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Title:Dosimetry and Toxicity Studies of the Novel Sulfonamide Derivative of Sulforhodamine 101([18F]SRF101) at a Preclinical Level. VOLUME: 12 ISSUE: 1. Author(s):Ingrid Kreimerman, Erick Mora-Ramirez, Laura Reyes, Manuel Bardiès, Eduardo Savio* and Henry Engler. Affiliation:Uruguayan Centre of Molecular Imaging (CUDIM), Radiopharmacy Department, Montevideo, Inserm, UMR1037 CRCT, F-31000 Toulouse, Uruguayan Centre of Molecular Imaging (CUDIM), Radiopharmacy Department, Montevideo, Inserm, UMR1037 CRCT, F-31000 Toulouse, Uruguayan Centre of Molecular Imaging (CUDIM), Radiopharmacy Department, Montevideo, Uruguayan Centre of Molecular Imaging (CUDIM), Radiopharmacy Department, Montevideo. Keywords:Preclinical evaluation, toxicity, dosimetry, [18F]SRF101, PET radiotracers, tissue-weighting factors.. Abstract:Background: The SR101 N-(3-[18F]Fluoropropyl) sulfonamide ([18F]SRF101) is a Sulforhodamine 101 derivative that was previously synthesised by our group. The fluorescent dye SR101 has been ...

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The purpose of the study is to investigate the possible benefits of giving the anti-HIV drug maraviroc to people who are taking darunavir/ritonavir alone for their HIV treatment. Many people successfully take only darunavir/ritonavir treatment for their HIV. However, there are some concerns that this treatment may not reach some areas of the body, such as the brain and spinal cord (central nervous system or CNS), as effectively as it does the bloodstream.. There is already a large clinical study looking at any differences between conventional HIV treatment with 3 drugs and single drug treatment with a protease inhibitor, also called PI monotherapy, such as darunavir/ritonavir. This includes differences in the effects on the CNS. However, this study will only be finished in 2013.. The investigators know that maraviroc can reach the CNS very effectively. The investigators in this study will investigate the effect of adding maraviroc to darunavir/ritonavir monotherapy by looking at levels of ...

TY - JOUR. T1 - 2-Amino-N-{4-[5-(2-phenanthrenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl] -phenyl} acetamide (OSU-03012), a celecoxib derivative, directly targets p21-activated kinase. AU - Porchia, Leonardo M.. AU - Guerra, Marcy. AU - Wang, Yu Chieh. AU - Zhang, Yunlong. AU - Espinosa, Allan V.. AU - Shinohara, Motoo. AU - Kulp, Samuel K.. AU - Kirschner, Lawrence S.. AU - Saji, Motoyasu. AU - Chen, Ching Shih. AU - Ringel, Matthew D.. PY - 2007/11. Y1 - 2007/11. N2 - p21-Activated kinases (PAKs) are regulators of cell motility and proliferation. PAK activity is regulated in part by phosphoinositide-dependent kinase 1 (PDK1). We hypothesized that reduced PAK activity was involved in the effects of 2-amino-N-{4-[5-(2-phenanthrenyl)-3-(trifluoromethyl)-1H-pyrazol-1- yl]-phenyl} acetamide (OSU-03012), a previously characterized PDK1 inhibitor derived from celecoxib. In three human thyroid cancer cell lines, OSU-03012 inhibited cell proliferation with reduced AKT phosphorylation by PDK1. OSU-03012 ...

In a previous study, we reported that the short-term treatment with celecoxib, a non-steroidal anti-inflammatory drug (NSAID) attenuates the activation of brain structures related to nociception and does not interfere with orthodontic incisor separation in rats. The conclusion was that celecoxib could possibly be prescribed for pain in orthodontic patients. However, we did not analyze the effects of this drug in periodontium. The aim of this follow-up study was to analyze effects of celecoxib treatment on recruitment and activation of osteoclasts and alveolar bone resorption after inserting an activated orthodontic appliance between the incisors in our rat model. Twenty rats (400-420 g) were pretreated through oral gavage with celecoxib (50 mg/kg) or vehicle (carboxymethylcellulose 0.4%). After 30 min, they received an activated (30 g) orthodontic appliance, set not to cause any palate disjunction. In sham animals, the appliance was immediately removed after introduction. All animals received ...

