ライフサイエンスコーパス: p.o.

1 p.o. treatment with OGT2378 starting 3 days before intra

2 chronically in chow [MF. tricyclic; 0.015%, p.o.] from day 6 to day 14 after tumor implantation.

3 FRE (200 and 400mgkg(-1), p.o.), in a dose-dependent manner, altered the biochemic

4 Compound 12 (2 mg kg(-1), p.o. mice) increased wakefulness representing novel phar

5 Among them, compound 19 (p.o.) improved GI tract motility by 75% while orally adm

6 10 (Th2-type) secretion after the high QS-21 p.o. dose than after low doses.

7 Currently, 3 of 4 i.p./s.c.- and 2 of 4 p.o. secondary passage-inoculated cats have developed ab

8 angiogenesis at a dose of 3 mg/kg (q.d. x 5, p.o., corresponding to 5.5 ng/mL at C(max)).

9 The compound was >50% p.o. bioavailable in rodents and dogs and did not alter

10 Here we describe a p.o. active, dual Src/Abl kinase inhibitor with potent a

11 Linomide is a p.o. active antiangiogenic agent that has been demonstra

12 SCH66336 is a p.o.-active, farnesyl protein transferase inhibitor.

13 we investigated the effect of perifosine, a p.o.-bioavailable ALK, on the cell cycle kinetics of imm

14 howed that like MSC, GGMSC was well absorbed p.o., with urinary excretion as the major route for elim

15 ministered either acrolein (5 mg/kg acrolein p.o.) or butylated hydroxylanisole (BHA) (0.45% in the d

16 ss tobacco use, in which NNK is administered p.o. rather than by inhalation.

17 NBI 35965 (10 mg/kg) administered p.o. or subcutaneously (s.c.) 1 h before intravenous CRF

18 Cyclosporin A was administered p.o. (10 mg/kg/day) starting from the day before TALL-10

19 idazole, and clarithromycin was administered p.o. at 8, 12, or 22 WPI.

20 13-MTD was administered p.o. once daily to the implanted mice for approximately

21 When folic acid was administered p.o. to mice that were mildly folate deficient, antitumo

22 sphorylation in xenografts when administered p.o. to athymic mice.

23 When administered p.o., compound 9 shows 50% trabecular bone protection wh

24 Administration p.o. of CEP-7055 at 2.57 to 23.8 mg/kg/dose b.i.d. resul

25 PSI (8 mg/kg) decreased motor activity after p.o. but not i.p. administration.

26 9 in CB17 SCID mouse intestine 11 days after p.o. inoculation.

27 delayed clearance of T3C9 7 to 11 days after p.o. inoculation.

28 ) levels in gastric luminal secretions after p.o. immunization was greater than after i.n. administra

29 which can be achieved in human tissues after p.o. administration, have not yet been defined.

30 (calculated EC(50) of 93 ng/mL, total) after p.o. administration to tumor-bearing mice.

31 Our goal was to discover and characterize an p.o. active VEGFR-2 small molecule inhibitor.

32 BMS-275291 is an p.o. bioavailable, sulfhydryl-based matrix metalloprotei

33 We show here that an p.o.-active small molecule kinase inhibitor of the 2-phe

34 14662 was administered both parenterally and p.o. and was active by all these routes.

35 .v. heparin immediately after transplant and p.o. warfarin as outpatients.

36 f LH in male castrate rats via both i.v. and p.o. dosing.

37 metabolite, EM-652, have been reported to be p.o. active nonsteroidal pure antiestrogens.

38 rm administration of SB 217242 (15 mg/kg BID p.o.).

39 Both p.o. and s.c. immunizations induced Chlamydia-specific s

40 xenografts, administration of anastrozole by p.o. gavage for 21 days elicited pronounced inhibition o

41 was inhibited in a dose-dependent manner by p.o. administration of EGCG in a dose range of 0.02% to

42 inoculated into cohorts of cats by the i.c., p.o., and intraperitoneal and subcutaneous (i.p./s.c.) r

43 nude mouse model of human pancreatic cancer, p.o. administration of gamma-T3 inhibited tumor growth a

44 Chronic p.o. administration of CEP-7055 at doses of 11.9 to 23.8

45 Chronic p.o. administration of CEP-7055 in preclinical efficacy

46 of c-Met deficiency were reversed by chronic p.o. administration of antioxidant N-acetyl-L-cysteine.

47 he mice were treated with MMF (100 mg/kgBW/d p.o.) for one week.

48 p II received cyclosporine (CsA, 15 mg/kg/d, p.o.) when I-FABP rose to > or = 80 ng/ml.

