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1 phatase and by purinergic receptor blockade (suramin).
2 -naphthylazo-6-nitro-4',8'-disulfonate), and suramin.
3 (s) underlying the antimitogenic activity of suramin.
4 tidase apyrase and the P2 receptor inhibitor suramin.
5 ure-assisted design of improved analogues of suramin.
6 arable or significantly improved relative to suramin.
7 nt made a complete recovery after 5 weeks of suramin.
8 ere then directly assessed in the absence of suramin.
9 ring raw beef, and successfully treated with suramin.
10 sphate 6-azophenyl-2',4'-disulfonic acid and suramin.
11 or in activation of RyR2 channels by Ca2+ or suramin.
12 d lysyl oxidase expression in the absence of suramin.
13 imal activity at pH 8--9 and is inhibited by suramin.
14 -specific P2X receptor antagonists, PPADS or suramin.
15 ith apyrase or blockade of P2 receptors with suramin.
16 nists XAMR 0721, periodate-oxidized ATP, and suramin.
17 tive randomized comparison of three doses of 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 (33% v 16%; P =.01) in patients who received suramin.
23 ation, but neither response was inhibited by suramin.
24 eparin interact with elicitor receptors like suramin.
25 of systemin was inhibited in the presence of suramin.
26  curve to increases in CO2 was reduced after suramin.
27 rine cytokines but can still be inhibited by suramin.
28 ch was blocked in the presence of 100 microM suramin.
29 hat was additive to insulin and inhibited by suramin.
30 on is sensitive to the purinergic antagonist suramin.
31 -) mice and C57BL/6 mice given injections of suramin.
32 ch is antagonistic to another anti-HAT drug, suramin.
33 re blocked by the P2Y(2) receptor antagonist suramin.
34 o eflornithine and increasing sensitivity to suramin.
35 as did treatment with the purinergic blocker suramin.
36 sphate 6-azophenyl-2',4'-disulfonic acid and suramin.
37 c application of the P2 receptor antagonists suramin (0.02 M) and pyridoxal-phosphate-6-azophenyl-2',
38 ts were abolished by the P2 receptor blocker suramin (0.02 M, 80 nA), which also reduced the baseline
39 n the presence of the P2-receptor antagonist suramin (0.1 mM), the amplitude of vasoconstrictions to
40 disulfonic acid (PPADS) (0.1-100 microM) and suramin (1-300 microM) inhibited contractions evoked by
41  treated i.v. with paclitaxel (15 mg/kg) and suramin (10 mg/kg) administered twice weekly for 3 weeks
42                                              Suramin (10 microm) and NF449 (3-300 nM) effectively blo
43 Pretreatment of Galpha12WT-NIH3T3 cells with suramin (100 microM), a receptor-uncoupling agent, inhib
44                                              Suramin (100 microm), Cibacron blue 3GA (100 microm), an
45              Purinergic receptor antagonists suramin (100 microm), PPADS (20-50 microm), and apyrase
46 brilliant blue G (BBG: 1 microM), but not by suramin (100 microM).
47 e were blocked by the P2 receptor antagonist suramin (100 microm).
48                           In the presence of suramin (100 micrometer) or gadolinium (100 micrometer),
49 es to ATP, 2MeSATP or ADP were unaffected by suramin (100 micrometer).
50              Microinjection in NTS of either suramin (100 pmol) or pyrinoxalphosphate-6-azophenyl-2',
51 voked a bradycardia which was antagonized by suramin (100 pmol).
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 , 4'-disulphonic acid (20 mg kg-1, i.v.) and suramin (80 mg kg-1, i.v. ) each antagonised both the ea
62       Apyrase (an agent of ADP degradation), suramin (a general P2 receptor antagonist), pyridoxal 5'
63 h higher than CM-cholesterol (P < 0.01), and suramin (a lipoprotein receptor antagonist) decreased ch
64                                              Suramin (a nonselective P(2)-purinoceptor antagonist; 10
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                                     However, suramin, a polycyclic anionic compound, selectively anta
72                                              Suramin, a polysulfonated naphthylurea, is known to be a
73                                              Suramin, a polysulfonated napthylurea, displaces both fo
74 netic analysis of the inhibition of SIRT5 by suramin, a potent sirtuin inhibitor previously shown by
75  APAP in insulin signaling were prevented by suramin, a PTP1B inhibitor, or rosiglitazone that decrea
76 imulated [Ca(2+)]i increase was inhibited by suramin, a purinergic 2Y-receptor inhibitor.
77                       In a rat model of CKD, suramin abrogated proteinuria, limited the decline of re
78 lglucosamine biosynthesis, all contribute to suramin action.
