Molecular target
Plasmodium Heme Polymerization
Antimalarial mechanism — parasite digests host hemoglobin, releasing toxic free heme, which is normally polymerized into inert hemozoin. Chloroquine and hydroxychloroquine inhibit this polymerization, killing the parasite via heme toxicity. Artemisinin acts via a complementary heme-iron radical mechanism.
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Pharmaceutical agents
Drugs that act on Plasmodium Heme Polymerization
These medications have Plasmodium Heme Polymerization among their molecular targets. Sharing a target is a mechanistic relationship — it does not make any plant below an alternative to, or substitute for, these drugs.
Botanical connections
Plants whose compounds act on Plasmodium Heme Polymerization
Each plant below contains a named compound documented to act on Plasmodium Heme Polymerization. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- QuinineCinchona alkaloid (quinoline)
Foundational antimalarial. Disrupts Plasmodium heme polymerization. Same compound as the prescription drug Qualaquin — pharmaceutical-grade quinine has standardized dosing while raw cinchona bark does not. QT prolongation, thrombocytopenia, hemolytic anemia (especially G6PD deficiency) are class concerns.
- QuinidineCinchona alkaloid (quinoline, stereoisomer)
Diastereomer of quinine with cardiac sodium-channel blocking activity — basis for quinidine's separate use as a Class IA antiarrhythmic. The same plant gave the pharmacopoeia TWO distinct prescription drugs from stereoisomers.
- Cinchonidine, cinchonineCinchona alkaloid
Auxiliary cinchona alkaloids with reduced antimalarial potency vs quinine.
- QuinineQuinoline alkaloid
Research reports accumulation in the Plasmodium falciparum digestive vacuole where it is investigated as an inhibitor of haem polymerisation (haemozoin formation), disrupting parasite detoxification. Also investigated for membrane-stabilising and sodium-channel effects contributing to antispasmodic properties. Stereochemical configuration at C-9 (erythro orientation) reported to be critical for antiplasmodial potency.
- QuinidineQuinoline alkaloid (stereoisomer of quinine)
Shares the antiplasmodial haem polymerisation inhibition mechanism with quinine. As a pharmaceutical agent, quinidine is classified as a class Ia antiarrhythmic: studies describe blockade of voltage-gated sodium channels (prolonging action potential), L-type calcium channel antagonism, and α1-adrenergic blocking activity. These cardiac effects are relevant to drug interaction risk.
- CinchonineQuinoline alkaloid
Included in the combination alkaloid preparation studied by Sowunmi et al. (1990). Shares the quinoline scaffold and is investigated for antiplasmodial activity via haem polymerisation inhibition, though reported to have lower potency than quinine or quinidine.
- LapacholNaphthoquinone
Research has investigated antimalarial activity via interference with Plasmodium heme polymerization, and in vitro cytotoxic activity ([1], [2], [3]).
- BerberineProtoberberine alkaloid
Berberine has been studied for inhibition of Plasmodium heme polymerization and broad anti-infective activity in preclinical models. Biosynthesis of berberine in A. mexicana via CYP719A13/CYP719A14 enzymes is characterized by Díaz Chávez et al. (2011).