: 47702.0112WO1 human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. [00106] In some embodiments, the total GA lesion area is measured about 6 months after treatment, about 1 year after treatment, about 18 months after treatment, and/or about 2 years after treatment. In some embodiments, the total GA lesion area is measured every time the C3-binding agent is administered. In some embodiments, the total GA lesion area is measured at time points chosen by the medical practitioner. In some instances, the reduction of the total GA lesion area is measured within 4 weeks, within 8 weeks, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of administering a first dose of the anti-C3 antibody. In some instances, the reduction of the total GA lesion area growth rate is measured after administering two or more doses (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 doses) of the anti-C3 antibody. In some instances, the reduction of the total GA lesion area growth rate is measured within 4 weeks, within 8 weeks, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of administering a final dose of the anti-C3 antibody (i.e., after termination of the administering of the anti-C3 antibody at the dose and the interval that does not cause adverse events in the human subject). [00107] In some instances of any of the foregoing methods, the adverse event not caused by the intravitreal injection is an increase (e.g., a measurable increase) in intraocular pressure (IOP), an increase in IOP that last longer than 24 hours, 48 hours, or 72 hours after injection, an increase (e.g., a measurable increase) in intraocular inflammation, CNV conversion or the development of neovascular AMD, the likelihood of CNV conversion, or ischemic neuropathy. [00108] Also provided herein is a method of reducing the decline in visual acuity in a human subject having GA (e.g., relative to an untreated subject), the method comprising Attorney Docket No.: 47702.0112WO1 administering to the human subject an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, wherein the administering is via intravitreal injection of the eye. In some instances, the dose and interval are 5 mg, 10 mg, 15 mg, 20 mg, 25 mg, or 30 mg, administered once every 4 weeks, 8 weeks, 10 weeks, 12 week, or 16 weeks, and the human subject has only extrafoveal GA lesions or has both foveal and extrafoveal GA lesions at the initiation of therapy. In some instances, the duration of therapy is at least 26 weeks, 52, weeks, 78 weeks, 104 weeks, 130 weeks, 156 weeks, or for the lifetime of the patient. In some instances, the antibody is administered at a dose and an interval that does not cause adverse events in the human subject. [00109] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of less than about 4 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of less than about 4 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of between about 4 mm ² and 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of between about 4 mm ² and 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of greater than about 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of greater than about 10.5 mm ² at the initiation of therapy. [00110] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject does not have CNV in the eye at the initiation of Attorney Docket No.: 47702.0112WO1 therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject does not have CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has CNV in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has banded or diffuse junctional hyperautofluorescence in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has banded or diffuse junctional hyperautofluorescence in the eye at the initiation of therapy. [00111] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a low luminance deficit (LLD) score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a LLD score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. [00112] Methods of measuring visual acuity are known in the art, such as, e.g., Snellen eye charts (see e.g., www.mdcalc.com/calc/10060/visual-acuity-testing-snellen-char t), ETDRS letters, use of a standardized chart to determine the smallest letters a person can read on the standardized chart. [00113] In some instances of any of the foregoing methods, the adverse event not caused by the intravitreal injection is an increase (e.g., a measurable increase) in intraocular pressure (IOP), an increase in IOP that last longer than 24 hours, 48 hours, or 72 hours after injection, an increase (e.g., a measurable increase) in intraocular inflammation, Attorney Docket No.: 47702.0112WO1 CNV conversion or the development of neovascular AMD, the likelihood of CNV conversion, or ischemic neuropathy. [00114] Also provided herein is a method of preventing development of choroidal neovascularization (CNV) in an eye of a human subject having GA, the method comprising administering to the human subject an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, wherein the administering is via intravitreal injection of the eye. In some instances, the eye is monitored for CNV about 6 months after treatment, about 1 year after treatment, about 18 months after treatment, and/or about 2 years after treatment. In some embodiments, the eye is monitored for CNV every time the C3-binding agent is administered. In some embodiments, the eye is monitored for CNV at time points chosen by the medical practitioner. In some instances, the eye does not develop CNV within 4 weeks, within 8 weeks, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of administering a first dose of the anti-C3 antibody. In some instances, the eye does not develop CNV after being administered one or more doses (e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 doses) of the anti-C3 antibody. In some instances, the eye does not develop CNV within 4 weeks, within 8 weeks, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of a final dose of the anti-C3 antibody (i.e., after termination of the administering of the anti-C3 antibody at the dose and the interval that does not cause adverse events in the human subject). In some instances, the eye does not develop leakage. In some instances, the eye does not develop severe leakage/ hyperfluorescence. In some instances, the dose and interval are 5 mg, 10 mg, 15 mg, 20 mg, 25 mg, or 30 mg, and administered once every 4 weeks, 8 weeks, 10 weeks, 12 week, or 16 weeks. In some instances, the duration of therapy is at least 26 weeks, 52, weeks, Attorney Docket No.: 47702.0112WO1 78 weeks, 104 weeks, 130 weeks, 156 weeks, or for the lifetime of the patient. In some instances, the antibody is administered at a dose and an interval that does not cause adverse events in the human subject. [00115] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of less than about 4 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of less than about 4 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of between about 4 mm ² and 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of between about 4 mm ² and 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a total GA lesion area of greater than about 10.5 mm ² at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a total GA lesion area of greater than about 10.5 mm ² at the initiation of therapy. [00116] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a low luminance deficit (LLD) score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a LLD score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. [00117] Methods of measuring CNV are described herein and known in the art, see, e.g., Guthrie et al., 2014, Microvasc Res 91:1-7, which is incorporated by reference Attorney Docket No.: 47702.0112WO1 herein in its entirety. In some instances, CNV is measured using fluorescein angiography (FA) and/or Spectral Domain Optical Coherence Tomography (SD-OCT). [00118] Also provided herein is a method of slowing/reducing the development of choroidal neovascularization (CNV) in an eye of a human subject having GA, including GA secondary to AMD, the method comprising administering to the human subject an antibody that specifically binds human complement component C3 (SEQ ID NO:2), wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, wherein the administering is via intravitreal injection of the eye. In some instances, the eye does not develop vascular leakage. In some instances, the eye does not develop severe vascular leakage/hyperfluorescence. Methods of measuring CNV are known in the art, see, e.g., Guthrie et al., 2014, Microvasc Res 91:1-7, which is incorporated by reference herein in its entirety. In some instances, the eye is monitored for CNV about 6 months after treatment, about 1 year after treatment, about 18 months after treatment, and/or about 2 years after treatment. In some embodiments, the eye is monitored for CNV every time the C3-binding agent is administered. In some embodiments, the eye is monitored for CNV at time points chosen by the medical practitioner. In some instances, the development of CNV is evaluated within 4 weeks, within 8 weeks, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of administering a first dose of the anti-C3 antibody. In some instances, the development of CNV is evaluated after administering two or more doses (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 doses) of the anti-C3 antibody. In some instances, the development of CNV is evaluated within 4 weeks, within 8 weeks, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of a final dose of the anti-C3 antibody (i.e., after termination of the administering of the anti- C3 antibody at the dose and the interval that does not cause adverse events in the human Attorney Docket No.: 47702.0112WO1 subject). In some instances, the dose and interval are 5 mg, 10 mg, 15 mg, 20 mg, 25 mg, or 30 mg, administered once every 4 weeks, 8 weeks, 10 weeks, 12 week, or 16 weeks. In some instances, the duration of therapy is at least 26 weeks, 52, weeks, 78 weeks, 104 weeks, 130 weeks, 156 weeks, or for the lifetime of the patient. In some instances, the antibody is administered at a dose and an interval that does not cause adverse events in the human subject. [00119] In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has banded or diffuse junctional hyperautofluorescence in the eye prior to administering the anti-C3 antibody. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has banded or diffuse junctional hyperautofluorescence in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 4 weeks, respectively, and the human subject has a low luminance deficit (LLD) score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the dose and interval are 15 mg and once every 8 weeks, respectively, and the human subject has a LLD score of at least 30 ETDRS letters in the eye at the initiation of therapy. [00120] In some instances of the foregoing methods, the human subject has a total GA lesion area of 2.5 mm ² to 17.5 mm ² in the eye at the initiation of therapy. In some instances, the human subject has a total GA lesion area of less than 4.0 mm ² in the eye at the initiation of therapy. In some instances, the human subject has a total GA lesion area of 4.0 mm ² to 10.5 mm ² in the eye at the initiation of therapy. In some instances, the human subject has a total GA lesion area of greater than 10.5 mm ² in the eye at the initiation of therapy. In some instances, the human subject has a total GA lesion area of 1 mm ² to 17.5 mm ² , 1 mm ² to 15 mm ² , 1 mm ² to 12.5 mm ² , 1 mm ² to 10 mm ² , 1 mm ² to 7.5 mm ² , 1 mm ² to 5 mm ² , 2.5 mm ² to 17.5 mm ² , 2.5 mm ² to 15 mm ² , 2.5 mm ² to 12.5 mm ² , 2.5 mm ² to 10 mm ² , 2.5 mm ² to 7.5 mm ² , 2.5 mm ² to 5 mm ² , 5 mm ² to 17.5 mm ² , 5 mm ² to 15 mm ² , 5 mm ² to 12.5 mm ² , 5 mm ² to 10 mm ² , 5 mm ² to 7.5 mm ² , 2.5 mm ² to 5 mm ² , 7.5 mm ² to 17.5 mm ² , 10 mm ² to 17.5 mm ² , 12.5 mm ² to 17.5 mm ² , 15 mm ² to 17.5 mm ² , 5 mm ² to 15 mm ² , 7.5 mm ² to 15 mm ² , 10 mm ² to 15 mm ² , 12.5 mm ² to 15 mm ² , 5 Attorney Docket No.: 47702.0112WO1 mm ² to 7.5 mm ² , or 5 mm ² to 10 mm ² in the eye at the initiation of therapy. In some instances, the human subject has a total GA lesion area of at least 0.5 mm ² , at least 1 mm ² , at least 1.5 mm ² , at least 2 mm ² , at least 2.5 mm ² , at least 3 mm ² , at least 4 mm ² , at least 5 mm ² , at least 7.5 mm ² , at least 10 mm ² , at least 15 mm ² , at least 20 mm ² , at least 30 mm ² , or at least 40 mm ² in the eye at the initiation of therapy. [00121] In some instances of the foregoing methods, the human subject has a single focal GA lesion in the eye at the initiation of therapy. In some instances, the single focal GA lesion area is less than 4.0 mm ² , 4.0-10.5 mm ² , or greater than 10.5 mm ² to 50 mm ² at the initiation of therapy. [00122] In some instances of the foregoing methods, the subject has multifocal GA lesions in the eye at the initiation of therapy. In some instances, the total lesion area in the eye is less than 4.0 mm ² , 4.0-10.5 mm ² , or greater than 10.5 mm ² to 50 mm ² at the initiation of therapy. [00123] In some instances of the foregoing methods, the human subject has a Best Corrected Visual Acuity (BCVA) score of at least 4, at least 9, at least 14, at least 19, at least 24, at least 29, at least 34, at least 39, at least 44, at least 49, at least 59, at least 59, or at least 64 early treatment diabetic retinopathy study (ETDRS) letters in the injected eye at the initiation of therapy. In some instances, the human subject has a BCVA score of 4 to 8 (20/800 Snellen equivalent), 9 to 13 (20/640 Snellen equivalent), 14 to 18 (20/500 Snellen equivalent), 19 to 23 (20/400 Snellen equivalent), 24 to 28 (20/320 Snellen equivalent), 29 to 33 (20/250 Snellen equivalent), 34 to 38 (20/200 Snellen equivalent), 39 to 43 (20/160 Snellen equivalent), 44 to 48 (20/125 Snellen equivalent), 49 to 53 (20/100 Snellen equivalent), 54 to 58 (20/80 Snellen equivalent), 59 to 63 (20/63 Snellen equivalent), or 64 to 68 (20/50 Snellen equivalent) ETDRS letters. In some instances, the human subject has 4 to 68, 4 to 63, 4 to 58, 4 to 53, 4 to 48, 4 to 43, 4 to 38, 4 to 33, 4 to 28, 4 to 23, 4 to 18, 4 to 13, or 4 to 8 ETDRS letters. In some instances, the human subject has 8 to 68, 8 to 63, 8 to 58, 8 to 53, 8 to 48, 8 to 43, 8 to 38, 8 to 33, 8 to 28, 8 to 23, 8 to 18, or 8 to 13 ETDRS letters. In some instances, the human subject has 13 to 68, 13 to 63, 13 to 58, 13 to 53, 13 to 48, 13 to 43, 13 to 38, 13 to 33, 13 to 28, 13 Attorney Docket No.: 47702.0112WO1 to 23, or 13 to 18 ETDRS letters. In some instances, the human subject has 18 to 68, 18 to 63, 18 to 58, 18 to 53, 18 to 48, 18 to 43, 18 to 38, 18 to 33, 18 to 28, or 18 to 23 to 18 ETDRS letters. In some instances, the human subject has 23 to 68, 23 to 63, 23 to 58, 23 to 53, 23 to 48, 23 to 43, 23 to 38, 23 to 33, or 23 to 28 ETDRS letters. In some instances, the human subject has 28 to 68, 28 to 63, 28 to 58, 28 to 53, 28 to 48, 28 to 43, 28 to 38, or 28 to 33 ETDRS letters. In some instances, the human subject has 33 to 68, 33 to 63, 33 to 58, 33 to 53, 33 to 48, 33 to 43, or 33 to 38 ETDRS letters. [00124] The GA lesion(s) in the eye(s) of the human subject treated in accordance with any one of the foregoing methods may be within or including the fovea, outside of the fovea (extrafoveal), or there may be GA lesion(s) in the fovea and outside of the fovea. In some instances of the foregoing methods, the human subject treated in accordance with any one of the foregoing methods is identified as having foveal lesions. In some instances, the subject is identified as having extrafoveal GA lesion(s). In some instances, the human subject treated in accordance with any one of the foregoing methods is identified as having both foveal and extrafoveal lesions. In some instances of the foregoing methods, the human subject is identified as having one or more (e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or more) foveal GA lesions at the initiation of therapy. In some instances, the human subject does not have any GA lesions in the fovea of the eye administered the anti-C3 antibody. In some instances, the human subject has one or more (e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or more) extrafoveal GA lesions at the initiation of therapy. In some instances, the human subject has one or more (e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or more) foveal GA lesions and one or more (e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or more) extrafoveal GA lesions at the initiation of therapy. [00125] In some instances of the foregoing methods, the human subject does not have choroidal neovascularization in the eye at the initiation of therapy. In some instances of the foregoing methods, the human subject has never had choroidal neovascularization (e.g., has never been diagnosed as having CNV) in the eye prior to the initiation of therapy. Attorney Docket No.: 47702.0112WO1 [00126] In some instances of the foregoing methods, the human subject has CNV in the eye prior to administering the anti-C3 antibody to the eye. [00127] In some instances, the human subject has banded or diffuse junctional hyperautofluorescence in the eye at the initiation of therapy. Methods of identifying banded or diffuse junctional hyperautofluorescence are known in the art; see, e.g., Holz et al., Am J Ophthalmol, 143:463-472 (2007), which is incorporated by reference herein in its entirety. [00128] In some instances, the human subject has a low luminance deficit (LLD) score of at least 10, at least 11, at least 12, at least 13, at least 14, at least 15, at least 16, at least 17, at least 18, at least 19, at least 20, at least 21, at least 22, at least 23, at least 24, at least 25, at least 26, at least 27, at least 28, at least 29, at least 30, at least 31, at least 32, at least 33, at least 34, at least 35, at least 36, at least 37, at least 38, at least 39, or at least 40 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of 10 to 40, 11 to 40, 12 to 40, 13 to 40, 14 to 40, 15 to 40, 20 to 40, 25 to 40, 30 to 40, 45 to 40, 10 to 35, 11 to 35, 12 to 35, 13 to 35, 14 to 35, 15 to 35, 16 to 35, 17 to 35, 18 to 35, 19 to 35, 20 to 35, 30 to 35, 10 to 30, 11 to 30, 12 to 30, 13 to 30, 14 to 30, 15 to 30, 16 to 30, 17 to 30, 18 to 30, 19 to 30, 20 to 30, 21 to 30, 22 to 30, 23 to 30, 24 to 30, 25 to 30, 26 to 30, 27 to 30, 28 to 30, 29 to 30, 10 to 25, 11 to 25, 12 to 25, 13 to 25, 14 to 25, 15 to 25, 16 to 25, 17 to 25, 18 to 25, 19 to 25, 20 to 25, 21 to 25, 22 to 25, 23 to 25, 24 to 25, 10 to 20, 11 to 20, 12 to 20, 13 to 20, 14 to 20, 15 to 20, 16 to 20, 17 to 20, 18 to 20, 19 to 20, 15 to 70, 15 to 60, 15 to 50, 15 to 40, 15 to 30, 20 to 70, 20 to 60, 20 to 50, 20 to 40, 30 to 70, 30 to 60, 30 to 50, or 30 to 40 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of at least 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of at least 20 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of at least 13 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of at least 12 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of at least 11 ETDRS Attorney Docket No.: 47702.0112WO1 letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of at least 10 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of 10 to 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of 13 to 30 ETDRS letters in the eye at the initiation of therapy. In some instances, the human subject has an LLD score of 10 to 40 ETDRS letters in the eye at the initiation of therapy. [00129] In some instances of the foregoing methods, the human subject has bilateral GA at the initiation of therapy. In some instances of the foregoing methods, the human subject has GA in the eye and CNV in a fellow eye at the initiation of therapy. In some instances, the human subject has GA in the eye and does not have CNV in a fellow eye at the initiation of therapy. [00130] Also provided herein is use of an antibody that specifically binds human complement component C3 (SEQ ID NO:2) in the manufacture of a medicament for treating GA in an eye of a human subject in need thereof, wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, and wherein the medicament is administered via intravitreal injection of the eye. [00131] Also provided herein is use of an antibody that specifically binds human complement component C3 (SEQ ID NO:2) in the manufacture of a medicament for slowing down growth of total GA lesion area in an eye of a human subject in need thereof, wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, and wherein the medicament is administered via intravitreal injection of the eye. [00132] Also provided herein is use of an antibody that specifically binds human complement component C3 (SEQ ID NO:2) in the manufacture of a medicament for Attorney Docket No.: 47702.0112WO1 improving visual acuity in an eye of a human subject having GA, , wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, and wherein the medicament is administered via intravitreal injection of the eye. [00133] Also provided herein is use of an antibody that specifically binds human complement component C3 (SEQ ID NO:2) in the manufacture of a medicament for preventing development of choroidal neovascularization in an eye of a human subject having GA, wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, and wherein the medicament is administered via intravitreal injection of the eye. [00134] Also provided herein is use of an antibody that specifically binds human complement component C3 (SEQ ID NO:2) in the manufacture of a medicament for slowing down development of choroidal neovascularization in an eye of a human subject having GA, wherein the antibody comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25, and wherein the medicament is administered via intravitreal injection of the eye. [00135] In some instances of the foregoing methods or uses, the anti-C3 antibody comprises a VH comprising a VH CDR1 comprising the amino acid sequence set forth in SEQ ID NO:121, a VH CDR2 comprising the amino acid sequence set forth in SEQ ID NO:14, and a VH CDR3 comprising the amino acid sequence set forth in SEQ ID NO:9, and a VL comprising a VL CDR1 comprising the amino acid sequence set forth in SEQ ID NO:10, a VL CDR2 comprising the amino acid sequence set forth in SEQ ID NO:11, and a VL CDR3 comprising the amino acid sequence set forth in SEQ ID NO:12. In some instances of the foregoing methods or uses, the anti-C3 antibody comprises a VH Attorney Docket No.: 47702.0112WO1 comprising the amino acid sequence set forth in SEQ ID NO:21 and a VL comprising the amino acid sequence set forth in SEQ ID NO:25. In some instances of the foregoing methods or uses, the anti-C3 antibody comprises a heavy chain comprising the amino acid sequence set forth in SEQ ID NO:29 and a light chain comprising the amino acid sequence set forth in SEQ ID NO:31. In some instances of the foregoing methods or uses, the anti-C3 antibody comprises a heavy chain consisting of the amino acid sequence set forth in SEQ ID NO:29 and a light chain consisting of the amino acid sequence set forth in SEQ ID NO:31. In some instances of the foregoing methods or uses, the anti-C3 antibody is formulated as a pharmaceutical composition, wherein the pharmaceutical composition comprises the anti-C3 antibody and a pharmaceutically acceptable carrier. In some instances, the pharmaceutical composition is sterile. In some instances, the pharmaceutical composition is formulated for intravitreal injection. [00136] In some instances of any of the foregoing methods and uses, the dose of the anti-C3 antibody is 5 to 20 mg. In some instances, the dose of the anti-C3 antibody is 5 to 20 mg, 5 to 15 mg, 5 to 10 mg, 7 to 20 mg, 7 to 15 mg, 7 to 10 mg, 10 to 20 mg, 10 to 15 mg, or 12 to 17 mg. In some instances, the dose of the anti-C3 antibody is about 15 mg. As used herein, “about” in the context of a dose means within 10% of the recited dose (e.g., about 15 mg means 13.5 mg to 16.5 mg). [00137] In some instances of any of the foregoing methods and uses, the dose of the anti-C3 antibody is 15 mg. [00138] In some instances of any of the foregoing methods and uses, the interval of administering the anti-C3 antibody is once every 4 to 16 weeks (e.g., once every 4 weeks, every 5 weeks, every 6 weeks, every 7 weeks, every 8 weeks, every 9 weeks, every 10 weeks, every 11 weeks, every 12 weeks, every 13 weeks, every 14 weeks, every 15 weeks, or every 16 weeks). In some instances, the interval of administering the anti-C3 