Nurix Therapeutics, Inc. · NASDAQ:NRIX
Nurix Therapeutics — Investor Day (May 2022)
147 slides from Nurix Therapeutics's investor day presentation, May 26, 2022
Slide 1: Leader in Targeted Protein Modulation: R&D Day
Exhibit 99.1 Leader in Targeted Protein Modulation Nurix Therapeutics Blazing a New Path in Medicine R&D Day New York, NY May 26, 2022
Slide 2: Welcome and Introduction
Welcome and Introduction Arthur T Sands, MD, PhD President, CEO and Board Director Nurix Therapeutics 2
Slide 3: Important Notice and Disclaimers
Important Notice and Disclaimers This presentation contains statements that relate to future events and expectations and as such constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. When or if used in this presentation, the words “anticipa
Slide 4: Cancer Connects Us All
Cancer Connects Us All 602,350 Deaths From Cancer in 2020 in the United States Nurix is committed to building a patient-focused, science-driven oncology company powered by our leadership position in Targeted Protein Modulation 4
Slide 5: Cancer Connects Us All
Cancer Connects Us All 602,350 Deaths From Cancer in 2020 in the United States How can targeted protein modulation drugs make a difference, how are they differentiated? Simply stated, our drugs are designed to work when other drugs do not…an important place to start 5
Slide 6: The War on Cancer Has a New Weapon
The War on Cancer Has a New Weapon Nurix is the Pioneer and Leader in Targeted Protein Modulation Small Molecule Antibodies Nucleic Acid- Adoptive Cell Inhibitors Based Therapies Therapy Therapeutic Targeted Protein Modulation (TPM) Proteins Antisense, RNAi DeTIL to Increase or Decrease Gene Therapy
Slide 7: Nurix Drugs Engage Ligases for the Treatment of Cancer
Nurix Drugs Engage Ligases for the Treatment of Cancer Targeted Protein Modulation: TPM = TPD + TPE A Powerful Targeted Protein Cellular System Elevation (TPE) Harness ligases to decrease specific protein levels Inhibit ligases to increase specific protein levels Targeted Protein Ubiquitin is ligate
Slide 8: Targeted Protein Modulation Addresses Key Limitations of Leading Modalities
Targeted Protein Modulation Addresses Key Limitations of Leading Cancer Therapy Modalities Resistance Mutations Targeted Scaffolding Functions Inhibitors Undruggable Targets Cell Exhaustion Immunotherapy Cell Expansion Cell Persistence 8
Slide 9: The Evolution of Nurix Therapeutics
The Evolution of Nurix Therapeutics Breakthrough Science, Breakthrough Drugs 2009 – 2015 2015 – 2019 2019 – 2022 Groundbreaking Science Building the Platform Drive to the Clinic Assembled initial scientific team Innovated DNA encoded library Signed Gilead collaboration: collection and DELigase $45M
Slide 10: Four Wholly Owned Clinical Programs with a Deep Pipeline
Nurix Is Advancing Four Wholly Owned Clinical Programs with a Deep Pipeline of Proprietary and Partnered Novel Targets Target/ MOA Drug Program Therapeutic Area Pre-Clinical Phase 1 Phase 2 Phase 3 Delivery NX-2127 BTK-IKZF B-Cell Malignancies Oral Degrader TPD NX-5948 BTK B-Cell Malignancies Oral D
Slide 11: Today's Agenda
Today's Agenda Part 1 Anthony Mato, MD, MSCE Director, CLL Program, Memorial Unmet Need in CLL Sloan Kettering Cancer Center First Targeted Protein Degradation Drugs in Hematologic Malignancies: NX-2127 & NX-5948 NX-2127: BTK Degrader With Robert J Brown, MD Immunomodulatory Activity & EVP, Head of
Slide 12: Today's Agenda
Today's Agenda Part 2 First Targeted Protein Elevation Drugs in Immuno-Oncology: NX-1607 & NX-0255 CBL-B: Master of the Immune Cristiana Guiducci, PhD Response SVP, Immunology and Oncology Research NX-1607: Biomarkers that Robert J Brown, MD Light the Way EVP, Head of Clinical Development DeTIL-0255
Slide 13: Today's Agenda
Today's Agenda Part 3 The Genesis: Powerful Gwenn M Hansen, PhD Chief Scientific Officer DELigase R&D Platform Hans van Houte Financial Snapshot Chief Financial Officer Conclusions Arthur T Sands, MD, PhD President, CEO and Board Director Q&A / Adjourn 13
Slide 14: The Team… Conquering Cancer
The Team… Conquering Cancer Arthur T Sands, MD, PhD Hans van Houte Gwenn M Hansen, PhD Stefani A Wolff President, Chief Executive Chief Financial Officer Chief Scientific Officer Chief Operating Officer and Officer, and Board Director Executive Vice President, Product Development Cristiana Guiducci,
Slide 15: Key Messages for Today
Key Messages for Today 1 2 3 We set the stage for the Resistance has We have next breakthrough met its match positive and in immune with targeted protein exciting findings modulation oncology from the first trial of a TPD in a hematologic with more to come from malignancy our powerful platform 15
Slide 16: Addressing the Unmet Needs in CLL in 2022
Bench-to-Bedside and Back: Addressing the unmet needs in Chronic Lymphocytic Leukemia in 2022 Anthony R. Mato, MD, MSCE Associate Attending Director, Chronic Lymphocytic Leukemia Program Memorial Sloan Kettering Cancer Center New York, New York 16
Slide 17: Chronic Lymphocytic Leukemia
Chronic Lymphocytic Leukemia ● CD5+ mature B-cell neoplasm ● Peripheral blood, lymph node and bone marrow compartments ● Median age at diagnosis: 72 years ● Most common leukemia in Western countries ● Heterogenous clinical presentation Remarkable Basic, Translational and Clinical Scientific Advances
Slide 18: Era of Targeted Therapies: Two Key Pathways
Era of Targeted Therapies: Two Key Pathways Targeted therapies are now standard of care options in the front-line and relapsed/refractory settings B-cell receptor signaling: Covalent, irreversible Bruton’s Tyrosine Kinase Inhibitors: ibrutinib & acalabrutinib Apoptotic Pathway: Bcl2-inhibitor veneto
Slide 19: Key Questions and Issues in Treating Relapsed CLL Patients
