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

August 4, 2021 Training the Immune

System to Fight Cancer December 6, 2021 Exhibit 99.1

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, the preclinical and clinical development of our product candidates, and other financial and operating information. 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. Disclaimer

Gerber et al., Biochemical Pharmacology

2016 Market estimates from PD-1 and PDL-1 Inhibitors Market Size in 2021 - MarketWatch, 360 Research The Modern-Day Challenge in Immuno-Oncology Majority of patients don't respond to PD-1/PD-L1 monotherapy1 Global PD-1/PD-L1 Market2

~$30B ~$90B 2020 2026

Adapted from Van der Woulde-LL, et al,

Trends in Cancer, 2017 Two Major Types of Non-Responders to PD-1 Blockade Green = T-cells Purple = tumor Non-Responders T-cells Absent T-cells Inactive or Outside Tumor Responders T-cells Inside Tumor

Generate anti-tumor T-cells Unleash

anti-tumor T-cells ImmunoPhage Platform Powerfully self-adjuvanted nanoparticle vaccine can drive B cell and T cell responses Multi-antigen vaccine enables personalized approach from "off-the-shelf" components Targets APCs

Enhanced through addition of immunostimulatory nanobodies & cytokines TMAb (Tumor Microenvironment Activated Biologics) Platform Next-generation tumor activated mAbs Binding only in the low-pH tumor microenvironment Target checkpoints

and/or other immune pathways Enable improved PK/PD and toxicity profiles Two Platforms to Unleash Anti-Cancer T-cell Activity

T cell APC Peptide TCR HLA T cell

Immune Checkpoint Focus on multi-antigen approach for HLA-mediated immunotherapy to GENERATE anti-tumor T-cells ImmunoPhage TMAb Target Cell Focus on novel immune checkpoints to UNLEASH anti-tumor T-cells T-Cells Are Central to Our Approach

and the Key to Unlocking Groundbreaking Clinical Activity

Two Platforms Provide Broad Pipeline

Opportunities TMAb* Platform ImmunoPhage Platform *Tumor Microenvironment Activated biologics **Consists of cash, cash equivalents and marketable securities In-house GMP manufacturing capabilities Business Development Strong Cash Position

Ended 3Q 2021: $156.7M** Positioned to Drive Value with Next Generation Product & Platform Development

Pipeline Utilizing Pioneering

ImmunoPhage Platform, TMAb Platform Program (Target) Indication Discovery IND-enabling Phase 1 / 2 Clinical TMAb SNS-101 (VISTA) Solid Tumors SNS-VSIG4 Solid Tumors ImmunoPhage SNS-401-NG (Multiple Tumor Antigens) Merkel Cell Carcinoma Head and Neck

Cancer Lung Cancer Melanoma Breast Cancer

TMAb (Tumor Microenvironment Activated

Antibodies that bind at

physiological pH may encounter a "sink" Prevents effective binding at the tumor and may lead to toxicity TMAb antibodies bypass tissue compartments other than the low-pH tumor microenvironment Potential for improved safety and clinical

activity profile pH 7.4 pH 7.4 pH 7.4 pH~ 6 Ph~ 6 pH~ 6 TMAb PLATFORM pH-sensitive Antibodies Only Bind Their Targets in the Low-pH Tumor Microenvironment The tumor microenvironment of pH ~6 is lower than physiological pH of 7.4 Sensei's

technology identifies pH-sensitive antibodies that bind only at the tumor

70-80% of patients do not achieve

increased survival with CPI monotherapy1 The immunosuppressive tumor microenvironment (TME) influences response to immune checkpoint blockade Innate immune cells such as myeloid cells are a key driver of immunosuppressive TME 1 Gerber, et al

Biochemical Pharmacology 2016 The Promise and Challenge of Immunotherapy Using the body's own immune system to attack cancer Capitalizing on immunological specificity and long-term memory Achieving durable cures with minimal toxicity THE

PROMISE THE CHALLENGE Targeting Immunosuppressive myeloid cells is a promising strategy to overcome resistance to checkpoint Inhibitor therapy

1 Lines et al. Cancer

research vol. 74,7 (2014) 2 Gao et al. Nature medicine vol. 23,5 (2017) VISTA: An Emerging Checkpoint Target on Myeloid Cells Target Overview: Large market opportunity B7 family ligand Extensive expression on myeloid cells1 Inhibition of

