Off-white to Yellow powder
10,11,7'-Trimethoxy-emetan-6'-ol,Hydrochlorid/cephaeline dihydrochloride/10,11,7'-trimethoxy-emet-1'-ene-9,6'-diol/Alangicine/10,11,7'-trimethoxy-emetan-6'-ol,dihydrochloride/10,11,7'-Trimethoxy-emetan-6'-ol,Dihydrochlorid/(-)-Cephaeline (dihydrochloride)
(-)-Cephaeline dihydrochloride is an enantiomer of Cephaeline dihydrochloride. Cephaeline dihydrochloride is a selective CYP2D6 inhibtor with IC50 of 121 μM.
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:5853-29-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Ex vivostudies have suggested that high dose proton pump inhibitors (PPI) may have negative inotropic effects in myocardial tissue. We sought to investigate this concept in a real?world clinical setting. In this case series, we enrolled critically ill patients in the coronary and cardiothoracic intensive care units who had a preexisting pulmonary artery (PA) catheter in place for hemodynamic monitoring and were on a PPI for prespecified clinical indications. Hemodynamic measurements were made at baseline and then at 15 minute intervals for 1 hour after PPI administration. A total of 18 patients were evaluated; 72% were male with a mean age of 59.9 years. A total of 9 patients were evaluated on 2 consecutive days, yielding 26 patient?exposures to the medication. The majority of patients (72%) were receiving 1 or more inotropic agents (n= 6), a vasopressor (n= 4), or both (n= 4). When compared to baseline values, there was no significant change in mean arterial pressure (baseline 80 ± 11 mm Hg), heart rate (87 ± 11 bpm), or Fick cardiac index (2.7 ± 1.8 L/min/m2). Mean PA pressure did decrease transiently at 45 minutes following PPI administration (28.5 ± 7.7 mm Hg at baseline vs 26.5 ± 7.5 mm Hg, P = 0.017), but is unlikely to be of clinical significance. In conclusion, these data suggest that IV PPIs do not immediately impact important hemodynamic parameters and are likely safe in a high?risk intensive care setting. Copyright ? 2010 Wiley Periodicals, Inc.
Case Report: The Effect of Proton Pump Inhibitor Administration on Hemodynamics in a Cardiac Intensive Care Unit
Anna M. Booher, MD,corresponding author 1 Michael Dorsch, PharmD, 1 and Hitinder S. Gurm, MBBS, FACC 1 , 2
The cyclophilins (CYPs) and FK506 binding proteins (FKBPs) are two families of distinct proline isomerases that are targets for a number of clinically important immunosuppressive drugs. Members of both families catalyze cis/trans isomerization of peptidyl-prolyl bonds, which can be a rate-limiting step during protein folding in vitro and in vivo. We demonstrate in Saccharomyces cerevisiae that heat shock causes a 2- to 3-fold increase in the level of mRNA encoded by the major cytoplasmic CYP gene, CYP1. The cloned CYP1 promoter confers heat-inducible expression upon a reporter gene, and transcriptional induction is mediated through sequences similar to the consensus heat shock response element. Disruption of CYP1 decreases survival of cells following exposure to high temperatures, indicating that CYP1 plays a role in the stress response. A second CYP gene, CYP2, encodes a cyclophilin that is located within the secretory pathway. Its expression is also stimulated by heat shock, and cells containing a disrupted CYP2 allele are more sensitive than wild-type cells to heat. By contrast, expression of the FKB1 gene, which encodes a cytoplasmic member of the yeast FKBP family, is neither heat responsive nor necessary for survival after exposure to heat stress.
Proline isomerases function during heat shock.
K Sykes, M J Gething, and J Sambrook
1993 Jun 15;
Cultured cells from individuals affected with Fanconi anemia (FA) exhibit spontaneous chromosome breakage and hypersensitivity to the cell killing and clastogenic effects of the difunctional alkylating agent diepoxybutane (DEB). We report here the correction of both of these DEB-hypersensitivity phenotypes of FA cells achieved by cotransfection of normal placental or Chinese hamster lung cell DNA and the plasmid pSV2-neo-SVgpt. Transfectants were selected for clonogenic survival after treatment with DEB at a dose of 5 micrograms/ml. At this dose of DEB, the clonogenicity of normal fibroblasts was reduced to 50% and that of FA fibroblasts was reduced to zero. DEB-resistant (DEBr) colonies selected in this system exhibited a normal response to DEB-induced chromosome breakage and resistance to repeated DEB treatment. The neo and gpt sequences were detected by Southern blot analysis of DNA from one of four DEBr colonies independently derived from transfection of human DNA and one of three DEBr colonies independently derived from transfection of Chinese hamster DNA. In addition, Alu-equivalent hamster sequences were detected in three of seven additional independently derived colonies from transfection of Chinese hamster DNA. The DEBr phenotype of these colonies was stably maintained over several subcultures. Our results demonstrate that DNA sequences that complement the two hallmark cellular phenotypes (cellular and chromosomal hypersensitivity to alkylating agents) of FA are present in human as well as Chinese hamster DNA. The cloning of these genes using transfection strategies can be expected to enable molecular characterization of FA.
Transfection of normal human and Chinese hamster DNA corrects diepoxybutane-induced chromosomal hypersensitivity of Fanconi anemia fibroblasts.
M Shaham, B Adler, S Ganguly, and R S Chaganti