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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 10 (Th2-type) secretion after the high QS-21 p.o. dose than after low doses.
5      Currently, 3 of 4 i.p./s.c.- and 2 of 4 p.o. secondary passage-inoculated cats have developed ab
6 angiogenesis at a dose of 3 mg/kg (q.d. x 5, p.o., corresponding to 5.5 ng/mL at C(max)).
7                        The compound was >50% p.o. bioavailable in rodents and dogs and did not alter
8                           Here we describe a p.o. active, dual Src/Abl kinase inhibitor with potent a
9                                Linomide is a p.o. active antiangiogenic agent that has been demonstra
10                                SCH66336 is a p.o.-active, farnesyl protein transferase inhibitor.
11  we investigated the effect of perifosine, a p.o.-bioavailable ALK, on the cell cycle kinetics of imm
12 howed that like MSC, GGMSC was well absorbed p.o., with urinary excretion as the major route for elim
13 ministered either acrolein (5 mg/kg acrolein p.o.) or butylated hydroxylanisole (BHA) (0.45% in the d
14 ss tobacco use, in which NNK is administered p.o. rather than by inhalation.
15            NBI 35965 (10 mg/kg) administered p.o. or subcutaneously (s.c.) 1 h before intravenous CRF
16               Cyclosporin A was administered p.o. (10 mg/kg/day) starting from the day before TALL-10
17 idazole, and clarithromycin was administered p.o. at 8, 12, or 22 WPI.
18                      13-MTD was administered p.o. once daily to the implanted mice for approximately
19             When folic acid was administered p.o. to mice that were mildly folate deficient, antitumo
20 sphorylation in xenografts when administered p.o. to athymic mice.
21                            When administered p.o., compound 9 shows 50% trabecular bone protection wh
22                               Administration p.o. of CEP-7055 at 2.57 to 23.8 mg/kg/dose b.i.d. resul
23 PSI (8 mg/kg) decreased motor activity after p.o. but not i.p. administration.
24 9 in CB17 SCID mouse intestine 11 days after p.o. inoculation.
25 delayed clearance of T3C9 7 to 11 days after p.o. inoculation.
26 ) levels in gastric luminal secretions after p.o. immunization was greater than after i.n. administra
27 which can be achieved in human tissues after p.o. administration, have not yet been defined.
28 (calculated EC(50) of 93 ng/mL, total) after p.o. administration to tumor-bearing mice.
29 Our goal was to discover and characterize an p.o. active VEGFR-2 small molecule inhibitor.
30                             BMS-275291 is an p.o. bioavailable, sulfhydryl-based matrix metalloprotei
31                         We show here that an p.o.-active small molecule kinase inhibitor of the 2-phe
32 14662 was administered both parenterally and p.o. and was active by all these routes.
33 .v. heparin immediately after transplant and p.o. warfarin as outpatients.
34 f LH in male castrate rats via both i.v. and p.o. dosing.
35 metabolite, EM-652, have been reported to be p.o. active nonsteroidal pure antiestrogens.
36 rm administration of SB 217242 (15 mg/kg BID p.o.).
37 xenografts, administration of anastrozole by p.o. gavage for 21 days elicited pronounced inhibition o
38  was inhibited in a dose-dependent manner by p.o. administration of EGCG in a dose range of 0.02% to
39 inoculated into cohorts of cats by the i.c., p.o., and intraperitoneal and subcutaneous (i.p./s.c.) r
40 nude mouse model of human pancreatic cancer, p.o. administration of gamma-T3 inhibited tumor growth a
41                                      Chronic p.o. administration of CEP-7055 at doses of 11.9 to 23.8
42                                      Chronic p.o. administration of CEP-7055 in preclinical efficacy
43 of c-Met deficiency were reversed by chronic p.o. administration of antioxidant N-acetyl-L-cysteine.
44 p II received cyclosporine (CsA, 15 mg/kg/d, p.o.) when I-FABP rose to > or = 80 ng/ml.
45  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
46 of this agent was evaluated after once daily p.o. administration to athymic mice bearing human xenogr
47                                   Once-daily p.o. x 10 days dosing routinely inhibited tumor growth (
48               The results suggest that daily p.o. doses of resveratrol at 0.5 or 1.0 g produce levels
49 el in in vivo angiogenesis assays that daily p.o. Linomide at 25 mg/kg/day inhibits angiogenesis indu
50   We have previously demonstrated that daily p.o. treatment with Linomide has antiangiogenic abilitie
51                    Celecoxib at 30 mg/kg/day p.o. inhibited angiogenesis (78.6%) and prostaglandin pr
52 tase inhibitor (ARI) (sorbinil; 25 mg/kg/day p.o.) and the sorbinil treatment was associated with sig
53 intravenously), cyclosporine (2.5 mg/ kg/day p.o.), or rapamycin (0.025 mg/kg/day intraperitoneally).
