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Exhibit 99.1 VISTA Science Symposium November 16, 2021 Sensei Presenters: Guest Speaker: John Celebi Prof. Robert Schreiber Chief Executive Officer Andrew M. Bursky and Jane M. Bursky Distinguished Professor of Pathology and Immunology, Professor of Molecular Microbiology and co-leader of the tumor Dr. Robert Pierce immunology program at the Siteman Comprehensive Chief Scientific Officer Cancer Center, Founding Director of the Center for Human Immunology and Immunotherapy Programs at Dr. Edward van der Horst The Washington University School of Medicine SVP, TMAb Antibody Development Sensei IOAB member

Disclaimer This presentation has been prepared by Sensei Biotherapeutics, Inc. (the “Company,” we, us ) and is made for informational purposes only. The information set forth herein does not purport to be complete or to contain all of the information you may desire. Statements contained herein are made as of the date of this presentation unless stated otherwise, and neither the delivery of this presentation at any time, nor any sale of securities, shall under any circumstances create an implication that the information contained herein is correct as of any time after such date or that information will be updated or revised to reflect information that subsequently becomes available or changes occurring after the date hereof. This presentation contains estimates and other statistical data made by independent parties and by us relating to market shares and other data about our industry. This presentation also contains forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995 that are based on our management's beliefs and assumptions and on information currently available to management. These forward-looking statements include, without limitation, statements regarding our industry, business strategy, plans, and the preclinical and clinical development of our product candidates. When used in this presentation, the words may, believes, intends, seeks, anticipates, plans, estimates, expects, should, assumes, continues, could, will, future and the negative of these or similar terms and phrases are intended to identify forward-looking statements. Forward-looking statements involve known and unknown risks, uncertainties and other factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward- looking statements. Risks and uncertainties that may cause actual results to differ materially include uncertainties inherent in the development of therapeutic product candidates, such as preclinical discovery and development, conduct of clinical trials and related regulatory requirements, our reliance on third parties over which we may not always have full control, and other risk and uncertainties that are described in our Annual Report on Form 10-K filed with the SEC on March 30, 2021 and our other Periodic Reports filed with the SEC. Forward-looking statements represent our management's beliefs and assumptions only as of the date of this presentation and include all matters that are not historical facts. Our actual future results may be materially different from what we expect. Except as required by law, we assume no obligation to update these forward-looking statements publicly, or to update the reasons actual results could differ materially from those anticipated in the forward-looking statements, even if new information becomes available in the future. Certain information contained in this presentation relates to, or is based on, studies, publications, surveys and other data obtained from third-party sources and the Company's own internal estimates and research. While the Company believes these third-party sources to be reliable as of the date of this presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. In addition, all of the market data included in this presentation involves a number of assumptions and limitations, and there can be no guarantee as to the accuracy or reliability of such assumptions. Finally, while we believe our own internal research is reliable, such research has not been verified by any independent source.

AGENDA Speaker Topics John Celebi • Welcome/TMAb Mission President & CEO Professor, Robert Schreiber, Ph.D. • VISTA biology Washington University School of Medicine Sensei IOAB member Robert Pierce, M.D. • SNS-101 preclinical data Chief Scientific Officer highlights from SITC Edward van der Horst, Ph.D. • Join for Q&A SVP, TMAb Antibody Development 3

Our TMAb (Tumor Microenvironment Activated biologics) Platform Mission Leverage unique features of the tumor microenvironment to selectively activate biologics that unleash clinically meaningful anti-cancer immune responses 4

The Modern-Day Challenge in Immuno-Oncology Majority of patients don’t respond to PD- 2 Global PD-1/PD-L1 Market 1 1/PD-L1 monotherapy 2026 2020 Survival Benefit 20-30% No Survival ~$90B ~$30B Benefit 70% 1. Gerber et al., Biochemical Pharmacology 2016 2. Market estimates from PD-1 and PDL-1 Inhibitors Market Size in 2021 – MarketWatch, 360 Research

Two Major Types of Non-Responders to PD-1 Blockade Responders Non-Responders T-cells Inactive or T-cells Inside Tumor T-cells Absent Outside Tumor Green = T-cells Purple = tumor 6 Adapted from Van der Woulde-LL, et al, Trends in Cancer, 2017

Two Platforms to Unleash Anti-Cancer T-cell Activity TODAY’S DISCUSSION TMAb™ (Tumor ImmunoPhage™ Platform Microenvironment Activated Biologics) Platform • Powerfully self-adjuvanted nanoparticle vaccine that drive • Next-generation tumor activated tumor-specific T cell mAbs responses