49 of 45 mg TAM/kg body weight and after daily p.o. dosing for 7 days with 5.0, 10.0, and 20.0 mg TAM/k

50 of this agent was evaluated after once daily p.o. administration to athymic mice bearing human xenogr

51 Once-daily p.o. x 10 days dosing routinely inhibited tumor growth (

52 The results suggest that daily p.o. doses of resveratrol at 0.5 or 1.0 g produce levels

53 el in in vivo angiogenesis assays that daily p.o. Linomide at 25 mg/kg/day inhibits angiogenesis indu

54 We have previously demonstrated that daily p.o. treatment with Linomide has antiangiogenic abilitie

55 p.) and choline fenofibrate (60 mg/kg daily, p.o.) in reversing and preventing the development of PIP

56 Celecoxib at 30 mg/kg/day p.o. inhibited angiogenesis (78.6%) and prostaglandin pr

57 tase inhibitor (ARI) (sorbinil; 25 mg/kg/day p.o.) and the sorbinil treatment was associated with sig

58 intravenously), cyclosporine (2.5 mg/ kg/day p.o.), or rapamycin (0.025 mg/kg/day intraperitoneally).

59 The median FK506 starting dose was 4 mg/day p.o.; the median average FK506 blood level, 12 ng/ml.

60 i.p.) or simvastatin (40 mg x kg(-) x day(-) p.o.) for 16 weeks.

61 v. day 0) or high dose of CsA (10 mg/kg/day, p.o., day 0-6).

62 salt of boron, was administered for 7 days, p.o., 21 days post-injury at a dose level of 4 mg/kg bod

63 Single-dose p.o. or s.c. administration of CEP-7055 or CEP-5214 to C

64 vated Wa human rotavirus administered either p.o. or parenterally is significantly less effective in

65 r weight, water-soluble agent with excellent p.o. absorption and bioavailability.

66 atients in the study group received MMF (1 g p.o. b.i.d.), tacrolimus (0.1 mg/kg p.o. b.i.d.), and a

67 rats on a control diet that were first given p.o. TAM at 45 mg/kg/day for 4 days.

68 androgen promotion model, Linomide was given p.o. at a daily dose as high as 25 mg/kg/day for at leas

69 in blocking and regressing tumors when given p.o. at doses of 0.45 or 0.65 g/kg in mouse chow.

70 soft agar colony formation, and, when given p.o. to nude mice, it effectively reduced tumor formatio

71 aximum approved adult dose of 4PBA, 19 grams p.o. divided t.i.d., given for 1 wk.

72 either PTF (800 mg q 8 hr for at least 24 h) p.o. or placebo, along with methylprednisolone (7 mg/kg)

73 Further, low but not high p.o. QS-21 doses triggered Ag-specific secretory IgA (S-

74 Injection of LPS (100 microgram kg-1, i.p.o.) induced a rise in body temperature which commenced

75 into a subcutaneous air pouch (intrapouch, i.p.o.) that does not lead to LPS appearance in the circul

76 More importantly, p.o. administration of CT52923 to nude mice caused a sig

77 In contrast to 5-FU, OGT 719 is p.o. bioavailable and has a plasma half-life between 1.5

78 he antimetastatic efficacy of CS-682 and its p.o. availability confer significant advantages and clin

79 started 24 h after induction of MR (60 mg/kg p.o. b.i.d.) and continued for three months.

80 ical control received tacrolimus (0.15 mg/kg p.o. b.i.d.) and the same steroid taper.

81 MMF (1 g p.o. b.i.d.), tacrolimus (0.1 mg/kg p.o. b.i.d.), and a standard steroid taper.

82 ] twice a day [BID]), voriconazole (10 mg/kg p.o. BID), liposomal amphotericin B (10 mg/kg intraperit

83 ceptor antagonist, spironolactone (200 mg/kg p.o. daily), or an antioxidant, either pyrrolidine dithi

84 LY231617 (50 mg/kg p.o. or 30 mg/kg i.p.) was administered either 30 min pr

85 Oral administration of selinexor (15 mg/kg p.o. QoDx3/week for 3weeks) resulted in complete cures (

86 e loss of Tsc1-induced mortality at 50 mg/kg p.o. twice a day.

