SIRT1 (IC50 = 297 nM); SIRT2 (IC50 = 1.15 μM); SIRT5 (IC50 = 22 μM)

In a dose-dependent and time-regulated manner, suramin sodium salt (also known as suramin hexasodium salt; 50-600 μg/mL; lasting 24-96 hours) suppresses cell proliferation and lowers lymphocyte viability [7]. mL; for 48 hours) causes HeLa cells to undergo apoptosis and express less mRNA [7]. One hour of 1 mg/mL suramin sodium salt suppresses phosphorylated ERK1/2 substantially [8]. HeLa and PM have IC50 values of 476 μg/mL and 319 μg/mL, respectively [7]. In Vero E6 cells, suramin sodium salt increases viral replication [5].

Suramin hexasodium salt (Suramin hexasodium salt; form 10 mg/kg; intravenously; twice weekly for 3 weeks) reverses established pulmonary hypertension (PH), consequently improving pulmonary artery pressure values and vascular structure Normal [8].

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Suramin (Sur) acts as an ecto-NTPDase inhibitor in Trypanosoma cruzi and a P2-purinoceptor antagonist in mammalian cells. Although the potent antitrypanosomal effect of Sur has been shown in vitro, limited evidence in vivo suggests that this drug can be dangerous to T. cruzi-infected hosts. Therefore, we investigated the dose-dependent effect of Sur-based chemotherapy in a murine model of Chagas disease. Seventy uninfected and T. cruzi-infected male C57BL/6 mice were randomized into five groups: SAL = uninfected; INF = infected; SR5, SR10, and SR20 = infected treated with 5, 10, or 20 mg/kg Sur. In addition to its effect on blood and heart parasitism, the impact of Sur-based chemotherapy on leucocytes myocardial infiltration, cytokine levels, antioxidant defenses, reactive tissue damage, and mortality was analyzed. Our results indicated that animals treated with 10 and 20 mg/kg Sur were disproportionally susceptible to T. cruzi, exhibiting increased parasitemia and cardiac parasitism (amastigote nests and parasite load (T. cruzi DNA)), intense protein, lipid and DNA oxidation, marked myocarditis, and mortality. Animals treated with Sur also exhibited reduced levels of nonprotein antioxidants. However, the upregulation of catalase, superoxide dismutase, and glutathione-S-transferase was insufficient to counteract reactive tissue damage and pathological myocardial remodeling. It is still poorly understood whether Sur exerts a negative impact on the purinergic signaling of T. cruzi-infected host cells. However, our findings clearly demonstrated that through enhanced parasitism, inflammation, and reactive tissue damage, Sur-based chemotherapy contributes to aggravating myocarditis and increasing mortality rates in T. cruzi-infected mice, contradicting the supposed relevance attributed to this drug for the treatment of Chagas disease.[7]

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Researchers evaluated whether RTK blockade by the nonspecific growth factor inhibitor, suramin, reversed advanced MCT-PH in rats via its effects on growth-factor signaling pathways. We found that suramin inhibited RTK and ERK1/2 phosphorylation in cultured human PA-SMCs. Suramin inhibited PA-SMC proliferation induced by serum, PDGF, FGF2, or EGF in vitro and ex vivo. Treatment with suramin from day 1 to day 21 after monocrotaline injection attenuated PH development, as shown by lower values for pulmonary artery pressure, right ventricular hypertrophy, and distal vessel muscularization on day 21 compared to control rats. Treatment with suramin from day 21 to day 42 after monocrotaline injection reversed established PH, thereby normalizing the pulmonary artery pressure values and vessel structure. Suramin treatment suppressed PA-SMC proliferation and attenuated both the inflammatory response and the deposition of collagen. Conclusions: RTK blockade by suramin can prevent MCT-PH and reverse established MCT-PH in rats. This study suggests that an anti-RTK strategy that targets multiple RTKs could be useful in the treatment of pulmonary hypertension [8].

Receptor tyrosine kinase phosphorylation assay [8]
PA-SMCs cultured in DMEM supplemented with 10% FCS were synchronized for 48 hours. After preincubation with suramin (1000 µg/mL) for 1 hour, the cells were stimulated with a combination of PDGF, EGF and FGF2 for 15 minutes at 37°C. The relative levels of tyrosine phosphorylation of the RTKs in the PA-SMCs were determined using the Proteome Profiler™ Human Phospho-RTK Array kit in accordance with the manufacturer's protocol. Briefly, cells were lysed in ice-cold lysis buffer and 150 µg of total protein was used for the assay. Densitometric quantification of the immunoblot dots was performed using semi-automated image analysis.

