REGIMEN DOSE

OF
SIMVASTATIN
Kelompok 2
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Kelompok 2
1. Nurfawardani (N012211012)
2. Haldi Nugraha HS (N012211014)
3. Syaadatun Nadiah (N012211015)
4. Zhavirah P. Saadjad
(N012211017)
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Table of Contents

01 02 03
PHARMACOKIN
What is ETIC & DOSSAGE
Simvastatin? PHARMACODIN
AMIC
BIOGRAPHY

04 05
INTERACTI PHARMACOGEN
ETIC
ONS
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Structure

WHAT IS
SIMVASTATIN?
Simvastatin is a group of drugs called
HMG CoA reductase inhibitors or
statins. Simvastatin is used to lower
cholesterol levels and is used to lower
the risk of stroke, heart attack, and other
heart complications. This drug is
lipophilic (Drugs.com & Ramsey, Laura https://pubchem.ncbi.nlm.nih.gov
B., et al, 2014).
PHARMACOKINETIC & PHARMACODINAMIC
BIOGRAPHY

1. Onset of action : >3 days

2. Peak effect : 2 weeks
3. Absorption : 85%
4. Protein binding :~95%
5. Metabolism : Hepatic via CYP3A4; extensive first-pass effect
6. Bioavailability : <5%
7. Half-life elimination: Unknown
8. Time to peak : 1.3-2.4 hours
9. Excretion : Feces (60%); urine (13%)
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DOSSAGE

ADULT PEDIATRIC GERIATRIC

 DOSSAGE ADULT
 Homozygous familial hypercholesterolemia: Oral: 40 mg
once daily in the evening or 80 mg/day.
 Prevention of cardiovascular events, hyperlipidemias:
Oral: 20-40 mg once daily in the evening; range: 5-80
mg/day
 Patients requiring only moderate reduction of LDL-
cholesterol: May be started at 10 mg once daily
 Patients requiring reduction of >45% in low-density
lipoprotein (LDL) cholesterol: May be started at 40 mg
once daily in the evening
 Patients with CHD or at high risk for CHD: Dosing should
be started at 40 mg once daily in the evening; simvastatin
should be started simultaneously with diet therapy

(DIH ed17, 2009 & Micromedex)

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DOSSAGE PEDIATRIC & GERIATRIC

PEDIATRIC
10 to 17 years: Initial, 10 mg
GERIATRIC
orally once in the evening; Administration Oral: Initial:
dose range, 10 to 40 mg daily; Maximum reductions in LDL-
cholesterol may be achieved with
MAX, 40 mg/day. Adjust at 4-
daily dose 20 mg
week or greater intervals to
meet goals of therapy (Medscape.com, DIH ed17,2009 &
Micromedex)
(Medscape.com & DIH ed17, 2009)
DOSE ADJUSTMENTS
AHA, 2016 INTERACTIONS
 PHARMACOGENETIC
SLCO1B1 (OATP1B1) CC genotype significantly increases AUCs
of parent drug and metabolites compared with the CT or TT genotypes This
polymorphism is proposed to reduce transport into the liver, the main site of
statin metabolism and elimination, resulting in elevated plasma
concentrations SLCO1B1 polymorphism is thought to have a lesser effect on
the more hydrophilic statins (eg, rosuvastatin, fluvastatin) compared with
those that are more lipophilic (eg, atorvastatin, simvastatin) Other genetic
polymorphisms of elimination (eg, CYP450, P-glycoprotein) for each
individual drug must also be considered, to explain variability for statin
clearance among patients that exhibit SCLO1B1 polymorphism SLCO1B1
CC genotype is most common in Caucasians and Asians (15%) Risk of
myopathy is 2.6- to 4.3-fold higher if the C allele is present and 16.9-fold
higher in CC homozygotes than in TT homozygotes.

(Postmus, Iris, et al, 2012, Ramsey, Laura B., et al, 2014 &
Medscape.com)
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