87 (capsaicin-induced flinch, ED50 = 0.33 mg/kg p.o.) and was antihyperalgesic in a model of inflammator

88 on of injury-induced firing, CDA54 (10 mg/kg p.o.) significantly reduced behavioral signs of neuropat

89 eptor-selective antagonist A192621 (25 mg/kg p.o.), but unaffected by the ET(A) receptor-selective an

90 ere treated with cyclosporine (CsA, 10 mg/kg p.o.), leflunomide (LFM, 20 mg/kg p.o.), or rapamycin (R

91 , 10 mg/kg p.o.), leflunomide (LFM, 20 mg/kg p.o.), or rapamycin (RPM, 6 mg/kg i.p.) for 14 or 21 day

92 of novel object recognition (MED = 10 mg/kg p.o.), thus providing efficacy in preclinical models of

93 tor-selective antagonist SB 234551 (25 mg/kg p.o.).

94 atalepsy at very low doses (MED = 0.04 mg/kg p.o.).

95 test in rats at low doses (MED = 0.63 mg/kg p.o.).

96 ain (brain-to-plasma ratio of 4.7; 0.4 mg/kg p.o., 2 h, 580 nmol/kg).

97 ain (brain-to-plasma ratio of 4.7; 0.4 mg/kg p.o., 2 h, 580 nmol/kg).

98 d the effect of chronic paroxetine (10 mg/kg p.o., 21 days) on the 5-HT1B and 5-HT1D autoreceptors co

99 e selective COX-2 inhibitor SC58125, 3 mg/kg p.o., attenuated the increase in PGE2 concentration.

100 Daily postischemic oral dosing (1 mg/kg p.o., b.i.d., beginning at 1 h after insult) decreased t

101 2-ME (150 mg/kg p.o., n = 20) inhibited bFGF and VEGF-induced neovascula

102 Treatment with 2-ME (75 mg/kg p.o., n = 9) for 1 month suppressed the growth of a huma

103 avioral alterations at doses up to 100 mg/kg p.o., supporting further investigation of this compound

104 treatment of Balb/c female mice (500 nmol/kg p.o. q.d.) grafted with 4T1 breast cancer cells ameliora

105 ase (45%) in total cholesterol at 1.0 mg/kg (p.o.) and showed a protective effect on bone relative to

106 controls with maximal efficacy at 1.0 mg/kg (p.o.).

107 Cebranopadol at a low dose of 25 ug/kg (p.o.) did not induce significant hyperactivity itself, b

108 e hind leg were treated with 2ME2 (75 mg/kg) p.o. for 5 days, and 2 Gy radiation fractions were deliv

109 he HEX fraction and betulinic acid (10mg/kg, p.o.), isolated from the AcOEt1 and AcOEt2 fractions.

110 (0.1-1mg/kg, p.o), carnosol (0.01-0.1mg/kg, p.o.) isolated from the HEX fraction and betulinic acid

111 ct of gallic acid (GA; 50, 100 and 200mg/kg, p.o. for 10 days) on memory deficit and cerebral oxidati

112 done administration (0, 15, and 30 mg/70 kg, p.o.).

113 ological response in vivo (ED50 = 1.9 mg/kg, p.o. in the capsaicin-induced flinch model in rats) and

114 ups and treated with OIFE (125 or 250 mg/kg, p.o.) and D-gal (50 mg/kg, i.p.) for eight weeks.

115 ion (minimum effective dose (MED) = 3 mg/kg, p.o.) and MK-801 induced disruptions of novel object rec

116 with the CSF1R inhibitor PLX3397 (40 mg/kg, p.o.) and submitted to behavioral sensitization or condi

117 at curcumin administration (10 and 20 mg/kg, p.o.) increased hippocampal neurogenesis in chronically

118 1 partial agonist RO5263397 (0.1,1,10 mg/kg, p.o.) on sleep/wake, EEG spectra, and LMA was determined

119 atase inhibitor COUMATE at a dose (10 mg/kg, p.o.) shown previously to cause almost complete inhibiti

120 the effect of LY2444296 (0, 3, and 10 mg/kg, p.o.) was tested on alcohol self-administration at 8 h o

121 acute effects of RO5263397 (0.1,1,10 mg/kg, p.o.) were assessed on a delayed-match-to-sample test of

122 6.25-400 microg/kg, i.v., and 0.25-16 mg/kg, p.o.), CG3509 (25-1600 microg/kg, i.v.), and TA0910 (25-

123 or behavioral responses (5, 10 and 20 mg/kg, p.o.), could alleviate or reverse the effects of stress

124 a dose that increased food intake (10 mg/kg, p.o.), induced Fos expression in the nucleus of the soli

125 uced thermal hyperalgesia, MED = 0.83 mg/kg, p.o.).

