Slide 1: Corporate Presentation
Corporate Presentation August 2026 NASDAQ L I S T E D ARVN © 2026 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: PROteolysis TAargeting Chimera ("PROTAC") prot
Slide 3: Igniting a transformative change
IGNITING A TRANSFORMATIVE CHANGE in the fight for patients with cancer and neurodegenerative diseases
Slide 4: Experienced team 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: ER and AR degraders highlight ability to develop valuable PROTAC degraders
ER and AR degraders highlight Arvinas’ ability to develop valuable PROTAC degraders ER: VEPPANUa AR: luxdegalutamide • Demonstrated signals of efficacy in late-line FDA approved VEPPANU (vepdegestrant) prostate cancer suggests potential for on May 1, 2026 positive efficacy in earlier-line settings •
Slide 6: PROTAC degraders harness 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 benefits over other modalities in oncology and neurology
PROTAC degraders have potential benefits that may provide advantages over other modalities in oncology and neurology BENEFITS IN BENEFITS OF BENEFITS IN ONCOLOGY Ability to overcome PROTAC PROTEIN DEGRADERS NEUROLOGY Blood-brain barrier evolving resistance Elimination (rather than inhibition)
Slide 8: Pipeline of differentiated PROTAC degraders in neurology and oncology
Arvinas’ pipeline includes differentiated PROTAC degraders in neurology and oncology PROGRAM* INDICATION(S) PRECLINICAL PHASE 1/1B PHASE 2 PHASE 3 APPROVED ARV-102 PSP, Parkinson’s Planned initiation of additional clinical trials in 2027** (LRRK2) Disease Phase 1 in HV/PD ARV-027 Spinal-Bulbar Phase
Slide 9: Committed to bringing valuable treatments and creating shareholder value
Committed to bringing valuable treatments for patients and creating value for shareholders Multiple Phase 1 • Targeting LRRK2 for neurodegeneration, polyQ-AR for spinal and bulbar muscular atrophy, BCL6 for hematological malignancies and HPK1 for solid tumors PROTAC Programs with Near-Term • Deliver
Slide 10: 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 11: Neurodegenerative diseases: an area of tremendous unmet need
Neurodegenerative diseases: An area of tremendous unmet need There are 20,000 – 25,000 Unmet need is high: patients in the U.S. living with • No approved disease-modifying therapies for multiple Progressive Supranuclear Palsy important target proteins (e.g., LRRK2, tau, α-synuclein) (PSP)1. implicat
Slide 12: PROTAC degraders could 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 13: LRRK2 implicated in PSP and Parkinson's disease
LRRK2 is implicated in both in progressive supranuclear palsy and Parkinson’s disease Progressive Supranuclear Palsy (PSP) Parkinson’s Disease (PD) • Rare progressive neurological disease that affects movement, balance, and cognitive • Neurodegenerative disease that affects function movement, balanc
Slide 14: Human genetics and biology rationale for LRRK2 degraders
Human genetics and biology create a strong rationale for differential biology of PROTAC LRRK2 degraders Progressive supranuclear palsy (PSP) is a tauopathy with rapid progression to death within 5-7 years • LRRK2 SNPs and variants are associated with tau pathology resembling PSP1 • LRRK2 genetic var
Slide 15: LRRK2 degradation may differentiate from kinase inhibition
PROTAC-induced LRRK2 degradation has the potential to differentiate from kinase inhibition ARV-102 degrades the entire LRRK LRRK2 is a large multidomain scaffolding kinase1-3 protein and differentiates from inhibitors 1 Protein-protein interaction (scaffolding) GTPase Kinase 2527 LRRK2 PROTAC Inhibi
Slide 16: ARV-102 increases lysosome 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 in patients with PDa; ARV-102 dose- dependently increased degradation efficiency and lysosome number vs kinase inhibitors ARV-102 increases lysosome ARV-102 incre
Slide 17: 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 18: ARV-102 shows 50x greater target and pathway engagement vs inhibitor
ARV-102 shows 50x greater target and pathway engagement, with enhanced potency, 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 19: ARV-102 degrades LRRK2 in NHP deep-brain regions
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 20: LRRK2 biomarkers reduced in non-human primate CSF
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 21: ARV-102 plasma and CSF exposure in Parkinson's patients
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 Day 1: 20 mg Day 1: 40 mg Day 1: 80 mg 10000 20 mg 40
Slide 22: Reductions of LRRK2 in PBMCs and BMP in urine