antibody is once every 4 weeks. In some instances, the interval of administering the anti- C3 antibody is once every 8 weeks. In some instances, the anti-C3 antibody is administered at the dose and interval for a period time, e.g., 2 months, 3 months, 4 months, 5 months, 6 months, 7 months, 8 months, 9 months, 10 months, 11 months, 12 Attorney Docket No.: 47702.0112WO1 months, or longer than 12 months. For example, in some instances, the anti-C3 antibody is administered at a dose of 15 mg once every four weeks for a total of 52 weeks (i.e., 15 mg once every four weeks over the course of 52 weeks, totaling 13 doses). As another example, in some instances, the anti-C3 antibody is administered at a dose of 15 mg once every eight weeks for a total of 52 weeks (i.e., 15 mg once every eight weeks over the course of 52 weeks, totaling 6 doses). In some instances, the dose and interval of administering the anti-C3 antibody is for a period time, e.g., 12 weeks, 16 weeks, 20 weeks, 24 weeks, 28 weeks, 32 weeks, 36 weeks, 40 weeks, 44 weeks, 48 weeks, 52 weeks, 56 weeks, 60 weeks, 64 weeks, 68 weeks, 72 weeks, 76 weeks, or 80 weeks. In some instances, the dose and interval of administering the anti-C3 antibody is for a period of 52 weeks (e.g., a dose of 15 mg once every 4 or 8 weeks or a total of 52 weeks). [00139] In some instances of any of the foregoing methods and uses, the dose and interval of administering the anti-C3 antibody is 15 mg once every 4 weeks. [00140] In some instances of any of the foregoing methods and uses, the dose and interval of administering the anti-C3 antibody is 15 mg once every 8 weeks. [00141] In some instances of any of the foregoing methods and uses, the human subject is at least 45 years, at least 50 years, at least 55 years, at least 60 years, at least 65 years, at least 70 years, at least 75 years, at least 80 years, or at least 85 years of age. In some instances, the human subject is at least 55 years of age. In some instances, the human subject is 45 to 100, 45 to 90, 45 to 80, 45 to 70, 45 to 60, or 45-55 years of age. In some instances, the human subject is 55 to 100, 55 to 90, 55 to 80, 55 to 70, or 55 to 65 years of age. In some instances, the human subject is 65 to 100, 65 to 90, 65 to 80, or 65 to 70years of age. In some instances, the human subject is 70 to 100, 70 to 90, 70 to 80, or 70 to 75 years of age. In some instances, the human subject is 75 to 100, 75 to 95, 75 to 90, 75 to 85, or 75 to 80 years of age. In some instances, the human subject is 80 to 100, 80 to 95, 80 to 90, or 80 to 95 years of age. In some instances, the human subject is 85 to 100, 85 to 95, or 85 to 90 years of age. In some instances, the human subject is 90 to 100 or 90 to 95 years of age. Attorney Docket No.: 47702.0112WO1 Adverse Events [00142] In some instances, the methods described herein comprise administering to the human subject an anti-C3 antibody at a dose and an interval that does not cause one or more (e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or more) adverse events (e.g., mild, moderate, severe, potentially life threatening) in the human subject. Adverse events may be characterized as mild, moderate, severe, or potentially life threatening. Mild adverse events are minor and do not cause significant discomfort to human subject or change in activities of daily living (ADL); human subject is aware of the symptoms, but the symptoms are easily tolerated. Moderate adverse events are an inconvenience or concern to the human subject and cause interference with ADL, but the human subject is able to continue with ADL. Severe adverse events significantly interfere with ADL and the human subject is incapacitated and/or unable to continue with ADL. Potentially life- threatening adverse events are events/reactions in which the human subject was at risk of death at the time of the event/reaction; it does not refer to events/reactions that hypothetically might have caused death if they were more severe. [00143] In some instances, the dose and interval do not cause one or more adverse events (e.g., mild, moderate, severe, potentially life threatening) within 1 day, within 2 days, within 3 days, within 4 days, within 5 days, within 6 days, within 1 week, within 2 weeks, within 3 weeks, within 1 month, within 2 months, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of administering a first dose of the anti-C3 antibody. In some instances, the dose and interval do not cause one or more adverse events (e.g., mild, moderate, severe, potentially life threatening) within 1 day, within 2 days, within 3 days, within 4 days, within 5 days, within 6 days, within 1 week, within 2 weeks, within 3 weeks, within 1 month, within 2 months, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of administering a first, second, third, fourth, fifth, sixth, seventh, eighth, ninth, tenth, eleventh, twelfth, or thirteenth dose of the anti-C3 antibody. In some instances, the dose Attorney Docket No.: 47702.0112WO1 and interval do not cause one or more adverse events (e.g., mild, moderate, severe, potentially life threatening) within 1 day, within 2 days, within 3 days, within 4 days, within 5 days, within 6 days, within 1 week, within 2 weeks, within 3 weeks, within 1 month, within 2 months, within 3 months, within 4 months, within 5 months, within 6 months, within 7 months, within 8 months, within 9 months, within 10 months, within 11 months, or within 12 months of administering a last dose of the anti-C3 antibody. [00144] Adverse events may be ocular (e.g., conjunctival, hemorrhage, eye pruritus, endophthalmitis, CNV development, intraocular inflammation, increased intraocular pressure lasting more than 60 minutes after administering the anti-C3 antibody) or non- ocular (e.g., basal cell carcinoma, benign prostatic hyperplasia, diarrhea, diverticulitis, headache, hypoesthesia, pneumonia, sciatica, ventricular extrasystoles). In some instances, the adverse event is endophthalmitis, CNV development, or intraocular inflammation in either eye. [00145] In some instances, the anti-C3 antibody is administered at a dose (e.g., 15 mg) and an interval (e.g., once every 4 weeks or once every 8 weeks) that does not increase the intraocular pressure (IOP) in the eye administered the anti-C3 antibody by more than 2.5%, more than 5%, more than 10%, more than 15%, more than 20%, more than 25%, or more than 30% relative to the intraocular pressure prior to administering the anti-C3 antibody to the eye (e.g., within 1 hour, within 1 day, within 1 week of prior to administering the anti-C3 antibody), wherein the IOP is measured 1, 2, 3, 4, 5, or more days after said administering. In some instances, the method does not cause a measurable increase in IOP. Methods of measuring IOP are known in the art, such as, e.g., Goldmann tonometry. In certain instances, the antibody is administered at a dose and interval that does not cause an increase in intraocular inflammation and/or that does not cause an increase in intraocular pressure that is measurable for more than 48 hours. Pharmaceutical Formulations [00146] The disclosure also provides compositions (e.g., pharmaceutical formulations) comprising any one of the anti-C3antibodies described herein. For example, an anti-C3 Attorney Docket No.: 47702.0112WO1 antibody of this disclosure comprises: a VH comprising VH CDR1, VH CDR2, and VH CDR3 from the amino acid sequence set forth in SEQ ID NO:21, and a VL comprising VL CDR1, VL CDR2, and VL CDR3 from the amino acid sequence set forth in SEQ ID NO:25. The CDRs can be based on any CDR definition known in the art (e.g., Kabat, Chothia, enhanced Chothia, contact, IMGT, etc.). In one instance, the anti-C3 antibody comprises a VH CDR1 comprising the amino acid sequence set forth in SEQ ID NO:121, a VH CDR2 comprising the amino acid sequence set forth in SEQ ID NO:14, a VH CDR3 comprising the amino acid sequence set forth in SEQ ID NO:9, a VL CDR1 comprising the amino acid sequence set forth in SEQ ID NO:10, a VL CDR2 comprising the amino acid sequence set forth in SEQ ID NO:11, and a VL CDR3 comprising the amino acid sequence set forth in SEQ ID NO:12. In some cases, the anti-C3 antibody comprises a VH comprising a sequence