Century Therapeutics, Inc. · NASDAQ:IPSC
Century Therapeutics — Investor Day (June 2022)
76 slides from Century Therapeutics's investor day presentation, Jun 13, 2022
Slide 1: Virtual R&D Day
@ CENTURY THERAPEUTICS Virtual R&D Day June 13, 2022
Slide 2: Forward-looking statements
2 Forward-looking statements This presentation contains forward-looking statements within the meaning of, and made pursuant to the safe harbour provisions of, The Private Securities Litigation Reform Act of 1995. All statements contained in this document, other than statements of historical facts or
Slide 3: Agenda
3 Agenda Building A Next-Generation iPSC Platform Lalo Flores, PhD, CEO GBM Landscape and Opportunity Shelia Singh, MD, PhD, Professor of Surgery and Biochemistry, Chief Pediatric Neurosurgeon at McMaster Children’s Hospital, the Division Head of Neurosurgery at Hamilton Health Sciences, and the Ina
Slide 4: Building A Next-Generation iPSC Platform
Building A Next-Generation iPSC Platform Lalo Flores, PhD ǀ CEO
Slide 5: Building a Next Generation Allogeneic Cell Therapy Platform
5 Building a Next Generation Allogeneic Cell Therapy Platform Gene Editing • Proprietary gene editing platform • CRISPR MAD7-derived gene editing for precise transgene integration Protein Engineering • Developing proprietary next-generation CARs • Universal tumor targeting platform iPSC Differentiat
Slide 6: With a Strong Foundation in Place, Century is Ready to Execute
6 With a Strong Foundation in Place, Century is Ready to Execute 2018 – 2021 Building know-how, optimizing processes 2022 iNK 3.0 and γδ iT product engines 2023-2024 Critical mass and readiness to file 5 INDs Company and platform building Transformational year with first IND filing Focus on pipeline
Slide 7: Common Progenitor Milestone Enables Cost, Time Efficiencies
7 Common Progenitor Milestone Enables Cost, Time Efficiencies Multiple gene edits Engineered iPSC iNK cell iPSC bank Cell engineering Manufacturing Common Progenitor iNK 3.0 CD34+ HSC T cell Reprogramming Reprogramming Differentiation NK cell • iPSC cell bank with 12 core 3.0 gene edits introduced i
Slide 8: Product candidate pipeline
Product iPSC Platform Targets Indications Expected IND Submission Discovery Preclinical Clinical Collaborator CNTY-101 iNK CD19 B-Cell Malignancies Mid 2022 CNTY-103 iNK CD133 Glioblastoma 2024 CNTY-102 iT CD19 + CD79b B-Cell Malignancies 2024 CNTY-104 iNK/iT Multi-specific Acute Myeloid Leukemia 20
Slide 9: Universal Tumor Antigen Receptor Targeting Platform (uTRAP)
9 Universal Tumor Antigen Receptor Targeting Platform (uTRAP) T Cell Signaling domains Tumor binding domain (antibody or soluble TCR) Cancer Cell Signaling domains Synthetic BAIT receptor Synthetic receptor binding domain T Cell LOCK AND KEY SYSTEM • Multifaceted tumor targeting platform • Compatibl
Slide 10: Century's Strategic Vision for Winning in Solid Tumors
10 Century’s Strategic Vision for Winning in Solid Tumors Building best-in-class γδ iT cell platform with up to 5 distinct tumor killing mechanisms CAR CD16 NKG2D Safety switch & tracer TCR UTRAP Tumor antigen/ TCR Stress ligands Antibody/tumor antigen ADCC Tumor antigen Non-HLA TCR target Cytokine
Slide 11: Anticipated Catalysts Over Next Months
11 Anticipated Catalysts Over Next 12 months Underpinned by strong balance sheet with platform synergies and operational excellence CNTY-101 Becoming clinical stage biotech company with most advanced allogeneic cell therapy • IND submission (Mid-2022) • Phase 1 (ELiPSE-1) start in B-cell malignancie
Slide 12: Targeting Clonal Heterogeneity in Treatment-refractory Brain Cancers
Targeting Clonal Heterogeneity in Treatment-refractory Brain Cancers with Rationally Designed Immunotherapies: Advances and Challenges AACR Meet-The-Expert Session April 10th, 2022 Sheila K. Singh MD PhD FRCS(C) McMaster University, Hamilton, ON, Canada
Slide 13: Glioblastoma is an aggressive disease
Glioblastoma is an aggressive disease 13 Most prevalent primary brain tumor in adults causing death Recurrent tumor Primary tumor Disease progression Standard of care (SoC): • Surgical resection • Radiation • Chemotherapy with Temozolomide Post-SoC Patients succumb to recurrent disease with a median
Slide 14: Glioblastoma (GBM) Overview
Glioblastoma (GBM) Overview FOCUS – Unmet need in brain cancer therapy • 9-month relapse period • 15 months median survival post-diagnosis • ~5% five-year relative survival 1. American Brain Tumor Association 2. Hexa Research 23Aug 2017 18Oct 2018 15Apr 2018 Primary GBM Recurrent GBM COMMERCIAL POTE
Slide 15: GBM Market landscape – Limited competition
GBM Market landscape – Limited competition A total of 139 drugs currently in clinical development in primary and recurrent GBM PHASE SMALL MOLECULES BIOLOGICS OTHERS (CAR-Ts, viruses, vaccines, etc Approved 3 (Temozolomide, carmustine/ carmustine implant) 3 (bevacizumab and 2 biosimilars) 0 Phase II
Slide 16: Glioblastoma: A Graveyard of Clinical Trials, or Unmet Opportunity?
