ライフサイエンスコーパス: suramin

1 phatase and by purinergic receptor blockade (suramin).

2 sphate 6-azophenyl-2',4'-disulfonic acid and suramin.

3 -naphthylazo-6-nitro-4',8'-disulfonate), and suramin.

4 (s) underlying the antimitogenic activity of suramin.

5 tidase apyrase and the P2 receptor inhibitor suramin.

6 ure-assisted design of improved analogues of suramin.

7 arable or significantly improved relative to suramin.

8 ere then directly assessed in the absence of suramin.

9 sphate 6-azophenyl-2',4'-disulfonic acid and suramin.

10 or in activation of RyR2 channels by Ca2+ or suramin.

11 d lysyl oxidase expression in the absence of suramin.

12 imal activity at pH 8--9 and is inhibited by suramin.

13 -specific P2X receptor antagonists, PPADS or suramin.

14 ith apyrase or blockade of P2 receptors with suramin.

15 nists XAMR 0721, periodate-oxidized ATP, and suramin.

16 tive randomized comparison of three doses of suramin.

17 ch is antagonistic to another anti-HAT drug, suramin.

18 nergistic interaction between paclitaxel and suramin.

19 ibition of SHP-1 by the reversible inhibitor suramin.

20 plete reversal in the presence of <20 microM suramin.

21 arbohydrate elicitors were also inhibited by suramin.

22 o eflornithine and increasing sensitivity to suramin.

23 (33% v 16%; P =.01) in patients who received suramin.

24 ation, but neither response was inhibited by suramin.

25 as did treatment with the purinergic blocker suramin.

26 eparin interact with elicitor receptors like suramin.

27 of systemin was inhibited in the presence of suramin.

28 curve to increases in CO2 was reduced after suramin.

29 nt made a complete recovery after 5 weeks of suramin.

30 ring raw beef, and successfully treated with suramin.

31 hat was additive to insulin and inhibited by suramin.

32 on is sensitive to the purinergic antagonist suramin.

33 -) mice and C57BL/6 mice given injections of suramin.

34 re blocked by the P2Y(2) receptor antagonist suramin.

35 c application of the P2 receptor antagonists suramin (0.02 M) and pyridoxal-phosphate-6-azophenyl-2',

36 ts were abolished by the P2 receptor blocker suramin (0.02 M, 80 nA), which also reduced the baseline

37 n the presence of the P2-receptor antagonist suramin (0.1 mM), the amplitude of vasoconstrictions to

38 disulfonic acid (PPADS) (0.1-100 microM) and suramin (1-300 microM) inhibited contractions evoked by

39 treated i.v. with paclitaxel (15 mg/kg) and suramin (10 mg/kg) administered twice weekly for 3 weeks

40 Suramin (10 microm) and NF449 (3-300 nM) effectively blo

41 Pretreatment of Galpha12WT-NIH3T3 cells with suramin (100 microM), a receptor-uncoupling agent, inhib

42 Suramin (100 microm), Cibacron blue 3GA (100 microm), an

43 Purinergic receptor antagonists suramin (100 microm), PPADS (20-50 microm), and apyrase

44 brilliant blue G (BBG: 1 microM), but not by suramin (100 microM).

45 e were blocked by the P2 receptor antagonist suramin (100 microm).

46 In the presence of suramin (100 micrometer) or gadolinium (100 micrometer),

47 es to ATP, 2MeSATP or ADP were unaffected by suramin (100 micrometer).

48 Microinjection in NTS of either suramin (100 pmol) or pyrinoxalphosphate-6-azophenyl-2',

49 voked a bradycardia which was antagonized by suramin (100 pmol).

50 d by apyrase, or by the P2 receptor agonists suramin (150 mum) or PPADS (50 mum) but were blocked by

51 nyl-2',4'-disulfonic acid (PPADS; 50 mum) or suramin (150 mum) were added to the extracellular buffer

52 Suramin (200 microM) or PPADS (200 microM) applied by in

53 e insensitive to block by the P2X antagonist suramin (300 microM) but were prevented by incubation in

54 PPADS (100 microM) and suramin (300 microM) reduced the peak neurogenic contrac

55 by the P(2X) purinergic receptor antagonist suramin (300-500 microM).

56 Suramin (40 microM) significantly increased the single c

57 2 receptor antagonists PPADS (10 microm) and suramin (5 microm).

