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1 20-30% by calcineurin inhibitors (FK506 and cyclosporine A).
2 nd is inhibited by the cyclophilin inhibitor cyclosporine A.
3 trast to the HBV inhibitors, telbivudine and cyclosporine A.
4 unosuppression with mycophenolate mofetil or cyclosporine A.
5 and therapy with the immunosuppressive agent cyclosporine A.
6 n infection was conducted in the presence of cyclosporine A.
7 ynthesis of the important cyclic polypeptide cyclosporine A.
8 me inhibitor Velcade or an immunosuppressant cyclosporine A.
9 disparity, followed by 12 days of high-dose cyclosporine A.
10 All animals were maintained on oral cyclosporine A.
11 iature swine treated with a 12-day course of cyclosporine A.
12 adation induced by the calcineurin inhibitor cyclosporine A.
13 as receptors for the immunosuppressive drug, cyclosporine A.
14 decreased sensitivity to the Rgg2 antagonist cyclosporine A.
15 vitro at a concentration 10 times lower than cyclosporine A.
16 imilar concentration as pharmaceutical grade cyclosporine A.
17 able and orally bioavailable natural product cyclosporine A.
18 s a target of the natural products FK506 and Cyclosporine A.
19 e cellular receptor of the immunosuppressant cyclosporine A.
20 e trough level (C0) and used higher doses of cyclosporine A.
21 transplantation (HCT) and a 45-day course of cyclosporine A.
22 e trough level (C0) and used higher doses of cyclosporine A.
23 tion of the Itpr2 promoter was attenuated by cyclosporine-A.
24 ts were randomized to receive an IV bolus of cyclosporine A (10 mg/kg) or normal saline (placebo, con
25 xic T-lymphocyte antigen-4 immunoglobulin or cyclosporine A (15 mg/kg), graft survival was significan
26 randomized to receive intravenous boluses of cyclosporine A (2.5, 10, or 25 mg/kg) or normal saline (
27 haride (3.0 mg/kg, intravenously; n = 8), or cyclosporine A (6.0 mg/kg, intravenously; n = 6) or tacr
32 loyed to determine whether pretreatment with cyclosporine A, a potent inhibitor of the mitochondrial
33 ubating cells with the cyclophilin inhibitor cyclosporine A, a treatment that triggered efficient ER
34 l other grafts were accepted with 12 days of cyclosporine A across both MHC-matched and MHC class I b
36 gher in recipients aged >44 years and taking cyclosporine A (adjusted hazard ratio = 1.44; P = 0.011)
37 orine A (TCD arm; n=201) or methotrexate and cyclosporine A after transplantation of T-replete marrow
41 ) or cyclophilin (using nonimmunosuppressive cyclosporine A analog) reduced tissue neutrophilia by up
43 clobetasol, or in combination with systemic cyclosporine A and anti-alphabeta-T-cell receptor antibo
45 on of immune tolerance--via oral delivery of cyclosporine A and azathioprine for two months at the ti
48 ath and ROS production were also reversed by cyclosporine A and diazoxide, chemicals that regulate th
50 ibitors of calcineurin/NFAT binding, such as cyclosporine A and FK506, are broadly used in organ tran
52 A-matched related donor and prophylaxis with cyclosporine A and methotrexate were associated with low
53 noclonal antibodies, total body irradiation, cyclosporine A and mycophenolate mofetil (12 doses), and
55 overy of powerful immunotherapeutics such as cyclosporine A and rapamycin that has allowed for the wi
56 Recipients were injected daily with 5 mg/kg cyclosporine A and received either 10 mg/kg prednisolone
57 Alisporivir (Debio-025) is an analogue of cyclosporine A and represents the prototype of a new cla
59 f the most commonly used immunosuppressants, cyclosporine A and tacrolimus (FK506), inhibit the activ
62 -dependent migration (including SP600125 and cyclosporine A) and differentiation (cyclosporine A only
65 ross a class I MHC disparity with 12 days of cyclosporine A, and two across a class I MHC disparity w
67 rapies using calcineurin inhibitors, such as cyclosporine A, are associated with a higher incidence o
70 iliximab (n=5), calcineurin inhibitor (CNI) (cyclosporine A)/basiliximab (n=4) or CNI (tacrolimus)-ba
71 vulnerability to mPT and in higher levels of cyclosporine A being required to inhibit mPTP opening.
