Company: ARVN
Filing Date: 2025-02-11
Form Type: 10-K
Source: 0001655759-25-000016
Chunk: 81

Company: ARVINAS, INC.
Filing Date: 2025-02-11
Form: 10-K
Item: Item 1
Chunk 81
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 and present initial data from the ongoing SAD portion of the Phase 1 clinical trial in patients with PD, and initiate the MAD cohort of the Phase 1 clinical trial in patients with PD, in 2025. 

Additional information regarding our preclinical and clinical progress with ARV-102 is included below in "Item 1. Business—Our Clinical Stage Programs—Neuroscience Program: ARV-102".

Pipeline 

In addition to our clinical product candidates, we are expanding our pipeline by utilizing our platform to potentially address historically undruggable targets. Unlike existing small molecule inhibitor therapies, our PROTAC targeted protein degraders can degrade proteins using any available binding site, including low-affinity active binding sites or non-functional binding sites, bringing biological utility to ligands that would otherwise be ineffective. While some gene-based medicines are also seeking to address undruggable targets, we believe that our PROTAC targeted protein degraders confer the advantages of traditional small molecule therapies, such as broad tissue distribution, multiple routes of administration, including oral delivery, a well-established development pathway and relative ease of manufacturing. 

We are further diversifying our pipeline by developing new PROTAC targeted protein degraders against targets for which we believe protein degradation offers advantages to existing therapeutic modalities, including PROTAC degraders that are designed to reach targets in deep brain regions and are capable of being delivered through multiple routes of administration, including oral delivery. We have engineered PROTAC targeted protein degraders that, in preclinical studies, have successfully achieved blood-brain barrier penetration, a key step in developing drugs with the potential to treat neurodegenerative diseases. We believe there are many other indications for which our PROTAC technology may be advantageous.

In the second quarter of 2023, we presented in vivo and in vitro data at the AACR Annual Meeting - Targeting RAS Special Conference that demonstrated that our PROTAC KRAS G12D degraders were potent, selective, and led to tumor stasis in a mouse xenograft model with intermittent dosing and that degradation of KRAS G12D provides an advantage versus inhibition in vitro and in vivo. Our KRAS G12D program is currently in preclinical development and we anticipate filing an IND application for our PROTAC KRAS G12D degrader in 2025.

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Other Programs: Luxdegalutamide (ARV-766) and Bavdegalutamide (ARV-110)

Luxdegalutamide (ARV-766