NGM621 is a Potent Inhibitory Anti-Complement C3 Antibody in Development for Treatment of Geographic Atrophy

Alexander Loktev, Iris Ngan, Kalyani Mondal, Yan Wang, Jian Luo, Darrin Lindhout, Bin Fan, Raj Haldankar, Jie Tang, Husam Younis, David Shen, Hui Tian, and Zhonghao Liu

NGM Biopharmaceuticals, South San Francisco, CA, USA

Poster # B0267

Financial Disclosures:

All authors are employees of NGM Biopharmaceuticals, South San Francisco, CA, USA

Poster # B0267

Geographic Atrophy (GA) is an Advanced Form of AMD

3

ChoroidalNeovascularization

GeographicAtrophy

Advanced AMDIntermediate AMD

Larger or more numerous drusen, +/- pigmentary changes

Early AMD

Small or intermediate drusen, +/- pigmentary changes

• GA is characterized by progressive and irreversible loss of photoreceptors, retinal pigment epithelium (RPE) and choriocapillaris

• GA is typically bilateral and lesion enlargement results in irreversible blindness

• GA affects ~5 million people globally and ~ 1 million people in the US

• Currently there are no effective treatments for GA CNV = choroidal neovascularizationFleckenstein et al, Ophthalmology 2018, 125(3): 369-390; Friedman et al, Arch Ophthalmol. 2004, 122: 564-572

4

Complement Activation is Associated with Development of Advanced AMD

Fritsche et al. Nat Genet 2016

NATURE GENETICS VOLUME 48 | NUMBER 2 | FEBRUARY 2016 135

variants (frequency among controls >1%) and 163,714 protein- altering variants (including 8,290 from known AMD-associated loci), which were mostly rare (88% with frequency among controls a1%). Imputation to the 1000 Genomes Project reference panel enabled examination of a total of 12,023,830 variants (Supplementary Table 3). Our final data set included a total of 43,566 subjects, consisting of 16,144 patients with advanced AMD and 17,832 control subjects of European ancestry for our primary analysis, as well as 6,657 Europeans with intermediate disease and 2,933 subjects with non-European ancestry (Supplementary Fig. 1 and Supplementary Table 3).

Altogether, our genotyped markers accounted for 46.7% (ref. 28) of variability in advanced AMD risk in the European-ancestry subjects (95% confidence interval (CI) = 44.5–48.8%). With respect to AMD subtypes, heritability estimates for choroidal neovascularization (h2 = 44.3%, CI = 42.2–46.5%) and geographic atrophy (h2 = 52.3%, CI = 47.2–57.4%) were similar; bivariate analyses29 showed a genetic correlation of 0.85 (CI = 0.78–0.92) between these disease subtypes.

Thirty-four susceptibility loci for AMDWe first conducted a genome-wide single-variant analysis of the >12 million genotyped or imputed variants (applying genomic control L = 1.13) comparing the 16,144 patients with advanced AMD and 17,832 controls of European ancestry (full results available online; see URLs). We obtained >7,000 variants with genome-wide significant associa-tion (P a 5 ! 10"8; Supplementary Fig. 2). Sequential forward selec-tion (Supplementary Fig. 3) identified 52 independently associated variants at P a 5 ! 10"8 (Supplementary Table 4 and Supplementary Data Set 1). These variants are distributed across 34 ‘locus regions’ (Fig. 1a), each extending across the identified and correlated vari-ants, including variants with r2 q0.5 and o500 kb with respect to the

index SNP (Supplementary Table 5). The 34 loci include 16 loci that reached genome-wide significance for the first time (new loci; Table 1) and overlap genes with compelling biology, such as extracellular matrix genes (COL4A3, MMP19 and MMP9), an ABC transporter linked to high-density lipoprotein (HDL) cholesterol (ABCA1) and a key activator in immune function (PILRB). Also included are 18 of the 21 AMD susceptibility loci that reached genome-wide significance previously6,9 (known loci; Table 1); between-study heterogeneity was low, particularly for the new loci (Supplementary Tables 6 and 7, and Supplementary Note).

