Arvinas, Inc. · NASDAQ:ARVN
Arvinas — Investor Presentation (November 2026)
49 slides from Arvinas's investor presentation, Nov 3, 2026
Slide 1: Corporate Presentation November 2026
© 2026 Arvinas. All rights reserved. N A S D A Q A R V N L I S T E D Corporate Presentation November 2026 Exhibit 99.2
Slide 2: 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") protein degraders having potential benefits tha
Slide 3: Igniting a transformative change in the fight against cancer and neurodegenerative disease
IGNITING A TRANSFORMATIVE CHANGE in the fight for patients with cancer and neurodegenerative diseases
Slide 4: History of firsts with our novel therapeutic modality: PROTAC
PROTAC:, proteolysis targeting chimera a. vepdegestrant, bavdegalutamide, luxdegalutamide (JSB462), ARV-102, ARV-393, ARV-806, ARV-027, ARV-6723 Our experienced and talented team is advancing a new therapeutic modality for patients 4 History of FIRSTS with our novel Clinical trials in oncology Disco
Slide 5: ER and AR degraders highlight ability to develop valuable PROTAC degraders
AR, androgen receptor; ER, estrogen receptor; ESR1, estrogen receptor 1 gene; ER+/HER2-, estrogen receptor-positive/human epidermal growth factor receptor 2-negative; FDA, Food and Drug Administration; mCRC, metastatic castrate resistant prostate cancer; mHSPC, metastatic hormone-sensitive prostate
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 6 COMPLEX FORMATION: Recognizing disease causing protein of interest 1 ITERATIVE ACTIVITY E3 ligase Ubiquitin Proteasome PROTEIN TAGGING: Tagging of target protein for degradation 2 PROTEIN
Slide 7: PROTAC degraders have potential benefits over other modalities
IM, intramuscular; IV, intravenous 1. Global Cancer Observatory: https://gco.iarc.fr/tomorrow/en/dataviz/isotype?years=2040; accessed 10/14/26. 2. Gammon, K. Neurodegenerative disease: Brain windfall. Nature 515, 299–300 (2014). PROTAC degraders have potential benefits that may provide advantages ov
Slide 8: Pipeline of differentiated PROTAC degraders in neurology and oncology
Out-licensed Programs PROGRAM* O N C O L O G Y ARV-393 (BCL6) ARV-6723 (HPK1) N E U R O L O G Y ARV-027 (polyQ-AR) ARV-102 (LRRK2) HV/SBMA HV, PD Arvinas’ pipeline includes differentiated PROTAC degraders in neurology and oncology PRECLINICAL PHASE 1/1B PHASE 2 PHASE 3 APPROVAL 8 AR, androgen recept
Slide 9: Our goal is to change treatment paradigms
Our goal is to change treatment paradigms Immuno-Oncology Engage the power of the immune system to establish new expectations Hematology Target transcriptions factor with an all oral or chemo-free options for patients Neurology Disease modifying therapies in neurology GOALS TO CHANGE T HE TREATME NT
Slide 10: Committed to bringing valuable treatments and creating shareholder value
BCL6, B-cell lymphoma 6; HPK1, hematopoietic progenitor kinase 1; LRRK2, leucine-rich repeat kinase 2; polyQ-AR, polyglutamine androgen receptor *Based on cash, cash equivalents, and marketable securities position as of September 30, 2026 Committed to bringing valuable treatments for patients and cr
Slide 11: ARV-393 PROTAC BCL6 degrader
ARV-393 PROTAC BCL6 degrader CLINICAL PROGRAMS: Hematology-Oncology ARV-393 is an investigational compound. Its safety and effectiveness have not been established.
