ライフサイエンスコーパス: tacrolimus

1 normalization of hyperglycemia caused by the tacrolimus.

2 s molecular targets of the immunosuppressant tacrolimus.

3 atients were on once-daily prolonged-release tacrolimus.

4 e outcomes with belatacept-based regimens to tacrolimus.

5 ating calcineurin activity in the absence of Tacrolimus.

6 ncreas allograft biopsies from recipients on tacrolimus.

7 h an initial 1-month treatment with low-dose tacrolimus.

8 llel, belatacept was stopped and switched to tacrolimus.

9 nrollment and were subsequently treated with tacrolimus.

10 in patients on once-daily prolonged-release tacrolimus.

11 tapered steroids, mycophenolate mofetil, and tacrolimus.

12 score achieved statistical significance with tacrolimus (27% reduction; P = 0.02), but was marginal w

13 volving pimecrolimus and 41 trials involving tacrolimus, 8 (20.5%) and 13 (31.7%), respectively, made

14 ys with prednisolone, mycophenolate mofetil, tacrolimus, a combination of these 3 drugs, everolimus,

15 We report the direct agonist effect of tacrolimus, a potent natural immunosuppressant with mult

16 Tacrolimus, a widely prescribed immunosuppressant drug f

17 Tacrolimus, a widely used immunosuppressant, accelerates

18 tina-a mouse model of HHT vascular pathology-tacrolimus activated endothelial Smad1/5/8 and prevented

19 In HUVECs, tacrolimus activated Smad1/5/8 and opposed the pro-angio

20 Sequestration of FKBP12 by rapamycin or tacrolimus activates hepcidin both in vitro and in murin

21 Tacrolimus activates TRPM8 channels in different species

22 nt adherence to and acceptance of once-daily tacrolimus (Advagraf) initiation in kidney and liver tra

23 Therefore, tacrolimus affects glucose metabolism through the butyra

24 kidney transplantation and were treated with tacrolimus alone (n = 3), a CRACM1 inhibitor (PRCL-02) (

25 Tacrolimus also causes side effects, however, such as hy

26 the immunosuppressive drugs cyclosporine and tacrolimus also inhibit BCR-mediated lytic induction but

27 In these cells, tacrolimus also inhibited Akt and p38 stimulation by vas

28 se models, we show that topical therapy with tacrolimus, an anti-T-cell immunosuppressive drug, is hi

29 ly assesses bioequivalence between innovator tacrolimus and 2 generics in individuals with a kidney o

30 Nine patients were on tacrolimus and a mycophenolic antimetabolite, and 70% we

31 as administered standard-dose cyclosporin or tacrolimus and an antimetabolite, mostly mycophenolate m

32 Animals treated initially with tacrolimus and converted to PRCL-02 monotherapy had a me

33 novel belatacept-based strategies employing tacrolimus and corticosteroid avoidance.

34 Ctc is a surrogate of cumulative exposure to tacrolimus and may be helpful for routine dose adjustmen

35 kg per day on days -3, -2, -1 in addition to tacrolimus and methotrexate as GVHD prophylaxis.

36 eria as the trial, but who were treated with tacrolimus and methotrexate at centres not participating

37 en is thus being prospectively compared with tacrolimus and methotrexate in a phase 3 randomised tria

38 d with controls receiving the combination of tacrolimus and methotrexate using a novel composite prim

39 14, and Sept 14, 2016, 224 controls received tacrolimus and methotrexate.

40 Patients received GVHD prophylaxis with tacrolimus and methotrexate.

41 ts show that adverse effects associated with tacrolimus and mycophenolate are complex, and recipient

42 The immunosuppressants tacrolimus and mycophenolate are important components to

43 eceived rituximab 1 month before transplant; tacrolimus and mycophenolate mofetil were started 1 week

44 harged on maintenance immunosuppression with tacrolimus and mycophenolate mofetil with/without steroi

45 h 288 kidney transplant recipients receiving tacrolimus and prednisone were randomized for 3 differen

46 novo kidney transplant recipients receiving tacrolimus and prednisone, the use of EVR was associated

47 ty, and functional assays in hiPSC-CMs using tacrolimus and rosiglitazone, drugs targeting pathways p

48 While tacrolimus and sirolimus (T/S)-based graft-versus-host d

49 ne patient is taking belatacept with lowered tacrolimus and sirolimus trough levels.

