ライフサイエンスコーパス: fluphenazine

1 s blocked by a dopamine receptor antagonist (fluphenazine).

2 pical application of the dopamine antagonist fluphenazine.

3 privation, amyloid beta peptide (25-35), and fluphenazine.

4 ects on plasma prolactin than risperidone or fluphenazine.

5 ng symptom progression and was comparable to fluphenazine.

6 acy and side effect profile of clozapine and fluphenazine.

7 e effect of the dopamine receptor antagonist fluphenazine (0.1-1.0 mg/kg) was also assessed for compa

8 Fluphenazine (10 or 50 microg/side), infused immediately

9 ly 10 mV in the hyperpolarizing direction by fluphenazine (3 microM for ND7/23 currents and 10 microM

10 y 14 days), which was supplemented with oral fluphenazine (5 mg twice daily) or a placebo when they f

11 The calmodulin inhibitor, fluphenazine (50 microM) inhibited CCh-stimulated PYK-2

12 eline while patients were being treated with fluphenazine and after 12 weeks of double-blind treatmen

13 complexes revealed substantial stability for Fluphenazine and Nintedanib with Sirt2.

14 conventional drugs, such as chlorpromazine, fluphenazine and pimozide, were more toxic than the atyp

15 -week, double-blind crossover trial in which fluphenazine and placebo were administered for 12 weeks

16 onth formulation), olanzapine, flupenthixol, fluphenazine, and paliperidone (1-month formulation).

17 ly haloperidol was inferior to aripiprazole, fluphenazine, and paliperidone.

18 he phenothiazine derivatives acetophenazine, fluphenazine, and periciazine, used clinically as antips

19 a or schizoaffective disorder who were given fluphenazine as the first treatment.

20 ribe our electrophysiological examination of fluphenazine at tetrodotoxin-sensitive (TTX-S) and resis

21 demonstrated significant reductions from the fluphenazine baseline in positive symptoms, total sympto

22 ll or Na(V)1.8 currents revealed a prominent fluphenazine block of sodium channel activity.

23 tion, the D1/D2 dopamine receptor antagonist fluphenazine blocked footshock-induced reinstatement whe

24 upenthixol, (+)-butaclamol, haloperidol, and fluphenazine but not SCH23390 or (-)-butaclamol decrease

25 efficacy and tolerability of topiramate and fluphenazine, but more rigorous studies are needed to fu

26 Fluphenazine, but not clozapine, increased metabolic rat

27 R showed a decrease in impulsivity following fluphenazine, but not following either amphetamine or me

28 (ii) Three structurally distinct inhibitors (fluphenazine, calmidazolium and a W-7 analogue) of the C

29 zophrenia were stabilized with a low dose of fluphenazine decanoate (5 to 10 mg every 14 days), which

30 cally stabilized on a maintenance regimen of fluphenazine decanoate for a mean of 16.7 months had the

31 r were randomly assigned to receive 25 mg of fluphenazine decanoate intramuscularly either every 2 we

32 omized to 1 of 3 medication strategies using fluphenazine decanoate under double-blind conditions: co

33 l temporal lobes, whereas clozapine, but not fluphenazine, decreased inferior prefrontal cortex activ

34 We explored the effects of tamoxifen (TAM), fluphenazine (FLU) and estradiol (E2) on ATP levels in H

35 d both radioligands in Acc and IC (30%-70%); fluphenazine had no effect.

36 trols and patients not receiving medication, fluphenazine hydrochloride- and clozapine-treated patien

37 which is comparable to the response rate to fluphenazine in the previous study.

38 butaclamol, haloperidol, chlorpromazine, and fluphenazine inhibited constitutive adenylyl cyclase act

39 Moreover, clozapine and fluphenazine inhibited glucose transport in the rat musc

40 y 2 weeks); or targeted, early intervention (fluphenazine only when symptomatic).

41 paliperidone-LAI 1-monthly, iloperidone-OS, fluphenazine-OS, brexpiprazole-OS, paliperidone-LAI 1-mo

42 or acceptability to other LAIs (bromperidol, fluphenazine, paliperidone [1-month formulation], pipoth

43 Fluphenazine (Prolixin(R)) is a potent phenothiazine-bas

44 Fluphenazine's apparent potency for blocking either ND7/

45 selectively increased MAD scores in WKY and fluphenazine selectively increased MAD scores in SHR.

46 ence [SMD], 0.04; 95% CI, -0.25 to 0.33) and fluphenazine (SMD, 0.15; 95% CI, -0.39 to 0.69) as well

47 These experiments show fluphenazine to be capable of blocking neuronal sodium c

48 atients compared diazepam with placebo (with fluphenazine treatment for a comparison group).

49 After a baseline fluphenazine treatment period, 29 patients participated

50 ients with schizophrenia received 4 weeks of fluphenazine treatment.

51 When fluphenazine was administered into the nucleus accumbens

52 exacerbation or relapse during this period, fluphenazine was openly withdrawn; participants were the

53 nyl-2-ethoxy-1,2-dihydroquinoline (EEDQ), or fluphenazine were microinjected into rat nucleus accumbe

54 gs, such as sertraline, trifluoperazine, and fluphenazine, were found to be direct inhibitors of the

55 Conversely, applying fluphenazine, which decreases brain dopamine levels, wea