79  of three patients suggests that evidence of suramin activity may be delayed.
80                                              Suramin, added to the internal solution of voltage-clamp
81                                              Suramin alone had no antitumor activity.
82 ut only RLC phosphorylation was inhibited by suramin/alpha,beta-meATP.
83 ase (MLCK) in smooth muscles, the effects of suramin/alpha,beta-methylene ATP (alpha,beta-meATP) (pur
84                                              Suramin also decreased the expression of multiple cytoki
85 ment with the purinergic receptor antagonist suramin also partly suppressed early regenerative signal
86                                    PPADS and suramin also reduced contractions to exogenous ATP (300
87                                              Suramin also reduced wave propagation from Muller cell t
88 d this response was blocked by coaddition of suramin, an inhibitor of FGF ligand-receptor interaction
89 um chemoresistance in solid tumors, and that suramin, an inhibitor of multiple growth factors includi
90                                              Suramin, an inhibitor of systemin receptor function, str
91                     We therefore screened 45 suramin analogs against a panel of seven PTPs, including
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 otherapy drugs that cause neuropathy include suramin and Dolostatin-10.
98                                         Both suramin and doxorubicin are potent (low-microM) DNA- and
99                             The results show suramin and heparin exerted multiple concentration-depen
100                                              Suramin and heparin yielded qualitatively and quantitati
101 ere sensitive to the P2 receptor antagonists suramin and iso-PPADS.
102 hosphate-6-azophenyl-2',4'-disulphonic acid, suramin and kynurenic acid) significantly decreased base
103                                              Suramin and NF449 are polysulfonates, with six and eight
104 that plays a key role in the binding of both suramin and NF449 to P2X(1) receptors.
105  mouse receptor, the sensitivity to block by suramin and NF449 was much increased for E138K, but not
106 8N, reduced the sensitivity to block by both suramin and NF449.
107  by the purported close binding proximity of suramin and nicotinamide, we prepared two sets of fragme
108  A, B, and C, and sulfated compounds such as suramin and pentosan efficiently extract TIMP-3 from the
109 ytes with P2 receptor antagonists, including suramin and periodate oxidized ATP (oATP), resulted in a
110 llular adhesion molecule-1 (ICAM-1), whereas suramin and PPADS decreased both ATPgammaS-induced and b
111                                              Suramin and PPADS often reduced ongoing activity, and bl
112 potentiated by ivermectin but insensitive to suramin and PPADS, and it permeated the large cation N-m
113                                              Suramin and PPADS, general P2Y receptor blockers, and MR
114 -induced currents were blocked by 100 microm suramin and pyridoxal phosphate 6-azophenyl-2',4'-disulf
115                                              Suramin and pyridoxal phosphate-6-azophenyl-2', 4'-disul
116 re was little or no effect on sensitivity to suramin and pyridoxal-phosphate-6-azophenyl-2,4-disulfon
117                  The P2 receptor antagonists suramin and pyridoxalphosphate-6-azophenyl-2'4'-disulfon
118 tly most effective inhibitory compounds were suramin and quercetin-3beta-d-glucoside sulfate.
119                    As a result of this data, suramin and radiation are now being administered concurr
120                                              Suramin and reactive blue 2 inhibited the peak amplitude
121 pyrase), and purinergic receptor inhibitors (suramin and reactive blue-2).
122                        This study shows that suramin and several structurally related compounds [8,8'
123 her investigation, and two known inhibitors, suramin and SirReal2, were profiled against substrates c
124 and nuclear influx of Myb3 were inhibited by suramin and SQ22536, respective inhibitors of the Galpha
125 enhancement of the efficacy of paclitaxel by suramin and support the use of nontoxic doses of suramin
126 erpretation can account for the results with suramin and TNP-ATP.
127 ATP signaling by the P2Y1 blockers, MRS2176, suramin, and apyrase, reduces Ca(2+) transients and reta
128 zumab, the purinergic P2 receptor antagonist suramin, and EDTA.
129        Sensitivity to the antagonists NF449, suramin, and PPADS was conferred by the nature of the ex
130  P2X1 receptor, which is inhibited by NF449, suramin, and pyridoxal-phosphate-6-azophenyl-2,4-disulfo
131 g bicuculline-resistant mPSCs are blocked by suramin, and their decay phase is briefer than that of G
132 phylline, but not the P2-receptor antagonist suramin, antagonized the effect of AP4A, suggesting that
133                             Two molecules of suramin appear to bind simultaneously to one molecule of
134                                              Suramin, apyrase (an ATP-hydrolyzing enzyme), and TTX su
135                             These actions of suramin are not consistent with simple competitive antag
136 ng therapy with the growth factor antagonist suramin as part of CALGB 9480.
