Suramin Sodium Salt (BAY-205) is a sodium salt form of suramin, a polysulphonated naphthylurea with potential antineoplastic activity. Suramin blocks the binding of various growth factors, including insulin-like growth factor I (IGF-I), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and tumor growth factor-beta (TGF-beta), to their receptors, thereby inhibiting endothelial cell proliferation and migration. This agent also inhibits vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (bFGF)-induced angiogenesis; retroviral reverse transcriptase; uncoupling of G-proteins from receptors; topoisomerases; cellular folate transport; and steroidogenesis.

SIRT2:1.15 μM, SIRT5:22 μM, DNA topo II:5 μM, SIRT1:297 nM

Suramin inhibits cell proliferation and DNA synthesis in cultured HeLa cells. The replication of SV40 DNA is completely abolished by 40 μM suramin. DNA polymerase α is sensitive to lower concentrations of suramin (IC50=8 μM) than is DNA polymerase δ (IC50=36 μM), whereas DNA polymerase β is relatively insensitive to the drug (IC50 of 90 μM)[1]. Suramin is a potent inhibitor of DNA strand exchange and ATPase activities of bacterial RecA proteins. Suramin inhibits RecA-catalysed proteolytic cleavage of the LexA repressor. The mechanism underlying such inhibitory actions of suramin involves its ability to disassemble RecA–single-stranded DNA filaments[2]. Suramin is a potent inhibitor of the nuclear enzyme DNA topoisomerase II. Suramin inhibits purified yeast topoisomerase II with an IC50 of about 5 μM[3].

Treatment with suramin shows lower values for pulmonary artery pressure, right ventricular hypertrophy, and distal vessel muscularization on day 21 compared to control rats. Suramin treatment suppresses PA-SMC proliferation and attenuates both the inflammatory response and the deposition of collagen[4].

The ATPase assay is performed in a 10 μL reaction mixture containing 20 mM Tris-HCl (pH 7.5), 1 mM DTT, 8 mM MgCl2, 5 μM M13 circular ssDNA, 2.5 μM RecA from the specified bacterial species and increasing concentrations of suramin. The reaction is initiated by the addition of 2 mM [α-32P]ATP, incubated for 30 min at 37°C and stopped by the addition of 25 mM EDTA[2].