| Indication |
For the treatment of menopausal and postmenopausal disorders and
alone or in combination with other hormones as an oral contraceptive. |
| Pharmacodynamics |
Levonorgestrel is a progestin or a synthetic form of the
naturally occurring female sex hormone, progesterone. In a woman's
normal menstrual cycle, an egg matures and is released from the ovaries
(ovulation). The ovary then produces progesterone, preventing the
release of further eggs and priming the lining of the womb for a
possible pregnancy. If pregnancy occurs, progesterone levels in the body
remain high, maintaining the womb lining. If pregnancy does not occur,
progesterone levels in the body fall, resulting in a menstrual period.
Levonorgestrel tricks the body processes into thinking that ovulation
has already occurred, by maintaining high levels of the synthetic
progesterone. This prevents the release of eggs from the ovaries. |
| 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 levonorgestrel will slow the frequency of release of gonadotropin
releasing hormone (GnRH) from the hypothalamus and blunt the
pre-ovulatory LH (luteinizing hormone) surge. |
| Absorption |
Levonorgestrel is not subjected to a "first-pass" effect and is virtually 100% bioavailable. |
| Volume of distribution |
- 260 L [Healthy Female Volunteers under Fasting Conditions]
- 1.8 L/kg
|
| Protein binding |
55% |
| Metabolism |
Hepatic |
| Route of elimination |
About 45% of levonorgestrel and its metabolites are excreted in
the urine and about 32% are excreted in feces, mostly as glucuronide
conjugates. |
| Half life |
Not Available |
| Clearance |
- 7.7 +/- 2.7 L/h [Healthy Female Volunteers under Fasting Conditions]
|
| Toxicity |
LD50 >5000 mg/kg (orally in rats) |
