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PubMed2003

Determination of selected human pharmaceutical compounds in effluent and surface water samples by high-performance liquid chromatography-electrospray tandem mass spectrometry.

A simple method is presented for the analysis of 13 pharmaceutical and pharmaceutical metabolite compounds in sewage effluents and surface waters. The pharmaceutical compounds were extracted using a genetic solid-phase extraction (SPE) procedure using Phenomenex Strata X as a stationary phase. Extracts were quantitatively analysed by four separate reversed-phase high-performance liquid chromatography-electrospray tandem mass spectrometry (HPLC-ESI-MS/MS) techniques and quantified by comparison with an internal standard ([13C]-phenacetin). Recoveries and limits of detection (LOD) for sulfamethoxazole (120%, 50 ng l(-1)), acetyl-sulfamethoxazole (56%, 50 ng l(-1)), trimethoprim (123%, 10 ng l(-1)), erythromycin (73%, 10 ng l(-1)), paracetamol (75%, 50 ng l(-1)), ibuprofen (117%, 20 ng l(-1)), clofibric acid (83%, 50 ng l(-1)), mefenamic acid (24%, 50 ng l(-1)), diclofenac (62%, 20 ng l(-1)), propranolol (45%, 10 ng l(-1)), dextropropoxyphene (63%, 20 ng l(-1)) and tamoxifen (42%, 10 ng l(-1)) were all acceptable. The recovery of lofepramine (4%) was too low to be of use in a monitoring programme. Application of the method to samples collected from UK sewage effluents and surface waters showed detectable concentrations of mefenamic acid, diclofenac, propranolol, erythromycin, trimethoprim and acetyl-sulfamethoxazole in both matrices. Ibuprofen and dextropropoxyphene were detected in sewage effluents alone. All other pharmaceutical compounds were below the methods limits of detection.

Chromatography, High Pressure Liquid↗
PubMed1982

Prostaglandin secretion by human endometrium in vitro.

Late proliferative (days 9 to 14) and midsecretory (days 18 to 24) human endometria were maintained in organ culture in the presence of 17 beta-estradiol and/or progesterone or mefenamic acid 17 beta-estradiol (0.1 to 1,000 ng/ml) increased prostaglandin F (PGF) secretion by both proliferative and secretory endometria. Progesterone (1,000 ng/ml) markedly inhibited PGF secretion by proliferative but not secretory endometrium. 17 beta-estradiol and progesterone had no effect on prostaglandin E (PGE) secretion by both types of endometrium. Secretion of both PGF and PGE by proliferative and secretory endometria was inhibited by mefenamic acid ( 1 microgram/ml). This was more apparent with PGF secretion and was detectable within the first 2 hours of culture. These findings indicate that the human endometrium is a rich source of PGF and PGE and that the production of PGF is regulated by gonadal steroids. These results support the concept that one mechanism of action of mefenamic acid in the treatment of dysmenorrhea is inhibition of prostaglandin production.

Adult↗
PubMed1998

Assessment of acrylic bone cement as a local delivery vehicle for the application of non-steroidal anti-inflammatory drugs.

Non-steroidal anti-inflammatory drugs (NSAIDs) have been widely used to reduce the inflammation and pain in patients suffering from arthritis. There is a possible use for these drugs in the treatment of inflammation associated with periodontitis. However, the propensity of NSAIDs to cause serious side effects, including gastrointestinal bleeding, has reduced their usefulness. The local application of NSAIDs can avoid these side effects by delivering low doses of drug directly to the affected site. Three NSAIDs (indomethacin, tolmetin and mefenamic acid) were incorporated into polymethylmethacrylate bone cement (PM MA) strips in a range of concentrations and their cytotoxicity, pattern of drug release and ability to suppress elevated levels of prostaglandin E2 (PGE2) in cultured human periodontal ligament fibroblasts (HPLF) assessed. The strips released between 10 and 30% of the total incorporated drug over 7 days, with the highest levels released by strips containing 20% w/w of drug. Strips containing 20% indomethacin and mefenamic acid released in excess of toxic levels in the first 24 h. Strips containing 20, 10 and 5% w/w NSAID significantly (P < 0.05) reduced the level of PGE2 expression by E. coli lipopolysaccharide (LPS) challenged cells, with only the 20% mefenamic acid strip performing significantly better than the other drugs. We conclude that local delivery of NSAIDs using PMMA as a sustained release vehicle is a possible additional tool in the treatment of periodontitis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Possible mechanism of hepatocyte injury induced by diphenylamine and its structurally related nonsteroidal anti-inflammatory drugs.

