The drug praziquantel (PZQ), discovered in the 1970s, is an essential medication for combating diseases caused by parasitic flatworms. PZQ is the therapeutic mainstay for the treatment of schistosomiasis, a socioeconomically devastating infection caused by flatworms of the Schistosoma genus that afflicts ~260 million people worldwide. Overall, the disease burden of schistosomiasis encumbers LMIC economies with an annual loss of 70 million disability-adjusted life years. The WHO classifies PZQ as one of the 100 essential medications used worldwide, requiring over 50 million tablets globally for treatment every year.

Any decrease in the effectiveness of PZQ as a cheap, effective drug will prove a significant public health challenge.

Although PZQ has been used clinically for over 40 years, the mechanism of action has remained elusive. In 2019, the Marchant Laboratory identified a putative target for the drug, a transient receptor potential ion channel in the melastatin subfamily, named TRPM_PZQ. While variation within the channel sequence may not affect PZQ action, some variant residues may impair PZQ action and potentially treatment efficacy. If such variants occurred de novo in natural schistosome populations or emerged in response to selection pressure evoked by mass drug administrative campaigns, resistance to PZQ as the sole clinical therapy may occur.

Here we have cataloged the effect of various mutations on TRPM_PZQ function. This dataset is meant to provide researchers a way to check the likely effect of any natural variation, allowing for surveillance of potential PZQ resistance.