50 alcoholic fatty liver disease and the use of tacrolimus and sirolimus were independently associated w

51 Generic Hi and Generic Lo with the Innovator tacrolimus and with each other.

52 oteins (streptavidin, anti-digoxigenin, anti-tacrolimus) and small molecules (biotin, digoxigenin, ta

53 rine-allopurinol, biologicals, methotrexate, tacrolimus) and were subsequently treated with TG as res

54 Prednisolone, tacrolimus, and mycophenolate mofetil modified fecal mic

55 phylaxis included post-HCT cyclophosphamide, tacrolimus, and mycophenolate mofetil.

56 e regurgitation, controlled with adalimumab, tacrolimus, and prednisone.

57 thermoreceptor endings are also activated by tacrolimus, and tacrolimus solutions trigger blinking an

58 P-1 and HepG2 cells were exposed in vitro to tacrolimus, and validation of genes involved in insulin

59 n all renal transplant patients treated with tacrolimus at our center from 2009 to 2013 was conducted

60 sirolimus, but not the calcineurin inhibitor tacrolimus, at levels routinely achieved in patients, re

61 Tacrolimus AUCtc was an independent predictor of eGFR de

62 s variability in a "Symphony" style low-dose tacrolimus based regime, by collecting data from 432 pat

63 secutive cohort of 455 LT patients receiving tacrolimus-based immunosuppression was studied (2008-201

64 nts (2004-2016) with the following criteria: tacrolimus-based immunosuppression, >1-year graft surviv

65 tized kidney transplant recipients receiving tacrolimus-based immunosuppressive therapy similar clini

66 increased skeletal muscle compared with the tacrolimus-based regimen.

67 ortality and allograft failure compared with tacrolimus-based regimens.

68 x hospitalization on belatacept-based versus tacrolimus-based regimens.

69 nd more severe acute rejection compared with tacrolimus-based therapy.

70 on (odds ratio [OR], 1.3; P < 0.01) and with tacrolimus-based versus ciclosporin-based immunosuppress

71 Immunosuppression was tacrolimus-based with antilymphocyte recipient pretreatm

72 equent under belatacept-based, compared with tacrolimus-based, immunosuppression.

73 Maintenance regimens were tacrolimus-based.

74 A prolonged-release tacrolimus, basiliximab, and mycophenolate mofetil immun

75 All patients received prolonged-release tacrolimus, basiliximab, mycophenolate mofetil and 1 bol

76 Drug Administration (FDA)-approved compound Tacrolimus, blocks calcineurin's activity toward those p

77 L36alpha siRNA-CYnLIP (p<0.05) comparable to Tacrolimus but markedly less than imiquimod-only treatme

78 nosuppressant drugs such as cyclosporine and tacrolimus but not rapamycin also inhibit BCR-mediated E

79 Together, these results suggest that tacrolimus causes hypertension predominantly by inhibiti

80 e association between individually estimated tacrolimus clearance (daily tacrolimus dose [mg]/trough

81 Patients with high tacrolimus clearance eliminate more drug within a dose i

82 Median tacrolimus coefficient of variation was 28%.

83 ipients were 1:1 randomized to belatacept or tacrolimus combined with basiliximab, mycophenolate mofe

84 istent with 5-year findings, subjects taking tacrolimus, compared with those taking cyclosporin, had

85 Low tacrolimus concentrations have been associated with high

86 Transient subtherapeutic tacrolimus concentrations may induce acute rejection epi

87 t concentration intervention in contemporary tacrolimus-containing regimens and future research to de

88 in in vitro MLR comparable to animals in the tacrolimus control arm.

89 tes mellitus (PTDM) with 2 prolonged-release tacrolimus corticosteroid minimization regimens.

