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At least 19 recordsLinked to original sources
PubMed1977

Quantitative determinations of codeine phosphate, guaifenesin, pheniramine maleate, phenylpropanolamine hydrochloride, and pyrilamine maleate in an expectorant by high-pressure liquid chromatography.

The quantitative determinations of codeine phosphate, guaifenesin, pheniramine maleate, phenylpropanolamine hydrochloride, and pyrilamine maleate in a liquid dosage form are described. All active and inactive ingredients (sodium benzoate and FD&C Yellow No. 5 dye) can be separated with high-pressure liquid chromatography except the two antihistamines, pheniramine maleate and pyrilamine maleate. Pheniramine maleate is determined colorimetrically, and pyrilamine maleate is determined either by difference or spectrophotometrically. The methods are simple short, accurate, and precise. The standard deviations are reported.

Chromatography, High Pressure Liquid↗
PubMed1978

Fluoremetric determination of methylergonovine maleate and ergonovine maleate in tablets and injections.

A column cleanup, followed by a shakeout and fluorometric determination, has been developed to determine methylergonovine maleate and ergonovine maleate in tablets and injections. The ether eluate is extracted with tartaric acid solution. An aliquot is diluted with sodium tartrate solution, and this solution is excited at 325 nm. The resulting fluorescence is measured at 432 nm. Results obtained using this method compare favorably with those from the official NF XIV procedure and a semiautomated procedure. Recoveries of 100 and 99% were obtained from one sample each of spiked excipient tablets of methylergonovine maleate and ergonovine maleate, respectively.

Ergonovine↗
PubMedDate not supplied

Comparative effect of dimethindene maleate and chlorpheniramine maleate on histamine-induced weal and flare.

Antihistaminic activity of 3 or 6 mg dimethindene maleate was compared with that of placebo and 12 mg chlorpheniramine maleate in 60 healthy volunteers in a randomized, crossover study. Activity of each drug was assessed by measuring 2 micrograms histamine-induced weal and flare areas. Compared with placebo, both doses of dimethindene and chlorpheniramine significantly (P less than 0.001) reduced weal area. Both doses of dimethindene (P less than 0.001) and chlorpheniramine (P less than 0.05) also significantly reduced flare area. Dimethindene (6 mg) brought about the maximum reduction in weal area (28.8%) and flare area (39.1%). Dimethindene (6 mg) also reduced weal area significantly (P less than 0.01) compared with chlorpheniramine and reduced flare area significantly (P less than 0.05) compared with 3 mg dimethindene. Using a 100 mm visual analogue scale for assessment of weal and flare intensities, 6 mg dimethindene again produced the maximum response. The study confirmed that the antihistamine activity of dimethindene was better than that of chlorpheniramine.

Adult↗
PubMed1979

Semiautomated method for the analysis of formulations of chlorpheniramine maleate and brompheniramine maleate.

The determination of chlorpheniramine maleate and brompheniramine maleate in tablets, capsules, injections, and elixirs has been automated. The active ingredient is dissolved in dilute HCl. The dilute acid solution is sampled, made basic with dilute NaOH, and extracted with isooctane. The isooctane phase is resampled and the drug is re-extracted into dilute HCl. The absorbance of the acidic aqueous layer is monitored at 265 nm. The method is an automated version of the general USP XIX assay for salts of organic nitrogenous bases. The results from the semiautomated procedure agree well with the USP XIX and NF XIV official methods. Recoveries were 100% from an authentic tablet material. The system is linear from 0 to 300% of declared potency. The procedure is free from common excipient and dye interferences. Precision data are included for both the automated and official methods.

Autoanalysis↗
PubMed1975

Semiautomated analysis of ergonovine maleate or methylergonovine maleate tablets and injections by colorimetric or fluorometric systems.

Two semiautomated analytical systems have been developed to determine ergonovine and methylergonovine maleate in single tablets and injections. The active ingredient is dissolved in a tartrate buffer. In the fluorometric method the stream is automatically diluted with tartrate buffer and excited with ultraviolet light; the resulting fluorescence is measured and recorded. In the colorimetric method, the stream is automatically made basic with sodium hydroxide and extracted with n-butanol. The extract is mixed with p-dimethylaminobenzaldehyde reagent. After reaction, the solution is mixed with sodium nitrite solution, and the developed color is measured at 550 nm. Recoveries of 100% were obtained from spiked placebos. Standard deviations for powdered tablet and injection samples ranged from 0.63 to 1.24%. Comparisons with the USP XVIII methods are presented.

