TAK-448 protected insulin resistant, obese mice against the development of hepatic steatosis:
H& E showing fatty liver.
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder worldwide that can progress to steatohepatitis (NASH), the leading reason for liver transplants. In the U.S., there are nearly 100 million affected by the disease, which includes children and adults. Since there is no FDA approved drug for NAFLD or NASH treatment, there is an urgent need to develop a novel and effective therapy.
Kisspeptins are peptides that circulate in the blood and bind KISS1R receptors. Scientists from the Rutgers University discovered that increasing KISS1R signaling by administration of the kisspeptin analog (TAK-488) in obese wild type insulin-resistant mice improves insulin resistance, protects against excess fat build-up in the liver (known as fatty liver or steatosis), lowers liver and serum triglycerides, and lowers serum free fatty acids. Moreover, livers from TAK-448 treated mice displayed lower levels of markers for inflammation and fibrosis. By contrast, loss of KISS1R in obese, insulin-resistant mice exacerbated steatosis, insulin-resistance, and metabolic profile.
- Novel therapy for the treatment and prevention of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH)
- First pharmacological compound for the treatment of NAFLD
- Long-lasting analog of kisspeptin-10, a naturally occurring peptide found in the blood
- Reduces hepatic lipids and inflammatory and fibrosis markers
- Reduces peripheral fat and lowers blood triglycerides and free fatty acids
- Protects against insulin resistance
Intellectual Property & Development Status:
Patent pending. Available for licensing and/or research collaboration.