FUCIDIN H CREAM

Product Information

Registration Status: Active

FUCIDIN H CREAM is approved to be sold in Singapore with effective from 1999-03-24. It is marketed by LEO PHARMA ASIA PTE LTD, with the registration number of SIN10834P.

This product contains Fusidic Acid 20mg/g, and Hydrocortisone 10mg/g in the form of CREAM. It is approved for TOPICAL use.

This product is manufactured by LEO Laboratories LTD 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.

Fusidic Acid
Hydrocortisone

Description

An antibiotic isolated from the fermentation broth of Fusidium coccineum. (From Merck Index, 11th ed) It acts by inhibiting translocation during protein synthesis.

Indication

For the treatment of bacterial infections.

Mechanism of Action

Fusidic acid works by interfering with bacterial protein synthesis, specifically by preventing the translocation of the elongation factor G (EF-G) from the ribosome. It also can inhibit chloramphenicol acetyltransferase enzymes.

Pharmacokinetics

Absorption
Sodium fusidic acid tablets have a 91% oral bioavailability. Absorption of the film-coated tablets is complete when compared to a solution, however oral absorption is variable. Oral fusidic acid hemihydrate (suspension) achieved a 22.5% bioavailability in pediatric patients following a 20 milligram/kilogram dose.
Distribution
Metabolism
Metabolites include dicarboxylic ester/acid, 3-keto fusidic acid, hydroxy fusidic acid, glucuronide fusidic acid and a glycol metabolite.
Elimination

Active Ingredient/Synonyms

Fucidate | Fucidin acid | Fusidate | Fusidic acid | Fusidine | Ramycin | Fusidic Acid |


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

The main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. [PubChem]

Indication

For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.

Mechanism of Action

Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

Pharmacokinetics

Absorption
Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption.
Distribution
Metabolism
Primarily hepatic via CYP3A4
Elimination

Toxicity

Side effects include inhibition of bone formation, suppression of calcium absorption and delayed wound healing

Active Ingredient/Synonyms

(11alpha,14beta)-11,17,21-trihydroxypregn-4-ene-3,20-dione | (11beta)-11,17,21-Trihydroxypregn-4-ene-3,20-dione | 11beta-hydrocortisone | 11beta,17alpha,21-Trihydroxy-4-pregnene-3,20-dione | 11β-hydrocortisone | 17-Hydroxycorticosterone | 4-Pregnen-11beta,17alpha,21-triol-3,20-dione | Cortisol | Hidrocortisona | Hydrocortisone | Hydrocortisonum | Kendall's compound F | Reichstein's substance M | Hydrocortisone |


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.

References

  1. Health Science Authority of Singapore - Reclassified POM
  2. Drugbank