CHAGAS DISEASE

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A silent parasite colonizes and degrades the heart tissue, leading to progressive disease and high mortality

Hourglass icon representing the decades-long progression of Chagas disease damage to heart tissue.

Persists within cardiac tissue and progressively damages myocardium over ~10–30 years

Anatomical heart icon representing serious cardiac complications in about 30% of Chagas cases.

~30% of cases: arrhythmia, cardiac arrest, cardiomyopathy, heart failure, emboli, and other conditions

Intestines icon representing gastrointestinal and nervous system complications of Chagas disease.

Additional organ systems vulnerable: GI (megacolon, megaesophagus), CNS

Mother holding child icon representing mother-to-child and other Chagas transmission routes.

Other forms of transmission: mother to child, blood donation, organ transplant, food-borne

Illustration of a triatomine bug ("kissing bug") transmitting the T. cruzi parasite, which then lives and replicates in heart muscle.
An estimated 300,000 people in the U.S. and 7-10 million people globally are infected with the parasite Trypanosoma cruzi (T. cruzi), which causes Chagas disease.
Chagas disease: A global threat with an expanding US prevalenceDot map of the U.S. showing Chagas disease cases by state, with the largest clusters in California, Texas, Florida, and New York.

T. cruzi replicates within heart muscle cells, digestive tract tissue, and other organs. Cells eventually burst open, allowing T. cruzi to spread to new sites. Twenty to thirty percent of those infected will eventually develop severe cardiac or gastrointestinal disease (e.g., sudden cardiac arrest, heart failure, stroke, or life-threatening GI enlargement), and ~30% will progress to Chagas cardiomyopathy, a chronic, destructive condition that can lead to sudden death. There is no way to predict who will progress, creating a strong imperative to treat all infected individuals.

There are no FDA-approved treatments for adults with chronic Chagas disease.

Diagram of oral AN2-502998 blocking T. cruzi mRNA processing, leading to parasite death.

AN2-502998: An oral, small molecule benzoxaborole targeting CPSF3

Diagram of oral AN2-502998 blocking T. cruzi mRNA processing, leading to parasite death.
AN2-502998 is an oral benzoxaborole with presumed mechanism of action being inhibition of CPSF3 in the T. cruzi parasite.

Preclinical highlights

Curative potential observed in multiple non-human primate studies.

Kills both actively dividing and dormant parasites faster than benznidazole in preclinical models.

Curative potential observed in multiple non-human primate studies.

Kills both actively dividing and dormant parasites faster than benznidazole in preclinical models.

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A Phase 2 proof-of-concept trial is anticipated to initiate in 2026, with topline data expected in the second half of 2027.

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