Diphenylamine is a common structure of nonsteroidal anti-inflammatory drugs (NSAIDs) to uncouple mitochondrial oxidative phosphorylation and to cause a decrease in hepatocellular ATP content and hepatocyte injury. The mechanism for acute cell injury induced by diphenylamine and its structurally related NSAIDs was investigated with rat liver mitochondria and freshly isolated hepatocytes, focusing on the relation to the uncoupling of oxidative phosphorylation. Incubation of mitochondria with diphenylamine as well as mefenamic acid and diclofenac caused pseudoenergetic mitochondrial swelling, indicating that these compounds induce mitochondrial membrane permeability transition. Diphenylamine also caused changes in safranine-binding spectra to mitochondria that was energized by succinate oxidation. This spectral shift indicates the loss of mitochondrial membrane potentials, which is known as one of the characteristics for uncouplers of oxidative phosphorylation, and also was caused by mefenamic acid and diclofenac. Incubation of hepatocytes with mefenamic acid, diclofenac, and diphenylamine diminished cellular ATP content, followed by leakage of lactose dehydrogenase from hepatocytes. Fructose, a low K(m) substrate for glycolysis, partially protected against the ATP depletion and hepatocyte injury induced by these compounds. Further addition of oligomycin, which blocks ATPase, pronounced the protection against cell injury. These results suggested that decreases in cellular ATP content, mainly caused by uncoupling of mitochondrial oxidative phosphorylation, were responsible for acute hepatocyte injury induced by diphenylamine and structurally related NSAIDs.

Adenosine Triphosphate↗
PubMed1987

Effect of tolfenamic acid on the metabolism of the main connective tissue components in rats.

Tolfenamic acid (Clotam) has been used in the therapy of rheumatic diseases for some years. Regarding its chemical structure it belongs to the group of fenamates. The effect of tolfenamic acid on the synthesis of collagen and proteoglycans in granulation tissue, skin or cartilage of rat weanlings was tested and compared with the action of mefenamic acid. According to the results obtained, tolfenamic acid is a potent inhibitor of collagen as well as proteoglycan syntheses. The concentrations of the constituents of proteoglycans, i.e. protein core, link protein as well as glycosaminoglycans were decreased in the tissue after treatment with tolfenamic acid. In comparison with mefenamic acid, if the same doses were used (50 mg and 100 mg/kg of body weight/day in in vivo experiments and 10 mg/g wet tissue in in vitro experiments), tolfenamic acid exhibits more distinct inhibitory effect. A general inhibitory effect of tolfenamic acid on proteosynthesis is suggested.

Animals↗
PubMed1995

Long-lasting activation of cation current by low concentration of endothelin-1 in mouse fibroblasts and smooth muscle cells of rabbit aorta.

