Post on 23-May-2020
transcript
Safe Harbor Statement
2
This presentation and the accompanying oral presentation contain “forward‐looking” statements within the meaning of the "safeharbor" provisions of the Private Securities Litigation Reform Act of 1995, including, but not limited to: the timing of the release of data from our clinical trials, including etokimab’s Phase 2b clinical trial in moderate-to-severe adult atopic dermatitis patients, etokimab’s Phase 2 clinical trial in adult chronic rhinosinusitis with nasal polyps patients and ANB019’s Phase 2 trials in GPP and PPP patients; the design of and our ability to launch a Phase 2b clinical trial of etokimab in eosinophilic asthma patients; the timing of an IND filing for ANB030, our new wholly-owned anti-inflammatory antibody program; the timing of a BLA filing for TESARO’s dostarlimab product candidate; and the milestones and success of our partnerships with TESARO (recently acquired by GlaxoSmithKline) and Celgene. Statements including words such as “plan,” “continue,” “expect,” or “ongoing” and statements in the future tense are forward-looking statements. These forward-looking statements involve risks and uncertainties, as well as assumptions, which, if they do not fully materialize or prove incorrect, could cause our results to differ materially from thoseexpressed or implied by such forward-looking statements. Forward-looking statements are subject to risks and uncertainties that may cause the company’s actual activities or results to differ significantly from those expressed in any forward-looking statement, including risks and uncertainties related to the company’s ability to advance its product candidates, obtain regulatory approval of and ultimately commercialize its product candidates, the timing and results of preclinical and clinical trials, the company’s ability to fund development activities and achieve development goals, the company’s ability to protect intellectual property and other risks and uncertainties described under the heading “Risk Factors” in documents the company files from time to time with the Securities and Exchange Commission. These forward-looking statements speak only as of the date of this presentation, and the company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date hereof.
Certain information contained in this presentation may be derived from information provided by industry sources. The Companybelieves such information is accurate and that the sources from which it has been obtained are reliable. However, the Company cannot guarantee the accuracy of, and has not independently verified, such information.
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AnaptysBio: Clinical-Stage Antibody Development CompanyFocused on Novel Antibody Medicines for Severe Inflammatory Diseases
3
TESARO
Celgene
Rapid Antibody Generation Platform Technology
~2.5 years
Antibody
Discovery
Preclinical &
Translational
IND or
Equivalent Filing
Antibody Medicines For Severe Diseases
Wholly-Owned Anti-Inflammatory Pipeline
Etokimab (ANB020, Anti-IL-33) Atopic Dermatitis, Eosinophilic Asthma & Chronic Rhinosinusitis with Nasal Polyps
ANB019 (Anti-IL-36R)Generalized Pustular Psoriasis & Palmoplantar Pustulosis
ANB030 (PD-1 Agonist)Inflammatory Diseases
Multiple Efficacy Readouts Anticipated From Wholly-Owned PipelineValidating Product Partnerships
Generated ~$80MM*
* As of March 31st 2019
ANB019 Generalized Pustular Psoriasis Phase 2: Top-line data
in mid 2019
Etokimab Atopic Dermatitis Phase 2b: Top-line data in H2 2019