90 Cibinetide, in combination with low-dose tacrolimus, could significantly improve long-term graft

91 A 10% increase in tacrolimus CV augmented the risk of acute rejection by 2

92 Overall, intrapatient tacrolimus CV was higher in AAs versus non-AAs (39.9 +/-

93 1 concentrations used to assess intrapatient tacrolimus CV.

94 lid organ transplant recipients who received tacrolimus developed hyperglycemia.

95 dually estimated tacrolimus clearance (daily tacrolimus dose [mg]/trough concentration [mug/L]) and b

96 ury at 7 months was reversed by reducing the tacrolimus dose to 14 mg twice per day.

97 A small adjustment of the tacrolimus dose was mandatory upon treatment initiation

98 pression and subsides when immunosuppressive tacrolimus doses are increased.

99 Tacrolimus dosing required adjustment during and after l

100 ata from 1106 patients initiating once-daily tacrolimus during posttransplant follow-up were analyzed

101 mber of immunosuppressive drugs, and dose of tacrolimus during the last 4 months of follow-up were pr

102 In cultured mouse DRG neurons, tacrolimus evokes an increase in intracellular calcium a

103 owed that early everolimus plus reduced-dose tacrolimus (EVR + rTAC) led to significantly better kidn

104 ant to receive everolimus + reduced-exposure tacrolimus (EVR + rTAC; n = 52) with corticosteroid with

105 o investigate the association between IPV in tacrolimus exposure and immune-mediated graft injury aft

106 High IPV in tacrolimus exposure beyond month 6 postliver transplanta

107 A high intrapatient variability (IPV) in tacrolimus exposure is associated with impaired long-ter

108 f transplant and explored how differences in tacrolimus exposure may modulate this risk.

109 ections of FDA-approved drugs, we identified tacrolimus (FK-506) as the most potent activator of ALK1

110 calcineurin inhibitor and immunosuppressant tacrolimus (FK-506) was prevented by Npas4 overexpressio

111 Mice received tacrolimus (FK-506, 0.1 mg/kg per day)/mycophenolate mof

112 Calcineurin inhibitors, such as tacrolimus (FK506) and cyclosporine, are widely used as

113 Cyclosporin A (CsA) and tacrolimus (FK506) are valuable immunosuppressants for a

114 Cyclosporin A (CsA) and tacrolimus (FK506) has been reported to reduce proteinur

115 nd that TRPM8 is a pharmacological target of tacrolimus (FK506), a macrolide immunosuppressant with s

116 own modulators of alphaS toxicity, including tacrolimus (FK506), isradipine, nilotinib, nortriptyline

117 e major tacrolimus metabolite 13-O-desmethyl tacrolimus for AUC, but it failed the EMA criterion.

118 ades of use, the optimal maintenance dose of tacrolimus for kidney transplant recipients is unknown.

119 nt F344 rats using mycophenolate mofetil and tacrolimus for partial lymphocyte-directed immunosuppres

120 e graft survival, for example, by optimizing tacrolimus formulation.

121 etic and clinical characteristics of generic tacrolimus formulations versus the reference drug (Progr

122 pression decreased significantly only in the tacrolimus group (P = 0.03).

123 Animals treated with tacrolimus have markedly improved lymphatic function wit

124 The pharmacokinetics of the Tacrolimus Hexal (TacHexal) formulation is similar to Pr

125 When treated with tacrolimus, however, BP and the renal abundance of phosp

126 R, 1.39; 95% CI, 1.02-1.90; P = .04), use of tacrolimus (HR, 2.31; 95% CI, 1.72-3.10; P < .001), and

127 mechanism underlying the diabetogenicity of tacrolimus in primary human beta-cells.

128 ic index generic immunosuppressants, such as tacrolimus, in transplant recipients.

