™ D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Investor Event 1 December 2022

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Disclaimer 2 Forward Looking Statements This presentation contains forward-looking statements. Statements we make in this presentation may include statements which are not historical facts and are considered forward-looking within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, which are usually identified by the use of words such as “anticipates,” “believes,” “estimates,” “expects,” “future,” “opportunity,” “proposed,” “targets,” “intends,” “may,” “plans,” “projects,” “seeks,” “should,” “will,” and variations of such words or similar expressions. 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D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Agenda 3 Gene Circuits to Engineer Next Generation Cell Therapies Tim Lu, MD, PhD – Co-founder & CEO Treatment Paradigm and Unmet Medical Need in AML Stephen A. Strickland, Jr., MD, MSCI - Director of Leukemia Research at the Sarah Cannon Transplant & Cellular Therapy Network Update on SENTI-202 For Heme Malignancies Kanya Rajangam, MD, PhD – Chief Medical and Development Officer (CMDO) Conclusions and Next Steps Tim Lu, MD, PhD – Co-founder & CEO Q&A

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Gene Circuits to Engineer Next Generation Cell Therapies Tim Lu, MD, PhD - Co-founder & CEO 4

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Senti’s Next Generation Gene Circuit Technologies for Cancer Cell Therapy 5 Broaden patient access Address efficacy AND safety Address large unmet needs across multiple solid and liquid tumors Enhance durability and persistence Increase specificity and dosing window Aim to.. NK Cells Logic Gating Regulator DialMulti-Arming Can be applied to: T Cells HSCsiPSCs Gene Circuits for Cell Therapy: NK Cells: Natural Killer Cells, iPSCs: induced pluripotent stem cells, HSCs: hematopoietic stem cells

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Today’s Cell Therapies Are Largely Guided by Single CAR System and Limited to a Small Set of Potential Therapeutic Targets 6 Only ~5% of potential surface proteins have been utilized in CAR therapies Heterogeneous antigen expression leading to tumor escape On-target / off-tumor killing leading to poor therapeutic window Two key limitations of today’s cell therapies

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Senti’s Gene Circuit Technology Has the Potential to Expand the Range of CAR Cell Therapies With Enhanced Efficacy and Precision 7 Expanding the range of potential therapeutics into the “empty” space Inhibitory CAR: NOT GATESenti’s next-gen capabilities Bivalent activating CAR: OR GATE

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Gene Circuits Designed to Solve for Key Cell Therapy Challenges 8 Senti’s Gene Circuit Solutions Cancer Cell Therapy Challenges Lack of NK cell expansion and persistence Antigen escape and tumor heterogeneity Dirty targets (on-target / off-tumor toxicity) Immunosuppressive tumor microenvironment Multi-Arming Autocrine and paracrine activation with proprietary Calibrated Release IL-15 (crIL-15) and other complementary cytokines (e.g., IL-21) Bivalent activating CAR with OR Logic GateLogic Gating Inhibitory CAR protects healthy cells with NOT Logic GateLogic Gating Pulsed Calibrated Release IL-12 with small molecule- controlled Regulator Dial Regulator Dial

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S NK Cells Compare Favorably to T Cell Based Therapies, While Gene Circuits Have Potential to Further Improve Efficacy, Safety, and Durability Further 9 NK cells are an attractive modality vs T cells • Extensive clinical experience with ~70 global peripheral blood derived unengineered NK cell therapy clinical trials1 • Well-tolerated with no/minimal CRS, neurotoxicity, GvHD • Anti-tumor activity including CR observed in R/R AML Key limitations noted with prior unengineered NK cell therapies • Limited persistence • Limited ability to cryopreserve • Scale-up manufacture Senti’s Gene Circuit technology, donor selection and scalable manufacturing aim to address these limitations Capabilities Current Auto T Cells Off-the-shelf potential with broad patient accessibility Designed with Logic Gates to achieve enhanced selectivity and safety Engineered with enhanced persistence   N/A ✓ ✓ ✓ Senti’s CAR-NK Cells Engineered to stimulate the patient immune system  ✓ 1 Lamers-Kok Journal of Hematology & Oncology 2022 CRS: cytokine release syndrome, GvHD: graft-versus-host disease, AML: acute myeloid leukemia