Glioblastoma: A Graveyard of Clinical Trials, or Unmet Opportunity? Post OP “Every surgeon carries within himself a small cemetery, where from time to time he goes to pray.” - Dr. René Leriche: from epigraph to “Do No Harm,” Dr. Henry Marsh • First-line standard of care was developed @ 20 years ago.
Slide 17: CAR T Cell Therapies for GBM: the Promise of Locoregional Delivery
CAR T Cell Therapies for GBM: the Promise of Locoregional Delivery Intracavitary Delivery of IL13aR2 CAR T Cells Intraventricular Delivery of IL13aR2 CAR T Cells Regression of Recurrent Multifocal Glioblastoma, Including Spinal Metastases
Slide 18: EGFR CAR T Cells for GBM: Continued Improvements
EGFR CAR T Cells for GBM: Continued Improvements to Overcome Technical Challenges
Slide 19: Lessons from GBM Treatment Failures
• Trusted therapeutic targets expressed in treatment-naïve, primary GBM may be selected against and evolve out of GBM recurrence: new therapeutic targets must be pursued that are relevant to recurrence. • Monotherapies will not likely succeed in eradicating such a rapidly evolving, highly heterogene
Slide 20: Mimicking GBM recurrence: mouse-adapted in vivo treatment protocol
EORTC/NCIC treatment scheme for glioblastoma patients Cranial Radiation TMZ (single dose) as sensitizer for radiation 1 hour pre-radiation Day 1 Day 3 Day 5 Day 19 TMZ (single dose) TMZ (single dose) Sacrifice Day (MRD) End point Sacrifice Day Patient-derived primary GBMs Immunodeficient mouse Mimic
Slide 21: Preclinical model of recurrent GBM
DMSO Primary tumor engraftment Chemoradiotherapy TMZ 2 Gy Tumor recurrence Control Treatment MRD Control 2 days post-treatment (MRD) Recurrence post-treatment H&E Preclinical model of recurrent GBM MRI
Slide 22: GBM program: A Translational Pipeline
GBM program: A Translational Pipeline Targeting clonal heterogeneity in treatment-refractory GBM with novel and empiric immunotherapies 22 June 9, 2022 PROJECT 1: Clonal dynamics and tracking Dr. Jason Moffat CORE 3: Platform for Advanced Cell Engineering Discover and validate novel cell surface mar
Slide 23: CD133, a marker of tumor initiating cells
CD133, a marker of tumor initiating cells O’Brien et al 2010, Clin. Can. Res. Intracranial xenografts 100 CD133+ BTICs Brain Tumor Initiating Cell (BTIC) model CD133, a marker of treatment-resistance in several human malignancies Jason Moffat Sheila Singh Parvez Vora Chitra Venugopal
Slide 24: CD133, a marker of treatment-resistant GBM
CD133, a marker of treatment-resistant GBM CD133 expression correlates with disease progression, metastasis, recurrence, and poor overall survival in several human malignancies 24
Slide 25: Engineering CD133-targeting immunotherapies
Engineering CD133-targeting immunotherapies 25
Slide 26: CD133-directed treatment significantly eliminates GBM tumor burden
CD133-directed treatment significantly eliminates GBM tumor burden CAR CON CART133 H&E stain hPBMCs hPBMCs + DATE1 H&E stain 0 50 100 150 0 25 50 75 100 Days P e r c e n t s u r v i v a l ( % ) PBS CD133 DATE*** BT428 Control DATEs + PBMCs 0 25 50 75 100 T u m o r v o l u m e ( m m 2 ) BT 9 3 5 ** C
Slide 27: Measuring the 'ON target OFF tumor' effect in humanized NSG mice
Measuring the ‘ON target OFF tumor’ effect in humanized NSG mice Vora et al 2020 Cell Stem Cell Transplant 15,000 CD34+ cells/mouse Hematopoietic stem cell enrichment from Lin-cord blood Validate CD133 expression in cord blood HSPCs pre-transplant Long-term human stem cell repopulation 12wk NSG Bone
Slide 28: ET001 treatment does not significantly reduce human HSPCs
ET001 treatment does not significantly reduce numbers of human HSPCs or impair haematopoiesis Vora et al 2020, Cell Stem Cell BM aspirate CAR CON CART133 0 5 10 15 P e r c e n t C D 3 4 p o s i t i v e c e l l s ( % ) n.s. n.s. * BM aspirate CAR CON CART133 0 25 50 75 100 P e r c e n t C D 1 3 3 o f
Slide 29: CD133 plays a redundant role in haematopoiesis?