VISTA may lead to activation of myeloid cells Excellent therapeutic combinability with CTLA-4 or PD-1/PD-L1 ICIs, especially in cold tumors2 VISTA expression correlates with poor survival rates across multiple cancers Novel development

program with no approved therapies Sensei's Competitive Advantage: Extensive understanding of VISTA biology and differentiated candidate antibody VISTA is a Negative Regulator of T cell Function Low pH tumor microenvironment

Increased Understanding of VISTA as

a Promising Target to Address the Needs of Patients with Cancer

VISTA's extracellular domain

is uniquely rich in histidines Histidines are protonated at low pH enabling VISTA to distinguish the active (acidic pH) and inactive (neutral pH) PSGL-1 binding interface 1. Johnston et al., Nature 2019 VISTA Checkpoint is Activated at the Low

pH of the Tumor Microenvironment Antibodies that block VISTA histidines: H153, H154 and H155 on interrupt PSGL-1 binding1

Block VISTA's interaction with

PSGL-1 at pH 6 within the tumor microenvironment Selectively bind VISTA at low pH to avoid: target mediated drug disposition on-target/off-tumor side effects Design an Fc-competent IgG engaging with Fc R on tumor-infiltrating myeloid cells Key

to Unlocking the Power of VISTA SNS-101

SNS-101 Inhibited Interaction of

VISTA to its Receptor, PSGL-1, in CD4/CD8 T-Cells at Low pH 6.0 PSGL-1 VISTA-Bio PE T-cell SA PSGL-1: VISTA Interaction on primary T-cells at pH 6.0 CD4 T-cells CD8 T-cells SITC 2021: Poster titled: Antagonistic pH-selective VISTA antibody SNS-101

potentiates anti-PD-1/PD-L1-induced anti-tumor immunity 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 suppress myeloid cells in the tumor microenvironment SNS-101: IND-Enabling Studies are Underway for SNS-101

R [RU] [Vista] - 7.5 nmol

- 0.2 nmol SNS-101 Has >600-Fold Selectivity for VISTApH6 ka = 4.59E+06 M-1s-1 Kd = 1.00E-03 s-1 KD = 2.18E-10 M SNS-101 ka = 7.11E+05 M-1s-1 Kd = 1.78E-04 s-1 KD = 2.5E-10 M SNS-101 [Vista] - 15 nmol - 0.2 nmol [Vista] -

7.5 nmol - 0.2 nmol [Vista] - 15 nmol - 0.2 nmol R [RU] Biophysical characterization demonstrates >600-fold selectivity for VISTA at pH 6.0 Picomolar binding at low pH No significant binding observed at physiological pH (7.4)

SITC 2021: Poster titled: Antagonistic pH-selective VISTA antibody SNS-101 potentiates anti-PD-1/PD-L1-induced anti-tumor immunity. pH7.4 pH 6.0 pH-dependent "benchmark" pH-dependent "benchmark" pH-independent

"benchmark" pH-independent "benchmark" ka = 1.45E+06 M-1S-1 Kd = 2.25E-03 S-1 KD = 1.55E-09 M [Vista] - 15 nmol - 0.2 nmol ka = 4.162E+05 M-1S-1 Kd = 9.27E-05 S-1 KD = 2.23E-10 M [Vista] - 15 nmol -

0.47 nmol pH 6.0 pH 7.4 Monovalent Affinity (KD) [nM] 0.218 132 (~No binding)

Proposed Mechanism of Action for

SNS-101 Fc-competent framework is required for optimal activity, but Fc R engagement in the blood may result in untoward "off tumor" activation (i.e. CRS) Non-pH dependent pH-dependent Blood Tumor Monocyte VISTA Non-pH sensitive mAb

Fc R SNS-101 Peripheral Sink and Activation CRS? T-cell PSGL-1 Monocyte Macrophage Macrophage Macrophage T-cell Macrophage Macrophage Macrophage Same Activation Activation No Activation No CRS Macrophage Pro-inflammatory Cytokines