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Senti’s Next Generation CAR-NK Cell Therapy Pipeline Tackles Hard to Treat Cancers With Gene Circuits 10 Program Target Indications Discovery IND enabling Phase 1 Gene Circuits SENTI-202 CD33 and/or FLT3 AML, MDS and other blood cancers ✓ Multi-Arming: designed for enhanced efficacy ✓ crIL-15: autocrine and paracrine activation ✓ OR GATE: bivalent activation ✓ NOT GATE selectivity: healthy cell protection SENTI-301A GPC3 HCC and other solid tumors ✓ Multi-Arming: designed for enhanced efficacy ✓ crIL-15: autocrine and paracrine activation SENTI-401 CEA CRC and other solid tumors ✓ Multi-Arming: designed for enhanced efficacy ✓ crIL-15: autocrine and paracrine activation ✓ NOT GATE selectivity: healthy cell protection ✓ IL-21: sustained anti-tumor function Additional Programs Undisclosed Other tumors Program candidates integrate Multi-Arming, Logic Gating and/or Regulator Dial Gene Circuits 2023 IND 2024 IND 2H 2023 IND MDS: myelodysplastic syndromes, HCC: hepatocellular carcinoma, CRC: colorectal cancerr

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S SENTI-202, a Novel, Multi-Armed, Off-The-Shelf, Selective CAR-NK Cell Therapy for Blood Cancers Including AML and MDS 11LSCs: Leukemic Stem Cells Multi-Armed, off-the-shelf, selective CAR-NK • OR GATE: bivalent CD33 and/or FLT3 activation → potential for deep and durable responses in acute myeloid leukemia (AML) and other blood cancers. • NOT GATE: inhibition by endomucin (EMCN) protective antigen selectively expressed on healthy hematopoietic stem cells (HSCs) → potential for improved safety and increased therapeutic window • crIL-15 → potential for increased persistence, autocrine and paracrine immune cell activation On track for IND in 2H 2023

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S EMCN Engagement Enables Protection of Healthy HSCs FLT3 OR CD33 Engagement Triggers Killing of Heterogeneous AML Cancer Cells SENTI-202 Logic Gates Are Designed to Achieve Deep Clearance of AML Blasts and LSCs While Sparing Healthy HSCs 12 CD33 FLT3 EMCNAntigen: Healthy HSC SENTI-202 CAR-NK Cell Safety AntigenInhibitory CAR (iCAR)Tumor-Associated AntigensActivating CAR (aCAR) SENTI-202 CAR-NK Cell AML Cancer Cells Blast Cell LSC Do Not Kill

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S crIL-15 Senti’s Proprietary crIL-15 Technology Aims to Enhances NK Cell Expansion, Persistence and Tumor Killing 13 1. CYTOKINE SECRETION ONLY (PARACRINE) Enhanced NK Cell Expansion, Persistence and Tumor Killing 3. CALIBRATED RELEASE (cr) (PARACRINE AND AUTOCRINE) Cell Therapies Using This Approach Combines 1 & 2 2. MEMBRANE-BOUND ONLY (AUTOCRINE) Secreted IL-15 can activate neighboring immune cells present in the local tumor microenvironment (TME) • Secreted IL-15 activates neighboring immune cells present in the local TME • Membrane-bound IL-15 on the cell surface increases NK cell activity/function Membrane-bound IL-15 on the cell surface leads to autocrine activity and increases CAR-NK cell activity/function IL-15 Membrane bound IL-15

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Scalable Manufacturing to Support Off-The-Shelf CAR-NK Products 14 Lentivi rus Outpatient use potential Patient Isolate from selected donors Thaw and infuse Scalable ~21 Day Process NK Cells Selected Donor Gene Circuit Engineered CAR-NK cells Engineer CryopreserveExpand Off-The-Shelf Gene Circuits 1 2 3 4 5 Easy to thaw vials Final product harvested and cryopreserved >100 doses per batch NK cells isolated from peripheral blood of selected donors NK cells efficiently engineered with Gene Circuits High post-thaw potency

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E STreatment Paradigm and Unmet Medical Need in AML Stephen A. Strickland, Jr., MD, MSCI - Director of Leukemia Research at the Sarah Cannon Transplant & Cellular Therapy Network 15