1. Recombinant human ETA receptors were expressed in a mouse fibroblast cell line (Ltk- cell) and functional coupling of the receptors with Ca2+ permeable channels at low concentrations of endothelin-1 (ET-1) was investigated using whole-cell recordings and monitoring the changes in intracellular free Ca2+ concentrations ([Ca2+]i) with a Ca2+ indicator, fluo-3. A similar type of coupling was investigated in freshly dispersed vascular smooth muscle cells (VSMCs) of rabbit thoracic aorta by use of whole-cell recordings. 2. In Ltk- cells expressing recombinant human ETA receptors, concentrations of ET-1 (10(-8) M, 10(-9) M) evoked an initial transient peak and a subsequent sustained elevation in [Ca2+]i whereas a lower concentration of ET-1 (10(-10) M) evoked only a sustained elevation of [Ca2+]i. After removal of extracellular Ca2+, ET-1 evoked only an initial peak without a sustained elevation of [Ca2+]i. The sustained elevation induced by 10(-10) M ET-1 was blocked by 300 microM mefenamic acid (a cation channel blocker) but not by 10 microM nifedipine (a blocker of voltage-operated Ca2+ channel). 3. In whole-cell recordings with Ltk- cells, a brief (3-5 min) application of ET-1 (10(-10) M) induced a sustained inward current at a holding potential of -60 mV. The current-voltage relationship revealed that the reversal potential of the ET-1-induced current was close to 0 mV (1.9 mV) and was not altered by reducing the concentration of Cl- in the bath solution, indicating that the current is carried by cations. The current was reversibly blocked by 300 microM mefenamic acid, and it persisted after all cations in the bath solution had been replaced by Ca2+ (5 or 30 mM) and nonpermeant cation N-methyl-D glucamine,indicating that the ET-1-activated channel is permeable to Ca2+. Activation of the current was independent of membrane potential and the current was induced even after addition of a high concentration (10 mM) of a Ca2+ chelator, EGTA, to the pipette solution.4. In whole-cell recordings from rabbit aortic VSMCs, ET-l (101-10 M) induced a sustained inward current at a holding potential of -60 mV. The reversal potential was - 12 mV and was not altered when the concentration of Cl- in the pipette solution was decreased, indicating that the current is carried by cations. Again activation of the current was independent of membrane potential and was observed even after addition of a high concentration (10 mM) of a Ca2+ chelator, EGTA to the pipette solution. The current was reversibly blocked by 300 microM mefenamic acid and was permeable to Ca2+,showing marked similarities to ET-1-induced cationic current in Ltk- cells.5. These results indicate that in Ltk- cells transfected with cDNA for recombinant ETA receptors andVSMCs, ETA receptors can functionally couple with a nonselective cation channel permeable to Ca2+.Thus the present data suggest that the cation channel plays an essential role in the sustained elevation of[Ca2+]i at low concentrations of ET-l by causing Ca2+ entry through the channel.

Aniline Compounds↗
PubMed1998

Efficacy of minor analgesics in primary dysmenorrhoea: a systematic review.

OBJECTIVE: To quantify the efficacy and safety of naproxen, ibuprofen, mefenamic acid, aspirin and acetaminophen (paracetamol) in the treatment of primary dysmenorrhoea through a systemic overview of randomised controlled trials. METHODS: MEDLINE, EMBASE and the Science Citation Index were searched for randomised controlled trials. Efficacy was assessed by measurement of pain relief, requirement for rescue analgesics, restriction of daily life and absence from work or school. The rate ratios of side effects were used to assess safety. RESULTS: Fifty-six trials describing 55 comparisons of analgesics with placebo and 12 direct comparisons with other analgesics met our inclusion criteria. Women taking naproxen were over three times more likely to have at least moderate pain relief than those taking placebo. Ibuprofen, mefenamic acid and aspirin were also superior to placebo but acetaminophen was not. The requirement for rescue analgesics, restriction of daily life and absence from work or school were less frequent with naproxen and ibuprofen than placebo but not with aspirin or acetaminophen. Direct comparisons did not show any difference between naproxen and ibuprofen. Side effects occurred more frequently only with naproxen when compared with placebo. CONCLUSION: Naproxen, ibuprofen, mefenamic acid and aspirin are all effective in primary dysmenorrhoea. Ibuprofen appears to have the most favourable risk-benefit ratio. Acetaminophen appears to be less effective than nonsteroidal anti-inflammatory drugs, but there was only one trial meeting our inclusion criteria and further studies are required.

Acetaminophen↗
PubMed2001

Determination of drug residues in water by the combination of liquid chromatography or capillary electrophoresis with electrospray mass spectrometry.

Methods for the determination of drug residues in water have been developed based on the combination of liquid chromatography (LC) or capillary electrophoresis (CE) with mass spectrometry (MS). For HPLC-MS two types of interfaces (pneumatically assisted electrospray ionization interface or an atmospheric pressure chemical ionization interface, respectively) were employed and compared in terms of detection limits. 2 mM Ammonium acetate at pH 5.5 and a methanol gradient was used for the HPLC-MS allowing the separation of a number of drugs such as paracetamol, clofibric acid, penicillin V, naproxen, bezafibrate, carbamazepine, diclofenac, ibuprofen and mefenamic acid. A 20 mM ammonium acetate solution, pH 5.1 was employed for the separation of clofibric acid, naproxen, bezafibrate, diclofenac, ibuprofen and mefenamic acid by CE-MS. Sample pretreatment was performed by solid-phase extraction (SPE) for HPLC-MS or by a combination of liquid-liquid extraction and SPE for CE-MS. The applicability of both the HPLC-MS and CE-MS method was demonstrated for several river water samples.