Slide 12: BCL6 degrader could address unmet needs in non-Hodgkin lymphoma
AITL, angioimmunoblastic T-cell lymphoma; BCL6, B-cell lymphoma 6; FL, Follicular Lymphoma; LBCL, Large B-Cell Lymphoma; NHL, non-Hodgkin lymphoma; nTFHL, nodal T-Follicular Helper Cell Lymphoma; POD24, progression of disease within 24 months of starting initial active treatment. 1. Sehn and Salles
Slide 13: Uncontrolled BCL6 activation is implicated in B-cell lymphomas
• Master Regulator – BCL6 represses genes that control cell proliferation, survival, and apoptosis during B-cell maturation1,2 • Disrupts B-Cell Function – Deregulated BCL6 alters cell signaling and cycle control, preventing proper B-cell differentiation1,3 • Drives Malignant Transformation – Abnorm
Slide 14: ARV-393 is an investigational oral PROTAC BCL6 degrader
BCL6, B cell lymphoma 6; DLBCL, diffuse large b-cell lymphoma; NHL, non-Hodgkin lymphoma; R/R, relapsed/refractory; SOC, standard of care 1. Gough et al., European Hematology Association (EHA) Poster P1256. June 2024, Madrid Spain. 2. Van Acker et al., American A ssociation for Cancer Research (AACR
Slide 15: ARV-393 potently degrades BCL6 in lymphoma cell lines
BCL6, B cell lymphoma 6; DLBCL, diffuse large b-cell lymphoma Gough et al., European Hematology Association (EHA) Poster P1256. June 2024, Madrid Spain. ARV-393 potently degrades BCL6 in human lymphoma cell lines 15 ARV-393, but not its E3-inactive analogue, robustly degrades BCL6 in the OCI-Ly1 mod
Slide 16: ARV-393 rapidly degrades BCL6 and overcomes high resynthesis rate
BCL6, B cell lymphoma 6 Gough et al., European Hematology Association (EHA) Poster P1256. June 2024, Madrid Spain. Preclinically, ARV-393 rapidly degrades BCL6 and overcomes its high resynthesis rate that drives tumor cell growth 16 0.001 0.01 0.1 1 10 0 20 40 60 80 100 120 ARV-393 Log10 [nM] B C L
Slide 17: ARV-393 induces sustained tumor growth inhibition and regressions in vivo
0 5 10 15 20 25 30 35 40 45 50 55 0 200 400 600 800 1000 1200 1400 1600 1800 2000 Day M e a n T u m o r v o l (m m 3 ) Vehicle ARV-393 1 mg/kg ARV-393 3 mg/kg ARV-393 10 mg/kg ARV-393 30 mg/kg PO QDx28 %TGI Day 26 67**** 103**** 92**** Daily dosing halted Off treatment, 30 mg/kg remains in regressio
Slide 18: BCL6 degradation drives antitumor activity by increasing gene expression
Signal Transduction PTPN6 (SHP1) B-cell Differentiation IRF4 Cell cycle CDKN1B (p27) • BCL6 Repression – BCL6 is a transcriptional repressor and expression of PTPN6, IRF4, and CDKN1B are repressed by it • Pathway Activation – Treatment with ARV-393 increased the expression of PTPN6, IRF4, and CDKN1B
Slide 19: ARV-393 induces tumor growth inhibition in PDX models of NHL subtypes
ABC, activated B cell-like; BCL6, B-cell lymphoma 6; DLBCL, diffuse large B-cell lymphoma; GCB, germinal center B cell-like; NHL, non-Hodgkin’s lymphoma; PDX, patient derived xenograft model; tFL, transformed follicular lymphoma; TGI, tumor growth inhibition *molecular classification according to Ly
Slide 20: Preclinical efficacy in a patient-derived rare T-cell lymphoma model
AITL, angioimmunoblastic T-cell lymphoma, also known as nodal T-follicular helper cell lymphoma, angioimmunoblastic-type; BCL6, B cell lymphoma 6; CHOP, Cyclophosphamide, hydroxydaunorubicin, vincristine sulfate, and prednisone; ns, not significant; SOC, standard of care; PDX, patient-derived xenogr
Slide 21: ARV-393 as combination partner for NHL treatment options
DLBCL, diffuse large B-cell lymphoma; R-CHOP, rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine sulfate, and prednisone; SOC, standard of care Acker et al., American Association for Cancer Research (AACR) Poster 1655/15. April 2025, Chicago. ARV-393 has the potential to be an attractive
Slide 22: ARV-393 with SOC chemotherapy/biologics drives tumor regressions
CDX, cell-derived xenograft; DLBCL, diffuse large B-cell lymphoma; IV, Intravenous; PO, oral; QD, once a day; R-CHOP, rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine sulfate, and prednisone; SOC, standard of care a. Rituximab 3 mg/kg was administered intravenously (IV) on days 1, 8, 15
Slide 23: ARV-393 with small molecule inhibitors drives tumor regressions
ABC, activated B-cell; BID, twice a day; CDX, cell-derived xenograft; DLBCL, diffuse large B-cell lymphoma; GCB, germinal center B-cell; IV, Intravenous; PO, oral; QD, once daily. **P<0.01; ***P<0.005; ****P<0.0001 (one-way ANOVA, Tukey’s multiple comparisons) Van Acker et al., American Association
Slide 24: Phase 1 trial of ARV-393 in relapsed/refractory NHL
Sequential assignment Previously treated adult patients with relapsed/refractory mature B-cell NHL or nTFHL-AI • ARV-393 is being evaluated in Phase 1 dose escalation study to assess its safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary antitumor activity as monothe
Slide 25: ARV-027 PROTAC polyQ-AR degrader
ARV-027 PROTAC polyQ-AR degrader CLINICAL PROGRAMS: Neurology ARV-027 is an investigational compound. Its safety and effectiveness have not been established.
