Simvastatin acid (Tenivastatin) calcium hydrate is a potent HMG-CoA reductase (HMGCR) inhibitor. Simvastatin acid calcium hydrate reduces Indoxyl sulfate-mediated reactive oxygen species (ROS) production in human cardiomyocytes. Simvastatin acid calcium hydrate can also modulates OATP3A1 expression in cardiomyocytes and HEK293 cells transfected with the OATP3A1 gene[1][2].
Rosuvastatin Calcium is a competitive inhibitor of HMG-CoA reductase with IC50 of 11 nM. IC50 Value: 11 nM [1]Target: HMG-CoA reductasein vitro: Rosuvastatin is relatively hydrophilic and is highly selective for hepatic cells; its uptake is mediated by the liver-specific organic anion transporter OATP-C. Rosuvastatin is a high-affinity substrate for OATP-C with apparent association constant of 8.5 μM [2]. Rosuvastatin inhibits cholesterol biosynthesis in rat liver isolated hepatocytes with IC50 of 1.12 nM. Rosuvastatin causes approximately 10 times greater increase of mRNA of LDL receptors than pravastatin [1]. Rosuvastatin (100 μM) decreases the extent of U937 adhesion to TNF-α-stimulated HUVEC. Rosuvastatin inhibits the expressions of ICAM-1, MCP-1, IL-8, IL-6, and COX-2 mRNA and protein levels through inhibition of c-Jun N-terminal kinase and nuclear factor-kB in endothelial cells [3].in vivo: Rosuvastatin (3 mg/kg) daily administration for 14 days decreases plasma cholesterol levels by 26% in male beagle dogs with normal cholesterol levels. In cynomolgus monkeys, Rosuvastatin decreases plasma cholesterol levels by 22% [1]. Rosuvastatin (20 mg/kg/day) administration for 2 weeks, significantly reduces very low-density lipoproteins (VLDL) in diabetes mellitus rats induced by Streptozocin [4]. Rosuvastatin shows antiatherothromhotic effects in vivo. Rosuvastatin (1.25 mg/kg) significantly inhibits thrombin-induced transmigration of monocvtes across mesenteric venules via inhibition of the endothelial cell surface expression of P-selectin, and increases the basal rate of nitric oxide in aortic segments by 2-fold times [5].
Simvastatin (MK 733) is a competitive inhibitor of HMG-CoA reductase with a Ki of 0.2 nM.
Pitavastatin Calcium is a potent hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor. Pitavastatin inhibits cholesterol synthesis from acetic acid with an IC50 of 5.8 nM in HepG2 cells.
Atorvastatin is an inhibitor of HMG-CoA reductase used as a cholesterol-lowering medication that blocks the production of cholesterol. Target: HMG-CoA reductaseAtorvastatin is an inhibitor of HMG-CoA reductase used as a cholesterol-lowering medication that blocks the production of cholesterol. 81 patients were randomly assigned to receive either placebo or 2.5, 5, 10, 20, 40, or 80 mg atorvastatin once daily for 6 weeks. Plasma LDL cholesterol reductions from baseline were dose related, with 25% to 61% reduction from the minimum dose to the maximum dose of 80 mg atorvastatin once a day [1]. Atorvastatin 10 mg daily is safe and efficacious in reducing the risk of first cardiovascular disease events, including stroke, in patients with type 2 diabetes without high LDL-cholesterol. No justification is available for having a particular threshold level of LDL-cholesterol as the sole arbiter of which patients with type 2 diabetes should receive statins [2].
Simvastatin-d3 is the deuterium labeled Simvastatin[1]. Simvastatin (MK 733) is a competitive inhibitor of HMG-CoA reductase with a Ki of 0.2 nM[2].
Simvastatin sodium is a lactone prodrug, can be hydrolysed to active hydroxy-acid by non-specific carboxyesterases or non-enzymatic processes. Simvastatin sodium shows a inhibition of HMG-CoA reductase with a Ki value of 0.12 nM[1][2].
