Slide 1: Corporate Presentation
Corporate Presentation August 2025 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: our potential receipt of milestone and royalty
Slide 3: Igniting a Transformative Change
IGNITING A TRANSFORMATIVE CHANGE in the fight for patients with cancer and neurodegenerative diseases
Slide 4: Our experienced and talented 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 In the clinic for oncology 6* programs ente
Slide 5: Multiple partnerships reinforce Arvinas' leadership position in PROTAC protein degradation
Multiple partnerships reinforce Arvinas’ leadership position in PROTAC protein degradation • Global co-development and co-commercialization agreement for vepdegestrant, our PROTAC estrogen receptor degrader • Arvinas and Pfizer to split profits 50/50 worldwide • Arvinas to book sales in the US • Glo
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 clear potential benefits over other modalities
PROTAC degraders have clear potential benefits that may provide advantages over other modalities in oncology and neurodegenerative diseases BENEFITS IN BENEFITS OF BENEFITS IN ONCOLOGY PROTAC PROTEIN DEGRADERS NEURODEGENERATION Ability to overcome Elimination (rather than inhibition) Blood-bra
Slide 8: Seeking to address two of the largest areas of significant 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 D E G E N E R AT I O N 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 i
Slide 9: Broad pipeline including the first pivotal trial for PROTAC degraders
Broad pipeline including the first pivotal trial for PROTAC degraders PROGRAM INDICATION PRECLINICAL PHASE 1/1B PHASE 2 PHASE 3 MARKET VERITAC-2 vepdegestrant monotherapy pivotal trial (2L+) Global co/co with Vepdegestrant BREAST CANCER (ARV-471; ER) Phase 1/2 combo trials with palbociclib, atirmoci
Slide 10: Strategically positioned for the next stage of growth
Strategically positioned for the next stage of growth Vepdegestrant Launch • Pursuing 2L+ ESR1 mutant indication with for vepdegestrant as Potential Focuses monotherapy; evaluating future combinations and patient populations Arvinas on Near-Term • Vepdegestrant is an investigational potential first-
Slide 11: Vepdegestrant (ARV-471)
CLINICAL PROGRAMS Vepdegestrant (ARV-471) Investigational PROTAC estrogen receptor degrader Vepdegestrant is an investigational compound. Its safety and effectiveness have not been established.
Slide 12: Breast cancer is the most common cancer in women
Breast cancer is the most common cancer in women IN THE U.S. WORLDWIDE ~317K Among women, breast cancer was the most commonly diagnosed cancer in 2022 with an estimated Estimated new 2.3M new cases comprising 11.6% of all cancer cases2 , cases in 20251 Breast Cancer is the leading 1 in 8 Second lead
Slide 13: 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 14: Vepdegestrant: Potential first PROTAC estrogen receptor degrader
VEPDEGESTRANT: Potential first • The first PROTAC to be evaluated in a Phase 3 pivotal study PROTAC estrogen • Vepdegestrant has a unique mechanism of action: a PROTAC that receptor degrader directly harnesses the ubiquitin-proteasome system to degrade ER • Preclinically, vepdegestrant yielded subst
Slide 15: Vepdegestrant is the first PROTAC degrader to demonstrate clinical benefit in a Phase 3 pivotal trial
Vepdegestrant is the first PROTAC degrader to demonstrate clinical benefit in a Phase 3 pivotal trial PROGRAM INDICATION PRECLINICAL PHASE 1/1B PHASE 2 PHASE 3 MARKET PARTNER VERITAC-2 vepdegestrant monotherapy pivotal trial (2L+) VERITAC vepdegestrant monotherapy dose expansion (2L+) TACTIVE-K vepd
Slide 16: Vepdegestrant has potential to be a 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 17: Phase 3 VERITAC-2 Results
Phase 3 VERITAC-2 Results ARVINAS
Slide 18: 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 19: VERITAC-2: Patient disposition
VERITAC-2: Patient disposition Randomized (1:1) All patients, n=624; ESR1m, n=270 Vepdegestrant Fulvestrant All patients, n=313 All patients, n=311 ESR1m, n=136 ESR1m, n=134 Discontinued treatment Discontinued treatment Treated Treated All patients/ESR1m, n=216/90 All patients, n=312 All patients, n
