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Research and Development

Arvinas scientific staff member preparing vials for testing

Our Pipeline

Our pipeline of proteolysis targeting chimeras, or PROTAC® protein degraders, are designed to harness the body’s own natural protein disposal system to selectively and efficiently degrade and remove disease-causing proteins.

See how Arvinas is deploying our PROTAC® protein degrader technology to target research for people living with devastating diseases.

PROTAC molecule from MOA
Arvinas scientific staff member preparing vials for testing

The agents set forth below are currently under investigation. Their safety and effectiveness for these investigational uses have not yet been established.

Program

Preclinical

Phase 1 / 1B

Phase 2

Phase 3

Oncology / Immuno-oncology Pipeline

Global partners with

ARV-471 is an investigational, oral PROTAC® protein degrader that targets the estrogen receptor (ER), a highly validated driver of ER+ breast cancer. In July 2021, Arvinas and Pfizer Inc. announced a global collaboration to develop and commercialize ARV-471. More information is available here.

ER+/HER2-Breast Cancer

Bavdegalutamide (ARV-110) is an investigational, oral PROTAC® protein degrader that targets the androgen receptor (AR), a highly validated driver of prostate cancer. More information is available here.

mCRPC

ARV-766 is an investigational, oral PROTAC® protein degrader that targets the androgen receptor (AR) and has a different profile than bavdegalutamide (ARV-110).

mCRPC

AR-V7 is a splice variant of the androgen receptor (AR). Our AR-V7-targeting PROTAC® protein degrader is a next-generation AR PROTAC® that would target both AR-V7 and full-length AR.

mCRPC

B-cell lymphoma 6 protein (BCL6) is a transcriptional repressor implicated in B cell lymphomas by facilitating B cell tolerance of rapid proliferation and somatic gene recombination via repressing cell cycle checkpoints, terminal differentiation, apoptosis, and the DNA damage response. PROTAC®-mediated degradation would address the scaffolding function of BCL6.

B-cell Malignancies

Kirsten rat sarcoma (KRAS) has historically been considered a “undruggable” target due to its lack of deep “pockets” and is associated with poor prognosis and resistance to standards of care in several tumor types. Arvinas is developing pan-KRAS mutant and mutant-specific KRAS degraders G12D and G12V.

NSCLC, CRC, Pancreatic

Myelocytomatosis (Myc) proteins are implicated in up to 70% of all human cancers. Targeting Myc indirectly, such as by inhibiting transcription modulators, has not been successful, but PROTAC®-mediated degradation has the potential to directly target and degrade Myc.

Solid Malignancies

Hematopoietic progenitor kinase 1 (HPK1) is a suppressor of T cell activation, and targeting HPK1 can enhance anti-tumor immune responses6 PROTAC®-mediated degradation has the potential to address the proposed scaffolding component of HPK1’s activity.

Solid Malignancies

Neuroscience Pipeline

All Arvinas programs are wholly owned.

Program

Preclinical

Phase 1 / 1B

Phase 2

Phase 3

Tau is a key disease driver in many tauopathies, including Alzheimer’s disease and progressive supranuclear palsy. Our PROTAC® protein degrader targets pathogenic tau without degrading healthy forms of tau. More information is available here.

FTLD-TAU, PSP, AD

The pathologic aggregation of α-synuclein is a key driver in many synucleinopathies, including Parkinson’s disease. Our PROTAC® protein degraders specifically degrade oligomeric forms of α-synuclein, which forms disease-causing aggregates. More information is available here.

MSA, Parkinson’s Disease

Huntington’s disease is caused by a mutation in the huntingtin (HTT) gene. PROTAC® degradation has the potential to allow the selective targeting of mutant HTT protein without impacting wild-type HTT protein.

Huntington’s Disease

Oncology / Immuno-oncology Pipeline

All Arvinas programs, with the exception of ARV-471, are wholly owned.

Program

Global partners with

ARV-471 is an investigational, oral PROTAC® protein degrader that targets the estrogen receptor (ER), a highly validated driver of ER+ breast cancer. In July 2021, Arvinas and Pfizer Inc. announced a global collaboration to develop and commercialize ARV-471. More information is available here.

