Anaptysbio, Inc. · NASDAQ:ANAB
Anaptysbio — Investor Presentation (February 2025)
45 slides from Anaptysbio's investor presentation, Feb 19, 2025
Slide 1: February 2025 Corporate Overview
February 2025 Corporate Overview
Slide 2: Forward-looking statements
This presentation and any accompanying oral presentation contains forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995, including, but not limited to: the timing of the release of data from the Company’s clinical trials
Slide 3: Pipeline overview and capital position
Cytokine Antagonists (available for out-license) 3 Immune Cell Modulators ANB033 (CD122 antagonist) P1 in Healthy Volunteers Rosnilimab (PD-1 depleter and agonist) P2b in Rheumatoid Arthritis P2 in Ulcerative Colitis Autoimmune and inflammatory diseases including dermatology, gastroenterology and rh
Slide 4: Antibody programs and anticipated milestones
Antibody Program Therapeutic Indication Development Stage and Anticipated Milestones IND Enabling Phase 1 Phase 2 Phase 3 Rosnilimab (PD-1 depleter and agonist) Rheumatoid Arthritis Ulcerative Colitis ANB033 (CD122 antagonist) Inflammatory Diseases ANB101 (BDCA2 modulator) Inflammatory Diseases 4 Fu
Slide 5: Rosnilimab (PD-1 Depleter and Agonist)
(PD-1 Depleter and Agonist) Rosnilimab
Slide 6: Rosnilimab potential in RA and UC
1. Expected by 2028 (Evaluate 29 Nov 2022); 2. Market research conducted by Ambit in 2022; 3. Expected by 2028 (Evaluate 21 Aug 2023); 4. Phase 3 registrational data from product labels. RA and UC are large commercial markets with high unmet need Potential first new differentiated class in RA in ove
Slide 7: Rosnilimab Week 14 vs competitors in bio-experienced patients
• By Month 3, treaters look for signal of response (i.e. ACR20) to treat through to Month 6 ― 70%+ ACR20 rate at Month 3 • However, treatment target is minimally LDA by Month 64 ― 69% (220/318) is highest ever rate of CDAI LDA reported already at Week 14 ― Some portion of the 31% LDA non-responders
Slide 8: Rosnilimab mechanism of action
8 Dendritic cell T cell T cell Activation MHCCD80/86 SHP2 TCRCD28 P PD-1 PD-L1 Rosnilimab Fc Receptor Rapidly engage homeostatic mechanisms to induce clinical response1 2 Rosnilimab aims to: Immune Cells Impacted Mechanism Immunologic Outcome PD-1high Tfh/Tph depletes downstream effect on B cells Pl
Slide 9: Rosnilimab restores immune homeostasis
9 Pre- treatment Post Rosnilimab RA Synovial Tissue PD-1neg PD-1neg PD-1int PD-1high Rosnilimab is designed to bring the immune system back to homeostasis and modify disease Pre- treatment Post Rosnilimab Healthy Periphery PD-1neg PD-1neg PD-1neg Treg PD-1int Treg PD-1high PD-1neg PD-1int PD-1int PD
Slide 10: PD-1 expressed on activated Teff and Tfh/Tph cells
Adapted from Akiyama et al, Ann Rheum Dis, 2023. 10 PD-1 is expressed preferentially on activated Teff and Tfh/Tph cells that mediate autoimmune pathology Lymphoid tissues Periphery Inflamed tissue 10 B cell PD-1high Tfh Plasma celllg lg lg PD-1high Tfh FDC Generation CXCL13 IL-21 PD-1high Tfh Type
Slide 11: PD-1+ T cells prevalent in RA and UC
Adapted from Nguyen et al, Human Pathology (2022) 126, 19e27; Guo et al, PLoS One 2018; 13(2). Roosenboom et al, Scand J of Gastro. 2021; 56(6):671-679. 1. Chen et al, Clinical and Translational Immunology, 2024. 11 PD-1+ T cells are prevalent in inflamed tissue and periphery in RA and UC RA UC AA 0
Slide 12: Reducing PD-1+ T cells impacts RA drivers