Pravastatin is an HMG-CoA reductase inhibitor against sterol synthesis with IC50 of 5.6 μM.Target: HMG-CoA reductasePravastatin (marketed as Pravachol or Selektine) is a member of the drug class of statins, used in combination with diet, exercise, and weight-loss for lowering cholesterol and preventing cardiovascular disease.Pravastatin is primarily used for the treatment of dyslipidemia and the prevention of cardiovascular disease. It is recommended to be used only after other measures such as diet, exercise, and weight reduction have not improved cholesterol levels.The evidence for the use of pravastatin is generally weaker than for other statins. The antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT), failed to demonstrate a difference in all-cause mortality or nonfatal myocardial infarction/fatal coronary heart disease rates between patients receiving pravastatin 40mg daily (a common starting dose) and those receiving usual care.
(3S,5R)-Fluvastatin sodium ((3S,5R)-XU 62-320) is the (3S,5R)-enantiomer of Fluvastatin. Fluvastatin is a first fully synthetic, competitive HMG-CoA reductase inhibitor with an IC50 of 8 nM. Fluvastatin protects vascular smooth muscle cells against oxidative stress through the Nrf2-dependent antioxidant pathway[1].
Ganoderenic acid K is a natural product, that can be isolated from fruiting bodies of Ganoderma lucidum. Ganoderenic acid K shows strong inhibitory activity against HMG-CoA reductase (HMGCR) with IC50 of 16.5 μM[1].
β-Amyrin palmitate shows HMG-CoA reductase inhibition[1]. And β-Amyrin palmitate has anti-diabetes mellitus activity[2].
2'-Ethyl Simvastatin (compound 6) is a Mevinolin analog, with HMG-CoA reductase inhibition[1].
(3R,5S)-Fluvastatin ((3R,5S)-XU 62-320) sodium is the 3R,5S-isomer Fluvastatin. Fluvastatin (XU 62-320 free acid) is a first fully synthetic, competitive HMG-CoA reductase inhibitor with an IC50 of 8 nM. Fluvastatin protects vascular smooth muscle cells against oxidative stress through the Nrf2-dependent antioxidant pathway[1][2][3].
Lovastatin-d3 hydroxy acid (Mevinolinic acid-d3) sodium is the deuterium labeled Lovastatin hydroxy acid sodium. Lovastatin hydroxy acid sodium (Mevinolinic acid sodium) is a highly potent inhibitor of HMG-CoA reductase with a Ki of 0.6 nM[1].
(rel)-Atorvastatin, a relative configuration of Atorvastatin. Atorvastatin is an orally active HMG-CoA reductase inhibitor, has the ability to effectively decrease blood lipids. Atorvastatin inhibits human SV-SMC proliferation and invasion with IC50s of 0.39 μM and 2.39 μM, respectively[1][2][3].
Simvastatin acid (Tenivastatin) is an orally active HMG-CoA reductase (HMGCR) inhibitor. Simvastatin acid can reduce cholesterol synthesis and lower blood cholesterol levels[1]. Simvastatin acid shows anti-proliferation activities against cancer cells and induces apoptosis[2].
(3S,5R)-Fluvastatin D6 sodium is the deuterium labeled (3S,5R)-Fluvastatin sodium. Fluvastatin is a first fully synthetic, competitive HMG-CoA reductase inhibitor with an IC50 of 8 nM. Fluvastatin protects vascular smooth muscle cells against oxidative stress through the Nrf2-dependent antioxidant pathway[1]
3α-Hydroxy pravastatin sodium is the major metabolite of Pravastatin. Pravastatin is a competitive HMG-CoA reductase inhibitor[1][2].
Atorvastatin lactone is a prodrug form of atorvastatin. Atorvastatin is an orally active 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor[1].