ER+/HER2-Breast Cancer – PHASE 2

Bavdegalutamide (ARV-110) is an investigational, oral PROTAC® protein degrader that targets the androgen receptor (AR), a highly validated driver of prostate cancer. More information is available here.

mCRPC – PHASE 2

ARV-766 is an investigational, oral PROTAC® protein degrader that targets the androgen receptor (AR) and has a different profile than bavdegalutamide (ARV-110).

mCRPC – PHASE 1/1B

AR-V7 is a splice variant of the androgen receptor (AR). Our AR-V7-targeting PROTAC® protein degrader is a next-generation AR PROTAC® that would target both AR-V7 and full-length AR.

mCRPC – PRECLINICAL

B-cell lymphoma 6 protein (BCL6) is a transcriptional repressor implicated in B cell lymphomas by facilitating B cell tolerance of rapid proliferation and somatic gene recombination via repressing cell cycle checkpoints, terminal differentiation, apoptosis, and the DNA damage response. PROTAC®-mediated degradation would address the scaffolding function of BCL6.

B-cell Malignancies – PRECLINICAL

Kirsten rat sarcoma (KRAS) has historically been considered a “undruggable” target due to its lack of deep “pockets” and is associated with poor prognosis and resistance to standards of care in several tumor types. Arvinas is developing pan-KRAS mutant and mutant-specific KRAS degraders G12D and G12V.

NSCLC, CRC, Pancreatic – PRECLINICAL

Myelocytomatosis (Myc) proteins are implicated in up to 70% of all human cancers. Targeting Myc indirectly, such as by inhibiting transcription modulators, has not been successful, but PROTAC®-mediated degradation has the potential to directly target and degrade Myc.

Solid Malignancies – PRECLINICAL

Hematopoietic progenitor kinase 1 (HPK1) is a suppressor of T cell activation, and targeting HPK1 can enhance anti-tumor immune responses. PROTAC®-mediated degradation has the potential to address the proposed scaffolding component of HPK1’s activity.

Solid Malignancies – PRECLINICAL

Neuroscience Pipeline

All Arvinas programs are wholly owned.

Program

Tau is a key disease driver in many tauopathies, including Alzheimer’s disease and progressive supranuclear palsy. Our PROTAC® protein degrader targets pathogenic tau without degrading healthy forms of tau. More information is available here.

FTLD-TAU, PSP, AD – PRECLINICAL

The pathologic aggregation of α-synuclein is a key driver in many synucleinopathies, including Parkinson’s disease. Our PROTAC® protein degraders specifically degrade oligomeric forms of α-synuclein, which forms disease-causing aggregates. More information is available here.

MSA, Parkinson’s Disease – PRECLINICAL

Huntington’s disease is caused by a mutation in the huntingtin (HTT) gene. PROTAC® degradation has the potential to allow the selective targeting of mutant HTT protein without impacting wild-type HTT protein.

Huntington’s Disease – PRECLINICAL

Smiling female patient touch chest while conversing with medical staff

Clinical Trials

Learn more about participating in one of our clinical trials.
Female patient smiling while female doctor reads chart and touches her shoulder

Rooted in Science. Guided by People.

We are committed to patients, families and caregivers, as we aim to delivery potentially transformative treatments through scientific innovation.
  1. Westaby et al. A New Old Target: Androgen Receptor Signaling and Advanced Prostate Cancer. Annual Review of Pharmacology and Toxicology. 2021 Aug;62:1, 131-153.
  2. Sobhani et al. AR-V7 in Metastatic Prostate Cancer: A Strategy beyond Redemption. Int J Mol Sci. 2021 May 24;22(11):5515
  3. Cardenas et al. The expanding role of the BCL6 oncoprotein as a cancer therapeutic target. Clin Cancer Res. 2017 February 15;23(4): 885-893.
  4. Moore, et al. RAS-targeted therapies: is the undruggable drugged? Nat Rev Drug Discov. August 2021;19(8): 522-552.
  5. Llombart, Mansour. Therapeutic targeting of “undruggable” MYC. EBioMedicine. 2022 Jan;75:103756.
  6. Sawasdikosol, Burakoff. A perspective on HPK1 as a novel immuno-oncology drug target. eLife. 2020 Sept 8;9: e55122
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