STATINE Struktur

STATINE

Bezeichnung:STATINE

CAS-Nr49642-07-1

Englisch Name:STATINE

CBNumberCB9272763

SummenformelC8H17NO3

Molgewicht175.23

MOL-Datei49642-07-1.mol

STATINE physikalisch-chemischer Eigenschaften

Schmelzpunkt	209 °C
alpha	D15 -20° (c = 0.64 in water)
Siedepunkt	306.53°C (rough estimate)
Dichte	1.1233 (rough estimate)
Brechungsindex	1.4476 (estimate)
storage temp.	2-8°C
Löslichkeit	0.5 M HCl: 50 mg/mL, clear, very faintly yellow
pka	3.97±0.10(Predicted)
Aggregatzustand	Solid
Farbe	White to off-white
Merck	13,8879

Sicherheit

Kennzeichnung gefährlicher	Xi
R-Sätze:	36/37/38
S-Sätze:	26-36
WGK Germany	3

Gefahreninformationscode (GHS)

STATINE Chemische Eigenschaften,Einsatz,Produktion Methoden

R-Sätze Betriebsanweisung:
R36/37/38:Reizt die Augen, die Atmungsorgane und die Haut.
S-Sätze Betriebsanweisung:
S26:Bei Berührung mit den Augen sofort gründlich mit Wasser abspülen und Arzt konsultieren.
S36:DE: Bei der Arbeit geeignete Schutzkleidung tragen.
Chemische Eigenschaften
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.
Nebenwirkungen
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.

STATINE Upstream-Materialien And Downstream Produkte

STATINE Anbieter Lieferant Produzent Hersteller Vertrieb Händler.

49642-07-1, STATINE Verwandte Suche:

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