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The effect of suramin , a well known antitrypanosomal drug and a novel experimental agent for the treatment of several cancers, on protein-tyrosine phosphatases (PTPases) has been examined. Suramin is a reversible and competitive PTPase inhibitor with Kis values in the low microM range, whereas the Kis for the dual specificity phosphatase VHR is at least 10-fold higher. Although suramin can also inhibit the activity of the potato acid phosphatase at a slightly higher concentration, it is 2-3 orders of magnitude less effective against the protein Ser/Thr phosphatase 1alpha and the bovine intestinal alkaline phosphatase. Suramin binds to the active site of PTPases with a binding stoichiometry of 1:1. Furthermore, when suramin is bound to the active site of PTPases, its fluorescence is enhanced approximately by 10-fold. This property has allowed the determination of the binding affinity of suramin for PTPases and several catalytically impaired mutant PTPases by fluorescence titration techniques. Thus, the active site Cys to Ser mutants bind suramin with similar affinity as the wild type, while the active site Arg to Ala mutant exhibits a 20-fold reduced affinity toward suramin. Interestingly, the general acid deficient Asp to Ala mutant PTPases display an enhanced affinity toward suramin, which is in accord with their use as improved "substrate-trapping" agents. That suramin is a high affinity PTPase inhibitor is consistent with the observation that suramin treatment of cancer cell lines leads to an increase in tyrosine phosphorylation of several cellular proteins. Given the pleiotropic effects of suramin on many enzyme systems and growth factor-receptor interactions, the exact in vivo actions of suramin require further detailed structure-activity investigation of suramin and its structural analogs.[1]

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Sirtuins are NAD(+)-dependent protein deacetylases and are emerging as molecular targets for the development of pharmaceuticals to treat human metabolic and neurological diseases and cancer. To date, several sirtuin inhibitors and activators have been identified, but the structural mechanisms of how these compounds modulate sirtuin activity have not yet been determined. We identified suramin as a compound that binds to human SIRT5 and showed that it inhibits SIRT5 NAD(+)-dependent deacetylase activity with an IC(50) value of 22 microM. To provide insights into how sirtuin function is altered by inhibitors, we determined two crystal structures of SIRT5, one in complex with ADP-ribose, the other bound to suramin. Our structural studies provide a view of a synthetic inhibitory compound in a sirtuin active site revealing that suramin binds into the NAD(+), the product, and the substrate-binding site. Finally, our structures may enable the rational design of more potent inhibitors.[3]

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The COVID-19 pandemic caused by nonstop infections of SARS-CoV-2 has continued to ravage many countries worldwide. Here we report that suramin , a 100-year-old drug, is a potent inhibitor of the SARS-CoV-2 RNA-dependent RNA polymerase (RdRp) and acts by blocking the binding of RNA to the enzyme. In biochemical assays, suramin and its derivatives are at least 20-fold more potent than remdesivir, the currently approved nucleotide drug for treatment of COVID-19. The 2.6 Å cryo-electron microscopy structure of the viral RdRp bound to suramin reveals two binding sites. One site directly blocks the binding of the RNA template strand and the other site clashes with the RNA primer strand near the RdRp catalytic site, thus inhibiting RdRp activity. Suramin blocks viral replication in Vero E6 cells, although the reasons underlying this effect are likely various. Our results provide a structural mechanism for a nonnucleotide inhibitor of the SARS-CoV-2 RdRp.[5]

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Suramin is a symmetric polyanionic naphthylurea originally used for the treatment of trypanosomiasis and onchocerciasis. Suramin and diverse analogues exhibit a broad range of biological actions in vitro and in vivo, including, among others, antiproliferative and antiviral activity. Suramin derivatives usually target purinergic binding sites. Class III histone deacetylases (sirtuins) are amidohydrolases that require nicotinamide adenine dinucleotide (NAD(+)) as a cofactor for their catalytic mechanism(.) Deacetylation of the target proteins leads to a change in conformation and alters the activity of the proteins in question. Suramin was reported to inhibit human sirtuin 1 (SIRT1). We tested a diverse set of suramin analogues to elucidate the inhibition of the NAD(+)-dependent histone deacetylases SIRT1 and SIRT2 and discovered selective inhibitors of human sirtuins with potency in the two-digit nanomolar range. In addition, the structural requirements for the binding of suramin derivatives to sirtuins were investigated by molecular docking. The recently published X-ray crystal structure of human SIRT5 in complex with suramin and the human SIRT2 structure were used to analyze the interaction mode of the novel suramin derivatives[2].

