The sodium-hydrogen exchanger isoform-1 (NHE-1) is the predominant isoform of the Na+/H+ exchanger and is expressed in the heart where it contributes to cardiomyocyte pH homeostasis.{22706} It plays an important role in the myocardial response to ischemia-reperfusion.{22816} Cariporide is a benzoylguanidine compound that inhibits NHE-1 with IC50 values ranging from 0.03-3.4 µM.{22706} It displays selectivity for NHE-1 over NHE-2, NHE-3, and NHE-5 (IC50s = 4.3-62, 1->100, and >30 µM, respectively).{22706} The cardioprotective efficacy of cariporide has been examined in clinical investigations of patients at risk for myocardial infarction.{22706,22816}
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A benzoylguanidine compound that selectively inhibits NHE-1 (IC50s range from 0.03-3.4 µM)
Formal name: N-(aminoiminomethyl)-4-(1-methylethyl)-3-(methylsulfonyl)-benzamide
Synonyms: HOE 642
Molecular weight: 283.3
CAS: 159138-80-4
Purity: ≥95%
Formulation: A crystalline solid
Product Type|Biochemicals|Transporter & Exchanger Modulators||Research Area|Cardiovascular System|Cardiovascular Diseases|Myocardial Infarction
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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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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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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