Slide 1: Corporate Presentation
Corporate Presentation February 2026 NASDAQ L I S T E D ARVN © 2025 Arvinas. All rights reserved.
Slide 2: Safe harbor and forward-looking statements
Safe harbor and forward-looking statements This presentation contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties, including statements regarding: the potential for vepdegestrant to be a first-
Slide 3: Igniting a transformative change
IGNITING A TRANSFORMATIVE CHANGE in the fight for patients with cancer and neurodegenerative diseases
Slide 4: Our experienced team is advancing a new therapeutic modality
Our experienced and talented team is advancing a new therapeutic modality for patients History of FIRSTS with our novel Promising preclinical results are translating PROTAC Strong, experienced therapeutic modality: into the clinic leadership team Discovery Clinical trials in oncology 7 programs ente
Slide 5: AR and ER degraders highlight Arvinas' ability to develop valuable PROTAC degraders
AR and ER degraders highlight Arvinas’ ability to develop valuable PROTAC degraders ER: vepdegestranta AR: luxdegalutamide • Positive efficacy and well-tolerated in • Demonstrated signals of efficacy in late-line Phase 1, 2 and 3 clinical trials prostate cancer suggests potential for ‒ First positiv
Slide 6: PROTAC degraders harness the body's natural machinery to degrade disease-causing proteins
PROTAC degraders harness the body’s natural machinery to degrade, not simply inhibit, disease-causing proteins E3 ligase PROTEIN TAGGING: 2 Tagging of target protein COMPLEX FORMATION: for degradation 1 Target Protein Recognizing disease Ubiquitin causing protein of interest ITERATIVE ACTIVITY PROTE
Slide 7: PROTAC degraders have potential benefits over other modalities
PROTAC degraders have potential benefits that may provide advantages over other modalities in oncology and neurology BENEFITS IN BENEFITS OF BENEFITS IN ONCOLOGY PROTAC PROTEIN DEGRADERS NEUROLOGY Ability to overcome Elimination (rather than inhibition) Blood-brain barrier evolving resistance
Slide 8: Seeking to address two of the largest areas of unmet need
Seeking to address two of the largest areas of significant unmet need for patients O N C O LO GY N E U R O LO GY By 2040 By 2040 30M 15M neurodegenerative diseases will be the LEADING CAUSE Leading to New cancer cases per year worldwide1 Cancer-related deaths per year1 #2 OF DEATH in developed count
Slide 9: Arvinas pipeline includes differentiated PROTAC degraders in neurology and oncology
Arvinas pipeline includes differentiated PROTAC degraders in neurology and oncology PROGRAM INDICATION PRECLINICAL PHASE 1/1B PHASE 2 PHASE 3 MARKET ARV-102 PSP, Parkinson’s Phase 1: Parkinson’s disease (LRRK2) Disease ARV-027 Spinal Bulbar Phase 1: SBMA (polyQ-AR) Muscular Atrophy ARV-806 Pancreati
Slide 10: Strategically positioned for the next stage of growth
Strategically positioned for the next stage of growth • Delivering innovative assets intended to differentiate from other therapies; investing High-Value Pipeline in highest value drivers across the pipeline of Differentiated • Best-in-class research engine sets up Arvinas for long-term impact Progr
Slide 11: ARV-102
CLINICAL PROGRAMS: Neurology ARV-102 PROTAC LRRK2 degrader ARV-102 is an investigational compound. Its safety and effectiveness have not been established.