Robust reductions of LRRK2 levels in PBMCs and BMP levels in urine were observed following multiple doses of ARV-102 treatment PBMC LRRK2 Urine BMP Day 28 Day 28 Time course 300 150 85.4% Placebo 20 mg 40 mg 80 mg 1500 CFB in LRRK2 protein levels (%) 78.1% 1000 100 500 200 50 CFB BMP levels (%) Mean
Slide 23: ARV-102 achieved more than ~50% LRRK2 degradation in the CNS
ARV-102 achieved more than ~50% LRRK2 degradation in the CNS at all dose levels Baseline LRRK2 in CSFa Change in participants with Parkinson’s diseaseb 50 200 Placebo 20 mg 40 mg 80 mg CFB in LRRK2 protein levels (%) LRRK2 in CSF (pg/mL) 40 150 33.9% 30 100 9.7% 20 50 -49.3% -48.3% -61.1% 0 10 -71.5
Slide 24: ARV-102 reduced endolysosomal and neuroinflammatory pathway proteins
ARV-102 reduced endolysosomal and neuroinflammatory pathway proteins that are elevated in LRRK2-related Parkinson’s disease1 • Multi-cohort CSF proteomics analysis identified lysosomal and microglial proteins associated with LRRK2 variants1 that are also reduced with ARV-102 treatment in healthy vol
Slide 25: Consistent reductions across predefined CSF protein panel at 80 mg
ARV-102 at 80 mg QD led to consistent reductions from baseline across the predefined panel of CSF proteins 50 Change in CSF protein levels (day 28) 50 Change in CD68 by dose (day 28) 25 25 0 0 CFB (%) CFB (%) -25 -25 -50 -50 -75 -75 Placebo (n=6) 80 mg (n=6) LRRK2 in CSF (median % CFB) -100 -100 C1Q
Slide 26: ARV-102 development plan in PSP and Parkinson's disease
Development plan for ARV-102 includes clinical trials in patients with progressive supranuclear palsy and Parkinson’s disease Status of Arvinas Trials with ARV-102 OBJECTIVES: Safety, Tolerability, PK, and PD Planned trials in 2027* (pending regulatory feedback) Phase 1: Healthy Volunteers Phase 1:
Slide 27: 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 28: SBMA caused by 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 a rare, genetically defined, neuromuscular disease • X-linked inheritance pattern and caused by a polyglutamine (polyQ
Slide 29: SBMA is a multisystemic disease with progressive 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 30: ARV-027 potent in vitro and in vivo 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 31: ARV-027 degrades polyQ-AR in muscle and rescues 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 32: Phase 1 trial of ARV-027 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 DOSE in healthy MULTIPLE DOSE in patients in healthy volunteers volunte
Slide 33: 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 34: 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 35: BCL6 activation 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 36: ARV-393 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 37: ARV-393 potently degrades BCL6 in 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 38: ARV-393 rapidly degrades BCL6 and overcomes resynthesis
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 39: 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 40: BCL6 degradation increases expression of repressed genes
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 41: ARV-393 induces tumor growth inhibition in PDX models
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 42: Preclinical efficacy in a rare 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 43: ARV-393 as an attractive combination partner in NHL
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 44: ARV-393 with SOC chemotherapy/biologics drives regressions in DLBCL
ARV-393, in combination with SOC chemotherapy/biologics, 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, QD x 28 Vehicle PO, QDx28
Slide 45: ARV-393 with small molecule inhibitors drives regressions in DLBCL
ARV-393, in combination with small molecule inhibitors, 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 Tazemetostat 300 mg/kg,
Slide 46: ARV-393 with glofitamab as chemotherapy-free approach
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 47: Phase 1 trial of ARV-393 in relapsed/refractory NHL
Arvinas is currently enrolling a Phase 1 clinical trial of ARV-393 in relapsed/refractory non-Hodgkin lymphoma • ARV-393 is being 28-day treatment cycles evaluated in an open- Previously treated label, first-in-human Dose escalation of ARV-393 orally Phase 1 dose escalation adult patients with Seque
Slide 48: ARV-6723
CLINICAL PROGRAMS: Oncology ARV-6723 PROTAC HPK1 degrader ARV-6723 is an investigational compound. Its safety and effectiveness have not been established.
