Background:

Suramin is a polysulfonated naphthylurea that inhibits the binding of calmodulin to recognition sites on the ryanodine receptor-1 (IC50 = 4.9 μM), blocks G protein coupling to GPCRs, and non-selectively antagonizes P2 purinergic receptors (10-100 μM).[1],[2[ Suramin also acts as a non-specific competitor of glycosaminoglycan binding to a variety of targets including TGFβ, PDGF, and FGF and additionally inhibits insulin-like growth factor-l, EGF, PKC activity, TNF, IL-2, transferrin, and Apo-B.[3] While originally used as an early stage treatment of trypanosome-caused onchocerciasis (African river blindness) and African trypanosomiasis (African sleeping sickness), suramin has been under clinical evaluation for its potential to regress a number of cancer cell lines, including non-small cell lung cancer, advanced breast cancer, hormone refractory prostate cancer, metastatic renal cell cancer, colorectal cancer, and high-grade gliomas.[3],[4],[5]

Reference:

[1]. Klinger, M., Bofill-Cardona, E., Mayer, B., et al. Suramin and the suramin analogue NF307 discriminate among calmodulin-binding sites Biochemistry Journal 355(3), 827-833 (2001).
[2]. Charlton, S.J., Brown, C.A., Weisman, G.A., et al. PPADS and suramin as antagonists at cloned P2Y- and P2U- purinoceptors British Journal of Pharmacology 118(3), 704-710 (1996).
[3]. Eisenberger, M.A., and Reyno, L.M. Suramin Cancer Treatment Reviews 20, 259-273 (1994).
[4]. Stein, C.A. Suramin: A novel antineoplastic agent with multiple potential mechanisms of action Cancer Research 53, 2239-2248 (1993).
[5]. McGeary, R.P., Bennett, A.J., Tran, Q.B., et al. Suramin: Clinical uses and structure-activity relationships Mini Rev.Med.Chem. 8(13), 1384-1394 (2008).