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STATINE

CAS No.
49642-07-1
Chemical Name:
STATINE
Synonyms
STATIN;STATINE;H-STA-OH;S)-Statine;LEU-STATINE;4S)-Statine;(S,S)-Statine;H-STA(3S,4S)-OH;(3S,4S)-STATINE;H-(3S,4S)-STA-OH
CBNumber:
CB9272763
Molecular Formula:
C8H17NO3
Molecular Weight:
175.23
MDL Number:
MFCD00037277
MOL File:
49642-07-1.mol
MSDS File:
SDS
Last updated:2023-05-18 11:31:11

STATINE Properties

Melting point 209 °C
alpha D15 -20° (c = 0.64 in water)
Boiling point 306.53°C (rough estimate)
Density 1.1233 (rough estimate)
refractive index 1.4476 (estimate)
storage temp. 2-8°C
solubility 0.5 M HCl: 50 mg/mL, clear, very faintly yellow
pka 3.97±0.10(Predicted)
Merck 13,8879
NCI Dictionary of Cancer Terms statin
FDA UNII YTC77XR1EK

SAFETY

Risk and Safety Statements

Symbol(GHS)  GHS hazard pictograms
GHS07
Signal word  Warning
Hazard statements  H319-H315-H335
Precautionary statements  P264-P280-P305+P351+P338-P337+P313P-P264-P280-P302+P352-P321-P332+P313-P362
Hazard Codes  Xi
Risk Statements  36/37/38
Safety Statements  26-36
WGK Germany  3

STATINE price More Price(1)

Manufacturer Product number Product description CAS number Packaging Price Updated Buy
American Custom Chemicals Corporation API0004236 STATINE 95.00% 49642-07-1 50MG $340.2 2021-12-16 Buy
Product number Packaging Price Buy
API0004236 50MG $340.2 Buy

STATINE Chemical Properties,Uses,Production

Chemical Properties

white powder

Mechanism of action

The statin family of six closely related hypocholesterolemic drugs are all potent competitive inhibitors of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase), the rate-limiting enzyme in cholesterol biosynthesis.The liver is their target organ, and decreased hepatic cholesterol synthesis ultimately leads to increased removal of LDL particles from the circulation. As a consequence, all other hypocholesterolemic drugs have been relegated to secondary status.
Clinical trials with lovastatin (Mevacor), simvastatin (Zocor) and pravastatin (Pravachol) provided much of the evidence supporting the observation that lowering of blood cholesterol lowers the risk of CHD. Reductions in CHD risk appear to be due to multiple consequences of inhibiting the cholesterol synthesis pathway. Drug-induced inhibition of hepatic cholesterol synthesis leads to lowering of liver cholesterol concentrations and feedback up-regulation at the gene level of both HMG CoA reductase and the LDL receptor (mechanisms IV and VII in Fig. 23.2). As long as the statin is present at adequate concentration in the liver, the extra HMG CoA reductase activity is not expressed. However, the increased hepatic LDL receptor protein results in increased rates of removal of LDL particles from the circulation by the liver, lowering of blood LDL-cholesterol levels, slowing of atherosclerosis, and decreased risk of heart attack.
The reduced risk of CHD achieved with the statins may also be due to drug actions independent of lowering blood cholesterol. Many important molecules besides cholesterol are generated by intermediates in the complex cholesterol synthesis pathway. These include the isoprenes geranylgeranyl and farnesyl, which are covalently attached to some proteins (isoprenylation) and target them to membranes where they function.The re-ported capacities of statins to inhibit proliferation of arterial wall smooth muscle cells and to improve endothelial cell functions may be due to inhibited protein isoprenylation in these cells secondary to HMG CoA reductase inhibition.

Clinical Use

With the possible exception of atorvastatin, the statins are used to lower LDL cholesterol in familial or polygenic ( multifactorial) hypercholesterolemia (type IIa) and in combination with triglyceride-lowering drugs to treat combined hyperlipidemia (type IIb) when both LDL and VLDL (very low density lipoproteins) are elevated. However, the statins probably should not be given with the fibrates (triglyceridelowering drugs, discussed later), since this combination may greatly increase statin toxicity. Atorvastatin, the most potent of the available statins, has also been shown to lower blood triglycerides significantly.
This effect may be due to decreasing hepatic cholesterol and cholesterol ester levels to such an extent that hepatic formation of VLDL is impaired.The statins also have been claimed to reduce blood cholesterol levels modestly in some patients with homozygous familial hypercholesterolemia, a condition often fatal in childhood or in early adulthood.
The statins may lower the risk of CHD by decreasing inflammation, an important component of atherogenesis. Lovastatin decreased elevated plasma levels of Creactive protein, a marker for cellular inflammation, and acute coronary events in patients with relatively low plasma cholesterol levels. Recent studies also suggest that use of statins may decrease the risk of stroke, dementia, and Alzheimer’s disease and may improve bone density in postmenopausal women. These broad actions may be related to the hypocholesterolemic, antiproliferative, antiinflammatory, or antioxidant properties of the statins or some combination of these properties.

Side effects

The statins generally appear to be well tolerated, with muscle pain and liver dysfunction seen in 1 to 2% of patients. However, the consequences of 20 to 30 years of continuous use are unknown. This fact has been dramatically reinforced by the recent recognition of a potentially fatal consequence of statin use. A relatively common side effect of the statins (perhaps 1% of patients) is myositis, that is, inflammation of skeletal muscle accompanied by pain, weakness, and high levels of serum creatine kinase. Rhabdomyolysis, i.e., disintegration of muscle with urinary excretion of myoglobin and kidney damage, was considered to be a rare and extreme toxic outcome. However, cerivastatin (Baycol) has now been withdrawn from the market by its manufacturer (Bayer) because of 31 deaths linked to fatal rhabdomyolysis. The risk of muscle damage is said to increase with simultaneous use of the triglyceride-lowering fibrates. Pravastatin may be less toxic than other statins because it does not readily penetrate extrahepatic cells and may be more confined to the liver after oral dosage.

34993-63-0
49642-07-1
Synthesis of STATINE from 5-METHYL-HEX-2-ENOIC ACID ETHYL ESTER

STATINE Suppliers

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STATIN STATINE H-STA(3S,4S)-OH H-STA-OH H-(3S,4S)-STA-OH LEU-STATINE (3S,4S)-4-AMINO-3-HYDRO-6-METHYLHEPTANOIC ACID (3S,4S)-(-)-STATINE (3S,4S)-STATINE (3S,4S)-4-AMINO-3-HYDROXY-6-METHYLHEPTANOIC ACID (3S,4S)-4-AMINO-3-HYDROXY-L-METHYLHEPTANOIC ACID Sta(3S,4S)-OH·HCl Statine Hydrochloride≥ 98% (TLC) (3S,4S)-(-)-Statine,98% (3S,4S)-4-Amino-3-hydroxy-6-methylheptanoic acid hydrochloride Statine *CAS 49642-07-1* (S,S)-Statine Heptanoic acid, 4-amino-3-hydroxy-6-methyl-, (3S,4S)- 4S)-Statine S)-Statine 49642-07-1 Unnatural Amino Acid Derivatives Peptide Synthesis Others Specialty Synthesis Amino Acids