UT-34 is a selective and orally active antagonist of second-generation pan-androgen receptor (AR) and degrader(IC50s of 211.7 nM, 262.4 nM and 215.7 nM for wild-type, F876L and W741L AR, respectively), and has anti-prostate cancer efficacy.

In LNCaP cells, UT-34 (3-10 μM; 24 hours) treatment inhibits the expression of PSA and FKBP5 and growth of LNCaP cells starting from 100 nM with maximum effect observed at 10 μM[1].In LNCaP cells UT-34 (0.1-10 μM; 24 hours; LNCaP cells) treatment results in a reduction of AR levels at 1000 nM [1]. Treatment of ZR-75-1 cells maintained in serum-containing growth medium with UT-34 results in downregulation of AR protein levels, but not estrogen receptor (ER) or progesterone receptor (PR) levels. Furthermore, in MDA-MB-453 breast cancer cells that express AR and glucocorticoid receptor (GR), UT-34 induces the downregulation of AR, but not GR[1]. UT-34 is an effective degrader of both AR and AR-V7.LNCaP-ARV7 cells were treated in the presence of 0.1 nM R1881 or 10 ng/mL doxycycline for 24 hours. Doxycycline induces the expression of EDN2, which is inhibited by UT-34, and UT-34 inhibits the expression of FKBP5 gene expression induced by R1881[1].

In NSG mice, UT-34 (20-40 mg/kg; oral administration; daily; for 14 days ) at 20 and 40 mg/kg reduces the seminal vesicle weight by 10%-20% and 50%-60 %, respectively[1]. in rats,UT-34 inhibits androgen-dependent tissues such as prostate and seminal vesicles , and the growth of Enzalutamide-resistant castration-resistant prostate cancer (CRPC) xenografts. In intact immunocompromised rats, UT-34 also induces tumor regression [1].