Vandetanib-d6 is intended for use as an internal standard for the quantification of vandetanib (Item No. 14706) by GC- or LC-MS. Vandetanib is a multi-kinase inhibitor that inhibits VEGFR2, VEGFR3, VEGFR1, EGFR, PDGFRβ, Tie-2, and FGFR1 in cell-free assays (IC50s = 40, 110, 1,600, 500, 1,100, 2,500, and 3,600 nM, respectively).{53195,24156} It also binds to 142 additional kinases in a panel of 442 kinases (Kds = 4.6-7,900 nM). Vandetanib (1 and 2.5 µM) induces apoptosis and cell cycle arrest at the G0/G1 phase in GEO colon and OVCAR-3 ovarian cancer cells.{53196} It inhibits proliferation of HAK1-B, KYN-2, and Huh7 hepatocarcinoma cells, as well as human umbilical vein endothelial cells (HUVECs), with IC50 values of 10, 8.1, 9.4, and 7.1 µM, respectively.{53197} Vandetanib (200 mg/kg) increases survival and decreases tumor angiogenesis and VEGFR2 levels in a D54MG glioblastoma mouse xenograft model.{53198} It reduces tumor growth in a variety of mouse xenograft models, including lung, colon, and breast cancer models, when administered at doses of 25, 50, and 100 mg/kg per day.{53195} Formulations containing vandetanib have been used in the treatment of medullary thyroid cancer.
Available on backorder
An internal standard for the quantification of vandetanib by GC- or LC-MS
Formal name: N-(4-bromo-2-fluorophenyl)-6-(methoxy-d3)-7-[[1-(methyl-d3)-4-piperidinyl]methoxy]-4-quinazolinamine
Synonyms:
Molecular weight: 481.4
CAS: 1174683-49-8
Purity: ≥99% deuterated forms (d1-d6)
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}
Available on backorder
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}
Available on backorder
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.
Available on backorder
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}
Available on backorder