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
The maintenance of embryonic stem cells in culture typically requires feeder cells and various exogenous factors found in serum. Murine embryonic stem (mES) cells can be maintained in the absence of feeder cells and serum but require the leukemia inhibitor factor (LIF) and bone morphogenic protein (BMP) to prevent differentiation and promote self-renewal. SC-1 is a small molecule activator of stem cell renewal that allows the propagation of OG2 mES cells for at least 10 passages in an undifferentiated state.{14533} The activity of SC-1 is mediated by the combined inhibition of RasGAP and ERK1 with Kd values of 98 and 212 nM, respectively.{14533} Inhibition of RasGAP increases Ras signaling via the PI3-kinase pathway which promotes self-renewal, whereas inhibition of ERK blocks differentiation.
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The maintenance of embryonic stem cells in culture typically requires feeder cells and various exogenous factors found in serum. Murine embryonic stem (mES) cells can be maintained in the absence of feeder cells and serum but require the leukemia inhibitor factor (LIF) and bone morphogenic protein (BMP) to prevent differentiation and promote self-renewal. SC-1 is a small molecule activator of stem cell renewal that allows the propagation of OG2 mES cells for at least 10 passages in an undifferentiated state.{14533} The activity of SC-1 is mediated by the combined inhibition of RasGAP and ERK1 with Kd values of 98 and 212 nM, respectively.{14533} Inhibition of RasGAP increases Ras signaling via the PI3-kinase pathway which promotes self-renewal, whereas inhibition of ERK blocks differentiation.
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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 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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