Etokimab Chronic Rhinosinusitis With Nasal Polyps Phase 2:
Top-line data in H2 2019
ANB019 Palmoplantar Pustulosis Phase 2: Top-line data in H1
2020
All programs generated internally using AnaptysBio’s proprietary antibody generation platform technology
Wholly-Owned and Partnered Product Pipeline6 AnaptysBio-Generated Antibodies Advanced to Clinic Since Q1 2016
4
Discovery Preclinical Phase 1 Phase 3
Atopic DermatitisPhase 2a Data Presented at
AAD and EAACI 2018
ATLAS: Phase 2b Top-Line
Data H2 2019
Eosinophilic AsthmaPhase 2a Data Presented at
EAACI 2019
Phase 2b To Be Initiated in
2019
Chronic Rhinosinusitis With
Nasal Polyps
ECLIPSE: Phase 2 Top-Line Data
H2 2019
Generalized Pustular
Psoriasis
GALLOP: Phase 2 Top-Line Data
Mid 2019
Palmoplantar PustulosisPOPLAR: Phase 2 Top-Line Data
H1 2020
ANB030: Anti-PD-1
AgonistInflammatory Diseases IND Filing H2 2019
Dostarlimab (TSR-042):
Anti-PD-1Immuno-Oncology
TSR-022: Anti-TIM-3 Immuno-Oncology
TSR-033: Anti-LAG-3 Immuno-Oncology TSR-042 Combination Trial
Ongoing
TSR-075: Anti-PD-1/
LAG-3 BispecificImmuno-Oncology
IND-Enabling Studies
Ongoing
CC-90006: Anti-PD-1
AgonistPsoriasis Ongoing
Undisclosed Inflammation Ongoing
Commercial RightsProgram Therapeutic Indication
ANB019: Anti-IL-36RPhase 1 Data Presented
at EAACI 2018
Phase 2
Development Stage & Anticipated Milestones
Etokimab (ANB020):
Anti-IL-33
BLA Filing Anticipated in H2 2019
TSR-042 Combination Trial Ongoing
Phase 1 Data Presented at
AAD and AAAAI 2017
Wholly-Owned Pipeline:
Etokimab (ANB020, Anti-IL-33)Moderate-to-Severe Atopic Dermatitis
Moderate-to-Severe Eosinophilic Asthma
Chronic Rhinosinusitis with Nasal Polyps
Atopic Diseases: Large Unmet Medical NeedIL-33-driven Disease Mechanism Affects Multiple Organ Systems
6
Inflammatory
Response to
Allergen
Skin
Atopic Dermatitis• 1.4 million adult atopic dermatitis patients in the US
• Estimate ~280,000 adults with moderate-to-severe atopic dermatitis
Lung
Eosinophilic Asthma• 19 million adult patients diagnosed with asthma in the US
• Estimate ~1.1M adults with severe asthma insufficiently controlled through standard-of-care
Atopic diseases occur through a common inflammatory response to an allergen, leading
to concomitant incidence of multiple atopic diseases amongst some patients
SinusChronic Rhinosinusitis with Nasal Polyps • 1.3 million adults diagnosed in the US
• Estimate ~400,000 adults inadequately controlled with standard-of-care
7
Etokimab: First-in-Class Anti-IL-33 AntibodyBroadly Applicable to Atopic Diseases
• IL-33 is an upstream driver of
atopic disease
– Human genetics validate key role of IL-33 in
atopic dermatitis and asthma
– Pro-inflammatory cytokine released upon
allergen contact with epithelium
– Activates downstream release of IL-4, IL-5
and IL-13
– Modulates IgE-mediated mast cell and
basophil degranulation
• Etokimab is a potentially first-in-
class anti-IL-33 cytokine
antibody
– Phase I healthy volunteer trial completed
without dose-limiting toxicities
– AnaptysBio pursuing development in
moderate-to-severe atopic dermatitis,
moderate-to-severe eosinophilic asthma
and chronic rhinosinusitis with nasal polyps 1. Cayrol et al. Curr Opin Immunol (2014) 31:312. Peine et al. Trends Immunol (2016) 37(5):3213. Saluja et al. Clin Transl Allergy (2015) 5:33
IL-33 acts as a gatekeeper of allergic response with demonstratedactivity in the initiation (activation of ILC2 cells)1, propagation (activationof allergen-specific T and B cells)2 and amplification (degranulation ofmast cells and basophils)3.