that is at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100% identical to the amino acid sequence set forth in SEQ ID NO:21 and a VL comprising a sequence that is at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100% identical to the amino acid sequence set forth in SEQ ID NO:25. In other cases, the anti-C3 antibody comprises a heavy chain comprising a sequence that is at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100% identical to the amino acid sequence set forth in SEQ ID NO:29 and a light chain comprising a sequence that is at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100% identical to the amino acid sequence set forth in SEQ ID NO:31. [00147] In some cases, the compositions (e.g., pharmaceutical formulations) comprise an anti-C3 antibody described herein at a concentration of 75 mg/mL to 175 mg/mL; L- histidine at a concentration of 10 mM to 30 mM; sucrose at a concentration of 5% to 10%; and PS20 at a concentration of 0.01% to 0.05%. In some cases, the composition Attorney Docket No.: 47702.0112WO1 (e.g., pharmaceutical formulation) has a pH of 5.0 to 6.0. In some cases, the composition (e.g., pharmaceutical formulation) is administered to a human subject in need thereof in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [00148] In certain cases, the compositions (e.g., pharmaceutical formulations) comprise an anti-C3 antibody described herein at a concentration of 75 mg/mL to 175 mg/mL; 0.50 to 1 mg/mL L-Histidine; 2 to 5 mg/mL L-Histidine monohydrochloride monohydrate; 75 to 100 mg/mL sucrose; and 0.1 to 0.5 mg/mL polysorbate 20. In some cases, the composition (e.g., pharmaceutical formulation) has a pH of 5.0 to 6.0. In some cases, the composition (e.g., pharmaceutical formulation) is administered to a human subject in need thereof in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [00149] In certain cases, the compositions (e.g., pharmaceutical formulations) comprise an anti-C3 antibody described herein at a concentration of 150 mg/mL; histidine at a concentration of 20 mM; sucrose at a concentration of 8.2%; and PS20 at a concentration 0.02%. In some cases, the composition (e.g., pharmaceutical formulation) has a pH of 5.5. In some cases, the composition (e.g., pharmaceutical formulation) is administered to a human subject in need thereof in a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl). [00150] The compositions (e.g., pharmaceutical formulations) described herein can be used to treat geographic atrophy. In some cases, the compositions (e.g., pharmaceutical formulations are used in a method treating geographic atrophy secondary to age-related macular degeneration in a human subject in need thereof. In some cases, the pharmaceutical composition is intravitreally administered to the human subject at a dose of 15 mg once every 4 weeks or once every 8 weeks. In certain cases, the compositions (e.g., pharmaceutical formulations are used in a method of stabilizing or reducing GA lesion size or lesion growth in a human subject in need thereof. In some cases, the pharmaceutical composition is intravitreally administered to the human subject at a dose of 15 mg once every 4 weeks or once every 8 weeks. In certain cases, the human subject Attorney Docket No.: 47702.0112WO1 in the above methods has a total GA lesion area in the eye of about 4.0 mm ² to about 10.5 mm ² . [00151] The compositions (e.g., pharmaceutical formulations) described herein can be provided in any delivery device (e.g. syringe, pump). In some cases, a pre-filled syringe is provided that can be used to intravitreally administer a fixed dose of 15 mg of the anti- C3 antibody. In some cases, the delivery device (e.g., syringe, pump) contains a volume of 50 to 100 µl (e.g., 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100 µl) of the pharmaceutical formulation. Kits [00152] Also provided are kits comprising an anti-C3 antibody described herein. In some instances, the kit comprises (a) a container comprising a composition (e.g., a pharmaceutical composition) comprising an anti-C3 antibody described herein, and optionally (b) informational material. In some instances, the informational material is descriptive, instructional, marketing or other material that relates to the methods described herein. In some instances, the composition comprising the anti-C3 antibody in the kit comprises the anti-C3 antibody at a dose that does not cause one or more adverse events (e.g., mild, moderate, severe, potentially life threatening) in the human subject. In some instances, the composition comprising the anti-C3 antibody in the kit comprises the anti-C3 antibody in an amount sufficient to administer a 15 mg dose to a human subject. In some instances, the kit further comprises a device suitable for administration of the composition, e.g., a syringe or other suitable delivery device. The device can be provided pre-loaded with the composition comprising the anti-C3 antibody or can be empty, but suitable for loading.

Attorney Docket No.: 47702.0112WO1 EXAMPLES Example 1 [00153] A randomized, double-masked multicenter study was performed in which subjects with GA secondary to AMD in one or both eyes were administered either the anti-C3 antibody identified as Hz38G10(G56A), as described herein, at a dose of 15 mg in 100 µl volume by intravitreal (IVT) injection, or a sham control, either every 4 weeks (Q4W; a total of 13 doses) or every 8 weeks (Q8W; a total of 7 doses) over a 52-week period. Only one eye of any given subject was chosen as the study eye. In the event both eyes were eligible, the eye with the worse visual function (lower BCVA value) was used as the study eye. If both eyes had the same visual function, the eye with the larger area of GA was selected as the study eye. In the event that both eyes have the same visual function and GA area, the right eye was selected. GA lesion area was measured by fundus autofluorescence (FAF). [00154] Study inclusion criteria included: (a) male or female (non-pregnant, non-lactating) subjects ≥ 55 of age; (b) standard luminance BCVA score of 34 letters or better using ETDRS charts at the starting distance of 4 meters (approximately 20/200 Snellen equivalent or better) in study eye; (c) Clinical diagnosis of GA secondary to AMD with the GA lesion meeting the following criteria as determined by the central reading center's assessment of FAF imaging at screening: (i) total GA area must be ≥ 2.5 and ≤ 17.5 mm ² ; (ii) if GA is multifocal, at least one focal lesion must be ≥ 1.25 mm ² (0.5 DA), with the overall area of GA ≥ 2.5 and ≤ 17.5 mm ² ; (iii) the entire GA lesion must be completely visualized on the macula- centered image and must be able to be imaged in its entirety and not contiguous with any areas of peripapillary atrophy; Attorney Docket No.: 47702.0112WO1 (iv) presence of banded or diffuse pattern of hyper-autofluorescence in the junctional zone of GA. Absence of hyper-autofluorescence in the junctional zone of the GA (i.e., pattern = none) is excluded; (v) well demarcated GA with no anatomical evidence (as assessed by FA and SD-OCT) of current or prior CNV in the study eye (d) clear ocular media and adequate pupil dilatation and fixation in both eyes to permit good quality photographic imaging; and (e) female subjects must be either of i) non-childbearing potential, defined as women who have had a hysterectomy, bilateral oophorectomy, medically documented ovarian failure, documented postmenopausal, or a follicle stimulating hormone > 40 mIU/mL, or ii) if of childbearing potential, defined as women with < 2 years of amenorrhea (absence of menstruation), then must have a negative serum pregnancy test at screening and urine pregnancy test at the Day 1 visit prior to first dose of study drug. [00155] The demographics and baseline ocular characteristics of the study subjects are provided in Table 2. Table 2: Q4W Q8W Sham Pooled Total Attorney Docket No.: 47702.0112WO1 Foveal Involved G _{A (%)} ^{62 (57.4%) 65 (62.5%) 66 (62.3%) 193 (60.7%)} Example 1A – Anti-C3 Therapy Reduces The Overall Growth Rate Of GA Lesions [00156] Slope analysis demonstrates that the Q4W and Q8W groups had a mean reduction of 6.3% and 6.5%, respectively, relative