Disease relevance of 4-Hydroxypropranolol

• Propranolol plasma levels and relief of migraine. Relationship between plasma propranolol and 4-hydroxypropranolol concentrations and clinical effects [1].
• Arylsulfatase from Helix pomatia and Aerobacter aerogenes completely hydrolyzed peak 4 to 4-hydroxypropranolol [2].

High impact information on 4-Hydroxypropranolol

• The pharmacokinetics of metabolites of avitriptan (N-desmethylavitriptan, methoxypyrimidinyl piperazine, and O-desmethylavitriptan) and the pharmacokinetics of 4-hydroxypropranolol were also assessed [3].
• Three genotypes showed distinct time profiles of plasma propranolol and 4-hydroxypropranolol [4].
• When propranolol and 4-hydroxypropranolol were incubated in combination with platelets in equal concentrations, there were synergistic effects on platelet aggregation and TXA2 generation [5].
• The kinetics of propranolol and its metabolite 4-hydroxypropranolol were determined together with heart rate and blood pressure responses in five cyanotic children on long-term propranolol therapy and after abrupt withdrawal [6].
• The concentration of drug that inhibited receptor binding by 50% (IC50) was l-propranolol, 1.5 micrograms/L; d-propranolol, 243 micrograms/L; and 4-hydroxypropranolol, 8.8 micrograms/L [7].

Chemical compound and disease context of 4-Hydroxypropranolol

• The relationship between propranolol and 4-hydroxypropranolol plasma concentrations and relief of migraine was assessed in 17 patients during treatment with oral racemic propranolol hydrochloride in doses of 40 to 240 mg/day [1].

Biological context of 4-Hydroxypropranolol

• There were no significant differences in the AUC of 4-hydroxypropranolol (4OHPPL) and its conjugates or the urinary excretion of conjugated 4OHPPL [8].
• These observations together with UV spectra before and after acid hydrolysis indicated peak 4 to be an acid- and heat-labile conjugate of 4-hydroxypropranolol with the conjugating group at the phenolic oxygen atom [2].
• No correlations were found between the mean arterial blood pressure (post-therapy) or the fall in blood pressure as a result of the P therapy (p much greater than 0.05) and P dose, peak P plasma concentrations, peak 4-hydroxypropranolol (4OHP) plasma concentrations or peak (P plus 4OHP) plasma concentrations [9].
• The mean peak levels of propranolol, propranolol glucuronide, 4-hydroxypropranolol, and 4-hydroxypropranolol glucuronide were not significantly different in the first, second, third trimesters and at least 3 months post partum [10].

Anatomical context of 4-Hydroxypropranolol

• During incubation with rat liver microsomes (1 mg of protein) fortified with an NADPH-generating system, 4-hydroxypropranolol (4-OH-PL) quickly disappeared from the reaction medium, but none of the possible metabolite peaks was detected under the high-performance liquid chromatographic conditions used [11].
• Stereoselective sulfate conjugation of racemic 4-hydroxypropranolol by human and rat liver cytosol [12].

Associations of 4-Hydroxypropranolol with other chemical compounds

• Propranolol and its oxidized metabolites 4-hydroxypropranolol (4-OH-P) and N-desisopropylpropranolol (nor-P) were analyzed using high-performance liquid chromatography and fluorometric detection [13].
• Silica gel high-performance liquid chromatography for the simultaneous determination of propranolol and 4-hydroxypropranolol enantiomers after chiral derivatization [14].
• Propranolol, 4-hydroxypropranolol and quinidine were eluted from 5 microns, C-18 reversed phase column with a mobile phase consisting of acetonitrile-methanol-phosphoric acid at pH 4 and detected with fluorescence detector [15].
• The derivatized products were separated on an Altex C18 column using a mixture of acetonitrile-water-phosphoric acid-triethylamine (58:42:0.1:0.06 and 50:50:0.15:0.06, v/v, for propranolol and 4-hydroxypropranolol, respectively) as mobile phase [16].

Gene context of 4-Hydroxypropranolol

• Involvement of SULT1A3 in elevated sulfation of 4-hydroxypropranolol in Hep G2 cells pretreated with beta-naphthoflavone [17].
• In summary, we found that both CYP1A2 and CYP2D6 catalyze formation of 4-hydroxypropranolol and that both enzymes exhibited racial differences in this reaction [18].
• An automated HPLC method is described for the simultaneous determination of propranolol, 4-hydroxypropranolol, and N-desisopropylpropranolol in plasma and urine before and after beta-glucuronidase/aryl sulfatase treatment [19].

Analytical, diagnostic and therapeutic context of 4-Hydroxypropranolol

• An active metabolite, 4-hydroxypropranolol and possibly other active compounds have been identified; the former only after oral administration [20].
• Concentrations of P, propranolol glucuronide (PG), 4-hydroxypropranolol (4P), 4-hydroxypropranolol glucuronide (4PG), 4-hydroxypropranolol sulfate (4PS), and naphthoxylactic acid (NLA) were determined by HPLC with fluorescence and UV detection [21].
• At the conclusion of the perfusion, 4-hydroxypropranolol was the major metabolite present and 5-hydroxypropranolol and N-desisopropylpropranolol were minor metabolites [22].

References