Chromatography, High Pressure Liquid↗
PubMed2005

Ibuprofen for the treatment of patent ductus arteriosus in preterm and/or low birth weight infants.

BACKGROUND: A patent ductus arteriosus (PDA) complicates the clinical course of preterm infants, increasing their risks of developing chronic lung disease (CLD), necrotizing enterocolitis (NEC), and intraventricular hemorrhage (IVH). Indomethacin is used as standard therapy to close a PDA, but is associated with reduced blood flow to the brain, kidneys and gut. Ibuprofen, another cyclo-oxygenase inhibitor, may be as effective with fewer side effects. OBJECTIVES: To determine the effectiveness and safety of ibuprofen compared to placebo or no intervention for closing a PDA in preterm and/or low birth weight infants. To determine the effectiveness and safety of ibuprofen compared to other cyclo-oxygenase inhibitors (including indomethacin, mefenamic acid) for closing a PDA in preterm and/or low birth weight infants. SEARCH STRATEGY: Randomized or quasi-randomized controlled trials (RCTs) comparing ibuprofen to placebo or indomethacin or mefenamic acid for therapy of PDA were identified by searching the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 2, 2005), MEDLINE (1996 - July 2005), CINAHL (1982 - July 2005), EMBASE (1980 - July 2005), reference lists of published RCTs and abstracts from the Pediatric Academic Societies and the European Society for Pediatric Research meetings published in Pediatric Research (1991 - April 2005). No language restrictions were applied. SELECTION CRITERIA: 1) DESIGN: Randomized or quasi-randomized controlled trials 2) POPULATION: Preterm (< 37 weeks gestational age) or low birth weight infants (< 2500 grams) with a clinically or echocardiographically diagnosed PDA 3) INTERVENTION: Administration of ibuprofen for the closure of PDA 4) OUTCOMES: At least one of the following outcomes were reported: failure to close a PDA, mortality, surgical ligation, intraventricular haemorrhage (IVH), periventricular leukomalacia (PVL), NEC, decreased urine output, retinopathy of prematurity (ROP), chronic lung disease (CLD), sepsis, days on supplementary oxygen. DATA COLLECTION AND ANALYSIS: At least two authors worked independently at each step of the original review, then compared results and resolved differences. The current update was conducted by one author (AO). Methodological quality of eligible studies was assessed according to blinding of randomization, of intervention and of outcome assessment, and completeness of follow up. Weighted treatment effects, calculated using RevMan 4.2, included typical relative risk (RR), typical risk difference (RD), number needed to treat (NNT) or harm (NNH), and weighted mean difference (WMD), all with 95% confidence intervals (CI). A fixed effect model was used for meta-analyses. Heterogeneity tests including I(2 )were performed to assess the appropriateness of pooling the data. MAIN RESULTS: No study using mefenamic acid was identified. One study compared ibuprofen to placebo but results were not reported unblinded to group. Eleven studies including 620 patients compared the effectiveness of ibuprofen to indomethacin for the closure of a PDA. There was no statistically significant heterogeneity of treatment effect for any of the outcomes. For the primary outcome (failure of ductal closure), there was no statistically significant difference between ibuprofen and indomethacin groups [typical RR 0.96 (95% CI 0.74, 1.25)]. There were no statistically significant differences in mortality, surgical duct ligation, duration of ventilator support, IVH, PVL, NEC, time to full enteral feeds, ROP, sepsis, duration of hospital stay or gastrointestinal bleed. For many of these outcomes the sample size was small and the estimates imprecise. The incidence of decreased urine output (< 1cc/kg/hr) was lower in the ibuprofen group as compared to the indomethacin group [NNT 9 (95% CI 5-14)]. This was the only statistically significant clinical finding favouring ibuprofen. CLD defined as oxygen requirement at 28 days post-natally was statistically significantly more likely to occur in the ibuprofen group [typical RR 1.37 (95% CI 1.01, 1.86); NNH 7 (95% CI 3 - 100)]. There was a similar trend for CLD at 36 weeks corrected gestational age. AUTHORS' CONCLUSIONS: We found no statistically significant difference in the effectiveness of ibuprofen compared to indomethacin in closing the PDA. Ibuprofen reduces the risk of oliguria. However, ibuprofen may increase the risk for CLD, and pulmonary hypertension has been observed in three infants after prophylactic use of ibuprofen. Based on currently available information ibuprofen does not appear to confer a net benefit over indomethacin for the treatment of a PDA. We conclude that indomethacin should remain the drug of choice for the treatment of a PDA. The most urgent research question to be answered is weather ibuprofen compared to indomethacin confers an improved rate of intact survival (survival without impairment) at 18 months corrected age.