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Rats administered doses up to 43 mg/kg/day in males and 52 mg/kg/day in females had no increases in tumor incidence, with the exception of a modest increase in the frequency of mammary gland fibroadenomas in female rats receiving doses ≥5.4 mg/kg (P,0.015). The highest doses of tamsulosin hydrochloride evaluated in the rat carcinogenicity study produced systemic exposures (AUC) in rats 3 times the exposures in men receiving the maximum therapeutic dose of 0.8 mg/day.. Mice were administered doses up to 127 mg/kg/day in males and 158 mg/kg/day in females. There were no significant tumor findings in male mice. Female mice treated for 2 years with the two highest doses of 45 and 158 mg/kg/day had statistically significant increases in the incidence of mammary gland fibroadenomas (P,0.0001) and adenocarcinomas (P,0.0075). The highest dose levels of tamsulosin hydrochloride evaluated in the mice carcinogenicity study produced systemic exposures (AUC) in mice 8 times the exposures in men receiving ...

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Absorption In clinical pharmacology studies in man, peak plasma concentrations of rosuvastatin were reached 3 to 5 hours following oral dosing. Both Cmax and AUC increased in approximate proportion to rosuvastatin dose. The absolute bioavailability of rosuvastatin is approximately 20%. Administration of rosuvastatin with food did not affect the AUC of rosuvastatin. The AUC of rosuvastatin does not differ following evening or morning drug administration. Distribution Mean volume of distribution at steady-state of rosuvastatin is approximately 134 liters. Rosuvastatin is 88% bound to plasma proteins, mostly albumin. This binding is reversible and independent of plasma concentrations. Elimination Rosuvastatin is primarily eliminated by excretion in the feces. The elimination half-life of rosuvastatin is approximately 19 hours.. Metabolism Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as metabolite. The major metabolite is N-desmethyl ...

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Several studies suggest that cyclooxygenase (COX)-2 plays a pivotal role in the progression of ischemic brain damage. In the present study, we investigated the effects of selective inhibition of COX-2 with nimesulide (12 mg/kg) and selective inhibition of COX-1 with valeryl salicylate (VAS, 12-120 mg/kg) on prostaglandin E2 (PGE2) levels, myeloperoxidase (MPO) activity, Evans Blue (EB) extravasation and infarct volume in a standardized model of transient focal cerebral ischemia in the rat. Postischemic treatment with nimesulide markedly reduced the increase in PGE2 levels in the ischemic cerebral cortex 24 h after stroke and diminished infarct size by 48 % with respect to vehicle-treated animals after 3 days of reperfusion. Furthermore, nimesulide significantly attenuated the blood-brain barrier (BBB) damage and leukocyte infiltration (as measured by EB leakage and MPO activity, respectively) seen at 48 h after the initial ischemic episode. These studies provide the first experimental evidence ...

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No. Therefore sulfonamides are selectively toxic to bacteria and other microorganisms. Against which microorganisms are sulfonamides effective? Gram-positive and gram-negative bacteria, Nocardia, Chlamydia trachomatis, some protozoa (malaria), Escherichia Coli, Klebsiella, Salmonella, Shigella, Enterobacter Are sulfonamide antibiotics bactericidal or bacteriostatic? Primarily bacteriostatic What are the adverse effects of sulfonamide antibiotics? Nausea; vomiting; diarrhea; phototoxicity; hemolysis (in individuals having glucose-6-phosphate dehydrogenase (G6PD) deficiency); hypersensitivity; Stevens-Johnson syndrome (incidence and severity of adverse effects greatly increase immunocompromised in AIDS patients) Why are sulfonamide antibiotics contraindicated in neonates? 25% How much drug is left after three half-lives? 5% During constant infusion, what percent of steady state is reached after one half-life? 50% During constant infusion, what percent of steady state is reached after two ...

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The sulfonamides are weakly acidic compounds that have a common chemical nucleus resembling p-aminobenzoic acid (PABA). Members of this group differ mainly in their pharmacokinetic properties and clinical uses. Pharmacokinetic features include modest tissue penetration, hepatic metabolism, and excretion of both intact drug and acetylated metabolites in the urine. Solubility may be decreased in acidic urine, resulting in precipitation of the drug or its metabolites. Because of the solubility limitation, a combination of 3 separate sulfonamides ...

