R&D DayNovember 11, 2022

2 This presentation contains forward-looking statements within the meaning of, and made pursuant to the safe harbourprovisions of, The Private Securities Litigation Reform Act of 1995. All statements contained in this document, other than statements of historical facts or statements that relate to present facts or current conditions, including but not limited to, statements regarding possible or assumed future results of operations, business strategies, research and development plans, regulatory activities, market opportunity, competitive position and potential growth opportunities are forward-looking statements. These statements involve known and unknown risks, uncertainties and other important 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. In some cases, you can identify forward-looking statements by terms such as “may,” “might,” “will,” “should,” “expect,” “plan,” “aim,” “seek,” “anticipate,” “could,” “intend,” “target,” “project,” “contemplate,” “believe,” “estimate,” “predict,” “forecast,” “potential” or “continue” or the negative of these terms or other similar expressions. The forward-looking statements in this presentation are only predictions. We have based these forward-looking statements largely on our current expectations and projections about future events and financial trends that we believe may affect our business, financial condition and results of operations. These forward-looking statements speak only as of the date of this presentation and are subject to a number ofrisks, uncertainties and assumptions, some of which cannot be predicted or quantified and some of which are beyond our control, including, among others: our ability to successfully advance our current and future product candidates throughdevelopment activities, preclinical studies, and clinical trials; our reliance on the maintenance on certain key collaborative relationships for the manufacturing and development of our product candidates; the timing, scope and likelihood of regulatory filings and approvals, including final regulatory approval of our product candidates; the impact of the COVID-19 pandemic on our business and operations; the performance of third parties in connection with the development of our product candidates, including third parties conducting our future clinical trials as well as third-party suppliers and manufacturers; our ability to successfully commercialize our product candidates and develop sales and marketing capabilities, if our product candidates are approved; and our ability to maintain and successfully enforce adequate intellectual property protection. These and other risks and uncertainties are described more fully in the “Risk Factors” section of our most recent filings with the Securities and Exchange Commission and available at www.sec.gov. You should not rely on these forward-looking statements as predictions of future events. The events and circumstances reflected in our forward-looking statements may not be achieved or occur, and actual results could differ materially from those projected in the forward-looking statements. Moreover, we operate in a dynamic industry and economy. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict all risk factors and uncertainties that we may face. Except as required by applicable law, we do not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise.Forward-looking statements

3 AgendaDelivering on a Next-Generation iPSC PlatformLalo Flores, PhD, CEONectin-4 directed therapies: Urothelial Cancer and BeyondJonathan Rosenberg, MD, Chief Genitourinary Oncology Service, Division of Solid Tumor Oncology; Enno W. ErcklentzChair, Memorial Sloan Kettering Cancer Center Rationale for iPSC-derived γδCAR-T cellsHy Levitsky, MD, President of Research & Development Century’s Gamma Delta iTCell PlatformMark Wallet, PhD, Vice President, Head of Immuno-OncologyCNTY-107, our γδiTProduct Candidate for the Treatment of Solid Tumors Expressing Nectin-4Luis Borges, PhD, CSOQ&A

Delivering on a Next-Generation iPSC PlatformLalo Flores, PhD ǀCEO

5 Positioned to Deliver Next-Generation Cell Therapies First IND (CNTY-101) deemed eligible to proceed by FDA, Poised to initiate Phase 1 imminentlyFoundational investment to establish in-house manufacturing Maintaining financial strength with cash runway into 2025 Advances with next generation iNK3.0 and gamma delta iTcell platforms

6 Century’s Key Areas of Internal Focus B cell malignanciesCNTY-101: Lead product candidate, CD19 targeted CAR-iNKCNTY-102: First γδiTcandidate, multi-specific (CD19 + CD79b) CAR-iTDesigned to increase proportion of patients achieving durable responses through multi-dosing regimens enabled by key Allo-EvasionTMedits GlioblastomaCNTY-103: CD133 CAR iNK for recurrent GBMAddress heterogeneity via multi-tumor antigen targeting and safety and technical trafficking challenges with locoregional deliveryCNTY-107: Nectin-4 targeted CAR GD iTLeveraging gamma deltaiTplatform designed to address several solid tumor indications with high expression of Nectin-4 and unmet need Nectin-4 + Solid tumors