Cell proliferation experiment[6]
Cell Types: HO-8910 PM ovarian cancer cells and HeLa cervical cancer cells
Tested Concentrations: 50, 100, 200, 300, 400, 500 and 600 μg/mL
Incubation Duration: 24, 48, 72 and 96 hrs (hours)
Experimental Results: Cell proliferation was inhibited in a dose- and time-dependent manner.

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Apoptosis analysis [6]
Cell Types: HeLa Cell
Tested Concentrations: 300 μg/mL
Incubation Duration: 48 hrs (hours)
Experimental Results: Induction of apoptosis.

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Western Blot Analysis[7]
Cell Types: PA-SMCs Cell
Tested Concentrations: 1 mg/mL
Incubation Duration: 1 hour
Experimental Results: Dramatically inhibited phosphorylated ERK1/2.

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Flow cytometry assessment of apoptosis [8]
Apoptosis was detected using the Annexin V-fluorescein isothiocyanate (FITC) Apoptosis Detection Kit I. PA-SMCs were treated with suramin (1000 µg/mL). After 24 h, the culture medium containing the detached cells was collected. The plates were rinsed with phosphate buffered saline (PBS), and the cells were detached using 0.05% trypsin/EDTA and combined with their medium and floating cells. The cells were washed twice in cold PBS and resuspended at a density of 106 cells/mL in the binding buffer provided. Each sample was incubated with 5 µL of each of the provided Annexin V-FITC and propidium iodide (PI) solutions for 15 min in the dark. The sample volumes were then increased to 500 µL, and the samples were run using CyAn.

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Isolation, culture, and proliferation tests of human PA-SMCs [8]
PA-SMCs were isolated and cultured as previously described. The cells were subjected to 48 hours of growth arrest in serum-free medium and were then treated with suramin 1 h before incubation with 10% FCS. We also tested the effect of suramin on the growth response to exogenous PDGF (10 ng/mL), EGF (10 ng/mL), or FGF2 (10 ng/mL). For each condition, the cells were incubated for 24 hours and PA-SMC proliferation was then measured by 5-bromo-2-deoxyuridine (BrdU) incorporation and by direct cell counting.

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Organ culture of human pulmonary arteries [8]
Ex vivo organ culture of human pulmonary arteries (hPA) was performed as previously described. Briefly, the arteries were obtained from patients, and segments 1 cm in length were prepared for ex vivo organ culture. The tissues were then incubated in culture medium that was either unsupplemented or supplemented with 10% FCS, suramin (1000 µg/mL), or masitinib (10-5 M) for ten days. The segments were fixed in 4% buffered paraformaldehyde and embedded in paraffin before being serially sectioned at 5 μm thickness and prepared for immunostaining and double immunofluorescence staining.

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Suramin, a polysulfonated naphthylurea widely used in the treatment of trypanosomiasis and onchocerciasis, is currently being investigated as an antitumor agent for the treatment of advanced cancer. Suramin exerts a wide variety of biological effects. We have shown that suramin inhibits cell proliferation and DNA synthesis in cultured HeLa cells. The replication in vitro of SV40 DNA is completely abolished by 40 microM suramin. The inhibition of DNA replication is due to inhibition of DNA polymerases alpha and delta, the replicative enzymes in eukaryotic cells. DNA polymerase alpha is sensitive to lower concentrations of suramin [concentration to achieve 50% inhibition (IC50) of 8 microM] than is DNA polymerase delta (IC50 36 microM), whereas DNA polymerase beta is relatively insensitive to the drug (IC50 of 90 microM). Suramin inhibits other replicative DNA polymerases such as Escherichia coli polymerase I (Klenow fragment) and Thermus aquaticus polymerase. Suramin is noncompetitive with both substrate deoxyribonucleotides and template-primers with respect to DNA polymerase inhibition. Much lower concentrations (8-30 microM) of the drug are required for 50% inhibition of DNA polymerases than for 50% inhibition of other enzymes such as protein kinase C and reverse transcriptase. These results show an important biological effect of this drug and indicate the need for more studies before its clinical use as an antitumor agent [6].