These studies indicate that laromustine readily undergoes base-catalyzed (nonenzymatic) conversion to methylisocyanate and 90CE, which further degrade to additional chloroethylating derivatives. Figure 1B shows the proposed formation of decomposition/metabolite product pathways of laromustine formed in in vitro systems. The rate at which [14C]laromustine (100 μ M) produces its metabolites/degradation products in the presence of NADPH-fortified HLMs was essentially the same as that in the absence of NADPH or the presence of boiled (heat-denatured) microsomes. Additionally, it remained consistent with the nonenzymatic rate of laromustine degradation in potassium phosphate buffer (Nassar et al., 2009). This suggests that laromustine metabolism/degradation is not significantly affected by human liver microsomal P450 enzymes and carboxylesterases.. Only the formation of C-7 required the presence of NADPH. C-7 appears to be decomposed or metabolized further, which suggests that P450 is a factor in ...

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Effects of the dual endothelin-receptor antagonist bosentan in patients with pulmonary hypertension: a randomised placebo-controlled study.

We have read with interest the study by Jackson et al,1 recently published in your journal, that investigated plasma and intracellular pharmacokinetics of darunavir/ritonavir (800/100 mg once daily) and raltegravir (800 mg once and 400 mg twice daily) alone or coadministered in a group of 24 HIV-infected individuals. The authors main conclusions were that no remarkable interactions between darunavir/ritonavir and raltegravir were observed. However, although no modification of raltegravir pharmacokinetic (PK) was observed after darunavir/ritonavir intensification, some darunavir PK parameters showed a significant change after raltegravir discontinuation. In particular, in patients taking darunavir/ritonavir 800/100 mg once daily plus raltegravir 400 mg twice daily plus 2 nucleoside reverse transcriptase inhibitors (NRTIs; n = 13, group 1), significantly higher darunavir area under the curve (AUC) and Ctrough were observed both in plasma (24% and 37% increase, respectively) and in intracellular ...

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Macitentan may be the lately approved dual endothelin-receptor antagonist (Period) for the treating symptomatic pulmonary arterial hypertension. hypertension sufferers with macitentan resulted in statistically significant improvements in useful class, workout tolerance, and hemodynamic variables, and a decrease in morbidity within an event-driven long-term trial. solid course=kwd-title Keywords: endothelin, endothelin receptor antagonists, macitentan, pulmonary arterial hypertension Pulmonary arterial hypertension Pulmonary arterial hypertension (PAH) is normally a intensifying and BRL-15572 supplier lethal disease seen as a remodeling from the pulmonary arterioles with consequent enhance from the pulmonary vascular level of resistance (PVR) with eventual best ventricular failing and ultimately loss of life. Furthermore, despite targeted remedies, the disease continues to be fatal.1 The organic history of PAH as well as the survival prices for patients experiencing this disease had been ...

TABLE-US-00001 TABLE 1 Example compounds and characterization Example LC-MS IC50Ox1 IC50Ox2 No Chemical Name tR in min; [M + H].sup.+ [nM] [nM] 1 (S)-1-(5-Bromo-thiophene-2-sulfonyl)-pyrrolidine-2- 0.86; 461.1 20 .sup.*2 10 .sup.*2 carboxylic acid (3-methylsulfanyl-phenyl)-amide 2 (S)-1-(5-Bromo-thiophene-2-sulfonyl)-pyrrolidine-2- 0.92; 499.1 149 104 carboxylic acid (3-trifluoromethoxy-phenyl)-amide 3 (S)-1-(3-Methoxy-benzenesulfonyl)-pyrrolidine-2- 0.81; 407.2 28 8 carboxylic acid (3-methylsulfanyl-phenyl)-amide 4 (S)-1-(4-Propyl-benzenesulfonyl)-pyrrolidine-2- 0.92; 419.3 91 47 carboxylic acid (3-methylsulfanyl-phenyl)-amide 5 (S)-1-(4-Methyl-3,4-dihydro-2H-benzo[1,4]oxazine-7- 0.83; 447.6 128 27 sulfonyl)-pyrrolidine-2-carboxylic acid (3-methylsulfanyl- phenyl)-amide 6 (S)-1-(4-Methoxy-benzenesulfonyl)-pyrrolidine-2- 0.80; 407.3 21 .sup.*3 3 .sup.*3 carboxylic acid (3-methylsulfanyl-phenyl)-amide 7 (S)-1-(3-Chloro-benzenesulfonyl)-pyrrolidine-2- 0.85; 411.2 8 2 carboxylic acid ...