58 Bilateral microinjection of suramin (50 nl, 0.02 M), a P2 purinoceptor antagonist, i

59 Suramin (500 mum), a broad-spectrum P2 receptor antagoni

60 The G-protein G(beta)gamma subunit blockers suramin (8,8'-[carbonylbis[imino-3,1-phenylen ecarbonyli

61 Apyrase (an agent of ADP degradation), suramin (a general P2 receptor antagonist), pyridoxal 5'

62 h higher than CM-cholesterol (P < 0.01), and suramin (a lipoprotein receptor antagonist) decreased ch

63 Suramin (a nonselective P(2)-purinoceptor antagonist; 10

64 gly inhibit HMGA2-DNA interactions including suramin, a century-old, negatively charged antiparasitic

65 Autocrine pathways were blocked with suramin, a general inhibitor of growth factor receptor b

66 enhanced their sensitivity to cisplatin; 3) suramin, a growth factor receptor antagonist that greatl

67 Treatment of adherent HKs with suramin, a heparin analogue, or inhibitors of phosphotyr

68 d by the polysulfonated naphtylurea compound suramin, a known inhibitor of cytokine and growth factor

69 Suramin, a nonselective P2 receptor antagonist, and MRS-

70 ice and C57BL/6 wild-type mice injected with suramin, a pharmacologic inhibitor of P2YR.

71 Suramin, a polysulfonated naphthylurea, is known to be a

72 Suramin, a polysulfonated napthylurea, displaces both fo

73 netic analysis of the inhibition of SIRT5 by suramin, a potent sirtuin inhibitor previously shown by

74 APAP in insulin signaling were prevented by suramin, a PTP1B inhibitor, or rosiglitazone that decrea

75 imulated [Ca(2+)]i increase was inhibited by suramin, a purinergic 2Y-receptor inhibitor.

76 In a rat model of CKD, suramin abrogated proteinuria, limited the decline of re

77 lglucosamine biosynthesis, all contribute to suramin action.

78 of three patients suggests that evidence of suramin activity may be delayed.

79 Suramin, added to the internal solution of voltage-clamp

80 Suramin alone had no antitumor activity.

81 ut only RLC phosphorylation was inhibited by suramin/alpha,beta-meATP.

82 ase (MLCK) in smooth muscles, the effects of suramin/alpha,beta-methylene ATP (alpha,beta-meATP) (pur

83 Suramin also decreased the expression of multiple cytoki

84 ment with the purinergic receptor antagonist suramin also partly suppressed early regenerative signal

85 PPADS and suramin also reduced contractions to exogenous ATP (300

86 Suramin also reduced wave propagation from Muller cell t

87 d this response was blocked by coaddition of suramin, an inhibitor of FGF ligand-receptor interaction

88 um chemoresistance in solid tumors, and that suramin, an inhibitor of multiple growth factors includi

89 Suramin, an inhibitor of systemin receptor function, str

90 We therefore screened 45 suramin analogs against a panel of seven PTPs, including

91 with 1 mum U46619 in the presence of 140 mum suramin and 1 mum prazosin.

92 P-induced vasodilation was inhibited by both suramin and 2',3'-O-(2,4,6-trinitrophenyl)-ATP (TNP-ATP)

93 Further, it is blocked by pre-incubation in suramin and by a selective protein kinase A inhibitor (H

94 ion are blocked by the purinergic antagonist suramin and by TTX.

95 that can be inhibited by pertussis toxin and suramin and can be desensitized by ATP and ADP, suggesti

96 olongs phosphorylation of p80 in response to suramin and changes in adhesion.

97 Both suramin and doxorubicin are potent (low-microM) DNA- and

98 The results show suramin and heparin exerted multiple concentration-depen

99 Suramin and heparin yielded qualitatively and quantitati

100 ere sensitive to the P2 receptor antagonists suramin and iso-PPADS.

101 hosphate-6-azophenyl-2',4'-disulphonic acid, suramin and kynurenic acid) significantly decreased base

102 Suramin and NF449 are polysulfonates, with six and eight

103 that plays a key role in the binding of both suramin and NF449 to P2X(1) receptors.

104 mouse receptor, the sensitivity to block by suramin and NF449 was much increased for E138K, but not

105 8N, reduced the sensitivity to block by both suramin and NF449.