Pro-inflammatory Cytokines

TMAb Platform Johnston et al,

Nature, 2019; Kineta website; Snyder et al, AACR Annual Meeting 2016; Pierre Fabre website; Hummingbird website SNS-101 Is a Differentiated Anti-VISTA Antibody SNS-101 VISTA.18 (BMS) KVA12.1 (Kineta) CI-8993; JNJ-61610588 (J&J/Curis) K01401-020;

W0180 (Pierre Fabre) HMBD-002 (Hummingbird) Inhibit PSGL-1 Binding Yes Yes unknown Yes unknown unknown pH Sensitive Binding Yes Yes No No No No Fc Active Yes (IgG1) No (IgG4) Yes (IgG1) Yes (IgG1) N/A No (IgG4) Stage Preclinical Preclinical

Preclinical Phase I Phase I IND submission Clinical Data / Notes Preclinical data presented at STIC IND-enabling studies underway N/A N/A JNJ initiated Phase I study in 2016 12 pts enrolled; initial dose 0.005 mg/kg Only patient treated at 0.3 mg/kg

experienced grade 3 CRS-associated encephalopathy; trial was halted Ongoing

Second TMAb program B7 family

related protein Expressed on macrophages Inhibits T-cell activation Novel therapeutic combinability with existing IO drugs Adapted from Zang et al., J Clin Invest. 2006 VSIG4: A Novel Next Generation Checkpoint Modulating the Tumor Microenvironment

No approved therapies against VSIG4

Ubiquitous viruses that infect

bacteria but not mammalian cells. Adept at activating the human immune system in multiple unique ways Bacteriophage

ImmunoPhage Platform Generating

Strong Antibody and T-cell Responses Bacteriophage virus is engineered and manufactured with both antigen and immune stimulatory viral DNA Viral DNA (self-adjuvant) Target antigen The ImmunoPhage bacteriophage is an icosahedron with a tail.

This configuration can be viewed as an activating signal to the immune system

Generating Strong Antibody and

T-cell Responses ImmunoPhages are taken-up by APCs and deliver three critical signals required to drive activation of T cells. Antigen cross presentation Positive co-stimulation Generation of Th1-biased immune response & cytokines CD28 CD80 T

cell receptor Antigen T- Cell Phage taken up by antigen presenting cells 1 2 3 1 2 3 Cytokines

Our ImmunoPhages can mount a

multi-modal attack on cancer, combining the benefits of a traditional vaccine with localized gene therapy Targeted therapeutic vaccine MHC-mediated immunity Bacteriophage have natural tropism for APCs Can be further targeted to APCs with non-antigen

capsid modifications Gene therapy vehicle Phage containing self-replicating RNA Used to deliver payloads consisting of immunomodulatory proteins or nanobodies Phortress library Personalized - yet off the shelf - medicines Pre-manufactured

cost effectively - then combined based on genetic profile ImmunoPhage A Multi-Pronged Approach to Address the Complexities of Cancer

33-46% disease-specific mortality

2,500 cases/yr with disease-specific mortality approaching 50% Vaccine combination therapy in adjuvant or neoadjuvant is attractive and feasible PD-1/PD-L1 refractory MCC remains unmet medical need with aggressive clinical course ~40% MCC patients

recur <24 months following definitive local treatment In these cases, expression of a viral antigen (oncogenic T-antigen) appears to be a strictly required tumor driver Researchers at UW have mapped MCPyV epitopes and determined CD8 T-cell, CD4

T-cell, and B-cell epitopes that are antigenic in the context of MCPyV+ MCC tumors. SNS-401-NG Development Collaboration with University of Washington to build first custom Merkel Cell Carcinoma (MCC) vaccine consisting of Merkel Cell Polyoma Virus

epitopes and other patient specific antigens SNS-401-NG: Building the First Custom Merkel Cell Polyoma Virus (MCPyV) ImmunoPhage MCC is a rare, aggressive neuroendocrine skin cancer Integration of MCPyV is present in ~80% of U.S. cases

Critical signals of dendritic cell

activation show dose-dependent increases when cells are exposed to increasing amounts of ImmunoPhages Mechanism of Action: Activation and Maturation of Dendritic Cells Dose-response of engineered lambda phage on human skin-derived DC cultures

Signal: Dendritic cell co-stimulatory molecules Signal: Cytokine secretion