By replacing the ovalicin of PROTAC-1 targeting METAP-2 with estradiol, which can bind to the estrogen receptor (ER), or dihydroxytestosterone (DHT), which can bind to the androgen receptor (AR), they attempted to induce the targeted degradation of ER, a breast cancer-associated protein, and AR, a prostate cancer-associated protein, respectively. Here, AR is linked to breast carcinoma.