Slide 12: Neurodegenerative diseases: An area of tremendous unmet need
Neurodegenerative diseases: An area of tremendous unmet need Unmet need is high: • No approved disease-modifying therapies for multiple In the U.S., there are ~8 million important target proteins (e.g., LRRK2, tau, α-synuclein) people living with Alzheimer’s, Parkinson’s, and Huntington’s diseases1-
Slide 13: PROTAC degraders could potentially revolutionize treatment of neurodegenerative diseases
PROTAC degraders could potentially revolutionize the treatment of neurodegenerative diseases Cross the Are orally administered blood-brain barriera Arvinas can engineer PROTAC degraders Reach targets in “deep brain” regions that: Selectively target mutant and/or wild-type proteins A novel PROTAC app
Slide 14: LRRK2 is implicated in Parkinson's disease and progressive supranuclear palsy
LRRK2 is implicated in both in Parkinson’s disease and progressive supranuclear palsy Parkinson’s Disease (PD) Progressive Supranuclear Palsy (PSP) • Rare progressive neurological disease that • Neurodegenerative disease that affects affects movement, balance, and cognitive movement, balance, and co
Slide 15: PROTAC-induced LRRK2 degradation as a potential treatment for PD and PSP
PROTAC-induced LRRK2 degradation as a potential treatment for idiopathic Parkinson’s disease and progressive supranuclear palsy Progressive supranuclear palsy (PSP) is a tauopathy with rapid progression to death within 5-7 years Mutations and increased expression of LRRK2 • LRRK2 genetic variants wi
Slide 16: LRRK2 degradation has potential to differentiate from kinase inhibition
PROTAC-induced LRRK2 degradation has the potential to differentiate from kinase inhibition PROTAC LRRK2 degrader differentiates from inhibitors LRRK2 is a large multidomain scaffolding kinase Inhibitor PROTAC 1 ARM ANK LRR ROC COR KIN WD40 2527 Kinase activity Protein-protein interaction (scaffoldin
Slide 17: ARV-102 increases lysosome functional degradative capacity and number in vitro
ARV-102 increases lysosome functional degradative capacity and number in vitro Lysosome function and number are reduced preclinically and patients with PDa; ARV-102 dose- dependently increased degradation efficiency and lysosome number vs kinase inhibitors ARV-102 increases lysosome ARV-102 increase
Slide 18: LRRK2 PROTAC degraders can reduce PSP-induced pathologic tau
In vitro and in vivo data suggest that Arvinas’ LRRK2 PROTAC degraders can reduce PSP-induced pathologic tau LRRK2 SNP accelerated time to death LRRK2 PROTAC reduced PSP induced LRRK2 PROTAC degraders reduced by 1 year in PSP1 pathologic AT8-tau, in vitro pathologic tau protein in vivo PS19 (~12 wee
Slide 19: ARV-102 shows better target engagement versus a LRRK2 inhibitor
ARV-102 shows better target engagement, enhanced potency, and pathway engagement versus a LRRK2 inhibitor in preclinical model Iterative and catalytic PROTAC advantage results in stronger LRRK2 reduction and RAB pathway engagement versus a LRRK2 kinase inhibitora LRRK2 Target Engagement RAB Pathway
Slide 20: ARV-102 degrades LRRK2 in deep-brain regions in non-human primates
ARV-102 degrades LRRK2 in NHP deep-brain regions in non-human primates Orally dosed ARV-102 reaches multiple “deep brain” regions in non-human In NHPs, CSF levels of LRRK2 can be used to primates (NHPs) and degrades LRRK2 up to 94% indicate levels of LRRK2 in cortex 94% 92% 83% decrease decrease dec
Slide 21: LRRK2 biomarkers reduced in non-human primate CSF after dosing
Putative LRRK2 biomarkers associated with disease are reduced in non-human primate CSF after dosing with ARV-102 Marker of pathologic Lysosomal hydrolase Lysosomal marker increased neuroinflammation implicated in Parkinson’s disease in glia in neuroinflammation IBA1 is reduced by ARV-102 Cathepsin B
Slide 22: In healthy volunteers, ARV-102 shows brain penetration and target engagement
In healthy volunteers, dose-dependent increases in ARV-102 and LRRK2 reductions in CSF indicate brain penetration and target engagement ARV-102 induced dose-dependent reductions in LRRK2 levels in CSF, with >50% LRRK2 reduction at single doses ≥60 mg (data not shown) and repeated doses ≥20 mg ARV-10
