Product Information
Registration Status: ActiveSIN15664P
CHOLIB FILM-COATED TABLET 145MG/20MG is approved to be sold in Singapore with effective from 2019-04-09. It is marketed by ABBOTT LABORATORIES (SINGAPORE ) PTE LTD, with the registration number of SIN15664P.
This product contains Fenofibrate 145mg, and Simvastatin 20mg in the form of TABLET, FILM COATED. It is approved for ORAL use.
This product is manufactured by Fournier Laboratories Ireland Limited in FRANCE, andMylan Laboratoires SAS (Primary & Secondary) in IRELAND.
It is a Prescription Only Medicine that can only be obtained from a doctor or a dentist, or a pharmacist with a prescription from a Singapore-registered doctor or dentist.
Product Reference
Important Note: For generic product, the SPC/PIL provided may not be brand specific.
{{/items}} {{^items}}Description
Fenofibrate is a prodrug of fenofibric acid, an antilipemic agent which reduces both cholesterol and triglycerides in the blood.
Indication
For use as adjunctive therapy to diet to reduce elevated LDL-C, Total-C,Triglycerides and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb)
Mechanism of Action
Fenofibrate exerts its therapeutic effects through activation of peroxisome proliferator activated receptor a (PPARa). This increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III. The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles, to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly.
Pharmacokinetics
- Absorption
- Fenofibrate is well absorbed from the gastrointestinal tract. After absorption, fenofibrate is mainly excreted in the urine in the form of metabolites, primarily fenofibric acid and fenofibric acid glucuronide
- Distribution
- In healthy adults, the volume of distribution is 30 L. The volume of distribution is 95 L in individuals with moderate renal impairment and creatinine clearance of 50 to 90 mL/min [FDA Label].
- Metabolism
- Elimination
Clearance
* 1.2 L/h [Eldery]
Toxicity
LD50=1600 mg/kg (Oral, in mice); Investigated as a teratogen and reproductive hazard.
Active Ingredient/Synonyms
2-(4-(4-Chlorobenzoyl)phenoxy)-2-methylpropanoic acid 1-methylethyl ester | Fenofibrato | Fenofibratum | Finofibrate | FNF | Isopropyl (4'-(p-chlorobenzoyl)-2-phenoxy-2-methyl)propionate | Isopropyl 2-(4-(4-chlorobenzoyl)phenoxy)-2-methylpropionate | Procetofen | Fenofibrate |
Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.
Description
Simvastatin is a lipid-lowering agent that is derived synthetically from the fermentation of Aspergillus terreus. It is a potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (hydroxymethylglutaryl COA reductases), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL receptors, it increases breakdown of LDL cholesterol. [PubChem]
Indication
For the treatment of hypercholesterolemia and for the reduction in the risk of cardiac heart disease mortality and cardiovascular events. It can also be used in adolescent patients for the treatment of heterozygous familial hypercholesterolemia.
Mechanism of Action
Simvastatin is a prodrug in which the 6-membered lactone ring of simvastatin is hydrolyzed in vivo to generate the beta,delta-dihydroxy acid, an active metabolite structurally similar to HMG-CoA (hydroxymethylglutaryl CoA). Once hydrolyzed, simvastatin competes with HMG-CoA for HMG-CoA reductase, a hepatic microsomal enzyme. Interference with the activity of this enzyme reduces the quantity of mevalonic acid, a precursor of cholesterol.
Pharmacokinetics
- Absorption
- Absorption of simvastatin, estimated relative to an intravenous reference dose, in each of two animal species tested, averaged about 85% of an oral dose. In animal studies, after oral dosing, simvastatin achieved substantially higher concentrations in the liver than in non-target tissues. However, because simvastatin undergoes extensive first-pass metabolism, the availability of the drug in the systemic is low. Peak plasma concentration occurs 1.3 - 2.4 hours after administration.
- Distribution
- Simvastatin can cross the blood-brain-barrier.
- Metabolism
- Hepatic, simvastatin is a substrate for CYP3A4. The major active metabolites of simvastatin are β-hydroxyacid metabolite and its 6'-hydroxy, 6'-hydroxymethyl, and 6'-exomethylene derivatives
- Elimination
Toxicity
The most common adverse reactions that lead to discontinuation of therapy include gastrointestinal disorders (0.5%), myalgia (0.1%), and arthralgia (0.1%).
Active Ingredient/Synonyms
2,2-Dimethylbutyric acid, 8-ester with (4R,6R)-6-(2-((1S,2S,6R,8S,8ar)-1,2,6,7,8,8a-hexahydro-8-hydroxy-2,6-dimethyl-1-naphthyl)ethyl)tetrahydro-4-hydroxy-2H-pyran-2-one | Simvastatin | Simvastatina | Simvastatine | Simvastatinum | Synvinolin | Simvastatin |
Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.