Animal/Disease Models: Adult male Wistar rat (200-225 g) [7]
Doses: 10 mg/kg
Route of Administration: IV; chemical [8]. Twice a week for 3 weeks
Experimental Results:Reversal of established pH, thereby normalizing pulmonary artery pressure values and vascular structure.

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Infection and Treatments [7]
Seventy animals were equally randomized into five groups: SAL = uninfected and untreated; INF = infected and untreated; SR5, SR10, and SR20 = infected and treated with 5, 10, or 20 mg/kg of the purinergic antagonist suramin . The infection was induced by intraperitoneal inoculation of 5000 T. cruzi trypomastigotes (Y strain). The parasites were obtained from mice previously infected with metacyclic trypomastigotes obtained from late stationary-phase cultures on liver infusion tryptose medium. The doses of suramin were based on (i) one-fourth, (ii) half, and (iii) the therapeutic dose (Sur, 20 mg/kg/day) for African trypanosomiasis. Suramin was dissolved in sterilized water and intraperitoneally administered for 15 consecutive days after confirmation of the infection by microscopic identification of parasites in blood samples from all inoculated mice. Control mice were concurrently treated with sterilized water. The animals were euthanized 48 h after the last treatment by cardiac puncture after deep anesthesia (ketamine 45 mg/kg and xylazine 5 mg/kg, i.p.).

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Treatment of animals with suramin [8]
For all experiments, adult male Wistar rats (200-225 g) were used. Pulmonary hypertension was induced by a single subcutaneous injection of monocrotaline (60 mg/Kg). Assessment of pulmonary hypertension was performed as previously described. Briefly, a polyvinyl catheter was introduced into the right jugular vein, then pushed through the RV into the pulmonary artery. A polyethylene catheter was inserted into the right carotid artery. PAP and systemic artery pressure were measured, the thorax was opened, and the left lung was immediately removed and frozen in liquid nitrogen. The heart was dissected and weighed for calculation of the RV hypertrophy index (RV/[LV + S]). The right lung was fixed in the distended state with formalin buffer. After routine processing and paraffin embedding, multiple sections from each lobe were stained with H&E. In each rat, 60 intra-acinar arteries were examined and categorized as nonmuscular (NM), partially muscular (PM), fully muscular (FM), or obliterated (FM+). [8]
To assess the potential preventive and curative effects of suramin , rats were randomly divided into four groups after MCT injection. In the preventive strategy, the treatment was started on the first day, and one group received 10 mg/kg suramin intravenously twice weekly for 3 weeks, while a second group received only the vehicle at the same time points. To assess the potential curative effects of suramin, rats were given MCT and were left untreated for 21 days before being randomly divided into two groups that were subsequently treated with either suramin or vehicle from day 21 to day 42 inclusive. The effect of suramin on survival was evaluated from the day 21 of MCT injection to day 42 corresponding to the treatment period.

Absorption, Distribution and Excretion
Poorly absorbed from the gastrointestinal tract.

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Metabolism / Metabolites
Little or no metabolism

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Biological Half-Life
Approximately 36 to 60 days

Protein Binding
Approximately 99.7%

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man TDLo intravenous 46 mg/kg/5W-I SENSE ORGANS AND SPECIAL SENSES: OTHER: EYE New England Journal of Medicine., 314(1455), 1986
mouse LD50 intravenous 620 mg/kg KIDNEY, URETER, AND BLADDER: CHANGES IN TUBULES (INCLUDING ACUTE RENAL FAILURE, ACUTE TUBULAR NECROSIS) Advances in Pharmacology and Chemotherapy., 15(289), 1978 [PMID:358805]

[1]. Suramin is an active site-directed, reversible, and tight-binding inhibitor of protein-tyrosine phosphatases. J Biol Chem. 1998 May 15;273(20):12281-7.

[2]. Structure-activity studies on suramin analogues as inhibitors of NAD+-dependent histone deacetylases (sirtuins). ChemMedChem. 2007 Oct;2(10):1419-31.

[3]. Structural basis of inhibition of the human NAD+-dependent deacetylase SIRT5 by suramin. Structure. 2007 Mar;15(3):377-89.

[4]. Suramin: a potent inhibitor of the reverse transcriptase of RNA tumor viruses. Cancer Lett. 1979 Nov;8(1):9-22.