Slide 23: Multidose ARV-102 reduced downstream LRRK2 pathway biomarkers
In healthy volunteers, multidose ARV-102 treatment led to reductions in downstream LRRK2 pathway biomarkers in blood cells and urine Phospho-Rab10T73 in PBMCs BMP Lysosomal Lipid in Urine Rab10, a GTPase involved in the lysosomal stress response, is a LRRK2 substrate and biomarker for downstream LRR
Slide 24: ARV-102 reduced lysosomal pathway markers versus placebo
In healthy volunteers, ARV-102 led to significant reductions in lysosomal pathway markers when compared to placebo CSF CD68 – example of dose-dependent reductions Placebo (n=10) ARV-102, 80 mg (n=9) CD68 in CSF: Placebo ARV-102 ✱✱ LRRK2 in CSF (median % CFB) 50 ✱✱✱ 50 ✱✱✱ ✱✱✱ ✱✱ ✱✱✱ ✱✱ 25 25 Change
Slide 25: In Parkinson's patients, ARV-102 exposure in plasma and CSF increased dose-dependently
In patients with Parkinson’s disease, exposure of ARV-102 in plasma and CSF increased in a dose-dependent manner, indicating brain penetration ARV-102 exposure (AUCinf and Cmax) increased in a dose-dependent manner in plasma and in CSF Plasma CSF 1000 50 mg 1000 1000 Mean plasma concentration (ng/mL
Slide 26: In Parkinson's patients, ARV-102 decreased LRRK2 in PBMCs
In patients with Parkinson’s disease, ARV-102 decreased LRRK2 protein levels in PBMCs after a single oral dose Median LRRK2 levels in PBMCs decreased 86% from baseline following a single 50-mg dose of ARV-102 and 97% after a 200-mg dose 50 50 Change from baseline (%) 0 -50 -50 -86% -100 -100 -97% Pl
Slide 27: Development plan for ARV-102 in Parkinson's disease and PSP
Development plan for ARV-102 includes clinical trials in patients with Parkinson’ disease and progressive supranuclear palsy Status of ARVINAS Trials with ARV-102 OBJECTIVES: Safety, Tolerability, PK, and PD Study ARV-102-101 HEALTHY VOLUNTEERS Study ARV-102-103 PARKINSON’S DISEASE SINGLE ASCENDING
Slide 28: ARV-027
CLINICAL PROGRAMS: Neurology ARV-027 PROTAC polyQ-AR degrader ARV-027 is an investigational compound. Its safety and effectiveness have not been established.
Slide 29: SBMA is caused by a CAG repeat expansion in the androgen receptor
Spinal bulbar muscular atrophy is caused by a trinucleotide CAG repeat expansion in the androgen receptor Muscle is heavily impacted in SBMA Spinal bulbar muscular atrophy (SBMA) is rare, genetically defined, neuromuscular disease • X-linked inheritance pattern and caused by a polyglutamine (polyQ)
Slide 30: SBMA is a multisystemic disease with progressive neuromuscular symptoms
SBMA is a multisystemic disease and patients suffer from progressive debilitating neuromuscular symptoms1 SBMA Disease Overview SBMA Natural History and Treatment Options Symptom Onset Life expectancy is modestly Onset typically occurs Diagnosis impacted (brugada / between 35 – 55 years aspiration p
Slide 31: ARV-027 is a potent PROTAC degrader of polyQ-AR
ARV-027 is a potent in vitro and in vivo PROTAC degrader of polyQ-AR, the root cause of SBMA1 ARV-027 induces degradation of polyQ-AR in myotubes derived ARV-027 induces degradation of AR in muscle from SBMA patient induced pluripotent stem cells tissue from male mice 150 150 DC50 (nM) = ~ 0.4 DC50
Slide 32: ARV-027 induced polyQ-AR degradation in muscle and rescued strength
In preclinical models, ARV-027 induced polyQ-AR degradation in muscle tissues and rescued strength and endurance Monomeric polyQ-ARa All Paw Grip Strengtha vehicle ARV-027 kDa Quadriceps AR100Q quadriceps LABC AR100Q levator ani/bulbocavernosus Quadriceps AR100Q LABC Endurance (Distance on Treadmill
Slide 33: First-in-human Phase 1 trial of ARV-027 is enrolling healthy volunteers
A first-in-human Phase 1 clinical trial of ARV-027 is currently enrolling healthy volunteers Status of ARVINAS Trials with ARV-027 OBJECTIVES: Safety, Tolerability, PK, and PD ARV-027 Phase 1 trial SINGLE ASCENDING DOSE MULTIPLE ASCENDING DOSE MULTIPLE ASCENDING DOSE in healthy volunteers in healthy
Slide 34: ARV-806
CLINICAL PROGRAMS: Oncology ARV-806 PROTAC KRAS G12D degrader ARV-806 is an investigational compound. Its safety and effectiveness have not been established.