Key Questions and Issues in Treating Relapsed CLL Patients What are the unmet needs in the R/R setting? Limitations of covalent BTK inhibitors and venetoclax Limitations of noncovalent BTK inhibitors No standard of care for double-refractory disease 19
Slide 20: Covalent BTK Inhibitors: Resistance and Intolerance
Covalent BTK inhibitors: Resistance and Intolerance Continue to be Major Reasons for Discontinuation Even with Second Generation Agents! Clinical Trials and Real-World Data 20
Slide 21: Years of Follow-Up in the RESONATE-2 Study
7 Years of Follow-Up in the RESONATE-2 Study Overall discontinuation rate at 7 years = 53% PFS: Ibrutinib vs Chlorambucil PFS in Patient Subgroups of Interest Efficacy • Ibrutinib-treated patients had an 84% reduction in risk of progression or death • Ibrutinib led to a 97% reduction in risk of PD o
Slide 22: Ibrutinib Discontinuation for Intolerance in the Real World
Ibrutinib Discontinuation For Intolerance in the “Real World Setting” 41% of patients discontinued ibrutinib at a median follow-up of 17 months Toxicity accounted for the majority of discontinuations (over half) in both F/L and R/R CLL patients Most common toxicities in R/R population: atrial fibril
Slide 23: Acquired Resistance to Covalent BTKi
Acquired Resistance to Covalent BTKi • Majority of patients have identified mutations in BTKC481 at the time of disease progression on ibrutinib; ~53-87% of patients • Mutations also identified in PLCG2, immediately downstream of BTK • BTKC481 mutations are also the main mechanism of resistance for
Slide 24: Treatment of CLL After Covalent BTKi
Treatment of CLL After Covalent BTKi • Venetoclax: oral BCL2-inhibitor • Front-line setting and relapsed setting including after cBTKi • Approved as fixed-duration therapy (24 months in R/R setting) Phase II study of venetoclax in CLL patients with prior ibrutinib Median PFS only 24.7 months Differe
Slide 25: Patients on Landmark R/R Studies
Patients on Landmark R/R Studies Were Not Treated on Chemotherapy-Free Pathways or With Prior Novel Agents Only 9 of 921 Agent Study Name Number Median Percent on Percent treated with ≥ 1 patients (~1%) from (Control Arm) treated (range) prior modern BTK, Ven or PI3K-i therapies chemotherapy 6 landm
Slide 26: Resistance and Intolerance Limit Covalent BTK Inhibitor Outcomes
Resistance and Intolerance Limit Covalent BTK Inhibitor Outcomes 1 Ibrutinib discontinuation from 4 prospective studies ● Options following covalent BTK inhibitor treatment are limited: ○ Covalent BTK inhibitor retreatment: Only effective in the context of covalent BTK intolerance, not progression ○
Slide 27: Double Exposed CLL Patients
Double Exposed CLL Patients The Cutting Edge of Unmet Needs in the Clinic Today 27
Slide 28: Management of the Double Refractory CLL Patient
Management of the Double Refractory CLL Patient – Poor Survival Outcomes! After BTKi → Venetoclax: PI3Ki did not result in durable remissions and therefore is not an acceptable SOC rd in the 3 line setting in modern era Double Refractory Pts Median PFS = 4 months! Median OS = 3.6 months 28 Mato et a
Slide 29: Noncovalent BTK Inhibitors
Noncovalent BTK Inhibitors 29
Slide 30: Several BTKi Options to Consider
Several BTKi Options to Consider with Differences in BTKi Specificity, MOA, and Potential for Off-target Effects Irreversible Zanubrutinib Ibrutinib Acalabrutinib Reversible Vecabrutinib Nemtabrutinib/ARQ-531 Pirtobrutinib/LOXO-305 Kaptein et al. Blood 2018;132(suppl 1):1871. 30
Slide 31: BTK Pretreated CLL/SLL Patient Characteristics
BTK Pretreated CLL/SLL Patient Characteristics a Characteristics N = 261 Baseline Molecular Characteristics Median age, y (range) 69 (36-88) Mutation status, n (%) Female, n (%) 84 (32) BTK C481-mutant 89 (43) Male, n (%) 177 (68) a ECOG PS , n (%) BTK C481-wildtype 118 (57) 0 138 (53) PLCG2-mutant
Slide 32: Pirtobrutinib Efficacy in BTK Pretreated CLL/SLL Patients
Pirtobrutinib Efficacy in BTK Pretreated CLL/SLL Patients Efficacy evaluable BTK pretreated n = 252 a CLL/SLL Patients b Overall Response Rate, % (95% CI) 68 (62-74) Best response CR, n (%) 2 (1) PR, n (%) 137 (54) PR-L, n (%) 32 (13) SD, n (%) 62 (25) Data cutoff date July 16, 2021. BTK, Bruton tyr
Slide 33: From the Clinic to the Lab: Mechanisms of Resistance to ncBTKi
From the Clinic to the Lab Mechanisms of Resistance to ncBTKi 33
Slide 34: Progression on Pirtobrutinib: MSK Cohort
Progression on Pirtobrutinib: MSK Cohort Mato et al. Abstract 391. ASH 2021. https://ash.confex.com/ash/2021/webprogram/Paper147599.html 34
Slide 35: Mechanisms of Resistance to Noncovalent BTKi
Mechanisms of Resistance to Noncovalent BTKi 35
Slide 36: Investigating Mechanisms of Resistance
Investigating Mechanisms of Resistance We sought to investigate genetic mechanisms of resistance to ncBTKi DNA Sequencing: DNA Sequencing baseline mutational profile Treatment with pirtobrutinib monotherapy NCT03740529 Screening EOT ● Collected patient samples at screening and at the time of disease
Slide 37: CLL Patients with POD on Pirtobrutinib
CLL Patients with POD on Pirtobrutinib 9 CLL pts with POD on PLCG2 or BTK pirtobrutinib mutations at POD • 100% with prior covalent BTKi (100% ibrutinib) • Prior lines of therapy: range 2-10 • Baseline BTK C481 mutation: 44.4% • Baseline PLCG2 mutation 33.3% • Treated with pirtobrutinib for 3-17 mon
Slide 38: Acquired BTK Mutations on Pirtobrutinib
Acquired BTK Mutations on Pirtobrutinib We identified novel acquired mutations in BTK at the time of disease progression including: ● BTK L528W ● BTK V416L ● BTK M437R ● BTK T474I ● BTK A428D These mutations cluster around the tyrosine kinase catalytic domain of BTK Additionally, several patients wi
Slide 39: Acquired BTK L528W in Multiple Subclones at Relapse
