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1 ing unexpected similarity to the activity of sulfasalazine.
2 , and auxiliary gas using the model compound sulfasalazine.
3 ficantly greater with TwHF extract than with sulfasalazine.
4 fficacy similar to positive-control compound sulfasalazine.
5 be prevented by the clinically relevant drug sulfasalazine.
6 oid in chronic arthritis, and broader use of sulfasalazine.
7 an be modified and down-regulated in vivo by sulfasalazine.
8 to penicillamine, 2 to allopurinol, and 1 to sulfasalazine.
9     Treatment of hepatic stellate cells with sulfasalazine (0.5-2.0 mmol/L) induced apoptosis of acti
10  (0.8 [95% confidence interval 0.6-110]) and sulfasalazine (0.7 [95% confidence interval 0.5-1.0]) di
11        TwHF extract, 60 mg 3 times daily, or sulfasalazine, 1 g twice daily.
12 flammation in vivo, we studied the effect of sulfasalazine (100 mg/kg/day by gastric gavage for 3 day
13 hloride followed by recovery with or without sulfasalazine (150 mg/kg) treatment.
14                                Mesalamine or sulfasalazine (2 mM), but not sulfapyridine, significant
15 7.5 to 17.5 mg per week), the combination of sulfasalazine (500 mg twice daily) and hydroxychloroquin
16 the important advance was the development of sulfasalazine, a drug initially used for the treatment o
17 reparation, or the pretreatment of AECs with sulfasalazine, a potent and specific inhibitor of NF-kap
18 sted IRR 2.51, 95% CI 1.29-4.89, P = 0.004), sulfasalazine (adjusted IRR 1.74, 95% CI 1.04-2.91, P =
19 p with a clinically approved candidate drug, sulfasalazine, already in hand.
20                                     Low-dose sulfasalazine also prevented morphologically evident tig
21                                              Sulfasalazine (also as a representative of the salicylat
22 hereas combined treatment with brequinar and sulfasalazine, an FDA-approved drug with ferroptosis-ind
23                      It also cooperated with sulfasalazine, an FDA-approved inhibitor of cystine xCT
24   In addition, 1 patient continued receiving sulfasalazine and 1 patient remained on a regimen of sul
25 ching a sensitivity of 0.03 and 1.3mug/L for sulfasalazine and atrazine, respectively.
26                                              Sulfasalazine and calpain inhibitor I, inhibitors of NF-
27 g group), and 14 of 35 patients treated with sulfasalazine and hydroxychloroquine (40 percent), P = 0
28 ct to clinical benefit, triple therapy, with sulfasalazine and hydroxychloroquine added to methotrexa
29            Other established DMARDs, such as sulfasalazine and hydroxychloroquine, have also demonstr
30 azine and 1 patient remained on a regimen of sulfasalazine and hydroxychloroquine.
31 rmore, some old drugs, such as methotrexate, sulfasalazine and intraarticular glucocorticoids, still
32            Our studies provide evidence that sulfasalazine and methotrexate may be described as a new
33 ation due to toxicity did not differ between sulfasalazine and methotrexate.
34                                              Sulfasalazine and metronidazole may prove to be useful,
35 e is experimental data to support the use of sulfasalazine and metronidazole.
36  by the system [Formula: see text] inhibitor sulfasalazine and rose bengal, but not by system L inhib
37 oved for treatment of inflammatory diseases, sulfasalazine and the antifolate methotrexate.
38 atment of ulcerative colitis (UC) began with sulfasalazine and was driven by sulfapyridine toxicity.
39 itis, combination therapy with methotrexate, sulfasalazine, and hydroxychloroquine is more effective
40 modifying antirheumatic drugs (methotrexate, sulfasalazine, and hydroxychloroquine) or etanercept plu
41 ither methotrexate alone or a combination of sulfasalazine, and hydroxychloroquine.
42 he triple combination of hydroxychloroquine, sulfasalazine, and methotrexate is very effective even i
43  MTX, 4) triple therapy (hydroxychloroquine, sulfasalazine, and MTX), 5) continuation of MTX monother
44 ase reports have suggested that minocycline, sulfasalazine, and penicillamine are associated with ant
45                 We conclude that mesalamine, sulfasalazine, and rosiglitazone significantly reduced t
46 c for the herbicide atrazine, the antibiotic sulfasalazine, and the vitamin biotin in mice and rabbit
47 alathion, pentachlorophenol, pyraclostrobin, sulfasalazine, and triclosan, achieving detection limits
48 dehyde content, leading to the inhibition of sulfasalazine- and erastin-induced ferroptosis.