106 by the purported close binding proximity of suramin and nicotinamide, we prepared two sets of fragme

107 A, B, and C, and sulfated compounds such as suramin and pentosan efficiently extract TIMP-3 from the

108 ytes with P2 receptor antagonists, including suramin and periodate oxidized ATP (oATP), resulted in a

109 llular adhesion molecule-1 (ICAM-1), whereas suramin and PPADS decreased both ATPgammaS-induced and b

110 Suramin and PPADS often reduced ongoing activity, and bl

111 potentiated by ivermectin but insensitive to suramin and PPADS, and it permeated the large cation N-m

112 Suramin and PPADS, general P2Y receptor blockers, and MR

113 creased contraction to EFS in the absence of suramin and prazosin.

114 -induced currents were blocked by 100 microm suramin and pyridoxal phosphate 6-azophenyl-2',4'-disulf

115 re was little or no effect on sensitivity to suramin and pyridoxal-phosphate-6-azophenyl-2,4-disulfon

116 The P2 receptor antagonists suramin and pyridoxalphosphate-6-azophenyl-2'4'-disulfon

117 tly most effective inhibitory compounds were suramin and quercetin-3beta-d-glucoside sulfate.

118 As a result of this data, suramin and radiation are now being administered concurr

119 Suramin and reactive blue 2 inhibited the peak amplitude

120 pyrase), and purinergic receptor inhibitors (suramin and reactive blue-2).

121 This study shows that suramin and several structurally related compounds [8,8'

122 her investigation, and two known inhibitors, suramin and SirReal2, were profiled against substrates c

123 and nuclear influx of Myb3 were inhibited by suramin and SQ22536, respective inhibitors of the Galpha

124 enhancement of the efficacy of paclitaxel by suramin and support the use of nontoxic doses of suramin

125 erpretation can account for the results with suramin and TNP-ATP.

126 ATP signaling by the P2Y1 blockers, MRS2176, suramin, and apyrase, reduces Ca(2+) transients and reta

127 zumab, the purinergic P2 receptor antagonist suramin, and EDTA.

128 Sensitivity to the antagonists NF449, suramin, and PPADS was conferred by the nature of the ex

129 P2X1 receptor, which is inhibited by NF449, suramin, and pyridoxal-phosphate-6-azophenyl-2,4-disulfo

130 g bicuculline-resistant mPSCs are blocked by suramin, and their decay phase is briefer than that of G

131 phylline, but not the P2-receptor antagonist suramin, antagonized the effect of AP4A, suggesting that

132 Two molecules of suramin appear to bind simultaneously to one molecule of

133 Suramin, apyrase (an ATP-hydrolyzing enzyme), and TTX su

134 These actions of suramin are not consistent with simple competitive antag

135 ng therapy with the growth factor antagonist suramin as part of CALGB 9480.

136 e utility of suramin, particularly high-dose suramin, as administered on this schedule.

137 he basis of the feasibility of administering suramin, as judged by the number of patients who develop

138 habeta-MethyleneADP enhanced the fade, while suramin at 50 micrometer prevented the early component o

139 The first step involves the binding of suramin at specific sites on the protein.

140 e significantly inhibited by oATP but not by suramin; ATP-induced apoptosis was significantly inhibit

141 s show that the inhibition is likely through suramin binding to the "AT-hook" DNA-binding motifs and

142 Suramin binds directly to a peptide that corresponds to

143 Results of the NMR experiments reveal that suramin binds to residues in the heparin binding pocket

144 Suramin bioavailability and function were demonstrated b

145 ttern of pH modulation of ATP activation and suramin blockade.

146 Luminal apyrase or suramin blocked the effects of forskolin but not ACh on

147 y genistein, but not G-protein inhibition by suramin, blocked FN-induced intracellular Ca(2+) signali

148 r HC067047 or purinergic receptor antagonist suramin blunted flow/pressure-evoked vasoconstriction, w

149 Cisplatin and suramin both result in apoptosis in dorsal root ganglion

150 (oATP) but not by the P2 receptor antagonist suramin; both ATP and BzATP increase intracellular Ca(2+

151 Transients were partially attenuated by 1 mm suramin but PPADS (80 microm) had no effect.

152 tment with the growth factor receptor poison suramin but was sensitive to treatment with the PI 3-K i