Slide 35: ARV-806 is a novel PROTAC KRAS G12D degrader
ARV-806 is a novel PROTAC KRAS G12D degrader with the potential to be a best-in-class therapy KRAS is one of the most frequently mutated human oncogenes and G12D is the most common mutation of the KRAS protein. ARV-806 has the potential to address high unmet need in solid tumors, such as pancreatic,
Slide 36: KRAS is a key regulator of cell growth; mutations lead to cancer
KRAS is a key regulator of cell growth, and KRAS mutations lead to cancer Normal Cell Cancer Cell Role of KRAS G12D in Cancer1,2 • KRAS is a GTPase that alternates between inactive Inactive KRAS Inactive KRAS and active states, regulating “OFF” GDP GDP several critical signaling KRAS Mutation pathwa
Slide 37: Metastatic cancers with KRAS G12D mutations have poor survival outcomes
Patients with metastatic cancers harboring KRAS G12D mutations have poor survival outcomes with no approved KRAS G12D-targeted therapy Key Tumors Harboring KRAS 5-year Survival Rate for Newly Diagnosed Patients Prevalence of KRAS G12D G12D Mutations Metastatic Setting1 Per Year in the US (2025)2 Mut
Slide 38: ARV-806 targets both ON and OFF forms of KRAS G12D
ARV-806 targets both ON and OFF forms of KRAS G12D • ARV-806 forms a ternary complex with both OFF (GDP-bound) and ON (GTP-bound) KRAS G12D • Targeting both OFF and ON KRAS G12D allows ARV-806 to eliminate this oncogenic protein from the cell • ARV-806 treatment directly leads to ubiquitination of K
Slide 39: ARV-806 is a potent, selective degrader of KRAS G12D
Preclinical data show ARV-806 is a highly potent, selective degrader of KRAS G12D ARV-806 degrades KRAS G12D with picomolar potency ARV-806 is selective for KRAS G12D Degradation of RAS Measured Degradation of KRAS G12D in GP2d Degradation of KRAS G12D by HiBit Signal3 Colorectal Cancer Cells Multip
Slide 40: ARV-806 anti-proliferative activity 25 times greater than KRAS inhibitors
Preclinically, ARV-806 demonstrates anti-proliferative activity 25 times greater than KRAS inhibitors and the leading clinical-stage degrader Proliferation KRAS G12D Levels ARV-806 >25-fold more potent than all G12D-targeting competitors ARV-806 >40-fold more potent KRAS G12D Levels AsPC-1 Pancreati
Slide 41: ARV-806 more potently induces pancreatic cancer cell death in vitro
ARV-806 more potently induces pancreatic cancer cell death in vitro relative to clinical-stage inhibitors and degrader ARV-806 more potently increases apoptosis (cell death) BIM Levels AsPC-1 Pancreatic Cancer Cells 600 ARV-806 (normalized to DMSO) KRAS G12D ON inhibitor 400 KRAS G12D OFF inhibitor
Slide 42: ARV-806 leads to robust degradation and signaling suppression in vivo
ARV-806 leads to robust and extended degradation and signaling suppression in vivo Proliferative marker (c-MYC) suppressed and pro-apoptotic KRAS G12D reduced >90% for 7 daysa marker (BIM) increased for 5 daysa % KRAS G12D ARV-806 concentration c-MYC BIM 150 10000 150 250 [ARV-806] (ng/g tissue) (no
Slide 43: ARV-806 robust responses in colorectal, pancreatic and lung cancer models
ARV-806 demonstrated robust responses at low doses in models of colorectal, pancreatic, and non-small cell lung cancers Pancreatic Cancer SW1990 KRAS G12D Xenograft Model ≥30% tumor volume reductions in 1000 800 Vehicle pancreatic and colorectal CDX models and a % change from baseline ARV-806 (3 mg/
Slide 44: Phase 1/2 trial of ARV-806 in KRAS G12D tumors is enrolling
A Phase 1/2 clinical trial of ARV-806 in KRAS G12D- mutated advanced solid tumors is currently enrolling Phase 1 dose escalation (part A, Phase 2 expansion and dose ARV-806 is being enrollment complete) optimization (part B) evaluated in an open- label, first-in-human Adults with KRAS G12D Phase 1/2
Slide 45: ARV-393
CLINICAL PROGRAMS: Hematology-Oncology ARV-393 PROTAC BCL6 degrader ARV-393 is an investigational compound. Its safety and effectiveness have not been established.
