1 ; N-(4-aminobutyl)-1-naphthalenesulfonamide; promethazine; 2-[N-(4-methoxybenzenesulfonyl)]amino-N-(4

2 und no difference between metoclopramide and promethazine after 24 hours (episodes of vomiting, 1 [IQ

3  The analytical approach was then applied to promethazine, an FDA-approved drug previously shown to i

4 ; loratadine and ropinirole (RR = 3.21); and promethazine and tegaserod (RR = 3.00).

5 ed for three different drugs: amitriptyline, promethazine, and methadone.

6 or moderate symptoms, pyridoxine-doxylamine, promethazine, and metoclopramide were associated with gr

7 phenothiazine neuroleptics (chlorpromazine & promethazine) as additive neuroprotectants, with the aim

8 lline, CGP35348 (GABAB receptor antagonist), promethazine, atropine, d-tubocurarine and suramin had n

9               Kinetic analysis revealed that promethazine delayed mPT induction in a manner qualitati

10 aneous quantitative analysis of three drugs (promethazine, enalapril, and verapamil) using deuterated

11 er MB derivatives, 2-chlorophenothiazine and promethazine, exert no effect on cellular bioenergetics

12 CTs compared corticosteroids with placebo or promethazine or metoclopramide in women with severe symp

13  0-5] for metoclopramide vs 2 [IQR, 0-3] for promethazine [P = .81], VAS [0-10 scale] for nausea, 2 [

14 combined intravenous midazolam, morphine and promethazine (Phenergan).

15                                Specifically, promethazine protected primary neuronal cultures subject

16 loratadine and simvastatin and tegaserod and promethazine were predicted to have a strong DDI through

17  (N-(6-aminohexyl)-1-naphthalenesulfonamide; promethazine), were also found to block activation of th

18  general structural class that inhibits mPT, promethazine, were protective in both in vitro and mouse