Sulfapyridine sodium
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| Category | Antibiotics |
| Catalog number | BBF-03887 |
| CAS | 127-57-1 |
| Molecular Weight | 271.27 |
| Molecular Formula | C11H10N3NaO2S |
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Description
Sulfapyridine sodium is the first-generation sulfa antibiotic, one of the first compounds used to treat pneumonia. It has anti-inflammatory effects and can be used for immunodeficiency research.
Specification
| Related CAS | 144-83-2 (free base) |
| Synonyms | Soludagenan; Sodium Sulfapyridine |
| IUPAC Name | sodium;(4-aminophenyl)sulfonyl-pyridin-2-ylazanide |
| Canonical SMILES | C1=CC=NC(=C1)[N-]S(=O)(=O)C2=CC=C(C=C2)N.[Na+] |
| InChI | InChI=1S/C11H10N3O2S.Na/c12-9-4-6-10(7-5-9)17(15,16)14-11-3-1-2-8-13-11;/h1-8H,12H2;/q-1;+1 |
| InChI Key | DAINBAXHBFSNCQ-UHFFFAOYSA-N |
Properties
| Antibiotic Activity Spectrum | bacteria |
| Boiling Point | 473.5°C at 760 mmHg |
Reference Reading
1. Diclofenac-β-cyclodextrin for colonic drug targeting: In vivo performance in rats
Abdul W Basit, Amélia C F Vieira, António M d'A Rocha Gonsalves, Francisco J Veiga, Sudaxshina Murdan, Arménio C Serra Int J Pharm . 2016 Mar 16;500(1-2):366-70. doi: 10.1016/j.ijpharm.2016.01.024.
The aim of this in vivo study was to assess the ability of the prodrug conjugate diclofenac-β-cyclodextrin to release diclofenac in the colon following oral administration, using sulfapyridine (a metabolite of sulfasalazine) as a marker of colonic absorption. Two groups of rats were used; the test rats received a suspension containing the two prodrugs, diclofenac-β-cyclodextrin and sulfasalazine, while the control rats received a suspension containing the corresponding free drugs, sodium diclofenac and sulfapyridine. The rats were fasted overnight with free access to water before and throughout the first 12h of the study. Blood was collected from the tail vein at pre-determined time points and the plasma analyzed for the concentrations of diclofenac and sulfapyridine. Following the oral administration of the two prodrugs, a more extended absorption profile was observed and Cmax was achieved 10h post-dose, in contrast to rapid absorption of the free drugs (tmax of diclofenac being 1.3h, and that of sulfapyridine being 2.1h). In addition to a later tmax, conjugation of diclofenac to β-cyclodextrin also resulted in a reduced Cmax and a reduced AUC. The same tmax for diclofenac-β-cyclodextrin as for sulfasalazine confirms the colonic metabolism of diclofenac-β-cyclodextrin. This study shows the potential of this new cyclodextrin-based prodrug to target and release diclofenac specifically in the colon following oral administration.
2. Amelioration of dextran sulfate sodium-induced chronic colitis by sulfasalazine salicylazosulfapyridine via reducing NF-kappaB transcription factor p65 recruitment to ICAM-1 gene promoters
Deng Hongzhu, Wenchang Zhao, Lijun Song Yakugaku Zasshi . 2010 Sep;130(9):1239-49. doi: 10.1248/yakushi.130.1239.
Sulfasalazine salicylazosulfapyridine (SASP), consisting of 5-aminosalicylic acid bound to sulfapyridine by a diazo bond, is an effective drug in the treatment of inflammatory bowel diseases (IBD). However, its mechanism of action remains a matter of debate. The objective of our work was to investigate SASP's effect on NF-kappaB signal transduction pathway in transcriptional regulation level. Repeated colitis was induced by administration of 4 cycles of 4% dextran sulfate sodium (DSS); The severity of colitis was assessed on the basis of clinical signs, colon length, and histology scores. Moreover, sIgA and haptoglobin (HP) were analyzed by enzyme linked immunosorbent assay, and ICAM-1 gene expression was analyzed by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR) using SYBA green I. NF-kappaB signal transduction proteins and transcriptional factor p65 interaction with promoter of ICAM-1 were assessed by western blotting and chromatin immunoprecipitation assay. SASP administration significantly attenuated the colitis signs and caused substantial reductions of HP expression, and maintained the level of cecum sIgA. SASP inhibited ICAM-1 gene expression and had no effect on MIF gene expression. Also, SASP was able to reduce p-IkBalpha protein expression; however, no change in the activation of IKKalpha, IKKbeta, p65, and IKBalpha was noted. SASP inhibited p65 recruitment to the gene ICAM-1 promoter. In conclusion, inhibition of NF-kappaB pathway signal proteins and blockade of p65 binding to gene ICAM-1 promoter might explain the effect and mechanisms of SASP at alleviating DSS-induced colitis in mice.
3. Photodegradation of sulfasalazine and its human metabolites in water by UV and UV/peroxydisulfate processes
Yuefei Ji, Lei Zhou, Jean-Marc Chovelon, Junhe Lu, Corinne Ferronato, Yan Yang, Lu Wang Water Res . 2018 Apr 15;133:299-309. doi: 10.1016/j.watres.2018.01.047.
The widespread occurrence of pharmaceuticals and their metabolites in natural waters has raised great concerns about their potential risks on human health and ecological systems. This study systematically investigates the degradation of sulfasalazine (SSZ) and its two human metabolites, sulfapyridine (SPD) and 5-aminosalicylic acid (5-ASA), by UV and UV/peroxydisulfate (UV/PDS) processes. Experimental results show that SPD and 5-ASA were readily degraded upon UV 254 nm direct photolysis, with quantum yields measured to be (8.6 ± 0.8) × 10-3and (2.4 ± 0.1) × 10-2mol Einstein-1, respectively. Although SSZ was resistant to direct UV photolysis, it could be effectively removed by both UV/H2O2and UV/PDS processes, with fluence-based pseudo-first-order rate constants determined to be 0.0030 and 0.0038 cm2mJ-1, respectively. Second-order rate constant between SO4·-and SSZ was measured as (1.33 ± 0.01) × 109M-1s-1by competition kinetic method. A kinetic model was established for predicting the degradation rate of SSZ in the UV/PDS process. Increasing the dosage of PDS significantly enhanced the degradation of SSZ in the UV/PDS process, which can be well predicted by the developed kinetic model. Natural water constituents, such as natural organic matter (NOM) and bicarbonate (HCO3-), influenced the degradation of SSZ differently. The azo functional group of SSZ molecule was predicted as the reactive site susceptible to electrophilic attack by SO4·-by frontier electron densities (FEDs) calculations. Four intermediate products arising from azo bond cleavage and SO2extrusion were identified by solid phase extraction-liquid chromatography-triple quadrupole mass spectrometry (SPE-LC-MS/MS). Based on the products identified, detailed transformation pathways for SSZ degradation in the UV/PDS system were proposed. Results reveal that UV/PDS could be an efficient approach for remediation of water contaminated by SSZ and its metabolites.
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Bio Calculators
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Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
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