54  The median FK506 starting dose was 4 mg/day p.o.; the median average FK506 blood level, 12 ng/ml.
55 i.p.) or simvastatin (40 mg x kg(-) x day(-) p.o.) for 16 weeks.
56 v. day 0) or high dose of CsA (10 mg/kg/day, p.o., day 0-6).
57                                  Single-dose p.o. or s.c. administration of CEP-7055 or CEP-5214 to C
58 vated Wa human rotavirus administered either p.o. or parenterally is significantly less effective in
59 r weight, water-soluble agent with excellent p.o. absorption and bioavailability.
60 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
61 rats on a control diet that were first given p.o. TAM at 45 mg/kg/day for 4 days.
62 androgen promotion model, Linomide was given p.o. at a daily dose as high as 25 mg/kg/day for at leas
63 in blocking and regressing tumors when given p.o. at doses of 0.45 or 0.65 g/kg in mouse chow.
64  soft agar colony formation, and, when given p.o. to nude mice, it effectively reduced tumor formatio
65 aximum approved adult dose of 4PBA, 19 grams p.o. divided t.i.d., given for 1 wk.
66 either PTF (800 mg q 8 hr for at least 24 h) p.o. or placebo, along with methylprednisolone (7 mg/kg)
67                    Further, low but not high p.o. QS-21 doses triggered Ag-specific secretory IgA (S-
68      Injection of LPS (100 microgram kg-1, i.p.o.) induced a rise in body temperature which commenced
69 into a subcutaneous air pouch (intrapouch, i.p.o.) that does not lead to LPS appearance in the circul
70                            More importantly, p.o. administration of CT52923 to nude mice caused a sig
71              In contrast to 5-FU, OGT 719 is p.o. bioavailable and has a plasma half-life between 1.5
72 he antimetastatic efficacy of CS-682 and its p.o. availability confer significant advantages and clin
73 started 24 h after induction of MR (60 mg/kg p.o. b.i.d.) and continued for three months.
74 ical control received tacrolimus (0.15 mg/kg p.o. b.i.d.) and the same steroid taper.
75 MMF (1 g p.o. b.i.d.), tacrolimus (0.1 mg/kg p.o. b.i.d.), and a standard steroid taper.
76 ] twice a day [BID]), voriconazole (10 mg/kg p.o. BID), liposomal amphotericin B (10 mg/kg intraperit
77 ceptor antagonist, spironolactone (200 mg/kg p.o. daily), or an antioxidant, either pyrrolidine dithi
78                           LY231617 (50 mg/kg p.o. or 30 mg/kg i.p.) was administered either 30 min pr
79   Oral administration of selinexor (15 mg/kg p.o. QoDx3/week for 3weeks) resulted in complete cures (
80 (capsaicin-induced flinch, ED50 = 0.33 mg/kg p.o.) and was antihyperalgesic in a model of inflammator
81 on of injury-induced firing, CDA54 (10 mg/kg p.o.) significantly reduced behavioral signs of neuropat
82 eptor-selective antagonist A192621 (25 mg/kg p.o.), but unaffected by the ET(A) receptor-selective an
83 ere treated with cyclosporine (CsA, 10 mg/kg p.o.), leflunomide (LFM, 20 mg/kg p.o.), or rapamycin (R
84 , 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
85 tor-selective antagonist SB 234551 (25 mg/kg p.o.).
86 d the effect of chronic paroxetine (10 mg/kg p.o., 21 days) on the 5-HT1B and 5-HT1D autoreceptors co
87 e selective COX-2 inhibitor SC58125, 3 mg/kg p.o., attenuated the increase in PGE2 concentration.
88      Daily postischemic oral dosing (1 mg/kg p.o., b.i.d., beginning at 1 h after insult) decreased t
89                              2-ME (150 mg/kg p.o., n = 20) inhibited bFGF and VEGF-induced neovascula
90                Treatment with 2-ME (75 mg/kg p.o., n = 9) for 1 month suppressed the growth of a huma
91 ase (45%) in total cholesterol at 1.0 mg/kg (p.o.) and showed a protective effect on bone relative to
92 controls with maximal efficacy at 1.0 mg/kg (p.o.).
93 e hind leg were treated with 2ME2 (75 mg/kg) p.o. for 5 days, and 2 Gy radiation fractions were deliv
94 he HEX fraction and betulinic acid (10mg/kg, p.o.), isolated from the AcOEt1 and AcOEt2 fractions.