En
rollm
en
t
n=
12 Placebo
IV Single Dose
Da
y -
21
Da
y -
7
Day 1
Da
y 1
5
Da
y 2
9
Da
y 5
7
Da
y 1
40
8
Etokimab Atopic Dermatitis Phase 2a Clinical TrialSingle Dose of Etokimab Administered on Day 1
Day 7
8
Da
y 1
13
Adult Moderate-to-Severe Atopic Dermatitis PatientsAverage baseline EASI score of 32
Patient Population
Clinical: EASI, 5-D pruritus, SCORAD, IGA, DLQI, safetyBiomarkers: Circulating eosinophils, ex-vivo IFN-g PD, granulocyte skin infiltrationKey Endpoints
Etokimab300mg IV Single Dose
EASI Scores Following Single Etokimab Dose Rapid Response & All Patients Achieved EASI-50 On Or Before Day 57
Timepoint
Average
% EASI Score
Reduction*
% Patients
Achieving
EASI-50*
% Patients
Achieving
EASI-75*
Day -21 (Baseline)
0% 0 0
Day 1 (Etokimab Dosing)
4% 0 0
Day 15 58%9 of 12 (75%)
3 of 12 (25%)
Day 29 61%10 of 12
(83%)4 of 12 (33%)
Day 57 62%9 of 12 (75%)
5 of 12 (42%)
Day 78 62%9 of 12 (75%)
2 of 12(17%)
Day 113 55%8 of 12(67%)
2 of 12(17%)
Day 140 45%5 of 12 (42%)
3 of 12 (25%)0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
Day -21 Day 1 Day 15 Day 29 Day 57 Day 78 Day 113 Day 140
% Patients Achieving EASI-50
% Patients Achieving EASI-75
Average % EASI Score Reduction
* Relative to baseline upon enrollment at Day -21
Time
9
10
0%
10%
20%
30%
40%
50%
60%
Day -21 Day 1 Day 15 Day 29 Day 57 Day 78 Day 113 Day 140
Average % 5-D Pruritus Score Reduction Average % SCORAD Reduction
Average % DLQI Reduction
IGA scores of zero or 1 (clear/almost clear skin) observed in 25% (3/12) of patients
TimepointAverage % 5-D Pruritus Score
Reduction*
Average % SCORAD
Reduction*
Average % DLQI
Reduction*
Day -21 (Baseline)
0% 0% 0%
Day 1 (Etokimab
Dosing)10% 3% 21%
Day 15 28% 37% 43%
Day 29 32% 40% 45%
Day 57 21% 38% 48%
Day 78 25% 40% 55%
Day 113 17% 38% 35%
Day 140 21% 32% 43%
* Relative to baseline upon enrollment at Day -21
Pe
rce
nta
ge
Time
Additional Efficacy Data5-D Pruritus, SCORAD, DLQI and IGA Scores
11
Timepoint% Blood
Eosinophil Reduction*
% Ex Vivo IL-33-Mediated IFN-g
Release Reduction*
% Patients AchievingEASI-50*
% Patients Achieving EASI-75*
Day -21(Baseline)
0% 0% 0% 0%
Day 1-4** 25% 98% 0% 0%
Day 15 37% Not measured 75% 25%
Day 29 40% Not measured 83% 33%
Day 57 39% 86% 75% 42%
Day 78 18% Not measured 75% 17%
Day 113 Not measured 27% 67% 17%
Day 140 16% 29% 42% 25%
* Average relative to baseline upon enrollment
** 6 to 72 hours post-etokimab dose
Etokimab-mediated eosinophil reduction is aligned with genotypic data from prior human IL-33 loss-of-function studies#
Inhibition of ex vivo IL-33-mediated interferon-gamma (IFN-g) release consistent with Phase 1 pharmacodynamic results
# Smith et al. (2017) A rare IL33 loss-of-function mutation reduces blood eosinophil counts and protects from asthma. PLoS Genet 13(3): e1006659.
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
Day -21 Day 1-4 Day 15 Day 29 Day 57 Day 78 Day 113 Day 140
Per
cen
tage
Day% Patients Achieving EASI-50 % Patients Achieving EASI-75
% Eosinophil Reduction % Ex Vivo IFN-g Release Reduction
Biomarker DataClinical Efficacy Consistent With Reduction of Blood Eosinophil Levels and Ex Vivo
Pharmacodynamic Assay
• Rapid and persistent EASI score improvement following single dose of etokimab- Rapid efficacy observed as early as Day 15
- Efficacy was maximized between Day 29 and Day 57
- All patients achieved at least EASI-50 response on or before Day 57
- EASI responses consistent with 5-D pruritus, SCORAD, DLQI and IGA scores
• Etokimab improved EASI scores irrespective of disease severity- Etokimab showed similar improvement in the seven of 12 patients with higher baseline EASI scores (treated with systemic
immuno-modulators pre-study) versus the five of 12 patient with lower baseline EASI scores that did not require systemic
therapy pre-study
