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  • In general: ℞ (Prescription only)
Pharmacokinetic data
Elimination half-lifeAbout 4-11 hours
ExcretionMainly Bile
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E number{{#property:P628}}
ECHA InfoCard{{#property:P2566}}Lua error in Module:EditAtWikidata at line 36: attempt to index field 'wikibase' (a nil value).
Chemical and physical data
Molar mass284.35 g/mol
3D model (JSmol)
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Dihydroartemisinin (also known as dihydroqinghaosu, artenimol or DHA) is a drug used to treat malaria. Dihydroartemisinin is the active metabolite of all artemisinin compounds (artemisinin, artesunate, artemether, etc.) and is also available as a drug in itself. It is a semi-synthetic derivative of artemisinin and is widely used as an intermediate in the preparation of other artemisinin-derived antimalarial drugs.[1] It is sold commercially in combination with piperaquine and has been shown to be equivalent to artemether/lumefantrine.[2]


The lactone of artemisinin could selectively be reduced with mild hydride-reducing agents, such as sodium borohydride, potassium borohydride, and lithium borohydride to dihydroartemisinin (a lactol) in over 90% yield. It is a novel reduction, because normally lactone cannot be reduced with sodium borohydride under the same reaction conditions (0-5 ˚C in methanol). Reduction with LiAlH4 leads to some rearranged products. It was surprising to find that the lactone was reduced, but that the peroxy group survived. However, the lactone of deoxyartemisinin resisted reduction with sodium borohydride and could only be reduced with diisobutylaluminium hydride to the lactol deoxydihydroartimisinin. These results show that the peroxy group assists the reduction of lactone with sodium borohydride to a lactol, but not to the alcohol which is the over-reduction product. No clear evidence for this reduction process exists.[citation needed]


Dihydroartemisinin is available as a fixed drug combination with piperaquine (each tablet contains 40 mg of dihydroartemisinin and 320 mg of piperaquine).

The adult dose is 1.6/12.8 mg/kg per dose (rounded up or down to the nearest half tablet) given at 0 h, 8 h, 24 h, and 48 h. Alternatively, the same total dose may be given once daily for three days.[3]

Antimalarial activity

In a systematic review of randomized controlled trials, both dihydroartemisinin-piperaquine and artemether-lumefantrine are very effective at treating malaria (high quality evidence). However, dihydroartemisinin-piperaquine cures slightly more patients than artemether-lumefantrine, and it also prevents further malaria infections for longer after treatment (high quality evidence). Dihydroartemisinin-piperaquine and artemether-lumefantrine probably have similar side effects (moderate quality evidence). The studies were all conducted in Africa. In studies of people living in Asia, dihydroartemisinin-piperaquine is as effective as artesunate plus mefloquine at treating malaria (moderate quality evidence). Artesunate plus mefloquine probably causes more nausea, vomiting, dizziness, sleeplessness, and palpitations than dihydroartemisinin-piperaquine (moderate quality evidence).[4]

Activity as experimental cancer chemotherapeutic

Accumulative research suggests that dihydroartemisinin and other artemisinin-based endoperoxide compounds may display activity as experimental cancer chemotherapeutics.[5] Recent pharmacological evidence demonstrates that dihydroartemisinin targets human metastatic melanoma cells with induction of NOXA-dependent mitochondrial apoptosis that occurs downstream of iron-dependent generation of cytotoxic oxidative stress.[6]

Commercial preparations

In combination with piperaquine:

  • Artekin (Holleykin)
  • Diphos ( Genix Pharma)
  • TimeQuin ( Sami Pharma )
  • Eurartesim (Sigma Tau; by Good Manufacturing Practices)
  • Duocotecxin (Holley Pharm)

Alone (not recommended by WHO due to risk of resistance development):

  • Cotecxin (Zhejiang Holley Nanhu Pharmaceutical Co.)


  1. Woo, Soon Hyung; Parker, Michael H.; Ploypradith, Poonsakdi; Northrop, John; Posner, Gary H. (1998). "Direct conversion of pyranose anomeric OH→F→R in the artemisinin family of antimalarial trioxanes". Tetrahedron Letters. 39 (12): 1533–6. doi:10.1016/S0040-4039(98)00132-4.
  2. Arinaitwe, Emmanuel; Sandison, Taylor G.; Wanzira, Humphrey; Kakuru, Abel; Homsy, Jaco; Kalamya, Julius; Kamya, Moses R.; Vora, Neil; et al. (2009). "Artemether‐Lumefantrine versus Dihydroartemisinin‐Piperaquine for Falciparum Malaria: A Longitudinal, Randomized Trial in Young Ugandan Children". Clinical Infectious Diseases. 49 (11): 1629–37. doi:10.1086/647946. PMID 19877969.
  3. Ashley, E. A.; McGready, R.; Hutagalung, R.; Phaiphun, L.; Slight, T.; Proux, S.; Thwai, K. L.; Barends, M.; et al. (2005). "A Randomized, Controlled Study of a Simple, Once-Daily Regimen of Dihydroartemisinin-Piperaquine for the Treatment of Uncomplicated, Multidrug-Resistant Falciparum Malaria". Clinical Infectious Diseases. 41 (4): 425–32. doi:10.1086/432011. PMID 16028147.
  4. Zani, B; Gathu, M; Donegan, S; Olliaro, PL; Sinclair, D (Jan 20, 2014). "Dihydroartemisinin-piperaquine for treating uncomplicated Plasmodium falciparum malaria". The Cochrane database of systematic reviews. 1: CD010927. doi:10.1002/14651858.CD010927. PMID 24443033.
  5. Efferth, Thomas (2006). "Molecular Pharmacology and Pharmacogenomics of Artemisinin and its Derivatives in Cancer Cells". Current Drug Targets. 7 (4): 407–21. doi:10.2174/138945006776359412. PMID 16611029.
  6. Cabello, Christopher M.; Lamore, Sarah D.; Bair, Warner B.; Qiao, Shuxi; Azimian, Sara; Lesson, Jessica L.; Wondrak, Georg T. (2011). "The redox antimalarial dihydroartemisinin targets human metastatic melanoma cells but not primary melanocytes with induction of NOXA-dependent apoptosis". Investigational New Drugs. 30 (4): 1289–301. doi:10.1007/s10637-011-9676-7. PMC 3203350. PMID 21547369.