Most (45/52) associated variants are common, showing fully conditioned odds ratios (ORs; from one model including all 52 variants) from 1.1 to 2.9 (Fig. 1b and Supplementary Table 4) with two interacting variants (Supplementary Note). We also observed seven rare variants with frequencies between 0.01 and 1% and ORs between 1.5 and 47.6 (Fig. 1b and Supplementary Table 4). All of these variants were also rare in individuals of non-European ancestry (Supplementary Table 8; see extended association results for non-Europeans in Supplementary Data Set 2). All seven rare variants are located in or near complement genes; they comprise four previously described nonsynonymous variants (CFH, p.Arg1210Cys; CFI, p.Gly119Arg; C9, p.Pro167Ser; C3, p.Lys155Gln)7–11 and three others (rs148553336, rs191281603 and rs35292876 in CFH) described here for the first time, including two for which the rare allele decreases disease risk. To ensure the validity of our results, we verified associa-tions of lead variants in sensitivity analyses that relied on alternate association tests, adjusted for age, sex or ten ancestry principal compo-nents, or that were restricted to population-based controls or controls q50 years of age (data not shown). Altogether, our genome-wide single-variant analysis nearly doubles the number of AMD-associated loci and variants.

a

COL4A3

COL8A1

SPEF2

VEGFA

KMT2E-SRPK2

PILRB-PILRA

TNFRSF10A

MIR6130-RORB

TRPM3

TGFBR1

RDH5-CD63

ACAD10

B3G

ALTL

RAD51BLIPC

CETP

CTR

B2-CTR

B1

NPLO

C4-TS

PAN10

TMEM97-VTN

C3

APOE

MMP9

C20orf85

SLC

16A8SYN3-TIMP3

CNN2

ABCA1

ARHGAP21

ARMS2-HTR

A1

CF1

C9

ADAMTS

9-AS

C2/CFB-SKIV2L800

600400200

20

15

–log

10 (P

)

10

5

0

12

34

56

7 9 11 13 15 17 19 21 X MT8 10

Chromosome12 14 16 18 20 22 Y

CFH

b50

Rare Common Rare

20

10

Odd

s ra

tio

5.0

3.0

2.01.51.21.0

0.01 0.1 1 10 50 90 99 99.9 99.99Risk allele frequency (controls) (%)

c8

6

4

2

01

23

45

67 9 11 13 15 17 21 X

Chromosome

SLC16A8

TIMP3CFH CFI C3CFH2CFH4CFH5

KCNT2

ASPMDXOCFBATF6B

8 10 12 14 1618 22

–log

10 (P

)

Figure 1 Genome-wide search identifies 34 loci and genes with rare variant burden for AMD. (a) We conducted a genome-wide single-variant association analysis for >12 million variants in 16,144 patients with advanced AMD versus 17,832 controls. Shown is the Manhattan plot exhibiting P values for association, highlighting new (P < 5 ! 10"8 for the first time; green) and known (blue) AMD loci (Table 1). The horizontal lines indicate genome-wide significance (P = 5 ! 10"8; red) or the y-axis break (P = 1 ! 10"20; gray). MT, mitochondrial DNA. (b) We computed the independent effect size (odds ratio) of each of the 52 identified variants (Supplementary Table 4). Shown are these effect sizes versus the frequency of the AMD risk-increasing allele and an 80% power curve (dashed line). (c) We conducted a genome-wide gene-based test for disease burden based on protein-altering variants, testing 17,044 RefSeq genes by the variable-threshold test51. Shown is the Manhattan plot with P values; the red dashed line indicates genome-wide significance (P a 0.05/17, 044 = 2.9 ! 10"6), and the yellow dashed line indicates significance across an AMD-associated locus (given 703 genes in the 34 AMD loci, P a 0.05/703 = 7.1 ! 10"5). No gene outside the 34 loci is genome-wide significant; 14 genes are significant across the AMD loci (blue), four of which remain significant after locus-wide conditioning (highlighted in bold; Supplementary Table 11).

