(Amlodipine Besilate Tablets)
Vamlo Tablets 10mg
Each tablet contains Amlodipine Besilate equivalent to Amlodipine 10 mg
Vamlo Tablets 5mg
Each tablet contains Amlodipine Besilate equivalent to Amlodipine 5 mg
Vamlo Tablets 10 mg:
White to off white, flat, beveled edge, round uncoated tablets with a score-line on one side. Diameter 10.5mm
Vamlo Tablets 5 mg:
White to off white, flat, beveled edge, round uncoated tablets with a score-line on one side. Diameter 8.0mm
VAMLO (Amlodipine Besilate) is a Calcium channel blocker. It is chemically designated (R. S.) 3-ethyl-5-methyl-2-(2-aminoethoxymethyl)-4-(2-chlorophenyl)-1,4-dihydro-6-methyl-3,5-pyridinedicarboxylate benzenesulphonate. Its empirical formula is C20H25CIN2O5C6H6O3S
and its molecular weight is 567.1.
Amlodipine is a calcium ion influx inhibitor (slow channel-blocker or calcium ion antagonist) and inhibits the transmembrane influx of calcium
ions into the cardiac and vascular smooth muscle.
The mechanism of the antihypertensive action of amlodipine is due to a direct relaxant effect on the vascular smooth muscle. The precise
mechanism by which amlodipine relieves angina has not been fully determined, but amlodipine reduces the total ischemic burden by the
following 2 actions:
1) Amlodipine dilates the peripheral arterioles and thus, reduces the total peripheral resistance (afterload) against which the heart works. Since
the heart rate remains stable, this unloading of the heart reduces myocardial energy consumption and oxygen requirements.
2) The mechanism of action of amlodipine probably involves dilation of the main coronary arteries and coronary arterioles, both in normal and
This dilatation increases myocardial oxygen delivery in patients with coronary artery spasm (Prinzmetal's or variant angina) and blunt smoking-
induced coronary vasoconstriction.
In patients with hypertension, once-daily dosing provides clinically significant reductions of blood pressure in both the supine and standing
positions throughout the 24-hr interval. Due to the slow onset of action, acute hypotension is not a feature of amlodipine administration.
In patients with angina, once-daily administration of amlodipine increases total exercise time, time to angina onset, and time to 1 mm ST
segment depression and decreases both angina attack frequency and nitroglycerine tablet consumption.
Amlodipine has not been associated with any adverse metabolic effects or changes in plasma lipids and is suitable for use in patients with
asthma, diabetes and gout.
Pharmacokinetics studies with cyclosporin have demonstrated that amlodipine does not significantly alter the pharmacokinetics of cyclosporin.
Hemodynamic studies and a controlled clinical trial in NYHA Class II-IV heart failure patients have shown that amlodipine did not lead to clinical
deterioration as measured by exercise tolerance, left ventricular ejection fraction and clinical symptomatology.
After oral administration of therapeutic doses, amlodipine is well absorbed with peak blood levels between 6-12 hrs post-dose. Absolute
bioavailability has been estimated to be between 64 and 80%. The volume of distribution was approximately 21 L/kg. Absorption of amlodipine is
unaffected by consumption of food.
The terminal plasma elimination half-life is about 35-50 hrs and is consistent with once-daily dosing. Steady-state plasma levels are reached
after 7-8 days of consecutive dosing. Amlodipine is extensively metabolized to inactive metabolites with 10% of the parent compound and 60%
of metabolites excreted in the urine.
In vitro studies have shown that approximately 97.5% of circulating amlodipine is bound to plasma proteins.
First-line treatment of hypertension and as the sole agent to control blood pressure in the majority of patients. Patients not adequately controlled
on a single antihypertensive agent may benefit from the addition of Vamlo, which has been used successfully in combination with a thiazide
diuretic, beta-adrenoceptor-blocking agent or an angiotensin-converting enzyme inhibitor.
Vamlo is indicated for the 1st-line treatment of myocardial ischemia, whether due to fixed obstruction (stable angina) and/or
vasospasm/vasoconstriction / (Prinzmetal's or variant angina) of coronary vasculature. Vamlo may be used where the clinical presentation
suggests a possible vasospastic/vasoconstrictive component but where vasospasm/vasoconstriction has not been confirmed. Vamlo may be
used alone, as monotherapy or in combination with other antianginal drugs in patients with angina that is refractory to nitrates and/or adequate
doses of beta-blockers.