7 Leapfrogging the Competition in Lymphoma Leverage iPSC technology to develop products•With multiple enhancements introduced with precision CRISPR gene editing•That can be manufactured at scale with antibody-like COGs•That can realize the durability benefit of repeat dosing because they can resist rejection TimeDisruptive InnovationGen 1.0 -autologous CAR TGen 3.0 and future –Century iPSC candidates Gen 2.0 -donor derived allogeneic, early iPSC candidates Set efficacy barIncremental benefits on access but durable CRs inferior to AutologousLarge opportunity for products that can exceed the Autologous efficacy bar.

8 Transforming the cell therapy treatment paradigm •AUC main predictor of duration of response•Variable cell expansion/exposure drives toxicity and suboptimal responses •Finite repeatdosing regimens have the potential to exceed bar set by autologous cell therapy and deliver more durable responses, ifthe cells are engineered to avoid host rejection (Allo-EvasionTM) Single dose of allogeneic NK cells unlikely to match αβautologous CAR T Illustrative curves

9 Advances with iNKand iTCell Platforms Showcased at SITCEmpowering iPSC-Derived iNKCells with Multiple Gene Edits to Improve Persistence and Anti-Tumor Efficacy (SITC Abstract 265) Multiple Targeting of Solid Tumors with iPSC-derived Gamma Delta CAR T Cells in Combination with Therapeutic Antibodies (SITC Abstract 262)γδ-EGFR-CAR-T cells demonstrate significant CAR-specific killing of ovarian tumor spheroidsCell FitnessTumor cell killingImaging + Cytokine support + Safety switch CD16NKG2DPSMAHLA-GHLA-EIL-15/IL15RAHSV-TK Safety switch HLA-I KOHLA-II KO CD70 KO Clonal iPSC line with 11 total genetic modifications show enhanced functionality in iNK3.0 common progenitor iNK3.0γδiT NKG2A KO

10 Winning in Solid Tumors Trafficking and infiltration γδiTcells -tissue homing TME / Immunosuppressive environment Requirement for chemotherapy conditioning Tumor heterogeneity •Novel conditioning regimens•Genetic engineeringChallengesCentury’s Solution Future engineering strategies •Engage endogenous immunity•Multi tumor targeting pathways CARCD16TCRCytokine supportAllo-Evasion TMEnhanced fitnessTracer TBD

11 CNTY-107: First in Class Nectin-4 Targeted GD iTCell TherapyNectin-4 has been validated by ADC approaches•Opportunity to address multiple Nectin-4 positive solid tumors•Potential indications include bladder, breast, pancreatic, non-small cell lung cancer, esophageal/gastric, head and neck, and/or ovarian cancersGD iTallogeneic therapies provide potential to improve upon ADC toxicity profile and efficacy•Intrinsic homing of GD iTcells to tissues and solid malignancies•Multi-tumor killing modalities to tackle heterogeneity Tumor cell killingImaging + Cytokine support + Safety switchAllo-EvasionTM Cell Fitness CNTY-107CNTY-107 Illustrative constructNectin-4

12 ProductiPSC PlatformTargetsIndicationsExpected IND SubmissionDiscoveryPreclinicalClinicalCollaboratorCNTY-101iNKCD19B-Cell MalignanciesCleared to proceed 3Q22CNTY-103iNKCD133Glioblastoma2024CNTY-102iT CD19 + CD79bB-Cell Malignancies2024CNTY-104iNK/iTMulti-specificAcute Myeloid Leukemia2024CNTY-106iNK/iTMulti-specificMultiple Myeloma2024CNTY-107iTNectin-4Solid Tumors2025Discovery Research ProgramsiNKTBDHematological Tumors2023iTTBDSolid TumorsTBD Hematologic TumorsSolid TumorsPipelineProduct candidate pipeline across cell platforms and targets in solid and hematologic cancers

13 Anticipated Catalysts Over Next 12 MonthsUnderpinned by strong balance sheet with platform synergies and operational excellenceCNTY-101•Phase 1 (ELiPSE-1) trial initiation in B-cell malignancies (by YE22)CNTY-101 Follow On (CNTY-102) •Present pre-clinical data at major medical meeting (2H23)CNTY-103•Disclose pre-clinical data of development candidate at major medical meeting (2H23)