A RT I C L E S

Variants in the complement pathway account for the majority of the known genetic risk for AMD

CFH C9 C2/CFB C3CFI

Pathological Dysregulation of Complement System Provides Rationale for Total Complement Inhibition for Treatment of GA

www.nature.com/scientificreports/

3SCIENTIFIC REPORTS | (2018) 8:7348ȁǣͷͶǤͷͶ;ȀͺͷͻͿ;ǦͶͷ;ǦͻͻͻͽǦ;

Figure 1. Complement C3 immunoreactivity on photoreceptor outer segments. (a) Cross-section through the retina of an 82 year old female donor diagnosed with GA 2 years prior to death. !e section captures a non-atrophic area, a transition zone of photoreceptor degeneration recognized by mislocalized rhodopsin (yellow "uorescence) and the atrophic area that lacks photoreceptors. !e GA lesion border (purple arrowhead) is noted by the decent of the external limiting membrane (ELM) towards the Bruch’s membrane (red arrowhead) and follows the GA transition zone where C3 immunoreactivity (red "uorescence) on POS was detected (boxed areas). Mislocalized rhodopsin in the atrophic zone likely represent degenerate rods. (b) Localization of C3 (red) and rhodopsin (yellow) immunoreactivity in a control donor eye (le# panels) and a donor eye diagnosed with GA with close-ups of boxed insets of non-atrophic, transition and border/atrophic zones as displayed in (a). Top panels show C3 staining (red), the second row of panels show rhodopsin staining merged with C3 staining and the third row of panels are bright$eld images indicating discontinuous RPE cells (black arrows). Bottom panels are close-ups of boxed inset of the non-atrophic zone showing C3 and rhodopsin staining in the POS layer. White arrowheads indicate C3 positive POS, green arrowheads indicate C3 staining in the choriocapillaris, orange arrowhead indicates sub-RPE neovasculature (right panel), yellow arrowheads indicate the external limiting membrane (ELM) and red arrowheads indicate the position of the Bruch’s membrane. (c) Dual immuno"uorescence of complement C3 (red) and red/green cone opsin (green) in the eye of an 86 year old female donor diagnosed with GA. !e image is taken ~1.2 mm from the edge of the GA lesion. Auto"uorescence of RPE cells, Bruch’s membrane and choroidal vascular lumen is shown in the CFP channel (purple). White arrowheads indicate C3 immunoreactivity on cone POS. Scale bar = 0.5 mm (a) and 50 µm (b,c). INL = inner nuclear layer; ONL = outer nuclear layer; ELM = external limiting membrane; POS = photoreceptor outer segments; RPE = retinal pigmented epithelium; Ch = choroid.

5

www.nature.com/scientificreports/

3SCIENTIFIC REPORTS | (2018) 8:7348ȁǣͷͶǤͷͶ;ȀͺͷͻͿ;ǦͶͷ;ǦͻͻͻͽǦ;

Figure 1. Complement C3 immunoreactivity on photoreceptor outer segments. (a) Cross-section through the retina of an 82 year old female donor diagnosed with GA 2 years prior to death. !e section captures a non-atrophic area, a transition zone of photoreceptor degeneration recognized by mislocalized rhodopsin (yellow "uorescence) and the atrophic area that lacks photoreceptors. !e GA lesion border (purple arrowhead) is noted by the decent of the external limiting membrane (ELM) towards the Bruch’s membrane (red arrowhead) and follows the GA transition zone where C3 immunoreactivity (red "uorescence) on POS was detected (boxed areas). Mislocalized rhodopsin in the atrophic zone likely represent degenerate rods. (b) Localization of C3 (red) and rhodopsin (yellow) immunoreactivity in a control donor eye (le# panels) and a donor eye diagnosed with GA with close-ups of boxed insets of non-atrophic, transition and border/atrophic zones as displayed in (a). Top panels show C3 staining (red), the second row of panels show rhodopsin staining merged with C3 staining and the third row of panels are bright$eld images indicating discontinuous RPE cells (black arrows). Bottom panels are close-ups of boxed inset of the non-atrophic zone showing C3 and rhodopsin staining in the POS layer. White arrowheads indicate C3 positive POS, green arrowheads indicate C3 staining in the choriocapillaris, orange arrowhead indicates sub-RPE neovasculature (right panel), yellow arrowheads indicate the external limiting membrane (ELM) and red arrowheads indicate the position of the Bruch’s membrane. (c) Dual immuno"uorescence of complement C3 (red) and red/green cone opsin (green) in the eye of an 86 year old female donor diagnosed with GA. !e image is taken ~1.2 mm from the edge of the GA lesion. Auto"uorescence of RPE cells, Bruch’s membrane and choroidal vascular lumen is shown in the CFP channel (purple). White arrowheads indicate C3 immunoreactivity on cone POS. Scale bar = 0.5 mm (a) and 50 µm (b,c). INL = inner nuclear layer; ONL = outer nuclear layer; ELM = external limiting membrane; POS = photoreceptor outer segments; RPE = retinal pigmented epithelium; Ch = choroid.