Adapted from Aletaha and Smolen, JAMA, 2018; 1. Chen et al, Clinical and Translational Immunology, 2024. 12 Reducing PD-1+ T cells broadly impacts multiple downstream, clinically validated drivers of RA pathogenesis >80% of T cells in RA synovium are PD-1+ • Similar findings are observed in treatmen
Slide 13: Rosnilimab optimizes PD-1+ T cell inhibitory signaling
Parmley S, et al. ECCO 2024. February 2024. 1. Adapted from Suzuki et al., Sci. Immunol. 8, eadd4947 (2023). 13 Dendritic cell T cell T cell Activation MHCCD80/86 SHP2 TCRCD28 P PD-1 PD-L1 Rosnilimab Fc Receptor #3, 4 Functional assay of antagonism or agonism1 Lilly epitope PD-L1 epitope Lilly PD-1
Slide 14: PD-1 Agonist Landscape
14 PD-1 Agonist Landscape Fc receptor binding affinity Depletion Agonism Membrane- proximal epitope S tr u ct u ra l ch a ra ct e ri st ic s Fu n ct io n a l o u tp u ts Rosnilimab is a best-in-class PD-1 depleter and agonist Lilly’s patent notes peresolimab’s “modest” activity and disclosed more po
Slide 15: Depletion and agonism reduce T cell proliferation and cytokines
15 1. Healthy donor purified DCs + autologous total T cells stimulated with anti-CD3, cultured for 3 days for assessment of T cell proliferation 2. Anti-CD3+ anti-CD28 stimulation of RA patient PBMCs for assessment of depletion and agonism MOA, representative data from N=8 donors. Two-way ANOVA, Tuk
Slide 16: Sustained ~90% reduction of PD-1high T cells
16 -100% -80% -60% -40% -20% 0% 20% 40% 60% C el l C o u n t (% C h a n g e fr o m B a se li n e) PD-1high T Cells PD-1+ T Cells Total Treg Total T Cell Representative Rosnilimab T Cell Impact Overall Population – 400mg Q4W1 Wk 0 Wk 6 Wk 12 10-wk off-drug follow-up Rosnilimab’s rapid and sustained ~
Slide 17: PD-1+ Tregs in disease
17 In disease, PD-1+ Tregs exhibit a dysregulated phenotype, which induce proinflammatory cytokines Very low % Tregs (<20%) are PD-1+ in RA synovium, even fewer are PD- 1high1 In Phase 2b RA trial, few PD-1+ Tregs were present in periphery and were reduced proportionally to PD-1+ T cells overall Min
Slide 18: Phase 2b RA trial design
18 Screening Period (up to 35 days) Blinded Placebo-Controlled Treatment Period (12 weeks) Follow-Up Period All-Active (10 weeks) Blinded All-Active Treatment Period (16 weeks) Week -5 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 34 38 Visit V1 V2 V3 V4 V5 V6 V7 V8 V9 V10 V11 V12 V13 V14 V15 V16 FUV1
Slide 19: Patient disposition
19 Patient disposition through Week 12 *ITT – Intent-to-Treat (all randomized participants) ITT* (n=424) Placebo, n=106 Naïve – n=62 (59%) Experienced – n=44 (42%) Discontinued treatment, n=9 (8%) Primary reason: Adverse events, n=1 Disease progression, n=0 Withdrawal of consent, n=7 Other, n=1 Comp
Slide 20: Baseline characteristics
20 Baseline Characteristic Placebo (n=106) 100mg Q4W (n=106) 400mg Q4W (n=107) 600mg Q2W (n=105) Overall (N=424) Age, years, mean (SD) 58 (11) 57 (10) 57 (12) 56 (11) 57 (11) Female, n (%) 83 (78%) 79 (75%) 79 (74%) 80 (76%) 321 (76%) Weight (kg), mean (SD) 78 (17) 78 (19) 81 (19) 77 (16) 78 (18) Ge
Slide 21: Black box warnings and blockbuster RA sales
Black box warnings for increasing SAE incidence of commercial products have not impeded blockbuster sales Black box warning ~30% infection rate vs. 28% placebo5 ~0.7% MACE rate vs. 0.4% placebo5 ~54% infection rate vs. 48% placebo5 ~0.2% MACE rate vs. 0.5% placebo5 Black box warning ~20% infection r
Slide 22: Adverse events through Week 12
22 Adverse Events through Week 12, n (%) Placebo (n=106) 100mg Q4W (n=106) 400mg Q4W (n=107) 600mg Q2W (n=105) Participants with any AE, n (%) 36 (34%) 51 (48%) 48 (45%) 38 (36%) Any SAE1 1 (1%) 1 (1%) 1 (1%) 3 (3%) Any Drug-Related SAE 1 (1%) 0 (0%) 0 (0%) 0 (0%) Severe AE2 2 (2%) 1 (1%) 0 (0%) 4 (