Slide 46: BCL6 degrader could address unmet needs in non-Hodgkin lymphoma
A PROTAC BCL6 degrader has the potential to address substantial unmet needs for patients with non-Hodgkin lymphoma (NHL) • Although a high proportion of patients achieve complete Large B-Cell remission, therapy resistance or relapse still occurs in 30–40% of Lymphoma patients, thus evidencing a need
Slide 47: Uncontrolled activation of BCL6 is implicated in B-cell lymphomas
Uncontrolled activation of BCL6 is implicated in development of B-cell lymphomas Healthy B-cells The Importance of BCL6 BCL6 “On” Normal B-cell in Lymphoma maturation Antigen Memory B-cells • Master Regulator – BCL6 represses genes that BCL6 “OFF” Plasma cells control cell proliferation, Naïve Antig
Slide 48: ARV-393 is an oral PROTAC degrader of BCL6
ARV-393 is an investigational oral PROTAC degrader that degrades BCL6, a classic “undruggable” protein Potent, orally bioavailable PROTAC small molecule degrader of BCL61 ARV-393 Degrades BCL6, a target that has long been considered “undruggable” Differentiated preclinical profile. ARV-393 potently
Slide 49: ARV-393 potently degrades BCL6 in human lymphoma cell lines
ARV-393 potently degrades BCL6 in human lymphoma cell lines ARV-393, but not its E3-inactive analogue, robustly degrades BCL6 ARV-393 exhibits picomolar degradation potency in quantitative in the OCI-Ly1 model of DLBCL immunocapture assay in multiple DLBCL cell lines 140 BCL6 levels (% DMSO) 120 100
Slide 50: ARV-393 rapidly degrades BCL6 and overcomes its high resynthesis rate
Preclinically, ARV-393 rapidly degrades BCL6 and overcomes its high resynthesis rate that drives tumor cell growth BCL6 protein is resynthesized rapidly – nearly back to baseline ARV-393 rapidly degrades >90% of BCL6 within 2 hours - levels at 2 hours post-ARV-393 washout degrading BCL6 faster than
Slide 51: ARV-393 induces tumor growth inhibition and regressions in vivo
ARV-393 induces dose-dependent and sustained tumor growth inhibition and regressions in vivo ARV-393 induces dose-dependent and sustained ARV-393 demonstrated >90% TGI TGI in OCI-Ly1 DLBCL CDX model 2200 PO QDx23 %TGI Daily dosing halted 2000 Vehicle 2000 PO QDx28 Day 26 ARV-393 3 mg/kg 1800 1800 Ve
Slide 52: BCL6 degradation increases expression of genes it represses
Preclinically, BCL6 degradation by ARV-393 drives antitumor activity by increasing gene expression normally repressed by BCL6 Signal Transduction B-cell Differentiation Cell cycle • BCL6 Repression – PTPN6 (SHP1) IRF4 CDKN1B (p27) BCL6 is a transcriptional repressor and 2000 **** expression of PTPN6
Slide 53: ARV-393 induces tumor growth inhibition in PDX models of NHL subtypes
Single agent ARV-393 induces tumor growth inhibition in PDX models of various non-Hodgkin lymphoma subtypes Breadth of efficacy beyond DLBCL demonstrated in multiple patient-derived xenograft (PDX) models with no body weight lossa ABC MCD* DLBCL 1500 tFL LY9605 Burkitt 4500 Double Hit (BCL6/MYC) 4 5
Slide 54: Preclinical efficacy of ARV-393 in a patient-derived T-cell lymphoma model
First preclinical evidence of efficacy with a BCL6-targeted degrader in a patient-derived model of a rare T-cell lymphoma with a high unmet need ARV-393 demonstrates evidence of significant efficacy (comparable to SOC romidepsin) in a chemo (CHOP) relapsed AITL PDX model Peripheral Blood Bone Marrow
Slide 55: ARV-393 potential combination partner for NHL treatment options