Acquired BTK L528W in Multiple Subclones at the Time of Relapse 39 Wang E*, Mi X*, Thompson MC*… Mato, AR*, Taylor J*, Abdel-Wahab O*, NEJM 2022
Slide 40: Suppressed BTK C481S but Acquired L528W at Relapse
Suppressed BTK C481S but Acquired L528W at the Time of Relapse (9.6%) 40 Wang E*, Mi X*, Thompson MC*… Mato, AR*, Taylor J*, Abdel-Wahab O*, NEJM 2022
Slide 41: Novel BTK Mutations Clustered Within the BTK Kinase Domain
Novel BTK Mutations Identified in Pirtobrutinib-Resistant Patients Clustered Within the BTK Kinase Domain 41 Wang E*, Mi X*, Thompson MC*… Mato, AR*, Taylor J*, Abdel-Wahab O*, NEJM 2022
Slide 42: Novel BTK Mutations Confer Broad Resistance to Noncovalent BTK Inhibitors
Novel BTK Mutations Confer Broad Resistance to Noncovalent BTK Inhibitors 42 Wang E*, Mi X*, Thompson MC*… Mato, AR*, Taylor J*, Abdel-Wahab O*, NEJM 2022
Slide 43: Novel BTK Mutations Impaired Binding of Inhibitors
Novel BTK Mutations Impaired Binding of Both Noncovalent and Covalent Inhibitors *Red values indicate mutants which decrease drug binding affinity by at least 10-fold 43 Wang E*, Mi X*, Thompson MC*… Mato, AR*, Taylor J*, Abdel-Wahab O*, NEJM 2022
Slide 44: Novel BTK Mutations Reduced Phosphorylation of BTK and PLCγ2
Many of the Novel Acquired BTK Mutations Reduced Phosphorylation of BTK and Downstream PLCγ2 44 Wang E*, Mi X*, Thompson MC*… Mato, AR*, Taylor J*, Abdel-Wahab O*, NEJM 2022
Slide 45: Kinase Dead BTK Mutants Still Enabled AKT, ERK, NF-κB Activation
Upon IgM Stimulation, “Kinase Dead” BTK Mutants Still Enabled AKT, ERK, and NF-κB Activation 45 Wang E*, Mi X*, Thompson MC*… Mato, AR*, Taylor J*, Abdel-Wahab O*, NEJM 2022
Slide 46: Next Steps & New Means to Inhibit BTK
Next Steps & New Means to Inhibit BTK 46
Slide 47: Discovery of Kinase Dead BTK Mutants
Discovery of Kinase Dead BTK Mutants How do kinase dead BTK mutant activate B-cell receptor signaling? Are cells dependent on mutant BTK? Can we target these BTK mutants? 47
Slide 48: Targeted Protein Degradation of BTK
Targeted Protein Degradation of BTK BTK Destroyed by the Proteasome Nurix degrader E2 Ubiquitin drugs BTK Degrader CRBN E3 recycling Ligase Complex BTK Poly Ubiquitinated BTK Ubiquitination of Protein 48
Slide 49: Effective Degradation of Wild-type and Mutant BTK Protein
Effective Degradation of Wild-type and Mutant BTK Protein with Nurix Compounds NX-2127 NX-2127 BTKi resistance mutations Wang, Mi, Thompson, et al. NEJM 2022 Both NX-2127 and NX-5948 degrade wild-type & drug resistant mutant forms of BTK 49
Slide 50: First Targeted Protein Degradation Drugs in Hematologic Malignancies
Leader in Targeted Protein Modulation First Targeted Protein Degradation Drugs in Hematologic Malignancies NX-2127 & NX-5948 R&D Day New York, NY May 26, 2022 50
Slide 51: NX-2127: BTK Degrader With Immunomodulatory Activity
NX-2127: BTK Degrader With Immunomodulatory Activity Robert J Brown, MD EVP, Head of Clinical Development Nurix Therapeutics 51
Slide 52: A First-In-Class Franchise of BTK Degraders
A First-In-Class Franchise of BTK Degraders: NX-2127 & NX-5948 BTK DEGRADATION BTK DEGRADATION & IMMUNOMODULATION NX-5948 NX-2127 (Oncology & Autoimmune) (Oncology) • Robust BTK degradation and • Active against multiple BTK inhibitor- immunomodulatory activity observed resistant mutations across all
Slide 53: NX-2127 Degrades Both BTK and Aiolos
NX-2127 Degrades Both BTK and Immunomodulatory Cereblon Neosubstrate Aiolos BTK Degradation in TMD8 Cells Aiolos Degradation in T Cells NX-2127 shows potent BTK degradation in TMD8 cells NX-2127 degradation of Aiolos in human T cells occurs at (human DLBCL cell line) a similar potency to lenalidomid
Slide 54: NX-2127 Is Active Against Ibrutinib-Resistant Tumor Cell Lines
NX-2127 Is Active Against Ibrutinib- Resistant Tumor Cell Lines TMD8 BTK-C481S BTK-C481 mutations are the most common resistance mutations to ibrutinib and other covalent BTK inhibitors NX-2127 may offer a therapeutic option for patients with resistance to BTK inhibitors 54
Slide 55: Resistance to Noncovalent BTK Inhibitors Presents a New Challenge
Resistance to Noncovalent BTK Inhibitors Presents a New and Growing Challenge to Treatment “Our data suggest potential new therapeutic approaches to overcome the newly described BTK inhibitor resistance mechanisms. For example, these data provide a rationale for therapies aimed at addressing the pot
Slide 56: Degraders Directly Address Emerging Resistance Mutations
Degraders Directly Address Emerging Resistance Mutations and BTK Scaffolding Activity BTK mutations identified from patients NX-2127 has demonstrated clinical activity progressing on the noncovalent in patients harboring a variety of BTK inhibitor pirtobrutinib mutations Nurix has confirmed the acti
Slide 57: Aiolos Overexpression Drives BTK Inhibitor Resistance in CLL
Aiolos (IKZF3) Overexpression Drives BTK Inhibitor Resistance in CLL, a Rationale for a Combination Strategy “Our results thus highlight IKZF3 oncogenic function in CLL via transcriptional dysregulation and demonstrate that this pro-survival function can be achieved by either somatic mutation or ove
Slide 58: BTK Degradation of 80%+ Drives Potent Anti-tumor Activity
BTK Degradation of 80%+ Drives Potent Anti-tumor Activity in Preclinical Models Ikaros and Aiolos degradation also achieve target range at therapeutic doses Aiolos Degradation in Ikaros Degradation in Tumor Growth BTK Degradation in TMD8 Tumor Tissue TMD8 Tumor Tissue Vehicle Peripheral B cells 10 m
Slide 59: NX-2127-001: Initial Phase 1a Clinical Findings
NX-2127-001: Initial Phase 1a Clinical Findings Meeting the Need in CLL 59
Slide 60: NX-2127-001 Trial Design and Active Sites