126 e selective A2AR antagonist KW6002 (3 mg/kg, p.o.); (iii) global A2AR deletion; and (iv) selective A2

127 In contrast, pramipexole dosing (1 mg/kg, p.o., 1 h after the last methamphetamine dose, plus dail

128 Two doses of VEGFR2-TKI (25 mg/kg, p.o., b.i.d.) resulted in a decrease of V(b) to 1.3 +/-

129 Pramipexole at the 1 mg/kg, p.o., dose level was able to significantly reduce the in

130 The leaf extract (170-510 mg/kg, p.o., LD(50) = 1732 mg/kg) and fractions demonstrated si

131 The animals received CHP, 25 mg/kg, p.o., or oxotremorine (OX), 0.2 mg/kg, s.c.

132 5 h), or chronic escalating (20 to 80 mg/kg, p.o.; for 3 weeks) drug administration.

133 Administration of A-889425 (10-300 mumol/kg, p.o.) alleviated grip force impairment in OA rats 3 week

134 ation of an active dose of Opra Kappa (10 mg p.o. daily, four consecutive days in comparison with an

135 drocortisone (30 mg p.o. each morning, 10 mg p.o. each evening; n=128).

136 To do this, we administered MDMA-HCl (100 mg p.o.) and, separately, placebo (ascorbic acid) in a rand

137 ree times a week) and ribavirin (400-1000 mg p.o. daily) for 12 months or more.

138 Ganciclovir (1000 mg p.o. t.i.d.; n=19) or acyclovir (200 mg p.o. b.i.d.; n=2

139 levels with nicotinic acid (NA) (100-150 mg p.o., q 30 min x 4 h) in type 2 diabetic patients and in

140 Lamivudine (150 mg p.o./d) was begun before transplantation in 10 patients,

141 By contrast, betaxolol (20 mg p.o.), a selective beta1-antagonist devoid of serotonerg

142 0 mg p.o. t.i.d.; n=19) or acyclovir (200 mg p.o. b.i.d.; n=23) was begun at transplantation and cont

143 g) were detected overall such that the 25 mg p.o. capsule demonstrated higher values as compared with

144 ps were detected (p < 0.001), with the 25 mg p.o. capsule exhibiting the largest value (5054 ng-hr/mL

145 orally [p.o.] tid) and hydrocortisone (30 mg p.o. each morning, 10 mg p.o. each evening; n=128).

146 ay central effects of pindolol (10 and 30 mg p.o.), a mixed beta(1/2)-adrenoceptor/5-hydroxytryptamin

147 intravenously every 2 weeks plus CABO 40 mg p.o. o.d. or SUN 50 mg p.o. o.d. (4 weeks each 6-week cy

148 randomized to receive pentoxifylline 400 mg p.o. t.i.d. or matching placebo for 1 year after cardiac

149 weeks plus CABO 40 mg p.o. o.d. or SUN 50 mg p.o. o.d. (4 weeks each 6-week cycle) until disease prog

150 f oral glucosamine at standard doses (500 mg p.o. t.i.d.) in lean (n = 20) and obese (n = 20) subject

151 t and reuptake inhibitor fenfluramine (60 mg p.o.) and 3 hours afterward.

152 a selective DRD3 antagonist (GSK598809 60 mg p.o.).

153 and after the COX inhibitor aspirin (600 mg p.o.).

154 randomized 1:1 to placebo or 2-HOBA (750 mg p.o. TID) 3 days before a planned AF ablation.

155 =18) and HS (n=14) received memantine 20 mg (p.o.) and placebo over 2 test days in a double-blind, ra

156 s the influence of CBD (0, 200, 400, 800 mg, p.o.) pretreatment on the reinforcing, subjective, cogni

157 hen mice were immunized with rUre (25 microg p.o. or rectally or 10 microg i.n.) plus heat-labile tox

158 g p.o. dose of QS-21, whereas the 250-microg p.o. dose also induced IgG2a and IgG3 Abs.

159 tly IgG1 followed by IgG2b for the 50-microg p.o. dose of QS-21, whereas the 250-microg p.o. dose als

160 were subchronically exposed to PAH mixtures (p.o.), and mutagenic potency (MP) values were determined

161 In the golden Syrian hamster model, p.o. sodium bicarbonate supplementation (5 mg/ml in drin

162 Moreover, p.o. immunization or infection with Chlamydia confers pr

163 administration of the AI letrozole (20 mug, p.o.) on cognition, anxiety, thermoregulation, brain est

164 Neither p.o. nor i.m. inoculation conferred significant protecti

165 OGT 719 is a novel p.o. bioavailable nucleoside analogue in which galactose

166 shed that treatment of the host with a novel p.o. inhibitor of glucosylceramide synthesis, the imino

167 study we demonstrate the ability of a novel, p.o.-administered cytosine analogue, CS-682, to effectiv

168 The ability of p.o. administered I3C to reverse MDR was also tested in

169 s serotype 3 clone 9 (T3C9) within 7 days of p.o. inoculation.