95  (0.1-1mg/kg, p.o), carnosol (0.01-0.1mg/kg, p.o.) isolated from the HEX fraction and betulinic acid
96 ct of gallic acid (GA; 50, 100 and 200mg/kg, p.o. for 10 days) on memory deficit and cerebral oxidati
97 done administration (0, 15, and 30 mg/70 kg, p.o.).
98 ological response in vivo (ED50 = 1.9 mg/kg, p.o. in the capsaicin-induced flinch model in rats) and
99 at curcumin administration (10 and 20 mg/kg, p.o.) increased hippocampal neurogenesis in chronically
100 atase inhibitor COUMATE at a dose (10 mg/kg, p.o.) shown previously to cause almost complete inhibiti
101 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-
102 or behavioral responses (5, 10 and 20 mg/kg, p.o.), could alleviate or reverse the effects of stress
103 a dose that increased food intake (10 mg/kg, p.o.), induced Fos expression in the nucleus of the soli
104 uced thermal hyperalgesia, MED = 0.83 mg/kg, p.o.).
105 e selective A2AR antagonist KW6002 (3 mg/kg, p.o.); (iii) global A2AR deletion; and (iv) selective A2
106    In contrast, pramipexole dosing (1 mg/kg, p.o., 1 h after the last methamphetamine dose, plus dail
107           Two doses of VEGFR2-TKI (25 mg/kg, p.o., b.i.d.) resulted in a decrease of V(b) to 1.3 +/-
108                  Pramipexole at the 1 mg/kg, p.o., dose level was able to significantly reduce the in
109          The animals received CHP, 25 mg/kg, p.o., or oxotremorine (OX), 0.2 mg/kg, s.c.
110 5 h), or chronic escalating (20 to 80 mg/kg, p.o.; for 3 weeks) drug administration.
111 Administration of A-889425 (10-300 mumol/kg, p.o.) alleviated grip force impairment in OA rats 3 week
112 ation of an active dose of Opra Kappa (10 mg p.o. daily, four consecutive days in comparison with an
113 drocortisone (30 mg p.o. each morning, 10 mg p.o. each evening; n=128).
114 To do this, we administered MDMA-HCl (100 mg p.o.) and, separately, placebo (ascorbic acid) in a rand
115 ree times a week) and ribavirin (400-1000 mg p.o. daily) for 12 months or more.
116                         Ganciclovir (1000 mg p.o. t.i.d.; n=19) or acyclovir (200 mg p.o. b.i.d.; n=2
117  levels with nicotinic acid (NA) (100-150 mg p.o., q 30 min x 4 h) in type 2 diabetic patients and in
118                           Lamivudine (150 mg p.o./d) was begun before transplantation in 10 patients,
119                By contrast, betaxolol (20 mg p.o.), a selective beta1-antagonist devoid of serotonerg
120 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
121 g) were detected overall such that the 25 mg p.o. capsule demonstrated higher values as compared with
122 ps were detected (p < 0.001), with the 25 mg p.o. capsule exhibiting the largest value (5054 ng-hr/mL
123 orally [p.o.] tid) and hydrocortisone (30 mg p.o. each morning, 10 mg p.o. each evening; n=128).
124 ay central effects of pindolol (10 and 30 mg p.o.), a mixed beta(1/2)-adrenoceptor/5-hydroxytryptamin
125  randomized to receive pentoxifylline 400 mg p.o. t.i.d. or matching placebo for 1 year after cardiac
126 f oral glucosamine at standard doses (500 mg p.o. t.i.d.) in lean (n = 20) and obese (n = 20) subject
127 t and reuptake inhibitor fenfluramine (60 mg p.o.) and 3 hours afterward.
128 a selective DRD3 antagonist (GSK598809 60 mg p.o.).
129  and after the COX inhibitor aspirin (600 mg p.o.).
130 =18) and HS (n=14) received memantine 20 mg (p.o.) and placebo over 2 test days in a double-blind, ra
131 s the influence of CBD (0, 200, 400, 800 mg, p.o.) pretreatment on the reinforcing, subjective, cogni
132 hen mice were immunized with rUre (25 microg p.o. or rectally or 10 microg i.n.) plus heat-labile tox
133 g p.o. dose of QS-21, whereas the 250-microg p.o. dose also induced IgG2a and IgG3 Abs.