72 re proline-containing peptide substrates and cyclosporine A bind and that are vital for the enzymatic
73 bunit ring and unhooks it from cyclophilin D/cyclosporine A binding sites in the ATP synthase F1, pro
75 was rescued upon MG132 treatment as well as cyclosporine A, but not by FK506 or bile acids, suggesti
76 leukin-8, and inhibited by dexamethasone and cyclosporine A, consistent with a role as a proinflammat
77 omplex systems, including the cyclic peptide cyclosporine A, constrained peptide systems, and heteroc
78 for 10 or 100 days or immunosuppressed with cyclosporine A continuously for 50 days and then withdra
80 L without a calcineurin inhibitor (33%), SRL+cyclosporine A (CsA) (33%), and SRL+tacrolimus (TAC) (34
83 monly prescribed topical treatments included cyclosporine A (CSA) 0.05 % (71/104, 68 %), fluoromethol
84 antly, a pharmacological inhibition of CN by cyclosporine A (CsA) ameliorated the alpha-syn-induced l
85 ses for CypA independence using Debio-025, a cyclosporine A (CsA) analog that disrupts CypA-capsid in
86 C3 and that received immunosuppression with cyclosporine A (CsA) and a predegenerated PNG (termed I-
87 ated in DHHC5-deficient hearts, inhibited by cyclosporine A (CsA) and adenosine, promoted by staurosp
89 whereas inhibitors of immunophilins, such as cyclosporine A (CsA) and FK506, inhibited CrkII, but not
90 ions, the inhibitory effects of TPR ligands, cyclosporine A (CsA) and FK506, on AR activity were not
92 til (MMF) are considered more efficient than cyclosporine A (CsA) and MMF, but recent studies have ch
93 f two commonly used immunosuppressive drugs, cyclosporine A (CsA) and sirolimus (SRL), on the develop
95 microperfusion due to the administration of cyclosporine A (CsA) and tacrolimus (Tac) can be evidenc
99 on of rituximab to corticosteroids (CSs) and cyclosporine A (CsA) as first-line therapy for newly dia
101 etreatment with the NFAT signaling inhibitor cyclosporine A (CsA) blocked NaBT-mediated PTEN inductio
102 f an investigational therapy for severe VKC, cyclosporine A (CsA) cationic emulsion (CE), an oil-in-w
103 s are administered the calcineurin inhibitor cyclosporine A (CsA) chronically and demonstrate an incr
104 in an era of lower prednisone doses, whether cyclosporine A (CsA) contributes, whether hypothalamic-p
105 ts who received the combination of sirolimus-cyclosporine A (CsA) demonstrated AVN, compared with 1.4
107 y, and we evaluated their ability to deliver cyclosporine A (CsA) for immunomodulatory applications.
109 To evaluate the treatment with topical 0.05% cyclosporine A (CsA) in patients with subepithelial corn
110 cardiovascular/metabolic risk profile versus cyclosporine A (CsA) in the Belatacept Evaluation of Nep
113 dro-N6-propyl-2,6-benzothiazole-diamine) and cyclosporine A (CSA) inhibited increases in ion conducta
120 ds of patients initiated on monotherapy with cyclosporine A (CsA) microemulsion require addition of s
121 mic or pharmacological postconditioning with cyclosporine A (CsA) might protect the kidney from letha
123 correlates with the variation in response to cyclosporine A (CsA) noted in some clinical trials.
124 tudy evaluated whether sirolimus (SRL), with cyclosporine A (CsA) or alone, affects TA, and examined
125 Patients with acute GvHD are treated with cyclosporine A (CsA) or tacrolimus (FK506), which not on
127 s of 3-8 or 6-12 ng/mL plus reduced-exposure cyclosporine A (CsA) or to mycophenolic acid (MPA) 1.44
128 rapy combined with the calcineurin inhibitor cyclosporine A (CsA) prolonged median primary graft surv
130 The peptidyl-prolyl isomerase inhibitor Cyclosporine A (CsA) selectively kills EGFR+ or HER2+ br
131 pressive action of the calcineurin inhibitor cyclosporine A (CsA) stems from the inhibition of nuclea
132 alcineurin inhibitors tacrolimus (FK506) and cyclosporine A (CSA) to enhance the activity of PHMB, am
133 after renal transplantation) conversion from cyclosporine A (CsA) to everolimus versus continued CsA
134 ty of rapamycin or the calcineurin inhibitor cyclosporine A (CSA) to promote chimerism in a murine ha
135 warm ischemia), and rats subjected to acute cyclosporine A (CSA) toxicity (50 mg/kg for 2 d intraper
136 the RNA-induced silencing complex (RISC) of cyclosporine A (CsA) treated and control human proximal
138 veral time points: (a) SRL (CNI-free) versus cyclosporine A (CsA) treatment de novo, (b) CsA+SRL vers
140 ive strategies combining tacrolimus (TAC) or cyclosporine A (CsA) with mycophenolate mofetil (MMF) an
145 ression with mycophenolate mofetil (MMF) and cyclosporine A (CsA), achieved stable engraftment of dog