ARV-393 has the potential to be an attractive combination partner for development of novel treatment options for non-Hodgkin lymphoma CHEMOTHERAPY-FREE AND IMPROVED CHEMOTHERAPY-FREE CHEMOTHERAPY OPTIONS AND ALL ORAL OPTIONS • Standard of Care Chemotherapy • R-CHOP ARV-393 Small molecule inhibitors
Slide 56: ARV-393 combination with chemotherapy and biologics drives tumor regressions
ARV-393 demonstrates activity in combination with SOC chemotherapy/ biologics and drives tumor regressions, including complete responses, in a preclinical model of aggressive DLBCL R-CHOP Rituximab Tafasitamab Polatuzumab vedotin 2200 2200 2200 2200 Vehicle PO, QDx28 Vehicle PO, QD x 28 Vehicle PO,
Slide 57: ARV-393 combination with small molecule inhibitors drives tumor regressions
ARV-393 demonstrates activity in combination with small molecule inhibitors and drives tumor regressions, including complete responses, in a preclinical model of aggressive DLBCL Venetoclax Tazemetostat Acalabrutinib 2400 Vehicle PO, QDx22 2000 Vehicle PO, QDx22 2200 1000 ARV-393 3 mg/kg, PO, QDx22
Slide 58: ARV-393 with glofitamab as a chemotherapy-free combination in DLBCL
Preclinical data support ARV-393 in combination with glofitamab as a chemotherapy-free combination approach in DLBCL* Change in tumor volume at endpoint (day 34) 2000 IgG 0.15 mg/kg IV QWx5 + vehicle PO QDx33 ARV-393 6 mg/kg PO QDx33 + IgG Glofitamab 0.15 mg/kg IV QWx5 + vehicle 1500 ARV-393 + glofi
Slide 59: Phase 1 trial of ARV-393 in relapsed/refractory NHL is enrolling
Arvinas is currently enrolling a Phase 1 clinical trial of ARV-393 in relapsed/refractory non-Hodgkin lymphoma • ARV-393 is being evaluated in an open- 28-day treatment cycles label, first-in-human Previously treated Phase 1 dose escalation Dose escalation of ARV-393 orally study to assess its safet
Slide 60: Vepdegestrant (ARV-471)
CLINICAL PROGRAMS: Oncology Vepdegestrant (ARV-471) Investigational PROTAC estrogen receptor degrader Vepdegestrant is an investigational compound. Its safety and effectiveness have not been established.
Slide 61: Unmet need in ER+/HER2- metastatic breast cancer
Unmet need in ER+/HER2- metastatic breast cancer ER+/HER2- breast cancer accounts for approximately 70% ER pathway mediates First-line treatments for ER+/HER2- No clear standard of the transcription of advanced or metastatic breast care in the second- genes that promote cancer are typically endocrin
Slide 62: Vepdegestrant: Potential first PROTAC estrogen receptor degrader
VEPDEGESTRANT: Potential • Vepdegestrant is the first PROTAC to be evaluated in a Phase 3 pivotal first PROTAC study, VERITAC-2 estrogen receptor • VERITAC-2 data presented at ASCO 2025, and simultaneously published in the New England Journal of Medicine, showed: degrader • Vepdegestrant was well to
Slide 63: Vepdegestrant potential best-in-class in 2L+ ESR1 mutant setting
Vepdegestrant has the potential to be best-in-class treatment in the 2L+, ESR1 mutant setting If approved, vepdegestrant has the potential to be: BEST-IN-CLASS TREATMENT without tradeoffs between efficacy, tolerability, and patient reported outcomes EFFICACY MEASURES TOLERABILITY REAL-WORLD APPLICAB
Slide 64: VERITAC-2: Global Phase 3 clinical trial of vepdegestrant
VERITAC-2: Global Phase 3 clinical trial of vepdegestrant 28-day Treatment Cycles Key Eligibility Criteria Primary Endpoints: • Age ≥18 years old • ER+/HER2- advanced or metastatic breast Vepdegestrant (n=313) • PFS by BICR in ‒ ESR1m population Randomization (1:1) cancer 200 mg orally (once daily)