CD133 plays a redundant role in haematopoiesis? “CD133-deficient HSCs (KO) can competitively and serially reconstitute immune cells and the HSC compartment of irradiated recipientmice” “Animals were viable and fertile but are affected with a retinal degeneration leading to blindness. No obvious hema
Slide 30: Phase I trial of CD133-specific CAR-T
NCT02541370: a phase I clinical trial of CD133-specific CAR-T for treatment of relapsed and/or chemotherapy refractory advanced malignancies Participant Overview [n=23] o 7 with pancreatic carcinomas o 2 with colorectal carcinomas o 14 with hepatocellular carcinoma (HCC) Dose escalation study result
Slide 31: Locoregional delivery can address CAR-T trafficking challenges
Locoregional delivery can address CAR-T trafficking challenges Non-Confidential Identifier Indication Therapy Sponsor NCT02208362 Relapsed GBM Anti-IL13Ra2 CAR-T City of Hope Medical Center NCT03283631 Relapsed GBM Anti-EGFRvIII CAR-T Duke University Medical Center NCT02442297 Relapsed GBM Anti-HER2
Slide 32: Engineering new allogeneic CAR T therapies for cancer patients
Engineering new allogeneic CAR T therapies for cancer patients
Slide 33: Enhanced Control of iNK Cells in the Treatment of GBM
Enhanced Control of iNK Cells in the Treatment of GBM Hy Levitsky, MD ǀ President, R&D
Slide 34: Major Challenges in Cell Therapy for GBM
34 Major Challenges in Cell Therapy for GBM • Clonal evolution of cancer cells driving antigen heterogeneity • The most abundant target antigens are also expressed at some level on normal tissues • The CNS is highly sensitive to features associated with immune effector function (e.g., cytokines, rap
Slide 35: Century's iNK platform engineered to provide control
35 Century’s iNK platform- Engineered to provide control to overcome these challenges • NK cells significantly less proliferative than T cells, reducing the risk of toxicities associated with rapid and extensive lymphocyte expansion in the brain • iNK clones selected for maximal serial killing capac
Slide 36: HSVtk-2A-PSMA Cassette
36 HSVtk-2A-PSMA Cassette • Single molecular construct enables co-expression and selection for intracellular HSV-tk, and surface membrane expressed PSMA • HSV-tk encodes an intracellular enzyme that converts ganciclovir (GCV) into GCV- triphosphate that inhibits DNA-polymerase, leading to cell death
Slide 37: PET Imaging for Quantitative Assessment of Cell Trafficking
37 PET Imaging for Quantitative Assessment of Cell Trafficking, Abundance, and Persistence PSMA PET Imaging of Prostate Cancer HSV-tk PET Imaging of CAR-T in GBM Correlation between PET signal strength and CAR-T accumulation in mouse model SCIENCE ADVANCES 3 Jul 2019 Vol 5,Issue 7 SCIENCE TRANSLATIO
Slide 38: Safety Switch
38 Safety Switch •Ability to rapidly eliminate the product upon encountering severe toxicities improves safety profile, broadens eligible patient populations, and partially de-risks pursuing novel targets that may have narrow therapeutic windows • Transgenic HSV-tk expression has been successfully u
Slide 39: Enhanced Control of iNK Cells To Address GBM
39 Enhanced Control of iNK Cells To Address GBM • Therapeutic control achieved through engineered product attributes enables the pursuit of the most challenging oncology settings, including GBM • These attributes include: • Selection of cell type (iNK) and clones with limited replicative capacity •
Slide 40: Century's iNK 3.0 platform iNK common progenitor and Next-Gen CNTY-103
Century’s iNK 3.0 platform iNK common progenitor and Next-Gen CNTY-103 Luis Borges, PhD ǀ CSO