Slide 49: ARV-6723 PROTAC degrader of HPK1
ARV-6723 is a potent PROTAC degrader of hematopoietic progenitor kinase 1 (HPK1), a central regulator of immune suppression HPK1 HPK1 degradation destroys both kinase and scaffold- mediated signaling, and may lead to: Biorender Increase immune function (T/dendritic cells) and immune attack (T/NK cel
Slide 50: Single oral dose of ARV-6723 shows sustained target degradation
Single dose of oral ARV-6723 showed profound and sustained target degradation and durable pathway engagement HPK1 Degradation Downstream Pathway Inhibition (pSLP76) Numbers indicate % degradation 100 Numbers indicate % inhibition Vehicle numbers indicate % inhibition 80 23 %pSLP76 Positive HPK1 inhi
Slide 51: ARV-6723 superior TGI vs anti-PD1 or HPK1 inhibitor
ARV-6723 shows superior TGI compared to either anti-PD1 or HPK1 inhibitor in high immunogenic tumor model Single agent ARV-6723 treatment showed superior single agent Combines with anti-PD1 to achieve complete activity to HPK1 inhibitor and anti-PD1 antibody* regressions (CRs)* 2000 Vehicle + Isotyp
Slide 52: ARV-6723 superior to anti-PD-1 plus anti-CTLA-4
Single-agent ARV-6723 demonstrates superior anti-tumor activity in pre-clinical models compared to anti-PD-1 + anti-CTLA-4 Tumor volume HPK1 protein expression, spleen 2500 Vehicle + IgG 6×10 -4 Vehicle + IgG ARV-6723 + IgG (normalized to β-actin and GAPDH) ARV-6723 + IgG Vehicle + anti-PD-1 ARV-672
Slide 53: ARV-6723 outperforms HPK1 inhibitor in ICI-resistant models
ARV-6723 outperforms an investigational HPK1 inhibitor in ICI- resistant models Tumor Growth Efficacy Studies LLC1-IFNy B16F10 KPCY-2699 Vehicle + IgG 2500 2500 Vehicle + IgG 1200 Vehicle + IgG ARV-6723 (30 mg/kg, ARV-6723 (30 mg/kg, QD) + ARV-6723 (30 mg/kg, BID) + IgG (TGI = IgG (TGI = 89%) 1000 2
Slide 54: Planned Phase 1/2 trial of ARV-6723
Planned Phase 1/2 clinical trial of ARV-6723 as monotherapy and in combination with pembrolizumab in advanced solid tumors 21-day treatment cycles ARV-6723 will be evaluated in a Phase 1/2 open-label study Previously treated Dose escalation of oral ARV-6723 daily to evaluate safety, tolerability, ad
Slide 55: Multiple value-driving milestones anticipated ahead
Multiple value-driving milestones anticipated ahead Anticipated milestones: Anticipated milestones: Upcoming milestones: Neurology Neuromuscular Oncology Upcoming milestones:Immuno-oncology ARV-102 ARV-027 ARV-393 ARV-6723 Oral LRRK2 degrader Oral polyQ-AR degrader Oral BCL6 degrader Oral HPK1 degra
Slide 56: For more information
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