Castration-resistant prostate cancer (CRPC) progresses through reactivation of androgen receptor (AR) signaling despite treatment with androgen receptor pathway inhibitors (ARPIs). Androgen receptor splice variant 7 (AR-V7) is a major mechanism of ARPI resistance and is associated with poor therapeutic responses and clinical outcomes. AR-V7 lacks the ligand-binding domain (LBD) but retains the N-terminal domain (NTD) and DNA-binding domain (DBD), enabling ligand-independent transcriptional activity. In this study, we developed hydrophobic tagging (HyT)-based degraders targeting AR-V7. AR-V7-targeting HyT compounds (KANT-HyT) were designed and synthesized by introducing various hydrophobic tags and linkers to an AR-NTD binding moiety. Their antiproliferative activity and AR/AR-V7 degradation were evaluated in AR-V7-positive prostate cancer cells. Among them, KANT-HyT-010 exhibited greater antiproliferative activity than the LBD-targeting inhibitor enzalutamide in 22Rv1 cells, with a GI₅₀ value of 7.20 μM. KANT-HyT-010 also induced concentration-dependent degradation of both full-length AR and AR-V7, with a DC₅₀ value of 5.86 μM for AR-V7. These findings demonstrate the feasibility of NTD-directed HyT-mediated degradation of AR-V7 and suggest AR-V7-targeted protein degradation as a potential strategy to overcome ARPI resistance in CRPC.