137 e utility of suramin, particularly high-dose suramin, as administered on this schedule.
138 he basis of the feasibility of administering suramin, as judged by the number of patients who develop
139 habeta-MethyleneADP enhanced the fade, while suramin at 50 micrometer prevented the early component o
140       The first step involves the binding of suramin at specific sites on the protein.
141 e significantly inhibited by oATP but not by suramin; ATP-induced apoptosis was significantly inhibit
142 f a suramin molecule, could not compete with suramin binding and oligomerization suggesting that the
143 n bound to protein provided evidence for two suramin-binding sites on each C9 and three on each C8 in
144                                              Suramin binds directly to a peptide that corresponds to
145   Results of the NMR experiments reveal that suramin binds to residues in the heparin binding pocket
146                                              Suramin bioavailability and function were demonstrated b
147 ttern of pH modulation of ATP activation and suramin blockade.
148                           Luminal apyrase or suramin blocked the effects of forskolin but not ACh on
149 y genistein, but not G-protein inhibition by suramin, blocked FN-induced intracellular Ca(2+) signali
150 r HC067047 or purinergic receptor antagonist suramin blunted flow/pressure-evoked vasoconstriction, w
151                                Cisplatin and suramin both result in apoptosis in dorsal root ganglion
152 (oATP) but not by the P2 receptor antagonist suramin; both ATP and BzATP increase intracellular Ca(2+
153 Transients were partially attenuated by 1 mm suramin but PPADS (80 microm) had no effect.
154 tment with the growth factor receptor poison suramin but was sensitive to treatment with the PI 3-K i
155 y chemoreceptor stimulation was depressed by suramin, but convergent excitatory inputs from pharyngo-
156  by the purinergic receptor (P2X) antagonist suramin, but they are totally unaffected by the alpha1 a
157                           We discovered that suramin (C51H40N6O23S6) bound to TIMP-3 with a KD value
158 e axonal neuropathies, tacrolimus and rarely suramin can result in a demyelinating neuropathy that ma
159                                              Suramin caused a significant block in the effect of 100
160                                              Suramin causes accumulation of lamellar inclusion bodies
161                                              Suramin, Cibacron blue 3GA, and apyrase attenuated hypox
162 philic medications (amiodarone, chloroquine, suramin, clofazimine, etc.) may produce a drug-induced l
163 er adjusting for treatment arm, the measured suramin concentration was not associated with clinical r
164 inct increase in G' and G'' as a function of suramin concentration.
165                 Relationships between plasma suramin concentrations and response, toxicity, and survi
166    Oligomerization could be reversed by high suramin concentrations, but 8-aminonaphthalene-1,3,6- tr
167 11 patients revealed that all reached target suramin concentrations.
168 s BBG and oxidized ATP, but not by 30 microM suramin, consistent with the actions of the P2X(7) recep
169 erally long-term release and, in the case of suramin, cross-linked hydrogels that can modulate cellul
170                                    Moreover, suramin decreased expression of the type II TGF-beta rec
171                                     However, suramin decreased TAG oxidation from both VLDL and CM wi
172                                    NF 007, a suramin derivative, induced medium alkalinization, indic
173       Single-drug therapy with paclitaxel or suramin did not reduce body weight.
174                                              Suramin did not reverse the enhancement of cisplatin-ind
175 sphate-6-azophenyl-2',4'-disulfonic acid and suramin) did not block adenosine- or AMP-evoked activati
176     Administration of a proapoptotic dose of suramin diminished the fungal burden.
177 ry compounds yielded several hits, including suramin, doxorubicin and ellagic acid.
178                           We also found that suramin effectively inhibited PRMT1 activity.
179 ethylene ATP, and the purinergic antagonist, suramin, effectively inhibited the local Ca2+ transients
180 rther showed that an inhibitor of aFGF/bFGF (suramin) enhanced the in vitro and in vivo activity of c
181 the determination of the binding affinity of suramin for PTPases and several catalytically impaired m
182                                   Release of suramin from scaffolds was determined using UV spectrosc
183                                  Addition of suramin (G protein-coupled receptor inhibitor) and ethyl
184 e patient who "progressed" after 12 weeks of suramin had a subsequent marked reduction in tumor size
185                                              Suramin had little effect on the mouse receptor.
186                              The addition of suramin had no effect in the absence of CM but reversed
187                                              Suramin has been widely used as an antagonist at P2X rec
188 cal promise in treatment of several cancers, suramin has many undesirable side effects.