VISTA (V-domain Ig suppressor of T cell activation) Target Overview: • Established immune checkpoint target to overcome checkpoint resistance • Large market opportunity • Extensive expression on normal myeloid cells Low pH tumor Sensei’s Competitive Advantage: microenvironment Leverage extensive understanding of VISTA biology to deliver a differentiated approach SNS-101: • A fully human monoclonal antibody that selectively binds active (low pH) VISTA, but not inactive VISTA in the blood • Potent inhibitor of PSGL-1 binding to VISTA • Fc-competent framework to deliver positive “kick” to suppressive myeloid cells in the tumor microenvironment 8

Leveraging a Team with Decades of Experience 9

Dr. Schreiber VISTA Biology VISTA (B7-H5) is recognized an important immune checkpoint and B7 family member that is expressed on myeloid cells, a hub of immunosuppressive activity, and is activated via binding to its receptor on T-cells (PSGL-1) at sub-physiologic pH

The Promise and Challenge of Immunotherapy Targeting Immunosuppressive myeloid cells is a promising strategy to overcome resistance to checkpoint Inhibitor therapy THE PROMISE THE CHALLENGE • Using the body’s own immune system to • 70-80% of patients do not achieve increased 1 attack cancer survival with CPI monotherapy • Capitalizing on immunological specificity and • The immunosuppressive tumor long-term memory microenvironment (TME) influences response to immune checkpoint blockade • Achieving durable cures with minimal toxicity • Innate immune cells such as myeloid cells are a key driver of immunosuppressive TME 11 1 Gerber, et al Biochemical Pharmacology 2016

VISTA Has Emerged as an Important Checkpoint Regulator Target Gao. J., et al Yuan, L., et.al

Patients with High Circulating Myeloid Cells Have Shown Lower Overall Survival When Treated with Checkpoint Blockade Ipilimumab-treated Melanoma Patients Nivolumab-treated Melanoma Patients MDSC ≤ 12.65 MDSC low MDSC > 12.65 MDSC high Kitano et al., Cancer Immunol Res. 2012 13 Weber et al., Cancer Immunol Res. 2016

VISTA may be a Compensatory Pathway Following Checkpoint Therapy Can targeting VISTA augment T-cell checkpoint blockade in refractory tumors? VISTA Increases on Prostate Tumor Cell Prostate Tumor Cell Infiltrates Increase Infiltrates Following Ipilumimab Treatment Following Ipilumimab Treatment Gao et al., Nat Med. 2017 14

VISTA Expression Increases in PBMC Subsets of Patients with Non-Small Cell Lung Cancer (NSCLC) 15 Cairns B et al, AACR Annual Meeting 2016.

VISTA Blockade Synergizes With PD-1/L-1 Pathway Inhibition CT26 Syngeneic Tumor Model Liu J. et al. PNAS 2015 16

VISTA is An Emerging Target on Myeloid Cells and Key Resistance Mechanism for PD-1/PD-L1 Blockade • VISTA is a B7 family (e.g., same protein VISTA is a Negative Regulator of T cell family as PD-L1) ligand expressed on Function at Low pH myeloid cells, a hub of immunosuppressive 1 activity T-cell • VISTA is a key player in controlling Myeloid cell checkpoint blockade • VISTA has been implicated in resistance to Low pH interaction 2 PD-1/PD-L1 inhibitors 1 Lines et al. Cancer research vol. 74,7 (2014) 17 2 Gao et al. Nature medicine vol. 23,5 (2017)

VISTA is an Emerging Target on Myeloid Cells and Key Resistance Mechanism for PD-1/PD-L1 Blockade • Tumors are typically lower in pH than Tumors are typically lower in pH than normal tissues normal tissues • At low pH, key amino acids in VISTA become protonated, changing its Tumor pH ~6-6.5 charge, and likely, its shape Normal physiological pH • This change activates VISTA enabling 7.4 VISTA to bind to PSGL-1 on T cells, engaging its checkpoint function 1 Lines et al. Cancer research vol. 74,7 (2014) 18 2 Gao et al. Nature medicine vol. 23,5 (2017)

The Binding of VISTA to PSGL-1 is pH Dependent Active VISTA Inactive VISTA 19 Adapted from Gao et al. Nature medicine vol. 23,5 (2017)

Dr. Schreiber VISTA has been difficult to drug due to its unique biology

VISTA is Expressed at High Levels on Human Monocytes and Neutrophils Flow Cytometry Analysis of VISTA Expression on Normal Human Peripheral Immune Cells 21 Snyder et al, 2016 AACR Annual Meeting, Oral Presentation