Autoanalysis↗
PubMed1985

Maleate effects on kidney peptidases and proteinuria of male and female rats. Histochemical and biochemical studies.

The effects of maleate on membrane-bound and lysosomal peptidases were studied histochemically in the kidney and biochemically in the kidney and the urine of male and female rats 6 h after the administration of two different doses of sodium maleate (150 and 300 mg/kg body weight). Additionally, the proteinuria of experimental animals was electrophoretically analysed to detect maleate-induced alterations in the urinary protein composition. The histochemistry of the brush-border peptidases (aminopeptidase A, gamma-glutamyltransferase) showed dose-dependent maleate effects in the late pars convoluta and the pars recta of the proximal tubule (blurring of the brush-border enzyme reaction pattern). The female animals were more severely affected by both maleate doses. After maleate treatment, enzyme-activity measurements in the kidney homogenate supernatant and urine indicated dose-dependent structural destruction of the proximal tubule, especially of brush-border membranes, and revealed an increase in enzyme excretion. Both the maleate-induced enzyme excretion and proteinuria were more pronouncedly increased in females than in males. Electrophoretic analysis of urinary proteins revealed alterations in the urinary-protein composition after maleate treatment, which favoured the excretion of proteins with a molecular weight higher than 20,000 daltons. Again, sex-related differences in the maleate effects were demonstrated. The results indicate that maleate causes alterations in the brush-border membranes and, especially at higher doses, results in cellular destruction selectively in the late proximal tubule of rat kidneys. Selectivity was also encountered in the maleate effects on urinary-protein composition, suggesting that the tubular alterations lead to an inhibition of the reabsorption of mainly high-molecular-weight proteins. Although the nature of the effects was independent of sex, it appears that females are less well protected against tubular damage caused by maleate.

Aminopeptidases↗
PubMed1976

Maleate-induced bicarbonaturia in the dog: a carbonic anhydrase-independene effect.

Studies were performed to characterize the renal effects of maleate in anesthetized dogs. Following the intravenous administration of maleate or maleic acid (50 mg/kg), mean fractional bicarbonate excretion (CHCO3/GFR) rose to as high as 26%. Na, K, and phosphate excretion also increased markedly, whereas C1 excretion remained low. An initial transient fall in urinary pH from 6.53 to 6.13 contrasted sharply with the rapid alkalinization of the urine induced by acetazolamide administration. During saline expansion CHCO3/GFR rose from 4 to 37% after maleate administration, whereas Cl excretion did not change significantly. During continuous carbonic anhydrase inhibition with acetazolamide, maleate administration resulted in a further rise in CHCO3/GFR from 22 to 35%. Whereas CPO4/GFR increased only from 1 to 3% during acetazolamide administration, this ratio reached 75% following the addition of maleate. Fumarate, the transisomer of maleate, and malonate, a well-known inhibitor of Krebs cycle, failed to affect bicarbonate excretion. This study demonstrates that maleate inhibits the fraction of bicarbonate reabsorption uncatalyzed by carbonic anhydrase. Impaired anionic reabsorption of bicarbonate or accelerated passive backflux of this ion into proximal tubular lumen are the two mechanisms that best explain the bicarbonaturia induced by maleate.

Acetazolamide↗
PubMed1992

Screening for microorganisms producing D-malate from maleate.

More than 300 microorganisms were screened for their ability to convert maleate into D-malate as a result of the action of maleate hydratase. Accumulation of fumarate during incubation of permeabilized cells with maleate was shown to be indicative of one of the two enzymes known to transform maleate. The ratio in which fumarate and malate accumulated could be used to estimate the enantiomeric composition of the malate formed. Many strains (n = 128) were found to be capable of converting maleate to D-malate with an enantiomeric purity of more than 97%. Pseudomonas pseudoalcaligenes NCIMB 9867 was selected for more detailed studies. Although this strain was not able to grow on maleate, permeabilized cells were able to degrade maleate to undetectable levels, with a concomitant formation of D-malate. The D-malate was formed with an enantiomeric purity of more than 99.97%.

Bacteria↗
PubMed1975

Identity of maleate-stimulated glutaminase with gamma-glutamyl transpeptidase in rat kidney.

