The Bcl 2 protein family plays a critical position in the regulation of apoptosis. For both materials, the IC50 value was calculated. Bcl XL and Bcl 2, two anti apoptotic members of the Bcl 2 protein family, do not only bring about cancer progression by inhibiting apoptosis, Checkpoint inhibitor but may also be responsible for the resistance of cancer cells against current cancer treatments. For that reason, Bcl 2 proteins are encouraging new targets in cancer treatment. Degterev et al. showed, that apoptosis induced by the materials BH3I 1 and BH3I 2, is similar to the cell death caused by an overexpression of professional apoptotic Bcl 2 family members, but does not lead to Bax insertion in to mitochondrial membranes. They concluded, that BH3I 1 and BH3I 2 induce apoptosis by inhibiting the heterodimerisation of Bcl XL/Bcl 2 and by publishing pro apoptotic Bcl 2 family members, which in turn trigger downstream apoptotic activities. Using as Urogenital pelvic malignancy lead compounds for a computerassisted assessment BH3I 1 and BH3I 2, we identified seven compounds. By application of a variety of bioinformatical strategies, the materials 1 and 5 showed best houses which may be tested by apoptosis assays in a variety of cell systems. Experimental effects of 3, 2, 4, 6 and 7 checked the theoretical predictions, which specified these compounds to become no promising anti cancer agents. To assess 1 and 5 together with the qualities of the lead compounds BH3I 1 and BH3I 2, cells, overexpressing Bcl XL proteins, were applied and it revealed, the lead compounds as well as their analogue, show Bcl XL reliance. In cells, overexpressing Bcl XL, a decreased quantity of apoptotic cells is detectable after-treatment with 5 and 1 as these cells contain more anti apoptotic Bcl XL. Its AG-1478 solubility analogue and bh3i 1 don’t show any Bax dependency, from which it can be concluded, that neither the lead design or substance 1 can induce a conformational change in Bax, which supports the thesis that both BH3Is directly interact with Bcl 2. BH3I 2 shows similar qualities as BH3I 1, referring to the induction of Bcl 2 dependent apoptosis. Between your lead design and its analogue, no significant difference in the quantity of hypodiploid cells is seen, although improved apoptosis is shown by the analogue, inducing abilities compared to BH3I 2 in other cell lines. Influencing the Bcl 2 induced apoptosis appears to be impossible in Bcl 2 and Bcl XL expressing cell lines. Particularly, it must be identified, that 5 shows a greater induction of apoptosis in Bak cells when compared with BH3I 2, and it seems that 5 can result in a heterodimerisation of Bax. This shows that an improvement of binding skills is possible and that this could even lead to a different mechanism of the induction of apoptosis, in comparison to the first buildings.