Cyclooxygenase Inhibitors↗
PubMed2005

Synthesis of thyroid hormone binding proteins transthyretin and albumin by human trophoblast.

CONTEXT: Mechanisms regulating materno-fetal transfer of thyroid hormone are not well understood. Modulation of trophoblast type 3 iodothyronine deiodinase (D3) may play an important role. OBJECTIVE: The objective of this study was to investigate trophoblast thyroid hormone binding proteins that may modulate interactions between D3 and T4. DESIGN: Placentas were obtained by informed consent from women delivering normal infants by repeat cesarean section at 38-40 wk gestation. T4 and T3 binding was examined in human placenta. Serum thyroid hormone binding proteins were identified by Western blotting, and their mRNA was examined by RT-PCR. Presence of these proteins in trophoblast was determined by immunocytochemistry and immunofluorescence. Cytosol was progressively purified to reveal additional thyroid hormone binding proteins that were identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry. Effects of mefenamic acid on placental deiodination were examined by HPLC. RESULTS: We detected high-affinity T4 and T3 binding in human placental cytosol. All three major serum-binding proteins, T4 binding globulin (TBG), transthyretin (TTR), and albumin, were present in cytosol. TTR mRNA and albumin mRNA were detected in human placenta, and TTR and albumin were identified histochemically in syncytiotrophoblasts. Neither TBG mRNA nor TBG was detected, suggesting that plasma TBG had contaminated the cytosol preparation. Low-affinity thyroid hormone binding proteins alpha-1-antitrypsin and alpha-1-acid glycoprotein were also identified. Addition of mefenamic acid, a potent inhibitor of thyroid hormone binding, to placental cytosol significantly enhanced deiodination of T4 by D3. CONCLUSIONS: Placenta produces a series of thyroid hormone binding proteins that may modify thyroid hormone deiodination and materno-fetal thyroid hormone transport.

Albumins↗
PubMed1984

Clinical features and management of analgesic poisoning.

Analgesic poisoning is a common medical emergency, and these drugs account for about 30% of self-poisoning in adults. Aspirin and paracetamol are taken most often, and can cause significant morbidity and mortality. However, problems with the hepatotoxicity of paracetamol have been greatly reduced by the introduction of effective treatment with agents such as N-acetylcysteine. The non-steroidal anti-inflammatory analgesics are not commonly taken in overdosage but the incidence of self-poisoning with mefenamic acid is increasing at an alarming rate. With the exception of phenylbutazone and mefenamic acid these drugs rarely seem to cause serious toxicity. The narcotic analgesics can cause profound respiratory depression and are the most dangerous drugs in overdosage.

Acetaminophen↗
PubMed2000

Inhibition of human liver phenol sulfotransferase by nonsteroidal anti-inflammatory drugs.

OBJECTIVE: The aim of this investigation was to study the inhibition of 11 nonsteroidal anti-inflammatory drugs (NSAIDs) on the human liver phenol sulfotransferases (HL-PST) and catechol sulfotransferase (HL-CST). METHODS: The activities of HL-PST and HL-CST were measured with 4 microM 4-nitrophenol and 60 microM dopamine (the sulfate acceptors) and 0.4 microM 3'-phosphoadenosine-5'-phosphosulfate [35S] (the sulfate donor). Samples of liver were obtained from five patients, aged 55-79 years, undergoing clinically indicated hepatectomy. The inhibition curves were constructed with at least five concentrations of the inhibitor. RESULTS: With the exception of piroxicam, NSAIDs inhibited HL-PST, and the estimates of the inhibitory concentration for 50% of responses (IC50; microM) were: 0.02 (mefenamic acid), 3.7 (diflunisal), 5.4 (nimesulide), 9.5 (diclofenac), 30 (salicylic acid), 41 (ketoprofen), 74 (indomethacin), 159 (ibuprofen), 245 (ketoralac) and 473 (naproxen). With 4-nitrophenol as the variable substrate, the inhibition of salicylic acid on HL-PST was non-competitive and the Ki and Kies were 18 microM and 21 microM (n = 5; P = 0.548), respectively. HL-CST was less susceptible than HL-PST to inhibition by NSAIDs, with only five drugs inhibiting this enzyme. The IC50 estimates for these drugs (microM) were 76 (mefenamic acid), 79 (diflunisal), 103 (indomethacin), 609 (salicylic acid) and 753 (diclofenac). CONCLUSION: The comparison of the IC50 estimates of HL-PST with the therapeutic plasma concentrations of NSAIDs corrected for the plasma unbound fraction was consistent with the view that mefenamic acid and salicylic acid, when administered at therapeutic doses, should impair the hepatic sulfation of those compounds that are substrates of phenol sulfotransferase.