Gamma-Glutamyl transpeptidase was purified from rat kidney by a procedure involving Lubrol extraction, acetone precipitation, ammonium sulfate fractionation, treatment with bromelain, and column chromatography on DEAE-cellulose and Sephadex G-100. The final preparation (enzyme III), which exhibits a specific activity about 8-fold higher than that of the purified rat kidney transpeptidase previously obtained in this laboratory (enzyme I), was apparently homogeneous on polyacrylamide gel electrophoresis. Enzyme III is a glycoprotein containing 10% hexose, 7% aminohexose, and 1.5% sialic acid; a tentative molecular weight value of about 70,000 was obtained by gel filtration. Enzyme III has a much lower molecular weight and a different amino acid and carbohydrate content than the less active rat kidney transpeptidase preparation previously obtained, but obtained, but the catalytic properties of these preparations are virtually identical. It is suggested that bromelain treatment may liberate the transpeptidase from a brush border complex that contains other proteins. An improved method is described for the isolation of the higher molecular weight form of the enzyme (enzyme I) in which affinity chromatography on concanavalin A-Sephrose is employed. The purified transpeptidase (enzyme III) is similar to the phosphate-independent maleate-stimulated glutaminase preparation obtained from rat kidney by Katunuma and colleagues with respect to amino acid and carbohydrate content, apparent molecular weight, and relative transpeptidase and maleate-stimulated "glutaminase" activities. Both of these enzyme preparations are much more active in transpeptidation reactions with glutathione and related gamma-glutamyl compounds than with glutamine. In the absence of maleate, the enzyme catalyzes the utilization of glutamine (by conversion to gamma-glutamylglutamine, glutamate, and ammonia) at about 2% of the rate observed for catalysis of transpeptidation between glutathione and glycylglycine; the utilization of glutamine occurs about 8 times more rapidly in the presence of 0.1 M maleate. The transpeptidation and maleate-stimulated glutaminase reactions catalyzed by both enzyme preprations are inhibited by 5 mM L-serine in the presence of 5 mM sodium borate. Studies on gamma-glutamyl transpeptidase and maleate-stimulated glutaminase in the kidneys of fetal rats, newborn rats, and rats after weaning showed parallel development of these activities. The evidence reported here and earlier work in this laboratory strongly support the conclusion that maleate-stimulated glutaminase activity is a catalytic function of gamma-glutamyl transpeptidase. The studies on the ontogeny of gamma-glutamyl transpeptidase and other data are considered in relation to the proposal that this enzyme is involved in amino acid and peptide transport. Its possible role in renal formation of ammonia is also discussed.

Aging↗
PubMed1979

Cardiovascular responses to diazepam and midazolam maleate in the dog.

Previous clinical studies establishing the efficacy of midazolam maleate (RO 21-3981), a new water-soluble benzodiazepine for induction of anesthesia, have not critically evaluated the effects of this agent on the cardiovascular system. The present study compares the cardiovascular effects of midazolam maleate and diazepam in conscious dogs. Systemic arterial, pulmonary arterial and central venous pressures, cardiac output, LVmax dP/dt, heart rate and regional coronary blood flow were measured 3 min following intravenous administration of diazepam (0.5, 1.0, and 2.5 mg/kg) or midazolam maleate (0.25, 1.0, and 10.0 mg/kg). Midazolam maleate increased heart rate 10--20 per cent with all three doses and decreased mean arterial blood pressure approximately 10--20 per cent at 1.0 and 10 mg/kg. Cardiac output was increased 10--12 per cent with all three doses of midazolam maleate, and LVmax dP/dt was decreased 13--16 per cent at the two higher doses. Diazepam at all three doses did not alter heart rate or mean arterial blood pressure. Diazepam, 1.0 and 2.5 mg/kg, produced significant (17 per cent) decreases in LVmax dP/dt, and 2.5 mg/kg produced a significant (10 per cent) increase in cardiac output. Neither drug in any dosage altered regional coronary blood flow, systemic or coronary vascular resistance, stroke volume, or stroke work. Maximum alterations in cardiovascular variables occurred with doses of midazolam maleate that are 10--15 times the recommended clinical induction dosage. It is concluded that in concentrations necessary for induction of anesthesia midazolam maleate has minimal effects on cardiovascular function.

Animals↗
PubMed1990

LY277359 maleate: a potent and selective 5-HT3 receptor antagonist without gastroprokinetic activity.