DO NOT DISTRIBUTE 1973 Cytarabine/ Daunorubicin (7+3) 2000 Gemtuzumab ozogamicin 1977 First bone marrow transplant 2002 Idarubicin 2017 Midostaurin, Gemtuzumab ozogamicin (re- approved), CPX- 351, Enasidenib 2010 Gemtuzumab ozogamicin (withdrawal) 2018 Ivosidenib, Gilteritinib, Venetoclax, Glasdegib 2020 Azacitidine (maintenance) History of FDA Approvals in AML: Small molecules against broad targets/pathways ADCs Monoclonal antibodies Cell therapies or immune cell engagers directed at AML cells Over 600 clinical trials recruiting in AML using various modalities: Cell therapies designed to improve transplant outcomes VaccinesRadiopharmaceuticals Small molecules for genetically defined subsets History of FDA Approvals and Current Clinical Trials in AML

DO NOT DISTRIBUTE Significant Unmet Need in AML Even with Recent Approvals 1 Clarivate source data 2022; 2 Mangan Ther Adv Hematology 2011; 3 Brandwein Figure from Brandwein Am J Blood 2020 5.3 months median OS 12.6% 5-year OS AML • ~14,000 patients are newly diagnosed with AML in the US1 • Treatment at diagnosis generally includes intensive chemotherapy consolidated with HCT for younger fitter patients, and hypomethylating agents with venetoclax for older unfit patients • Even with initial intensive treatment, 20-40% of patients fail to respond to up-front AML therapy while ~50% of those who attain an initial CR eventually relapse2 • Prognosis at relapse is grim with ~5-10 months overall survival in R/R AML patients and limited standard of care options that includes FLT3, IDH1/2 inhibitors if relevant mutations are present3

DO NOT DISTRIBUTE AML Is a Heterogenous Disease and Requires Multi-Antigen Targeting SC-DARIC-33 JEZ-567 PRGN-3006 Targets Expressed on AML Blasts And/Or LSCs ICG-144 Target Antigen Expression on Various Cells1 Antigen LSCs Blasts HSCs CD33 (SIGLEC3) +/- + +/- FLT3 (CD135) + +/- + CLL-1 (CLEC12A) +/- + - CD123* +/- + +/- CD38 - + - NKG2D ligands - + - AML targets are notoriously heterogenous: CAR targets in AML and CAR cell therapies currently in clinical trials2: Targeting LSCs Is Critical in the Treatment of AML but Most CAR-Based Therapies Target Only One Antigen Leading To Incomplete Clearance of Leukemic Blasts and Stem Cells (LSCs), Tumor Escape and Eventual Patient Relapse 1 Valent Stem Cell Trans. Med. 2020, 2 Marvin-Peek Cancers 2022 * Note: CD123 is highly expressed in endothelial cells

DO NOT DISTRIBUTE The Need to Limit On-Target / Off-Tumor Toxicity in AML ESAs = Erythropoiesis-stimulating agents, G-CSF = Granulocyte colony stimulating factor Myelosuppression Anemia Thrombocytopenia Neutropenia Consequence Fatigue Risk of bleeding Risk of infection Targeting HSPCs leads to… • Common AML targets are largely expressed on cancer cells AND healthy hematopoietic stem and progenitor (HSPC) cells leading to on-target, off-tumor toxicity • Targeting HSPCs results in prolonged aplasia and myelosuppression leading to anemia, thrombocytopenia, neutropenia, and attendant complications like bleeding and infections • There is an urgent need for novel AML therapies with minimal bone marrow toxicities from off tumor effects CD123 CD123 CLL-1 Leukemic stem cells (LSCs) Leukemic blast cells Hematopoietic stem cell (HSC) Multipotent progenitor (MPP) cell Common lymphoid progenitor (CLP) cell Common myeloid progenitor (CMP) cell

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E SUpdate on SENTI-202 For Heme Malignancies Kanya Rajangam, MD, PhD - CMDO 20

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S SENTI-202 for CD33 and/or FLT3 Expressing Blood Cancers Including AML 21 7,860 7 20,216 Protein Coding Genes 40 2,611 Membrane proteins High expression in AML Low non-hematopoietic expression Manual curation FLT3 and CD33 2,152 112 Confirm high AML expression Low healthy tissue expression Optimization for AML subpopulation coverage Proven Targets • FLT3 and/or CD33 expressed in ~95% of AML • Targeting FLT3 and CD33 with an OR GATE has potential of increased efficacy and deeper remission, due to decreased likelihood of tumor antigen escape • Rigorous bioinformatics approach was used to identify CD33 and FLT3 as an optimal aCAR pair to provide broad coverage of blasts and LSCs Bioinformatics approach to identify aCAR pair

