Desogestrel

Desogestrel is a Contraceptive belonging to the pharmacology class of Progestins..

Desogestrel can be used in the treatment of prevention of pregnancy

Desogestrel is rapidly absorbed from the gastrointestinal tract with absolute bioavailability of 70% and enters breast milk (as etonogestrel). Plasma protein binding: 95-99% (as etonogestrel), mainly to albumin and to a lesser extent to sex hormone binding globulin which gets metabolised in the liver and the intestinal mucosa via hydroxylation and dehydrogenation into its active metabolite, etonogestrel (3-keto-desogestrel); undergoes further metabolism via sulfate and glucuronide conjugation and get excreted via urine and faeces (as free steroid hormone or as conjugates) with approx 30 hours (as etonogestrel).

The common side effects of Desogestrel includes: Bleeding pattern alterations (e.g. spotting, irregular bleeding, heavy bleeding, oligomenorrhoea, amenorrhoea), ectopic pregnancy, thromboembolism, hypertension, depression, breast cancer; implant or IUD expulsion, Carbohydrate intolerance, chloasma .

Desogestrel is available in the form of Tablets

The molecule is available in India, Japan, Germany, China.

Oral:

Desogestrel is believed to act as an emergency contraceptive principally by preventing ovulation or fertilization (by altering tubal transport of sperm and/or ova). In addition, it may inhibit implantation (by altering the endometrium). It is not effective once the process of implantation has begun.

Desogestrel is approved for use in the following clinical indications:

Prevention of pregnancy: Prevention of pregnancy following unprotected intercourse or possible contraceptive failure.

Prevention of pregnancy:

Oral: One 1.5 mg tablet as soon as possible within 72 hours of unprotected sexual intercourse or known or suspected contraceptive failure.

Tablets

Desogestrel may be contraindicated in the following conditions:-

• Known or suspected sex-steroid sensitive malignancies.
• Undiagnosed vaginal bleeding.
• Active venous thromboembolic disorder.
• Acute porphyria.
• Severe hepatic impairment (active or history).

The adverse reactions related to Desogestrel can be categorized as

Common Adverse effects:

Breakthrough bleeding, venous thromboembolism (e.g. DVT, pulmonary embolism), hypertension, SLE, porphyria, chloasma; depressed mood and depression of endometriosis

Less Common Adverse effects:

Contact lens intolerance, Nausea, vomiting.

Rare Adverse effects:

Ectopic pregnancy, Breast pain, irregular menstruation, amenorrhea, dysmenorrhea, ovarian cyst, decreased libido.

The clinically relevant drug interactions of Desogestrel is briefly summarized here:

Decreased contraceptive efficacy with enzyme inducers (e.g. barbiturates, bosentan, carbamazepine, phenytoin, primidone, rifampicin, efavirenz, felbamate, griseofulvin, oxcarbazepine, topiramate, and rifabutin).

May increase the plasma concentrations with CYP3A4 inhibitors (e.g. ketoconazole, erythromycin, diltiazem).

May increase or decrease the plasma concentrations with HIV protease inhibitors (e.g. ritonavir), agents for hepatitis C virus (e.g. boceprevir), and non-nucleoside reverse transcriptase inhibitors (e.g. nevirapine).

May increase the plasma and tissue levels of ciclosporin.

May decrease the plasma and tissue levels of lamotrigine.

The most common side effects of Desogestrel includes: Bleeding pattern alterations (e.g. spotting, irregular bleeding, heavy bleeding, oligomenorrhoea, amenorrhoea), ectopic pregnancy, thromboembolism, hypertension, depression, breast cancer; implant or IUD expulsion, Carbohydrate intolerance, chloasma.

Symptoms: Nausea, vomiting, and slight vaginal bleeding in young women.

Pharmacodynamics:

Desogestrel is a progestogen structurally related to Desogestrel. It inhibits ovulation and increases the viscosity of cervical mucous to produce its contraceptive effect.

Pharmacokinetics:

Absorption: Rapidly absorbed from the gastrointestinal tract. Absolute bioavailability: 70%. Time to peak plasma concentration: Approx 1-2 hours.

Distribution: Enters breast milk (as etonogestrel). Plasma protein binding: 95-99% (as etonogestrel), mainly to albumin and to a lesser extent to sex hormone binding globulin.

Metabolism: Metabolized in the liver and the intestinal mucosa via hydroxylation and dehydrogenation into its active metabolite, etonogestrel (3-keto-desogestrel); undergoes further metabolism via sulfate and glucuronide conjugation.

Excretion: Via urine and faeces (as free steroid hormone or as conjugates). Elimination half-life: Approx 30 hours (as etonogestrel).

1. https://www.uptodate.com/contents/ Desogestrel -drug-information?search= Desogestrel &source=panel_search_result&selectedTitle=1~148&usage_type=panel&kp_tab=drug_general&display_rank=1#F154338
2. https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/022352s017lbl.pdf
3. https://www.medicaid.nv.gov/Downloads/provider/ Desogestrel _2015-1215.pdf
4. https://www.mims.com/india/drug/info/ Desogestrel ?type=full&mtype=generic#mechanism-of-action