p-Hydroxyatorvastatin-D5 calcium salt - CAS 214217-88-6
Catalog number:
Main Product
Molecular Formula:
C33H33FN2O6 2Na
Molecular Weight:
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p-Hydroxyatorvastatin-D5 calcium salt; 4-Hydroxy atorvastatin disodium salt
A metabolite of Atorvastatin, a selective, competitive HMG-CoA reductase inhibitor. Atorvastatin is the only drug in its class specfically indicated for lowering both elevated LDL-cholesterol and triglycerides in patients with hypercholesterolemia.
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1.Ion Channels in Obesity: Pathophysiology and Potential Therapeutic Targets.
Vasconcelos LH1, Souza IL1, Pinheiro LS1, Silva BA2. Front Pharmacol. 2016 Mar 30;7:58. doi: 10.3389/fphar.2016.00058. eCollection 2016.
Obesity is a multifactorial disease related to metabolic disorders and associated with genetic determinants. Currently, ion channels activity has been linked to many of these disorders, in addition to the central regulation of food intake, energetic balance, hormone release and response, as well as the adipocyte cell proliferation. Therefore, the objective of this work is to review the current knowledge about the influence of ion channels in obesity development. This review used different sources of literature (Google Scholar, PubMed, Scopus, and Web of Science) to assess the role of ion channels in the pathophysiology of obesity. Ion channels present diverse key functions, such as the maintenance of physiological homeostasis and cell proliferation. Cell biology and pharmacological experimental evidences demonstrate that proliferating cells exhibit ion channel expression, conductance, and electrical properties different from the resting cells.
2.Modeling the formation of the quench product in municipal solid waste incineration (MSWI) bottom ash.
Inkaew K1, Saffarzadeh A2, Shimaoka T3. Waste Manag. 2016 Apr 11. pii: S0956-053X(16)30103-9. doi: 10.1016/j.wasman.2016.03.019. [Epub ahead of print]
This study investigated changes in bottom ash morphology and mineralogy under lab-scale quenching conditions. The main purpose was to clarify the mechanisms behind the formation of the quench product/layer around bottom ash particles. In the experiments, the unquenched bottom ashes were heated to 300°C for 1h, and were quenched by warm water (65°C) with different simulated conditions. After having filtered and dried, the ashes were analyzed by a combination of methodologies namely, particle size distribution analysis, intact particle and thin-section observation, X-ray diffractometry, and scanning electron microscope with energy dispersive X-ray spectroscopy. The results indicated that after quenching, the morphology and mineralogy of the bottom ash changed significantly. The freshly quenched bottom ash was dominated by a quench product that was characterized by amorphous and microcrystalline calcium-silicate-hydrate (CSH) phases. This product also enclosed tiny minerals, glasses, ceramics, metals, and organic materials.
3.Diuretics for Hypertension: A Review and Update.
Roush GC1, Sica DA2. Am J Hypertens. 2016 Apr 5. pii: hpw030. [Epub ahead of print]
This review and update focuses on the clinical features of hydrochlorothiazide (HCTZ), the thiazide-like agents chlorthalidone (CTDN) and indapamide (INDAP), potassium-sparing ENaC inhibitors and aldosterone receptor antagonists, and loop diuretics. Diuretics are the second most commonly prescribed class of antihypertensive medication, and thiazide-related diuretics have increased at a rate greater than that of antihypertensive medications as a whole. The latest hypertension guidelines have underscored the importance of diuretics for all patients, but particularly for those with salt-sensitive and resistant hypertension. HCTZ is 4.2-6.2 systolic mm Hg less potent than CTDN, angiotensin-converting enzyme inhibitors, beta blockers, and calcium channel blockers by 24-hour measurements and 5.1mm Hg systolic less potent than INDAP by office measurements. For reducing cardiovascular events (CVEs), HCTZ is less effective than enalapril and amlodipine in randomized trials, and, in network analysis of trials, it is less effective than CTDN and HCTZ-amiloride.
4.Trypanocidal action of bisphosphonium salts through a mitochondrial target in bloodstream form Trypanosoma brucei.
Alkhaldi AA1, Martinek J2, Panicucci B2, Dardonville C3, Zíková A2, de Koning HP1. Int J Parasitol Drugs Drug Resist. 2015 Dec 11;6(1):23-34. doi: 10.1016/j.ijpddr.2015.12.002. eCollection 2016.
Lipophilic bisphosphonium salts are among the most promising antiprotozoal leads currently under investigation. As part of their preclinical evaluation we here report on their mode of action against African trypanosomes, the etiological agents of sleeping sickness. The bisphosphonium compounds CD38 and AHI-9 exhibited rapid inhibition of Trypanosoma brucei growth, apparently the result of cell cycle arrest that blocked the replication of mitochondrial DNA, contained in the kinetoplast, thereby preventing the initiation of S-phase. Incubation with either compound led to a rapid reduction in mitochondrial membrane potential, and ATP levels decreased by approximately 50% within 1 h. Between 4 and 8 h, cellular calcium levels increased, consistent with release from the depolarized mitochondria. Within the mitochondria, the Succinate Dehydrogenase complex (SDH) was investigated as a target for bisphosphonium salts, but while its subunit 1 (SDH1) was present at low levels in the bloodstream form trypanosomes, the assembled complex was hardly detectable.
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CAS 214217-88-6 p-Hydroxyatorvastatin-D5 calcium salt

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