Slide 23: Rosnilimab significantly decreased CRP
23 -1.0 -9.7 -10.1 -7.6 -2.3 -9.6 -10.0 -9.7 -12.0 -10.0 -8.0 -6.0 -4.0 -2.0 0.0 Placebo Rosnilimab 100mg Q4W Rosnilimab 400mg Q4W Rosnilimab 600mg Q2W M e a n C h a n g e f ro m B a se li n e • Clear and consistent on target reduction at all rosnilimab doses • No immunological change on placebo at
Slide 24: Mean change in DAS28-CRP
24 -3.0 -2.5 -2.0 -1.5 -1.0 -0.5 0.0 Week 0 Week 2 Week 4 Week 6 Week 8 Week 10 Week 12 Week 14 M e a n C h a n g e f ro m B a se li n e • All rosnilimab doses statistically significant at Week 12 • All rosnilimab doses continue to improve into Week 14 with no evidence of flattening • Following Week
Slide 25: CDAI LDA responses
25 31% 46% 50% 38% 0% 10% 20% 30% 40% 50% 60% Placebo Rosnilimab 100mg Q4W Rosnilimab 400mg Q4W Rosnilimab 600mg Q2W % o f P a ti e n ts • Physicians minimally seek to achieve LDA by 6-months • Approximately half of rosnilimab-treated patients achieved LDA by Week 12 CDAI, a compositive assessment,
Slide 26: ACR50 and ACR70 responses
26 33% 44% 36% 47% 0% 10% 20% 30% 40% 50% 60% 70% 80% Placebo Rosnilimab 100mg Q4W Rosnilimab 400mg Q4W Rosnilimab 600mg Q2W % o f P a ti e n ts 27% 65% 61% 73% 0% 10% 20% 30% 40% 50% 60% 70% 80% Placebo Rosnilimab 100mg Q4W Rosnilimab 400mg Q4W Rosnilimab 600mg Q2W % o f P a ti e n ts 23% 52% 56% 5
Slide 27: ACR responses over time in CDAI LDA responders
0% 20% 40% 60% 80% 100% A C R 5 0 a s a % o f C D A I LD A R e sp o n d e rs Wk0 Wk2 Wk4 Wk6 Wk8 Wk10 Wk12 Wk14 Wk16 W18 Wk20 Wk22 Wk24 Wk26 Wk28 0% 20% 40% 60% 80% 100% A C R 7 0 a s a % o f C D A I LD A R e sp o n d e rs Wk0 Wk2 Wk4 Wk6 Wk8 Wk10 Wk12 Wk14 Wk16 W18 Wk20 Wk22 Wk24 Wk26 Wk28 Complete
Slide 28: DAS28-CRP over time in CDAI LDA responders
-3.5 -3 -2.5 -2 -1.5 -1 -0.5 0 M e a n C h a n g e f ro m B a se li n e f o r D A S 2 8 -C R P Wk0 Wk2 Wk4 Wk6 Wk8 Wk10 Wk12 Wk14 Wk16 W18 Wk20 Wk22 Wk24 Wk26 Wk28 Mean Change in DAS28-CRP Over Time CDAI LDA Responders vs. Overall Population 69% (220/318) of patients achieved CDAI LDA at Week 14 and
Slide 29: Next steps for rosnilimab in RA
Screening Period (up to 35 days) Blinded Placebo-Controlled Treatment Period (12 weeks) Follow-Up Period (10 weeks) Blinded All-Active Treatment Period (16 weeks) Week -5 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 34 38 Rosnilimab SC 100mg Q4W Rosnilimab SC 400mg Q4W Rosnilimab SC 600mg Q2W Placebo
Slide 30: PD-1+ T cells drive UC pathogenesis
Adapted from Gastroenterology & Hepatology Volume 18, Issue 8 August 2022. 1. Chen et al, Clinical and Translational Immunology, 2024. 30 PD-1+ T cell activation broadly impacts multiple clinically validated drivers of UC pathogenesis • >40% of T cells in lamina propria in UC are PD-1+ • 2x increase
Slide 31: Rosnilimab efficacy in murine colitis model
Therapeutic dosing of rosnilimab demonstrated efficacy in a murine model of colitis PD-1high Tph cells are reduced with remission in UC1,2 31 Tph impact seen in RA Phase 2b trial relevant to UC biology and correlates to reduction of remission % P D -1 h ig h T p h c e ll s % P D -1 h ig h T p h c e
Slide 32: Depletion and agonism in UC patient cells
Reduction of Tfh/Tph cytokine 0 25 50 75 100 0 0.1 1 10 100 Antibody (nM) C XC L1 3 & IL -2 1 (% Is ot yp e C on tro l) IL-21 CXCL13 Clinical range Reduction of inflammatory cytokine Agonism of PD-1+ T cellsDepletion of PD-1high T Cells Parmley et. al. UEGW 2024. October 2024; Anti-CD3+ anti-CD28 st
Slide 33: UC lacks highly effective treatment options