129 BMP signaling protects human beta-cells from tacrolimus-induced beta-cell dysfunction in vitro.

130 This tacrolimus-induced glucose metabolic disorder was caused

131 Whether the tacrolimus-induced gut microbiota is involved in the reg

132 insights for the prevention and treatment of tacrolimus-induced hyperglycemia in transplant recipient

133 Tacrolimus-induced phosphorylated SMAD1/5 acts in synerg

134 Here we show that tacrolimus induces loss of human beta-cell maturity and

135 In cultured cells, tacrolimus inhibited dephosphorylation of NCC.

136 with cibinetide (120 ug/kg), with or without tacrolimus injection (0.4 mg/kg/d) during days 4-14 afte

137 tudy design, we observed equivalence between tacrolimus innovator and 2 generic products as well as b

138 ondary outcomes were the association between tacrolimus IPV on (1) loss of renal function per year of

139 ipients, transplanted between 2000 and 2015, tacrolimus IPV was calculated from at least 5 tacrolimus

140 e tacrolimus (PR-T) versus immediate-release tacrolimus (IR-T)-based immunosuppression.

141 Tacrolimus is a widely used immunosuppressive drug that

142 Tacrolimus is an inhibitor of the phosphatase calcineuri

143 ications for lymphedema treatment as topical tacrolimus is FDA-approved for other chronic skin condit

144 agent followed by mycophenolate mofetil and tacrolimus is presently the most frequently used immune

145 Although tacrolimus is the basis of most maintenance immunosuppre

146 The effect of an immunosuppressant, Tacrolimus, is also confirmed in the same experimental s

147 Compared with tacrolimus, KT recipients aged <=44 years receiving cycl

148 Tacrolimus level variability is a strong risk factor for

149 h high HLA alloimmune risk should not target tacrolimus levels <5 ng/ml unless essential, and monitor

150 a series of thresholds <6 ng/ml and the mean tacrolimus levels before dnDSA development in the contex

151 Theoretically, tacrolimus levels consistently outside the target therap

152 This suggests that highly variable tacrolimus levels predict worse outcomes postrenal trans

153 t in allograft dysfunction as subtherapeutic tacrolimus levels predispose to episodes of acute reject

154 match score were less likely to tolerate low tacrolimus levels without developing dnDSA.

155 rmediate- and high-risk patients with a mean tacrolimus <6 ng/ml versus >8 ng/ml had increased risk o

156 globulin induction and mycophenolate mofetil-tacrolimus maintenance immunosuppression were analyzed.

157 nalysis, recipient age <40 years, the use of tacrolimus/mammalian target of rapamycin immunosuppressi

158 SCABE criteria were also met for the major tacrolimus metabolite 13-O-desmethyl tacrolimus for AUC,

159 Bioequivalence of the major tacrolimus metabolite was also assessed.

160 ily not to exceed 1 g from day 5 to day 35); tacrolimus, methotrexate, and bortezomib (bortezomib 1.3

161 clophosphamide, 0.98 (0.76-1.27; p=0.92) for tacrolimus, methotrexate, and bortezomib, and 1.10 (0.86

162 omly assigned to the three study arms: 89 to tacrolimus, methotrexate, and bortezomib; 92 to tacrolim

163 grade 3 and 68 (76%) had grade 4 events with tacrolimus, methotrexate, and bortezomib; and 18 (20%) h

164 ansplantation cyclophosphamide; 73 [82%] for tacrolimus, methotrexate, and bortezomib; and 78 [85%] f

165 avenously on days 1, 4, and 7 after HCT); or tacrolimus, methotrexate, and maraviroc (maraviroc 300 m

166 thotrexate, and bortezomib; and 78 [85%] for tacrolimus, methotrexate, and maraviroc) and cardiac (43

167 grade 3 and 63 (68%) had grade 4 events with tacrolimus, methotrexate, and maraviroc.

168 bortezomib, and 1.10 (0.86-1.41; p=0.49) for tacrolimus, methotrexate, and maraviroc.

