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PubMed1985

Local and systemic tolerability of suprofen. Experience with intravenous administration and infusion in healthy volunteers (2nd comm.).

12 healthy male volunteers who had given consent to the study each received in a randomized cross-over design 13 applications of 2-methyl-4-(2-thienylcarbonyl)-phenyl acetic acid (suprofen, Suprol) injection solution 200 mg/ml at 8 a.m. and at 2 p.m. as i.v. bolus injections or as infusions. It could be demonstrated, that suprofen given as multiple dose i.v. bolus injections or as multiple infusion doses was well tolerated. The peak plasma concentrations after i.v. bolus injections were in the range of 16.3 to 42.3 micrograms/ml (mean 26.5) and after 2 h between 1.3 and 9.8 micrograms/ml (mean 3.2). 1.5 h after the start of infusion (end of the infusion) the plasma concentrations were in the range of 4.0 and 11.2 micrograms/ml (mean 7.2) with a infusion rate of 4.6 mg/min for the first 30 min and then of 1.1 mg/min for about 57 additional min. At 2.5 h after the infusion applications the mean plasma level was 2.0 micrograms/ml. There was no indication of accumulation nor accelerated elimination during the 7-day period. There was no statistically significant difference between the plasma elimination after the last injection of the 7-day period and the plasma elimination after i.v. single injection as well as from the elimination after the last infusion of the 7-day period.

Adult↗
PubMed1985

Pharmacokinetics and bioavailability of suprofen injection solution after intravenous application versus capsules on six healthy male volunteers.

In a three-way cross-over study six healthy male volunteers received intravenously 50 mg and 100 mg suprofen as a bolus injection and orally 200 mg as one capsule. The plasma level curves could be fitted to a two-compartimental model by means of the computer program NONLIN. The pharmacokinetic parameter estimates did not show dose dependency. The absolute bioavailability of suprofen taken as one capsule was 92.2% based on AUC-values and did not indicate a first-pass effect. The plasma input curve was determined by point-area deconvolution. Assuming first order input a half-life of 23 min could be derived based on point-area deconvolution. Different dissolution models based on USP XX are discussed in relation to the kinetic data generated.

Adult↗
PubMed1975

Suprofen, a potent antagonist of acetic acid-induced writhing in rats.

A new standardized acetic acid-induced writhing test in rats is described in detail and its methodology is discussed briefly. The described method has proved to be useful for evaluating the anti-writhing activity of narcotic analgesics, non-narcotic anti-inflammatory compounds and narcotic-antagonists with analgesic activity. A direct quantitative comparison of anti-writhing activity was made between orally administered acetyl-salicylic acid, phenylbutazone, indometacin, tolmetin, ketoprofen and alpha-methyl-4-(2-thienylcarbonyl)benzeneacetic acid (suprofen) in a specially designed experiment. Among the known non-narcotic, non-steroidal anti-inflammatory compounds suprofen appeared to be the most potent antagonist of acetic acid-induced writhing in rats, about 200 to 300 times as potent as acetyl-salicylic acid and phenylbutazone, 15 to 30 times as potent as indometacin and tolmetin, and about 6 times as potent as ketoprofen.

Acetates↗
PubMed1975

Suprofen, a potent antagonist of ultraviolet-erythema in guinea-pigs.

A standardized ultraviolet erythema test in guinea-pigs is described in detail. The erythema reaction to 120 sec of UV irradiation was assessed after 1, 2 and 4 h. A direct quantitative comparison of the anti-erythema effect was made between phenylbutazone, indometacin, tolmetin, ketoprofen and alpha-methyl-4-(2-thienylcarbonyl)benzeneacetic acid (suprofen) in a specially designed experiment. All compounds were given by oral gavage 1 h before irradiation. Among the compounds studied suprofen was the most potent antagonist of ultraviolet-induced erythema in guinea-pigs, i.e. about 45 times tolmetin, 25 times phenylbutazone, 10 times indometacin and 5 times ketoprofen activity.

Animals↗
PubMed1975

The activity of suprofen on nystatin-induced paw oedema in rats.

Subplantar injection of nystatin into the rat paw induces acute paw oedema of long duration. In this test the anti-inflammatory activity of alpha-methyl-4-(2-thienylcarbonyl)benzeneacetic acid (suprofen) has been studied using doses from 1.25 up to 160 mg/kg. The lowest dose significantly reducing paw diameter increases was 2.5 mg/kg; more intense and longer lasting reductions appeared progressively with increasing doses. The dose producing 50% inhibition of diameter increase was 2.70 mg/kg 1 h and 1.5 h after administration (lowest ED50). Comparative lowest ED50-values for simultaneously tested reference compounds were 6.2 mg/kg for indometacin, 34 mg/kg for phenylbutazone and 38 mg/kg for acetyl-salicylic acid. Within the first 2 h after administration suprofen exhibited anti-inflammatory activity from 2 to 14 times as potent as did the reference compounds.