Slide 41: iNK 3.0 Common Progenitor
41 iNK 3.0 Common Progenitor Multiple New Features for Enhanced Functionality Tumor cell killing Allo- Evasion Cell Fitness Imaging + Cytokine support + Safety switch iNK CP Boldface: iNK 3.0-specific gene edits Common Progenitor Features ENGINEERING PROFILE Step Gene Edit Rationale 1 KO NKG2A Poten
Slide 42: The iPSC Common Progenitor Enables Cost and Time Efficiencies
42 The iPSC Common Progenitor Enables Significant Cost and Time Efficiencies One Common Progenitor Different CARs Multiple Product Candidates
Slide 43: iNK 3.0 Multiple Mechanisms for Tumor Cell Killing
43 iNK 3.0 Cell Platform Has Multiple Built-In Mechanisms for Tumor Cell Killing PATHWAYS FOR TUMOR KILLING 1. CAR-mediated killing 2. ADCC (Antibody-dependent cellular cytotoxicity) 3. NKG2D-mediated killing though recognition of stress ligands 1 2 3
Slide 44: iNK 3.0 Enhanced Allo-Evasion Features
44 iNK 3.0 Enhanced Allo-Evasion Features X X X X Allo-Evasion 3.0 • Deletion of β2M designed to eliminate HLA-I expression and prevents recognition by CD8 T cells • Knock out of CIITA designed to eliminate HLA-II expression and prevents recognition by CD4 T cells • Knock-in of HLA-E and HLA-G preve
Slide 45: iNK Cells Lacking HLA-I Are Not Recognized by Allogeneic CD8 T cells
45 iNK Cells Lacking HLA-I Are Not Recognized by Allogeneic CD8 T cells iNK Cells Expressing HLA-I Cause Allogeneic CD8 T Cell Activation, But Not HLA-I Null iNK Cells CD25 Expression by CD8 T Cells
Slide 46: Lack of HLA-I Can Lead to Elimination by Allogeneic NK Cells
46 Lack of HLA-I on iNK Cells Can Lead to Their Elimination by Allogeneic NK Cells Activating ligand HLA-I Inhibitory receptor Activating receptor HLA-E HLA-G NKG2A KIRs, LIRs iNK Cells Protected iNK Cells Protected iNK Cells Killed
Slide 47: Expression of HLA-E + HLA-G Offers Better Protection
47 Expression of HLA-E + HLA-G Offers Better Protection From NK Cell Killing HLA-E HLA-G NKG2A KIRs, LIRs Activating ligand Activating receptor Proof-of-Concept Study with HLA-I Null K562 Cells Engineered with HLA-E and HLA-G 0.125 0.25 0.5 1 2 4 8 16 32 0 20 40 60 80 100 Donor RC01 Ratio (E:T) % K
Slide 48: Membrane-Bound IL-15/IL-15RA Enhances iNK Persistence in vitro
48 Membrane-Bound IL-15/IL-15RA Enhances iNK Cell Persistence in vitro sIL15 IL15-TM _1X IL15RA/IL15 0 3 6 9 12 F o l d e x p a n s i o n sIL15 IL15-TM_1X IL15RA/IL15 0 20 40 60 0 20 40 60 80 100 Time (hr) N o r m a l i z e d T a r g e t c o u n t ( % o f c e l l l i n e a l o n e c o n t r o l ) IL
Slide 49: Engineered IL-15/IL-15RA Enhances iNK Persistence in vivo
49 Engineered IL-15/IL-15RA Enhances iNK Cell Persistence in vivo sIL-15 IL-15-TM _1X IL-15RA/IL-15 0 1000 2000 3000 4000 5000 14-Day Lung iNK Persistence i N K p e r 1 0 0 , 0 0 0 L i v e C e l l s sIL-15 IL-15-TM_1X IL-15RA/IL-15 sIL-15 IL-15-TM _1X IL-15RA/IL-15 0 200 400 600 800 14-Day Periphera
Slide 50: Engineered NKG2D Expression Enhances Tumor Killing
50 Engineered NKG2D Expression on iNK Cells Enhances Tumor Killing NKG2D Non-engineered iNK cells NKG2D-engineered iNK cells Engineered iNK Cells Express Higher Levels of NKG2D 0 20 40 60 80 0 20 40 60 80 100 Time (hr) % T u m o r C e l l G r o w t h Non-engineered iNK NKG2D-engineered iNK NKG2D-Eng
Slide 51: High-affinity CD16 Augments CAR-Mediated Killing
51 High-affinity CD16 Augments CAR-Mediated Killing of Tumor Cells Through Antibody-Dependent Cellular Cytotoxicity (ADCC) 0 5 10 15 20 25 0 1000000 2000000 3000000 4000000 5000000 Time (Hours) R a j i t u m o r c e l l d e n s i s t y iNK + Ctrl Ab iNK + Rituximab CAR/CD16-iNK + Ctrl Ab CAR/CD16-iN