Slide 20: 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 21: Vepdegestrant met the primary endpoint in patients with ESR1 mutations
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 22: Vepdegestrant did not meet the primary endpoint in the ITT population
Vepdegestrant did not meet the primary endpoint in the ITT population 100 Vepdegestrant Fulvestrant Vepdegestrant n=313 n=311 90 Fulvestrant Median follow-up, months 7.4 7.2 80 Events, n (%) 186 (59) 198 (64) 70 Median PFS by BICR, months 3.7 3.6 (95% CI) (3.6–5.3) (2.2–3.8) 60 Stratified HR (95%
Slide 23: Statistically significant improvements in CBR and ORR in the ESR1 mutant population
Vepdegestrant showed statistically significant improvements in CBR and ORR in the ESR1 mutant populationc Patients With ESR1m All Patients CBRa ORRb CBRa ORRb 80 80 70 Odds ratio: 2.88 70 (95% CI: 1.57–5.39) 60 60 Odds ratio: 1.29 P<0.001c 42.1 (95% CI: 0.89–1.91) 50 50 P=0.16c Odds ratio: 5.45 % ±
Slide 24: Consistent PFS benefit across pre-specified subgroups in the ESR1m population
Consistent PFS benefit across pre-specified prognostic characteristics/ baseline disease demographics in the ESR1m populationa Events/n Subgroup Vepdegestrant Fulvestrant HR (95% CI) All patients (stratified) 79/136 95/134 0.57 (0.42–0.77) Age, years <65 50/86 66/88 0.51 (0.35–0.74) ≥65 29/50 29/46
Slide 25: Vepdegestrant was generally well-tolerated with low rates of discontinuation
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 26: High unmet need remains for improved treatment options in 2L+, ESR1 mutant setting
High unmet need remains for improved treatment options for patients in 2L+, ESR1 mutant setting Current treatment landscape in 2L+, ESR1 mutant mBC ~20K patients treated each year in the U.S. EFFICACY MEASURES TOLERABILITY REAL-WORLD APPLICABILITY • HCPs seeking additional benefits • GI-related even
Slide 27: Vepdegestrant has the potential to be best-in-class in the 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 28: 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 29: ARV-102
CLINICAL PROGRAMS ARV-102 PROTAC LRRK2 degrader ARV-102 is an investigational compound. Its safety and effectiveness have not been established.
Slide 30: Neurodegenerative diseases: An area of tremendous unmet need
Neurodegenerative diseases: An area of tremendous unmet need ~8 Unmet need is high: • No approved disease-modifying therapies for multiple million important target proteins (e.g., LRRK2, tau, α-synuclein) implicated in the pathology of various neurodegenerative diseases4 • Blood-brain barrier penetr
Slide 31: PROTAC degraders could potentially revolutionize the 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 32: LRRK2 in Parkinson's disease and Progressive Supranuclear Palsy
LRRK2 in Parkinson’s disease and Progressive Supranuclear Palsy Parkinson’s disease (PD) Progressive Supranuclear Palsy (PSP) • Neurodegenerative disorder that • Rare progressive neurological disorder that affects movement, balance, and affects movement, balance, and cognitive coordination function
Slide 33: LRRK2 is important for lysosome function, and altered LRRK2 leads to multiple pathologies
Leucine-rich repeat kinase-2 (LRRK2) is important for lysosome function, and altered LRRK2 leads to multiple pathologies LRRK2 is required for healthy structure and function Mutated or over-expressed LRRK2 leads of intracellular lysosomes1,2 to multiple pathologies • LRRK2 is a multi-domain scaffold
Slide 34: PROTAC-induced LRRK2 degradation has the potential to differentiate from kinase inhibition
PROTAC-induced LRRK2 degradation has the potential to differentiate from kinase inhibition A PROTAC LRRK2 degrader has multiple opportunities Degrading the complete LRRK2 protein (rather than inhibiting to differentiate from other therapeutic modalities kinase activity) may impact multiple pathways
Slide 35: PROTAC LRRK2 degrader shows better target engagement versus a LRRK2 inhibitor in mice
PROTAC LRRK2 degrader shows better target engagement, enhanced potency and pathway engagement versus a LRRK2 inhibitor in G2019S KI mice Iterative and catalytic PROTAC advantage results in stronger LRRK2 and RAB pathway engagement versus a LRRK2 kinase inhibitora LRRK2 Target Engagement RAB Pathway
Slide 36: In human microglia, ARV-102 degrades wild type and G2019S LRRK2
