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Not as a general rule. Research suggests male-biased malaria parasite genes may evolve faster, raising a hypothesis that female parasite targets could be more evolutionarily durable in some contexts. But the key study concerned vaccine targets, not a clinical comparison of female-selective and male-selective drugs. Separate drug experiments found mature male gametocytes more vulnerable to the tested transmission-blocking compounds.
What the claim is based on
Khan, Reece, Waters, Janse and Kaczanowski compared genomic data across several Plasmodium species with proteomic data from parasite life-cycle stages. They found accelerated adaptive evolution in genes expressed mainly or exclusively in male parasites. The authors proposed that host immune pressures—including effects that can reduce gametocyte fertility, particularly male fertility—might help explain the pattern.
Their conclusion was about evolutionary vulnerability: they argued that vaccines targeting males could be more vulnerable to parasite evolution than vaccines targeting females or both sexes. The study did not test whether female-targeting drugs produce better outcomes in patients. Read the study.
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1Fix the driver behind crashes, sound loss and screen glitches2Repair Windows errors before they cause bigger problems3Scan for outdated or missing drivers - takes under a minuteWhy that does not settle which drugs should target
Evolutionary durability and drug susceptibility are different questions
A target can be less prone to evolutionary change yet still be harder to affect with a particular compound. Conversely, a parasite form can be highly susceptible to a drug without that result establishing that it is the most durable target over the long term. The evolutionary study and drug-response experiments examine different properties.
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The central evidence is about vaccines
The authors’ stated warning was specific: “Specifically, vaccines targeting males will be more vulnerable to parasite evolution than those targeting females or both sexes.” That conclusion does not demonstrate that a female-selective antimalarial would be superior in clinical use.
A University of Edinburgh summary broadened the implication to designing drugs and vaccines to target the slower-evolving female form. That is a researcher’s summary of the possible application, not clinical evidence that female-targeting drugs outperform other approaches. Read the University of Edinburgh summary.
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What drug-response experiments found
A 2013 experimental study of mature Plasmodium falciparum gametocytes reported different responses between the sexes. For the transmission-blocking drugs tested, mature male gametocytes were more vulnerable than female gametocytes. The authors therefore identified males as the more vulnerable target for those compounds and that parasite stage—not as a universal target for every antimalarial or for treating a patient’s blood-stage infection. Read the drug-response study.
This result does not contradict the finding about faster evolution in male-biased genes: susceptibility to tested drugs and the pace of adaptive evolution are not interchangeable measures. A 2024 review of transmission-blocking small-molecule development likewise describes activity across compounds and parasite stages, including selective and shared-sex effects, rather than a universal female-only strategy. Read the 2024 review.
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How to evaluate a proposed target
“Antimalarial” can refer to interventions acting at different points in the parasite’s life cycle. Male and female sexual forms both contribute to reproduction and transmission through mosquitoes; blocking that process is distinct from clearing disease-causing blood-stage parasites in a patient.
- Stage: Does the intervention act on asexual blood stages, gametocytes, gametes, or parasites in the mosquito?
- Sex activity: Does it affect males, females, or both—and at what stage?
- Outcome: Does the evidence show an effect on a patient’s infection, interruption of onward transmission, or both?
- Evidence model: Is the result from an in-vitro assay, an animal model, or clinical evidence?
- Evolution: Does the work measure resistance or evolutionary vulnerability, rather than infer it from sex-specific gene patterns?
Results should be compared on the same axes. A compound’s effect on mature gametocytes in a laboratory assay cannot by itself establish clinical benefit or long-term evolutionary durability.
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What readers should take away
The evidence supports a focused hypothesis: some female parasite targets may be less evolutionarily vulnerable in some contexts, particularly the vaccine-target question examined by Khan and colleagues. It does not establish that antimalarial drugs should generally target female parasites. Drug activity varies by compound and parasite stage, and the tested transmission-blocking drugs in one study favored mature male gametocytes as a more vulnerable target.
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