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].
(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].
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].
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].
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].
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].
Nicodicosapent is a fatty acid niacin conjugate that is also an inhibitor of the sterol regulatory element binding protein (SREBP), a key regulator of cholesterol metabolism proteins such as PCSK9, HMG-CoA reductase, ATP citrate lyase, and NPC1L1.
Pravastatin-d3 (CS-514-d3) sodium salt is the deuterium labeled Pravastatin sodium salt. Pravastatin (CS-514) sodium salt is a competitive HMG-CoA reductase inhibitor against sterol synthesis with IC50 of 5.6 μM[1][2].
Pitavastatin (NK-104) is a potent HMG-CoA reductase inhibitor, Pitavastatin inhibited cholesterol synthesis from acetic acid with an IC50 of 5.8 nM in a human liver cancer cell line (HepG2).IC50 value: 5.8 nM(cholesterol synthesis from aceticacid in HepG2) [1]Target: HMG-CoA reductasein vitro: Pitavastatin inhibited cholesterol synthesis from aceticacid with an IC50 of 5.8 nM in a human liver cancer cell line (HepG2), which indicates that is 2.9 and 5.7 times as potent as simvastatin and atorvastatin, respectively. When the inhibitory activity interms of the ED50 was compared with that of simvastatin,pitavastatin showed a 3-fold stronger activity in the rat and 15-fold stronger activity in a guinea pig model.22 The inhibitory effect of pitavastatin on sterol synthesis is thought to be liver-selective [1]. pitavastatin reduces total and phosphorylated tau levels in a cellular model of tauopathy, and in primary neuronal cultures. The decrease caused by pitavastatin is reversed by the addition of mevalonate, or geranylgeranyl pyrophosphate. The maturation of small G proteins, including RhoA was disrupted by pitavastatin, as was the activity of glycogen synthase kinase 3β (GSK3β), a major tau kinase [4].in vivo: Intravenous treatment with pitavastatin-incorporated nanoparticles, but not with control nanoparticles or pitavastatin alone, inhibited plaque destabilization and rupture associated with decreased monocyte infiltration and gelatinase activity in the plaque[2].The EAM model was established in BALB/c mice by immunization with murine α-myosin heavy chain. Mice were fed pitavastatin (5 mg/kg) or vehicle once daily for 3 weeks from day 0 to day 21 after immunization [3].
Hesperetin 7-O-glucoside is produced by the enzymatic conversion of Hesperidin. Hesperetin 7-O-glucoside is a potent human HMG-CoA reductase inhibitor and also effectively inhibits the growth of Helicobacter pylori. Antihypertensive effect[1][2].
Bemfivastatin (PPD 10558) hemicalcium is an orally active lipid-lowering agent and HMG-CoA reductase inhibitor. Bemfivastatin hemicalcium enhances the activity of liver extracts. Bemfivastatin hemicalcium has no-observed adverse effect levels (NOAEL) with dosages of ≥320 mg/kg/d (rat developmental toxicity), ≥12.5 mg/kg/d (rabbit maternal toxicity), ≥25 mg/kg/d (rabbit developmental toxicity), respectively. Bemfivastatin hemicalcium can be used in the study of statin-related hypercholesterolemic myalgia in statin-intolerant patients.
Fluvastatin (Leschol) inhibits HMG-CoA reductase activity with IC50 of 8 nM.IC50 value: 8 nMTarget: HMG-CoA reductaseFluvastatin is a competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMGCR), the enzyme that catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Human hepatocellular carcinoma cell (HCC) studies indicate that Fluvastatin induces G2/M phase arrest. In the presence of Fluvastatin, HCC cells show a decrease of Bcl-2 and procaspase-9 expression, and an increase in Bax, cleaved caspase-3, and cytochrome c. Fluvastatin is antilipemic and is used to reduce plasma cholesterol levels and prevent cardiovascular disease.
Rosuvastatin D3 Sodium is deuterium labeled Rosuvastatin, which is a competitive inhibitor of HMG-CoA reductase with IC50 of 11 nM.
Fluvastatin sodium is a competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMGCR), used to treat hypercholesterolemia and to prevent cardiovascular disease.Target: HMGCR Fluvastatin is a competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMGCR), the enzyme that catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Human hepatocellular carcinoma cell (HCC) studies indicate that Fluvastatin induces G2/M phase arrest. In the presence of Fluvastatin, HCC cells show a decrease of Bcl-2 and procaspase-9 expression, and an increase in Bax, cleaved caspase-3, and cytochrome c. Fluvastatin is antilipemic and is used to reduce plasma cholesterol levels and prevent cardiovascular disease.
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].
(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]
Clinofibrate (S-8527) is a hypelipidemic agent and a HMG-CoA reductase inhibitor.
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].
Rosuvastatin 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].
Rosuvastatin Sodium is a competitive HMG-CoA reductase (HMGCR) inhibitor, with an IC50 of 11 nM. Rosuvastatin Sodium potently blocks hERG current with an IC50 of 195 nM[2]. Rosuvastatin Sodium reduces the expression of the mature hERG and the interaction of heat shock protein 70 (Hsp70) with the hERG protein. Rosuvastatin Sodium effectively lowers low-density lipoprotein (LDL) cholesterol, triglycerides, and C-reactive protein levels[1][2][3].
L-157012 is a HMG-CoA reductase (HMGCR) inhibitor. L-157012 is also a cholesterol-lowering agent[1].
SR12813 is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, with an IC50 value of 0.85 μM.
Meglutol is an antilipemic agent which lowers cholesterol, triglycerides, serum beta-lipoproteins and phospholipids, and inhibits the activity of hydroxymethylglutarryl CoA reductases, which is the rate limiting enzyme in the biosynthesis of cholesterol.
Cerivastatin sodium 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 sodium reduces low-density lipoprotein cholesterol levels. Cerivastatin sodium also inhibits proliferation and invasiveness of MDA-MB-231 cells, mainly by RhoA inhibition, and has anti-cancer effect[1][2].
Bemfivastatin (PPD 10558) is an orally active, HMG-CoA Reductase (HMGCR) inhibitor, also known as Statin. Bemfivastatin enhances the activity of liver extraction. Bemfivastatin exhibits little developmental toxicity effects in pregnant rats and rabbits via daily oral doses during organogenesis period. The no observed adverse effect level (NOAEL) are ≥320 mg/kg/day for rats developmental toxicity, 12.5 mg/kg/day for rabbits maternal toxicity, and 25 mg/kg/day for rabbits developmental toxicity, respectively. Bemfivastatin can be used for research on Statin-related hypercholesterolemic myalgia with inability to tolerate statins[1][2].
Atorvastatin lactone D5 is a deuterated form of Atorvastatin lactone (HY-101873). Atorvastatin lactone is a prodrug form of atorvastatin. Atorvastatin is an orally active 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor[1].