Slide 65: Baseline characteristics of the VERITAC-2 population
Baseline characteristics of the VERITAC-2 population representative of the real-world second-line setting in the U.S. Patients With ESR1m All Patients Patients With ESR1m All Patients Vepdegestrant Fulvestrant Vepdegestrant Fulvestrant Vepdegestrant Fulvestrant Vepdegestrant Fulvestrant Characterist
Slide 66: Vepdegestrant met primary endpoint with ~3-month mPFS improvement
Vepdegestrant met the primary endpoint with a ~3-month mPFS improvement in patients with tumors harboring ESR1 mutations 100 Vepdegestrant Fulvestrant Vepdegestrant n=136 n=134 90 Fulvestrant Median follow-up, months 7.4 6.0 80 Events, n (%) 79 (58) 95 (71) 70 Median PFS by BICR, months 5.0 2.1 6-
Slide 67: Statistically significant improvements in CBR and ORR in ESR1 mutant population
Vepdegestrant showed statistically significant improvements in CBR and ORR in the ESR1 mutant population Patients With ESR1m CBRa ORRb 80 70 Odds ratio: 2.88 (95% CI: 1.57–5.39) 60 P<0.001c 42.1 50 % ± 95% CI Odds ratio: 5.45 40 (95% CI: 1.69–22.73) P=0.001c 30 20.2 18.6 20 4.0 10 0 Vepdegestrant Fu
Slide 68: Vepdegestrant generally well-tolerated with low discontinuation rates
Vepdegestrant was generally well-tolerated, with low rates of discontinuation and dose reductions; majority of TRAEs Gr 1/2 Overview TEAEs in >10% of Patients in Either Group Vepdegestrant Fulvestrant Vepdegestrant Fulvestrant TEAEs, % (n=312) (n=307) (n = 312) (n = 307) Any grade 87 81 TEAE, % Any
Slide 69: Reduced risk of definitive deterioration in overall health status
Vepdegestrant significantly reduced risk of clinically meaningful definitive deterioration in measures of overall health status compared to fulvestrant in patients with ESR1 mutations VERITAC-2: Patient Reported Outcomes in patients with ESR1 mutations TTDD in EORTC QLQ-C30 TTDD in EQ-5D-5L VAS 100
Slide 70: Lower risk of clinically meaningful deterioration in pain
The risk of clinically meaningful deterioration in pain was significantly lower with vepdegestrant compared to fulvestrant across all pain measures evaluated in patients with ESR1 mutations VERITAC-2: Patient Reported Outcomes in patients with ESR1 mutations Vepdegestrant (n = 127) Fulvestrant (n=12
Slide 71: Vepdegestrant potential best-in-class treatment in ESR1 mutant breast cancer
Vepdegestrant has potential to be a best-in-class treatment in ESR1 mutant ER+/HER2- advanced or metastatic breast cancer Novel treatment options are needed for the ~20k patientsa in the US with ESR1-mutated ER+/HER2- advanced or metastatic breast cancer in the 2L+ setting In VERITAC-2, vepdegestran
Slide 72: Positive VERITAC-2 results support potential registration
Positive results from VERITAC-2 Phase 3 clinical trial support a potential registration Potential to address high unmet need for patients with tumors harboring an ESR1 mutation in 2L+ setting Vepdegestrant showed a clinically meaningful median PFS benefit over fulvestrant, a current standard of care
Slide 73: Multiple upcoming value-driving milestones
Arvinas is a leader in developing PROTAC degraders with potential best-in- class profiles, with multiple upcoming value-driving milestones PROTAC degraders designed to provide advantages over other modalities in oncology and neurology 2H 2025 Anticipated Milestones 1H 2026 Anticipated Milestones 2H
Slide 74: For more information
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