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S SENTI-202 Has Shown Robust Preclinical Anti-Tumor Activity 22 Vehicle Unengineered NK Cells SENTI-202 CAR- NK Cells Day: 7 28 34 Significant in vitro killing of leukemia cell line Robust suppression of tumor in AML MV4-11 xenotransplantation model Broad in vitro killing of primary AML and MDS tumor cells AML #1 0 10 20 30 40 50 60 70 80 90 100 Blasts LSCs Blasts LSCs Blasts LSCs Blasts % A M L/ M D S C el l K ill in g Unengineered NK Cells SENTI-202 CAR-NK Cells AML #2 AML #3 MDS 0 20 40 60 80 100 1:4 1:2 1:1 2:1 4:1 % C yt o to xi ci ty E:T Ratio Unengineered NK Cells SENTI-202 CAR-NK Cells

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Senti’s Discovery Platform Identified EMCN as a Key Protective Antigen for Healthy HSCs 23 Surface Protein 0% EMCN on primary AML LSCs EMCN Si d e Sc at te r (S SC ) 70% EMCN on primary HSCs Challenge Solution and Validation FLT3 is expressed on healthy HSCs 7,680 1 20,216 Protein Coding Genes 15 115 Membrane proteins High HSC/AML expression ratio Confirm low AML expression Manual curation EMCN The NOT GATE uses EMCN as a Protective Antigen input to differentiate between healthy HSCs and AML cells AML Blasts AML LSCs Neutrophils Healthy HSCs AML Blasts AML LSCs Neutrophils Healthy HSCs

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Senti’s Discovery Platform Identified LIR1 as the Optimal iCAR ICD for SENTI-202 24 Systematic approach to identify optimal iCAR ICD for SENTI-202 using a screen of native inhibitory proteins Anti-FLT3 scFV CD28 CD3ZH TM Native inhibitory receptors Native binding domains Anti-EMCN scFV Inhibitory domain H TM Native TM and inhibitor domains ITMs Activating CAR (aCAR) Inhibitory CAR (iCAR) On- tumor Off- tumor Comparative analysis between NOT gates with different iCAR ICDs identified LIR1 as optimal ICD for SENTI-202 On-target killing O ff -t u m o r ki lli n g 1- Screening and Identification of iCAR 2- Killing Assays 3- Logic Analysis Screen of anti-EMCN iCARs with various transmembrane and intracellular domains

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S SENTI-202 Preclinical Selectivity via Inhibitory CAR Binding Endomucin to Protect Healthy Primary Human HSCs 25 In vitro protection of healthy primary human HSC fraction expressing EMCN 0 10 20 30 40 50 60 CD33 and/or FLT3 CAR-NK Cells SENTI-202 CAR-NK Cells % K ill in g (L e u ke m ia ) 0 5 10 15 20 25 30 35 40 45 50 CD33 and/or FLT3 CAR-NK Cells SENTI-202 CAR-NK Cells % K ill in g (E M C N + H SC s)

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S SENTI-202 Preclinical Selectivity via EMCN iCAR Protects Model Healthy Cells In Vivo from aCAR-Mediated Killing 26 I.V. injection Blood draw After 27 days N o rm al iz e d C o u n ts N o rm al iz e d C o u n ts N o rm al iz e d C o u n ts Unengineered NK Cells OR Gated CAR-NK Cells SENTI-202 CAR-NK Cells SENTI-202 CAR-NK Cells “Healthy” Cells Cancer Cells50:50 “Healthy” Cells Spared Cancer Cells Killed

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Calibrated Release IL-15 (crIL-15) Increases Persistence and Activation of Both CAR-NK and Immune Cells in Tumor Milieu 27 0 2,000 4,000 6,000 sIL-15 CAR-NK crIL-15 CAR-NK Pa ra cr in e A ct iv it y (p ST AT 5 M FI ) Phospho STAT5 levels increased in T cells exposed to supernatant from either crIL-15 or sIL-15 CAR-NK cell culture crIL-15: IL-15 released by local proteases → autocrine and paracrine effects crIL-15 has paracrine activity and activates resting immune cells crIL-15 increases persistence of CAR- NK cells 0 0.2 0.4 0.6 0.8 1 0 5 10 15 20 25 V ia b le C el ls ( e6 ) Days in Culture crIL-15 increases CAR-NK serial killing compared to secreted IL-15 crIL-15 CAR-NK Cells Unengineered NK Cells sIL-15: secreted wild-type IL-15 0 1 2 3 4 5 0 1 2 3 4 5 6 7 8 9 Tu m o r C el l A b u n d an ce Days Vehicle Unengineered NK Cells crIL-15 CAR-NK Cells sIL-15 CAR-NK Cells Cancer cells added Cancer cells added Cancer cells added