146 terestingly, the calcineurin inhibitor (CNI) cyclosporine A (CsA), an immunosuppressant used to preve
147 treated with immunosuppressant drugs such as cyclosporine A (CsA), an inhibitor of calcineurin phosph
148 more than that of M6G (80.31 +/- 21.75 muM); Cyclosporine A (CsA), an inhibitor of OATP2B1, can inhib
150 kin-2 receptor antagonists, tacrolimus (FK), cyclosporine A (CSA), and mycophenolate mofetil/sodium (
151 splant recipients treated with prednisolone, cyclosporine A (CsA), and mycophenolate sodium (MPS) for
153 free protocol was compared with a sirolimus, cyclosporine A (CsA), and prednisone-based immunosuppres
154 re swine can be induced by a short course of cyclosporine A (CsA), and that this stable tolerance is
155 f timing and duration of cardiac exposure to cyclosporine A (CsA), another putative mitochondrial pro
156 ugs, such as mycophenolate mofetil (MMF) and cyclosporine A (CsA), are often used together after HSCT
158 y side effect of the immunosuppressive drug, cyclosporine A (CsA), can be a major issue in transplant
159 on, we tested an anti-inflammatory compound, cyclosporine A (CsA), for its ability to block JCV infec
160 of AM19 and AM1c9, secondary metabolites of cyclosporine A (CsA), have been associated with nephroto
161 , following treatment with the PPI inhibitor cyclosporine A (CsA), or overexpression of a dominant-ne
162 ith immunosuppressive reagents that included cyclosporine A (CSA), rapamycin (RAP), mycophenylate mof
163 atients taking immunosuppressive drugs, like cyclosporine A (CsA), that inhibit calcineurin are highl
164 in mice treated with a potent SC activator, cyclosporine A (CSA), which inhibits the phosphatase cal
166 s of fibrosis-related IL-6-type cytokines in cyclosporine A (CsA)-induced gingival overgrowth (GO).
167 In this study, we examined the effects of cyclosporine A (CsA)-induced immune suppression during e
168 mavirus 1 (MmuPV1) infection caused cSCCs in cyclosporine A (CsA)-treated mice, even in the absence o
177 )/mycophenolate sodium+tacrolimus (TAC), MMF+cyclosporine A (CsA); mammalian target of rapamycin inhi
178 Recipients were immunosuppressed either with cyclosporine A (CsA, 1.5 mg/kg/day subcutaneously) or wi
179 nd during infusion (6, 12, or 24 mg/kg/h) of cyclosporine A (CsA, a P-glycoprotein [P-gp] inhibitor).
182 pening during the preconditioning phase with cyclosporine-A (CsA, 0.2 micromol/L) or sanglifehrin-A (
183 tide) and a model hydrophobic macromolecule (Cyclosporine A, CsA), herein we provide a mechanistic un
185 reviously shown that a 12-day treatment with cyclosporine A (CyA) facilitates induction of tolerance
186 from four AD patients who had received oral cyclosporine A (CyA) treatment for up to 17 months regar
188 to cyclosporine A monotherapy, CMPD 167 with cyclosporine A delayed alloantibody production, suppress
191 rkat cells or treatment of Jurkat cells with cyclosporine A eliminated the Vif-sensitive inhibition a
192 (also called niacinamide), minocycline, and cyclosporine A exhibited a uniform protective effect.
193 degrees C) or by treatment with substrates (cyclosporine A, FK506), modulators (tariquidar), or smal
196 findings may explain why patients receiving cyclosporine A for immunosuppressive therapy display exc
197 mus, KT recipients aged <=44 years receiving cyclosporine A had a higher risk of graft loss (adjusted
200 ochondrial permeability transition inhibitor cyclosporine A, has a requirement for mitochondrial Ca(2
203 regeneration and recruitment are impeded by cyclosporine A immunosuppression, and (4) donor GFP-posi
204 no reconstruction, VBP-allo with and without cyclosporine A immunosuppression, VBP autotransplantatio
207 ucted from June 22, 2010, to March 13, 2013 (Cyclosporine A in Out-of-Hospital Cardiac Arrest Resusci
210 s also enhanced viral resistance to the drug cyclosporine A, indicating a reduced dependence of the c
213 he immunosuppressants tacrolimus (FK506) and cyclosporine A inhibit calcineurin and have potent antif
215 this occurs independently of cyclophilin D (cyclosporine A insensitive) rather it is through decreas
216 tion were observed both in mice treated with cyclosporine, a known stimulator of the HCM response, an
217 or PLCgamma2 or inhibiting calcineurin with cyclosporine A leads to increased expression of PD-1 lig
220 ) and ACI donors (group 5) were treated with cyclosporine A monotherapy (16 mg/kg/day, tapered to 2 m
225 maintenance immunosuppression consisting of cyclosporine A, mycophenolate mofetil, and steroids.
