| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
Cell lines | LNCap, C4-2, PC3, DU145 and 22RV1 cell lines |
Preparation Method | Different concentration gradients of various compounds (MDV3100， Afatinib, Erlotinib, Sorafenib, Gefitinib) were added to each group. The control group was treated with 0.1% DMSO. The cells were continuously treated for 72h, then supplemented with 10μL MTT solution for 4h. |
Reaction Conditions | 0-100μM |
Applications | MDV3100 moderately inhibited the proliferation of PC3 and DU145 cells, both of which are androgen-independent PCa cell lines. Moreover, it also inhibited proliferation in the androgen-dependent LNCap, 22RV1 and C4-2 cell lines, with IC50values of 1.74, 39.79 and 49.17μM, respectively. |
Animal models | Male nude mice, Four-week-old |
Preparation Method | 6.0×106C4-2B-ENZR cells, or 3.0×10622Rv1 cells were injected subcutaneously into the mice. After the mice were surgically castrated, they were randomized into four groups (n=5/group) and treated as follows: (1) vehicle control (PBS, i.p.); (2) MDV3100 (10mg/kg, p.o.); (3) KIF15-IN-1 (10mg/kg, i.p.); (4) MDV3100 (10mg/kg, p.o.) + KIF15-IN-1 (10mg/kg, i.p.). Tumor tissues were harvested and weighed after 4 weeks of treatment. Tumor size was measured twice a week. |
Dosage form | (1) vehicle control (PBS, i.p.); (2) MDV3100 (10mg/kg, p.o.); (3) KIF15-IN-1 (10mg/kg, i.p.); (4) MDV3100 (10mg/kg, p.o.) + KIF15-IN-1 (10mg/kg, i.p.)/p> |
Applications | C4-2B-ENZR and 22Rv1 tumors treated with MDV3100 alone showed no difference to the control groups (MDV3100 vs. control; C4-2B-ENZR, 1145±119.3 vs. 1269±182mm3; 22Rv1, 1455±127.5 vs. 1547±97.93mm3). However, KIF15-IN-1 treatment reduced the tumor volume (C4-2B-ENZR, 633.5±85.3mm3; 22Rv1, 905.4±124.5mm3), and the combination of MDV3100 and KIF15-IN-1 induced further inhibition in tumor growth (C4-2B-ENZR,246.3±67.42mm3; 22Rv1, 481.5±87.82mm3). |
| 文献引用 | |
| 产品描述 | MDV3100(enzalutamide) is a second-generation AR antagonist with an IC50of 36nM in LNCaP prostate cells[1,2]. MDV3100 could reduce androgen binding to AR, inhibit AR transport to the nucleus and prevent the binding of AR to androgen response elements[2]. MDV3100 combined with TKIs exerted a synergistic effect on a variety of PCa cells. MDV3100 combined with afatinib could suppress the proliferation and migration of 22RV1 cells, as well as cause their cell cycle arrest and apoptosis[2]. MDV3100 probed the bone microenvironment that led to stronger cancer cell adaptive responses and osteomimicry than bicalutamide. MDV3100 presented with better treatment response, in line with MDV3100 delaying time to bone-related events and MDV3100 extending survival in mCRPC[3]. MDV3100 promoted macrophage migration to PCa cells that consequently led to enhanced PCa cell invasion in human (C4-2B/THP1) and mouse (TRAMP-C1/RAW264.7) PCa cells–macrophages co-culture systems[4] MDV3100 combination with KIF15 inhibitors significantly suppressed MDV3100-resistant PCa cell growth and xenograft progression. KIF15 inhibitors may enhance the sensitivity of prostate tumors to MDV3100 treatment, and rationalize a combination therapy of KIF15 inhibitors with MDV3100 to treat CRPC patients[5]. The antitumor efficacy of MDV3100 can be substantially improved by methylselenol prodrug, which also downregulates AR-FL and AR-Vs in vivo[6]. MDV3100 prolonged overall survival of metastatic CRPC patients who progressed after chemotherapy in a Phase III trial[7] References: |
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