Aged↗
PubMedDate not supplied

Synthesis and evaluation of some acyloxyethyl mefenamates as possible prodrugs.

Various acyloxyethyl mefanamates were synthesized and evaluated for potential application as prodrugs. Their kinetics of hydrolysis were examined in aqueous solutions of pH 1.0 and 7.4 and in human plasma at 37 degrees C. Among the synthesized compounds, the beta-carboxypropionylethyl mefenamate and the pivaloyloxyethyl mefenamate show high stability against enzymatic and non enzymatic hydrolysis. On the other hand the acetyloxyethyl mefenamate shows t1/2s of 1.4 h, 1.41 h and 3.61 h in human plasma, solutions of pH 7.4 and pH 1.0 respectively; However, its hydrolysis to mefenamic acid in plasma was not quantitative. Preliminary in vivo study shows that acetyloxyethyl mefenamate gave plasma concentration of mefenamic acid lower than that of control after oral administration. The calculated AUC0-inf for the acetyloxyethyl and control were 45 and 85 micrograms.h/ml respectively.

Acylation↗
PubMed1985

Differential effect of prostaglandin synthetase inhibitor pretreatment on pentylenetetrazol-induced seizures in rat.

Release of prostaglandins (PGs) from brain tissue increases during experimentally-induced and spontaneous seizures. However, whether PGs or other arachidonic acid metabolites have a role in induction of seizures is still unclear. The effectiveness of pretreatment with PG synthetase inhibitors on pentylenetetrazol (PTZ)-induced models of epilepsy was investigated in free-moving rats with chronically-implanted supracortical electrodes. The effects on the electrocortical and motor manifestations of both a subconvulsive (30 mg.kg-1) and a convulsive (60 mg.kg-1) dose of PTZ were examined. Mefenamic acid (15 or 50 mg.kg-1), meclofenamic acid (15 or 50 mg.kg-1), ibuprofen (30 or 90 mg.kg-1) and paracetamol (300 or 450 mg.kg-1) delayed the onset of PTZ-induced convulsions. But mefenamic acid and meclofenamic acid also potentiated the excitatory effects of both subconvulsive and convulsive doses of PTZ. Indomethacin (3, 10 or 30 mg.kg-1) had no significant effect. The results suggest that the differential effects were produced by actions not related to the cyclo-oxygenase inhibition although the more consistent decrease of convulsive behavior may have resulted from inhibition of PG synthesis.

Acetaminophen↗
PubMed2005

Dendrimers of citric acid and poly (ethylene glycol) as the new drug-delivery agents.

Citric acid-polyethylene glycol-citric acid (CPEGC) triblock dendrimers as biocompatible compounds containing G(1), G(2) and G(3) were applied as the drug-delivery systems. Some of the small size molecules and drugs are trapped with the above-synthesized dendrimers. The guest molecules, which are hydrophobic when trapped into the suitable sites of dendrimers, are becoming soluble in aqueous solution. The quantity of trapped molecules and drugs such as 5-amino salicylic acid (5-ASA), pyridine, mefenamic acid, and diclofenac was measured. The drug/dendrimer complexes remained in room temperature for about 10 months and after this long time they were stable and the drugs were not released. Also, the controlled release of the above-mentioned molecules and drugs in vitro conditions was investigated. The structure definition and controlled release of the molecules and drugs were carried out using different spectroscopy methods.

Biocompatible Materials↗