169 rolimus, methotrexate, and bortezomib; 92 to tacrolimus, methotrexate, and maraviroc; 92 to tacrolimu

170 comparing tacrolimus/sirolimus (Tac/Sir) vs tacrolimus/methotrexate (Tac/Mtx) as graft-versus-host d

171 Tacrolimus minimization is usually restricted to patient

172 Tacrolimus minimization should be universally attempted

173 cording to AUCtc, 33.7% of patients received tacrolimus minimization, 44.8% conventional exposure, an

174 Patients were stratified as tacrolimus minimization, conventional, or high exposure,

175 tor (PRCL-02) (n = 6) alone, or with initial tacrolimus monotherapy followed by gradual conversion at

176 Two patients were weaned to a low-dose tacrolimus monotherapy together with monthly belatacept

177 Animals receiving tacrolimus monotherapy were e on day 100 without rejecti

178 from mycophenolate mofetil and maintained on tacrolimus monotherapy.

179 Immunosuppression consisted of basiliximab, tacrolimus, mycophenolate mofetil, and corticosteroids i

180 ppression after transplantation consisted of tacrolimus, mycophenolate mofetil, and glucocorticoids.

181 had grade 3 and 67 (73%) grade 4 events with tacrolimus, mycophenolate mofetil, and post-transplantat

182 Tacrolimus, mycophenolate mofetil, and post-transplantat

183 toxicities were haematological (77 [84%] for tacrolimus, mycophenolate mofetil, and post-transplantat

184 RFS was 0.72 (90% CI 0.54-0.94; p=0.044) for tacrolimus, mycophenolate mofetil, and post-transplantat

185 crolimus, methotrexate, and maraviroc; 92 to tacrolimus, mycophenolate mofetil, and post-transplantat

186 ly assigned (1:1:1) by random block sizes to tacrolimus, mycophenolate mofetil, and post-transplantat

187 antithymyocyte globulin, methylprednisolone, tacrolimus, mycophenolate mofetil, and prednisone were c

188 uring the first 3 years postoperatively were tacrolimus, mycophenolate, and steroids, and later, tacr

189 1.79, 95% CI 1.09-2.93, compared with use of tacrolimus/mycophenolate mofetil) and following a diagno

190 fective in deceased donor KTRs maintained on tacrolimus/mycophenolate mofetil-based regimen along wit

191 bitor (CNI)-based immunosuppressive regimen (tacrolimus) (n = 21), or an investigational arm using lo

192 5%, P = 0.04) due to higher trough levels of Tacrolimus on month 3 (9.48 versus 7.30 ng/mL, P = 0.023

193 The effects of tacrolimus on purified TRPM8 in lipid bilayers demonstra

194 The actions of tacrolimus on TRPM8 resemble those of menthol but likely

195 n Norway recipients were treated either with tacrolimus,= or donor kidneys underwent 1h-HOPE-treatmen

196 , burning sensation was more pronounced with tacrolimus (P = 0.002).

197 lium decreased significantly in both groups (tacrolimus, P = 0.003; methylprednisolone, P = 0.008), w

198 Tacrolimus pharmacokinetics is similar with TacHexal and

199 Tacrolimus PK was measured by ultraperformance liquid ch

200 s standard GVHD prophylaxis (cyclosporine or tacrolimus plus methotrexate or mycophenolate) or standa

201 Anti-GvHD prophylaxis of tacrolimus, post-transplant cyclophosphamide, and CD28 b

202 nsplantation outcomes with prolonged-release tacrolimus (PR-T) versus immediate-release tacrolimus (I

203 suppressive protocol included thymoglobulin, tacrolimus, prednisone, and mycophenolate mofetil.

204 nti-thymocyte globulin-mycophenolate mofetil-tacrolimus protocol.

205 The calcineurin inhibitor FK506 (tacrolimus) reduced cell death and lateral transfer in v

206 ce of dnDSA development than recipients on a tacrolimus regimen.

207 Tacrolimus repurposing has therefore therapeutic potenti

208 ession levels; both patients who were taking tacrolimus required immunosuppression dose adjustments d

209 Conventional/high exposure to tacrolimus resulted in a more pronounced eGFR decline wi

210 ation treatment with cibinetide and low-dose tacrolimus significantly improved long-term graft surviv

211 mus, mycophenolate, and steroids, and later, tacrolimus, sirolimus, and steroids.

