The predetermined regulatory range of 90% CI for bioequivalence was 0.80 to
1.25. The 90% confidence intervals for log transformed data for C-max, AUC(0-t) and AUC(0-infinity) for test A vs. reference were 82.11-98.91, 86.29-102.17 and 86.34-102.59 respectively whereas for test B vs. reference were 104.39-125.76, 94.78-112.22 and 92.85-110.33 respectively. The results of this study suggest that the test A was bioequivalent to reference product, whereas test B was not as per regulatory defined criteria.”
“AimTubal ectopic pregnancy (tEP) must be diagnosed as early LY294002 order as possible because it is one of the leading causes of pregnancy-related death in the first trimester. The aim of this study was to evaluate the diagnostic value of serum total creatine kinase (CK) and its isoforms in diagnosis of tEP.
MethodsThe study included 32 tEP cases, and gestational age-matched intrauterine (IU) abortion and normal pregnancy
cases (n=31 each). Serum total CK and CK-MB fraction HSP990 were measured by the principle of spectrophotometry and CK-MM fraction was calculated from the above parameters. Serum -hCG was measured using chemiluminescent immunoassay. All study parameters were measured at the time of presentation.
ResultsSerum -hCG levels were significantly low in patients with both tEP and IU abortion than normal pregnancy. Women with tEP had higher concentrations of total CK, CK-MM and lower concentrations of CK-MB% compared to both gestational age-matched IU pregnancy controls and IU abortion. Receiver-operator characteristic analysis revealed that the optimal cut-off for total CK, CK-MM and CPK-MB% as predictors of ruptured EP were 147IU/L, 135IU/L and 10%, respectively, with the former two having higher specificity, and latter high sensitivity.
ConclusionEstimation of PF-6463922 CK and its CK isoenzyme fractions can aid in quick and accurate diagnosis of tEP.”
“JI-101, chemically 1-[1-(2-amino-pyridin-4-ylmethyl)-1H-indol-4-yl]-3-(5-bromo-2-methoxy-phenyl)-urea hydrochloride, is a novel orally active kinase inhibitor, which
has shown potent in vitro and in vivo anticancer activity against a variety of cancer cell lines and xenografts. It is currently entering Phase II clinical development for the treatment of solid tumors. The aim of the study is to assess the metabolic stability of JI-101 in various pre-clinical and human liver microsomes, to identify the major CYPs (cytochrome beta 450) involved in the metabolism of JI-101 and identification of putative metabolites. We have also studied the pharmacokinetics, tissue distribution and excretion of JI-101 in Sprague Dawley rats. JI-101 was found to be stable in various liver microsomes tested. JI-101 is highly permeable and not a substrate for P-gp (permeability glycoprotein). JI-101 excreted through bile along with its mono-and di-hydroxy metabolites.