NX-2127-001 Trial Design and Active Sites • Memorial Sloan Kettering Cancer Dose Escalation Potential Dose Expansion Center • MD Anderson Cancer Center Objectives: - Assess safety and tolerability • City of Hope: Duarte, California CLL with BTK C481 mutation (n≈20) - Identify maximum tolerated dose
Slide 61: Heavily Pretreated Patient Population
Heavily Pretreated Patient Population, Including Double-Refractory CLL Patients NX-2127-001 Overall Population CLL Non-CLL Characteristics (N = 21)** (N = 13) (N=7) Median Age, years (range) 76.0 (61 - 92) 76 (65 – 86) 77 (67 - 92) Female, n(%) 7 (33.3%) 7 (53.8%) 0 Male, n(%) 14 (66.7%) 6 (46.2%) 7
Slide 62: Robust BTK Degradation Across All Dose Levels
Robust BTK Degradation Observed with NX-2127 Across All Dose Levels and Malignancies NX-2127-001 Cohort 1-100 mg Cohort 2-200 mg Cohort 3- 300 mg % BTK remaining in CD19+ B cells % BTK remaining in CD19+ B cells % BTK remaining in CD19+ B cells 100 100 100 80 80 80 60 60 60 40 40 40 Therapeutic rang
Slide 63: Rapid and Sustained Degradation of BTK in CLL
Rapid and Sustained Degradation of BTK in Patients with CLL NX-2127-001 Therapeutic range Target BTK degradation achieved by Day 15 BTK degradation is sustained (steady state) for all starting BTK levels Data Cut April 8, 2022 63
Slide 64: NX-2127 Demonstrates Greater Ikaros Degradation
NX-2127 Demonstrates Greater Ikaros Degradation, Consistent with Cereblon Immunomodulatory Activity NX-2127-001 % Ikaros Remaining Healthy Donor Example 100 mg at C1D8 (ex vivo positive control) CLL Patient 100 80 60 Range of Ikaros -Ikaros -Ikaros decrease seen 40 with lenalidomide 20 Franssen et a
Slide 65: Lenalidomide Achieves 46-63% Ikaros Degradation
Lenalidomide Treatment Achieves 46-63% Ikaros Degradation in Immune Cells Ikaros decreases: • 63% median decrease in both CD4+ and CD8+ T cells • 59% median decrease in NK cells • 46% median decrease in B cells Ikaros levels in patients with MM treated with lenalidomide +low-dose cyclophosphamide an
Slide 66: Durable Benefit in CLL Patients With Median of 6 Prior Treatments
NX-2127-001: Durable Benefit In CLL Patients With A Median of 6 Prior Treatments No. Prior BTK- Cycle (28 Days) Prior Targeted BTK /BCL2 Prior 1 2 3 4 5 6 7 8 9 10 11 12 13 Lines Venetoclax Therapy Mutations 2 No ibrutinib BTK: C481R, L528W 5 No ibrutinib None Detected 8 Yes ibrutinib BTK: T474I • P
Slide 67: Positive Initial Findings in CLL Support Expansion at 100 mg
NX-2127-001 Phase 1a: Positive Initial Findings in CLL Support Expansion at 100 mg • Meaningful clinical benefit in CLL patients with a median of 6 prior lines of therapy • Biologic activity including nodal reductions and/or lymphocytosis observed in all patients treated • Responses in patients with
Slide 68: Safety Observations By Dose
Safety Observations By Dose: All Patients, Grade ≥ 3 NX-2127-001 Adverse Event 100mg (N=10) 200mg (N=6) 300mg (N=3) Preferred Term, Grade ≥3 n (%) n (%) n (%) Additional safety observations: Neutropenia 1 (10%) 3 (50%) 2 (66.7%) • Dose limiting toxicity observed at Hypertension 0 (0%) 1 (16.7%) 0 (0
Slide 69: Preliminary Findings Support Expansion of CLL Cohorts at 100mg
Preliminary Positive Clinical Findings Support Expansion of CLL Cohorts at the 100mg Dose Robust BTK degradation achieved in all patients Immunomodulatory activity achieved in all patients Expansion Favorable safety profile at dose selected for expansion cohorts dose declared in CLL at 100mg Meaning
Slide 70: Phase 1 First-in-Human Clinical Trial Design
NX-2127-001: Phase 1 First-in-Human Clinical Trial Design Phase 1a continues in NHL and Phase 1b CLL cohort initiated at 100mg Dose Escalation Cohort Expansion (Phase 1a) (Phase 1b) Indications Initiated CLL, MCL, MZL, WM, FL, DLBCL CLL (n≈40) Failed 2 or more prior treatments including a BTK inhibi
Slide 71: NX-2127 & NX-5948 Multiple Market Opportunities
NX-2127 & NX-5948 Multiple Market Opportunities Stefani A Wolff COO, EVP of Product Development Nurix Therapeutics 71
Slide 72: Nurix Portfolio of Degraders Poised To Take a Leadership Position
Nurix Portfolio of Degraders Poised To Take a Leadership Position NX-2127 NX-5948 BTK degrader + BTK degrader in B-cell immunomodulatory activity diseases (malignancies in B-cell malignancies and autoimmune) • Potential across lines of therapy • Beachhead in CLL • Opportunity in autoimmune • Near te
Slide 73: Multi-Billion-Dollar Revenue Opportunity Within B-cell Therapy
Multi-Billion-Dollar Revenue Opportunity Within the B-cell Therapy Universe for • B-cell directed therapies represent almost $18B in revenue in 2021 NX-2127 and NX-5948 • BTK inhibitors worth $8.4B in 2021 and expected to grow 90% to $16B by BTK inhibitors sales ($ in B) $20.0 2026 $15.0 • Anti-CD20
Slide 74: B-Cell Malignancies Opportunity
B-Cell Malignancies Opportunity BTK Degrader OPPORTUNITIES Growing # of BTK inhibitors are a standard of care in certain patients post BTKi hematologic malignancies (e.g., CLL, WM, MCL, MZL) Mutation escape across multiple BTKi BTK degraders address key unmet needs arising from New modality/ approac
Slide 75: NX-2127 Combines Two Blockbuster MOAs
NX-2127 Combines Activity of Two Blockbuster MOAs: BTK Inhibition and Immunomodulation Immuno- Established Targets BTK modulatory (e.g., Ibrutinib-$7B) Both (e.g., lenalidomide-$13B) B-CELL MALIGNANCIES ANNUAL INCIDENCE (US & EU) Aggressive; MCL DLBCL high unmet Chronic Lymphocytic Leukemia (CLL) 39
Slide 76: Potential Positioning Across All Lines of Therapy in CLL
Potential Positioning of Nurix BTK Degrader Franchise Across All Lines of Therapy in CLL Newly Diagnosed CLL Diagnosis Treatment Future CIT BTK inhibitors (BTKi) NX-2127 / Venetoclax Positioning (rituximab-based NX-5948 (mono + Gazyva + BTKi-based combination 1st Line regimens) and/or combo) regimen
