Product Information
Registration Status: ActiveSIN06136P
MERCILON TABLET is approved to be sold in Singapore with effective from 1991-06-19. It is marketed by MSD PHARMA (SINGAPORE) PTE LTD, with the registration number of SIN06136P.
This product contains Desogestrel 0.15mg, and Ethinylestradiol 0.02mg in the form of TABLET. It is approved for ORAL use.
This product is manufactured by N V ORGANON in IRELAND, andORGANON (IRELAND) LTD in NETHERLANDS.
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 synthetic progestational hormone used often as the progestogenic component of combined oral contraceptive agents. [PubChem]
Indication
For the prevention of pregnancy in women who elect to use this product as a method of contraception.
Mechanism of Action
Binds to the progesterone and estrogen receptors. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Once bound to the receptor, progestins like desogestrel will slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH (luteinizing hormone) surge.
Pharmacokinetics
- Absorption
- Following oral administration, the relative bioavailability of desogestrel, as measured by serum levels of etonogestrel, is approximately 84%. The absolute oral bioavailability is about 76%.
- Distribution
- Metabolism
- Desogestrel is rapidly and completely metabolized by hydroxylation in the intestinal mucosa and on first pass through the liver. It is primarily metabolized to 3α-hydroxydesogestrel with small amounts of 3β-hydroxydesogestrel being formed. Both of these metabolites are then rapidly oxidized to its active metabolite, etonogestrel (3-ketodesogestrel). Other metabolites (e.g. 2-hydroxydesogestrel) with no pharmacologic action have also been identified. Desogestrel and some of its metabolites (e.g. 3β-hydroxydesogestrel, 15β-hydroxydesogestrel) may also undergo glucuronide and sulfate conjugation. Early in vitro studies demonstrated that CYP2C9 and possibly CYP2C19 were involved in the conversion of desogestrel to 3α-hydroxydesogestrel and 3β-hydroxydesogestrel (PMID 9864282); however, later clinical studies conducted in humans refuted this result (PMID 15963096). The latter study indicates that CYP3A4 plays an important role in metabolizing etonogestrel. Thus, strong CYP3A4 inhibitors or inducers could result in increased side effects or therapeutic failure, respectively.
- Elimination
Toxicity
Symptoms of overdose include nausea and vaginal bleeding.
Active Ingredient/Synonyms
13-Ethyl-11-methylene-18,19-dinor-17alpha-pregn-4-en-20-yn-17-ol | Cerazette | Desogestrelum | Desogestrel |
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
A semisynthetic alkylated estradiol with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally and is often used as the estrogenic component in oral contraceptives. Ethinyl estradiol is marketed mostly as a combination oral contraceptive under several brand names such as Alesse, Tri-Cyclen, Triphasil, and Yasmin. The FDA label includes a black box warning that states that combination oral contraceptives should not be used in women over 35 years old who smoke due to the increased risk of serious cardiovascular side effects.
Indication
For treatment of moderate to severe vasomotor symptoms associated with the menopause, female hypogonadism, prostatic carcinoma-palliative therapy of advanced disease, breast cancer, as an oral contraceptive, and as emergency contraceptive.
Mechanism of Action
Estrogens diffuse into their target cells and interact with a protein receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. This cascade is initiated by initially binding to the estrogen receptors. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH).
Pharmacokinetics
- Absorption
- Rapid and complete absorption follows oral intake of ethinyl estradiol (bioavailability 43%).
- Distribution
- Metabolism
- Hepatic. Quantitatively, the major metabolic pathway for ethinyl estradiol, both in rats and in humans, is aromatic hydroxylation, as it is for the natural estrogens.
- Elimination
Toxicity
Oral, mouse LD50: 1737 mg/kg. Symptoms of overdose include nausea and vomiting, and withdrawal bleeding may occur in females. The FDA label includes a black box warning that states that combination oral contraceptives with ethinyl estradiol should not be used in women over 35 years old who smoke due to the increased risk of serious cardiovascular side effects.
Active Ingredient/Synonyms
17-ethinyl-3,17-estradiol | 17-ethinyl-3,17-oestradiol | 17-ethinylestradiol | 17alpha-Ethinyl estradiol | 17α-ethynylestradiol | Ethinylestradiol | Ethinylestradiolum | Ethinyloestradiol | Ethynyl estradiol | Etinilestradiol | Ethinyl Estradiol |
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.