Sulfamethoxazole-d4 is intended for use as an internal standard for the quantification of sulfamethoxazole (Item No. 23613) by GC- or LC-MS. Sulfamethoxazole is a sulfonamide antibiotic.{38582} It inhibits growth of E. coli (MIC = 10 μg/ml) and clinical isolates of methicillin-resistant S. aureus (MRSA; MICs = 25-50 μg/ml).{38583,38584} Sulfamethoxazole, in combination with trimethoprim (Item No. 16473) at a ratio of 20:1, inhibits growth of MRSA in vivo in mice (MIC = 0.8 μg/ml; ED50s = 6.4 and 9.6 mg/kg for two MRSA strains).{38584} In a mouse model of urinary tract infection with E. coli, a combination of sulfamethoxazole and trimethoprim decreases recurrent infection when administered for 10 days.{38585} Sulfamethoxazole acts by inhibiting dihydropteroate synthase (DHPS), which converts pteridine and 4-aminobenzoic acid (PABA; Item No. 18659) to dihydropteroate, an intermediate in folate biosynthesis. It inhibits recombinant P. carinii DHPS (IC50 = 23 nM; Ki = 7.5 nM) and folate biosynthesis in situ by 48.6%. Formulations containing sulfamethoxazole and trimethoprim have been used to treat bronchitis, prostatitis, and urinary tract infections among other infectious conditions.
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An internal standard for the quantification of sulfamethoxazole by GC- or LC-MS
Formal name: 4-amino-N-(5-methyl-3-isoxazolyl)-benzene-2,3,5,6-d4-sulfonamide
Synonyms:
Molecular weight: 257.3
CAS: 1020719-86-1
Purity: ≥99% deuterated forms (d1-d4); ≤1% d0
Formulation: A solid
1,2-Dipalmitoyl-sn-glycero-3-PC (DPPC) is a zwitterionic glycerophospholipid commonly used in the formation of lipid monolayers, bilayers, and liposomes for use in a variety of applications.{14480,24261,14478,14479} It has been used in the formation of proteoliposomes for implantation of γ-glutamyl transpeptidase into human erythrocyte membranes.{14478} Incorporation of glycosphingolipid antigens into DPPC-containing liposomes increases the immunogenicity of the antigens in mice.{14479}
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The PtdIn phosphates play an important role in the generation and transduction of intracellular signals.{8344,4096,14518} PtdIns-(3,4,5)-P3-biotin is an affinity probe which allows the PIP3 to be detected through an interaction with the biotin ligand. This design allows PtdIns-(3,4,5)-P3-biotin to serve as a general probe for any protein with a high affinity binding interaction with inositol-(3,4,5)-triphosphate phospholipids, such as phosphatidylinositol 3-kinase, PTEN, or PH-domain-containing proteins.
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The PtdIn phosphates play an important role in the generation and transduction of intracellular signals.{8344,4096,14518} PtdIns-(3,4,5)-P3-biotin is an affinity probe which allows the PIP3 to be detected through an interaction with the biotin ligand. This design allows PtdIns-(3,4,5)-P3-biotin to serve as a general probe for any protein with a high affinity binding interaction with inositol-(3,4,5)-triphosphate phospholipids, such as phosphatidylinositol 3-kinase, PTEN, or PH-domain-containing proteins.
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The tetracycline repressor (TetR) is a transcriptional regulator which normally binds tightly to its palindromic tetO operator DNA, blocking gene expression.{17508} Tet causes the repressor to dissociate from the DNA, allowing transcription to occur. A novel reverse TetR (revTetR) requires tetracycline as a co-repressor to bind tetO and block transcription.{17509,17510} Anhydrotetracycline (hydrochloride) is a powerful effector in both the tetracycline repressor (TetR) and reverse TetR (revTetR) systems, binding the Tet repressor 35-fold more strongly than Tet.{17508,17511} Moreover, anhydrotetracycline poorly binds the 30S ribosomal subunit, compared to Tet,{17512} so it does not act as a general inhibitor of translation and is a poor antibiotic. Perhaps related to this, the concentration of anhydrotetracycline that inhibits eukaryotic cell growth is more than a 1,000-fold above the dose that alters transcription through TetR.{17508}
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