Slide 77: Considerable Growth in CLL Patients Previously Treated with BTKi
Considerable Growth in CLL Patients Previously Treated with BTK Inhibitors ~70% increase of prior BTKi patients by 2030 18,000 CLL Patients 11,000 CLL Patients 2020 2030 77
Slide 78: NX-2127 Path to Market and Expansion
NX-2127 Path to Market and Expansion Initial Opportunity Expansion Clear unmet need in later lines of CLL Earlier line CLL if degradation and dual per FDA at recent ODAC meeting activity drive superior responses Third-line double-exposed CLL MCL for high unmet need where current (post-BTKi and post-
Slide 79: Nurix Is Creating a BTK Degrader Franchise
Nurix Is Creating a BTK Degrader Franchise: NX-2127 and NX-5948 Potential for BTK degraders to take share from established, blockbuster markets (BTK inhibitors and anti-CD20s) Nurix is the leader in this new modality – BTK degradation Multiple pathways for success in hematology/oncology Autoimmune i
Slide 80: Q&A: BTK Portfolio and CLL
ry nurix Q&A BTK Portfolio and CLL =o
Slide 81: First Targeted Protein Elevation Drugs in Immuno-Oncology
Leader in Targeted Protein Modulation First Targeted Protein Elevation Drugs in Immuno-Oncology NX-1607 & DeTIL-0255 R&D Day New York, NY May 26, 2022 81
Slide 82: CBL-B: Master of the Immune Response
CBL-B: Master of the Immune Response Cristiana Guiducci, PhD SVP, Immunology and Oncology Research Nurix Therapeutics 82
Slide 83: First-in-Class Targeted Protein Elevation Drugs: CBL-B Inhibitors
First-in-Class Targeted Protein Elevation Drugs CBL-B Inhibitors Highlight the properties and Rationale for targeting CBL-B mechanism of action of in oncology Nurix’s CBL-B inhibitors Development of highly optimized proximal NX-1607-101 initial clinical biomarkers and their use experience in the cli
Slide 84: A Better Immuno-Oncology Target
A Better Immuno-Oncology Target: A CBL-B Inhibitor Can Revolutionize Cancer Treatment The ultimate goal of cancer immunotherapy is to generate a coordinated immune system response against cancer associated antigens Immune checkpoint agents such as anti-PD-1/PD-L1 have demonstrated impressive long-la
Slide 85: Targeting CBL-B Enhances Antitumor Response
Targeting CBL-B Enhances Antitumor Response A Master Orchestrator of the Immune System CBL-B mediated mechanisms strongly restrains a productive anti-tumor response Lymph node T cell CBL Blood CBL-B inhibition increases: Tumor • DC and NK infiltration and function Dying Tumor DC tumor • T cell primi
Slide 86: NX-1607 Mechanism of Action: Intramolecular Glue
NX-1607 Mechanism of Action: Intramolecular Glue CBL-B is in Equilibrium Between Closed and Opened State E2 Y363 Y363 RING TKB TKB Closed State Opened State INACTIVE 86
Slide 87: NX-1607 Mechanism of Action: Intramolecular Glue
NX-1607 Mechanism of Action: Intramolecular Glue Substrate protein E2 E2 Y363 p Y363 pY363 1. Kinase RING TKB TKB TKB 2. E2/substrate Closed State Opened State Phosphorylation locks INACTIVE CBL-B in the ACTIVE Conformation Immune Response 87
Slide 88: NX-1607 Mechanism of Action: Intramolecular Glue
NX-1607 Mechanism of Action: Intramolecular Glue Substrate protein E2 E2 Y363 p NX-1607 Y363 pY363 1. Kinase RING RING TKB TKB TKB TKB 2. E2/substrate NX-1607 acts as an Closed State Opened State Phosphorylation locks intramolecular glue INACTIVE CBL-B in the ACTIVE forcing CBL-B in its Conformation
Slide 89: NX-1607 Increases IL-2 and IFN-γ Secretion in T cells
NX-1607 Increases IL-2 and IFN-�� Secretion in TCR Stimulated Primary Human T cells IL-2 Anti-CD3 IL-2 Anti-CD3/CD28 NX-1607 increases TCR stimulation-dependent production of IL-2 and IFN-�� in primary human T cells IFN-�� Anti-CD3 IFN-�� Anti-CD3/CD28 NX-1607 has no impact in the absence of T cell
Slide 90: Single-Agent NX-1607 Induces Antitumor Response in Multiple Models
Single-Agent NX-1607 Induces Antitumor Response in Multiple Models NX-1607 NX-1607 NX-1607 Reduced Tumor Volume Prolonged Survival Reduced Tumor Volume Colorectal Triple-Negative Breast B Cell Lymphoma NX-1607 30 mg/kg day 7 to 46 NX-1607 30 mg/kg day 16 to 28 Shaded area indicates dosing period 90
Slide 91: NX-1607 and Anti-PD-1 Synergize in Multiple Tumor Models
NX-1607 and Anti-PD-1 Synergize to Enhance Anti-tumor Effects and Survival of Mice in Multiple Tumor Models Colorectal (CT26) Colorectal (MC38) Triple-Negative Breast (4T1) Vehicle NX-1607 anti-PD-1 NX-1607+anti-PD-1 Shaded area indicates dosing period: NX-1607 (30 mg/kg, PO daily) and anti-PD-1 twi
Slide 92: NX-1607 Induces T and NK Cell Intratumoral Infiltration
NX-1607 Treatment Induces Dose Dependent T and NK Cell Intratumoral Infiltration and Enhanced Function Vehicle NX-1607 10 mg/kg NX-1607 30 mg/kg * p<0.05; ** p < 0.01; *** p < 0.001 Tumor-bearing mice treated for 18 days with NX-1607 at 10 or 30 mg/kg. Tumor microenvironment profiled using NanoStrin
Slide 93: NX-1607 Increases Pro-Inflammatory Cytokines in Human NK cells
NX-1607 Increases Secretion of Pro-Inflammatory Cytokines in Human NK cells IFN-�� TNF-⍺ NX-1607 increases stimulation-dependent production of IFN-�� and TNF-⍺ in primary human NK cells NX-1607 has no impact in the Baseline Response absence of NK cell stimulation, as measured by cytokine release NK
Slide 94: NX-1607 and Rituximab Enhance Anti-tumor Activity
Combination of NX-1607 and Rituximab Enhances Anti-tumor Activity in a Human NHL Animal Model NX-1607 Strongly Potentiate Rituximab-Directed NK Cell ADCC Against Tumor Cells NX-1607-mediated NK activation NK depletion abrogates NX-1607 and potentiates rituximab antitumor activity NX-1607 + Rituximab
Slide 95: NX-1607: Biomarkers that Light the Way
NX-1607: Biomarkers that Light the Way Robert J Brown, MD EVP, Head of Clinical Development Nurix Therapeutics 95
Slide 96: What Makes a Good Clinical Biomarker?