to the combined sham group, in the change in absolute lesion area (i.e., measured in mm ² ) by week 52. However, neither of these effects reached statistical significance. [00157] Secondary analysis using MMRM methodology, adjusted for covariates, helped to correct for the baseline GA lesion size imbalance. The covariates include lesion size, focality, foveal involvement, and CNV in the fellow eye. The results of the MMRM analysis are shown in Table 3 and demonstrate that a statistically-significant reduction in GA lesion growth was measured at week 24 in both the Q4W (19.8%; p=0.027) and Q8W (15.6%; p=0.084) groups relative to sham. There was no statistically- significant difference between the Q4W and Q8W groups at that time point. The effect diminished at 52 weeks and did not reach statistical significance. Attorney Docket No.: 47702.0112WO1 Table 3 Q ^4W Q8W Sham Pooled (n=108) (n=104) (n=106) ) Example 1B – Post-hoc Analysis Demonstrates A Robust Treatment Effect In Subjects Having GA Lesions Of Moderate Size. [00158] In order to further understand the treatment effect of anti-C3 therapy, and to mitigate the effects of the imbalanced initial lesion size among treatment groups (see, Table 2), a post -hoc analysis was performed. It is known that both small GA lesions and large GA lesions may not grow in a linear manner; each tending towards slower growth than moderate-sized lesions. Accordingly, a post-hoc analysis was performed on by sub- dividing each treatment group by initial GA lesion size: <4 mm ² (small lesions), 4-10.5 mm ² (moderate lesions), and >10.5 mm ² (large lesions). As shown in Table 4, the variability in initial lesion size that caused the imbalance without the subdivision of groups is driven by initial lesion size variability in the small and large lesion size subgroups, and particularly in the Q4W group (italicized). Furthermore, the moderate lesion size subgroups were balanced on initial lesion size. Attorney Docket No.: 47702.0112WO1 Table 4 Subgroup Treatment N Mean Lesion Std. Dev. Min Lesion Max Size (mm ² ) Size (mm ² ) Lesion 2) [00159] MMRM analysis of the GA lesion size change from baseline then was performed on all subgroups and the results are showing in FIGS.1A-1C. FIGS 1A and 1B illustrate that no statistically significant treatment effect was observed in the small lesion and large lesion subgroups, respectively. In contrast, FIG.1C illustrates a robust and statistically-significant treatment effect for reducing the GA lesion size growth rate in both the Q4W and Q8W groups relative to sham group in subjects having a moderate initial lesion size. There was no statistically-significant difference between the Q4W and Q8W treatment arms in this subgroup analysis. [00160] A further post-hoc quartile analysis was performed using both the MMRM and slope analyses. These analyses excluded only the quartile of patients with the largest lesions at the initiation of therapy (see, Table 5). The initial lesions size cut-off for the upper quartile is 9.64 mm ² . As shown in FIG.2A, MMRM analysis of the lower three quartiles identified reductions in the GA lesion area growth of 17.8% (p=0.055) and Attorney Docket No.: 47702.0112WO1 15.3% (p=0.133) at 24 weeks, and 13.9% (p=0.086) and 12.2% (p=0.146) at 52 weeks in the Q4W and Q8W groups, respectively. Similarly and as shown in FIG.2B, slope analysis of the combined lower three quartiles reveals that GA lesion area growth was reduced at 52 weeks by 13.7% (p=0.105) and 12.0% (p=0.166) in the Q4W and Q8W groups, respectively. Table 5 Adjusted Treatment Arm (N) Baseline GA Lesion Area Mean (SD) Example 1C – Post-hoc FAF Re-grading And Analysis Demonstrates A Robust Treatment Effect. [00161] The foregoing post-hoc analyses indicated significant variability in lesion size across all treatment groups which led to an imbalance in initial total lesion size, and that much of the variability stemmed from patients having large lesions. In particular, it was observed that the lesion growth trajectory in the sham group appeared to slow in the second six-month period. Some individual patients GA growth curves were atypical, showing a plateau or negative growth trajectory. And, GA lesion growth appear to be most impacted by specific GA lesion types (i.e., large and complex versus small and central). Therefore, the results may have been impacted by high patient variability and grading methodologies. In view of these observations, we undertook to better understand the patients enrolled and the reading center methodologies. [00162] All fundus autofluorescence (FAF) images from the study were reanalyzed by a single blinded observer. An ETDRS grid was placed on the FAF to define the grading field and GA was measured only within the grid. This led to GA areas being excluded from both contiguous and non-contiguous lesions. Satellite GA lesions were included Attorney Docket No.: 47702.0112WO1 only if they exceeded 430 µm in diameter. The following entry criteria violations were used and 54 patients did not meet the initial eligibility criteria: (i) entire GA not fully contained in image window (n=19) (ii) junctional hyper-autofluorescence not diffuse or banded pattern (n=29) (iii) GA not well demarcated (n=1) (iv) GA too large (n=5). These inclusion errors are distributed similarly across treatment arms. [00163] MMRM analysis, as described in Example 1B, was performed on the reanalyzed patient dataset. The results are shown in FIG.3A and demonstrate a similar but slightly more robust result. Specifically, GA lesion growth at the 24-week timepoint was reduced by 20.8% (p=0.037) and 19.3% (P=0.120) in the Q4W and Q8W treatment arms, respectively, relative to sham. At the 52-week timepoint, GA lesion growth was reduced by 11% and 9.5% in the Q4W and Q8W treatment arms, respectively, relative to sham. [00164] This patient dataset then was divided into quartiles based on initial lesion sizes. The middle two quartiles of patients (initial lesion sizes of 4.17 – 9.64 mm ² ) then were further assessed using a post-hoc MMRM and slope analysis As shown in FIG.3B, MMRM analysis of the middle two quartiles identified reductions in the GA lesion area growth of 26% (p=0.013) and 24.4% (p=0.022) at 24 weeks, and 20.6% (p=0.024) and 16.6% (p=0.071) at 52 weeks in the Q4W and Q8W groups, respectively. Similarly, slope analysis revealed reductions in the GA lesion area growth of 21.9% (p=0.020) and 16.8% (p=0.070) at 52 weeks in the Q4W and Q8W groups, respectively (FIG.3C). Table 6 Adjusted Treatment Arm (N) Baseline GA Lesion Area Mean (SD) Attorney Docket No.: 47702.0112WO1 Example 1D – Anti-C3 Therapy Reduces The Growth Rate Of Non-multifocal GA Lesions. [00165] Subgroup analysis was performed on each group based on the focality of lesions at the initiation of treatment. Multifocal GA lesions were those identified with two or more discrete lesions in the treated eye. The results for the change in lesion area at week 52 are provided in Table 7 and demonstrate that the anti-C3 therapy produced a strong trend towards a reduction in lesion size growth at 52 weeks in subjects having non-multifocal lesions. Table 7 Q ^4W Q8W Sham Pooled Example 1E – Anti-C3 Therapy Did Not Cause Intraocular Inflammation Or Other Significant Adverse Events. [00166] All subjects were assessed for adverse events including intraocular inflammation (IOI) in the study eye. IOI is defined as inflammation, anterior chamber cells, vitreous cells, endophthalmitis, vitritis, retinal vasculitis, and retinal vein occlusion. Attorney Docket No.: 47702.0112WO1 As shown in Table 8, the current anti-C3 therapies did not result in elevated IOI relative to the sham group. Table 8 Q4W Q8W Pooled Pooled Sham (n 108) (n 104) Treatment Arms Arms (n=106) Example 1F – Anti-C3 Therapy Reduced The CNV Conversion Rate In Study Eyes. [00167] Both the study eye and the fellow (non-study) eye of all subjects were monitored for the conversion of GA (dry AMD) into CNV and neovascular AMD over the course of the study. As shown in Table 9, the anti-C3 therapy reduced the incidence of CNV conversion in the study eye relative to sham, and the rate of CNV conversion in the fellow eye and sham arm was similar.