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The aim of this study was to evaluate whether rosuvastatin (HMG-CoA reductase inhibitor) modulates the carbohydrate and lipid metabolism, the development of non-alcoholic fatty liver disease (NAFLD), and the increase in body mass in a model of diet-induced obesity. Male C57Bl/6 mice (3-months-old) were fed a high-fat diet (HF, 60% lipids) or the standard chow (SC, 10% lipids) for 15 weeks. The animals were then treated with 10 mg/kg/day (HF-R10 group), 20 mg/kg/day (HF-R20), or 40 mg/kg/day (HF-R40) of rosuvastatin for five weeks. The HF diet led to glucose intolerance, insulin resistance, weight gain, increased visceral adiposity with adipocyte hypertrophy, and hepatic steatosis (micro and macrovesicular). The rosuvastatin treatment decreased the adiposity and the adipocyte size in the HF-R10 and HF-R20 groups. In addition, rosuvastatin changed the pattern of fat distribution in the HF-R40 group because more fat was stored subcutaneously than in visceral depots. This redistribution improved the fasting

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Results: 70 subjects (86% male, 66% white, mean (SD) CD4 cell count 537.3 (191.5) per mm3) were randomized, of whom 26 (DRV/r) and 31 (Atripla) completed the 48 week study on the allocated treatment. The mean (SD) difference between baseline and week 48 25[OH]D was 5.0 (5.9) ng/mmol for DRV/r and 1.2 (6.0) for Atripla. After adjustment for baseline 25[OH]D and demographics, at week 48 DRV/r monotherapy was associated with a +3.5 (95% CI 0.5, 6.4) ng/mmol increase in 25[OH]D compared to Atripla (p=0.02). Subjects in the DRV/r arm experienced increases in BMD (mean between-arm difference (0.02 [0.003, 0.04] g/cm2 at the lumbar spine, p=0.03, and 0.03 [0.006, 0.06] g/cm2 at the neck of femur, p=0.02), and reductions in parathyroid hormone (PTH) (-20.4 [-38.8, -2.0] ng/l, p=0.03), bone-specific alkaline phosphatase (-7.1 [-9.7, -4.5]) IU/L, p< 0.0001) and serum type 1 pro-collagen (-16.9 [-26.5, -7.4] ug/L, p=0.0008), as compared with subjects on Atripla. No significant difference in RTD (urine ...

Bosentan increases exercise capacity and improves haemodynamics in patients with pulmonary hypertension, suggesting that endothelin has an important role in pulmonary hypertension.

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No drugs have been approved for the treatment of patients with pulmonary hypertension (PH) secondary to idiopathic pulmonary fibrosis (IPF), particularly those with idiopathic honeycomb lung. This study was conducted to investigate the long-term efficacy and safety of bosentan for PH based on changes in prognosis and respiratory failure. IPF patients with borderline or less severe PH and completely organized honeycomb lung were randomized (1:1) to bosentan or no treatment for PH for 2 years and assessed at baseline and every 6 months for respiratory failure, activities of daily living (ADL), lung and heart functions by right cardiac catheterization, and other parameters. An interim analysis was performed, however, following detection of a significant survival benefit favoring bosentan therapy. Significant differences were noted for the bosentan-treated (n = 12) vs. untreated (n = 12) groups in hospital-free survival (603.44 ± 50.074 days vs. 358.87 ± 68.65 days; hazard ratio [HR], 0.19; P = 0.017) and

Several lines of evidence support the role of COX-2-dependent PGE2 in colon tumorigenesis (Wang and Dubois, 2010). Thus, in FAP, the administration of the selective COX-2 inhibitor celecoxib (400 mg/b.i.d.) was associated with a significant reduction of the number of colorectal polyps by approximately one-third (Steinbach et al., 2000). However, marked variability in the response to celecoxib was noted (Steinbach et al., 2000). We hypothesized that the inhibition of vascular COX-2-dependent PGI2 may contribute to the variable response to celecoxib in this setting. In fact, PGI2 may control angiogenesis by preventing endothelial activation and platelet release of angiogenic factors present in α-granules (Menter et al., 1987). Thus, we performed the present study to investigate the biosynthesis of PGI2 and TXA2, two key mediators of CV homeostasis (Grosser et al., 2006), and PGE2, a well known mediator of inflammation and tumorigenesis (Wang and Dubois, 2010) in intestinal neoplasia. We aimed to ...