Animals↗
PubMed1975

The antipyretic effect of suprofen in rats with yeast-induced fever.

The antipyretic activity of alpha-methyl--4-(2-thienylcarbonyl)benzeneacetic acid (suprofen) was studied in rats with comparable hyperthermia after s.c. injection of brewer's yeast. The lowest dose effectively reducing fever is 5 mg/kg and restoration of normal body temperature is obtained with 40 mg/kg. Hypothermia is not observed even after treatment with 160 mg/kg. The ED50 (with confidence limits), which reduces fever below 39 degrees C in 50% of the animals, at the time of peak hyperthermia is 10.0 (6.6--15.2) mg/kg. ED50's of simultaneously studied reference compounds are 5.7 (3.9--8.3) mg/kg for indometacin, 38 (24--61) mg/kg for tolmetin, 76 (47--121) mg/kg for phenylburazone and 113 (75--170) mg/kg for acetyl-salicylic acid. Two to four times higher doses of these compounds restore normal body temperature but further increase of the dose induces hypothermia, which is particularly pronounced for acetyl-salicylic acid and phenylbutazone. Suprofen is a potent antipyretic agent, devoid of hypothermic activity even at 32 times the lowest effective dose.

Analgesics↗
PubMed1993

Metal complexes of anti-inflammatory drugs. Part VIII: Suprofen complex of copper(II).

The preparation and properties of the copper(II) complex Cu(SUP)2.H2O are reported for the anti-inflammatory drug Suprofen (SUP). The diffuse reflectance spectra and magnetic moment are consistent with a dinuclear structure as found for [Cu(aspirinate)2(H2O)]2. The copper(II) complex exhibits an increased superoxide dismutase activity compared with the parent drug molecule in the nitroblue tetrazolium assay.

Copper↗
PubMed1994

Molecular mechanism of drug photosensitization. 5. Photohemolysis sensitized by Suprofen.

Red blood cell lysis photosensitized by Suprofen (SPF) and the photolysis of the drug were investigated. The photohemolysis process occurs at a higher rate in anaerobic than aerobic conditions. The effect of additives demonstrates the involvement of free radicals and, to a lesser extent, singlet oxygen and hydroxyl radicals in the process. Photolysis of the drug at 310-390 nm in deaerated buffered solutions (pH 7.4) leads to a decarboxylation process with the formation of p-ethylphenyl 2-thienyl ketone (I), whereas in aerated solutions formation of photoproduct I and of the photoproducts p-acetylphenyl 2-thienyl ketone (II) and p-(1-hydroxyethyl)phenyl-2-thienyl ketone (III) occurs. The photodegradation products, which were separated and characterized, show a moderate lytic and photolytic activity. The rate of SPF photodegradation decreases in the presence of oxygen and increases in the presence of hydrogen donors. The overall results lead us to propose a mechanism of SPF photodegradation and a hemolysis scheme in which cell damage is provoked principally by the direct attack of drug radicals and secondarily by singlet oxygen and hydroxyl radicals.

Aerobiosis↗
PubMed2004

UV-induced drug release from photoactive REV sensitized by suprofen.

In order to achieve local administration of drugs, calcein (CAL) encapsulated reverse phase evaporation vesicles (REV) carrying photoactive destabilization agent suprofen (SPF) in the lipid bilayer were prepared. Effect of both UV-A and UV-B photoactivation of liposomal membrane incorporated SPF on the destabilization of the liposome bilayer and the release of encapsulated CAL was investigated. Standard REV of phosphatidylcholine (PC):cholesterol (CHOL) in 7:3 molar ratio, and photoactive REV of PC:CHOL:SPF, and DPPC:CHOL:SPF in 7:3:3 molar ratio were prepared. CAL encapsulation efficiency (EE (%)) and in situ release was studied. SPF incorporation in the PC REV membrane led to approximately 5% increase in the EE (34%) in comparison to standard REV (29%). EE decreased (21%) when DPPC was used to replace PC. Exposure to UV-B caused the highest CAL release. The lowest release was from the unexposed REV. DPPC led to a higher liposomal membrane stability (lower CAL release) than PC. A linear relationship was observed between UV-B exposure duration and REV permeability. This study revealed that membrane destabilization of SPF incorporated REV was best achieved upon photoactivation of the membrane-localized SPF by a 40 min exposure to UV-B.