189 cid hexasodium salt), a structural analog of suramin, has an increased affinity for TIMP-3 and increa
190 gene survivin and two model polyanion drugs (suramin, heparin).
191                                          The suramin:hFGF-1 binding stoichiometry is estimated to be
192 hropathy, administration of a single dose of suramin immediately after ureteral obstruction abolished
193 activities can be inhibited by the polyanion suramin in a rapidly reversible manner.
194                   We report the structure of suramin, in complex with the heparin-binding site of vac
195                                Cisplatin and suramin induce a length, dose, and time-dependent axonal
196                                              Suramin induced high-affinity trimerization of C8 (Kd =
197                                              Suramin-induced C8 oligomerization may be the primary re
198 city, while some patients with tacrolimus or suramin-induced demyelinating neuropathy may respond to
199 trypsin digestion analysis data suggest that suramin-induced oligomerization of hFGF-1 occurs in two
200 ing excitation-contraction coupling and that suramin-induced potentiation of voltage-gated Ca(2+) rel
201 yme activity, was remarkably unable to block suramin-induced reversion.
202 c activity of both fI and the SP domain, but suramin inhibited only fI and not the SP domain.
203 s of polyionic ligands such as protamine and suramin inhibited the interaction.
204 cultured renal interstitial fibroblasts with suramin inhibited their activation induced by TGF-beta1
205 s the molecular interactions responsible for suramin inhibition of heparin binding, which could be of
206                                              Suramin inhibits fI directly at concentration of 1 mM.
207                                        Since suramin inhibits growth factor signaling pathways and in
208 th factors with their receptors, but whether suramin inhibits the progression of renal fibrosis is un
209  knowledge, this is the first study in which suramin interaction sites on FGF have been characterized
210  in this structure, and other details of VCP-suramin interactions, might provide useful structural in
211    Using a radioreceptor assay, we show that suramin interfered with the binding of the systemin anal
212                                              Suramin ionically cross-linked MDP into a fibrous meshwo
213                                              Suramin is a competitive inhibitor of heparin binding to
214                                              Suramin is a compound that inhibits the interaction of s
215                                              Suramin is a large naphthyl-polysulfonate compound that
216                                              Suramin is a novel agent that has demonstrated prelimina
217   Collectively, these findings indicate that suramin is a potent antifibrotic agent that may have the
218            It has previously been shown that suramin is a potent, reversible, and competitive inhibit
219                                By extension, suramin is proposed to stabilize the unbound state and t
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                                              Suramin may make an effective therapeutic agent for cont
225 n, cAMP/protein kinase A pathway inhibitors, suramin, MDL12330A, or H89 suppressed bile acid-mediated
226  trisulfonate (ANTS2- ), which mimics half a suramin molecule, could not compete with suramin binding
227 y relevant doses of the other anti-HAT drugs suramin, nifurtimox or melarsoprol, but a significant in
228 ze-exclusion chromatography data reveal that suramin oligomerizes hFGF-1 to form a stable tetramer.
229 ls), we sought to investigate the effects of suramin on the phenotype of transformed cells and the ro
230 with this, TF up-regulation was inhibited by suramin or by siRNA silencing of P2Y(2) receptor, but no
231 ) by Asp(-); both currents were prevented by suramin or DIDS pretreatment.
232           Blocking G-protein activation with suramin or intracellular GDP-beta-S, but not intracellul
233  photoreceptors with the G protein uncoupler suramin or pertussis toxin, which inactivates Gi/o/z pro
234 apyrase and blockade of P2Y-purinoceptors by suramin or reactive blue 2 inhibited both beta-blocker-i
235 addition of an anti-FGF-2 blocking antibody, suramin, or treatment with either sodium chlorate or hep
236                      In the isolated retina, suramin (P2 receptor antagonist) reduces the frequency o
237 ved raise questions regarding the utility of suramin, particularly high-dose suramin, as administered
238 and opioid analgesic intake were greater for suramin plus HC (rank sum P =.0001).
239                    Outpatient treatment with suramin plus HC is well tolerated and provides moderate
240 nts were allowed to cross-over to open-label suramin plus HC.
241 460 HRPC patients were randomized to receive suramin plus hydrocortisone (n = 229) or placebo plus hy
242                                              Suramin plus hydrocortisone and androgen deprivation has
243 , and TTPP, both in the entire group and the suramin plus hydrocortisone group at all three landmarks
244  data from a multicenter randomized trial of suramin plus hydrocortisone versus hydrocortisone alone.
245     In this prospective, randomized trial of suramin plus hydrocortisone versus placebo plus hydrocor
246 provement in a randomized phase III trial of suramin plus hydrocortisone versus placebo plus hydrocor
247 treated by combined androgen deprivation and suramin plus hydrocortisone.