153 y chemoreceptor stimulation was depressed by suramin, but convergent excitatory inputs from pharyngo-

154 by the purinergic receptor (P2X) antagonist suramin, but they are totally unaffected by the alpha1 a

155 We discovered that suramin (C51H40N6O23S6) bound to TIMP-3 with a KD value

156 e axonal neuropathies, tacrolimus and rarely suramin can result in a demyelinating neuropathy that ma

157 Suramin caused a significant block in the effect of 100

158 Suramin causes accumulation of lamellar inclusion bodies

159 Suramin, Cibacron blue 3GA, and apyrase attenuated hypox

160 philic medications (amiodarone, chloroquine, suramin, clofazimine, etc.) may produce a drug-induced l

161 er adjusting for treatment arm, the measured suramin concentration was not associated with clinical r

162 inct increase in G' and G'' as a function of suramin concentration.

163 Relationships between plasma suramin concentrations and response, toxicity, and survi

164 11 patients revealed that all reached target suramin concentrations.

165 s BBG and oxidized ATP, but not by 30 microM suramin, consistent with the actions of the P2X(7) recep

166 erally long-term release and, in the case of suramin, cross-linked hydrogels that can modulate cellul

167 Moreover, suramin decreased expression of the type II TGF-beta rec

168 However, suramin decreased TAG oxidation from both VLDL and CM wi

169 NF 007, a suramin derivative, induced medium alkalinization, indic

170 Single-drug therapy with paclitaxel or suramin did not reduce body weight.

171 Suramin did not reverse the enhancement of cisplatin-ind

172 sphate-6-azophenyl-2',4'-disulfonic acid and suramin) did not block adenosine- or AMP-evoked activati

173 Administration of a proapoptotic dose of suramin diminished the fungal burden.

174 Although we found little evidence that suramin disrupts glycolytic or glycosomal pathways, we n

175 ry compounds yielded several hits, including suramin, doxorubicin and ellagic acid.

176 We also found that suramin effectively inhibited PRMT1 activity.

177 ethylene ATP, and the purinergic antagonist, suramin, effectively inhibited the local Ca2+ transients

178 rther showed that an inhibitor of aFGF/bFGF (suramin) enhanced the in vitro and in vivo activity of c

179 Release of suramin from scaffolds was determined using UV spectrosc

180 Addition of suramin (G protein-coupled receptor inhibitor) and ethyl

181 e patient who "progressed" after 12 weeks of suramin had a subsequent marked reduction in tumor size

182 Suramin had little effect on the mouse receptor.

183 The addition of suramin had no effect in the absence of CM but reversed

184 Suramin has been widely used as an antagonist at P2X rec

185 cal promise in treatment of several cancers, suramin has many undesirable side effects.

186 We conclude that suramin has multiple and complex effects on trypanosomes

187 cid hexasodium salt), a structural analog of suramin, has an increased affinity for TIMP-3 and increa

188 gene survivin and two model polyanion drugs (suramin, heparin).

189 The suramin:hFGF-1 binding stoichiometry is estimated to be

190 hropathy, administration of a single dose of suramin immediately after ureteral obstruction abolished

191 activities can be inhibited by the polyanion suramin in a rapidly reversible manner.

192 We report the structure of suramin, in complex with the heparin-binding site of vac

193 Cisplatin and suramin induce a length, dose, and time-dependent axonal

194 Suramin-induced C8 oligomerization may be the primary re

195 ory mechanisms in drug-challenged cells, the suramin-induced collapse of cellular ATP ultimately lead

196 city, while some patients with tacrolimus or suramin-induced demyelinating neuropathy may respond to

197 trypsin digestion analysis data suggest that suramin-induced oligomerization of hFGF-1 occurs in two

198 ing excitation-contraction coupling and that suramin-induced potentiation of voltage-gated Ca(2+) rel

199 Significantly, the vast majority of suramin-induced proteins were normally more abundant in

200 yme activity, was remarkably unable to block suramin-induced reversion.

201 c activity of both fI and the SP domain, but suramin inhibited only fI and not the SP domain.

