Pitavastatin Calcium 50 mg


HMG-CoA reductase

SKU: BSV-S1759-50

Pitavastatin calcium, a novel member of the medication class of statins, is a calcium salt formulation of pitavastatin which is a highly effective HMG-CoA reductase inhibitor.

Target: HMG-CoA reductase, cholesterol esters

Chemical name: (3R,5S,6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)-3-quinolinyl]-3,5-dihydroxy-6-heptenoic acid,calcium salt (2:1)

Formula: C50H46CaF2N2O8

Molecular weight: 880.98

Size: 50 mg

Purity: 99.53 %

Solubility: 51 mg/mL (DMSO)

Storage: 3 years -20°C powder, 2 years -80°C in solvent

In vitro:
Pitavastatin significantly reduces both intracellular levels and synthesis of cholesterol esters. Pitavastatin is found to enhance LDL-receptor expression in vitro, as well as the amount of LDL binding to the LDL-receptor. Pitavastatin also exhibits more potent induction of LDL receptor mRNA expression compared with simvastatin and atorvastatin. Pitavastatin has many pleiotropic effects in vitro and in vivo, including deterring progression of atherosclerosis via inhibition of thromboxane synthesis, inhibition of migration/proliferation of vascular smooth muscle cells induced by angiotensin II, and stabilization of atherosclerotic plaque. [1] Pitavastatin is able to activate PPARα and induce HDL apoA-I through inducing inhibition of the Rho-signaling pathway. [2] Pitavastatin (1 μM) treatment for 48 h is able to enhances bone morphogenetic protein-2 BMP-2 (2.5-fold) and osteocalcin (10-fold) expression by inhibition of Rho-associated kinase in human osteoblasts[3]. Pitavastatin inhibits growth and colony formation of liver cancer Huh-7 cells and SMMC7721 cells. It induces arrest of liver cancer cells at the G1 phase. Increased proportion of sub-G1 cells is observed after pitavastatin treatment. Pitavastatin promotes caspase-9 cleavage and caspase-3 cleavage in liver cancer cells. Pitavastatin could regulate NF-κB and anti-inflammation in hepatocellular carcinoma cells. Pitavastatin could induce autophagic cell death in glioma cells and promote sensitivity of cells to radiotherapy. It could inhibit cell proliferation and induce cell apoptosis in cholangiocarcinoma cells as well[5].

In vivo:
Pitavastatin decreases the tumor growth and improved the survival of tumor-bearing mice[5]. Pitavastatin exerts a protective effect on dilated cardiomyopathy possibly through down-regulating the circulating and local RAS, followed by inhibition of PKCb2 phosphorylation, and consequently promoting the phosphorylation of PLB as well as the activity and the expressions of SERCA2a and RyR2, whereby heart function is preserved in the development of DCM[6].

[1] Ahmad H, et al. Cardiol Rev, 2010, 18(5):264-267.
[2] Martin G, et al. J Clin Invest, 2001, 107(11), 1423-1432.
[3] Ohnaka K, et al. Biochem Biophys Res Commun, 2001, 287(2), 337-342.
[4] Olsson AG, et al. Cardiovasc Drug Rev. 2002, 20(4):303-28.
[5] You HY, et al. Onco Targets Ther. 2016, 9:5383-8.
[6] Hu W, et al. Acta Pharm. 2014, 64(1):105-15.