www.nature.com/scientificreports/

1 2SCIENTIFIC REPORTS | (2018) 8:7348ȁǣͷͶǤͷͶ;ȀͺͷͻͿ;ǦͶͷ;ǦͻͻͻͽǦ;

Figure 8. Both classical/lectin and alternative complement pathways contribute to retinal degeneration. (a) Inhibition of complement-mediated rabbit red blood cell hemolysis by mouse serum using anti-mouse CFD blocking antibody (a-fD). (b) C4+/+ and C4!/! mice were treated with anti-CFD (a-fD) or isotype control (Ctrl) Ab to address the contribution of CP/MBL and AP to in!ammation and retinal degeneration. C5a and CCL2 concentrations were measured in retinal homogenates 24 hours a"er NaIO3 administration, n = 5–6, Naïve = no NaIO3. For CCL2 graph not signi#cant (n.s.) comparisons are indicated, otherwise comparisons are signi#cant. (c) Flow cytometry analysis of CD11b+CD45hi cells in the neural retina 3 days a"er NaIO3 treatment in C4+/+ or C4!/! treated with Ctrl or a-fD (n = 5). Naïve = no NaIO3 (d) E$ect of complement inhibition on retinal loss measured by SD-OCT 7 days a"er NaIO3 administration, n = 10. (e) Quanti#cation of rod photoreceptors 7 days a"er NaIO3 administration in C4+/+ or C4!/! treated with Ctrl or a-fD (n = 5). Naïve = no NaIO3 (f) E$ect of complement inhibition on retinal morphology in H&E stained horizontal sections through the retina, 7 days a"er NaIO3 administration. (g) Complement inhibition and POS length measured in horizontal sections along the temporal-nasal axis of the mouse retina 7 days a"er NaIO3 administration in C4+/+ or C4!/! treated with Ctrl or a-fD. Naïve = no NaIO3. Error bars indicate ± SEM, n = 8–10. (h) Dark adapted ERG a-wave and b-wave amplitudes 7 days following NaIO3 treatment in C4+/+ or C4!/! treated with Ctrl or a-fD (n = 5). Naïve = no NaIO3, n = 17–18. Data from two experiments were pooled *p < 0.05, **p < 0.01, ***p < 0.001, or ****p < 0.0001, 2-way ANOVA with Tukey’s multiple comparisons test. All experiments were repeated at least twice.

www.nature.com/scientificreports/

1 2SCIENTIFIC REPORTS | (2018) 8:7348ȁǣͷͶǤͷͶ;ȀͺͷͻͿ;ǦͶͷ;ǦͻͻͻͽǦ;

Figure 8. Both classical/lectin and alternative complement pathways contribute to retinal degeneration. (a) Inhibition of complement-mediated rabbit red blood cell hemolysis by mouse serum using anti-mouse CFD blocking antibody (a-fD). (b) C4+/+ and C4!/! mice were treated with anti-CFD (a-fD) or isotype control (Ctrl) Ab to address the contribution of CP/MBL and AP to in!ammation and retinal degeneration. C5a and CCL2 concentrations were measured in retinal homogenates 24 hours a"er NaIO3 administration, n = 5–6, Naïve = no NaIO3. For CCL2 graph not signi#cant (n.s.) comparisons are indicated, otherwise comparisons are signi#cant. (c) Flow cytometry analysis of CD11b+CD45hi cells in the neural retina 3 days a"er NaIO3 treatment in C4+/+ or C4!/! treated with Ctrl or a-fD (n = 5). Naïve = no NaIO3 (d) E$ect of complement inhibition on retinal loss measured by SD-OCT 7 days a"er NaIO3 administration, n = 10. (e) Quanti#cation of rod photoreceptors 7 days a"er NaIO3 administration in C4+/+ or C4!/! treated with Ctrl or a-fD (n = 5). Naïve = no NaIO3 (f) E$ect of complement inhibition on retinal morphology in H&E stained horizontal sections through the retina, 7 days a"er NaIO3 administration. (g) Complement inhibition and POS length measured in horizontal sections along the temporal-nasal axis of the mouse retina 7 days a"er NaIO3 administration in C4+/+ or C4!/! treated with Ctrl or a-fD. Naïve = no NaIO3. Error bars indicate ± SEM, n = 8–10. (h) Dark adapted ERG a-wave and b-wave amplitudes 7 days following NaIO3 treatment in C4+/+ or C4!/! treated with Ctrl or a-fD (n = 5). Naïve = no NaIO3, n = 17–18. Data from two experiments were pooled *p < 0.05, **p < 0.01, ***p < 0.001, or ****p < 0.0001, 2-way ANOVA with Tukey’s multiple comparisons test. All experiments were repeated at least twice.