Attorney Docket No.: 47702.0112WO1 Table 9 Q ^4W Q8W Sham Pooled (n=108) (n=104) (n=106) Example 2 Anti-C3 Antibody Pharmaceutical Formulation [00168] After detailed and careful experimentation testing multiple different excipients, Applicant arrived at a pharmaceutical formulation of the anit-C3 antibody that can be administered intravitreally at high concentrations. The pharmaceutical formulation comprises the anti-C3 antibody at a concentration of 150 mg/mL; L-histidine at a concentration of 20 mM; sucrose at a concentration of 8.2%; and PS20 at a concentration 0.02%.The pharmaceutical formulation has a pH of 5.5. The anti-C3 antibody comprises a VH and VL, wherein the VH comprises the three VH-CDRs of Hz38G10(G56A) and the VL comprises the three VL-CDRs of Hz38G10(G56A). See, Table 1. [00169] Provided below are exemplary sequences. Human C3 amino acid sequence with predicted signal sequence in bold (SEQ ID NO:1) MGPTSGPSLLLLLLTHLPLALGSPMYSIITPNILRLESEETMVLEAHDAQGDVPVTVTVH DFPGK KLVLSSEKTVLTPATNHMGNVTFTIPANREFKSEKGRNKFVTVQATFGTQVVEKVVLVSL QSGYL FIQTDKTIYTPGSTVLYRIFTVNHKLLPVGRTVMVNIENPEGIPVKQDSLSSQNQLGVLP LSWDI PELVNMGQWKIRAYYENSPQQVFSTEFEVKEYVLPSFEVIVEPTEKFYYIYNEKGLEVTI TARFL YGKKVEGTAFVIFGIQDGEQRISLPESLKRIPIEDGSGEVVLSRKVLLDGVQNPRAEDLV GKSLY Attorney Docket No.: 47702.0112WO1 VSATVILHSGSDMVQAERSGIPIVTSPYQIHFTKTPKYFKPGMPFDLMVFVTNPDGSPAY RVPVA VQGEDTVQSLTQGDGVAKLSINTHPSQKPLSITVRTKKQELSEAEQATRTMQALPYSTVG NSNNY LHLSVLRTELRPGETLNVNFLLRMDRAHEAKIRYYTYLIMNKGRLLKAGRQVREPGQDLV VLPLS ITTDFIPSFRLVAYYTLIGASGQREVVADSVWVDVKDSCVGSLVVKSGQSEDRQPVPGQQ MTLKI EGDHGARVVLVAVDKGVFVLNKKNKLTQSKIWDVVEKADIGCTPGSGKDYAGVFSDAGLT FTSSS GQQTAQRAELQCPQPAARRRRSVQLTEKRMDKVGKYPKELRKCCEDGMRENPMRFSCQRR TRFIS LGEACKKVFLDCCNYITELRRQHARASHLGLARSNLDEDIIAEENIVSRSEFPESWLWNV EDLKE PPKNGISTKLMNIFLKDSITTWEILAVSMSDKKGICVADPFEVTVMQDFFIDLRLPYSVV RNEQV EIRAVLYNYRQNQELKVRVELLHNPAFCSLATTKRRHQQTVTIPPKSSLSVPYVIVPLKT GLQEV EVKAAVYHHFISDGVRKSLKVVPEGIRMNKTVAVRTLDPERLGREGVQKEDIPPADLSDQ VPDTE SETRILLQGTPVAQMTEDAVDAERLKHLIVTPSGCGEQNMIGMTPTVIAVHYLDETEQWE KFGLE KRQGALELIKKGYTQQLAFRQPSSAFAAFVKRAPSTWLTAYVVKVFSLAVNLIAIDSQVL CGAVK WLILEKQKPDGVFQEDAPVIHQEMIGGLRNNNEKDMALTAFVLISLQEAKDICEEQVNSL PGSIT KAGDFLEANYMNLQRSYTVAIAGYALAQMGRLKGPLLNKFLTTAKDKNRWEDPGKQLYNV EATSY ALLALLQLKDFDFVPPVVRWLNEQRYYGGGYGSTQATFMVFQALAQYQKDAPDHQELNLD VSLQL PSRSSKITHRIHWESASLLRSEETKENEGFTVTAEGKGQGTLSVVTMYHAKAKDQLTCNK FDLKV TIKPAPETEKRPQDAKNTMILEICTRYRGDQDATMSILDISMMTGFAPDTDDLKQLANGV DRYIS KYELDKAFSDRNTLIIYLDKVSHSEDDCLAFKVHQYFNVELIQPGAVKVYAYYNLEESCT RFYHP EKEDGKLNKLCRDELCRCAEENCFIQKSDDKVTLEERLDKACEPGVDYVYKTRLVKVQLS NDFDE YIMAIEQTIKSGSDEVQVGQQRTFISPIKCREALKLEEKKHYLMWGLSSDFWGEKPNLSY IIGKD TWVEHWPEEDECQDEENQKQCQDLGAFTESMVVFGCPN Human C3 amino acid sequence without predicted signal sequence (SEQ ID NO:2) SPMYSIITPNILRLESEETMVLEAHDAQGDVPVTVTVHDFPGKKLVLSSEKTVLTPATNH MGNVT FTIPANREFKSEKGRNKFVTVQATFGTQVVEKVVLVSLQSGYLFIQTDKTIYTPGSTVLY RIFTV NHKLLPVGRTVMVNIENPEGIPVKQDSLSSQNQLGVLPLSWDIPELVNMGQWKIRAYYEN SPQQV FSTEFEVKEYVLPSFEVIVEPTEKFYYIYNEKGLEVTITARFLYGKKVEGTAFVIFGIQD GEQRI SLPESLKRIPIEDGSGEVVLSRKVLLDGVQNPRAEDLVGKSLYVSATVILHSGSDMVQAE RSGIP IVTSPYQIHFTKTPKYFKPGMPFDLMVFVTNPDGSPAYRVPVAVQGEDTVQSLTQGDGVA KLSIN THPSQKPLSITVRTKKQELSEAEQATRTMQALPYSTVGNSNNYLHLSVLRTELRPGETLN VNFLL RMDRAHEAKIRYYTYLIMNKGRLLKAGRQVREPGQDLVVLPLSITTDFIPSFRLVAYYTL IGASG QREVVADSVWVDVKDSCVGSLVVKSGQSEDRQPVPGQQMTLKIEGDHGARVVLVAVDKGV FVLNK Attorney Docket No.: 47702.0112WO1 KNKLTQSKIWDVVEKADIGCTPGSGKDYAGVFSDAGLTFTSSSGQQTAQRAELQCPQPAA RRRRS VQLTEKRMDKVGKYPKELRKCCEDGMRENPMRFSCQRRTRFISLGEACKKVFLDCCNYIT ELRRQ HARASHLGLARSNLDEDIIAEENIVSRSEFPESWLWNVEDLKEPPKNGISTKLMNIFLKD SITTW EILAVSMSDKKGICVADPFEVTVMQDFFIDLRLPYSVVRNEQVEIRAVLYNYRQNQELKV RVELL HNPAFCSLATTKRRHQQTVTIPPKSSLSVPYVIVPLKTGLQEVEVKAAVYHHFISDGVRK SLKVV PEGIRMNKTVAVRTLDPERLGREGVQKEDIPPADLSDQVPDTESETRILLQGTPVAQMTE DAVDA ERLKHLIVTPSGCGEQNMIGMTPTVIAVHYLDETEQWEKFGLEKRQGALELIKKGYTQQL AFRQP SSAFAAFVKRAPSTWLTAYVVKVFSLAVNLIAIDSQVLCGAVKWLILEKQKPDGVFQEDA PVIHQ EMIGGLRNNNEKDMALTAFVLISLQEAKDICEEQVNSLPGSITKAGDFLEANYMNLQRSY TVAIA GYALAQMGRLKGPLLNKFLTTAKDKNRWEDPGKQLYNVEATSYALLALLQLKDFDFVPPV VRWLN EQRYYGGGYGSTQATFMVFQALAQYQKDAPDHQELNLDVSLQLPSRSSKITHRIHWESAS LLRSE ETKENEGFTVTAEGKGQGTLSVVTMYHAKAKDQLTCNKFDLKVTIKPAPETEKRPQDAKN TMILE ICTRYRGDQDATMSILDISMMTGFAPDTDDLKQLANGVDRYISKYELDKAFSDRNTLIIY LDKVS HSEDDCLAFKVHQYFNVELIQPGAVKVYAYYNLEESCTRFYHPEKEDGKLNKLCRDELCR CAEEN CFIQKSDDKVTLEERLDKACEPGVDYVYKTRLVKVQLSNDFDEYIMAIEQTIKSGSDEVQ VGQQR TFISPIKCREALKLEEKKHYLMWGLSSDFWGEKPNLSYIIGKDTWVEHWPEEDECQDEEN QKQCQ DLGAFTESMVVFGCPN Human C3 and C3b beta chain (amino acids 23-667) (SEQ ID NO:3) SPMYSIITPNILRLESEETMVLEAHDAQGDVPVTVTVHDFPGKKLVLSSEKTVLTPATNH MGNVT FTIPANREFKSEKGRNKFVTVQATFGTQVVEKVVLVSLQSGYLFIQTDKTIYTPGSTVLY RIFTV NHKLLPVGRTVMVNIENPEGIPVKQDSLSSQNQLGVLPLSWDIPELVNMGQWKIRAYYEN SPQQV FSTEFEVKEYVLPSFEVIVEPTEKFYYIYNEKGLEVTITARFLYGKKVEGTAFVIFGIQD GEQRI SLPESLKRIPIEDGSGEVVLSRKVLLDGVQNPRAEDLVGKSLYVSATVILHSGSDMVQAE RSGIP IVTSPYQIHFTKTPKYFKPGMPFDLMVFVTNPDGSPAYRVPVAVQGEDTVQSLTQGDGVA KLSIN THPSQKPLSITVRTKKQELSEAEQATRTMQALPYSTVGNSNNYLHLSVLRTELRPGETLN VNFLL RMDRAHEAKIRYYTYLIMNKGRLLKAGRQVREPGQDLVVLPLSITTDFIPSFRLVAYYTL IGASG QREVVADSVWVDVKDSCVGSLVVKSGQSEDRQPVPGQQMTLKIEGDHGARVVLVAVDKGV FVLNK KNKLTQSKIWDVVEKADIGCTPGSGKDYAGVFSDAGLTFTSSSGQQTAQRAELQCPQPAA Human C3 alpha chain (amino acids 672-1663) (SEQ ID NO:4) Attorney Docket No.: 47702.0112WO1 SVQLTEKRMDKVGKYPKELRKCCEDGMRENPMRFSCQRRTRFISLGEACKKVFLDCCNYI TELRR QHARASHLGLARSNLDEDIIAEENIVSRSEFPESWLWNVEDLKEPPKNGISTKLMNIFLK DSITT WEILAVSMSDKKGICVADPFEVTVMQDFFIDLRLPYSVVRNEQVEIRAVLYNYRQNQELK VRVEL LHNPAFCSLATTKRRHQQTVTIPPKSSLSVPYVIVPLKTGLQEVEVKAAVYHHFISDGVR KSLKV VPEGIRMNKTVAVRTLDPERLGREGVQKEDIPPADLSDQVPDTESETRILLQGTPVAQMT EDAVD AERLKHLIVTPSGCGEQNMIGMTPTVIAVHYLDETEQWEKFGLEKRQGALELIKKGYTQQ LAFRQ PSSAFAAFVKRAPSTWLTAYVVKVFSLAVNLIAIDSQVLCGAVKWLILEKQKPDGVFQED APVIH QEMIGGLRNNNEKDMALTAFVLISLQEAKDICEEQVNSLPGSITKAGDFLEANYMNLQRS YTVAI AGYALAQMGRLKGPLLNKFLTTAKDKNRWEDPGKQLYNVEATSYALLALLQLKDFDFVPP VVRWL NEQRYYGGGYGSTQATFMVFQALAQYQKDAPDHQELNLDVSLQLPSRSSKITHRIHWESA SLLRS EETKENEGFTVTAEGKGQGTLSVVTMYHAKAKDQLTCNKFDLKVTIKPAPETEKRPQDAK NTMIL EICTRYRGDQDATMSILDISMMTGFAPDTDDLKQLANGVDRYISKYELDKAFSDRNTLII YLDKV SHSEDDCLAFKVHQYFNVELIQPGAVKVYAYYNLEESCTRFYHPEKEDGKLNKLCRDELC RCAEE NCFIQKSDDKVTLEERLDKACEPGVDYVYKTRLVKVQLSNDFDEYIMAIEQTIKSGSDEV QVGQQ RTFISPIKCREALKLEEKKHYLMWGLSSDFWGEKPNLSYIIGKDTWVEHWPEEDECQDEE NQKQC QDLGAFTESMVVFGCPN Human C3b alpha chain (amino acids 749-1663) (SEQ ID NO:5) SNLDEDIIAEENIVSRSEFPESWLWNVEDLKEPPKNGISTKLMNIFLKDSITTWEILAVS MSDKK GICVADPFEVTVMQDFFIDLRLPYSVVRNEQVEIRAVLYNYRQNQELKVRVELLHNPAFC SLATT KRRHQQTVTIPPKSSLSVPYVIVPLKTGLQEVEVKAAVYHHFISDGVRKSLKVVPEGIRM NKTVA VRTLDPERLGREGVQKEDIPPADLSDQVPDTESETRILLQGTPVAQMTEDAVDAERLKHL IVTPS GCGEQNMIGMTPTVIAVHYLDETEQWEKFGLEKRQGALELIKKGYTQQLAFRQPSSAFAA FVKRA PSTWLTAYVVKVFSLAVNLIAIDSQVLCGAVKWLILEKQKPDGVFQEDAPVIHQEMIGGL RNNNE KDMALTAFVLISLQEAKDICEEQVNSLPGSITKAGDFLEANYMNLQRSYTVAIAGYALAQ MGRLK GPLLNKFLTTAKDKNRWEDPGKQLYNVEATSYALLALLQLKDFDFVPPVVRWLNEQRYYG GGYGS TQATFMVFQALAQYQKDAPDHQELNLDVSLQLPSRSSKITHRIHWESASLLRSEETKENE GFTVT AEGKGQGTLSVVTMYHAKAKDQLTCNKFDLKVTIKPAPETEKRPQDAKNTMILEICTRYR GDQDA TMSILDISMMTGFAPDTDDLKQLANGVDRYISKYELDKAFSDRNTLIIYLDKVSHSEDDC LAFKV HQYFNVELIQPGAVKVYAYYNLEESCTRFYHPEKEDGKLNKLCRDELCRCAEENCFIQKS DDKVT LEERLDKACEPGVDYVYKTRLVKVQLSNDFDEYIMAIEQTIKSGSDEVQVGQQRTFISPI KCREA Attorney Docket No.: 47702.0112WO1 LKLEEKKHYLMWGLSSDFWGEKPNLSYIIGKDTWVEHWPEEDECQDEENQKQCQDLGAFT ESMVV FGCPN Human C3a (amino acids 672-748) (SEQ ID NO:6) SVQLTEKRMDKVGKYPKELRKCCEDGMRENPMRFSCQRRTRFISLGEACKKVFLDCCNYI TELRR QHARASHLGLAR Hz38G10(G56A) Heavy chain amino acid sequence with signal sequence in bold (SEQ ID NO:28) MDMRVPAQLLGLLLLWLRGARCQVQLVQSGAEVKKPGASVKVSCKASGYTFTDFYMDWVR QAPGQ RLEWMGYIYPHNAGTTYNQQFTGRVTITVDKSASTAYMELSSLRSEDTAVYYCARRGGFD FDYWG QGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVH TFPAV LQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPA LAGGP SVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNS TYRVV SVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQV SLTCL VKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVM HEALH NHYTQKSLSLSPGK Hz38G10 Light chain amino acid sequence with signal sequence in bold (SEQ ID NO:30) MDMRVPAQLLGLLLLWLRGARCDIQMTQSPSSLSASVGDRVTITCKASENVDTYVSWYQQ KPGKA PKLLIYGASNRYTGVPSRFSGSGSGTDFTFTISSLQPEDIATYHCGQSHSYPLTFGQGTK