202 cultured renal interstitial fibroblasts with suramin inhibited their activation induced by TGF-beta1

203 s the molecular interactions responsible for suramin inhibition of heparin binding, which could be of

204 Suramin inhibits fI directly at concentration of 1 mM.

205 Since suramin inhibits growth factor signaling pathways and in

206 th factors with their receptors, but whether suramin inhibits the progression of renal fibrosis is un

207 knowledge, this is the first study in which suramin interaction sites on FGF have been characterized

208 in this structure, and other details of VCP-suramin interactions, might provide useful structural in

209 Using a radioreceptor assay, we show that suramin interfered with the binding of the systemin anal

210 Suramin ionically cross-linked MDP into a fibrous meshwo

211 Suramin is a competitive inhibitor of heparin binding to

212 Suramin is a compound that inhibits the interaction of s

213 Suramin is a large naphthyl-polysulfonate compound that

214 Suramin is a novel agent that has demonstrated prelimina

215 Collectively, these findings indicate that suramin is a potent antifibrotic agent that may have the

216 It has previously been shown that suramin is a potent, reversible, and competitive inhibit

217 carry multiple "AT-hook" DNA-binding motifs, suramin is expected to inhibit HMGA1-DNA interactions as

218 By extension, suramin is proposed to stabilize the unbound state and t

219 Here we observed that suramin is rapidly accumulated in trypanosome cells prop

220 Suramin is thus a promising scaffold for the development

221 This study demonstrates that suramin is well tolerated by patients with recurrent hig

222 monstrating the generality of this approach, suramin led to the formation of the best hydrogels per u

223 The larger than anticipated flexibility of suramin manifested in this structure, and other details

224 n, cAMP/protein kinase A pathway inhibitors, suramin, MDL12330A, or H89 suppressed bile acid-mediated

225 y relevant doses of the other anti-HAT drugs suramin, nifurtimox or melarsoprol, but a significant in

226 ze-exclusion chromatography data reveal that suramin oligomerizes hFGF-1 to form a stable tetramer.

227 ls), we sought to investigate the effects of suramin on the phenotype of transformed cells and the ro

228 with this, TF up-regulation was inhibited by suramin or by siRNA silencing of P2Y(2) receptor, but no

229 ) by Asp(-); both currents were prevented by suramin or DIDS pretreatment.

230 Blocking G-protein activation with suramin or intracellular GDP-beta-S, but not intracellul

231 photoreceptors with the G protein uncoupler suramin or pertussis toxin, which inactivates Gi/o/z pro

232 apyrase and blockade of P2Y-purinoceptors by suramin or reactive blue 2 inhibited both beta-blocker-i

233 addition of an anti-FGF-2 blocking antibody, suramin, or treatment with either sodium chlorate or hep

234 In the isolated retina, suramin (P2 receptor antagonist) reduces the frequency o

235 ved raise questions regarding the utility of suramin, particularly high-dose suramin, as administered

236 and opioid analgesic intake were greater for suramin plus HC (rank sum P =.0001).

237 Outpatient treatment with suramin plus HC is well tolerated and provides moderate

238 nts were allowed to cross-over to open-label suramin plus HC.

239 460 HRPC patients were randomized to receive suramin plus hydrocortisone (n = 229) or placebo plus hy

240 Suramin plus hydrocortisone and androgen deprivation has

241 , and TTPP, both in the entire group and the suramin plus hydrocortisone group at all three landmarks

242 data from a multicenter randomized trial of suramin plus hydrocortisone versus hydrocortisone alone.

243 In this prospective, randomized trial of suramin plus hydrocortisone versus placebo plus hydrocor

244 provement in a randomized phase III trial of suramin plus hydrocortisone versus placebo plus hydrocor

245 treated by combined androgen deprivation and suramin plus hydrocortisone.

246 Binding of suramin possibly involves formation of solvent-exposed n

247 oxin) and polyanionic compounds (Evans Blue, suramin, PPNDS).

248 The currents were inhibited by suramin, pyridoxal-5-phosphate-6-azo-2',4'-disulfonic ac

249 TP, were blocked by P2Y receptor antagonists suramin, pyridoxal-phosphate-6-azophenyl-2',4'-disulfona

250 Suramin+RB2 or levamisole produced a significant rightwa

251 ished by antagonism of purinergic receptors (suramin+RB2) or TXA2 receptor (SQ29548), or by intratrac

252 n of 4 weeks or longer due to any persistent suramin-related toxicity.