Simultaneous Inhibition of Classical and Alternative Complement Pathways is Protective in Rodent

Retinal Degeneration Model

Complement Deposition on Photoreceptors Precedes their Degeneration in Human GA

non-atrophic GA lesion border

Ø Unsuccessful late stage clinical trials with alternative pathway complement inhibitors in GA provide rationale for developing inhibitors of all complement activation pathways

Katschke et al. Sci. Reports 2018 Katschke et al. Sci. Reports 2018

• Pathological activation of complement system is strongly implicated in development and progression of GA secondary of AMD

• Preclinical retinal degeneration models show greatest benefit from inhibition of both classical and alternative complement pathways

NGM621 Targets Complement C3, Blocking All Three Pathways of Complement Activation

6

C2

C4

Classical Pathway

LectinPathway

AlternativePathway

Factor BFactor D

C3b

C5 C5 convertase

C3a

C5a

• Inflammation• Chemotaxis• Vascular permeability

• Phagocytosis• Tissue recruitment• Ag presentation

Cell lysis

NGM621Inhibition at C3 may provide superior

efficacy for treatment of GA C3

Membrane AttackComplex (MAC)

Anti-C5 Abs do not block all activities mediated by C3b / C3a

Alternative pathway inhibitors do not block classical/lectin pathway

Opsonization

Discovery and Engineering of NGM621: A Potent Anti-Complement C3 Antibody

7

• NGM621 is a humanized monoclonal antibody selected for Ø High affinity binding to intact C3 determined by surface plasmon resonance (SPR)Ø Complete and potent inhibition of C3a release in biochemical assayØ Completed and potent inhibition of complement activation via alternative and classical pathways in

hemolytic assays

NGM Hybridoma Antibody Discovery Platform

[Antibody] Log(nM)

Hem

olys

is (%

)

Complement Hemolytic Assays

-1 0 1 2 30

5 0

1 0 0

H u m a n C 3 h e m o ly tic C P a s s a y

L o g (n M )

pe

rce

nt

lys

is n

orm

to

no

in

hib

itio

n

3 8 G 10

3 D 8

1 5 C 1 2

mAb 1

mAb 2

mAb 3

Binding by SPR

[Antibody] (nM)

3.0

Resp

onse

(RLU

x 1

05)

2.0

1.0

C3a Release Assay

0 .0 0 1 0 .0 1 0 .1 1 1 0 1 0 0 1 0 0 0 1 0 0 0 00

1 0 0 0 0 0

2 0 0 0 0 0

3 0 0 0 0 0

H u m a n C 3 a re le a s e a s s a y

m A b (n M )

RL

U

3 8 G 10

3 D 8

1 5 C 1 2

mAb 1

mAb 2

mAb 3

• Fc receptor effector function eliminated • Inhibitory activity is identical for common C3 SNPs (A80G and P292G)• Favorable biophysical properties

• High solubility and low viscosity• Excellent long-term stability

NGM621 Binds to Intact Human and Cynomolgus Monkey C3 with High Affinity

8

Binding to Cyno C3 at 37°C

0 2 0 0 4 0 0 6 0 0 8 0 0 1 0 0 00

5 0

1 0 0

1 5 0

2 0 0

2 5 0

N G M 6 2 1 B in d in g H u m a n C 3 a t 3 7 C

T im e (s )

Re

sp

on

se

[R

U]

R a w d a taF itte d d a ta

Time (s)

Resp

onse

(RU

)

0 2 0 0 4 0 0 6 0 0 8 0 0 1 0 0 00

5 0

1 0 0

1 5 0

2 0 0

N G M 6 2 1 B in d in g C y n o C 3 a t 3 7 C

T im e (s )

Re

sp

on

se

[R

U]

R a w d a taF itte d d a ta

Time (s)

Resp

onse

(RU

)

