Suramin sodium
[CAS# 129-46-4]

Identification

• Classification: API >> Antineoplastic agents
• Name: Suramin sodium
• Synonyms: 8,8'-Carbonylbisimino-3,1-phenylenecarbonylimino-(4-methyl-3,1-phenylene)carbonyliminobis-1,3,5-naphthalenetrisulfonic acid hexasodium
• Molecular Formula: C₅₁H₃₄N₆Na₆O₂₃S₆
• Molecular Weight: 1429.17
• CAS Registry Number: 129-46-4
• EC Number: 204-949-3
• SMILES: CC1=C(C=C(C=C1)C(=O)NC2=C3C(=CC(=CC3=C(C=C2)S(=O)(=O)[O-])S(=O)(=O)[O-])S(=O)(=O)[O-])NC(=O)C4=CC(=CC=C4)NC(=O)NC5=CC=CC(=C5)C(=O)NC6=C(C=CC(=C6)C(=O)NC7=C8C(=CC(=CC8=C(C=C7)S(=O)(=O)[O-])S(=O)(=O)[O-])S(=O)(=O)[O-])C.[Na+].[Na+].[Na+].[Na+].[Na+].[Na+]

Properties

• Solubility: water: soluble 50 mM, DMSO: 10 mM (Expl.)

Safety Data

• Hazard Symbols: GHS07 Warning
• Hazard Statements: H317
• Precautionary Statements: P261-P272-P280-P302+P352-P321-P333+P317-P362+P364-P501

Hazard Classification

Hazard	Class	Category Code	Hazard Statement
Skin sensitization	Skin Sens.	1	H317

Discovory and Applicatios

Suramin sodium is a polyanionic naphthylurea compound originally developed in the early 20th century by Bayer for the treatment of parasitic diseases. It was introduced in 1916 as a therapeutic agent against African trypanosomiasis, also known as sleeping sickness, caused by *Trypanosoma* species and transmitted by the tsetse fly. The drug emerged from structural modifications of earlier dyes such as trypan blue, with the aim of reducing toxicity and improving efficacy. Suramin’s development marked a significant milestone in medicinal chemistry, being among the earliest examples of rational drug design in antiparasitic therapy.

Suramin sodium is the water-soluble salt form of suramin and exhibits a complex symmetric structure containing multiple sulfonic acid groups. These sulfonate moieties confer the molecule with high aqueous solubility and enable strong electrostatic interactions with biological macromolecules. Its mechanism of action is multifaceted, involving inhibition of several enzymes and pathways in both host and parasite cells. Suramin non-selectively binds to proteins such as growth factor receptors, DNA and RNA polymerases, and G-protein coupled receptors, leading to the disruption of cell signaling and metabolic processes. This broad binding capability underlies both its pharmacological activity and its toxicity.

Suramin sodium remains on the World Health Organization’s list of essential medicines for its role in treating early-stage African trypanosomiasis, especially infections caused by *Trypanosoma brucei rhodesiense*. It is typically administered intravenously and does not cross the blood-brain barrier effectively, limiting its use to the hemolymphatic phase of the disease. For the meningoencephalitic stage, other agents such as melarsoprol are preferred.

In addition to its antiparasitic role, suramin sodium has attracted research interest for its potential applications in oncology and viral infections. It has demonstrated inhibitory effects on various tumor cell lines in vitro by interfering with growth factor signaling, such as blocking fibroblast growth factor (FGF) and epidermal growth factor (EGF) receptors. Clinical trials in cancer patients during the late 20th century showed limited therapeutic benefit due to poor tumor selectivity and systemic toxicity. Nevertheless, these studies laid the groundwork for the development of other polyanionic anticancer compounds.

In virology, suramin has been investigated as an entry and replication inhibitor for a range of viruses, including HIV, Zika, Chikungunya, and more recently, SARS-CoV-2. It interferes with viral RNA polymerases and viral-host cell attachment processes, although its lack of specificity and potential toxicity have prevented clinical adoption in these indications. Current interest focuses on using suramin as a molecular probe or scaffold for drug development rather than a direct antiviral agent.

Suramin has also been studied in the context of neurodevelopmental disorders. A small exploratory clinical trial involving children with autism spectrum disorder suggested transient improvements in core symptoms following suramin administration. This has been attributed to modulation of purinergic signaling pathways, which are hypothesized to be dysregulated in some neurodevelopmental conditions. However, given suramin’s broad biological activity and narrow therapeutic index, further research is required to confirm its safety and efficacy in these contexts.

From a chemical standpoint, suramin sodium’s synthesis is complex, involving stepwise formation of the symmetrical urea-linked disulfonated aromatic system. Its stability and extensive protein binding make it long-acting in the body, but these same properties contribute to its cumulative toxicity, particularly affecting renal and adrenal function during prolonged treatment.

Due to its historical significance, broad biological activity, and complex molecular structure, suramin sodium remains a molecule of continued interest in medicinal chemistry. While its clinical use is largely restricted to a specific parasitic indication, its legacy extends across pharmacological disciplines and continues to inform drug discovery efforts targeting growth factors, nucleotides, and viral enzymes.

References

1994. ATP antagonists cibacron blue, basilen blue and suramin alter sound-evoked responses of the cochlea and auditory nerve. Hearing Research, 78(2).
DOI: 10.1016/0378-5955(94)90024-8

1991. The Effects of Basic Fibroblast Growth Factor and suramin on Cell Motility and Growth of Rat Prostate Cancer Cells. The Journal of Urology, 145(1).
DOI: 10.1016/s0022-5347(17)38291-5

1991. A pilot study of suramin in the treatment of metastatic renal cell carcinoma. Cancer, 67(6).
DOI: 10.1002/1097-0142(19910315)67:6<1509::aid-cncr2820670608>3.0.co;2-f