What Makes a Good Clinical Biomarker? Proximal to the target As the first to target Dose-responsive CBL-B, Nurix is leading the field in biomarker Directly relates to the biologic mechanism of action discovery for this new mechanism of action Translates from animal models to humans 96
Slide 97: Proprietary Biomarkers Measure CBL Inhibition
Proprietary Biomarkers Measure CBL Inhibition Agnostic screening campaigns identified robust, reproducible and novel proximal biomarkers of CBL-B inhibition ⇢ Ubiscan identified direct ubiquitination substrates of CBL-B E3 ligase ⇢ Phosphoscreen demonstrated increased levels of activated proteins ca
Slide 98: Overview of UbiScan Technology
Overview of UbiScan Is a Method to Identify Direct UbiScan Technology Ubiquitination Substrates 1. CBL-B ubiquitinates proteins and targets them for degradation 2. Proteins that are ubiquitinated can be detected by ubiscan because they have GG or “diGly scar” 3. Antibodies recognizing the “scar” can
Slide 99: UbiScan Identified Direct CBL Substrates in TCR Signaling
UbiScan Identified Direct CBL Substrates Within the T Cell Receptor (TCR) Signaling Cascade Other E3 substrates 6- Decreased signal represents direct substrates ubiquitinated by CBL-B 4- ligase activity CD3z 2- 0- Lyn (kinase for HS1) -2- ZAP70 -4- Inhibiting CBL-B decreases ubiquitination of import
Slide 100: Phospho-Protein Flow Cytometry Assay Identified Proximal Biomarkers
Phospho-Protein Flow Cytometry Assay Identified Proximal Biomarkers • Stimulated human PBMCs with or without CBL-B inhibition pPLCγ2 • Cells were stained with a panel pHS1 (Substrate of phospho-specific antibodies for Lyn) for proteins downstream the TCR signaling pZAP70 • Expression levels were as
Slide 101: Signals Specific to Stimulated T Cells
Signals Identified in Ubiscan & Phosphoscreen Were Specific to Stimulated T Cells In presence of CBL inhibitor, stimulation of the TCR results in the phosphorylation of: ZAP70 • Key organizer of downstream TCR signaling PLCγ2 • Expressed in both T cells and B cells • Associates with LAT and SLP-76 &
Slide 102: Dose Dependent Biomarker Increases Correlate with Antitumor Effects
Dose Dependent Increases of CBL-B Proximal Biomarker Correlates with Antitumor Effects of NX-1607 Pharmacodynamic relationship in mice Antitumor activity in mice following NX-1607 dosing NX-1607 ** **** 100 2800 2000 80 1200 1000 60 Efficacious 800 40 Range 600 20 400 0 0.1 1 10 100 200 NX-1607 (mg/
Slide 103: NX-1607-101: Phase 1 Clinical Trial Design
NX-1607-101: Phase 1 first-in-human clinical trial design Two-Part Phase 1 Monotherapy Trial of NX-1607 in Relapsed or Refractory Tumors Cohort Expansion Dose Escalation Objectives: Melanoma • Assess safety and tolerability Squamous Cell Carcinoma of the Head • Identify maximum tolerated dose and Ne
Slide 104: NX-1607-101 Initial Clinical Experience
NX-1607-101 Initial Clinical Experience Dose escalation is ongoing Consistent with preclinical models, we are observing dose-dependent increases of proximal biomarkers Expect to select Phase 1b dose in H2 2022 Clinical update in mid-2022 will report PK and biomarkers 104
Slide 105: CBL-B Inhibition: Centerpiece of Immuno-Oncology Therapy
CBL-B Inhibition Has the Potential To Be the Small Molecule Centerpiece of Immuno-Oncology Therapy Post-ICI (Melanoma, NSCLC, Prostate, MSS Colorectal Ovarian, Gastric DLBCL (including Richter’s) TNBC, Meso, Urothelial, etc) Low-Immunogenicity Tumors Suppressive TME Acquired Resistance T-Cell Dysfun
Slide 106: CBL-B Inhibition: Potential Combinations
CBL-B Inhibition Has the Potential To Be the Small Molecule Centerpiece of Immuno-Oncology Therapy Post-ICI (Melanoma, NSCLC, Prostate, MSS Colorectal Ovarian, Gastric DLBCL (including Richter’s) TNBC, Meso, Urothelial, etc) Low-Immunogenicity Tumors Suppressive TME Acquired Resistance T-Cell Dysfun
Slide 107: CBL-B Inhibition: Combinations with DeTIL-0255
CBL-B Inhibition Has the Potential to Be the Small Molecule Centerpiece of Immuno-Oncology Therapy Post-ICI (Melanoma, NSCLC, Prostate, MSS Colorectal Ovarian, Gastric DLBCL (including Richter’s) TNBC, Meso, Urothelial, etc) Low-Immunogenicity Tumors Suppressive TME Acquired Resistance T-Cell Dysfun
Slide 108: DeTIL-0255: Drug Enhanced Cell Therapy in the Clinic
DeTIL-0255: Drug Enhanced Cell Therapy in the Clinic Michael T Lotze, MD, FACS Chief Cellular Therapy Officer Nurix Therapeutics 108
Slide 109: Drug-Enhanced Tumor Infiltrating Lymphocytes (DeTIL-0255)
Drug-Enhanced Tumor Infiltrating Lymphocytes (DeTIL-0255) A one-time patient-derived cell therapy 109
Slide 110: TIL T Cell Therapy with Durable Responses
Tumor Infiltrating Lymphocytes (TIL) – T Cell Therapy with Durable Responses and Potential to Cure Patients with Solid Tumors TIL for Patient with Median Sponsor N ORR CR% Metastatic Melanoma OS NCI US 43 49% 12% 62 NCI US Autologous Reactive TIL 51 45% 24% 36.6 NCI US 20 35% 5% n/
Slide 111: TIL Less Effective in the Post-Checkpoint Setting
TIL Administration Has Been Less Effective in the Post-Checkpoint Setting For Patients With Solid Tumors TIL has the potential to cure patients with solid tumors Checkpoint inhibitor therapy has reduced the efficacy of subsequent TIL administration The current TIL regimen is not suitable for most so
Slide 112: DeTIL-0255 Designed To Overcome Limitations of TIL Therapy