134 tly IgG1 followed by IgG2b for the 50-microg p.o. dose of QS-21, whereas the 250-microg p.o. dose als
135 were subchronically exposed to PAH mixtures (p.o.), and mutagenic potency (MP) values were determined
136          In the golden Syrian hamster model, p.o. sodium bicarbonate supplementation (5 mg/ml in drin
137                                      Neither p.o. nor i.m. inoculation conferred significant protecti
138                           OGT 719 is a novel p.o. bioavailable nucleoside analogue in which galactose
139 shed that treatment of the host with a novel p.o. inhibitor of glucosylceramide synthesis, the imino
140 study we demonstrate the ability of a novel, p.o.-administered cytosine analogue, CS-682, to effectiv
141                               The ability of p.o. administered I3C to reverse MDR was also tested in
142 s serotype 3 clone 9 (T3C9) within 7 days of p.o. inoculation.
143                       Finally, the effect of p.o. administered resveratrol on N-methyl-N-nitrosourea-
144                         The effectiveness of p.o. OGT2378 in this murine model suggests that inhibiti
145                             These effects of p.o.-administered green tea or caffeine on early adaptiv
146                                  Toxicity of p.o. administered CAI most commonly consisted of dose-re
147 no detectable ISTLs in the genital tracts of p.o.- or s.c.-infected mice.
148                          PSI 8 mg/kg s.c. or p.o., but not i.p., caused neuronal loss in the substant
149 prion diseases frequently originate by oral (p.o.) infection.
150 owing either intraperitoneal (i.p.) or oral (p.o.) administration, as well as activity in the mouse a
151 r mice given the vaccine by either the oral (p.o.), intranasal (i.n.), or rectal route.
152 ities were observed for 18 and 19 upon oral (p.o.) administration to rats (18, ED50 = 3.9 mg/kg; 19,
153 ginally (i.v.), intranasally (i.n.), orally (p.o.), or subcutaneously (s.c.) with C. trachomatis.
154 inoculated intracerebrally (i.c.) or orally (p.o.) with CWD-infected deer brain.
155           NBI 35965 administered per orally (p.o.) in rats (1, 3, 10 or 30 mg/kg) inhibited dose-depe
156  (n=132), or together with K (400 mg orally [p.o.] tid) and hydrocortisone (30 mg p.o. each morning,
157 osaconazole (10 mg/kg of body weight orally [p.o.] twice a day [BID]), voriconazole (10 mg/kg p.o. BI
158 ause systemic disease in mice after peroral (p.o.) inoculation and primary replication in the intesti
159 biotic pigs were inoculated twice perorally (p.o.) (group 1) or intramuscularly (i.m.) (group 2) or t
160 ance) for (R)-18 in mice (i.p.) and in rats (p.o.) were 6.0 and > 130, respectively.
161 efractory solid tumors, 49 patients received p.o. administered CAI daily or every other day.
162 ice were acutely administered by oral route (p.o.) with fractions, essential oil or isolated compound
163                          A highly selective, p.o. bioavailable irreversible inhibitor of epidermal gr
164 0%) was sustained for >4 hours with a single p.o. dose of 33 mg/kg.
165 icacy and associated mechanisms of long-term p.o. silibinin feeding against spontaneous intestinal tu
166                 Our results demonstrate that p.o.-administered noscapine significantly inhibits the p
167                                We found that p.o. administration of EGCG at doses of 0.08% or 0.16% i
168                          Here we report that p.o. administration of QS-21 with the vaccine protein te
169                             We now show that p.o. gavage of garlic constituent diallyl trisulfide (DA
170 female athymic BALB/c nu/nu mice showed that p.o. administration of 2-MeO-E(2) at 30 mg/kg body weigh
171                   The results suggested that p.o. administered tea or caffeine may have decreased tum
172 tly under development, as represented by the p.o. administered prodrug capecitabine, the gene silenci
173 patients with squamous cell carcinoma of the p.o. tongue, there was a significant correlation between
174               Mice were treated with various p.o. doses of CS-682 on a five times per week schedule u
175 ell xenografts with riluzole for 18 days via p.o. gavage or i.v. injection leads to inhibition of tum
176  or sulforaphane (9 micromol/day for 1 week, p.o.) was generated using the Murine Genome U74Av2 oligo
177            Six-week-old APC(min/+) mice were p.o. fed with vehicle control (0.5% carboxymethyl cellul
178  i.v. route were modestly protected, whereas p.o. and s.c. groups were indistinguishable in this rega
179              Efficacy was also achieved with p.o. administration of HTI-286.
180 is a promising cancer therapeutic agent with p.o. bioavailability.
181 umans by pairing a distinctive beverage with p.o. administration of dexamethasone.
182              Pretreatment of SKH-1 mice with p.o.-administered 0.6% green tea (6 mg of lyophilized te
183 tinctively flavored beverage was paired with p.o. administration of dexamethasone.
184 ntrations were achieved in all patients with p.o. Neoral.

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