Nectin-4 directed therapies: Urothelial cancer and beyondJonathan Rosenberg, MDChief, Genitourinary Oncology ServiceMemorial Sloan Kettering Cancer CenterNew York, NY

Cisplatin eligible Cisplatin ineligible Gemcitabine/carboplatin PDL1 high: Atezolizumab Platinum ineligible Pembrolizumab or atezolizumab Enfortumabvedotin SD/PR/CR:Avelumab maintenance PD: Pembrolizumab Accelerated approval: Sacituzumab govitecanFGFR2/3 mutation: Erdafitinib Metastatic urothelial carcinoma Cisplatin-based chemotherapy-Gemcitabine/cisplatin-ddMVAC Landscape of advanced urothelial cancer treatment

•Calcium-independent immunoglobulin-like cell adhesion molecule•Nectinsare cell surface protein involved in polarity, proliferation, differentiation, and migration•Expressed during development in multiple cell types (epithelial, immune, neuronal)•Nectin-4 expression is evident in multiple cancers, although restricted in normal tissues•Soluble nectin-4 is potential prognostic biomarker in breast and gastric cancer•Overexpression in multiple cancers including breast, gastric, urothelial, Nectin - 4 Taai, et al AnnuRev Cell Dev Biol. 2008;24:309-42.Fabre-Lafay, et al. BMC Cancer. 2007;7:73Okumura et al. Cornea. 2018;37:633-640 Zhang et al. Oncol Lett .. 201;1:9 9 iliary and ovarian cancers •Normal tissue expression in skin, cornea (low levels), esophagus

Nectin - 4 prevalence in cancer Source: https://www.proteinatlas.org/ENSG00000143217-NECTIN4/pathology

Nectin - 4 prevalence in cancer N%Ab usedRefHead and Neck Squamous cell ancer15913.8% negative53.5% weak 32.7% medium-highAbcam clone EPR15613-68Oncotarget.2022; 13:1166-1173Esophageal cancer9266% H score ≥70AF2659Cancer Cell Int. 2019; 19:106Luminal B Her2 Negative Breast cancer147IRS scores:23.8% negative18.3% low 40.1% moderate 17.7% highclone N4.61 (MERCK, DAB150)PatholRes Pract. 2017; 213:1102-1108Breast cancer14064.3% positive35.7% negativeAF2659Folia HistoCyto2011; 49:26–33Non-small cell lung cancer42258% strong positive 28% weak Positive14% absentclone 19–33Cancer Res. 2009. 15; 69: 6694-703

Nectin-4 staining* in urothelial cancer EV 101: J Clin Oncol 2020 38 1041-1049EV 201: J Clin Oncol 2021 39 6_suppl 394*M22-321b41.1 (developed by Agensys, not commercially available)Required in EV-101 (phase I study of EV in urothelial and other Nectin-4 positive cancers)Urothelial cancer: Median H-score, 290; range, 0-300; 4th percentile H-score, 150EV-201: median H-score 275

Nectin - 4: role in cancer •Nectin-4 knockdown reduces migration, spheroid formation, cell proliferation•Plays a role in epithelial-mesenchymal transition•Upon association with Afadin, Nectin-4 induces PI3K/AKT activation, and cellular proliferation via PI3K/AKT pathway•Nectin-4 interacts with ERBB2 and trastuzumab resistant splice variants, and leads to activation of PI3K/AKT signaling •Implicated in stemness, angiogenesis, and metastasisBoylan, et al. Oncotarget. 2017; 8:9717-9738Siddarthet al. Int J BiochemCell biol. 2017; 89:985-94Zhang, et al. Hum Pathol. 2018;72:107-116 Kedashiro et al. Sci Rep. 2019;9:18997

Enfortumab Vedotin : Nectin - 4 Targeted Therapy

Enfortumab vedotin anti - tumor activity EV-101Phase IORR 43%EV-201Phase 2 ORR 44%

EV - 301: EV improves survival compared to standard chemotherapy Powles, Rosenberg, et al. NEJM2021PFS 5.55 vs. 3.71 months; hazard ratio for progression or death, 0.62; 95% CI, 0.51 to 0.75; P<0.001)EV ORR 40.6%

Common enfortumab vedotin toxicities include fatigue, rash, neuropathy; hyperglycemia occurs and may be severe Powles and Rosenberg, et al. NEJM2021

MMAE Payload - related side effects Powles and Rosenberg, et al. NEJM2021

Nectin - 4 on - target side effects Powles and Rosenberg, et al. NEJM2021 Overlapping?