In human microglia, ARV-102 degrades wild type and G2019S LRRK2, a kinase activating mutation linked to increased Parkinson’s disease risk ARV-102 Potently Degrades LRRK2 in a Human Patient Model of Parkinson’s Disease • LRRK2 is 2X overexpressed in iPD microglia LRRK2 Degradation in G2019S iPSC-Mic
Slide 37: ARV-102 degrades wild type and G2019S LRRK2 and engages the lysosomal pathway in PBMCs
PROTAC LRRK2 degrader ARV-102 degrades wild type and G2019S LRRK2 and engages the lysosomal pathway in PBMCs LRRK2 PROTAC, but not a LRRK2 inhibitor, PROTAC LRRK2 degraders induce induces reduction of pathologic AT8-tau in vitro pathologic tau protein reduction in vivo Reduction of pathologic (AT8)
Slide 38: ARV-102 degrades LRRK2 and engages the lysosomal pathway in PBMCs
PROTAC LRRK2 degrader ARV-102 degrades wild type and G2019S LRRK2 and engages the lysosomal pathway in PBMCs PROTAC-induced LRRK2 degradation aligns with effects on target and pathway engagement in human PBMCs PROTAC Target Engagement Lysosome Pathway Engagement (shown by LRRK2 Degradation) (shown b
Slide 39: ARV-102 crosses the blood brain barrier and degrades deep brain regions in non-human primates
ARV-102 readily crosses the blood brain barrier and degrades multiple deep brain regions in non-human primates ARV-102 achieves >83% LRRK2 degradation in deep brain regions after oral dosing Striatum 200 94% 92% 83% decrease decrease decrease 150 Cortex LRRK2 Protein (% of Vehicle) Striatum 100 Cere
Slide 40: Equivalent PK/PD supports measuring CSF LRRK2 as a surrogate for brain LRRK2
Equivalent PK/PD supports the utility of measuring CSF LRRK2 as a surrogate for monitoring LRRK2 reductions in the brain PK/PD of LRRK2 are reduced in both cortex and CSF following oral dosing in NHP LRRK2 (% Vehicle) Plasma-free ARV-102 (M) Data as presented at the Michael J. Fox Foundation Confere
Slide 41: ARV-102 increases lysosome functional degradative capacity and number in vitro
ARV-102 increases lysosome functional degradative capacity and number in vitro ARV-102 increases lysosome ARV-102 increases lysosome • Mutant familial PD and degradation in A549 cells number in A549 cells increased LRRK2 expression “puts the 125 125 LRRK2 PROTAC ARV-102 LRRK2 Inhibitor MLi2 brakes”
Slide 42: PROTAC LRRK2 degraders induce reduction of downstream pathologic tau
PROTAC LRRK2 degraders induce reduction of downstream pathologic tau in vitro and in vivo LRRK2 PROTAC, but not a LRRK2 inhibitor, PROTAC LRRK2 degraders induce induces reduction of pathologic AT8-tau in vitro pathologic tau protein reduction in vivo Reduction of pathologic (AT8) Tau induced by LRRK
Slide 43: Oral ARV-102 crosses the blood-brain barrier and reduces CSF LRRK2 levels in NHPs
Oral ARV-102 Crosses the Blood-Brain Barrier and Reduces CSF LRRK2 levels in NHPs PK/PD of LRRK2 are reduced in cortex and CSF CSF LRRK2 levels are reduced in ported NHP study following following oral dosing in NHP ARV-102, 10 mg/kg oral single daily dose 200 NHP 1 1 Cyno NHP 2 2 Cyno 150 NHP 3 3 Cy
Slide 44: A single dose of ARV-102 induced reductions in CSF pathway biomarkers in NHPs
A single dose of ARV-102 induced unprecedented reductions in CSF pathway biomarkers in NHPs IBA1: A marker of pathologic Cathepsin B: A lysosomal hydrolase neuroinflammation implicated in PD 150 • ARV-102 is dosed orally, Cyno 1 crosses the blood-brain Cyno 2 Cyno 3 barrier, and degrades LRRK2 % Bas
Slide 45: ARV-102 is being evaluated in a Phase 1 clinical trial
ARV-102 is currently being evaluated in a Phase 1 clinical trial in patients with Parkinson's disease Study ARV-102-103 patients with Study ARV-102-101 HEALTHY VOLUNTEERS PARKINSON’S DISEASE OBJECTIVES: Safety, tolerability, PK, and PD of ARV-102 SINGLE ASCENDING DOSE MULTIPLE ASCENDING DOSE SINGLE
Slide 46: Dose-dependent ARV-102 exposure and LRRK2 reductions in CSF indicate brain penetration
Dose-dependent increases in ARV-102 exposure and substantial LRRK2 reductions in CSF indicate brain penetration 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-102 in CSF Change in CSF L
Slide 47: ARV-393
CLINICAL PROGRAMS ARV-393 PROTAC BCL6 degrader ARV-393 is an investigational compound. Its safety and effectiveness have not been established.
