Product Information
Registration Status: ActiveSIN10834P
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.
Product Reference
Important Note: For generic product, the SPC/PIL provided may not be brand specific.
{{/items}} {{^items}}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.