• Biomarker data consistent with etokimab EASI score improvement- Etokimab-mediated eosinophil reduction is aligned with genotypic data from prior human IL-33 loss-of-function studies
- Ex vivo IL-33-mediated IFN-g release consistent with Phase 1 pharmacodynamic assay results
• Etokimab was well-tolerated and no drug-related safety signals observed- Most frequent adverse event was dizziness in 17% of patients post-placebo versus headache in 25% of patients post-
etokimab
- A single serious adverse event of depression reported on Day 140 post-etokimab, which was consistent with the patient’s
pre-trial history of depression, and was deemed not drug-related
12
Etokimab Atopic Dermatitis Phase 2a Clinical TrialSummary
13
ATLAS: Etokimab Atopic Dermatitis Phase 2b TrialTop-line Data Anticipated in H2 2019
Etokimab 600mg SC Loading Dose + 300mg SC q4w Maintenance Dose
Ran
do
miz
atio
nn
=30
0
Etokimab 300mg SC Loading Dose + 150mg SC q4w Maintenance Dose
Etokimab 20mg SC q4w Maintenance Dose
Placebo
Etokimab 300mg SC Loading Dose + 150mg SC q8w Maintenance Dose
Treatment Period Monitoring Period
Moderate-to-Severe Adult Atopic DermatitisBaseline EASI ≥16, BSA ≥10%, IGA ≥3
Patient Population
Wee
k 0
Wee
k 1
6
Wee
k 2
4
Primary: % change in EASISecondary: EASI-50, EASI-75, IGA, SCORAD, Pruritus NRS, safety
Key EndpointsWeek 16
ClinicalTrials.gov: NCT03533751
14
Etokimab Eosinophilic Asthma Phase 2a TrialSingle Dose of Etokimab or Placebo Administered on Day 1
Etokimab 300mg IV Single Dose + High Dose ICS/LABA n=12
Ran
do
miz
atio
nn
=25
Placebo Single Dose + High Dose ICS/LABA n=13
Adults with severe asthma (according to GINA 2016)Pre-bronchodilator FEV1 <80% of predictedBlood eosinophils ≥300 cells/microliter≥1 asthma exacerbation in past year requiring rescue medicationStably maintained on ICS/LABA dose for at least 3 months prior to screening
Patient Population
Efficacy: % change in FEV1 relative to baselineBiomarker: change in blood eosinophil levelsSafety
Key Endpoints
ClinicalTrials.gov: NCT03469934
Da
y 1
(B
ase
line
)
Da
y 1
27
Da
y 2
Da
y 8
Da
y 2
2
Da
y 3
6
Da
y 6
4
Day 8
5
Da
y 1
06
0%
2%
4%
6%
8%
10%
12%
14%
16%
18%
1 8 15 22 29 36 43 50 57 64 71 78 85 92 99 106 113 120 127
Etokimab Placebo
15
FEV1 Improvement Relative to Baseline After Single DoseRapid and Sustained Lung Function Improvement In Etokimab Arm
Timepoint
FEV1 Improvement Relative to Baseline
Etokimab Placebo Net
Day 2 12% 4% 8%
Day 8 9% 5% 4%
Day 22 16% 8% 8%
Day 36 14% 8% 6%
Day 64 15% 4% 11%
Day 85 9% 7% 2%
Day 106 11% 11% 0%
Day 127 13% 8% 5%
2
Day
Imp
rove
men
t R
elat
ive
to B
asel
ine
(0.80)
(0.70)
(0.60)
(0.50)
(0.40)
(0.30)
(0.20)
(0.10)
-
1 8 15 22 29 36 43 50 57 64 71 78 85 92 99 106 113 120 127
Etokimab Placebo
16
Timepoint
ACQ-5 Score Reduction Relative to Baseline
Etokimab Placebo Net
Day 8 -0.62 -0.09 -0.52
Day 22 -0.48 -0.25 -0.24
Day 36 -0.60 -0.12 -0.48
Day 64 -0.67 -0.12 -0.54
Day 85 -0.67 -0.18 -0.48
Day 106 -0.72 -0.44 -0.27
Day 127 -0.77 -0.36 -0.41
ACQ-5 Score Reduction Relative to Baseline After Single DoseEtokimab Arm Achieved Minimal Clinically Important Difference (MCID) of 0.50 Score
Reduction Relative to Baseline
Day
Red
uct
ion
Rel
ativ
e to
Bas
elin
e
MCID
-50%
-40%
-30%
-20%
-10%
0%
10%
20%
1 8 15 22 29 36 43 50 57 64 71 78 85 92 99 106 113 120 127
Etokimab Placebo
17
Blood Eosinophil Reduction Relative to Baseline After Single DoseConsistent With Phase 2a Atopic Dermatitis Trial
Timepoint
Blood Eosinophil Reduction Relative to Baseline
Etokimab Placebo Net
Day 2 -22% 9% -31%
Day 8 -34% -15% -19%
Day 22 -30% -10% -20%
Day 36 -43% 1% -44%
Day 64 -40% 6% -46%
Day 85 -36% -7% -29%
Day 106 -19% -13% -6%
Day 127 -24% -16% -8%2
Day
Red
uct
ion
Rel
ativ
e to
Bas
elin
e
18
Etokimab Eosinophilic Asthma Phase 2a TrialSummary
• Single dose of etokimab resulted in rapid and sustained improvement in FEV1 and