49 thelial cell line, A549 cells, the effect of sulfasalazine appeared to be mediated in part by inhibit
50                       Hydroxychloroquine and sulfasalazine are compatible with nursing.
51 ent studies have shown that methotrexate and sulfasalazine are relatively safe and effective for JRA.
52 on, 45% of patients in the EI group received sulfasalazine as opposed to 14% in the CT group (chi(2)
53 ely reversed the anti-inflammatory effect of sulfasalazine (at concentrations <1 microM in this in vi
54  signaling, while inhibition of NF-kappaB by sulfasalazine attenuated nucleosome-induced macrophage a
55 reatment with pyrrolidine dithiocarbamate or sulfasalazine attenuated the iNOS-dependent production o
56 ent with > or = 1 DMARD (hydroxychloroquine, sulfasalazine, auranofin, intramuscular gold, D-penicill
57 gy employing bacteria-mediated drug release (sulfasalazine, Azulfidine(R)) was evaluated alongside a
58 antiinflammatory effects of methotrexate and sulfasalazine both in vitro and in vivo, but the mechani
59 ed antiinflammatory agents, methotrexate and sulfasalazine, both in vitro and in vivo.
60 ease was inhibited using either S-(4)-CPG or sulfasalazine, both potent blockers of system xC.
61 O-AS1 weakened the anti-tumor sensitivity to sulfasalazine by inhibiting ferroptosis both in vitro an
62                                 By contrast, sulfasalazine clearly inhibited HRV-16 induction of mRNA
63 with RA were being treated with methotrexate-sulfasalazine combined therapy, and two of the patients
64  for rheumatoid arthritis, with 51 receiving sulfasalazine compared with 38 receiving placebo; and 3)
65                                              Sulfasalazine completely blocked the development of tact
66 upport the concept that passive antibody and sulfasalazine could be an effective and specific adjunct
67 th the clinically approved anti-inflammatory sulfasalazine decreases tumor growth, revealing a therap
68 came evident that many patients treated with sulfasalazine developed intolerance to the drug and, in
69                With several medications (eg, sulfasalazine, diazo-bonded 5-aminosalicylates [ASA], me
70  68 receiving placebo; 2) a 37-week trial of sulfasalazine for rheumatoid arthritis, with 51 receivin
71 ts, 3 subjects with sickle cell disease took sulfasalazine (given orally at 1 g every 8 hours), and t
72  group and 32.8% (CI, 21.3% to 46.0%) of the sulfasalazine group met the ACR 20 response criteria (P=
73 ure to methotrexate, thiopurines, anti-TNFs, sulfasalazine, hydroxychloroquine, abatacept, or rituxim
74                     Two drugs (proguanil and sulfasalazine) implicated in viral replication were show
75 ered individually, both passive antibody and sulfasalazine improved pulmonary function and enhanced P
76               A review of therapeutic use of sulfasalazine in children with chronic arthritis, includ
77  Companion studies were also performed using sulfasalazine in sickle transgenic mice to verify its ef
78 antiinflammatory effects of methotrexate and sulfasalazine in the murine air pouch model of inflammat
79                                              Sulfasalazine increased the exudate adenosine concentrat
80           Multivariable analysis showed that sulfasalazine increased the vaccine response (by 1.49-fo
81  is a critical mediator of methotrexate- and sulfasalazine-induced antiinflammatory activity in vitro
82              It has recently been shown that sulfasalazine inhibits 5-aminoimidazole-4-carboxamidorib
83 onsistent with the in vitro observation that sulfasalazine inhibits AICAR transformylase.
84                                              Sulfasalazine is moderately effective for ankylosing spo
85           The anti-inflammatory mechanism of sulfasalazine is not well understood.
86                          One of these drugs, sulfasalazine, is clinically used to treat inflammatory
87 exate plus cyclosporine, hydroxychloroquine, sulfasalazine, leflunomide, etanercept, and infliximab.
88                  These results indicate that sulfasalazine, like methotrexate, enhances adenosine rel
89 ere developed consisting of either a similar sulfasalazine-like prodrug formulation requiring luminal
90                               Treatment with sulfasalazine markedly decreased the number of leukocyte
91 actile allodynia in experimental diabetes by sulfasalazine may stem from its ability to regulate both
92             Moreover, treatment with 5-ASAs (sulfasalazine/mesalamine) shows a high association with
93 e frequently for myocarditis, and ribavirin, sulfasalazine, methotrexate, omalizumab, and heparin for
94                                              Sulfasalazine might be useful in the treatment of nocice
95 rences between methotrexate, leflunomide and sulfasalazine monotherapies; early disease-modifying ant
96 based drugs (aspirin, sodium salicylate, and sulfasalazine) on the development of early stages of dia
97 ination therapy with either methotrexate and sulfasalazine or methotrexate and cyclosporine is being
98 s (limited to methotrexate, leflunomide, and sulfasalazine) or among anti-tumor necrosis factor drugs
99 ocked by inhibitors to NF-kappaB activation (sulfasalazine) or PI 3-kinase (LY294002), and both inhib