253 cells with high salt, protamine, heparin, or suramin released significant VEGF, suggesting that hepar

254 Introduced about a century ago, suramin remains a frontline drug for the management of e

255 ecular basis of the trypanocidal activity of suramin remains unclear, but some evidence suggests broa

256 inhibited by compounds such as CAY10566 and suramin, respectively.

257 01), and duration of response was longer for suramin responders (median, 240 v 69 days; P =.0027).

258 our results suggest that HMGA2 may be one of suramin's cellular targets.

259 ient P2Y1R-mediated relaxation followed by a suramin-sensitive contraction.

260 duces PKB/Akt activation in an SB203580- and suramin-sensitive manner, suggesting p38 MAPK-dependent

261 d UDP (0.1-1000 micrometer) evoked sustained suramin-sensitive vasoconstrictions.

262 e parasite population lead to differences in suramin sensitivity, a drug commonly used to treat this

263 urintricarboxylic acid (ATA) (IC50=1.4 muM), suramin sodium salt (IC50=3.6 muM), NF 023 hydrate (IC50

264 to suramin-treated cells completely reversed suramin stimulation of lysyl oxidase mRNA levels.

265 adenosine 3',5'-bisphosphate (MRS-2179), and suramin, suggesting that ATP released by neural cells ac

266 hat are insensitive to ATP or the antagonist suramin, suggesting uncoupling of the pore and the ligan

267 nteractions and hydrogen bonding between the suramin sulfonated groups and Arg/Lys residues play crit

268 in a higher proportion of patients receiving suramin than placebo (43% v 28%; P =.001), and duration

269 In the presence of suramin, there was a significant increase in esterificat

270 We also found suramin to be a potent inhibitor (IC(50) = 1.5 microm) o

271 The addition of suramin to Histoplasma-infected DC inhibited PL-fusion a

272 owth factor receptors that can interact with suramin to interfere with ligand binding.

273 The addition of suramin to paclitaxel therapy enhanced the antitumor eff

274 with the non-selective purinergic antagonist suramin to test the role of purinergic signaling in C57B

275 sidues play critical roles in the binding of suramin to the "AT-hook" DNA-binding motifs.

276 to receive low-, intermediate-, or high-dose suramin (total doses 3.192, 5.320, and 7.661 g/m(2), res

277 Finally, the addition of FGF-2 to suramin-treated cells completely reversed suramin stimul

278 8-day fixed dosing schedule (one cycle), and suramin treatment cycles were repeated every 6 months fo

279 Suramin treatment resulted in a more normal phenotype as

280 life nor performance status was decreased by suramin treatment, and overall survival was similar.

281 surface glycoprotein (ISG75) family mediates suramin uptake, and the AP1 adaptin complex, lysosomal p

282 Analysis of the experimental results of suramin using quantitative pharmacology (QP) modeling in

283 d in vivo interaction between paclitaxel and suramin, using human PC3-LN cells which, upon i.v. injec

284 in the uptake of the antitrypanosomal drug, suramin, via invariant surface glycoprotein 75, and in t

285 h pressures, the combination of prazosin and suramin virtually abolished constrictions.

286 Suramin was administered on a 78-day fixed dosing schedu

287 Although high-dose suramin was associated with higher objective and PSA res

288 The pH-dependent blocking activity of suramin was changed at this heteromeric receptor, althou

289 The P2X antagonist suramin was only able to block partially the 2-meSATP-st

290 The inhibition of medium alkalinization by suramin was reversible in the presence of high concentra

291 The effect of suramin was selective to purinergic receptors because th

292 nhibitors of in vitro VahC mART activity and suramin was the best inhibitor (IC(50) = 20 muM).

293 was used to hydrolyze extracellular ATP, and suramin was used to block apical P2Y ATP receptors.

294 phosphate, heparin, clodronate, trypan, and suramin, we demonstrate the utility of this strategy.

295 mycin SV, doxycycline, and another molecule, suramin, which binds but does not inhibit Cu(II)-induced

296 Suramin, which is a noncompetitive antagonist at wild-ty

297 c fibroblast growth factor (hFGF-1) binds to suramin with high affinity in the nanomolar range.

298 information for interpreting interactions of suramin with many proteins.

299 min and support the use of nontoxic doses of suramin with paclitaxel in the treatment of lung cancer.

300 rs that shares some structural elements with suramin yet is smaller than the latter.