ACQ-5 score reduction through at least Day 64
- Eosinophil reduction data consistent with prior atopic dermatitis Phase 2a trial
• Clinical trials to date support infrequent dosing of etokimab across atopic diseases
• Asthma exacerbations were observed post-Day 64 in one etokimab-dosed patient and
two placebo-dosed patients
- Rescue therapies, including short-acting beta agonist (SABA) and oral corticosteroids, were utilized in the
management of each exacerbation occurrence
• Etokimab was generally well-tolerated and no serious adverse events reported
- No treatment-emergent adverse events were deemed to be etokimab-related
- The most frequent treatment-emergent adverse events reported in the etokimab arm were moderate strep throat
in two patients
- Placebo-dosed patients reported the most frequent treatment-emergent adverse events as mild vomiting in two
patients, mild and moderate asthma exacerbations in two patients and mild cough in two patients
Company plans to conduct a Phase 2b multi-dose, subcutaneously-administered,
placebo-controlled, double-blinded clinical trial to test multiple dose levels and dosing
frequencies of etokimab in 300-400 eosinophilic asthma patients
19
ECLIPSE: Etokimab CRSwNP Phase 2 TrialTop-Line Data Anticipated in H2 2019
Adult Chronic Rhinosinusitis with Nasal PolypsBaseline NPS ≥5 and SNOT-22 >7
Patient Population
Etokimab 300mg SC Loading Dose + 150mg SC q4w Maintenance Dose + MFNS
Ran
do
miz
atio
nn
=10
0
Placebo + MFNS
Etokimab 300mg SC Loading Dose + 150mg SC q8w Maintenance Dose + MFNS
Treatment Period Monitoring Period
Week 0
Week 1
6
Week 2
4
Primary: change in NPS relative to baselinePrimary: change in SNOT-22 relative to baseline
Key EndpointsWeek 16
ClinicalTrials.gov: NCT03614923
MFNS = mometasone furoate nasal spray
Wholly-Owned Pipeline:
Anti-IL-36R (ANB019)
Adult Generalized Pustular Psoriasis
Adult Palmoplantar Pustulosis
Normal IndividualsIL-36 cytokine signaling balanced by
function IL-36 receptor antagonist
Disease PatientsUncontrolled signaling due to dysfunctional
IL-36 receptor antagonist or elevated IL-36
cytokine levels
Treated PatientsAnti-IL-36R antibody has the potential to
dampen disease by blocking the IL-36 receptor
IL-36 Dysfunction Mediates Severe Inflammatory DiseaseGenetic Association with Generalized Pustular Psoriasis
21
Dampened
Inflammatory Response
Generalized Pustular Psoriasis or
Palmoplantar Pustulosis
Balanced
Inflammatory Response
• GPP is a systemic, life-threatening
inflammatory disease characterized by
widespread pustules - Patients have a high fever and elevated levels of
serum CRP and inflammatory cytokines (e.g. IL-8)
• Severe GPP patients can die from
cardio-pulmonary failure, exhaustion,
toxicity and infection- No approved therapies for treatment of GPP
• Affects approximately 3,000 patients in
the United States
Generalized Pustular Psoriasis (GPP)Orphan Disease Associated with IL-36 Receptor Antagonist Mutations
22
Palmoplantar Pustulosis (PPP)Orphan Disease Associated With Elevated IL-36 Cytokine Levels
• Severe inflammation of hands
and feet– Significant pain and inability to stand,
walk or work
• No approved therapeutic options
in this indication
• PPP is an orphan disease that
affects approximately 150,000
patients in the United States
23
• 72 healthy volunteers dosed in single ascending dose (SAD) and multiple ascending dose
(MAD) cohorts - 36 dosed with a single subcutaneous or intravenous ANB019 doses ranging between 10mg to 750mg
- 18 dosed with 4 weekly intravenous ANB019 doses ranging between 40mg to 300mg
- 18 dosed with placebo across SAD and MAD cohorts
• Safety- No dose limiting toxicities or serious adverse events observed
- Most frequent adverse events in SAD cohorts were upper respiratory tract infections in 10 of 36 (28%) subjects
