17-phenyl trinor Prostaglandin F2α-d4 (17-phenyl trinor PGF2α-d4) contains four deuterium atoms at the 3, 3′, 4, and 4′ positions. It is intended for use as an internal standard for the quantification of 17-phenyl trinor PGF2α by GC- or LC-mass spectrometry. 17-phenyl trinor PGF2α is a metabolically stable analog of PGF2α and is a potent agonist for the FP receptor. It binds to the FP receptor on ovine luteal cells with a relative potency of 756% compared to that of PGF2α.{2058} At the rat recombinant FP receptor expressed in CHO cells 17-phenyl trinor PGF2α inhibits PGF2α binding with a Ki of 1.1 nM.{1374} The isopropyl ester of 17-phenyl trinor PGF2α-d4 is slightly better than PGF2α isopropyl ester in reducing the intraocular pressure in the cat eye without any irritation.{1107}
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An internal standard for the quantification of 17-phenyl trinor PGF2α by GC- or LC-MS.
Formal name: 9α,11α,15S-trihydroxy-17-phenyl-18,19,20-trinor-prosta-5Z,13E-dien-1-oic-3,3,4,4-d4 acid
Synonyms: 17-phenyl trinor PGF2α-d4|Bimatoprost (free acid)-d4
Molecular weight: 392.5
CAS: 58976-50-4
Purity: ≥99% deuterated forms (d1-d4)
Formulation: A solution in methyl acetate
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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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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Cyclin-dependent kinases (CDKs) are key regulators of cell cycle progression and are therefore promising targets for cancer therapy. (R)-Roscovitine is a potent inhibitor of Cdk2/cyclin E with an IC50 value of 0.1 µM.{14988} It also inhibits Cdk7/cyclin H, Cdk5/p35, and cell division cycle (cdc)/cyclin B with IC50 values of 0.49, 0.16, and 0.65 µM, respectively.{14987,14988,14991} (R)-Roscovitine inhibits the growth of rapidly proliferating cells with an average IC50 value of 15.2 µM against a panel of 19 human tumor cell lines.{14988} In murine models of polycystic kidney disease, (R)-roscovitine effectively inhibited disease progression at doses of 50-100 mg/kg.{14564}
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