OUR SCIENCE
OUR SCIENCE
Arvinas’ PROTAC Discovery Engine
Forging New Frontiers in Drug Discovery
From the founding of Arvinas in 2013 to the first PROTAC pivotal trial, we have firmly established ourselves as a leader in induced proximity research.
We focus on developing treatments for diseases with high unmet medical need across oncology and neurology, selecting targets based on patient genetics and their role as central drivers of disease pathways.
Our PROTAC Discovery Engine has led to the development and approval of the first FDA approved PROTAC therapy, a type of heterobifunctional protein degrader therapy, as well as a robust pipeline, driving some of the most significant breakthroughs in targeted protein degradation within the industry:
- Orally bioavailable degraders
- Degraders that penetrated the blood-brain barrier
- First-in-human safety data
- First-in-human pharmacokinetic and pharmacodynamic data
- First-in-human efficacy data
- First FDA-approved PROTAC, a type of heterobifunctional protein degrader therapy
Our focus on execution has put seven PROTAC degraders into clinical trials as of early 2026 – with more on the way.
While proud of our accomplishments, we do not rest on them. The PROTAC Discovery Engine undergoes tireless improvement and refinement to better meet tomorrow’s challenges.
Arvinas’ PROTAC Discovery Engine – A Clinically Proven Approach
Our PROTAC Discovery Engine is an interlocking suite of tools and expertise that assists with our goal of creating and advancing clinical-stage programs with the potential to help patients. Click below to learn more.
Human biology anchors target selection
Deep E3 ligase expertise
High-throughput, scalable, multi-model oral/BBB optimized chemistry
Structural biology
Global proteomics profiling
Artificial intelligence (AI) and ML multiparametric model integration
Ligand ID technologies
Pharmacodynamic (PD) and efficacy models in oncology and neurology with prospective pharmacokinetic (PK)/PD modeling
If you’re inspired, please take a look at the current list of opportunities to join our team.
- Guduru, S.K.R. et al, DNA-Encoded Library (DEL) Selection Identifies a Distinct DDB1 Ligand Binding Site. ACS Med. Chem. Lett. 17, 757-767 (2026).
- Lopez-Arroyo, A. Preclinical Activity of an Orally Bioavailable PROTAC Pan-KRAS Degrader Versus Inhibitors in Mutant KRAS Models (AACR RAS); March 5-8, 2026; Los Angeles, United States.
- Gough, S., The PROTAC Mode of Action Makes Therapeutic Targeting of BCL6 Possible (Keystone Symposium: Proximity Based Biologics and Therapeutics); February 23-26, 2026; Banff, Canada.
- Cacace, A. LRRK2 Degradation in the Brain Reprograms Lysosomal and Neurodegenerative Pathways – discovery to clinical translation (Keystone Symposium: Autophagy: Mechanisms to Therapy); February 2-5, 2026; Keystone, United States.
- Snyder, L.B. et al., Preclinical evaluation of bavdegalutamide (ARV-110), a novel PROteolysis TArgeting chimera androgen receptor degrader. Mol. Cancer Ther. 24, 511-522 (2025).
- Hickey, C.M. et al., Co-opting the E3 ligase KLHDC2 for targeted protein degradation by small molecules. Nat. Struct. Mol. Biol. 31, 311-322 (2024).
- Gough, S.M. et al., Oral estrogen receptor PROTAC vepdegestrant (ARV-471) is highly efficacious as monotherapy and in combination with CDK4/6 or PI3K/mTOR pathway inhibitors in preclinical ER+ breast cancer models. Clin. Cancer Res. 30, 3549-3563 (2024).
- Gregory, J.A., Hickey, C.M., Chavez, J. & Cacace, A.M. New therapies on the horizon: Targeted protein degradation in neuroscience. Cell Chem. Biol. 31, 1688-1698 (2024).
- Kelly, K. Development of Potent, Orally Bioavailable PROTAC LRRK2 Degrader Molecules as Potential Disease Modifying Therapeutics for Neurodegeneration (Biennial International LRRK2 Meeting); June 18-21, 2024; Crete, Greece.
- Sherman, D. The Discovery of ARV-393, a Potent, Orally Bioavailable BCL6-Targeting PROTAC for the Treatment of NHL (AACR Annual Meeting); April 5-10, 2024; San Diego, United States.
- Hornberger, K.R. & Araujo, E.M.V. Physicochemical Property Determinants of Oral Absorption for PROTAC Protein Degraders. J. Med. Chem. 66, 8281-8287 (2023).
- Chirnomas, D., Hornberger, K.R. & Crews, C.M. Protein degraders enter the clinic – a new approach to cancer therapy. Nature Rev. Clin. Oncol. 20, 265-278 (2023).
- Digianantonio, K. Small Molecule PROTAC Hijacking and Structural Characterization of an E3 Ligase, KLHDC2, for Targeted Protein Degradation (CSHL Ubiquitins, Autophagy & Disease); April 25-29, 2023; Cold Spring Harbor, United States.
- Snyder, L.B. Discovery of ARV-766, an Androgen Receptor Degrading PROTAC for the Treatment of Men with Metastatic Castration Resistant Prostate Cancer (AACR Annual Meeting); April 14-19, 2023; Orlando, United States.
- Harbin, A. The Arvinas PROTAC Discovery Engine: PROTAC Biophysical Characterization Fuels The Discovery Of Target And E3 Ligase Ligands For Optimized PROTAC Degrader Molecules (ACS National Meeting); March 26-30, 2023; Indianapolis, United States.
- Smith, K. KRAS-Targeted PROTAC Degraders Are Broadly Efficacious Against KRAS Dependent Tumor Models (AACR Special Conference Targeting RAS); March 5-8, 2023; Philadelphia, United States.
- PROTAC Protein Degraders: Bridging the Divide from Chemical Biology Tools to Clinical Candidates. In Inducing Targeted Protein Degradation, ed. Cromm, P. (Wiley, 2022).
- Wang, J.; Ishchenko, A.; Zhang, W., Razavi, A. & Langley, D. A highly accurate metadynamics Dissociation Free Energy method to calculate protein-protein and protein-ligand binding potencies. Sci. Rep. 12, 2024 (2022).
- Bekes, M., Langley, D.R. & Crews, C.M. PROTAC targeted protein degraders: the past is prologue. Nat. Rev. Drug Discov. 21, 181-200 (2022).