dosed with ANB019 versus 6 of 12 (50%) subjects dosed with placebo, and headache in 10 of 36 (28%)
subjects dosed with ANB019 versus 3 of 12 (25%) subjects dosed with placebo
- In MAD cohorts, most frequent adverse event was headache in seven of 18 (39%) subjects dosed with
ANB019 versus one of six (17%) subjects dosed with placebo
• Pharmacokinetics- Half-life of 28 days, similar between subcutaneous and intravenous route of administration
• Pharmacodynamics- Complete inhibition of ex vivo IL-36 cytokine stimulus for 85 days post-single dose of ANB019 at certain dose
levels
ANB019 Phase I Healthy Volunteer Clinical TrialFavorable Safety, Pharmacokinetic and Pharmacodynamic Profile
24
Phase 1 data supports advancement into patient studies
25
GALLOP: ANB019 Generalized Pustular Psoriasis Phase 2 TrialTop-Line Data Anticipated Mid 2019
Adult Generalized Pustular Psoriasis PatientsBaseline JDA Score ≥7
Patient Population
JDA Severity Score ImprovementSafety
Key EndpointsWeek 4 & 16
Scre
en
ing
n=1
0 ANB019 750mg IV Loading Dose + 100mg SC q4w Maintenance Dose
Treatment Period Monitoring PeriodW
eek 0
Week 1
6
Week 2
4
26
ANB019 200mg SC Loading Dose + 100mg SC q4w Maintenance Dose
Ran
do
miz
atio
nn
=50
Placebo
Adult Moderate-to-Severe Palmoplantar PustulosisPatient
Population
PPPASI Score Improvement Safety
Key EndpointsWeek 16
POPLAR: ANB019 Palmoplantar Pustulosis Phase 2 TrialTop-Line Data Anticipated H1 2020
Treatment Period Monitoring PeriodW
eek 0
Week 1
6
Week 2
4
28
ANB030: PD-1 Agonist AntibodyNovel Anti-Inflammatory Mechanism Through Inhibitory Checkpoint Receptor
• PD-1 is a key inhibitory immune
checkpoint receptor responsible for
down-regulating T-cell mediated immune
responses
• Insufficient PD-1 signaling is associated
with human inflammatory diseases
- Genetic mutations in the PD-1 pathway can
increase susceptibility to various
inflammatory conditions*
• We hypothesize that augmenting PD-1
signaling through ANB030 treatment has
the potential to suppress human
inflammatory diseases
- Designed to down-regulate autoreactive T
cells by mimicking the function of PD-L1
• We anticipate filing an ANB030 IND in
H2 2019
Activated T Cell
PD-1
PD-1 antagonist antibodies block
PD-1 signaling
Increase T cell activity for
immuno-oncology
PD-1 agonist antibodies increase
PD-1 signalingDecrease T cell activity to treat inflammatory
diseases
Compensate for high PD-L1
expression by tumor cells
Compensate for low PD-L1 expression
* Okazaki and Honjo. Intern Immunol. 2007.
ANB030 mimics the function of PD-L1, restoring PD-1-mediated negative signaling on activated T cells, and has the potential to suppresses human inflammatory diseasesNegative Signal
Anticipated Effect of ANB030 In Inflammatory
Disease Patients
29
Activated T cells are down-regulated by PD-1 mediated negative signaling, leading to controlled immune responses in healthy individuals
Activated T Cell
MHC
An
tigen
TCR
PD-L1PD-1Negative Signal
Antigen Presenting Cell
Healthy Individuals
Insufficient negative signaling, which could occur due to low PD-L1 expression, leads to excess T cell activity and inflammatory diseases
Low PD-L1
PD-1Insufficient Signal
Inflammatory Disease Patients
ANB030
ANB030: PD-1 Agonist AntibodyAugments PD-1 Signaling To Suppress Inflammatory Diseases
30
ANB030: Generated Using AnaptysBio’s Technology PlatformChallenging Antibody Profile; Key Preclinical Properties De-Risked
• AnaptysBio’s somatic
hypermutation platform is
uniquely positioned to
discover novel therapeutic
antibodies
• PD-1 agonist antibodies are
challenging to discover due to
the unique binding properties
required to augment signaling
through checkpoint receptors
• ANB030 has been preclinically
de-risked for key
pharmacological and
manufacturability properties
ANB030 Property Preclinical Profile