DeTIL-0255: Cell Therapy Product Designed To Overcome Major Limitations of Current TIL Therapy Desirable phenotype with mixture of increased stem-like T cells and potent effector T cells DeTIL-0255 can integrate effectively in a regimen for patients with virtually any cancer type 112
Slide 113: More Effective Expansion of Potent and Stem-like DeTIL-0255
More Effective Expansion of Potent and Stem-like Human DeTIL-0255 Compared with TIL • Increased diversity, cell number, and stem-like properties • Decreased exhaustion • Enhanced effector function • Increased activation Whelan et al Poster 98 SITC 2021 113
Slide 114: Potency Assay Designed to Meet Regulatory Requirements
Potency Assay Prospectively Designed to Meet Regulatory Requirements Tumor-specific Demonstrates the biologic activity of DeTIL-0255 Reproducible Developed prospectively Matrix testing of DeTIL-0255 properties including phenotype and function Ongoing validation in our clinical trial 114
Slide 115: Universal DeTIL-0255 Expansion Across Tumor Types
Universal DeTIL-0255 Expansion Allowing Application to Multiple Tumor Types Pilot Runs All tumors harbor TIL which can be expanded in pilot and full-scale runs Pilot scale: 100% of 105 tumors demonstrate T cell expansion Full-scale runs Full-scale: 100% of 13 tumors demonstrate successful DeTIL-0255
Slide 116: Introduction of DeTIL-0255 into the Clinic
Introduction of DeTIL-0255 into the Clinic Drug-enhanced TIL product utilizes our proprietary CBL-B inhibitor in manufacturing Cellular therapy with phenotypic and functional properties associated with superior activity in conventional TIL therapies 100% success rate in pilot and full-scale manufact
Slide 117: DeTIL-0255-201: First-in-Human Clinical Trial
DeTIL-0255-201: First-in-Human Clinical Trial Robert J Brown, MD EVP, Head of Clinical Development Nurix Therapeutics 117
Slide 118: DeTIL-0255-201: Phase 1 Clinical Trial Design
DeTIL-0255-201: Phase 1 First-in-Human Clinical Trial Design Two-Part Phase 1 Monotherapy Trial of DeTIL-0255 in Relapsed or Refractory Gynecological Cancers Safety Run in (3-6 patients) Cohort Expansion Objectives: Platinum Resistant Epithelial • Assess safety and tolerability Ovarian Cancer • Asse
Slide 119: Successful Infusion in First Patient
Successful Infusion in First Patient In DeTIL-0255-201 First patient with ovarian cancer has cleared DLT period and awaiting tumor assessment Successful expansion and desirable phenotype including CD4+ and CD8+ T cells with characteristics of memory and stem-like cells Successfully manufactured DeTI
Slide 120: DeTIL-0255 Holds the Promise of Superior Antitumor Activity
DeTIL-0255 Holds the Promise of Superior Antitumor Activity in the Clinic Displays characteristics associated with better outcomes in TIL therapy ⇢ Superior stem-like and memory phenotype ⇢ Enhanced effector function ⇢ Increased persistence and activity Clinical trial with DeTIL-0255 designed to dem
Slide 121: The Genesis: Powerful DELigase R&D Platform
Leader in Targeted Protein Modulation The Genesis: Powerful DELigase R&D Platform Gwenn M Hansen, PhD Chief Scientific Officer Nurix Therapeutics 121
Slide 122: Platform Enables Two Complementary Protein Modulation Approaches
Our Platform Enables Two Complementary Protein Modulation Approaches for Therapeutic Discovery Targeted Protein E3 ligases are the rheostat of the Elevation proteome Ligase Modulators can either Decrease Eliminate or Enhance Protein Dosage a pathway function Increase Protein Dosage Our CBL and BTK d
Slide 123: Key Questions About Nurix's Platform
Key Questions About Nurix’s Platform How is Nurix advancing the field of ligase discovery to become the leader in Targeted Protein Modulation? What is driving the productivity of Nurix’s DELigase platform? Why did Nurix focus on and internalize DEL technology? How is Nurix innovating to address the
Slide 124: Unique TPM Opportunities from Additional E3 Ligases
Unique TPM Opportunities Can Be Unlocked by Harnessing or Inhibiting Additional E3 Ligases Precedented TPD ligases Unlock novel targets and pathways Nurix TPM Discovery Improve target coverage and Ligases selectivity as Targets 125 NX-2127 Ibrutinib 100 75 50 Overcome inhibitor resistance 25 0 Compo
Slide 125: Most Comprehensive Ligase Discovery Pipeline
Nurix Has the Most Comprehensive Ligase Discovery Pipeline Ligand Ligand Degrader DC Clinic Optimization Profiling Discovery nominatio n CBL Inhibitors and BTK Degraders 20 Ligases 60 Ligases in 11 Ligases Discovery Pipeline 27 Ligases Examples: Selectively expressed vs Broadly-expressed Multiple li
Slide 126: DELigase Protein Modulation Discovery Platform
Nurix’s DELigase Protein Modulation Discovery Platform DEL Discovery Rational and Direct-to-Cell Scaled Screening for Empirical Chemistry Biology Capabilities in vivo exposure M e a n U n b o u n d D ru g C o n c e n tra tio n in P la s m a 1 0 .1 0 .0 1 0 .0 0 1 D C = 0 .0 0 5 u M 9 0 0 .0 0 0 1 0
Slide 127: Integrated Discovery Engine To Unlock Relevant Targets
Integrated Discovery Engine To Unlock Relevant Targets 2. Versatile Discovery 3. Efficient Follow-up 1. Proprietary Starting Points – Simultaneous identification of – Combinatorial design enables • Designed for Difficult Targets unique mechanisms of action automation and computation • Drug-Like – No
Slide 128: Custom Scaffold-Based DELs Identify Binders
Custom Scaffold-Based DELs Enable Nurix To Identify Binders to Challenging Protein Surfaces Our proprietary scaffold DELs Commercial DEL designs Nurix scaffold designs provide unique geometry and high show high pocket possess little sp3 sp3 character, allowing molecules to complementarity achieve op
