Professional role
a professor of pharmacology at Case Western Reserve School of Medicine[1]
EY
PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable.
Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job.
are now taking steps to study how PfNCR1 interacts with various inhibitors
Reviewed sources document are now taking steps to study how PfNCR1 interacts with various inhibitors. Explore attributed publications and research affiliations.
Explore researchare now taking steps to study how PfNCR1 interacts with various inhibitors[1]
Sources are listed once and connected to each accepted claim they support. Excerpts preserve the source language used in the review.
7 source claims · Reviewed Sep 9, 2026
Biographical context: PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable.
That’s an important finding because a parasite needs just the right amount of cholesterol to survive and grow in its host, said Edward Yu, a professor of pharmacology at Case Western Reserve School of Medicine and the study’s lead researcher. PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable. Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job. This disrupts the parasite’s ability to control its cholesterol levels, potentially killing it. “This breakthrough is a big step forward in developing new malaria treatments,” Yu said. “By focusing on PfNCR1, scientists could develop drugs that the parasite finds difficult to develop resistance to, advancing our fight against one of the deadliest and most persistent illnesses in the world.” To better understand PfNCR1’s structure and identify proteins that directly interact with it, Yu and his team are now taking steps to study how PfNCR1 interacts with various inhibitors. This information could lead to a new approach of designing drugs to fight malaria more effectively.
Biographical context: Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job.
That’s an important finding because a parasite needs just the right amount of cholesterol to survive and grow in its host, said Edward Yu, a professor of pharmacology at Case Western Reserve School of Medicine and the study’s lead researcher. PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable. Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job. This disrupts the parasite’s ability to control its cholesterol levels, potentially killing it. “This breakthrough is a big step forward in developing new malaria treatments,” Yu said. “By focusing on PfNCR1, scientists could develop drugs that the parasite finds difficult to develop resistance to, advancing our fight against one of the deadliest and most persistent illnesses in the world.” To better understand PfNCR1’s structure and identify proteins that directly interact with it, Yu and his team are now taking steps to study how PfNCR1 interacts with various inhibitors. This information could lead to a new approach of designing drugs to fight malaria more effectively.
Identity: Edward Yu
That’s an important finding because a parasite needs just the right amount of cholesterol to survive and grow in its host, said Edward Yu, a professor of pharmacology at Case Western Reserve School of Medicine and the study’s lead researcher. PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable. Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job. This disrupts the parasite’s ability to control its cholesterol levels, potentially killing it. “This breakthrough is a big step forward in developing new malaria treatments,” Yu said. “By focusing on PfNCR1, scientists could develop drugs that the parasite finds difficult to develop resistance to, advancing our fight against one of the deadliest and most persistent illnesses in the world.” To better understand PfNCR1’s structure and identify proteins that directly interact with it, Yu and his team are now taking steps to study how PfNCR1 interacts with various inhibitors. This information could lead to a new approach of designing drugs to fight malaria more effectively.
Professional role: a professor of pharmacology at Case Western Reserve School of Medicine
That’s an important finding because a parasite needs just the right amount of cholesterol to survive and grow in its host, said Edward Yu, a professor of pharmacology at Case Western Reserve School of Medicine and the study’s lead researcher. PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable. Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job. This disrupts the parasite’s ability to control its cholesterol levels, potentially killing it. “This breakthrough is a big step forward in developing new malaria treatments,” Yu said. “By focusing on PfNCR1, scientists could develop drugs that the parasite finds difficult to develop resistance to, advancing our fight against one of the deadliest and most persistent illnesses in the world.” To better understand PfNCR1’s structure and identify proteins that directly interact with it, Yu and his team are now taking steps to study how PfNCR1 interacts with various inhibitors. This information could lead to a new approach of designing drugs to fight malaria more effectively.
Professional role: the study’s lead researcher
That’s an important finding because a parasite needs just the right amount of cholesterol to survive and grow in its host, said Edward Yu, a professor of pharmacology at Case Western Reserve School of Medicine and the study’s lead researcher. PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable. Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job. This disrupts the parasite’s ability to control its cholesterol levels, potentially killing it. “This breakthrough is a big step forward in developing new malaria treatments,” Yu said. “By focusing on PfNCR1, scientists could develop drugs that the parasite finds difficult to develop resistance to, advancing our fight against one of the deadliest and most persistent illnesses in the world.” To better understand PfNCR1’s structure and identify proteins that directly interact with it, Yu and his team are now taking steps to study how PfNCR1 interacts with various inhibitors. This information could lead to a new approach of designing drugs to fight malaria more effectively.
Official profile: Official profile
That’s an important finding because a parasite needs just the right amount of cholesterol to survive and grow in its host, said Edward Yu, a professor of pharmacology at Case Western Reserve School of Medicine and the study’s lead researcher. PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable. Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job. This disrupts the parasite’s ability to control its cholesterol levels, potentially killing it. “This breakthrough is a big step forward in developing new malaria treatments,” Yu said. “By focusing on PfNCR1, scientists could develop drugs that the parasite finds difficult to develop resistance to, advancing our fight against one of the deadliest and most persistent illnesses in the world.” To better understand PfNCR1’s structure and identify proteins that directly interact with it, Yu and his team are now taking steps to study how PfNCR1 interacts with various inhibitors. This information could lead to a new approach of designing drugs to fight malaria more effectively.
Research interests: are now taking steps to study how PfNCR1 interacts with various inhibitors
That’s an important finding because a parasite needs just the right amount of cholesterol to survive and grow in its host, said Edward Yu, a professor of pharmacology at Case Western Reserve School of Medicine and the study’s lead researcher. PfNCR1 acts like a transporter, he said, moving cholesterol around to keep the parasite’s membrane stable. Yu’s team found that a compound known as MMV009108 can physically block the transporter, preventing it from doing its job. This disrupts the parasite’s ability to control its cholesterol levels, potentially killing it. “This breakthrough is a big step forward in developing new malaria treatments,” Yu said. “By focusing on PfNCR1, scientists could develop drugs that the parasite finds difficult to develop resistance to, advancing our fight against one of the deadliest and most persistent illnesses in the world.” To better understand PfNCR1’s structure and identify proteins that directly interact with it, Yu and his team are now taking steps to study how PfNCR1 interacts with various inhibitors. This information could lead to a new approach of designing drugs to fight malaria more effectively.