Slide 52: Pivoting to iNK 3.0 to Create Next-Gen CNTY-103
52 Pivoting to the iNK 3.0 Platform to Create Next-Gen CNTY-103 Is Expected to Improve the Likelihood of Clinical Success The iNK 3.0 Platform incorporates multiple features that are highly relevant for the treatment of GBM Pivoting to the iNK 3.0 platform is expected to improve the likelihood of cl
Slide 53: Next-Gen CNTY-103 Built-in Mechanisms for Anti-tumor Activity
53 Next-Gen CNTY-103 Has Multiple Built-in Mechanisms for Enhanced Anti-tumor Activity Tumor Killing 1. CD133 CAR-mediated tumor cell killing 2. CD16-mediated killing using Abs against tumor antigens (EGFR, HER2, CD70, others) 3. NKG2D-mediated killing though recognition of stress ligands (MICA/B, U
Slide 54: Century's Novel Universal Targeting Receptor Adaptor Platform
Century’s Novel Universal Targeting Receptor Adaptor Platform Jill Carton, PhD ǀ Executive Director of CAR Engineering and Protein Sciences
Slide 55: Century's Protein Sciences Capabilities
55 Century's Protein Sciences Capabilities Drive Sophisticated Therapeutic Solutions Antibody Discovery Century Therapeutics’ proprietary Phage Display Library for novel humanized VHH tumor target binders Protein Biochemistry Protein stability and biophysical characteristics designed to produce safe
Slide 56: Universal CAR Platforms Extend the Versatility of Conventional CARs
56 Universal CAR Platforms Extend the Versatility of Conventional CARs Universal CAR has two components: 1. CAR that binds a tag on a soluble protein 2. Soluble protein that binds to the tumor cell antigen and the CAR Effector cell mediated tumor cell killing is only activated when the soluble prote
Slide 57: uTRAP is Versatile and Flexible
57 Century’s Novel Universal Targeting Receptor Adaptor Platform (uTRAP) is Versatile and Flexible uTRAP is built on highly adaptable, single domain VHH proteins 1. BAIT CAR • Inactive in circulation • Inactive in the presence of tumor cells
Slide 58: uTRAP Built on Single Domain VHH Proteins
58 uTRAP is built on highly adaptable, single domain VHH proteins 1. BAIT CAR • Inactive in circulation • Inactive in the presence of tumor cells 2. Bispecific Anti-Idiotype Targeting (BAIT) Protein • Exploits the high specificity of an anti-Idiotype antibody • Adaptable binding affinity to the CAR
Slide 59: BAIT Proteins Engineered for Diverse Functions
59 BAIT Proteins are Engineered for Diverse Functions and Used With a Single Cell Line BAIT CAR Common Progenitor Cell
Slide 60: uTRAP Platform Mediates Potent Cytotoxicity In Vitro
60 Century’s uTRAP Platform Mediates Potent Cytotoxicity In Vitro Killing of NALM6 EGFR+ Cells through uTRAP engineered T-Cells In the presence of EGFR BAIT proteins BAIT protein engineering can modulate functionality
Slide 61: In vivo Proof of Concept Studies with uTRAP
61 In vivo Proof of Concept Studies with Century’s uTRAP Platform Initiated uTRAP in vivo efficacy studies in IPSC- derived iNK and iT cells are initiated In vivo studies with Peripheral Blood T-cells
Slide 62: uTRAP Addresses Multiple Clinical Challenges
62 Century’s uTRAP Addresses Multiple Clinical Challenges Advantage Extend the target landscape Tunable potency and temporal regulation of BAIT protein increases control of target engagement Antibody and TCR BAIT formats access cell surface and intracellular targets Address tumor heterogeneity Solub
Slide 63: uTRAP Strategy to Tackle Tumor Heterogeneity in Glioblastoma
