PMM-302

PMM-302 (PMMB-302) inhibits the proliferation of HeLa, MDA-MB-231, MCF-7, A549, Calu-3, H460, and H1650 cancer cells with IC₅₀ values of 8.05, 4.72, 7.12, 2.71, 16.02, 5.34, and 5.45 μM, respectively; its IC₅₀ against non-cancerous L0-2 cells is 93.81 μM^[1].
PMM-302 (0-8 μM; 24 h) dose-dependently induces G2/M phase cell cycle arrest in A549 cells, with the proportion of cells in G2/M phase increasing from approximately 11.30% in the control group to approximately 23.16%, 34.42%, and 44.53% at 2, 4, and 8 μM, respectively^[1].
PMM-302 (4 μM; 0-36 h) time-dependently increases the proportion of cells in G2/M phase in A549 cells, reaching 53.40% at 36 h^[1].
PMM-302 (0-4 μM; 24 h) dose-dependently induces apoptosis in A549 cells, with the proportion of late apoptotic cells increasing to 39.0% at 4 μM^[1].
PMM-302 (4 μM; 0-36 h) time-dependently increases the proportion of apoptotic cells in A549 cells^[1].
PMM-302 (0-8 μM) downregulates Bcl2, Bcl-XL, and FADD and upregulates cleaved caspase-3 and cleaved caspase-9 in a concentration-dependent manner in A549 cells, supporting its apoptosis-inducing effect^[1].
PMM-302 (0-8 μM) downregulates the telomerase core proteins DKC1 and NHP2 as well as TERT mRNA in A549 cells, and inhibits telomerase-related activity in a dose-dependent manner, with the most pronounced downregulation of DKC1 and NHP2 at 8 μM; its telomerase inhibitory effect is weaker than that of BIBR1532 at the same concentration^[1].
Molecular docking predicts that PMM-302 localizes to the telomerase active site and forms 1 hydrogen bond with THR232^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.