Several 5-hydroxytryptamine (5-HT3) receptor antagonists have been described. In addition to 5-HT3 receptor antagonist activity, many of these agents also possess gastroprokinetic activity. In the present report, we identify compound LY277359 maleate as a potent, p.o. active, highly selective 5-HT3 receptor antagonist lacking gastroprokinetic effects. LY277359 maleate was a potent and selective antagonist of 2-methyl 5-HT-induced contraction in the guinea pig ileum (KB = 1.6 nM), a response mediated by activation of 5-HT3 receptors. Given both i.v. (0.0003, 0.001 and 0.003 mg/kg) and p.o. (0.01 and 0.03 mg/kg), LY277359 maleate inhibited the bradycardic response to i.v. administered 5-HT in urethane-anesthetized rats. The duration of antagonism of 5-HT-induced bradycardia persisted beyond 6 hr after p.o. administration of LY277359 maleate (0.03 mg/kg p.o.). In contrast to its potent 5-HT3 receptor antagonist activity, LY277359 maleate, in doses up to 1 mg/kg p.o., did not affect gastric emptying in rats, suggesting minimal, if any, gastroprokinetic activity of LY277359 maleate. This is in contrast to another 5-HT3 receptor antagonist, zacopride, which did produce a marked increase in gastric emptying in rats at doses of 0.1 mg/kg p.o. and higher. LY277359 maleate (0.03 and 0.1 mg/kg i.v. and 0.07, 0.1, 0.3 and 1.0 mg/kg p.o.) did have effects consistent with other 5-HT3 antagonists, to inhibit cisplatin-evoked emesis in dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effects of proglumetacin maleate and its major metabolites on allergic air pouch inflammation in rats.

The mechanism of the anti-inflammatory effect of proglumetacin maleate, a novel indomethacin derivative, was examined in vivo in an allergic air pouch inflammation model in rats. Proglumetacin maleate did not affect the volume of pouch exudate 6 h after immunological challenge, irrespective of whether it was administered orally or locally, but it caused dose-dependent inhibition 24 h after challenge. It also caused dose-dependent reduction of leukocyte migration into the pouch exudate both 6 and 24 h after challenge. It markedly decreased the prostaglandin E2 content of the pouch exudate, but tended to increase the leukotriene B4 content. The main metabolites of proglumetacin maleate, desproglumideproglumetacin maleate and indomethacin, had effects similar to those of proglumetacin maleate on these four parameters on an equimolar dose basis. Unlike these three drugs, dexamethasone decreased the leukotriene B4 content of the pouch exudate. These results suggest that the action of proglumetacin maleate is qualitatively the same as that of indomethacin in vivo; that is, it inhibits cyclo-oxygenase in inflammatory sites.

Administration, Oral↗
PubMed1992

Antihistaminic efficacy of Ranitidine with & without Dimethendine maleate on histamine-induced cutaneous reactions.

The effect of Ranitidine, the H2-receptor antagonist, was investigated on cutaneous response to intradermal injection of histamine in healthy volunteers in a controlled, randomized, cross over study. The response was compared with that of the H1-receptor blocker; Dimethendine maleate used alone and in combination with the two antagonists. Reduction in the wheal area was significant in subjects pretreated with Ranitidine alone (P less than 0.05), and Dimethendine maleate alone (P less than 0.05); the combination of the two antagonists, did not produce additional reduction. Reduction in erythema area was not significant with Dimethendine maleate alone, but significant with Ranitidine alone (P less than 0.01). With the combination of the two antagonists the reduction was not more significant than with Ranitidine alone. The flare response scoring on visual analogue scale was not reduced significantly by Dimethendine maleate alone but reduced significantly by Ranitidine alone (P less than 0.10), and by combination of Ranitidine and Dimethendine maleate (P less than 0.05). Thus, Ranitidine appears to be more effective than Dimethendine maleate in reducing the erythema area and intensity of flare response and equieffective in reducing wheal response to histamine injection.

Adult↗
PubMed1976

Additive inhibition of renal bicarbonate reabsorption by maleate plus acetazolamide.

The effects of two potent inhibitors of renal bicarbonate reabsorption--maleate and acetazolamide--were investigated in the rat using clearance techniques. Acetazolamide given in high dose (50 mg/kg body wt) inhibited fractional bicarbonate reabsorption by ca. 30%, maleate (2.58 nmol/kg body wt) by 25%, and maleate plus acetazolamide by 54-72%. GFR was depressed, and urine volume was increased by both drugs in an additive manner. Maleate was equally effective as inhibitor of HCO3- reabsorption in the presence and absence of carbonic anhydrase activity. It is suggested that the site of action of both drugs is predominantly proximal, but they act on different steps in the transcellular HCO3- transport. A hypothetical mechanism of maleate action is presented, which takes into account the changes in passive HCO3- flux through the basolateral membrane.

