January 2024 Corporate Overview Nasdaq: ANAB

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, including rosnilimab’s Phase 2b clinical trial in rheumatoid arthritis and Phase 2 clinical trial in ulcerative colitis and ANB032’s Phase 2b clinical trial in atopic dermatitis; the timing of IND filings for ANB033 and ANB101; whether any of the Company’s product candidates will be best in class or optimized; the potential to receive any additional royalties from the GSK collaboration; the Company’s ability to find a licensing partner for imsidolimab or etokimab and the timing of any such transaction; and the Company’s projected cash runway. 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 its results to differ materially from those expressed 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 Company believes 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. The trademarks included herein are the property of the owners thereof and are used for reference purposes only. Such use should not be construed as an endorsement of such products. 2 Safe harbor statement

Best-in-class immune cell modulating antibodies 3 Immune Cell Modulators Imsidolimab (IL-36R) Positive P3 data reported in GPP Etokimab (IL-33) P2b/3-ready in epithelial driven diseases ANB033 (CD122 antagonist) ANB101 (BDCA2 modulator) IND-enabling Rosnilimab (PD-1 agonist) P2b in Rheumatoid Arthritis P2 in Ulcerative Colitis ANB032 (BTLA agonist) P2b in Atopic Dermatitis Cytokine Antagonists (legacy programs for out-licensing) Autoimmune and inflammatory diseases including dermatology, gastroenterology and rheumatology Strong capital position GSK immuno-oncology financial collaborationResearch-driven Cash runway to YE 2026 YE 2023 cash of ~$417MM Significant royalty potentialPreclinical pipeline of immunology targets

Antibody Program Therapeutic Indication Development Stage and Anticipated Milestones Lead Optimization IND Enabling Phase 1 Phase 2 Phase 3 Rosnilimab (PD-1 agonist) Rheumatoid Arthritis Ulcerative Colitis ANB032 (BTLA agonist) Atopic Dermatitis ANB033 (CD122 antagonist) Inflammatory Diseases ANB101 (BDCA2 modulator) Inflammatory Diseases Legacy Programs Available for Out-licensing Imsidolimab (IL-36R antagonist) Generalized Pustular Psoriasis (GPP) Etokimab (IL-33 antagonist) Epithelial Driven Diseases 4 C yt ok in e A n ta g on is ts P2b initiated Q3 2023 Top-line data mid 2025 P2 initiated Q4 2023 Top-line data H1 2026 P2b initiated Q2 2023 Top-line data YE 2024 IND submission H1 2024 GEMINI-1 and GEMINI-2 at medical conf H2 2024 GEMINI-1 BLA Q3 2024 P2b/3 ready Out-license in 2024 No further internal investment Im m u n e C el l M od u la to rs Immune cell modulator development Three P2 trials ongoing across three therapeutic areas; Top-line AD data expected by YE 24 IND submission H2 2024

Immune cells (e.g., T cells, B cells, dendritic cells) Checkpoint receptors (e.g., PD-1, BTLA) Treat inflammation: Down-regulate immune cells Teff=T effector cells; Tph cells=Peripheral helper cells; Tfh cells=Follicular helper cells. 5 Checkpoint agonists “hit the brakes” to restore immune balance and deliver differentiated outcomes Membrane-proximal binding epitope and optimized Fc receptor binding affinity enables tight immune synapse and best-in-class potency Rosnilimab (PD-1 agonist) targets PD-1+ T cells through 3 MOAs: 1. Deplete PD-1high Teff cells 2. Deplete PD-1high Tfh/Tph cells 3. Agonize PD-1int Teff cells ANB032 (BTLA agonist) modulates activated immune cells: 1. Agonize T cells (Th1, Th2, Th17, Th22) 2. Modulate dendritic cells 3. Agonize B cells

Fc receptor binding affinity Depletion Binding properties Agonism Membrane- proximal epitope 6 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 PD-1 Agonist BTLA Agonist Lilly’s LY-3361237 (IgG4 PAA1) ANB032 (IgG4) Lilly’s Peresolimab (IgG1k) Rosnilimab (IgG1k) Decreased2 Significantly Decreased2 1. IgG4 PAA (S228P/F234A/L235A) is a variation of IgG4 specifically engineered to eliminate FcγR affinity 2. Membrane-distal binding epitope results in wider immune synapse, contributing to significantly weaker agonism and less potent depletion 3. Depletion of PD-1high Teff and Tfh/Tph cells is expected to contribute to PD-1 agonist clinical efficacy. However, given the broader expression profile of BTLA on T cells, B cells and DCs, a non- depleting antibody is preferred None3 None3 Anaptys’ checkpoint agonists have a combination of attributes contributing to best-in-class potency Significantly Decreased2

8 Rosnilimab’s impact in inflamed tissue and periphery has potential to deliver differentiated efficacy and safety 2. Reduce PD-1+ T cell activation 1. Reduce PD-1high Teff cells 3. Reduce PD-1high Tfh/Tph cells Relevant Approved Treatments1 Rosnilimab’s 3 MOAs impact on T cells Immunologic outcomes Reduce plasma cell generation & autoantibody levels Reduce T cell migration, proliferation & cytokine secretion (IL-6) (S1P) (α4β7) (CD-80) (TNF) These treatments only target a subset of the immunologic outcomes driven by rosnilimab 1Other efficacious treatments have less specific MOAs causing safety liabilities, including Rinvoq (JAKs), Rituxan (broad B cell depleter), Lemtrada (broad lymphocyte depleter)