Pravastatin sodium is an HMG-CoA reductase inhibitor against sterol synthesis with IC50 of 5.6 μM.Target: HMG-CoA reductasePravastatin (marketed as Pravachol or Selektine) is a member of the drug class of statins, used in combination with diet, exercise, and weight-loss for lowering cholesterol and preventing cardiovascular disease.Pravastatin is primarily used for the treatment of dyslipidemia and the prevention of cardiovascular disease. It is recommended to be used only after other measures such as diet, exercise, and weight reduction have not improved cholesterol levels.The evidence for the use of pravastatin is generally weaker than for other statins. The antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT), failed to demonstrate a difference in all-cause mortality or nonfatal myocardial infarction/fatal coronary heart disease rates between patients receiving pravastatin 40mg daily (a common starting dose) and those receiving usual care.
Atorvastatin hemicalcium trihydrate is an orally active HMG-CoA reductase inhibitor, has the ability to effectively decrease blood lipids. Atorvastatin hemicalcium trihydrate inhibits human SV-SMC proliferation and invasion with IC50s of 0.39 μM and 2.39 μM, respectively[1][2][3].
Lovastatin is a cell-permeable HMG-CoA reductase inhibitor used to lower cholesterol.
L-669,262, a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, with an IC50 of 0.10 ng/mL for rat liver HMG-CoA[1].
(Rac)-5-Keto Fluvastatin (3-Hydroxy-5-Keto Fluvastatin) is an impurity of Fluvastatin (XU 62320). Fluvastatin is a HMG-CoA reductase inhibitor with an IC50 of 8 nM[1].
Cerivastatin is a synthetic lipid-lowering agent and a highly potent, well-tolerated and orally active HMG-CoA reductase inhibitor, with a Ki of 1.3 nM/L. Cerivastatin reduces low-density lipoprotein cholesterol levels. Cerivastatin also inhibits proliferation and invasiveness of MDA-MB-231 cells, mainly by RhoA inhibition, and has anti-cancer effect[1][2][3].
Clinofibrate (S-8527) is a hypelipidemic agent and a HMG-CoA reductase inhibitor.
Ganomycin I is a dual inhibitor of α-Glucosidase and HMG-CoA reductase. Ganomycin I can also inhibits HIV protease. Ganomycin I exhibits anti-diabetic and anti-osteoclastogenesis effects[1][2].
Mevastatin (Compactin; ML236B) inhibits HMGCR (HMG-CoA reductase) (Ki for acid form is 1 nM) which in turn inhibits isoprenoid biosynthesis and therefore blocks protein isoprenylation and reduces plasma cholesterol levels in humans. IC50 value: 1 nM (Ki)Target: HMGCRMevastatin induces apoptosis, arrests cancer cells in G1 phase and downregulates cdk 2, 4, and 6, cyclin D1 and E1, p21 and p27. Mevastatin suppresses TNF-induced NF-κB activation (IC50 = ~17 uM), which potentiates apoptosis in human myeloid leukemia cells and thus, may be useful in treating cancer.
QH536 (Compound 29) is a potent HMGCR degrader with an EC50 of 0.22 μM. QH536 has no side-effect of inducing cholesterol accumulation in cells. QH536 shows anti-inflammatory and can be used for cardiovascular disease and nonalcoholic steatohepatitis research[1].
(3S,5R)-Rosuvastatin is the (3S,5R)-enantiomer of Rosuvastatin. Rosuvastatin is a competitive HMG-CoA reductase inhibitor with an IC50 of 11 nM[1]. Rosuvastatin potently blocks human ether-a-go-go related gene (hERG) current with an IC50 of 195 nM[2]. Rosuvastatin reduces the expression of the mature hERG and the interaction of heat shock protein 70 (Hsp70) with the hERG protein. Rosuvastatin is very effective in lowering low-density lipoprotein (LDL) cholesterol, triglycerides, and C-reactive protein levels[3].