Binding potency to human PD-1
Picomolar KD,~10,000x stronger than PD-L1
In Vitro FunctionalActivity
>100x more potent IC50 than PD-L1
Binding epitope Does not block PD-1 binding to PD-L1
In Vivo EfficacyDemonstrated in xenogeneic
mouse model of graft-versus-host disease
ManufacturabilityHigh expression, stable at high
concentrations
Non-Human Primate Pharmacology
Robust half-life and subcutaneousbioavailability
In Vitro SHM Iterative Antibody Evolution
Somatic Hypermutation (SHM) PlatformProprietary Platform Incorporates in vitro SHM and Iterative Antibody Evolution
32
In vitro SHM permits access to biological targets that have been difficult
to address with prior antibody technologies
• Unprecedented antibody diversity through SHM
– In situ antibody diversity generation outside of the constraints of an in vivo environment
• High potency & functional activity
– Only small doses may be required to convey therapeutic effect in vivo
• Reliable manufacturability
– Increased probability of successful clinical and commercial manufacturing
• Speed: ~2.5 years from novel target to IND (or equivalent) filing
– Enables rapid development of potentially first-in-class therapeutic antibodies to emerging
target biology
33
Somatic Hypermutation (SHM) PlatformAdvantages Over Competing Antibody Technologies
TESARO Immuno-Oncology
Partnership
• 3 mono-specific and 1 bi-specific programs under development
• Potential milestone payments of ~$1.1 billion
• Tiered single-digit royalties
Successful Partnership Track-RecordReceived ~$80MM in Cash from Partnerships Through March 31st 2019
34
Celgene Inflammation Partnership
• 2 programs under development
• Potential milestone payments of ~$106 million
• Single-digit royalties
Anticipated MilestonesMultiple Additional Efficacy Readouts Anticipated From Wholly-Owned Pipeline
36
Program Milestone Timing
Etokimab
(anti-IL-33)
Moderate-to-Severe Adult
Atopic Dermatitis Phase 2a Trial
Top-line data announced October 2017
Detailed data presented at AAD and EAACI 2018
ATLAS: Moderate-to-Severe Adult
Atopic Dermatitis Phase 2b TrialTop-line data anticipated in H2 2019
Severe Adult Eosinophilic
Asthma Phase 2a Trial
Top-line data presented September 2018
Detailed data presented at EAACI 2019
Moderate-to-Severe Eosinophilic
Asthma Phase 2b TrialTo be initiated in 2019
ECLIPSE: Adult Chronic Rhinosinusitis with
Nasal Polyps Phase 2 TrialTop-line data anticipated in H2 2019
ANB019
(anti-IL-36R)
Healthy Volunteer Top-line Phase I TrialTop-line data announced November 2017
Detailed data presented at EAACI 2018
GALLOP: GPP Phase 2 Trial Top-line data anticipated in mid 2019
POPLAR: PPP Phase 2 Trial Top-line data anticipated in H1 2020
ANB030
(anti-PD-1 Agonist)IND Filing H2 2019
Cash, cash equivalents and investments of approximately $484MM as of March 31st 2019
AnaptysBio: Clinical-Stage Antibody Development CompanyFocused on Novel Antibody Medicines for Severe Inflammatory Diseases
37
TESARO
Celgene
Rapid Antibody Generation Platform Technology
~2.5 years
Antibody
Discovery
Preclinical &
Translational
IND or
Equivalent Filing
Antibody Medicines For Severe Diseases
Wholly-Owned Anti-Inflammatory Pipeline
Etokimab (ANB020, Anti-IL-33) Atopic Dermatitis, Eosinophilic Asthma & Chronic Rhinosinusitis with Nasal Polyps
ANB019 (Anti-IL-36R)Generalized Pustular Psoriasis & Palmoplantar Pustulosis
ANB030 (PD-1 Agonist)Inflammatory Diseases
Multiple Efficacy Readouts Anticipated From Wholly-Owned PipelineValidating Product Partnerships
Generated ~$80MM*
* As of March 31st 2019
ANB019 Generalized Pustular Psoriasis Phase 2: Top-line data
in mid 2019
Etokimab Atopic Dermatitis Phase 2b: Top-line data in H2 2019
Etokimab Chronic Rhinosinusitis With Nasal Polyps Phase 2:
Top-line data in H2 2019
ANB019 Palmoplantar Pustulosis Phase 2: Top-line data in H1
2020