A class of phosphane gold(I) compounds, made of azoles and phosphane ligands, was evaluated for a screening on the regards of Breast Cancer cell panels (BC). The compounds possess N-Au-P or Cl-Au-P bonds around the central metal, and they differ for the presence of aprotic or protic polar groups in the azoles and/or the phosphane moieties to tune their hydrophilicity. Among the six candidates, only the compounds having the P-Au-N environment and not displaying neither the hydroxyl nor carboxyl groups in the ligands were found active. The compounds were screened by MTT tests in SKBR3, A17, and MDA-MB231 cancer cells, and two compounds (namely the 4,5-dicyano-imidazolate-1yl-gold(I)-(triphenylphosphane, 5, and 4,5-dichloro-imidazolate-1yl-gold(I)-triphenylphosphane, 6) were found very cytotoxic, with the most active with an IC₅₀ value of 3.46 μM in MDA-MB231 cells. By performing enzymatic assays in the treated cells lysates, the residual enzymatic activity of dihydrofolate reductase (DHFR) has been measured after cell treatment for 4 or 12 h in comparison with control cells. Upon 12 h of treatment, the activity of DHFR was significantly reduced in both SKBR3 and A17 cells by compounds 5 and 6, but not in human MDA-MB231 cells; interestingly, it was found remarkably high after 4 h of treatment, revealing a time dependence for the DHFR enzymatic assays. The DHFR inhibition data have been compared to those for the thioredoxin reductase (TrxR), the most recognized molecular target for gold compounds. For this latter, similar residual activities (i.e., 37 and 49% for the match of SKBR3 cells and compound 5 or 6, respectively) were found. Binding studies on the regards of ct-DNA (calf-thymus-DNA) and of plasma transporters proteins, such as BSA (bovine serum albumin) and ATF (apo transferrin), were performed. As expected for gold compounds, the data support strong binding to proteins (K_sv values range: 1.51 ÷ 2.46 × 10⁴ M⁻¹) and a weaker interaction with ct-DNA's minor groove (K_sv values range: 1.55 ÷ 6.12 × 10³ M⁻¹).

对一类由吡咯和膦配体制成的膦金（I）化合物进行了评估，以筛选乳腺癌细胞组（BC）。这些化合物在中心金属周围具有N-Au-P或Cl-Au-P键，它们在吡咯和/或膦部分中存在非质子或质子极性基团，以调节其亲水性而有所不同。在这六个候选物中，只有具有P-Au-N环境并且在配体中既不显示羟基也不显示羧基的化合物才被发现具有活性。通过MTT测试在SKBR3，A17和MDA-MB231癌细胞中筛选了这些化合物，以及两种化合物（即4,5-二氰基咪唑盐-1基-金（I）-（三苯基膦，5和4,5-发现二氯-咪唑基-1基-金（I）-三苯基膦，具有很强的细胞毒性，最活跃的是IC₅₀MDA-MB231细胞中的3.46μM值。通过在处理过的细胞裂解物中进行酶促测定，与对照细胞相比，在细胞处理4小时或12小时后，已测量了二氢叶酸还原酶（DHFR）的残留酶促活性。处理12小时后，化合物5和6在SKBR3和A17细胞中DHFR的活性均显着降低，而在人MDA-MB231细胞中则没有。有趣的是，在处理4小时后发现其显着较高，这表明了DHFR酶法测定的时间依赖性。已将DHFR抑制数据与硫氧还蛋白还原酶（TrxR）的数据进行了比较，硫氧还蛋白还原酶（TrxR）是最公认的金化合物分子靶标。对于后者，发现了相似的残余活性（即，分别为SKBR3细胞和化合物5或6的匹配的37％和49％）。进行了关于ct-DNA（小牛胸腺DNA）和血浆转运蛋白（例如BSA（牛血清白蛋白）和ATF（载脂蛋白转铁蛋白））的结合研究。正如对金化合物的预期一样，数据支持与蛋白质的牢固结合（K_sv值范围：1.51÷2.46×10 ⁴ M ^-1）和与ct-DNA的小沟的相互作用较弱（K _sv值范围：1.55÷6.12×10 ³ M ^-1）。