Following remission on induction therapy, one third to one half of patients relapse within 1 year1 1. Phase 3 registrational data from product labels; 2 Prometheus Bioscience corp. presentation Mar 2023; 3. Roivant corp presentation Jan 2023; 4. Teva corp presentation Dec 2024; 5. Remission measured
Slide 34: Rosnilimab Phase 2 UC trial design
[Optional for Responders] Blinded Treatment Extension Period (TEP) (26 weeks) Rosnilimab Phase 2 in moderate-to-severe UC Top-line data anticipated Q4 2025 Screening Period (up to 35 days) Blinded Placebo- Controlled Treatment Period (12 weeks) Follow-Up Period (10 weeks) Blinded All-Active Treatmen
Slide 35: ANB033 (CD122 antagonist)
Autoimmune and Inflammatory Diseases ANB033 (CD122 antagonist)
Slide 36: ANB033 CD122 antagonist mechanism
36 CD122 is a shared beta subunit of the receptors for IL-15 and IL-2 CD122 antagonist mAb will potently inhibit IL-15 and IL-2 biology Both IL-15 and IL-2 mediate: • Proliferation and survival of T cell subsets, particularly CD8+ TEMRA, and NK cells • Inflammatory cytokine secretion (IFNγ) during T
Slide 37: ANB033 durable survival in GVHD model
GVHD (severe phenotype) model in human IL-15 transgenic mouse supports T cell and NK cell survival • ANB033 preclinical data suggests targeted elimination of pathogenic T cells and reduction of tissue infiltrating T cells leading to a more potent and durable response than belatacept • Belatacept (GV
Slide 38: ANB101 (BDCA2 modulator)
Autoimmune and Inflammatory Diseases ANB101 (BDCA2 modulator)
Slide 39: ANB101 BDCA2 modulator of pDC function
ANB101 will potently inhibit interferon secretion and immune activation 39 Activated pDCs bridge innate and adaptive immunity • Secrete Type I IFN (1000x increase over other cell types) • Present antigens to adaptive immune system pDCs enriched in tissue in rheumatology and other inflammatory diseas
Slide 40: GSK Immuno-Oncology Financial Collaboration
JemperliTM (dostarlimab, PD-1 Antagonist) Cobolimab (TIM-3 Antagonist) GSK Immuno- Oncology Financial Collaboration
Slide 41: Jemperli capped non-recourse monetization
“Jemperli – only” capped non-recourse monetization • Jemperli receivables payable to Sagard until cumulative $600MM paydown by Mar. 31, 20311,2 • ~$90MM paid to Sagard as of early January 2025 • Projected cumulative $600MM paydown by 2029 based on Wall Street Consensus3 Potential royalties and miles
Slide 42: Jemperli quarterly performance and royalty upside
$31 $57 $73 $101 $137 $170 $190 $0 $50 $100 $150 $200 Q2 2023 Q3 2023 Q4 2023 Q1 2024 Q2 2024 Q3 2024 Q4 2024 S a le s (i n U S D m il li o n s) Jemperli Quarterly Performance1 Consensus projections of Jemperli imply significant royalty upside to Anaptys post-Sagard paydown 1. GSK earnings presentat
Slide 43: Additional dostarlimab and cobolimab opportunities
Lung cancer2 • 2L NSCLC: P3 COSTAR trial (docetaxel vs dostarlimab + docetaxel vs docetaxel + dostarlimab + cobolimab) • Top-line data expected in H1 2025 • Significant U.S. market opportunity with 237,000 new NSCLC diagnoses/year1 Additional dostarlimab royalty opportunities • P3: LA unHNSCC monoth
Slide 44: Etokimab (IL-33 antagonist) Legacy Program for Out-Licensing
Etokimab (IL-33 antagonist) Legacy Program for Out-Licensing
Slide 45: Etokimab: IL-33 inhibiting IgG1 antibody
Etokimab: IgG1 antibody that inhibits the active form of IL-33 • Binding affinity of etokimab is <1 pM; best-in-class based on competitor affinities published in patents and literature • Targeting IL-33 cytokine rather than IL-33 receptor (ST2) has potential to not only modify disease, but also driv