Systematic (IUPAC) name
8,8'-{Carbonylbis[imino-3,1-phenylenecarbonylimino(4-methyl-3,1-phenylene)carbonylimino]}di(1,3,5-naphthalenetrisulfonic acid)
Clinical data
Trade names Antrypol, 309 F or 309 Fourneau, Bayer 205, Moranyl, Naganin, Naganine
Legal status
Routes of
CAS Registry Number  Y
ATC code P01 QP51
PubChem CID:
DrugBank  N
ChemSpider  Y
Chemical data
Formula C51H40N6O23S6
Molecular mass 1297.29

Suramin is an antiparasitic drug developed by Oskar Dressel and Richard Kothe of Bayer, Germany in 1916, and is still sold by Bayer under the brand name Germanin. The formula of suramin was kept secret by Bayer for commercial reasons, however, it was elucidated and published in 1924 by Ernest Fourneau and his team of the Pasteur Institute.[1]:378-379[2]

It is on the health system.[3]


  • Medical uses 1
    • Protozoa 1.1
    • Helminthiasis 1.2
  • Adverse reactions 2
  • Chemistry 3
  • Research 4
  • References 5
  • External links 6

Medical uses


It is used for treatment of human sleeping sickness caused by trypanosomes.[4]


It has been used in the treatment of onchocerciasis.[5]

Adverse reactions

The most frequent adverse reactions are nausea and vomiting. About 90% of patients will get an urticarial rash that disappears in a few days without needing to stop treatment. There is a greater than 50% chance of adrenal cortical damage, but only a smaller proportion will require lifelong corticosteroid replacement. It is common for patients to get a tingling or crawling sensation of the skin with suramin. Suramin will cause clouding of the urine which is harmless: patients should be warned of this to avoid them becoming alarmed.

Kidney damage and exfoliative dermatitis occur less commonly.

Suramin has been applied clinically to HIV/AIDS patients resulting in a significant number of fatal occurrences and as a result the application of this molecule was abandoned for this condition.[6]


The molecular formula of suramin is C51H40N6O23S6. It is a symmetric molecule in the center of which lies a urea (NH–CO–NH) functional group. Suramin contains eight benzene rings, four of which are fused in pairs (naphthalene), four amide groups (in addition to the urea) and six sulfonic acid groups. When given as drug, it is usually as the sodium sulfonate, with six sodium ions on the sulfonate groups rather than hydrogens.


Suramin was studied as a possible treatment for prostate cancer in a clinical trial.[7]

It has been studied in a mouse model of autism[8][9][10]

Suramin is also used in research as a broad-spectrum antagonist of P2 receptors[11][12] and agonist of Ryanodine receptors.[13]

Its effect on telomerase has been investigated.[14]

It may have some activity against RNA viruses.[15]

In addition to antagonism of P2 receptors, Suramin inhibits the activation of heterotrimeric G proteins in a variety of other GPCRs with varying potency. It prevents the association of heteromeric G proteins and therefore the receptors guanine exchange functionality (GEF). With this blockade the GDP will not release from the Gα subunit so it can not be replaced by a GTP and become activated. This has the effect of blocking downstream G protein mediated signaling of various GPCR proteins including rhodopsin, the A1 adenosine receptor, and the D2 dopamine receptor.[16]


  1. ^ Walter Sneader. Drug Discovery: A History. John Wiley & Sons, 2005 ISBN 9780471899792
  2. ^ Fourneau, E.; Th; Vallée, J. (1924). "Sur une nouvelle série de médicaments trypanocides". C. R. Séances Acad. Sci. 178: 675. 
  3. ^ "WHO Model List of EssentialMedicines" (PDF). World Health Organization. October 2013. Retrieved 22 April 2014. 
  4. ^ Darsaud A, Chevrier C, Bourdon L, Dumas M, Buguet A, Bouteille B (January 2004). "Megazol combined with suramin improves a new diagnosis index of the early meningo-encephalitic phase of experimental African trypanosomiasis". Trop. Med. Int. Health 9 (1): 83–91.  
  5. ^ Anderson J, Fuglsang H (July 1978). "Further studies on the treatment of ocular onchocerciasis with diethylcarbamazine and suramin". Br J Ophthalmol 62 (7): 450–7.  
  6. ^ "Lack of response to suramin in patients with AIDS and AIDS-related complex." 82. Mar 1987. pp. 615–20.  
  7. ^ Ahles TA, Herndon JE, Small EJ, et al. (November 2004). "Quality of life impact of three different doses of suramin in patients with metastatic hormone-refractory prostate carcinoma: results of Intergroup O159/Cancer and Leukemia Group B 9480". Cancer 101 (10): 2202–8.  
  8. ^
  9. ^
  10. ^
  11. ^ Abbracchio MP, Burnstock G, Boeynaems JM, Barnard EA, Boyer JL, Kennedy C, Knight GE, Fumagalli M, Gachet C, Jacobson KA, Weisman GA. (September 2006). "International Union of Pharmacology LVIII: update on the P2Y G protein-coupled nucleotide receptors: from molecular mechanisms and pathophysiology to therapy". Pharmacol Rev. 58 (3): 281–341.  
  12. ^ Khakh BS, Burnstock G, Kennedy C, King BF, North RA, Séguéla P, Voigt M, Humphrey PP. (March 2001). "International union of pharmacology. XXIV. Current status of the nomenclature and properties of P2X receptors and their subunits". Pharmacol Rev. 53 (1): 107–118.  
  13. ^ Wolner I, Kassack MU, Ullmann H, Karel A, Hohenegger M (October 2005). "Use-dependent inhibition of the skeletal muscle ryanodine receptor by the suramin analogue NF676". Br. J. Pharmacol. 146 (4): 525–33.  
  14. ^ Erguven M, Akev N, Ozdemir A, Karabulut E, Bilir A (August 2008). "The inhibitory effect of suramin on telomerase activity and spheroid growth of C6 glioma cells". Med. Sci. Monit. 14 (8): BR165–73.  
  15. ^ Mastrangelo E, Pezzullo M, Tarantino D, Petazzi R, Germani F, Kramer D, Robel I, Rohayem J, Bolognesi M, Milani M (2012) Structure-based inhibition of norovirus RNA-dependent RNA-polymerases. J Mol Biol
  16. ^ Beindl W, Mitterauer T, Hohenegger M, Ijzerman AP, Nanoff C, Freissmuth M. (August 1996). "Inhibition of receptor/G protein coupling by suramin analogues". ol. Pharmacology. 50 (2): 415–23.  

External links

  • Suramin bound to proteins in the PDB
  • Drug information
  • Suramin, drug information by JBC Online
  • Suramin in treating patients with recurrent bladder cancer
  • National Cancer Institute