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Objectives: The objective of this study was to assess whether a lower dose than the currently used one of darunavir/ritonavir might achieve good CSF concentrations and contribute to inhibition of CNS viral replication. Patients and methods: This was a substudy of a randomized, open, multicentre study (eudraCT 2011-006272-39), comparing the efficacy and safety of 800/100 mg of darunavir/ritonavir (darunavir 800) versus 600/100 mg of darunavir/ritonavir (darunavir 600) once daily plus tenofovir/emtricitabine or abacavir/lamivudine in 100 virologically suppressed patients. Paired blood and CSF samples were obtained. Total plasma darunavir concentrations were determined by HPLC, and CSF concentrations by liquid chromatography-tandem MS. Viral load (VL) was determined in plasma and CSF (limit of detection = 40 copies/mL) by PCR. Results: Sixteen patients were enrolled. The median (range) of darunavir CSF concentrations in darunavir 600 (n = 8) and darunavir 800 (n = 8) patients was 17.08 (5.79-30.19) ...

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Purpose: Neuroblastoma is the most common and deadly solid tumor of childhood. Cyclooxygenase-2 is expressed in clinical neuroblastoma tumors and cell lines and inhibitors of this enzyme induce apoptosis in human neuroblastoma cells in vitro and in neuroblastoma xenografts in vivo. We hypothesized that the cyclooxygenase-2- specific inhibitor celecoxib could enhance the cytotoxic effect of chemotherapeutic drugs currently used in neuroblastoma treatment. Furthermore, we investigated if prophylactic treatment with celecoxib could prevent neuroblastoma tumor development in vivo. Experimental Design: Neuroblastoma cell cytotoxicity of chemotherapeutic drugs in combination with celecoxib was examined. In vivo, athymic rats carrying established SH-SY5Y xenografts were treated with celecoxib in combination with irinotecan, doxorubicin or etoposide, or with either drug alone. For prevention studies, rats received celecoxib in the diet, 250 to 2,500 ppm, from the time of tumor cell injection. Results: ...

Introduction Cyclooxygenase-2 (COX-2) is frequently over-expressed in primary breast cancer. In transgenic breast cancer models, over-expression of COX-2 leads to tumour formation while COX-2...

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This Phase IIIb study was conducted to evaluate the safety, efficacy and pharmacokinetics of darunavir/cobicistat 800/100 mg once daily in HIV-1-infected adults with no darunavir RAMs who also received two fully active N[t]RTIs. We showed that darunavir/cobicistat 800/150 mg once daily was well tolerated, and the pharmacokinetics, virologic and immunologic responses were consistent with previously published data for darunavir/ritonavir 800/100 mg once daily.. Through Week 24, the onset of any grade 3 or 4 AEs regardless of causality was low (6% in the overall population). Five out of 313 patients (2%), all of whom were treatment-naïve, experienced any study drug-related grade 3 AE through Weeks 24 and 48. No patients experienced grade 4 drug-related AEs. The most commonly reported AEs of all grades during the study, diarrhea, nausea, upper respiratory tract infection and headache, have all been reported previously for darunavir and cobicistat [5-8, 15, 16]. Renal laboratory assessments showed ...

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Results of a new 12-week study combining iloprost and bosentan showed improvements in patients with pulmonary arterial hypertension (PAH). University of Michigan Medical Center researchers followed 65 PAH patients being treated with the endothelian receptor antagonist bosentan. Thirty-two patients began taking inhaled iloprost in addition to bosentan; 33 received bosentan plus placebo. At the end of 12 weeks, the bosentan-iloprost group could walk 98 feet farther in their 6-minute walk test. Eleven of the 32 in the combination-therapy group showed improvement, and none of them showed signs of clinical deterioration. PAH is characterized by a progressive narrowing of the blood vessels in the lungs and can be fatal. Symptoms, which only get worse over time, include shortness of breath, fatigue, weakness, dizziness, and fainting. The report can be found in the December 2006 issue of the American Journal of Respiratory and Critical Care Medicine. Ms. Farley is a freelance medical writer based in ...

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