212 se 3 clinical trial (BMT CTN 0402) comparing tacrolimus/sirolimus (Tac/Sir) vs tacrolimus/methotrexat

213 ndings are also activated by tacrolimus, and tacrolimus solutions trigger blinking and cold-evoked be

214 hamide 50 mg/kg on days 3 and 4, followed by tacrolimus starting on day 5 and mycophenolate mofetil s

215 Immunosuppression was based on CNI (tacrolimus), steroids and alternatively mycophenolic aci

216 Immunosuppression was based on CNI (tacrolimus), steroids and alternatively Mycophenolic Aci

217 Finally, tacrolimus stimulated Smad1/5/8 signaling in C2C12 cells

218 Previously, we reported that tacrolimus stimulates the renal thiazide-sensitive sodiu

219 Lastly, only the 1 mg tacrolimus strength was utilized in this study.

220 )-insensitive mutants were also activated by tacrolimus, suggesting a different binding site.

221 tment groups: (i) everolimus (EVR) + reduced tacrolimus (TAC) (n = 245); (ii) TAC control (n = 243) o

222 munosuppressive drug concentrations, such as tacrolimus (TaC) and cyclosporin A (CsA), is important i

223 Tacrolimus (Tac) and Cyclosporine (CsA) levels obtained

224 Tacrolimus (Tac) and Cyclosporine A (CyA) calcineurin in

225 Agouti into Lewis rats applying single-dose tacrolimus (TAC) at varying concentrations.

226 f whom 31 initiated cyclosporin (CsA) and 47 tacrolimus (Tac) based immunosuppression.

227 , with little long-term data from the modern tacrolimus (TAC) era using lower doses.

228 Tacrolimus (Tac) is an effective anti-rejection agent in

229 Tacrolimus (TAC) is the most important agent for mainten

230 Tacrolimus (Tac) is widely used to prevent rejection and

231 engraftment and function and protect against tacrolimus (Tac) toxicity.

232 95% CI, 1.78-9.73) had a negative effect and tacrolimus (TAC) use (HR, 0.55; 95% CI, 0.31-0.99) had a

233 with the hydrophobic anti-inflammatory drug Tacrolimus (TAC), a calcineurin inhibitor.

234 The patient's ability to absorb cyclosporin, tacrolimus (Tac), enteric-coated mycophenolate sodium (E

235 rolimus (SRL) + mycophenolate (MPA) or SRL + tacrolimus (Tac), relative to the control-regimen: Tac +

236 Tacrolimus (TAC)-based regimens are the most common amon

237 ients exposed to immunosuppressants, such as tacrolimus (TAC).

238 ransplant patients on cyclosporin A (CsA) or tacrolimus (Tac).

239 ansplant patients were randomized to generic tacrolimus (TacHexal) or Prograf in a 6-month open-label

240 ransplantation with concomitant reduction in tacrolimus targets.

241 level (Ctrough, 3-8 ng/mL), prednisone, and tacrolimus (TCL) (target Ctrough, 2-5 ng/mL).

242 Calcineurin can be inhibited with Tacrolimus through the recruitment and inhibition of the

243 BSX and could permit lower trough levels of Tacrolimus, thus reducing occurrence of PTD.

244 ing thiopurines, methotrexate, cyclosporine, tacrolimus, TNF-alpha antagonists, vedolizumab, tofacitn

245 treated by switching immunosuppression from tacrolimus to sirolimus.

246 oid taper, and maintenance mycophenolate and tacrolimus, to 2 arms using maintenance belatacept.

247 alence for the narrow therapeutic index drug tacrolimus translates from healthy volunteers to individ

248 ed for use of belatacept in combination with tacrolimus, transplant center effects, and differing app

249 idence was higher in belatacept-treated than tacrolimus-treated 55% versus 10% (P = 0.006).