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Proposed Phase 1 Study in R/R CD33+ And/or FLT3+ Malignancies With Focus on AML 28 Proposed Phase 1 study anticipated to enroll R/R CD33+ and/or FLT3+ heme malignancies • Modified “3+3” study design • Enroll patients who have received at least 1 prior treatment including targeted agents if FLT3, IDH1/2 mutation+ • 2 of 3 patients at each dose level with AML • Disease specific expansion cohorts for AML and MDS Planned study endpoints • Safety, DLT, identify recommended Phase 2 dose • Efficacy using standard ELN 2022 criteria for AML and other disease specific consensus criteria • PK, pharmacodynamics including endomucin protection, immunogenicity Lymphodepletion Fludarabine Cyclophosphamide SENTI-202 2-3 dose levels of cells Efficacy Additional cycles+ -5 to -3 0 7 14 28Days Planned Study Treatment/ Cycle Planned data- driven seamless Phase 1 to pivotal design

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E SConclusions and Next Steps Tim Lu, MD, PhD - Co-founder & CEO 29

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S SENTI-202 Can Potentially Fulfill AML Treatment Gap 30 Multi-Arming Multi-Antigen Targeting Healthy Cell Protection Redosing Potential Scalable Manufacturing SENTI-202 Calibrated release IL-15 enhances NK cell expansion, persistence, and tumor killing Simultaneously targeting FLT3 and/or CD33 via Logic Gating to drive deeper clearance of AML blasts and LSCs and prevent antigen escape and patient relapse Protection of healthy HSCs via EMCN NOT Gate to minimize on-target/off-tumor toxicity, prevent myelosuppression and allow for repeat dosing Potential to increase durability and response by re- dosing patients Rigorous screening and selection of GMP donors to minimize variability

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S SENTI-202 Aims to Fill Key Unmet Need of Targeting Both AML Blasts and AML LSCs 311 HSC toxicity was observed for several preclinical FLT3-targeted therapies, including CAR-T, ADCs and BiTes Select AML Cell Therapy Candidates in Development Manufacturer Modality MOA / Target1 Allogeneic CAR-T cells CD123 NKG2D ligands FLT3 OR CD33 NOT EMCN + + ✓ CAR-NK Cells iPSC-derived NK Cells CAR-NK Cells -- + Autologous CAR-T cells CLL-1 + Target Blasts +/- - ✓ - +/- Target LSCs We believe that by selectively targeting FLT3 (LSCs) and/or CD33 (blasts), we have the potential to provide AML patients with significantly deeper and longer remissions. Our clinical program initially enrolls patients with R/R CD33 and/or FLT3 positive heme malignancies with focus on AML with the potential to expand into earlier lines of therapy NKX101 FT538 UCART12 SENTI-202 KITE-222

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S YTD Progress and Planned Milestones in the Next 12 Months 32 SENTI-202 IND in 2H 2023 Pre-clinical data updates from multiple CAR-NK programs planned at key scientific meetings in 2023 GMP facility buildout on track to enable clinical manufacturing of CAR-NK cells in 2023 Continue to anticipate cash runway into 2024

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Gene Circuits Can Vastly Expand the Universe of Cancer Targets and Tumors That Can Be Addressed With Cell Therapies 33 Heme Malignancies Solid Tumors N ee d f o r H ea lt h y C el l P ro te ct io n FLT3* CD33* CEA* Target GPC3* OR GATE to enhance efficacy and deepen response Multi-Arming +/- Regulator Dial to overcome immunosuppressive TME NOT GATE enables expansion to dirty targets Logic Gating Multi-Arming Gene Circuit Technologies * Senti’s current CAR-NK programs Target Target Target Target TargetTarget Target Target Target Target Target Target Target Target Target Target Target CD19 BCMA Approved autologous CAR-T cell therapies Regulator Dial

D E C E M B E R 2 0 2 2 IN V E ST O R E V E N T | SE N T I B IO SC IE N C E S Q&A 34