Slide 129: Computational Methods To Discover Potent CRBN Binders
Leveraging Computational Methods To Search Beyond DEL Space to Discover Potent and Diverse CRBN Binders Nurix’s Discovery Workflow Allows Access to Chemical Space Beyond Existing Compound Collections BB 1 BB BB Traditional Hit 3 2 Resynthesis Machine Learning and Similarity Virtual DEL Screen for Au
Slide 130: Predicting Solubility with Machine Learning
Predicting Solubility in Unique Chemical Space with Machine Learning Problem: Experiment vs Prediction: Degraders occupy non-traditional Degraders 2 R = 0.44 Small Molecules chemical space Leading Degraders Chem- Small Molecules informatics Solution: Software Application of modern machine learning f
Slide 131: Automation to Define Parameters of Degrader Design
Nurix Is Applying Automation to Better Define the Parameters of Degrader Design to Advance our Programs to the Clinic Challenge: Identifying and optimizing degraders remains largely an empirical process Target Binder DESIGN SCOPE SYNTHESIZE AT SCALE Theoretical range of Automation enables Nurix degr
Slide 132: Lead-Like Aurora A Degraders Discovered by Automation
Lead-Like Aurora A Degraders Discovered by Applying Automation to Nurix’s Compound Synthesis Workflow Power of Applying Automation to Quickly Identify Ideal Design Space Desired Dmax A Aurora A Binders: B C D Binder 1 E F Binder 2 G H Binder 3 I J K Size of point = potency L M N O P Q In collaborati
Slide 133: Collaboration Pipeline Demonstrates Value of Platform
Collaboration Pipeline Has Demonstrated Value of Platform, Particularly with Targets Considered Undruggable Ligand Degrader Cellular In vivo Oral DC Discovery Discovery Profiling Profiling exposure nomination Druggable Targets Difficult-to-Drug Targets Nurix’s discovery platform is unlocking truly n
Slide 134: Degraders Solve Inhibitor Resistance
Nurix Is Confirming the Value of Degraders to Solve Inhibitor Resistance NX-2127 kills lymphoma cells NX-2127 degrades multiple novel BTK harboring BTK-C481S mutation mutations emerging post BTKi-treatment 125 NX-2127 WT 125 Ibrutinib C481S 100 100 L528W 75 75 V416L M437R 50 50 25 25 0 0 Compound (n
Slide 135: Leading the Field of Protein Modulation
Leading the Field of Protein Modulation Delivering multiple modalities of therapeutics across the broadest target space Largest pipeline of E3 ligase targets Best in class for integrating DEL within a discovery engine incorporating automation, machine learning, and structure-based drug design Proven
Slide 136: Financial Snapshot & Conclusions
Leader in Targeted Protein Modulation Financial Snapshot & Conclusions Building From a Position of Strength R&D Day New York, NY May 26, 2022 136
Slide 137: Financial Snapshot
Financial Snapshot Hans van Houte Chief Financial Officer Nurix Therapeutics 137
Slide 138: Nurix Is in a Strong Financial Position
Nurix Is in a Strong Financial Position $386M in cash and investments on February 28, 2022 R&D collaboration details: • Funded through key readouts for all four clinical programs • Execution on R&D collaborations drives success-based cash flow • Gilead $55M upfront and $2.3B in additional payments i
Slide 139: Funding Through Equity and Collaboration Revenue
Nurix Continues To Successfully Fund Through Appropriate Mix of Equity and Collaboration Revenue at Every Stage of Growth Equity Capital Collaborations Series A: $6M Celgene collaboration: $150M Series B: $25M Gilead collaboration: $45M Series C: $17M Sanofi collaboration: $55M Series D: $120M Sanof
Slide 140: Delivering Key Clinical Milestones in 2022
Delivering Key Clinical Milestones in 2022 Targeted Protein Degradation Targeted Protein Elevation NX-5948 NX-1607 DeTIL-0255 NX-2127 ✓ Dose first patient in • Present Phase 1a ✓ Dose first patient in ✓ Initiate Phase 1b trial Phase 1a trial in PK/PD in mid-2022 Phase 1 trial in H1 in mid-2022 H1 20
Slide 141: Delivering Key Clinical Milestones in 2022
Delivering Key Clinical Milestones in 2022 Targeted Protein Degradation Targeted Protein Elevation NX-5948 NX-1607 DeTIL-0255 NX-2127 ✓ Dose first patient in • Present Phase 1a ✓ Dose first patient in ✓ Initiate Phase 1b trial Phase 1a trial in PK/PD in mid-2022 Phase 1 trial in H1 in mid-2022 H1 20
Slide 142: A Bright Future
A Bright Future Arthur T Sands, MD, PhD President, CEO and Board Director Nurix Therapeutics 142
Slide 143: Key Messages for Today
Key Messages for Today 1 2 3 We set the stage for the Resistance has We have next breakthrough met its match positive and in immune with targeted protein exciting findings modulation oncology from the first trial of a TPD in a hematologic with more to come from malignancy our powerful platform 143
Slide 144: What to Expect From Nurix in 2022 and Beyond
What to Expect From Nurix in 2022 and Beyond Advancing technology and pipeline to remain leaders in Targeted Protein Modulation 2022-BEYOND CONQUERING CANCER Driving toward definitive clinical results Nurix is committed to building a patient-focused, science-driven Building commercial-ready organiza
Slide 145: Thank You
Thank You 145
Slide 146: nurix
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Slide 147: Leader in Targeted Protein Modulation
Leader in Targeted Protein Modulation Nurix is committed to building a patient-focused, science-driven oncology company powered by our leadership position in Targeted Protein Modulation R&D Day New York, NY May 26, 2022 147