Slide 26: SBMA is caused by a CAG repeat expansion in the androgen receptor
SBMA is a genetically-defined disease caused by a trinucleotide CAG repeat expansion in the androgen receptor (polyQ-AR) 26 SBMA Natural History and Treatment OptionsSBMA Disease Overview There are no approved therapies for SBMA in the U.S. • Current treatment focuses on symptom management only, inc
Slide 27: ARV-027 is a potent degrader of polyQ-AR
ARV-027 is a potent in vitro and in vivo PROTAC degrader of polyQ-AR, the root cause of SBMA1 27 -2 -1 0 1 2 3 0 50 100 150 log (ARV-027) nM p o ly Q -A R ( % o f v e h ic le ) DC50 (nM) = ~ 0.4 Dmax = ~ 90% ARV-027 induces degradation of polyQ-AR in myotubes derived from SBMA patient induced plurip
Slide 28: ARV-027 rescued strength and endurance in a preclinical SBMA model
28 In preclinical models, ARV-027 induced polyQ-AR degradation in muscle tissue and rescued strength and endurance in a rapidly progressing model of SBMAa polyQ-AR, polyglutamine-expanded androgen receptor; SBMA, spinal-bulbar muscular atrophy. a. AR100Q SBMA mouse model. Chivet et al. 2020. Gregory
Slide 29: Status of Arvinas trials with ARV-027
Status of Arvinas Trials with ARV-027 AR, androgen receptor; PK; Pharmacokinetics; PD, pharmacodynamics; SBMA; spinal bulbar muscular atrophy A first-in-human Phase 1 clinical trial of ARV-027 is currently enrolling healthy volunteers 29 OBJECTIVES: Safety, Tolerability, PK, and PD ARV-027 Phase 1 t
Slide 30: ARV-6723 PROTAC HPK1 degrader
CLINICAL PROGRAMS: Oncology ARV-6723 PROTAC HPK1 degrader ARV-6723 is an investigational compound. Its safety and effectiveness have not been established.
Slide 31: HPK1 degradation may strengthen the immune response across the cancer-immunity cycle
HPK1 degradation may help strengthen the immune response by acting at multiple points in the cancer-immunity cycle 31 3. Immune cells recognize cancer and activate T cells 4. Immune cells enter the tumor 1. T cell directed killing of cancer cells 2. Cancer cells call the immune system 5. Rewiring of
Slide 32: ARV-6723 is a potent PROTAC degrader of HPK1
ARV-6723 is a potent PROTAC degrader of HPK1, a central regulator of immune suppression 32 Increase immune function (T/dendritic cells) and immune attack (T/NK cells) Counter activation of T cell exhaustion Block suppressive TME (PGE2, Adenosine) Reprogram the TME to unleash immune response Tumor Mi
Slide 33: Single oral dose of ARV-6723 showed sustained target degradation
Single dose of oral ARV-6723 showed profound and sustained target degradation and durable pathway engagement in preclinical models 33 V eh ic le H P K 1 In hi bi to r 75 m pk A R V -6 72 3 10 m pk A R V -6 72 3 30 m pk 0 20 40 60 80 100 % p S L P 7 6 P o s it iv e 48 77 23 numbers indicate % inhibit
Slide 34: ARV-6723 outperforms an investigational HPK1 inhibitor in ICI-resistant models
ARV-6723 outperforms an investigational HPK1 inhibitor in ICI- resistant models Arvinas Confidential and Proprietary 34 0 5 10 15 0 500 1000 1500 2000 2500 LLC1-IFNy Days of treatment T u m o r V o lu m e ( m m 3 ) Vehicle + IgG ARV-6723 (30 mg/kg, QD) + IgG (TGI= 57%) Investigational HPK1i (75 mg/k
Slide 35: HPK1 degrader could work after αPD-1 progression and in combination
Preclinical work suggests that an HPK1 degrader could work after αPD-1 progression, in combination with αPD-1, and ahead of αPD-1 35αPD-1, anti-programmed death-1; HPK1, hematopoietic progenitor kinase 1; IO, immuno-oncology. 1. Van Acker et al. American Association for Cancer Research (AACR) Poster
Slide 36: Phase 1/2 trial of ARV-6723 in advanced solid tumors
Sequential assignment Previously treated adult patients with advanced solid tumors who have received prior immunotherapy ARV-6723 is being evaluated in a Phase 1/2 open-label study to evaluate safety, tolerability, pharmacokinetics, and preliminary anti-tumor activity administered as monotherapy and
Slide 37: ARV-102 PROTAC LRRK2 degrader
ARV-102 PROTAC LRRK2 degrader CLINICAL PROGRAMS: Neurology ARV-102 is an investigational compound. Its safety and effectiveness have not been established.