Delayed-Action Preparations↗
PubMed1999

Effect of nonenzymatic glycation of albumin and superoxide dismutase by glucuronic acid and suprofen acyl glucuronide on their functions in vitro.

Acyl glucuronides bind irreversibly to plasma proteins, and one mechanism proposed for this covalent binding is similar to that for glycation of protein by reducing sugars. Because glycation of protein by glucose and other reducing sugars can alter protein function, this lead to the hypothesis that the glycation of proteins by acyl glucuronides may cause similar effects. When human serum albumin (HSA) was incubated with 0.5 M glucose for 5 days, the unbound fractions of diazepam and warfarin were increased by 41 and 35%, respectively, less than that caused by glucuronic acid which increased the unbound fractions by 90% for diazepam and 420% for warfarin. When HSA was incubated with suprofen glucuronide (SG) at a much lower concentration of 0.005 M for only 24 h, the effects on the unbound fractions of diazepam and warfarin to HSA were altered dramatically with increases of 340 and 230%, respectively. After incubation of superoxide dismutase (SOD) with 0.5 or 1 M reducing sugars for 14 days, the enzyme activity decreased to 82 and 61% of initial levels at day 14, respectively, whereas glucuronic acid almost completely inactivated the enzyme activity over the same period. Even at a very low concentration (0.005 M) of SG, SOD activity was reduced significantly to 11% of initial levels by day 14, which was comparable to the effect by 0.5 and 1.0 M concentrations of glucuronic acid. Sodium dodecyl sulfate polyacrylamide gel electrophoresis and matrix associated laser desorption/ionization time of flight mass spectrometry indicated that several equivalents of reducing sugars or SG became attached to albumin after incubation. These results suggest that acyl glucuronides may affect the function of proteins by the formation of glycated protein in vivo and may be associated with the toxicity of xenobiotics metabolized to labile acyl glucuronides.

Animals↗
PubMed2000

Photoreactivity of tiaprofenic acid and suprofen using pig skin as an ex vivo model.

The skin is repeatedly exposed to solar ultraviolet radiation. Photoreaction of drugs in the body may result in phototoxic or photoallergic side effects. Non-steroidal anti-inflammatory drugs, such as tiaprofenic acid (TPA) and the closely related isomer suprofen (SUP) are frequently associated with photosensitive disorders; they may mediate photosensitised damage to lipids, proteins and nucleic acids. Using ex vivo pig skin as a model, we investigated the photodegradation of TPA and SUP, and photobinding of these drugs to protein by means of HPLC analysis and drug-directed antibodies. Both with keratinocytes, which were first isolated from the pig skin and thereafter exposed to UVA and with keratinocytes which were isolated from pig skin after the skin was UVA exposed, time-dependent photodegradation of TPA and SUP was found, beside photoadduct formation to protein. The results of this work show that: (a) TPA and SUP were photodecomposed with similar efficiency; major photoproducts detected were decarboxytiaprofenic acid (DTPA) and decarboxysuprofen (DSUP), respectively. (b) Both drugs form photoadducts, as concluded from recognition by drug-specific antibodies. Pig skin appears to be a good model for studying the skin photosensitising potential of drugs.

Animals↗
PubMed2001

Disposition of suprofen enantiomers in the cat.

Suprofen (SPF) is a non-steroidal anti-inflammatory drug (NSAID), which belongs to the 2-arylpropionic acids subclass. As a result of their chiral characteristics, these compounds have shown a marked enantioselective behaviour with a high degree of interspecies variation. They are mainly eliminated by glucuronidation. Plasma, biliary and urine disposition of SPF was investigated in the cat after intravenous administration of the racemate (dose 2 mg/kg). Both enantiomers exhibited similar disposition profiles in plasma with no evidence of chiral inversion. During bile sampling time, recovered acylglucuronides of R (-) and S (+) SPF were less than 1% of the total dose administered. Only free SPF was recovered in the urine, representing 0.12% of the administered racemic SPF dose. The results indicate that neither chiral inversion nor glucuronidation predominate in SPF disposition in cats.

Animals↗
PubMed2001

Protective effects of suprofen and its methyl ester against inactivation of rabbit kidney carbonyl reductase by phenylglyoxal.