Content of this presentation is copyrightand responsibility of the author. Permission is required for re-use. EV - 103 Cohort K: Enfortumab vedotin + pembrolizumab leads to deep and durable responses in newly diagnosed cisplatin - ineligible patients with advanced urothelial cancer Jonathan E. Rosenberg, MDBICR: Blinded Independent Central Review; CPS: Combined Positive Score; CR: Complete Response; PD-L1: Programmed Death-Ligand 1 PR: Partial Response•Activity seen regardless of PD-L1 statuso27/44(61.4%) cORR in CPS<10o21/31 (67.7%) cORR in CPS≥10 EV-103 Cohort A:•ORR 73.3% •PFS 12.3 mo•DOR 25.6 mo•OS 26.1 moHoimeset al. JCO 2022ORR 64.5%

Content of this presentation is copyrightand responsibility of the author. Permission is required for re-use. EV+P: Nectin - 4 Expression and Best Overall Response •Nectin-4 was detected in tumor tissue from 94.6% of patients who had adequate tissue for testingJonathan E. Rosenberg, MDActivity seen regardless of Nectin-4 expression level

Cisplatin ineligible Gemcitabine/carboplatin PDL1 high: Atezolizumab Enfortumab+ pembrolizumab Metastatic urothelial carcinoma Enfortumab moves to first line: Anticipated accelerated approval with EV - 103 Cohort K ull approval pending results of EV-30 comparing gemcitabine and platinum to enfortumabpembrolizumabNCT043

Potential mechanisms of resistance to Enfortumab vedotin •Luminal urothelial cancers may have higher Nectin-4 levelsClin Cancer Res. 2021 Sep 15;27(18):5123-5130.•MDR-1/P-glycoprotein overexpression likely leads to MMAE export from cancer cellMol Cancer Ther.(2022) 21 (7): 1227–1235.•Downregulation of Nectin-4 expression on cell surface•Eur UrolOncol. 2022 Feb 22;S2588-9311 (Online ahead of print).•Clin Cancer Res. 2021 Sep 15;27(18):5123-5130. •Clinical data is limited-3 patients with progression on EV retain Nectin-4 expression in post-treatment biopsies•UrolOncol. 2021 39(10): 619-22.

Other Nectin - 4 targeted thearpies : bicyclic compounds in early phase trials •Constrained bicyclic peptides or “bicycles”•Linear peptide cyclized around a trivalent scaffold•Can be used to deliver cytotoxics, or bind to other proteins/immune molecules•Smaller than ADC’s, more able to penetrate tumors Upadhyaya et al. J ImmunotherCancer. 2021;9:e001762Hurovet al. J ImmunotherCancer. 2021;9:e002883Rigby et al. Mol Cancer Ther. 2022;Epub ahead of print BT8009

Future landscape for Nectin-4 directed therapy:Nectin-4 directed therapy moves earlier in the urothelial cancer disease course•EV-103 cohort K and EV-302 seek to move EV to first-line therapy•KN-B15, KN-905 (EV/pembrolizumab) and VOLGA (EV/durva/treme) testing EV in muscle invasive localized disease•Nectin-4 expression may be preserved in EV refractory tumors•Subsequent opportunities include late-line disease states •Accelerated approval still possible in areas of unmet need (multiply refractory patients)•EV-202 (NCT04225117)is testing enfortumabin multiple diseases:•Breast cancer, lung cancer, gastric/GE junction, esophageal cohorts

Rationale for iPSC-derived γδ αǀPresident, R&D

34 γδ T cells in Homeostasis and Host Defense of Epithelial Barrier TissuesNature Reviews Immunology volume17,pages 733–745 (2017) γδT cells make up between 1-20% of peripheral blood T cells, but comprise the majority ofT cells that reside in tissues