100  ANCA seroconversion induced by minocycline, sulfasalazine, or penicillamine.
101 gitis; Child-Pugh classification; and use of sulfasalazine, other 5-aminosalicylic acid preparations,
102  use of MTX monotherapy with the addition of sulfasalazine plus hydroxychloroquine (or etanercept, if
103 n therapies (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroquine) at week 24 if the
104 ept, immediate oral triple therapy (MTX plus sulfasalazine plus hydroxychloroquine), or step-up from
105 ion therapy (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroquine).
106 ver, combination treatment with antibody and sulfasalazine produced a more rapid improvement, with re
107                   The anti-inflammatory drug sulfasalazine programs macrophages for enhanced Pneumocy
108           A single in vivo administration of sulfasalazine promoted accelerated recovery from fibrosi
109 on and targets of the anti-inflammatory drug sulfasalazine prompted us to investigate its effect on n
110 atients continued receiving TwHF extract and sulfasalazine, respectively, during the 24 weeks of the
111 is of Pneumocystis Both passive antibody and sulfasalazine resulted in the suppression of Th1 cytokin
112                   We examined the effects of sulfasalazine, salicylates, and the poly(ADP-ribose) pol
113 with FDA-approved rheumatoid arthritis drugs sulfasalazine (SAS) and auranofin: in MYCN-amplified, pa
114 e tumor and the ensuing hyperexcitability by sulfasalazine (SAS), a US Food and Drug Administration-a
115 CT activity with the pharmacologic inhibitor sulfasalazine (SASP).
116              Mechanistic studies showed that sulfasalazine selectively blocks nuclear factor-kappaB-d
117                                In these mice sulfasalazine significantly reduced CEC expression of va
118          In humans with sickle cell disease, sulfasalazine significantly reduced CEC expression of VC
119                      Further, both 5-ASA and sulfasalazine significantly reduced the growth of the fa
120  SLC7A11, as cotreatment with its inhibitor, sulfasalazine, significantly reduce extracellular RSSH r
121 flammation, so we tested the hypothesis that sulfasalazine similarly promotes intracellular AICAR acc
122                                              Sulfasalazine (SSZ) an FDA approved anti-inflammatory ag
123               We investigated the effects of sulfasalazine (SSZ) and its metabolites, sulfapyridine (
124                   To compare the efficacy of sulfasalazine (SSZ) with its two moieties, 5-aminosalicy
125 ne model either alone or in combination with Sulfasalazine (SSZ), a standard therapy for ulcerative c
126  were randomized to receive step-up therapy (sulfasalazine [SSZ] monotherapy, then after 3 months, me
127 L3), approved drugs (for example, sorafenib, sulfasalazine, statins and artemisinin), ionizing radiat
128 er the inhibitor of kappaB kinase suppressor sulfasalazine stimulates hepatic myofibroblast apoptosis
129 a in diabetic mice lacking expression of the sulfasalazine target nuclear factor-kappaB (NF-kappaB) p
130              We also evaluated the levels of sulfasalazine targets in sciatic nerves and dorsal root
131 g intraarticular corticosteroids followed by sulfasalazine therapy if resistant demonstrated reduced
132 ion use was excellent, ranging from 0.71 for sulfasalazine to 0.96 for methotrexate.
133 vioral findings, sciatic nerves and DRG from sulfasalazine-treated diabetic rats displayed a decrease
134                                              Sulfasalazine treatment also increased inosine levels in
135                                    Moreover, sulfasalazine treatment promoted a marked increase in sp
136 ly reversed the anti-inflammatory effects of sulfasalazine treatment.
137 zepine, phenobarbital, phenytoin, primidone, sulfasalazine, triamterene, and trimethoprim) during the
138  cholangitis, severity of liver disease, and sulfasalazine use (adjusted odds ratio, 0.14 [CI, 0.03 t
139 icular corticosteroid injections followed by sulfasalazine versus conservative therapy in patients wi
140                                              Sulfasalazine was a combination designer drug consisting
141 needed for nuclear factor-kappaB inhibition, sulfasalazine was able to prevent TNF-alpha-induced barr
142                                              Sulfasalazine was able to reduce glutathione levels in t
143                                              Sulfasalazine was administered in both groups for persis
144 FMLP) to endothelial cells preincubated with sulfasalazine was inhibited in a dose-dependent manner.
145  we hypothesized that combining antibody and sulfasalazine would have the dual benefit of enhancing f

 
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