63 uTRAP Enables a Therapeutic Strategy to Tackle Tumor Heterogeneity in Glioblastoma BAIT Protein 1 BAIT Protein 2 BAIT Protein 3 BAIT CAR Common Progenitor Cell
Slide 64: MAD7 CRISPR Nuclease for iPSC Genome Engineering
MAD7 CRISPR Nuclease for iPSC Genome Engineering Michael Naso, PhD ǀ VP Cell Engineering
Slide 65: Century's End-to-End Platform
65 Multiple gene edits Engineered iPSC iNK cell iT cell iPSC bank Gene editing, protein engineering Manufacturing Century’s End-to-End Platform Has the Key Components to Realize Potential of iPSC Engineered iPSC MCB Differentiation CD34+ HSC T cell NK cell Reprogramming Reprogramming Differentiation
Slide 66: Product Candidate Engineering Requires a Reliable CRISPR Nuclease
66 Product Candidate Engineering Requires a High Functioning and Reliably Sourced CRISPR Nuclease Attribute Preference for product candidate engineering Double-stranded gDNA cleavage High efficiency in iPSCs Fidelity Low off-target cutting Gene insertion High efficiency HDR in iPSCs PAM site recogni
Slide 67: MAD7 is a Novel Class Type V-A CRISPR Nuclease
67 MAD7 is a Novel Class 2 Type V-A CRISPR Nuclease High structural homology to Cpf1 (Cas12a), low sequence identity (~30%) T-rich PAM site similar to Cpf1 Single molecule gRNA Staggered DNA cutting to facilitate HDR Target DNA recognition Target DNA cleavage
Slide 68: MAD7 Produced in House in E. Coli
68 MAD7 Produced in House In E. Coli and is Functionally Equivalent to Industry Standard Cpf1 Knock-out efficiency of MAD7 is as efficient as Cpf1 Purified MAD7 activity is maintained for >6 months at -80C Multi-step column purification yields homogenous MAD7 protein MAD7 RNPs function comparably to
Slide 69: MAD7 Facilitates HDR at Multiple Loci in iPSCs
69 Mad7 Facilitates HDR at Multiple Loci in iPSCs at Efficiencies Seen with Cpf1 Not for further distribution HDR efficiency with MAD7 is equivelent to Cpf1 High HDR efficiency with MAD7 at multiple loci Locus 1 Locus 2 Locus 3 Transgene 1 Transgene 2 Transgene 3 HDR
Slide 70: MAD7 is a High-Fidelity CRISPR Nuclease
70 MAD7 is a High-Fidelity CRISPR Nuclease with Off-Target Rates at Least as Good as Cpf1 Not for further distribution Guide-seq off-target analysis Guide-seq characterization revealed very low frequency of off- target cutting, comparable to Cpf1, in iPSCs SNP CNV array analysis • SNP microarray CNV
Slide 71: We Have Pivoted to MAD-7 for All Product Candidates
71 We Have Pivoted to MAD-7 for Platform and Pipeline Engineering of All Product Candidates No impact on viability or pluripotency after multiple uses of MAD7 in iPSCs Process used to make common progenitor iPSC clone for CAR insertion to support multiple programs
Slide 72: We Continue to Optimize and Evolve Our MAD7 Platform
72 We Continue to Optimize and Evolve Our Mad7 Platform Increasing protein production yield and long-term stability PAM site evolution Increased HDR efficiencies with further protein engineering MAD7-on and MAD7-off fusions for gene regulation strategies Not for further distribution
Slide 73: Concluding Remarks
Concluding Remarks Lalo Flores, PhD ǀ CEO
Slide 74: Emerging leader in allogeneic cell therapies for cancer
74 Emerging leader in allogeneic cell therapies for cancer Comprehensive iPSC cell platform With end-to-end capabilities to develop iNK and γδiT cell candidates Financial Strength Cash runway into 2025 Ended 1Q22 with cash, cash equivalents, and investments of $466.4M Toolbox to address solid tumors
Slide 75: Century Therapeutics
CENTURY THERAPEUTICS
Slide 76: Thank you
CENTURY Thank you THERAPEUTICS