Acetazolamide↗
PubMed1990

DNA damage and sequence specificity of DNA binding of the new anti-cancer agent 1,4-bis(2'-chloroethyl)-1,4-diazabicyclo-[2.2.1] heptane dimaleate (Dabis maleate)

The DNA damage and the sequence specificity of guanine-N7 alkylation produced by the novel, positively charged, antineoplastic agent 1,4-bis(2'-chloroethyl)-1,4-diazabicyclo-[2.2.1] heptane dimaleate (Dabis maleate) and its uncharged tertiary amine analogue 1,4-bis(2'-chloroethyl)-1,4-diazacyclohexane (Dabis analogue) were investigated in L1210 cells and isolated DNA. Both compounds are cytotoxic in vitro causing an arrest of L1210 cells in G2/M phase of the cell cycle. In isolated DNA, Dabis maleate alkylates guanine at the N7-position with some differences in specificity compared to other alkylating agents (e.g. nitrogen mustard). Significant differences are also evident between Dabis maleate and Dabis analogue, suggesting that Dabis analogue is not the sole alkylating species of Dabis maleate. Using the alkaline elution technique a moderate number of DNA interstrand cross-links were detected in L1210 cells treated with both compounds, which were completely repaired within 24 h. Dabis maleate and Dabis analogue do not cause DNA single strand breaks or DNA protein cross-links at the doses at which DNA interstrand cross-links were detected.

Animals↗
PubMed1975

Timolol maleate, a new beta-adrenergic receptor blocking agent.

Some pharmacodynamic properties of an oxypropanolamine substituted novel heterocyclic compound are described. Initial studies involve comparison of the racemic mixture, dl-timolol maleate, with the beta-adrenergic receptor blocking agent propranolol in the rat, dog and cat. dl-Timolol maleate is shown to be a potent inhibitor of cardiovascular beta-adrenergic receptors activated by isoproterenol or adrenergic nerve stimulation. Blockade of alpha-adrenergic receptors is not observed even after extremely high doses. The compound is approximately 3 times more potent than propranolol in suppressing isoproterenol-induced cardioacceleration by the i.v. route of administration. dl-Timolol maleate is also extremely well absorbed when given orally, being then about 10 times more active than propranolol. Unlike propranolol, neither dl-timolol maleate nor its optical isomers possess demonstrable local anesthetic activity. Similar to propranolol and other beta-adrenergic receptor blocking agents, activity of the compound resides predominantly in the l-isomer (timolol maleate.

Adrenergic beta-Antagonists↗
PubMed1992

Brush border membrane proteins in experimental Fanconi's syndrome induced by 4-pentenoate and maleate.

Fanconi's syndrome was investigated using brush border membrane (BBM) vesicles isolated from dog kidney. Sodium-dependent uptake of glucose, phosphate, and amino acids and protein phosphorylation were studied in BBM isolated from normal and from 4-pentenoate- and maleate-treated animals. The time course of D-glucose and phosphate uptake, in BBM vesicles, remained unchanged, indicating that both treatments had no effect on carrier properties, and that permeabilities to these substrates and to sodium were not modified. Furthermore, sodium-dependent transport of alanine, phenylalanine, proline, glycine, and glutamate into vesicles remained unaltered by either treatment. 4-Pentenoate treatment caused modifications of the phosphorylation pattern of BBM proteins: the phosphorylation of two proteins (61 and 74 kDa) was increased and that of two others (48 and 53 kDa) was decreased. Maleate treatment caused an increase in the phosphorylation for the same 61-kDa protein, which was also affected by 4-pentenoate treatment, suggesting that phosphorylation of this protein could be related to a mechanism involved in both 4-pentenoate- and maleate-induced Fanconi's syndrome. These changes were also observed in the presence of sodium fluoride and L-bromotetramisole, indicating that the modification of phosphorylation was not due to a difference in phosphatase activities. These results suggest that Fanconi's syndrome induced by 4-pentenoate or maleate is not caused by an inhibition of BBM Na(+)-dependent transport systems. Our results also suggest that protein phosphorylation may play an important role in the molecular defect involved in Fanconi's syndrome.

Animals↗