[5]. Structural basis for inhibition of the SARS-CoV-2 RNA polymerase by suramin. Nat Struct Mol Biol. 2021 Mar;28(3):319-325.

[6]. Suramin affects DNA synthesis in HeLa cells by inhibition of DNA polymerases. Cancer Res. 1990 Dec 15;50(24):7754-7.

[7]. Purinergic Antagonist Suramin Aggravates Myocarditis and Increases Mortality by EnhancingParasitism, Inflammation, and Reactive Tissue Damage in Trypanosoma cruzi-Infected Mice. Oxid Med Cell Longev. 2018 Sep 30;2018:7385639.

[8]. The beneficial effect of suramin on monocrotaline-induced pulmonary hypertension in rats. PLoS One. 2013 Oct 15;8(10):e77073.

[9]. Suramin and NF449 Are IP5K Inhibitors That Disrupt IP6-mediated Regulation of Cullin RING Ligase and Sensitize Cancer Cells to MLN4924/pevonedistat. J Biol Chem. 2020 Jun 3;jbc.RA120.014375.

Suramin sodium is an organic sodium salt that is the hexasodium salt of suramin. It is an FDA approved drug for African sleeping sickness and river blindness. It has a role as an antinematodal drug, a trypanocidal drug, an antineoplastic agent, an angiogenesis inhibitor, an apoptosis inhibitor, an EC 2.7.11.13 (protein kinase C) inhibitor, a GABA antagonist, a GABA-gated chloride channel antagonist, a purinergic receptor P2 antagonist and a ryanodine receptor agonist. It contains a suramin(6-).
Suramin Sodium 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.
A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties.
See also: Suramin (annotation moved to).

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Suramin is a member of the class of phenylureas that is urea in which each of the amino groups has been substituted by a 3-({2-methyl-5-[(4,6,8-trisulfo-1-naphthyl)carbamoyl]phenyl}carbamoyl)phenyl group. An activator of both the rabbit skeletal muscle RyR1 and sheep cardiac RyR2 isoform ryanodine receptor channels, it has been used for the treatment of human African trypanosomiasis for over 100 years. It has a role as a ryanodine receptor agonist, a GABA-gated chloride channel antagonist, a GABA antagonist, an apoptosis inhibitor, an antineoplastic agent, an angiogenesis inhibitor, a purinergic receptor P2 antagonist, an EC 2.7.11.13 (protein kinase C) inhibitor, an antinematodal drug and a trypanocidal drug. It is a member of phenylureas, a secondary carboxamide and a naphthalenesulfonic acid. It is functionally related to a naphthalene-1,3,5-trisulfonic acid. It is a conjugate acid of a suramin(6-).
A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties. Suramin is manufactured by Bayer in Germany as Germanin®.
Suramin has been reported in Strychnos spinosa with data available.
Suramin is 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. (NCI04)
A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties.

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Drug Indication
For treatment of human sleeping sickness, onchocerciasis and other diseases caused by trypanosomes and worms.

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Mechanism of Action
The mechanism is unknown, but the trypanocidal activity may be due to the inhibition of enzymes involved with the oxidation of reduced nicotinamide-adenine dinucleotide (NADH), which functions as a co-enzyme in many cellular reactions, such as respiration and glycolysis, in the trypanosome parasite. Suramin's action in the treatment of onchocerciasis is macrofilaricidal and partially microfilaricidal. It may also act as an antagonist of P2 receptors and as an agonist of Ryanodine receptors. It also can inhibit follicle-stimulating hormone receptors.

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Suramin--a well-known antitrypanosomal agent--was found to exert a strong inhibitory effect on the RNA-directed DNA polymerase (reverse transcriptase) activity of several oncornaviruses such as Moloney murine leukemia virus, murine Rauscher leukemia viruses, Moloney murine sarcoma virus and avian myeloblastosis virus. Inhibition of enzyme activity was obtained with both endogenous viral RNA and (A)n . oligo(dT) as the template-primer. Suramin effected a 50% inhibition of the reverse transcriptase activity of oncornaviruses at a concentration range of 0.1--1 microgram/ml. In this aspect it compared favorably to ethidium bromide, another trypanocide drug which is considered as one of the most powerful inhibitors of oncornaviral DNA polymerases. The inhibition of reverse transcriptase activity by suramin was competitive with the template-primer, (A)n . oligo(dT), suggesting that the drug may interact with the template-primer binding site of the enzyme.[4]