Suprofen (SP) was little reduced by rabbit kidney carbonyl reductase, whereas its methyl ester (SPM) was an efficient substrate of the enzyme. To account for the differential catalytic activities for SP and SPM, the protective effects of these compounds against the inactivation of the enzyme by phenylglyoxal (PGO) were compared. Since the carboxyl group of SP is negatively charged and one essential arginine residue is known to be located in the NADPH-binding site of the enzyme, the protection of SP against the inactivation of the enzyme by PGO is expected to be more effective than that of SPM lacking a carboxyl group. However, the protective effects of SP and SPM were very similar. These results suggest that in spite of evidence for the binding of SP to the coenzyme-binding site, the carboxyl group of SP fails to interact with one essential arginine residue located in the site.

Alcohol Oxidoreductases↗
PubMed1994

Photocontact allergy due to suprofen.

A 79-year-old Japanese woman developed edematous erythema on sun-exposed areas 3 months after applying Sulprotin ointment, which contains 1% suprofen (SP), a phenylacetic acid derivative. A patch test with Sulprotin ointment as it was negative, but a photopatch test with Sulprotein ointment as is was positive. A photopatch test with 10-3% SP was positive, as was that obtained with an SP analogue, 3% ketoprofen, but that with the ointment base of Sulprotin was negative. Photopatch tests with other SP analogues such as flurbiprofen, ibuprofen, and pranoprofen were negative. She developed abnormal erythema with monochromatic irradiation in the range from 320 to 380 nm on the uninvolved abdominal skin where 1% SP had been applied 24 hours (h) before irradiation. The action spectrum for this erythema agreed with the absorption spectrum of SP in the range of UVA. The MED after applying SP was below that after applying w. pet. in the range from 250 to 290 nm and from 300 to 320 nm. Positive intracutaneous test results were obtained with an irradiated mixture of human serum albumin (HSA) and SP at 48 and 72 h after injection and negative ones with a mixture of HSA and irradiated SP.

Aged↗
PubMed1995

Molecular mechanism of drug photosensitization. 7. Photocleavage of DNA sensitized by suprofen.

Ultraviolet-A irradiation of a suprofen (2-[4-2(2-thenoyl) phenyl]propionic acid) (SPF) buffered solution (pH 7.4) in the presence of supercoiled pBR322 DNA leads to single strand breaks with the formation of an open circular form and subsequent linearization of the plasmid. On the basis of agarose gel electrophoresis data of samples irradiated in an air-saturated solution or in an oxygen-modified atmosphere, and the effects of sodium azide, D20, mannitol, copper(II), superoxide dismutase, 2-H-propanol, deferoxamine and surfactants, we suggest a photosensitization mechanism involving singlet oxygen and free radicals. The higher rate of photocleavage in nitrogen compared to that in an air-saturated solution and the results obtained from oxygen consumption measurements support the hypothesis that both the type I and type II photosensitization mechanisms are operative and that oxygen quenches the excited state of the irradiated drug. The photosensitization model applied was in agreement with that previously applied to cell membrane SPF photoinduced damage. Interaction of the drug with DNA, studied through circular dichroism and fluorescence anisotropy, probably occurs through a surface binding mode. The experimental techniques used for assessing the photodamaging activity of this drug may be useful for screening of phototoxic compounds in the environment and for determining the active species involved.

Binding Sites↗
PubMed1986

Suprofen-induced acute renal failure.

A case report of acute flank pain with reversible renal failure in a young adult after taking three doses of suprofen is presented. Blood urea nitrogen and serum creatinine values returned to normal from significantly elevated levels on admission.

Acute Kidney Injury↗
PubMed2000

Sequence specificity of alkali-labile DNA damage photosensitized by suprofen.

On irradiation at UVB wavelengths, in aerated neutral aqueous solution, the anti-inflammatory drug suprofen (SP) photosensitizes the production of alkali-labile cleavage sites in DNA much more efficiently than direct strand breaks. It is active at submillimolar concentrations despite having no significant binding affinity for DNA. Gel sequencing studies utilizing 32P-end-labeled oligonucleotides have revealed that piperidine-sensitive lesions are formed predominantly at the positions of guanine (G) bases, with the extent of modification being UV dose- and SP concentration-dependent. Quite distinct patterns of G-specific damage are observed in single-stranded and duplex DNA molecules. The uniform attack at all G residues in single-stranded DNA, which is enhanced in D2O, is compatible with a Type-II mechanism. SP is a known generator of singlet oxygen whose participation in the reaction is supported by the effects of quenchers and scavengers. In duplex DNA, piperidine-induced cleavage occurs with high selectivity at the 5'-G of GG and (less prominently) GA doublets. This behavior is characteristic of a Type-I process involving electron transfer from DNA to photoexcited SP molecules. The ability of SP to sensitize the formation of Type-I and Type-II photo-oxidation products from 2'-deoxyguanosine attests to the feasibility of competing mechanisms in DNA.

Alkalies↗