Tafenoquine and primaquine do not exhibit clinical neurologic signs associated with central nervous system lesions in the same manner as earlier 8-aminoquinolines
- Malar J. 2018 Nov 6;17(1):407. doi: 10.1186/s12936-018-2555-3.
- 1. Fast-Track Drugs & Biologics, North Potomac, MD, 20878, USA.
- 2. Clinical Network Services Pty Ltd, 88/4 Jephson Road, Toowong, 4066, Queensland, Australia.
- 3. 60°Pharmaceuticals LLC, 1025 Connecticut Ave NW, Suite 1000, Washington, DC, 20036, USA. [email protected].
- 4. Pegasus Research, 4103, Bottmingen, Switzerland.
Background: Tafenoquine was recently approved for Plasmodium vivax radical cure (KRINTAFEL™) and malaria prevention (ARAKODA™).
Methods: A review of the non-clinical and clinical literature was conducted to assess whether tafenoquine (and primaquine) exhibit the same neurologic lesions and associated clinical signs as earlier 8-aminoquinolines, as has been alleged in recent opinion pieces.
Results: Plasmocid, pamaquine and pentaquine damage specific neuro-anatomical structures in Rhesus monkeys and humans leading to corresponding deficits in neurologic function. Neurologic therapeutic indices for these 3 drugs calculated based on monkey data were well correlated with human data. Despite 60 years of use, there is no evidence that primaquine exhibits similar neurotoxicity in humans.
Discussion/conclusions: Extrapolation of data from Rhesus monkeys to humans, and the available clinical data, suggest that tafenoquine also does not exhibit pamaquine, pentaquine or plasmocid-like clinical neurologic signs in humans.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Parasite