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Inositol hexakisphosphate (IP6) is an abundant metabolite synthesized from inositol 1,3,4,5,6-pentakisphosphate (IP5) by the single IP5 2-kinase (IP5K). Genetic and biochemical studies have shown that IP6 usually functions as a structural cofactor in protein(s) mediating mRNA export, DNA repair, necroptosis, 3D genome organization, HIV infection, and cullin-RING ligase (CRL) deneddylation. However, it remains unknown whether pharmacological perturbation of cellular IP6 levels affects any of these processes. Here, we performed screening for small molecules that regulate human IP5K activity, revealing that the antiparasitic drug and polysulfonic compound suramin efficiently inhibits IP5K in vitro and in vivo The results from docking experiments and biochemical validations suggested that the suramin targets IP5K in a distinct bidentate manner by concurrently binding to the ATP- and IP5-binding pockets, thereby inhibiting both IP5 phosphorylation and ATP hydrolysis. NF449, a suramin analog with additional sulfonate moieties, more potently inhibited IP5K. Both suramin and NF449 disrupted IP6-dependent sequestration of CRL by the deneddylase COP9 signalosome, thereby affecting CRL activity cycle and component dynamics in an IP5K-dependent manner. Finally, nontoxic doses of suramin, NF449, or NF110 exacerbate the loss of cell viability elicited by the neddylation inhibitor and clinical trial drug MLN4924/pevonedistat, suggesting synergistic ef-fects. Suramin and its analogs provide structural templates for designing potent and specific IP5K inhibitors, which could be used in combination therapy along with MLN4924/pevonedistat. IP5K is a potential mechanistic target of suramin, accounting for suramin's therapeutic effects.[9]

C51H34N6NA6O23S6

1429.17

1427.938

C, 42.86; H, 2.40; N, 5.88; Na, 9.65; O, 25.75; S, 13.46

129-46-4

Suramin;145-63-1

8514

Typically exists as Off-white to light brown solid at room temperature

11.61

6

23

10

92

2940

0

O=C(NC1=CC(C(NC2=CC(C(NC3=CC=C(S(=O)([O-])=O)C4=CC(S(=O)([O-])=O)=CC(S(=O)([O-])=O)=C34)=O)=CC=C2C)=O)=CC=C1)NC5=CC(C(NC6=CC(C(NC7=CC=C(S(=O)([O-])=O)C8=CC(S(=O)([O-])=O)=CC(S(=O)([O-])=O)=C78)=O)=CC=C6C)=O)=CC=C5.[Na+].[Na+].[Na+].[Na+].[Na+].[Na+]

VAPNKLKDKUDFHK-UHFFFAOYSA-H

InChI=1S/C51H40N6O23S6.6Na/c1-25-9-11-29(49(60)54-37-13-15-41(83(69,70)71)35-21-33(81(63,64)65)23-43(45(35)37)85(75,76)77)19-39(25)56-47(58)27-5-3-7-31(17-27)52-51(62)53-32-8-4-6-28(18-32)48(59)57-40-20-30(12-10-26(40)2)50(61)55-38-14-16-42(84(72,73)74)36-22-34(82(66,67)68)24-44(46(36)38)86(78,79)80;;;;;;/h3-24H,1-2H3,(H,54,60)(H,55,61)(H,56,58)(H,57,59)(H2,52,53,62)(H,63,64,65)(H,66,67,68)(H,69,70,71)(H,72,73,74)(H,75,76,77)(H,78,79,80);;;;;;/q;6*+1/p-6

sodium 8,8'-((3,3'-((3,3'-(carbonylbis(azanediyl))bis(benzoyl))bis(azanediyl))bis(4-methylbenzoyl))bis(azanediyl))bis(naphthalene-1,3,5-trisulfonate)

NSC-34936l; NSC34936 ; NSC 34936;Suramin Hexasodium; BAY 205; BAY-205; BAY205; Germanin; NF 060; NF-060; NF060; Suramin; Farma; Fourneau; 129-46-4; suramin hexasodium salt; Suramin sodium salt; Antrypol; Germanin; Naganin;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~83.33 mg/mL (~58.31 mM)
H2O : ~50 mg/mL (~34.99 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (1.46 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (1.46 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: 100 mg/mL (69.97 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)