High VISTA Expression on Monocytes and Neutrophils Results in Sub-Optimal PK and may Decrease the Therapeutic Window Case Study + • Antibodies binding VISTA cells CI-8993 Clinical Ongoing Clinical Study (e.g. monocytes) at physiological • Phase 1 Dose Escalation Study pH result in rapid elimination from • 12 patients enrolled with advanced refractory solid circulation through targeted- tumors mediated drug disposition • Initial dose of 0.005 mg/kg and above • Low-grade transient Cytokine Release Syndrome (TMDD) (CRS) seen at 0.15 mg/kg and above • Study halted after 1 DLT at sub-therapeutic dose level • Efficacious drug occupancy levels may be difficult to reach and potentially narrow the therapeutic window Adapted from Curis Corporate presentation 2021 22

The VISTA Checkpoint Itself is Only ON Under Low pH Conditions 1 Antibodies that block VISTA histidines H153, H154 and H155 interrupt PSGL-1 binding VISTA’s extracellular domain is uniquely 1 rich in histidines PSGL-1 Histidines are protonated at low pH enabling VISTA to distinguish the active (acidic pH) and inactive (neutral pH) PSGL-1 interface 23 1. Johnston et al., Nature 2019

Engagement of FcƔR may be Required for Optimal Activity of Anti-VISTA Monoclonal Antibodies JNJ-61610588 VSTB140 Fc competent IgG1 Fc silent IgG2���� 24 Snyder et al., AACR Annual Meeting 2016

Summary Reasons Why VISTA Has Been Difficult to Drug Historically • VISTA is expressed at high levels on monocytes and neutrophils • For non-pH-dependent blocking antibodies, high expression on monocytes and neutrophils results in a sub-optimal PK due to target-mediated clearance and may decrease the therapeutic window • The VISTA checkpoint itself is only ON under low pH conditions • VISTA’s immune checkpoint function is only active (i.e. capable of binding PSGL-1 at low pH) • Other receptors for VISTA are active at physiologic pH but do not appear to function as immune checkpoints • Engagement of FcƔR may be a prerequisite for optimal activity of anti-VISTA antibodies • Fc silent antibodies are not effective at T cell proliferation ex vivo or anti-tumor activity in vivo despite picomolar binding affinity to VISTA • Engagement in the blood may result in untoward “off tumor” activation (i.e. CRS) 25

Dr. Rob Pierce SITC 2021: SNS-101 Preclinical Data Poster Presentation

pH-sensitive Antibodies Primarily Bind Their Antibodies in the Low pH Tumor Microenvironment TMAb Platform The tumor microenvironment of pH ̴ 6.0 is lower than Sensei’s technology identifies pH-sensitive antibodies physiological pH of 7.4 that bind primarily at the tumor pH 7.4 • Antibodies that bind at physiological pH may encounter a “sink” • Prevents effective binding at the tumor and may lead to toxicity pH 6.0 • Sensei’s technology selectively targets pH-sensitive antibodies to bypass tissue compartments other than the low-pH tumor microenvironment: pH 6.0 • Potential for improved safety and pH 6.0 clinical activity profile 27

SNS-101 Inhibited Interaction of VISTA to its Receptor, PSGL-1, in CD4/CD8 T-Cells at Low pH 6.0 PSGL-1: VISTA Interaction on primary T-cells at pH 6.0 T-cell PE PSGL-1 VISTA-Bio SA 28 SITC 2021: Poster titled: Antagonistic pH-selective VISTA antibody SNS-101 potentiates anti-PD-1/PD-L1-induced anti-tumor immunity. CD8 T-cells CD4 T-cells

SNS-101 Identified Based on Stringent Cell-Based Assay Candidate profile: no significant binding at pH 7.4 pH6.0 29