35 Abundance of γδ Ovarian CancerColorectal Cancer18,000 human tumor samplesacross 39 malignanciesDFS

36 γδ T cells: At the Interface of Innate and Adaptive Immunity Yazdanifaret al Cells2020,9(5), 1305Dranoff , Nature Reviews Cancer, 4, 11-22,2004

37 γδ TCRs Do Not Recognize Classical HLA And Are Not Alloreactive Clinical Evidence •Partial HLA-mismatched allo-HCT with αβT cell depleted grafts showed improved DFS as a function of the number of γδT cells (median 11 x 106/kg) infused with no increase in GVHD1-4•γδT cell enriched donor lymphocyte infusion post allo-HST (up to 83 x 106/kg), no GVHD5•Recent or ongoing studies of adoptive transfer of allogeneic ex vivo expanded γδT cells (with or without genetic engineering)6,7,81Lamb et al. Cytotherapy.1999;1(1):7-19, 2Godder et al. Bone Marrow Transplant.2007;39(12):751-757, 3Otto et al. J Immunother.2005;28(1):73-78, 4Lang et al. Bone Marrow Transplant.2015;50(Suppl 2):S6-S10, 5Radestad et al, J Immunol Res.2014:5787416Lin et al., Signal Transduction Targeted Ther(2020) 5(1):215, 7Xu et al, Cell Mol Immunol(2021) 18(2):427–398 Neelapu, et al. J Clin Oncol 40, 2022 (suppl 16; abstr7509), Nabors, et al. J Clin Oncol 40, 2022 (suppl 16; abstr2044), Xu, et al. Cell Mol Immunol 2021 Feb;18(2):427-439

38 Multiple Potential Mechanisms for Tumor Recognition Both Intrinsic and SyntheticBlood(2018) 131 (10): 1063–1072.

39 gd TCRCD8aCD16NKG2CNKG2DNKp30NKp44NKp46NKG2A 0255075100 Percent positive (CD3+ cells)Delta 1 Delta 2 Diverse Innate Mechanisms for Tumor TargetingN=13 clinical grade TiPSC lines at T cell stage (post differentiation); All lines are Vγ9

40 γδCAR-iTcells mediate ADCC 020406080 0200000400000600000 8000001000000 Hours Red objects(CD19+ CD20+)Green objects(CD19ko CD20+)Tumor cell death IsoIsoRituxObin 020406080 0100000020000003000000 5×1061×1071.5×1072×107 Hours Anti-CD19 CARCD16 (FcRγRIII)

41 Key TakeawaysThe biological properties of γδT cells make them an ideal platform for genetically modified cell therapy of cancers •Innate receptors provide multiple orthogonal mechanisms for tumor recognition•Functional Fc receptors enable combination therapies with monoclonal antibodies•Tissue tropism and long-lived persistence favor prolonged tumor surveillance•Expansion capacity in response to antigen and cytokines mirror αβT cells (and is > than NK cells)•Allogeneic sources can be utilized with little risk of GVHD•Differentiation from iPSCs yields highly potent immune effectors

γδT Cell PlatformMark Wallet, PhD ǀVP Immuno-Oncology

43 iPSC-derived Therapeutics are Developed from Unique Cells and Processes

44 iPSC-derived Therapeutics are Developed from Unique Cells and Processes iPSC-derivedT cells

45 iPSC-derived Therapeutics are Developed from Unique Cells and Processes iPSC-derivedT cells1. ReprogrammingγδT cells into TiPSC3. Differentiationof TiPSC into high-yield, high-purityγδCAR-T cells2. Engineering TiPSCfor enhanced fitness4. Pre-clinicalstudies exhibitingpotent activity ofγδCAR-T cellsagainst solid tumorsToday’s updateon T cell platform:5. Leveraging Century’sT cell platform for CNTY-107[Luis Borges, CSO]

46 1. Reprogramming γδT cells into TiPSC Banked cells fromhealthy donors Dozens of TiPSClines for clinical use Narrowed to twolead lines for initialclinical programs TCRs sequenced,cloned, and testedfor allo-reactivity Single blood donationenables developmentan entire platform withmultiple productsVγ9/Vδ1Vγ9/Vδ2Vγ9/Vδ1Screened for T cell differentiation and function

