Product Information
Registration Status: ActiveSIN12607P
TRI-LUMA CREAM is approved to be sold in Singapore with effective from 2004-10-19. It is marketed by GALDERMA SINGAPORE PTE LTD, with the registration number of SIN12607P.
This product contains Fluocinolone Acetonide 0.1mg/g,Hydroquinone 40mg/g, and Tretinoin 0.5mg/g in the form of CREAM. It is approved for TOPICAL use.
This product is manufactured by HILL DERMACEUTICALS in UNITED STATES, and INC. in CANADA.
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
A glucocorticoid derivative used topically in the treatment of various skin disorders. It is usually employed as a cream, gel, lotion, or ointment. It has also been used topically in the treatment of inflammatory eye, ear, and nose disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p732). It is also being investigated by Sivida and Alimera, under the brand name Medidur, as a sustained release intraocular implant for the treatment of diabetic macular edema.
Indication
For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also for the treatment of chronic non-infectious uveitis affecting the posterior segment of the eye (Retisert).
Mechanism of Action
Fluocinolone Acetonide is a corticosteroid that 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. Cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In another 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. Like other glucocorticoid agents Fluocinolone acetonide acts as a physiological antagonist to insulin by decreasing glycogenesis (formation of glycogen). It also promotes the breakdown of lipids (lipolysis), and proteins, leading to the mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating glucose concentrations (in the blood). There is also decreased glycogen formation in the liver.
Pharmacokinetics
- Absorption
- Rapidly absorbed (15 minutes)
- Distribution
- Metabolism
- Primarily hepatic, corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys.
- Elimination
Active Ingredient/Synonyms
6alpha-fluorotriamcinolone acetonide | 6alpha,9alpha-difluoro-16alpha-hydroxyprednisolone 16,17-acetonide | 6α-fluorotriamcinolone acetonide | 6α,9α-difluoro-16α-hydroxyprednisolone 16,17-acetonide | acétonide de fluocinolone | acetónido de fluocinolona | fluocinolon acetonid | fluocinolone 16,17-acetonide | fluocinoloni acetonidum | Fluocinolone Acetonide |
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
Monobenzone is the monobenzyl ether of hydroquinone used medically for depigmentation. Monobenzone occurs as a white, almost tasteless crystalline powder, soluble in alcohol and practically insoluble in water. The topical application of monobenzone in animals increases the excretion of melanin from the melanocytes. The same action is thought to be responsible for the depigmenting effect of the drug in humans. Monobenzone may cause destruction of melanocytes and permanent depigmentation.
Indication
Used topically to treat the loss of skin color (vitiligo).
Mechanism of Action
Monobenzone is a depigmenting agent whose mechanism of action is not fully understood. The topical application of monobenzone in animals, increases the excretion of melanin from the melanocytes. The same action is thought to be responsible for the depigmenting effect of the drug in humans. Monobenzone may cause destruction of melanocytes and permanent depigmentation. This effect is erratic and may take one to four months to occur while existing melanin is lost with normal sloughing of the stratum corneum. Hyperpigmented skin appears to fade more rapidly than does normal skin, and exposure to sunlight reduces the depigmenting effect of the drug. The histology of the skin after depigmentation with topical monobenzone is the same as that seen in vitiligo; the epidermis is normal except for the absence of identifiable melanocytes.
Active Ingredient/Synonyms
4-(Benzyloxy)phenol | 4-(Benzyloxyl)phenol | 4-(Phenylmethoxy)phenol | 4-Benzyloxy-phenol | 4-Benzyloxyphenol | Benzyl p-hydroxyphenyl ether | Hydrochinon monobenzylether | Hydroquinone benzyl ether | Hydroquinone monobenzyl ether | Monobenzona | Monobenzone | Monobenzonum | MONOBENZYL ether OF hydroquinone | Monobenzyl hydroquinone | p-(Benzyloxy)phenol | p-Hydroxyphenyl benzyl ether | Monobenzone |
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
Tretinoin, also known as all-trans-retinoic acid (ATRA), is a naturally occurring derivative of vitamin A (retinol). Retinoids such as tretinoin are important regulators of cell reproduction, proliferation, and differentiation and are used to treat acne and photodamaged skin and to manage keratinization disorders such as ichthyosis and keratosis follicularis. Tretinoin also represents the class of anticancer drugs called differentiating agents and is used in the treatment of acute promyelocytic leukemia (APL).
Indication
For the the induction of remission in patients with acute promyelocytic leukemia (APL), French-American-British (FAB) classification M3 (including the M3 variant); For the topical treatment of acne vulgaris, flat warts and other skin conditions (psoriasis, ichthyosis congenita, icthyosis vulgaris, lamellar icthyosis, keratosis palmaris et plantaris, epidermolytic hyperkeratosis, senile comedones, senile keratosis, keratosis follicularis (Darier's disease), and basal cell carcinomas.); For palliative therapy to improve fine wrinkling, mottled hyperpigmentation, roughness associated with photodamage.
Mechanism of Action
Tretinoin binds to alpha, beta, and gamma retinoic acid receptors (RARs). RAR-alpha and RAR-beta have been associated with the development of acute promyelocytic leukemia and squamous cell cancers, respectively. RAR-gamma is associated with retinoid effects on mucocutaneous tissues and bone. Although the exact mechanism of action of tretinoin is unknown, current evidence suggests that the effectiveness of tretinoin in acne is due primarily to its ability to modify abnormal follicular keratinization. Comedones form in follicles with an excess of keratinized epithelial cells. Tretinoin promotes detachment of cornified cells and the enhanced shedding of corneocytes from the follicle. By increasing the mitotic activity of follicular epithelia, tretinoin also increases the turnover rate of thin, loosely-adherent corneocytes. Through these actions, the comedo contents are extruded and the formation of the microcomedo, the precursor lesion of acne vulgaris, is reduced. Tretinoin is not a cytolytic agent but instead induces cytodifferentiation and decreased proliferation of APL cells in culture and in vivo. When Tretinoin is given systemically to APL patients, tretinoin treatment produces an initial maturation of the primitive promyelocytes derived from the leukemic clone, followed by a repopulation of the bone marrow and peripheral blood by normal, polyclonal hematopoietic cells in patients achieving complete remission (CR). The exact mechanism of action of tretinoin in APL is unknown.
Pharmacokinetics
- Absorption
- 1-31% (topical)
- Distribution
- Metabolism
- Hepatic
- Elimination
Active Ingredient/Synonyms
(all-e)-3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)-2,4,6,8-nonatetraenoic acid | 3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexene-1-yl)-2,4,6,8-nonatetraenoic acid (ecl) | Acide retinoique (french) (dsl) | AGN 100335 | All Trans Retinoic Acid | All Trans-Retinoic Acid | all-(e)-Retinoic acid | all-trans-beta-Retinoic acid | all-trans-Retinoic acid | all-trans-Tretinoin | all-trans-Vitamin a acid | all-trans-Vitamin a1 acid | ATRA | beta-Retinoic acid | Eudyna | RETINOIC acid | Retionic Acid | Ro 1-5488 | Stieva-a | trans-Retinoic acid | Tretin m | Tretinoin | Tretinoina | Trétinoïne | Tretinoine (french) (einecs) | Tretinoinum | Vitamin A acid | Tretinoin |
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.