BRAND NAME:- Z ROSU-FB10(ROSUVASTATIN 10 MG + FENOFIBRATE)
COMPOSITION: – ROSUVASTATIN 10 MG + FENOFIBRATE
1.ROSUVASTATIN:- It is a hypolipidaemic statin which competitively inhibits the conversion of 3-hydroxy-3-methyl glutaryl coenzyme A (HMG CoA) to mevalonate. The drug exerts it`s action by specific inhibition of enzyme; 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMG CoA reductase) and reduces cholesterol synthesis up to 50% at therapeutic doses. This results in compensatory increase in low density lipoprotein (LDL) receptor expression in liver which ultimately leads to increased receptor mediated uptake and catabolism of intermediate density lipoprotein(IDL) and low density lipoprotein (LDL). It causes dose dependent lowering of LDL cholesterol and reduces hepatic synthesis of very low density lipoprotein (VLDL) and lowers plasma triglyceride levels. It also increases high density lipoprotein (HDL) levels.
2.FENOFIBRATE:- It is prodrug which has greater LDL (low density lipoprotein) cholesterol lowering potential. It lowers circulating triglyceride levels by activating lipoprotein lipase which is a key enzyme in the degradation of VLDL (very low density lipoprotein) cholesterol. This effect is exerted through paroxisome proliferator-activated receptor alpha (PPARalpha) which enhances lipoprotein lipase synthesis and fatty acid oxidation. It also reduces hepatic triglyceride synthesis. It also reduces VLDL levels and increases HDL (high density lipoprotein) cholesterol. The increase in HDL cholesterol is partly due to transfer of surface lipid components from catabolised VLDL to HDL and also due to increased production of HDL apoproteins by liver.
Rationale for combination- rosuvastatin significantly decreases serum TGs , total cholestrol , LDL-C , non -HDL cholesterol and apoliproprotein B ApoB levels. Fenobibrate a fibric acid derivative is used as anti-hyperlipedemic agent due to the lipid modifying property.
Thus the combination of rosuvastatin and fenofibrate gives the synergistic action in reducing LDL-C and increasing HDL- cholesterol levels
· Absorption: Readily absorbed orally, and bioavailability is about 20%.
· Distribution: Widely distributed in a protein bound form,
· Metabolism: Not significantly metabolized in liver, only about 10% is metabolized in liver.
· Excretion: Excreted mainly through bile.
· Absorption: Well absorbed orally, food increases the absorption.
· Distribution: Widely distributed in a protein bound form
· Metabolism: Metabolized by ester hydrolysis to active metabolite which undergoes glucuronide conjugation in liver.
· Excretion: Excreted mainly through urine and a small portion is excreted through feces.
· Hypercholesterolemia as an adjunct to diet
· Mixed dyslipidaemia as an adjunct to diet
Hyper lipidaemia (Type IIa, IIb, III, IV, and V) unresponsive to diet alone