248                                   Binding of suramin possibly involves formation of solvent-exposed n
249 oxin) and polyanionic compounds (Evans Blue, suramin, PPNDS).
250               The currents were inhibited by suramin, pyridoxal-5-phosphate-6-azo-2',4'-disulfonic ac
251 TP, were blocked by P2Y receptor antagonists suramin, pyridoxal-phosphate-6-azophenyl-2',4'-disulfona
252                                              Suramin+RB2 or levamisole produced a significant rightwa
253 ished by antagonism of purinergic receptors (suramin+RB2) or TXA2 receptor (SQ29548), or by intratrac
254 n of 4 weeks or longer due to any persistent suramin-related toxicity.
255 cells with high salt, protamine, heparin, or suramin released significant VEGF, suggesting that hepar
256 01), and duration of response was longer for suramin responders (median, 240 v 69 days; P =.0027).
257                            Pretreatment with suramin resulted in the loss of Raf-1 from c-N-ras immun
258 ient P2Y1R-mediated relaxation followed by a suramin-sensitive contraction.
259 duces PKB/Akt activation in an SB203580- and suramin-sensitive manner, suggesting p38 MAPK-dependent
260 d UDP (0.1-1000 micrometer) evoked sustained suramin-sensitive vasoconstrictions.
261 e parasite population lead to differences in suramin sensitivity, a drug commonly used to treat this
262 urintricarboxylic acid (ATA) (IC50=1.4 muM), suramin sodium salt (IC50=3.6 muM), NF 023 hydrate (IC50
263 to suramin-treated cells completely reversed suramin stimulation of lysyl oxidase mRNA levels.
264 adenosine 3',5'-bisphosphate (MRS-2179), and suramin, suggesting that ATP released by neural cells ac
265 in a higher proportion of patients receiving suramin than placebo (43% v 28%; P =.001), and duration
266                           In the presence of suramin, there was a significant increase in esterificat
267                                We also found suramin to be a potent inhibitor (IC(50) = 1.5 microm) o
268                              The addition of suramin to Histoplasma-infected DC inhibited PL-fusion a
269 owth factor receptors that can interact with suramin to interfere with ligand binding.
270                              The addition of suramin to paclitaxel therapy enhanced the antitumor eff
271 with the non-selective purinergic antagonist suramin to test the role of purinergic signaling in C57B
272 ddition of the P(2) purinoceptor antagonist, suramin, to the assay medium.
273 to receive low-, intermediate-, or high-dose suramin (total doses 3.192, 5.320, and 7.661 g/m(2), res
274            Finally, the addition of FGF-2 to suramin-treated cells completely reversed suramin stimul
275 8-day fixed dosing schedule (one cycle), and suramin treatment cycles were repeated every 6 months fo
276                                              Suramin treatment resulted in a more normal phenotype as
277 life nor performance status was decreased by suramin treatment, and overall survival was similar.
278 surface glycoprotein (ISG75) family mediates suramin uptake, and the AP1 adaptin complex, lysosomal p
279      Analysis of the experimental results of suramin using quantitative pharmacology (QP) modeling in
280 d in vivo interaction between paclitaxel and suramin, using human PC3-LN cells which, upon i.v. injec
281 rmore, because only EDG-3 was antagonized by suramin, variations in receptor structure may determine
282  in the uptake of the antitrypanosomal drug, suramin, via invariant surface glycoprotein 75, and in t
283 h pressures, the combination of prazosin and suramin virtually abolished constrictions.
284                                              Suramin was administered on a 78-day fixed dosing schedu
285                           Although high-dose suramin was associated with higher objective and PSA res
286        The pH-dependent blocking activity of suramin was changed at this heteromeric receptor, althou
287                           The P2X antagonist suramin was only able to block partially the 2-meSATP-st
288   The inhibition of medium alkalinization by suramin was reversible in the presence of high concentra
289                                The effect of suramin was selective to purinergic receptors because th
290 nhibitors of in vitro VahC mART activity and suramin was the best inhibitor (IC(50) = 20 muM).
291 was used to hydrolyze extracellular ATP, and suramin was used to block apical P2Y ATP receptors.
292  phosphate, heparin, clodronate, trypan, and suramin, we demonstrate the utility of this strategy.
293  and also of the fluorescence enhancement of suramin when bound to protein provided evidence for two
294 mycin SV, doxycycline, and another molecule, suramin, which binds but does not inhibit Cu(II)-induced
295           Nevertheless, the anticancer agent suramin, which blocks collagenase synthesis by interferi
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.

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