Slide 38: Unmet need in neurodegenerative diseases is high
38 There are ~60,000 patients in the EU4, US, UK and Japan living with Progressive Supranuclear Palsy (PSP)1, 2. Globally, there are an estimated ~65 million people living with Alzheimer’s, Parkinson’s, and Huntington’s diseases2-4 Unmet need is high: • No approved disease-modifying therapies for mu
Slide 39: PROTAC degraders could potentially revolutionize treatment of brain diseases
Arvinas can engineer PROTAC degraders that: a. In preclinical and clinical studies, dose-dependent increases in exposure in cerebral spinal fluid after single and multiple doses of ARV-102 indicated brain penetration. PROTAC degraders could potentially revolutionize the treatment of neurodegenerativ
Slide 40: LRRK2 is implicated in PSP and Parkinson's disease
Progressive Supranuclear Palsy (PSP) • Rare progressive neurological disease that affects movement, balance, and cognitive function; rapid progression to death within 5-7 years • Characterized by tauopathy (accumulation of abnormal forms of the microtubule-associated protein tau)1 • Preclinical data
Slide 41: LRRK2 degradation may differentiate from kinase inhibition
LRRK2 PROTAC Inhibitor PROTAC-induced LRRK2 degradation has the potential to differentiate from kinase inhibition LRRK2 is a large multidomain scaffolding kinase1-3 LRRK2, leucine-rich repeat kinase 2 1. Rocha EM, et al. Trends Neurosci. 2022;45(3):224-36. 2. Kluss JH, et al. Biochem Soc Trans. 2019
Slide 42: ARV-102 shows 50x greater target engagement versus a LRRK2 inhibitor
LRRK2, Leucine-rich repeat kinase 2 a. G2019S familial Parkinson’s Disease mouse model. Data presented at 2023 Keystone Summit: Autophagy and Neurodegeneration. ARV-102 shows 50x greater target and pathway engagement, with enhanced potency, versus a LRRK2 inhibitor in preclinical model 42 -10 -9 -8
Slide 43: LRRK2 and BMP reductions in patients with Parkinson's disease
• Robust reductions of LRRK2 levels in PBMCs and BMP levels in urine were observed following multiple doses of ARV-102 treatment, with BMP levels returning towards baseline after 2 weeks of follow-up • Peripheral pharmacodynamic biomarker results in participants with Parkinson’s disease were consist
Slide 44: ARV-102 achieved over 50% LRRK2 degradation in CSF of PD patients
• Baseline levels of LRRK2 in CSF were higher in participants with Parkinson’s disease than in healthy volunteers • Median LRRK2 reductions of ~50% or greater were achieved in participants with Parkinson’s disease starting at daily ARV- 102 doses of 20 mg ARV-102 achieved more than ~50% LRRK2 degrad
Slide 45: ARV-102 decreased CSF biomarkers of endolysosomal function
C1QTNF1,complement C1q tumor necrosis factor-related protein 1; CBLN4, cerebellin 4 precursor; CD68, cluster of differentiation 68; CSF, cerebrospinal fluid; CTSH, cathepsin H; ENTPD1, ectonucleoside triphosphate diphosphohydrolase 1; GPNMB, glycoprotein nonmetastatic melanoma protein B; GRN, granul
Slide 46: ARV-102: achieving biomarker advancements previously unreachable
In a Phase 1 trial in patients with Parkinson’s disease, decreases in CSF LRRK2 levels correlated with: • Improvements in pathway measures of endolysosomal, neuroinflammatory, and synaptic function • The magnitude of change in ASH, which is an eye movement abnormality associated with Parkinson’s dis
Slide 47: Development plan for ARV-102 in PSP and Parkinson's disease
Status of Arvinas Trials with ARV-102 AD/PD, International Conference on Alzheimer's and Parkinson's Diseases and related neurological disorders; MDS, Movement Dis orders Society; PK; Pharmacokinetics; PD, pharmacodynamics; PSP, progressive supranuclear palsy *Discussions with health authorities are
Slide 48: Multiple value-driving milestones anticipated ahead
48 The agents listed on this slide are investigational. Their safety and effectiveness for these investigational uses have not been established. BCL6, B-cell lymphoma 6; DLBCL, diffuse large b-cell lymphoma; HPK1, hematopoietic progenitor kinase 1; LRRK2, leucine-rich repeat kinase 2; PD, Parkinson’
Slide 49: For more information
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