47 1. Reprogramming γδT cells into TiPSC Each TiPSC line is clonal-Arises from a single T cell-Carries a single monoclonal TCR gene rearrangement Lead γδTCR lacks allo-reactivity Anti-TCR Pos CTLAllogenic PBMCsAnti-TCR Pos CTLAllogenic PBMCs 02040 6080100 Activation condition% GFP+ (activated)TCR-less control γδ TCR Banked cells fromhealthy donors Single blood donationenables developmentan entire platform withmultiple products Dozens of TiPSClines for clinical use Narrowed to twolead lines for initialclinical programs TCRs sequenced,cloned, and testedfor allo-reactivityVγ9/Vδ1Vγ9/Vδ2Vγ9/Vδ1Screened for T cell differentiation and function

48 2. Engineering TiPSCfor Enhanced Fitness + CD19 CAR forPOC studies 0100200300 05×1061×107 Time Elapsed (hours)Tumor growth (red object intensity)γδCAR-T + recombinant IL-15 γδCAR-T Sustained serial killing in presence of recombinant IL-15~ 4 roundsserial killing14+ rounds serial killing

49 2. Engineering TiPSCfor Enhanced Fitness + CD19 CAR forPOC studies Sustained serial killing with engineered IL15/IL15RA 05×1061×107 DaysTumor growth (red object intensity)01234567891011121314151617γδ CAR-T CAR-T + engineered IL15/IL15RA Tumor Alone γδ CAR-T + recombinant IL15

50 3. Differentiation of TiPSCinto High-yield / High-purity T cells γ δ TiPSC w/ IL15 γδ HPC γ δ TiPSC w/o CAR γ δ HPC w/o CAR γ δ TiPSC w/o CAR γ δ HPC w/o CAR EGFR CAR98% 0714212835 02550 75100 Day of Differentiation% Positive EGFR-CARCD3 Yield from batch shown:1 iPSC →281,931 γδCAR-T cells91%IL15/IL15RA IL15/IL15RA Gene EditAnti-EGFR CAR Gene EditDifferentiation of γδCAR-T cells

51 4. Preclinical Studies Exhibiting Potent Activity of γδCAR-T Cells Against Solid Tumors SKOV-3OVCAR-3 EGFR Solid Tumor Models(Ovarian) 2:11:11:21:4 01020304050607080 90100 % Cytolysis γδ-CAR-T γδT (no CAR) 2:11:11:21:4 01020 30405060708090100 % Cytolysis 2:11:11:21:4Targetonly 0100200300400500 600700 IFNγ (pg/mL) 2:11:11:21:4Targetonly 050100150200250 TNF (pg/mL) E:T Ratio 2:11:11:21:4Targetonly 050100150200 IFNγ (pg/mL) 2:11:11:21:4Targetonly 01020304050 60 70 TNF (pg/mL) E:T Ratioγδ-CAR-T γδT (no CAR)SKOV-3OVCAR-3 γδ-CAR-T 0306090120150 05.0×1061.0×1071.5×107 Time (h)RCU x μm2/ Image γδT (no CAR)Target cells only γδT (no CAR)γδ-CAR-T CAR-mediated killing of solid tumor monolayersCAR-mediated killing ofOVCAR-3 3D spheroids OVCAR-3 xenograft in NSG mice10e6 EGFR-specific IL-15RA/IL-15 engineered CAR-T Day 4 0102030 01×1082×108 Study DaysAvg Radiance [p/s/cm²/sr]Control γδ CAR-T Day 8Day 11Day 15Day 18Day 22Day 25Day 28Day 31 ControlγδCAR-TDorsalVentralDorsalVentral OVCAR-3tumor controlTumor + CAR-Tversus+iPSC-derived γδCAR-T cells control ovarian cancer in vivo

52 Summary•Century has developed a fully in-house iPSC-derived γδT cell platform•Technical advances have enabled successful proof of concept for pre-clinical utility of γδCAR-T cells for solid tumors•The team is well-positioned to develop a solid tumor program for the clinic

CNTY-107, our γδiTProduct Candidate for the Treatment of Solid Tumors Expressing Nectin-4Luis Borges, PhD ǀCSO

