Company: ARVN
Filing Date: 2025-10-24
Form Type: 8-K
Source: 0001628280-25-046259
Chunk: 1

Company: ARVINAS, INC.
Filing Date: 2025-10-24
Form: 8-K
Item: Item 8.01
Chunk 1
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Item 8.01 Other Events.

On October 24, 2025, the Company issued a press release announcing preclinical data for ARV-806, a PROTAC KRAS G12D degrader. These data were presented at the 2025 Triple Meeting in Boston, Massachusetts. ARV-806 is designed to target both the ON and OFF forms of KRAS G12D, which is the most common mutation of the KRAS protein. ARV-806 has the potential to address high unmet need in solid tumors, such as pancreatic, colorectal and non-small cell lung cancer.

Key highlights from the presentation at the 2025 Triple Meeting include the following:

• In vitro, ARV-806 degraded KRAS G12D with picomolar potency across pancreatic, colorectal, and lung cancer cell lines, but did not induce degradation of wild-type and other mutant rat sarcoma ("RAS") isoforms.

• ARV-806 is differentiated from other KRAS G12D targeting agents in development and has potential to be a best-in-class therapy for KRAS G12D mutated cancers due to:

◦ Catalytic activity, which allows it to overcome upregulation, a common mechanism of resistance to inhibitor treatment

◦ Compared with clinical-stage KRAS G12D ON and OFF inhibitors and another clinical-stage G12D degrader, ARV-806 demonstrated:

▪>25-fold greater potency in reducing cancer cell proliferation,

▪>40-fold higher potency in degrading KRAS G12D protein (versus the comparable clinical-stage G12D degrader), and

▪>10-fold lower concentrations required to induce pro-apoptotic BIM expression.

• Following a single intravenous dose in a colorectal tumor xenograft model, ARV-806 degraded >90% of KRAS G12D for seven days, with parallel suppression of c-MYC (a key driver of cancer cell proliferation) and induction of BIM (Bcl-2-interacting mediator of cell death, a pro-apoptotic factor) for ≥5 days.

• ARV-806 demonstrated robust efficacy responses at low doses in tumor models including: ≥30% tumor volume reductions in pancreatic and colorectal cell line-derived xenograft ("CDX") models and a patient-derived xenograft ("PDX") model of lung cancer.

These data demonstrate sustained pharmacodynamic activity consistent with long-lasting target degradation, which the Company believes supports intermittent clinical dosing. The Company is