Buy Aerocort Inhaler (Levalbuterol with Beclomethasone Dipropionate) online

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Cheap Levalbuterol/Levosalbutamol and Beclomethasone 50 mcg + 50 mcg / dose




A population pharmacokinetics (PPK) model was developed using plasma concentrations of (R)-salbutamol obtained from 632 asthmatic patients, aged 4 to 81 years, in three large trials. There is PPK model-derived pharmacokinetic parameters for (R)-salbutamol in paediatric and adolescent / adult patients receiving a 90 mcg dose of inhaled levosalbutamol or a 180 mcg dose of inhaled racemic salbutamol. These pharmacokinetic data indicate that mean exposure to (R)-salbutamol was 1316% less in adult and 3032% less in paediatric patients given inhaled levosalbutamol as compared to those given a comparable dose of racemic salbutamol. When compared to adult patients, paediatric patients given 90 mcg of levosalbutamol had a 17% lower mean exposure to (R)-salbutamol.

Metabolism and Elimination

Information available in published literature suggests that the primary enzyme responsible for the metabolism of salbutamol enantiomers in humans is sulphotranferase 1A3 (SULT1A3). When racemic salbutamol was administered either intravenously or via inhalation after oral charcoal administration, there was a 3- to 4-fold difference in the area under the concentration time curves (AUC) between the (R)- and (S)-salbutamol enantiomers, with (S)-salbutamol concentrations being consistently higher. However, after either inhalation or oral administration without charcoal pre-treatment, the differences were 8 to 24-fold, suggesting that (R)-salbutamol is preferentially metabolized in the gastrointestinal tract, presumably by SULT1A3.

The primary route of elimination of salbutamol enantiomers is through renal excretion (80100%) of either the parent compound or the primary metabolite. Less than 20% of the drug is detected in the faeces. Following intravenous administration of racemic salbutamol, between 2546% of the (R)-salbutamol fraction of the dose was excreted as unchanged (R)-salbutamol in the urine.

Beclomethasone Dipropionate:


When administered via inhalation (via metered dose inhaler), systemic absorption of unchanged beclomethasone dipropionate (BDP) occurs through the lungs with negligible oral absorption of the swallowed dose. There is extensive conversion of BDP to its active metabolite B-17-MP within the lung prior to absorption. The systemic absorption of B-17-MP arises from both lung deposition and oral absorption of the swallowed dose. The absolute bioavailability following inhalation is approximately 60% of the nominal dose for B-17-MP. BDP is absorbed rapidly with peak plasma concentrations first being observed (Tmax) at 0.3h. B-17-MP appears more slowly with a Tmax of 1 h. There is an approximately linear increase in systemic exposure with increasing inhaled dose. When administered orally the bioavailability of BDP is negligible but pre-systemic conversion to B-17-MP results in approximately 40% of the dose being absorbed as B-17-MP.


The tissue distribution at steady state for beclomethasone dipropionate is moderate (20L), but more extensive for B-17-MP (424L). Plasma protein binding is moderately high (87%).


It is cleared very rapidly from the systemic circulation, owing to extensive first-pass metabolism. The main product of metabolism is the active metabolite (B-17-MP). Minor inactive metabolites, beclomethasone-21-monopropionate (B-21-MP) and beclomethasone (BOH) are also formed, but these contribute little to systemic exposure.


The elimination of beclomethasone dipropionate and B-17-MP are characterized by high plasma clearance (150 and 120 L/h), with corresponding terminal elimination half-lives of 0.5 hours and 2.7 hours. Following oral administration of titrated beclomethasone dipropionate, approximately 60% of the dose was excreted in the faeces within 96 hours, mainly as free and conjugated polar metabolites. Approximately 12% of the dose was excreted as free and conjugated polar metabolites in the urine.

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