KD = 0.34 nM KD = 0.4 nM

Binding affinity between NGM621 and human or cynomolgus monkey C3 measured by SPR at 37°C

Binding to Human C3 at 37°C

NGM621 Affinity to C3 Cleavage Fragments is Significantly Lower Compared to Affinity to Intact C3

9

• During complement activation, and inactivation by host factors, C3 is sequentially proteolyzed into fragments C3a, C3b/iC3b, C3c and C3d

• C3 fragments play role physiological functions including inflammation, activation of adaptive immune system, opsonization, phagocytosis and cell lysis

• NGM621 is >100 fold selective for intact C3 over C3b and other C3 proteolytic products

Time (s)

Resp

onse

(RU

)

NGM621 Binding to Human C3 and C3b

NGM621 Potently Inhibits Classical and Alternative Complement Activation Pathways

10

0 1 2 3 4-20020406080100120

Log Concentration (nM)

Hem

olys

is (%

) NGM621 CPIC50 = 74.1 nM

NGM621 Inhibition of Classical Pathway (CP) Hemolytic Assay• C3 depleted human serum supplemented

with 150 nM human C3• Lysis of sheep erythrocytes coated with

anti-sheep IgM• Requires Mg++ and Ca++

0 1 2 3 4-20020406080100120

NGM621 Inhibition of Alternative Pathway (AP) Hemolytic Assay• C3 depleted human serum supplemented

with 150 nM human C3• Lysis of rabbit erythrocytes• Requires Mg++ and chelation of Ca++

NGM621 APIC50 = 37 nM

Log Concentration (nM)

Hem

olys

is (%

)

• Canonical hemolytic assays allow for functional analysis of complement inhibitors• C3 concentration in vitreous humor of GA patients was reported to be 150 nM (Loyet, K. M., et al., 2012)

C2

C4

Classical Pathway

LectinPathway

AlternativePathway

C3b

C5 C5 convertase

C3a

C5a

C3

Factor BFactor D

MAC

Hemolysis

C3 convertase

Intravitreally Administered NGM621 Inhibits LPS-mediated Complement Activation in Cynomolgus Monkey

11

• Durability and in vivo efficacy of NGM621 after intravitreal injection (IVT) in Cynomolgus Monkey eye was assessed based on inhibition of C3a release, a proximal product of complement C3 proteolysis

• C3a protein concentration was measured in aqueous humor (AH) samples• In the healthy eye baseline levels of C3 proteolysis and C3a production are low• A carefully optimized low dose of LPS was used to transiently activate complement

Treatment groups (n=12 eyes per treatment group)• Vehicle or NGM621 8 mg/eye• AH samples collected prospectively

C3a concentration in AH samples were measured by ELISA and normalized to baseline (day -3) concentration

Testing NGM621 in vivo Activity in the Eye of Cynomolgus Monkeys

Day -3Baseline

AH

Day 1

NGM621 IVT

22 23 28

AH AH AHLPS IVT

AH C

3a (f

old

chan

ge

from

bas

elin

e)

NGM621 Inhibits Complement Activation up to 4 Weeks in Cynomolgus Monkey Eyes

LPS IVT

Day 22 Day 23 Day 280.5

1

2

4

8

16

Vehicle

NGM621 8 mg/eye

NGM621: A Potent Anti-Complement C3 Antibody

12

NGM621 Molecule AttributesType Humanized IgG1 monoclonal antibody

Target Binds & inhibits Complement C3

Molecular Weight ~150 kDa

Affinity (Biacore binding) KD = 0.34 nM, >100 specific to C3 over C3b

Potency (hemolytic assays) AP IC50 =37nM; CP IC50 =74nM (150 nM C3 concentration)

Effector Function 2-point mutations in the Fc region eliminate effector function

Concentration 15mg, 100ul IVT dose (150 mg/mL)

Formulation Liquid

Route of Administration IVT Injection

• Currently completing the first-in-human open-label single dose (SD) and multidose (MD) Phase 1 study of 15 GA patients (NCT04014777)

• Favorable safety and tolerability supports continued development of the maximum tolerated dose in Phase 2b study in GA

• Preclinical evidence suggest anti-angiogenic effect of C3 inhibition – see ARVO Abstract/Video Presentation # B0268

Thank you!

Contact information: Zhonghao Liu: zlui@ngmbio.com

Poster # B0267

Novel Biology.Powerful Medicines.Transformative Impact.