226 ependent of immunosuppressive therapy (using cyclosporine A, mycophenolate mofetil, or azathioprine a
233 ural Terminology codes and prescriptions for cyclosporine A ophthalmic emulsion were used to identify
234 ell treatment with the calcineurin inhibitor cyclosporine A or a NFAT-specific inhibitor led to a sha
235 aling pathway in lymphoma cells, either with cyclosporine A or anti-CD1d blocking antibody, prolonged
236 hat short term (4-6 h) treatment with 15 muM cyclosporine A or FK506 rescues the pre-formed immature
237 eliorated in T4C3 cells by pretreatment with cyclosporine A or FK506, implicating the calcium-depende
238 ation in its catalytic site, antagonism with cyclosporine A or FK506, or intracellular perfusion with
239 264)K variant was rescued by the addition of cyclosporine A or infection of a cyclophilin A-deficient
240 indicated that inhibition of calcineurin by cyclosporine A or knockdown of NFATc4 using small interf
241 si(m), and were protected from cell death by cyclosporine A or ppif ablation, implicating the mitocho
243 three specific calcineurin inhibitors FK506, cyclosporine A, or calcineurin inhibitory peptide preven
244 Ca(2+) signaling or calcineurin with BAPTA, cyclosporine A, or FK506 prevented activation of NF-kapp
245 c acid, the calcineurin inhibitors FK506 and cyclosporine A, or use of acinar cells from calcineurin
246 pulses of cyclophosphamide, vincristine, or cyclosporine A; or salvage splenectomy are considered.
247 p treatment with dexamethasone (P < 0.01) or cyclosporine A (P < 0.01) significantly lowered MS adhes
248 ecedented strategy for preparing polylactide-cyclosporine A (PLA-CsA) NPs (termed CsA-NPs) through Cs
249 tch1+/- mice with immunosuppressive doses of cyclosporine A plus prednisolone for 4-1/2 mo increased
250 nts spanned four immunosuppressive eras: pre-cyclosporine A (pre-CsA) era (16%), CsA era (23%), tacro
251 In contrast, reduction of p53 levels or cyclosporine A pretreatment of mice prevents this comple
253 tructive jaundice, prostaglandin inhibitors, cyclosporine A, radiocontrast dyes and volatile anesthet
255 with chaperone Hsp70, and the treatment with cyclosporine A reduces the association of mutant P-gp, t
257 ion with costimulation blockade and low-dose cyclosporine A resulted in a complete deletion of periph
258 ith phosphatase inhibitors (okadaic acid and cyclosporine A) resulted in a modest inhibition of the T
259 toxicity equivalents of model P-gp inhibitor cyclosporine A) revealed high inhibitory potential of po
260 tochondrial Ca(2+) influx, by mPTP inhibitor cyclosporine A, sanglifehrin, and in cyclophilin D knock
262 ha treated mice underwent calcium-dependent, cyclosporine A-sensitive swelling, which was prevented b
263 ells markedly induced COX-2 expression via a cyclosporine A-sensitive, calcineurin/NFAT-dependent pat
264 gamma-inducing effect of NcAg was blocked by cyclosporine, a specific ligand for CyP, in a dose-depen
266 eta-turns of the orally bioavailable peptide cyclosporine A, suggests that the introduction of bioact
268 currently available immunosuppressive agents cyclosporine A, tacrolimus, and rapamycin have potent an
269 ation with either T-cell depleted marrow and cyclosporine A (TCD arm; n=201) or methotrexate and cycl
273 wever, we demonstrate that a brief course of cyclosporine A to rat renal allograft recipients promote
275 rtrophy group (n = 5), and aortic-banded and cyclosporine A- treated cardiomyopathy group (n = 5).
280 keratin 16 (K16) mRNA] at baseline and after cyclosporine A treatment in 25 moderate to severe AD pat
284 late of diabetes development; tacrolimus and cyclosporine A treatments were associated with increased
285 kidneys long-term after 12 days of high-dose cyclosporine A, uniformly accepted donor-major histocomp
286 er patients, in women, in patients receiving cyclosporine A versus tacrolimus, and in patients with b
289 yl-Val-Ala-Asp-(OMe) fluoromethyl ketone and cyclosporine A, we also showed that AD198-induced PLS3 p
290 ender, cardiovascular disease before LT, and cyclosporine A were associated with the risk of long-ter
294 T-cell IFN-gamma production were ablated by cyclosporine A, which inhibits signaling through the T-c
296 2 expression in HGFs, whereas treatment with cyclosporine-A, which inhibited CD147 expression, reduce
297 -principle, the known binding interaction of Cyclosporine A with cyclophilin A protein in a yeast cel
298 sporivir, a nonimmunosuppressive analogue of cyclosporine A with potent cyclophilin inhibition proper
299 ation with or without immunosuppression with cyclosporine A (with cyclosporine A, n=6; no cyclosporin