LEIKR TVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDS KDSTY SLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC Cynomolgus monkey C3 amino acid sequence with predicted signal sequence in bold (SEQ ID NO:32) MGLTSGPSLLLLLLIHLPLALGTPMYSMITPNVLRLESEETVVLEAHDANGDVPVTVTVH DFPGK KLVLSSEKTVLTPATSHMGSVTIRIPANKEFKSEKGHNKFVTVQATFGAQVVEKVVLVSL QSGYL FIQTDKTIYTPGSTVLCRIFTVNHKLLPVGRTVVVNIENPDGIPVKQDSLSSQNQFGILP LSWDI Attorney Docket No.: 47702.0112WO1 PELVNMGQWKIRAYYENSPQQVFSTEFEVKEYVLPSFEVIVEPTEKFYYIYNQKGLEVTI TARFL YGKKVEGTAFVIFGIQDGEQRISLPESLKRIQIEDGSGDAVLSRKVLLDGVQNPRPEDLV GKSLY VSVTVILHSGSDMVQAERSGIPIVTSPYQIHFTKTPKYFKPGMPFDLMVFVTNPDGSPAY RVPVA VQGEDAVQSLTQGDGVAKLSINTHPSQKPLSITVRTKKRELSEAEQATRTMEAQPYSTVG NSNNY LHLSVPRAELRPGETLNVNFLLRMDRTQEAKIRYYTYLIMNKGKLLKVGRQVREPGQDLV VLPLS ITTDFIPSFRLVAYYTLIGANGQREVVADSVWVDVKDSCVGSLVVKSGQSEDRQPLPGQQ MTLKI EGDHGARVGLVAVDKGVFVLNKKNKLTQSKIWDVVEKADIGCTPGSGKDYAGVFSDAGLT FASSS GQQTAQRAELQCPQPAARRRRSVQLAEKRMDKVGQYPKELRKCCEHGMRENPMRFSCQRR TRYIT LDEACKKAFLDCCNYITELRRQHARASHLGLARSNLDEDIIAEENIVSRSEFPESWLWKI EELKE APKNGISTKLMNIFLKDSITTWEILAVSLSDKKGICVADPFEVTVMQDFFIDLRLPYSVV RNEQV EIRAVLYNYRQNQELKVRVELLHNPAFCSLATAKRRHQQTVTIPPKSSLSVPYVIVPLKT GQQEV EVKAAVYHFFISDGVRKSLKVVPEGIRMNKTVAVRTLDPERLGQEGVQREDVPPADLSDQ VPDTE SETRILLQGTPVAQMTEDAIDAERLKHLIVTPSGCGEQNMITMTPTVIAVHYLDETEQWE KFGPE KRQGALELIKKGYTQQLAFRQPSSAFAAFLNRAPSTWLTAYVVKVFSLAVNLIAIDSQVL CGAVK WLILEKQKPDGVFQEDAPVIHQEMTGGFRNTNEKDMALTAFVLISLQEAKEICEEQVNSL PGSIT KAGDFLEANYMNLQRSYTVAIAAYALAQMGRLKGPLLNKFLTTAKDKNRWEEPGQQLYNV EATSY ALLALLQLKDFDFVPPVVRWLNEQRYYGGGYGSTQATFMVFQALAQYQKDVPDHKELNLD VSLQL PSRSSKIIHRIHWESASLLRSEETKENEGFTVTAEGKGQGTLSVVTMYHAKAKGQLTCNK FDLKV TIKPAPETEKRPQDAKNTMILEICTRYRGDQDATMSILDISMMTGFVPDTDDLKQLANGV DRYIS KYELDKAFSDRNTLIIYLDKVSHSEDDCIAFKVHQYFNVELIQPGAVKVYAYYNLAESCT RFYHP EKEDGKLNKLCRDELCRCAEENCFIQKLDDKVTLEERLDKACEPGVDYVYKTRLVKAQLS NDFDE YIMAIEQIIKSGSDEVQVGQQRTFISPIKCREALKLEERKHYLMWGLSSDFWGEKPNLSY IIGKD TWVEHWPEEDECQDEENQKQCQDLGTFTENMVVFGCPN Cynomolgus monkey C3 amino acid sequence without predicted signal sequence (SEQ ID NO:33) TPMYSMITPNVLRLESEETVVLEAHDANGDVPVTVTVHDFPGKKLVLSSEKTVLTPATSH MGSVT IRIPANKEFKSEKGHNKFVTVQATFGAQVVEKVVLVSLQSGYLFIQTDKTIYTPGSTVLC RIFTV NHKLLPVGRTVVVNIENPDGIPVKQDSLSSQNQFGILPLSWDIPELVNMGQWKIRAYYEN SPQQV FSTEFEVKEYVLPSFEVIVEPTEKFYYIYNQKGLEVTITARFLYGKKVEGTAFVIFGIQD GEQRI SLPESLKRIQIEDGSGDAVLSRKVLLDGVQNPRPEDLVGKSLYVSVTVILHSGSDMVQAE RSGIP IVTSPYQIHFTKTPKYFKPGMPFDLMVFVTNPDGSPAYRVPVAVQGEDAVQSLTQGDGVA KLSIN Attorney Docket No.: 47702.0112WO1 THPSQKPLSITVRTKKRELSEAEQATRTMEAQPYSTVGNSNNYLHLSVPRAELRPGETLN VNFLL RMDRTQEAKIRYYTYLIMNKGKLLKVGRQVREPGQDLVVLPLSITTDFIPSFRLVAYYTL IGANG QREVVADSVWVDVKDSCVGSLVVKSGQSEDRQPLPGQQMTLKIEGDHGARVGLVAVDKGV FVLNK KNKLTQSKIWDVVEKADIGCTPGSGKDYAGVFSDAGLTFASSSGQQTAQRAELQCPQPAA RRRRS VQLAEKRMDKVGQYPKELRKCCEHGMRENPMRFSCQRRTRYITLDEACKKAFLDCCNYIT ELRRQ HARASHLGLARSNLDEDIIAEENIVSRSEFPESWLWKIEELKEAPKNGISTKLMNIFLKD SITTW EILAVSLSDKKGICVADPFEVTVMQDFFIDLRLPYSVVRNEQVEIRAVLYNYRQNQELKV RVELL HNPAFCSLATAKRRHQQTVTIPPKSSLSVPYVIVPLKTGQQEVEVKAAVYHFFISDGVRK SLKVV PEGIRMNKTVAVRTLDPERLGQEGVQREDVPPADLSDQVPDTESETRILLQGTPVAQMTE DAIDA ERLKHLIVTPSGCGEQNMITMTPTVIAVHYLDETEQWEKFGPEKRQGALELIKKGYTQQL AFRQP SSAFAAFLNRAPSTWLTAYVVKVFSLAVNLIAIDSQVLCGAVKWLILEKQKPDGVFQEDA PVIHQ EMTGGFRNTNEKDMALTAFVLISLQEAKEICEEQVNSLPGSITKAGDFLEANYMNLQRSY TVAIA AYALAQMGRLKGPLLNKFLTTAKDKNRWEEPGQQLYNVEATSYALLALLQLKDFDFVPPV VRWLN EQRYYGGGYGSTQATFMVFQALAQYQKDVPDHKELNLDVSLQLPSRSSKIIHRIHWESAS LLRSE ETKENEGFTVTAEGKGQGTLSVVTMYHAKAKGQLTCNKFDLKVTIKPAPETEKRPQDAKN TMILE ICTRYRGDQDATMSILDISMMTGFVPDTDDLKQLANGVDRYISKYELDKAFSDRNTLIIY LDKVS HSEDDCIAFKVHQYFNVELIQPGAVKVYAYYNLAESCTRFYHPEKEDGKLNKLCRDELCR CAEEN CFIQKLDDKVTLEERLDKACEPGVDYVYKTRLVKAQLSNDFDEYIMAIEQIIKSGSDEVQ VGQQR TFISPIKCREALKLEERKHYLMWGLSSDFWGEKPNLSYIIGKDTWVEHWPEEDECQDEEN QKQCQ DLGTFTENMVVFGCPN Human IgG1 constant region (SEQ ID NO:34) ASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSS GLYSL SSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFL FPPKP KDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLT VLHQD WLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGF YPSDI AVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYT QKSLS LSPGK Human IgG1 constant region E233A/L235A (SEQ ID NO:35) Attorney Docket No.: 47702.0112WO1 ASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSS GLYSL SSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPALAGGPSVFL FPPKP KDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLT VLHQD WLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGF YPSDI AVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYT QKSLS LSPGK Human IgG1 constant region L234A/L235A (SEQ ID NO:36) ASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQS SGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAA GGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPP SREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTV DKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK Rat C3 amino acid sequence with predicted signal sequence underlined (SEQ ID NO:37) MGPTSGSQLLVLLLLLASSLLALGSPMYSIITPNVLRLESEETFILEAHDAQGDVPVTVT VQDFL KKQVLTSEKTVLTGATGHLNRVFIKIPASKEFNADKGHKYVTVVANFGATVVEKAVLVSF QSGYL FIQTDKTIYTPGSTVFYRIFTVDNNLLPVGKTVVIVIETPDGVPIKRDILSSHNQYGILP LSWNI PELVNMGQWKIRAFYEHAPKQTFSAEFEVKEYVLPSFEVLVEPTEKFYYIHGPKGLEVSI TARFL YGKNVDGTAFVIFGVQDEDKKISLALSLTRVLIEDGSGEAVLSRKVLMDGVRPSSPEALV GKSLY VSVTVILHSGSDMVEAERSGIPIVTSPYQIHFTKTPKFFKPAMPFDLMVFVTNPDGSPAR RVPVV TQGSDAQALTQDDGVAKLSVNTPNNRQPLTITVSTKKEGIPDARQATRTMQAQPYSTMHN SNNYL HLSVSRVELKPGDNLNVNFHLRTDAGQEAKIRYYTYLVMNKGKLLKAGRQVREPGQDLVV LSLPI TPEFIPSFRLVAYYTLIGANGQREVVADSVWVDVKDSCVGTLVVKGDPRDNRQPAPGHQT TLRIE GNQGARVGLVAVDKGVFVLNKKNKLTQSKIWDVVEKADIGCTPGSGKNYAGVFMDAGLTF KTNQG LQTDQREDPECAKPAARRRRSVQLMERRMDKAGQYTDKGLRKCCEDGMRDIPMPYSCQRR ARLIT QGESCLKAFMDCCNYITKLREQHRRDHVLGLARSDVDEDIIPEEDIISRSHFPESWLWTI EELKE PEKNGISTKVMNIFLKDSITTWEILAVSLSDKKGICVADPYEITVMQDFFIDLRLPYSVV RNEQV Attorney Docket No.: 47702.0112WO1 EIRAVLFNYREQEKLKVRVELLHNPAFCSMATAKKRYYQTIEIPPKSSVAVPYVIVPLKI GLQEV EVKAAVFNHFISDGVKKILKVVPEGMRVNKTVAVRTLDPEHLNQGGVQREDVNAADLSDQ VPDTD SETRILLQGTPVAQMAEDAVDGERLKHLIVTPSGCGEQNMIGMTPTVIAVHYLDQTEQWE KFGLE KRQEALELIKKGYTQQLAFKQPISAYAAFNNRPPSTWLTAMWSRSFSLAANLIAIDSQVL CGAVK WLILEKQKPDGVFQEDGPVIHQEMIGGFRNTKEADVSLTAFVLIALQEARDICEGQVNSL PGSIN KAGEYLEASYLNLQRPYTVAIAGYALALMNKLEEPYLTKFLNTAKDRNRWEEPGQQLYNV EATSY ALLALLLLKDFDSVPPVVRWLNDERYYGGGYGSTQATFMVFQALAQYRADVPDHKDLNMD VSLHL PSRSSPTVFRLLWESGSLLRSEETKQNEGFSLTAKGKGQGTLSVVTVYHAKVKGKTTCKK FDLRV TIKPAPETAKKPQDAKSSMILDICTRYLGDVDATMSILDISMMTGFIPDTNDLELLSSGV DRYIS KYEMDKAFSNKNTLIIYLEKISHSEEDCLSFKVHQFFNVGLIQPGSVKVYSYYNLEESCT RFYHP EKDDGMLSKLCHNEMCRCAEENCFMHQSQDQVSLNERLDKACEPGVDYVYKTKLTTIELS DDFDE YIMTIEQVIKSGSDEVQAGQERRFISHVKCRNALKLQKGKQYLMWGLSSDLWGEKPNTSY IIGKD TWVEHWPEAEERQDQKNQKQCEDLGAFTETMVVFGCPN Human IgG1 constant region L234A/L235A/P329G (SEQ ID NO:109) ASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQS SGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAA GGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALGAPIEKTISKAKGQPREPQVYTLPP SREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTV DKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK [00170] Although the foregoing present disclosure has been described in some detail by way of illustration and example for purposes of clarity of understanding, the descriptions and examples should not be construed as limiting the scope of the present disclosure. The embodiments of the present disclosure described herein are intended to be merely exemplary, and those skilled in the art will recognize numerous equivalents to the specific procedures described herein. All such equivalents are considered to be within the scope of the present disclosure and are covered by the embodiments. Attorney Docket No.: 47702.0112WO1 [00171] All publications, patents, patent applications, internet sites, and accession numbers/database sequences including both polynucleotide and polypeptide sequences cited herein are hereby incorporated by reference in their entirety for all purposes to the same extent as if each individual publication, patent, patent application, internet site, or accession number/database sequence were specifically and individually indicated to be so incorporated by reference.