54 CNTY-107, Next-Generation Product Candidate For The Treatment Of Nectin-4 Expressing Cancers Trafficking and infiltration γ9δ1iT cells, subset of γδT cells that preferentially home to tissues TME / Immunosuppressive environment Sufficient homeostatic cytokine support for enhanced persistence Tumor heterogeneity ChallengesCentury’s Solution CD16 helps maximize combinations with antibodies that modulate TMEThree major pathways for tumor targeting: Nectin-4 CAR, CD16, and innate receptorsCNTY-107 γδiT cells -tissue homing Novel conditioning regimens Engineering Future engineering strategiesEngage innate, endogenous immunity Multi tumor targeting pathwaysCells engineered with homeostatic cytokine IL15/IL15Rα and Allo-EvasionTM CNTY-107

55 Engineering Profile of CNTY-107 Tumor cell killing Imaging + Cytokine support + Safety switch Cell Fitness ENGINEERING PROFILEStepGene EditRationale1KOβ2M Allo-EvasionKIHLA-E-2A-HLA-GAllo-Evasion2KONKG2A KO landing pad, potential to block inhibitory signalKIIL15/IL15RαHomeostatic cytokine support3KOCD70KO landing pad, potential to increase cell fitnessKICD16Tumor killing through ADCC4SHLCLYBLSafe harbor locus (SHL)KIPSMA+HSV-TKPSMA for cell tracing, HSV-TK as a safety switch5SHLAAVS1Safe harbor siteKINectin-4 -CARTumor targeting6KOCIITAAllo-Evasion Allo-Evasion

56 CNTY-107 Has Multiple Built-In Mechanisms for Tumor Killing PATHWAYS FOR TUMOR KILLING1.CAR-mediated killing2.ADCC (Antibody-dependent cellular cytotoxicity)3.Innate receptors (NCRs, others) mediated killing though recognition of stress ligands 1 2 3

57 Nectins Nectins are cell adhesion molecules (CAMs) involved in Ca2+-independent cell-cell interactions The Nectin family includes four Nectins •Nectins 1-3 are enriched in normal adult tissues•Nectin-4 is mostly expressed during fetal development and its expression declines in adult tissues (low expression levels in skin, bladder, placenta, oral mucosa, and tonsils)Nectins interact with other cell surface molecules including cadherins, integrins and growth factor receptors•These interactions help modulate cell adhesion, migration, and proliferationNectin-4 dimers bind to Nectin-1 or Nectin-4 on adjacent cellsNectin-4 also binds TIGIT on immune cells and this interaction leads to inhibition of NK cellsInteractions of Nectins and Cadherins Interact to Form Adherens Junctions and Promote Cell AdhesionFigure adapted from Takai et al, Nat Rev Mol Cell Biol, 2008 Adherens junction

58 Nectin-4 Expression in Cancer •Nectin-4 is expressed in high frequency in bladder, breast, lung, pancreatic, ovarian, head & neck, and esophageal cancers•The highest levels of expression of Nectin-4 are seen in bladder, breast, lung and pancreatic cancers•Clinical validation of Nectin-4 as a tumor target has been demonstrated by the approval Enfortumab vedotin for the treatment of urothelial cancer From Challita-Eid et al., Cancer Research, 2016 IHC Analysis of the Expression of Nectin-4 in a Panel of 2,394 Human Tumor Specimens Tumor HistologyModerate to High ExpressionBladder60%Breast53%Pancreatic37%Lung27%Tumors With the Highest Expression of Nectin-4

59 Nectin-4 Expression Levels On Human Skin Keratinocytes Is Lower Than In Most Tumor Cell Lines JurkatUM-UC-3TCCSUP Human KeratinocytesHeLaT245367SW780A431 HT1197K562OVCAR3CAPAN2OE19RT4T47DHT1376CHO-Nectin4BeadsNectin-4 PE Cell LineOriginRankingUM-UC-3Bladder cancerNegativeTCCSUPBladder cancerJURKATT cellHeLaCervical cancerT24Bladder cancerLow(50-250)Human keratinocytesNormal skin5637Bladder cancerHT1197Bladder cancerMedium(3,000 -10,000)SW780Bladder cancerK562CMLA431Breast cancerCAPAN2Pancreatic cancerOVCAR3Ovarian cancerOE19Esophageal cancerRT4Bladder cancerHT1376Bladder cancerHigh(10,000+)T47DBreast cancerCHO-Nectin4Chinese Hamster OvaryNectin-4 Expression in Multiple Cells Ranking Of Tumor Cells Based On Nectin-4 Expression Level

