A study administering ganirelix to healthy adult females (n=15) found the mean (SD) elimination half-life (t1/2) to be 16.2(1.6) hours, volume of distribution/absolute bioavailability (Vd/F) 76.5(10.3) liters, maximum serum concentration (Cmax) 11.2(2.4) ng/mL, and the time until maximum concentration (tmax) 1.1(0.2) hours. One 250 µg injection of ganirelix resulted in a mean absolute bioavailability of 91.1%. Chemistry
Ganirelix is derived from GnRH, with amino acid substitutions made at positions 1, 2, 3, 6, 8, and 10. History
The European Commission gave marketing authorization for ganirelix throughout the European Union to N.V. Organon in May 2000. See also
Gonadotropin-releasing hormone receptor § Antagonists

References
External links
"Ganirelix". Drug Information Portal. U.S. National Library of Medicine. "Ganirelix acetate". Drug Information Portal. U.S. National Library of Medicine.
Genetic counseling, prenatal testing, and preimplantation genetic diagnosis is available.In females, the cells expressing the mutated IKBKG gene due to lyonization selectively die around the time of birth, so the X-inactivation is extremely skewed.IP is caused by mutations in a gene called NEMO (NF-κB essential modulator). Diagnosis
The diagnosis of IP is established by clinical findings and occasionally by corroborative skin biopsy. Molecular genetic testing of the NEMO IKBKG gene (chromosomal locus Xq28) reveals disease-causing mutations in about 80% of probands. Such testing is available clinically. In addition, females with IP have skewed X-chromosome inactivation; testing for this can be used to support the diagnosis. Many people in the past were misdiagnosed with a second type of IP, formerly known as IP1. This has now been given its own name: Hypomelanosis of Ito (incontinentia pigmenti achromians). This has a slightly different presentation: swirls or streaks of hypopigmentation and depigmentation. It is not inherited and does not involve skin stages 1 or 2. Some 33–50% of patients have multisystem involvement—eye, skeletal, and neurological abnormalities. Its chromosomal locus is at Xp11, rather than Xq28. Treatment
There does not yet exist a specific treatment for IP. Treatment can only address the individual symptoms. History
This disorder was first reported by Swiss dermatologist Bruno Bloch in 1926 and American dermatologist Marion Sulzberger in 1928. See also
List of cutaneous conditions
List of radiographic findings associated with cutaneous conditions
List of dental abnormalities associated with cutaneous conditions

References
External links
GeneReview/NIH/UW entry on Incontinentia Pigmenti