1. Adapted from Suzuki et al., Sci. Immunol. 8, eadd4947 (2023). 9 Dendritic cell T cell T cell Activation MHCCD80/86 SHP2 TCRCD28 P PD-1 PD-L1 Rosnilimab Fc Receptor # 4 Functional assay of antagonism or agonism1 Lilly epitope Rosnilimab Lilly PD-1 agonist PD-L1 epitope Lilly PD-1 agonistRosnilimab Rosnilimab epitope Rosnilimab optimizes PD-1+ T cell inhibitory signaling by enabling tight immune synapse formation “A shared feature of agonist mAbs is recognition of the membrane-proximal extracellular region…” and “…activity depends on Fc receptor–supported crosslinking” Suzuki, et al. 2023

1. Healthy donor T cells + NK cells (1:5 ratio) + antibody in in-vitro ADCC assay, representative data from N=5 donors. 2. Healthy donor purified DCs + autologous total T cells stimulated with anti-CD3, cultured for 3 days for assessment of T cell proliferation Two-way ANOVA. Tukey’s multiple comparison test. ****P<0.0001, ***p<0.001, **p<0.01, *p<0.05. 10 Depletion (NK cell-mediated ADCC)1 Agonism (DCs + total T cells; no ADCC)2 0 25 50 75 100 0 0.1 1 10 100 Antibody (nM) % P D 1+ T c el ls (n or m al iz ed to Is ot yp e) Clinical range ** **** * 0.1 1 10 100 0 25 50 75 100 Antibody (nM) % P ro lif er at in g T ce lls (n or m al iz ed to is ot yp e) 0 Clinical range Isotype control Rosnilimab Lilly PD-1 agonist **** * Rosnilimab demonstrates potent depletion and agonism at clinically relevant concentrations

11 PD-1 expression on both CD4 and CD8 T cells correlates with activation state Rosnilimab targets only a small proportion of T cells In healthy volunteers: ―Deplete PD-1high T cells: ~5-8% of total T cells ―Agonize remaining PD-1int T cells: ~15% of total T cells P D -1 + T c e ll s CD3 PD-1high PD-1int PD-1neg Pre-treatment Rosnilimab Day 15 depletion agonism Pre-treatment Rosnilimab Day 15 Illustrative T cell composition change PD-1neg PD-1neg PD-1negTreg PD-1int Treg PD-1high PD-1neg PD-1int PD-1intPD-1high Treg PD-1neg Data illustrative, based on Phase 1 data from healthy volunteer study. Data on file with Anaptys. Rosnilimab restores immune balance bringing T cell composition to a less activated state

1. AA=Alopecia Areata; 2. Results shown from 400mg subcutaneous dose (single dose in healthy and monthly dose in AA). 12 Rosnilimab P2a AA patients Rosnilimab P1 healthy volunteers Consistent PD-1+ T cell effect2 • >90% reduction of PD-1high T cells • >50% reduction of PD-1+ T cells Overall T cell composition in less activated state • Positive bias to Treg ratio AA patients are in a low systemic inflammatory state • Represented by no significant increase in peripheral PD-1+ T cells relative to healthy controls        Dosing Treg Total T cells PD-1+ T cells PD-1high T cells  Potent and sustained reduction in peripheral PD-1+ T cells for >30 days across P1 HV and P2a AA1 studies

SAD=Single ascending dose; MAD=Multiple ascending doses; RO=Receptor occupancy; PK=Pharmakokinetics, SC = subcutaneous. 1. MAD cohort no SAEs; SAD cohorts 2 SAEs unrelated to rosnilimab as follows: Obstructive pancreatitis occurred in a placebo subject and Coronavirus infection occurred in drug 400 mg SC cohort on Day 24 until Day 31; participant recovered and discontinued from the study, and AE was deemed unrelated to rosnilimab. 2. Lilly peresolimab Phase 2 data in RA, published in NEJM (A Phase 2 Trial of Peresolimab for Adults with Rheumatoid Arthritis | NEJM). 13 Rosnilimab, and overall PD-1 agonist class, well- tolerated with no dose limiting tox observed to date Rosnilimab Phase 1: 144 healthy volunteers (HV) in SAD and MAD cohorts • Supports monthly SC dosing • Favorable safety and tolerability ― No SAEs related to rosnilimab1 ― No carcinogenic events observed ― No infection risk signal Rosnilimab P2a in alopecia areata (AA) for Q4W SC dosing for 6 months was well tolerated with no significant safety signals PD-1 agonist class: consistent tolerability profile to date • Competitor PD-1 programs no carcinogenic events or infection risk signal • >100+ RA patients treated with Lilly PD-1 agonist (highest dose of 700 mg IV over 6 months) showed tolerable profile2 Abatacept, targeting all T cells, has not shown clinically relevant carcinogenic increases in decades of commercial use