60 Selection of VHH Binders to Build Nectin-4 CAR VHH LibraryNot for further distributionLlama VHH antibodies Biophysicalanalysis Cell binding (FACS) CAR engineering and selection In vitro and in vivo screens 20 VHH binders identified Tissue specificity (Retrogenix) Final CAR selectionCentury’s Proprietary VHH LibrariesLlama VHH Library ScreensAssay Screening Flow to Select Nectin-4 Binders and CARs

61 Century’s Nectin-4 CARs Distinguish Between Cells Expressing Low vs. Moderate to High Levels Of Nectin-4 0.00.51.01.52.02.5 0204060 80100 TUCCSUPE:TCytotoxicity (%target killed) 0.00.51.01.52.02.5 020406080100 T24E:TCytotoxicity (%target killed)UTD P2026 P2017 P2117 P3106 P3107 P3108 P3110 P3113 P3821 P3822 P4016 P4017 P4018 0.00.51.01.52.02.5 0204060 80 T47DE:TCytotoxicity (%target killed)UTD P2026 P2017 P2117 P3106 P3107 P3108 P3110 P3113 P3821 P3822 P4016 P4017 P4018 0.00.51.01.52.02.5 020406080100 OVCARE:TCytotoxicity (%target killed) Century’s Nectin-4 CARsDo Not Kill Cells Expressing Low Levels of Nectin-4Century’s Nectin-4 CARsKill Cells Expressing Moderate to HighLevels of Nectin-4(Moderate Levels)(High Levels)(Very Low Levels)(Low Levels)Panel of Nectin-4 CARsPanel of Nectin-4 CARs

62 CNTY-107 Nectin-4 CARs Mediate Robust Anti-Tumor Activity in VivoNovember 8, 2022•5x106OVCAR-3 cells implanted subcutaneously in the right flank •Mice randomized after tumors reached 75-125 mm3•Mice treated with 5x106CAR-T cells Treatment GroupDay 28 % TGIDay 28 P-ValueP3108 -NECM_1780.80.0003P3107 -NEC_M_882.80.0002P3110 -NEC_M_4686.40.0001P3106 -NEC_M_588.50.0001P2117 -DB01-C1089.20.0007P3113 -NEC_S_3161.10.0116P2026 –Enfortumab-CAR94.7<0.0001All CAR Constructs Mediated Statistically Significant Tumor Growth Inhibition (TGI)In Vivo Evaluation of the Anti-tumor Activity Nectin-4 CARs Using Peripheral Blood CAR-T CellsOVCAR-3 Ovarian Tumor Xenograft Model 0102030 050010001500 Study DaysTumor Volume (mm3) ± SEMUTD ControlP3108; NECM_17P3106; NEC_M_5P3113; NEC_S_31P3107; NEC_M_8P2117; DB01-C10P3110; NEC_M_46P2026; Enfortumab-CAR

63 CNTY-107 Next Steps and Milestones Complete Engineering of the γδ γδ δ βα

64 CNTY-107 Preliminary Clinical Strategy•Initial Phase I clinical study is planned to be run as a basket trial that will include multiple Nectin-4 positive cancers•Cancers under consideration include bladder, breast, pancreatic, non-small cell lung cancer, esophageal, head and neck, and/or ovarian cancers•Dose-escalation will be done in the basket trial•The clinical trial will be designed to expand in any indication with acceptable tox and clinical responses•To enrich for potential responders among selected indications, we are developing an IHC-based Nectin-4 screening assay to potentially help select patients•We will develop our own fit-for-trial IHC assay•Ability to evaluate combination therapies•Combination therapy cohorts could be indication-specific (e.g., HER-2 antibody for breast cancer) or "generic”, addressing modulation of the TME (e.g., PD-L1 antibody, Avelumab)

Thank you

Q&A