250 All syngeneic and tacrolimus-treated grafts survived until endpoint.

251 RCL-02 monotherapy but not compared with the tacrolimus-treated group.

252 Hyperglycemia was observed in a tacrolimus-treated mouse model, with reduction in taxono

253 on rate was compared between belatacept- and tacrolimus-treated patients and immunological biomarkers

254 be particularly effective for lowering BP in tacrolimus-treated patients with hypertension.

255 Cellular rejection was minimized by tacrolimus treatment from day -1.

256 Tacrolimus treatment reduced skin inflammation and block

257 Acute tacrolimus treatment transiently increases hepcidin in w

258 munosuppressive activity but was inferior to tacrolimus treatment with respect to suppressing immune

259 We evaluated mean TAC C0 (tacrolimus trough concentration) and TAC time in therape

260 Tacrolimus trough concentrations (mean/variability), as

261 en into account (other covariates, including tacrolimus trough concentrations, were nonsignificant).

262 ic variants were found to be associated with tacrolimus trough concentrations.

263 d HLA-DR/DQ dnDSA had a higher proportion of tacrolimus trough levels <5 ng/ml, which continued to be

264 Tacrolimus trough levels along the first year were not d

265 Tacrolimus trough levels along the first year were not d

266 antibody (dnDSA) development correlates with tacrolimus trough levels and the recipient's individuali

267 e conclude that HLA-DR/DQ eplet mismatch and tacrolimus trough levels are independent predictors of d

268 We analyzed the frequency of tacrolimus trough levels below a series of thresholds <6

269 nal transplant recipients with 50,011 serial tacrolimus trough levels had HLA-DR/DQ eplet mismatch de

270 Mean tacrolimus trough levels in the 6 months before dnDSA de

271 Baseline characteristics and mean tacrolimus trough levels were comparable between arms.

272 n adherence assessed by self-report or SD of tacrolimus trough levels.

273 acrolimus IPV was calculated from at least 5 tacrolimus trough samples obtained between months 6 and

274 nfounders (tacrolimus trough, variability of tacrolimus trough, de novo donor-specific antibody devel

275 formed, adjusting for potential confounders (tacrolimus trough, variability of tacrolimus trough, de

276 gnosis with PBC or at liver transplantation, tacrolimus use, and biochemical markers of cholestasis a

277 s) and small molecules (biotin, digoxigenin, tacrolimus) using the same platform.

278 cipients; little is known about intrapatient tacrolimus variabilities impact on racial disparities.

279 High tacrolimus variability (CV >40%) was a significant expla

280 Tacrolimus variability 6 to 12 months after renal transp

281 High intrapatient tacrolimus variability has been associated with worse cl

282 We investigated the effect of tacrolimus variability in a "Symphony" style low-dose ta

283 ion in AAs was reduced by 46% when including tacrolimus variability in modeling and reduced by 40% fo

284 Tacrolimus variability is a significant explanatory vari

285 These data demonstrate that intrapatient tacrolimus variability is strongly associated with acute

286 High tacrolimus variability may identify a subset of patients

287 Tacrolimus variability was a significant risk factor for

288 Intrapatient tacrolimus variability was assessed using the coefficien

289 Tacrolimus variability was not associated with late cyto

290 Cumulative exposure to tacrolimus was calculated as the area under curve of tro

291 Tacrolimus was continued at least until day 90 and was t

292 venous bolus on days 3, 6, and 11 after HCT; tacrolimus was given intravenously at a dose of 0.05 mg/

293 Topical tacrolimus was more effective than methylprednisolone in

294 150 mumol/L, not significant), whereas mean tacrolimus was similar (7.32 vs. 7.22 ng/mL, n.s.).

295 rsistence of CMV viremia under belatacept vs tacrolimus were compared.

296 In total, 638 patients treated with oral tacrolimus were included in the analysis.

297 Importantly, dose adjustments for tacrolimus were necessary for maintaining sufficient tro

298 Recipients treated with tacrolimus who developed HLA-DR/DQ dnDSA had a higher pr

299 nth 5 posttransplant or to continue standard tacrolimus with mycophenolate mofetil (sTAC/MMF) and ste

300 contrast, immune activation was prevented by tacrolimus with significantly improved recipient surviva