Slide 48: A PROTAC 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 49: Multiple subsets of NHL include potentially BCL6-dependent disease
Multiple subsets of NHL include potentially BCL6-dependent disease Incidence of Non-Hodgkin Lymphoma in the U.S. (~80-85,0001, 100%) B-cell Lymphoma (85 - 90%) T- and NK-cell Lymphoma Aggressive Non-Hodgkin B-Cell Lymphoma Indolent Non-Hodgkin B-Cell (10 - 15%) (~50%) Lymphoma (~40%) nTFHL-AI Large
Slide 50: Uncontrolled activation of BCL6 is implicated in development of 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 51: ARV-393 is an investigational 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 52: 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 53: ARV-393 rapidly degrades BCL6 and overcomes its high resynthesis rate
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 the cell can re
Slide 54: Oral ARV-393 induces dose-dependent tumor growth inhibition and regressions in vivo
Oral ARV-393 induces dose-dependent and sustained tumor growth inhibition (TGI) and regressions in vivo ARV-393 induces dose-dependent and sustained BCL6 degradation >90% is required for optimal TGI (>100%) TGI in OCI-Ly1 DLBCL CDX model 2200 PO QDx23 %TGI 2000 Vehicle Daily dosing halted **** 2000
Slide 55: BCL6 degradation drives antitumor activity by increasing expression of repressed genes
BCL6 degradation by ARV-393 drives antitumor activity by increasing expression of genes 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, IRF4, and
Slide 56: Single agent ARV-393 induces tumor growth inhibition in PDX models of NHL
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 57: First preclinical evidence of efficacious BCL6 degrader in a rare T-cell lymphoma model
First preclinical evidence of an efficacious BCL6-targeted degrader in a patient-derived model of a rare T-cell lymphoma with a high unmet need ARV-393 demonstrates significant efficacy (comparable to SOC romidepsin) in a chemo (CHOP) relapsed AITL PDX model Peripheral Blood Bone Marrow Spleen ✱✱ ✱✱
Slide 58: ARV-393 has potential to be an attractive combination partner for 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 59: ARV-393 activity in combination with SOC chemotherapy and biologics
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 60: ARV-393 activity in combination with small molecule inhibitors
ARV-393 demonstrates activity in combination with small molecule inhibitors and drives tumor regressions, including complete responses, in preclinical models of aggressive DLBCL Venetoclax Tazemetostat Acalabrutinib 2400 Vehicle PO, QDx22 2000 Vehicle PO, QDx22 2200 1000 ARV-393 3 mg/kg, PO, QDx22 T
Slide 61: Phase 1 clinical 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 evaluated in an open- label, first-in-human Phase 1 dose escalation study to assess its safety, tolerability, 28-day treatment cycles Previously treated pharmacokinetics
Slide 62: ARV-806
CLINICAL PROGRAMS ARV-806 PROTAC KRAS G12D degrader ARV-806 is an investigational compound. Its safety and effectiveness have not been established.
Slide 63: 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 is commonly altered in pancreatic, colorectal, and lung cancers, among others; G12D is the most common mutation of the KRAS protein KRAS G12D A
Slide 64: KRAS is a key regulator of cell growth, and KRAS 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 • KRAS is a GTPase that alternates between inactive Inactive KRAS Inactive KRAS and active states, regulating “OFF” GDP GDP several critical signaling KRAS Mutation pathways
Slide 65: Metastatic cancers harboring 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 Prevalence of KRAS G12D Newly Diagnosed Patients G12D Mutations Metastatic Setting Mutations Per Year in the US (2
Slide 66: PROTAC KRAS G12D degrader shows greater potency than an inhibitor in vitro
Versus an inhibitor, a PROTAC KRAS G12D degrader demonstrated greater potency at inducing cell death and blocking cell proliferation in vitro Induction of cell death Cell proliferation block Arvinas’ PROTAC KRAS G12D degrader demonstrated greater potency Arvinas’ PROTAC KRAS G12D degrader demonstrat
Slide 67: Extended PD of a KRAS G12D degrader may allow intermittent dosing
Extended PD of a PROTAC KRAS G12D degrader may allow for intermittent dosing, which may improve tolerability and facilitate combination treatments GP2d Xenograft Model Panc04.03 Xenograft Model of Colorectal Cancer of Pancreatic Cancer • Arvinas’ PROTAC KRAS GP2d Colorectal Cancer Xenograft Panc04.0
Slide 68: Phase 1/2 clinical trial of ARV-806 in KRAS G12D-mutated solid tumors
A Phase 1/2 clinical trial of ARV-806 in KRAS G12D- mutated advanced solid tumors is currently enrolling ARV-806 is being evaluated in an open- Phase 2 Expansion label, first-in-human Phase 1 Dose escalation and dose optimization Phase 1/2 clinical trial to assess its safety, Adults with previously
Slide 69: Transforming Tomorrow with Major Milestones
TRANSFORMING TOMORROW WITH MAJOR MILESTONES PROTAC degraders designed to provide advantages over other modalities in oncology and neurodegenerative diseases Leaders in PROTAC Degraders with Potential Best-in-Class Pipeline and Research Engine 2H 2025 anticipated milestones 1H 2026 anticipated milest
Slide 70: For More Information
FOR MORE INFORMATION Press/Media | pr@arvinas.com Investors | ir@arvinas.com Business Development | bd@arvinas.com Careers | careers@arvinas.com NASDAQ L I S T E D ARVN © 2025 Arvinas. All rights reserved.