|Systematic (IUPAC) name|
|Half-life||5.2 ± 1.7 (range 0.4 to 5.5) minutes|
|(what is this?)|
Amodiaquine has been shown to be more effective than chloroquine in treating chloroquine-resistant Plasmodium falciparum malaria infections and may afford more protection than chloroquine when used as weekly prophylaxis. Amodiaquine, like chloroquine, is generally well tolerated. Although licensed, this drug is not marketed in the United States, but is widely available in Africa. Its use, therefore, is probably more practicable in long-term visitors and persons who will reside in Africa.
Amodiaquine is a histamine N-methyltransferase inhibitor.
It is on the World Health Organization's List of Essential Medicines, the most important medications needed in a basic health system.
It is bioactivated hepatically to its primary metabolite, N-desethylamodiaquine, by the cytochrome p450 enzyme CYP2C8. Among amodiaquine users, several rare but serious side effects have been reported and linked to variants in the CYP2C8 alleles. CYP2C8*1 is characterized as the wild-type allele, which shows an acceptable safety profile, while CYP2C8*2, *3 and *4 all show a range of “poor metabolizer” phenotypes. People who are poor metabolizers of amodiaquine display lower treatment efficacy against malaria, as well as increased toxicity. Several studies have been conducted to determine the prevalence of CYP2C8 alleles amongst malaria patients in East Africa, and have tentatively shown the variant alleles have significant prevalence in that population. About 3.6% of the population studied showed high risk for a poor reaction to or reduced treatment outcomes when treated with amodiaquine. This information is useful in developing programs of pharmacovigilance in East Africa, and have important clinical considerations for prescribing antimalarial medications in regions with high CYP2C8 variant frequency.
Recent research suggests that amodiaquine targets malignant melanoma cells through induction of autophagic-lysosomal and proliferative blockade sensitizing cancer cells to starvation- and chemotherapy-induced cell death.
- CDC recommendations for travel to areas with malaria
- "WHO Model List of EssentialMedicines". World Health Organization. October 2013. Retrieved 22 April 2014.
- Kerb, Reinhold; Fux; Morike; Kremsner; Gil; Gleiter; Schwab (2009). "Pharmacogenetics of antimalarial drugs: effect on metabolism and transport". Lancet Infectious Disease 9 (12): 760–774. doi:10.1016/S1473-3099(09)70320-2.
- Elyazar, Iqbal; Hay, Baird (April 2011). "Malaria Distribution, Prevalence, Drug Resistance, and control in Indonesia". Advanced Parasitology. Advances in Parasitology 74 (74): 41–175. doi:10.1016/B978-0-12-385897-9.00002-1. ISBN 9780123858979.
- Roederer, Mary; Mcleod, Juliano (2011). "Can pharmacogenetics improve malaria". Bulletin of World Health Organization 89 (11): 838–845. doi:10.2471/BLT.11.087320.
- Qiao, S.; Tao, S.; Rojo De La Vega, M.; Park, S. L.; Vonderfecht, A. A.; Jacobs, S. L.; Zhang, D. D.; Wondrak, G. T.; Rojo de la Vega M (2013). "The antimalarial amodiaquine causes autophagic-lysosomal and proliferative blockade sensitizing human melanoma cells to starvation- and chemotherapy-induced cell death". Autophagy 9 (12): 2087–2102. doi:10.4161/auto.26506. PMID 24113242.