## 3 Results and Discussion
### Antiproliferative Assay  
The antiproliferative activity evaluation of the synthesized triphenyl imidazole derivatives was made with the sulforhodamine B (SRB) assay. The tumoral cell lines employed were adherent epithelial cells from different anatomic origins. All results were expressed as growth inhibition 50 (GI\({}_{50}\)), as the concentration needed to inhibit the 50% of cell population, and calculated and expressed as micromolar (\(\mu\)M). As positive controls, different antitumor drugs were employed such as cisplatin, etoposide, and camptothecin, and imidazole was used as the structural reference of the synthesized compounds. The obtained results from the evaluation of the 13 synthesized compounds with the SRB assay against the tumor cell lines (Table 2) showed no selectivity by any specific line. Based on the results in Table 2 and the GI\({}_{50}\) range (Figure 3), the most active compounds of the series were **10** and **11**. As initial highlights, imidazole had no inhibitory activity in the compounds employed as controls; on the other hand, one of the most resistant cell lines against the synthesized compounds and drugs was A549, which corresponds to lung adenocarcinoma, and this is in agreement with the literature, as it has been documented that lung type cancers are usually chemotherapy resistant, even to one of the most used antitumor drugs, taxol [43]. From the 13 synthesized compounds, lower activity was shown from derivative **1**, this being the triphenyl imidazole bearing no substitutions, as against five of the six evaluated cell lines, it showed no significant activity, and a low one against SW1573 (89 \(\mu\)M). Likewise, between the molecules with one methoxy substitution **4** (_p_-OMe), **5** (_m_-OMe) and **6** (_o_-OMe), which are position isomers, only **5** showed a low activity against SW1573 with an GI\({}_{50}\) of 76 \(\mu\)M, while **4** and **6** presented no significant activity against all of the evaluated cell lines. Following these general low active compounds, derivatives **9** (_o_-Cl) and **12** (_o_-NO\({}_{2}\)) were partially active, as they presented different degrees of activity, but against only a couple of cell lines. Compound **9** showed good to moderate activity only against two cell lines, which were HeLa with a GI\({}_{50}\) of 7.7 \(\mu\)M and SW1573 with 17 \(\mu\)M; compound **12** presented activity against the same cell lines with GI\({}_{50}\) of 6.1 and 66 \(\mu\)M respectively. The following molecules with better results were the compounds **3** (_p_-OH), **7** (_m_-OMe, _p_-OH), **8** (_m_-OMe, _p_-OMe), and **13** (anthracene), as these molecules presented activity against all evaluated cell lines, the only exception being **13** against lines T-47D and WiDr; however, **13** also showed one of the best particular results, this being a GI\({}_{50}\) of 4.2 \(\mu\)M against SW1573. In the case of **3**, activity was shown against all analyzed cell lines, with HeLa being the most sensitive with a GI\({}_{50}\) of 13 \(\mu\)M, followed by  
Figure 2: Xantine oxidase inhibitory activity of synthesized compounds **1–13**. Allopurinol served as the reference compound. Bars are mean \(\pm\) SD, n = 3. SW1573 and HBL-100 with 15 and 16 \(\upmu\)M, respectively, while in the rest of the lines, the results were between 19 and 22 \(\upmu\)M.  
With molecules **7** and **8**, very similar GI\({}_{50}\) values could be seen between them. Comparing them against monosubstituted compounds **4**, **5**, and **6** (which have a methoxy group in different positions), **7** and **8** showed that di-substitution enhanced the antiproliferative activity against these cell lines, these being substitutions of the hydroxy and methoxy type. In the literature, compound **8** was reported to show antiproliferative activity against the breast cancer cell line MDA-MB-231 with a GI\({}_{50}\) of 21 \(\upmu\)M [44]. This value is consistent with the results obtained in our study.