170 ing that is important for the development of p.o. subunit vaccines to target Chlamydia and possibly o

171 Finally, the effect of p.o. administered resveratrol on N-methyl-N-nitrosourea-

172 The effectiveness of p.o. OGT2378 in this murine model suggests that inhibiti

173 These effects of p.o.-administered green tea or caffeine on early adaptiv

174 in the vaginal washes and fecal extracts of p.o.-immunized animals.

175 Vaginal secretions of p.o.-immunized animals neutralize Chlamydia in vivo, res

176 Toxicity of p.o. administered CAI most commonly consisted of dose-re

177 no detectable ISTLs in the genital tracts of p.o.- or s.c.-infected mice.

178 PSI 8 mg/kg s.c. or p.o., but not i.p., caused neuronal loss in the substant

179 prion diseases frequently originate by oral (p.o.) infection.

180 30.0 mg/kg) was first tested following oral (p.o.) administration.

181 owing either intraperitoneal (i.p.) or oral (p.o.) administration, as well as activity in the mouse a

182 infected via intranasal (i.n.) or per-oral (p.o.) Chlamydia inoculation and that unlike the female r

183 r mice given the vaccine by either the oral (p.o.), intranasal (i.n.), or rectal route.

184 ities were observed for 18 and 19 upon oral (p.o.) administration to rats (18, ED50 = 3.9 mg/kg; 19,

185 ginally (i.v.), intranasally (i.n.), orally (p.o.), or subcutaneously (s.c.) with C. trachomatis.

186 inoculated intracerebrally (i.c.) or orally (p.o.) with CWD-infected deer brain.

187 NBI 35965 administered per orally (p.o.) in rats (1, 3, 10 or 30 mg/kg) inhibited dose-depe

188 (n=132), or together with K (400 mg orally [p.o.] tid) and hydrocortisone (30 mg p.o. each morning,

189 osaconazole (10 mg/kg of body weight orally [p.o.] twice a day [BID]), voriconazole (10 mg/kg p.o. BI

190 ause systemic disease in mice after peroral (p.o.) inoculation and primary replication in the intesti

191 biotic pigs were inoculated twice perorally (p.o.) (group 1) or intramuscularly (i.m.) (group 2) or t

192 ance) for (R)-18 in mice (i.p.) and in rats (p.o.) were 6.0 and > 130, respectively.

193 efractory solid tumors, 49 patients received p.o. administered CAI daily or every other day.

194 ice were acutely administered by oral route (p.o.) with fractions, essential oil or isolated compound

195 A highly selective, p.o. bioavailable irreversible inhibitor of epidermal gr

196 0%) was sustained for >4 hours with a single p.o. dose of 33 mg/kg.

197 icacy and associated mechanisms of long-term p.o. silibinin feeding against spontaneous intestinal tu

198 Our results demonstrate that p.o.-administered noscapine significantly inhibits the p

199 We found that p.o. administration of EGCG at doses of 0.08% or 0.16% i

200 Here we report that p.o. administration of QS-21 with the vaccine protein te

201 We now show that p.o. gavage of garlic constituent diallyl trisulfide (DA

202 female athymic BALB/c nu/nu mice showed that p.o. administration of 2-MeO-E(2) at 30 mg/kg body weigh

203 The results suggested that p.o. administered tea or caffeine may have decreased tum

204 tly under development, as represented by the p.o. administered prodrug capecitabine, the gene silenci

205 patients with squamous cell carcinoma of the p.o. tongue, there was a significant correlation between

206 Mice were treated with various p.o. doses of CS-682 on a five times per week schedule u

207 ell xenografts with riluzole for 18 days via p.o. gavage or i.v. injection leads to inhibition of tum

208 or sulforaphane (9 micromol/day for 1 week, p.o.) was generated using the Murine Genome U74Av2 oligo

209 Six-week-old APC(min/+) mice were p.o. fed with vehicle control (0.5% carboxymethyl cellul

210 i.v. route were modestly protected, whereas p.o. and s.c. groups were indistinguishable in this rega

211 Efficacy was also achieved with p.o. administration of HTI-286.

212 is a promising cancer therapeutic agent with p.o. bioavailability.

213 umans by pairing a distinctive beverage with p.o. administration of dexamethasone.

214 Pretreatment of SKH-1 mice with p.o.-administered 0.6% green tea (6 mg of lyophilized te

215 tinctively flavored beverage was paired with p.o. administration of dexamethasone.

216 ntrations were achieved in all patients with p.o. Neoral.