pH6 SNS-101 Has >600-Fold Selectivity for VISTA • Biophysical characterization demonstrates pH 6.0 pH 7.4 >600-fold selectivity for VISTA at pH 6.0 132​ • Picomolar binding at low pH Monovalent Affinity (K ) [nM]​ 0.218​ (~No D binding) • No significant binding observed at physiological pH (7.4) pH7.4 pH 6.0 pH-independent pH-dependent pH-dependent pH-independent SNS-101 SNS-101 “benchmark” “benchmark” “benchmark” “benchmark” -1 -1 -1 -1 -1 -1 -1 -1 k = 4.59E+06 M s k = 1.45E+06 M S k = 7.11E+05 M s k = 4.162E+05 M S a a a a -1 -1 -1 -1 K = 1.00E-03 s K = 2.25E-03 S K = 1.78E-04 s K = 9.27E-05 S d d d d K = 2.18E-10 M K = 1.55E-09 M D K = 2.5E-10 M K = 2.23E-10 M D D D [Vista] – 7.5 nmol – 0.2 nmol [Vista] – 7.5 nmol – 0.2 nmol [Vista] – 15 nmol – 0.2 nmol [Vista] – 15 nmol – 0.2 nmol [Vista] – 15 nmol – 0.2 nmol [Vista] – 15 nmol – 0.47 nmol 30 SITC 2021: Poster titled: Antagonistic pH-selective VISTA antibody SNS-101 potentiates anti-PD-1/PD-L1-induced anti-tumor immunity. R [RU] R [RU]

+ SNS-101 Does Not Significantly Bind to VISTA Monocytes at pH 7.4 • VISTA+ monocytes are one of the main causes of TMDD • Non-pH sensitive VISTA mAbs bind to monocytes at pH 7.4 thus allowing TMDD and have potential for on-target/off-tumor toxicity VISTA Copy Number: Kasumi-3: 70,202 CD14+ Monocytes: ~103,000 31

Proposed Mechanism of Action for SNS-101 Fc-competent framework is required for optimal activity, but FcƔR engagement in the blood may result in untoward “off tumor” activation (i.e. CRS) Non-pH dependent pH-dependent Monocyte Macrophage Blood Monocyte Peripheral Sink and Activation No Activation CRS? No CRS Pro-inflammatory Pro-inflammatory Cytokines Cytokines T-cell Macrophage T-cell Macrophage Macrophage Same Macrophage Tumor Macrophage Macrophage Activation Activation Non-pH VISTA PSGL-1 FcƔR SNS-101 sensitive mAb 32

‘High-bar’ In Vivo Screening Test of SNS-101 Activity 1-week Administration Black Line (IgG Control human & ratl) Antibodies were administered I.P. 2/wk for 1 week Blue Line (IgG Control human & rat anti-mPD-1) at 40 mg/kg total (20 mg/kg each)​ Red Line (rat anti-mPD-1 & anti-VISTA) 33 SITC 2021: Poster titled: Antagonistic pH-selective VISTA antibody SNS-101 potentiates anti-PD-1/PD-L1-induced anti-tumor immunity.

SNS-101 Is a Differentiated Anti-VISTA Antibody TMAb Platform K01401-020; SNS-101 VISTA.18 KVA12.1 CI-8993; JNJ-61610588 HMBD-002 W0180 (BMS) (Kineta) (J&J/Curis) (Hummingbird) (Pierre Fabre) Inhibit PSGL-1 Yes Yes unknown Yes unknown unknown Binding pH Sensitive Yes Yes No No No No Binding Fc Active Yes (IgG1) No (IgG4) Yes (IgG1) Yes (IgG1) N/A No (IgG4) Stage Preclinical Preclinical Preclinical Phase I Phase I IND submission • JNJ initiated Phase I study in 2016 • Preclinical data • 12 pts enrolled; initial dose presented at STIC 0.005 mg/kg • Ongoing; no data • First-patient to Clinical Data / • IND-enabling studies • N/A • N/A reported be dosed in • Only patient treated at 0.3 Notes underway 4Q’21 mg/kg experienced grade 3 CRS-associated encephalopathy; trial was halted 34 Johnston et al, Nature, 2019; Kineta website; Snyder et al, AACR Annual Meeting 2016; Pierre Fabre website; Hummingbird website

Key to Unlocking the Power of VISTA 1. Block VISTA’s interaction with PSGL-1 at pH 6 within the tumor microenvironment 2. Selectively bind VISTA at low pH to avoid: • target mediated drug disposition • on-target/off-tumor side effects 3. Design an Fc-competent IgG engaging with FcƔR on tumor- infiltrating myeloid cells IND-Enabling Studies are Underway for SNS-101 35

Question & Answer Session

VISTA Science Symposium November 16, 2021 Sensei Presenters: Guest Speaker: John Celebi Prof. Robert Schreiber Chief Executive Officer Andrew M. Bursky and Jane M. Bursky Distinguished Professor of Pathology and Immunology, Professor of Molecular Microbiology and co-leader of the tumor Dr. Robert Pierce immunology program at the Siteman Comprehensive Chief Scientific Officer Cancer Center, Founding Director of the Center for Human Immunology and Immunotherapy Programs at Dr. Edward van der Horst The Washington University School of Medicine SVP, TMAb Antibody Development Sensei IOAB member