Figures & data
Figure 1. Reported pyrimidine-based anticancer molecules and design rationale for anticancer 2,5-diamino-4-pyrimidinol derivatives.
![Figure 1. Reported pyrimidine-based anticancer molecules and design rationale for anticancer 2,5-diamino-4-pyrimidinol derivatives.](/cms/asset/60f00f5c-3078-4291-84af-eb5db1a44b22/ienz_a_1699554_f0001_c.jpg)
Table 1. General structure and specific examples of the compounds being evaluated for their antiproliferative effects in this report.
Table 2. GI50 values (μM) exhibited by selected compounds over M-NFS-60 murine myeloblastic leukaemia cell line.
Table 3. % Inhibition of kinase reactions of a panel of kinases by 10 μM doses of compound 6e.
Figure 2. Measured % growth inhibition of various hematological cancers triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 2. Measured % growth inhibition of various hematological cancers triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/89658fb1-52cf-47ca-9da5-a368270a1c95/ienz_a_1699554_f0002_c.jpg)
Figure 3. Measured % growth inhibition of various NSCLC cells triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 3. Measured % growth inhibition of various NSCLC cells triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/fb27830f-7743-4fbe-9a86-2d29c3875a90/ienz_a_1699554_f0003_c.jpg)
Figure 4. Measured % growth inhibition of various colon cancers triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 4. Measured % growth inhibition of various colon cancers triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/3ed2e000-b923-4a55-956b-741b916f12da/ienz_a_1699554_f0004_c.jpg)
Figure 5. Measured % growth inhibition of various brain cancer cell lines triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 5. Measured % growth inhibition of various brain cancer cell lines triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/7413e76e-4a12-46aa-b260-d3629b40aa91/ienz_a_1699554_f0005_c.jpg)
Figure 6. Measured % growth inhibition of various melanoma cell lines triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 6. Measured % growth inhibition of various melanoma cell lines triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/9dd66a9f-1dcc-48ae-97c8-2b74d1df3c3b/ienz_a_1699554_f0006_c.jpg)
Figure 7. Measured % growth inhibition of various ovarian cancer cell lines triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 7. Measured % growth inhibition of various ovarian cancer cell lines triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/d0cb1d23-f551-4e44-8179-d41be6e11eaa/ienz_a_1699554_f0007_c.jpg)
Figure 8. Measured % growth inhibition of various renal cancer cells triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 8. Measured % growth inhibition of various renal cancer cells triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/41995991-a768-4d35-813f-5d3b7c9a74aa/ienz_a_1699554_f0008_c.jpg)
Figure 9. Measured % growth inhibition of various prostate cancer cell lines triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 9. Measured % growth inhibition of various prostate cancer cell lines triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/e037c0ee-aadb-4921-82c7-89668e0668fe/ienz_a_1699554_f0009_c.jpg)
Figure 10. Measured % growth inhibition of various breast cancer cells triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 10. Measured % growth inhibition of various breast cancer cells triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/57f56f24-a33d-4232-bb92-8105830bd677/ienz_a_1699554_f0010_c.jpg)
Figure 11. Average % values of measured growth inhibition of nine cancer diseases triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.
![Figure 11. Average % values of measured growth inhibition of nine cancer diseases triggered by 10 µM doses of compounds 6a–h and hit compound 4. Values are the averages of duplicate assays.](/cms/asset/5d569182-3805-48fa-8d99-caaf93731eaf/ienz_a_1699554_f0011_c.jpg)
Table 4. In vitro measured effective permeability (Pe) of compound 6e as well as verapamil and ranitidine using PAMPA-GIT.
Figure 12. Calculated binding modes and interactions of compound 6e: (A) Compound 6e docked within kinase binding site of CSF1R (PDB code: 3KRJ); (B) Predicted interactions of compound 6e within the binding pocket of CSF1R (PDB code: 3KRJ); (C) Compound 6e docked within substrate-binding site of DAPK1 (PDB code: 4TXC); (D) Predicted interactions of compound 6e within the substrate binding pocket of DAPK1 (PDB code: 4TXC).
![Figure 12. Calculated binding modes and interactions of compound 6e: (A) Compound 6e docked within kinase binding site of CSF1R (PDB code: 3KRJ); (B) Predicted interactions of compound 6e within the binding pocket of CSF1R (PDB code: 3KRJ); (C) Compound 6e docked within substrate-binding site of DAPK1 (PDB code: 4TXC); (D) Predicted interactions of compound 6e within the substrate binding pocket of DAPK1 (PDB code: 4TXC).](/cms/asset/33e126e6-a10a-40b0-a3f6-6b72109daa91/ienz_a_1699554_f0012_c.jpg)