Search
  • 網站搜尋
亞洲知識產權資訊網為知識產權業界提供一個一站式網上交易平台,協助業界發掘知識產權貿易商機,並與環球知識產權業界建立聯繫。無論你是知識產權擁有者正在出售您的知識產權,或是製造商需要購買技術以提高操作效能,又或是知識產權配套服務供應商,你將會從本網站發掘到有用的知識產權貿易資訊。
返回搜索結果

In Utero Prevention Of Congenital Heart Disease By Metabolic Intervention


技術優勢

This chemical is already FDA-approved for alternate indications No current strategies to decrease risk of congenital heart disease More effective than controlling maternal blood glucose levels


技術應用

Prevention of congenital heart disease


詳細技術說明

Professor Nakano and coworkers have discovered an in utero treatment to prevent CHD. A chemical screen revealed that high maternal glucose levels interfered with development of heart muscle cellsviaa key regulatory pathway. By inhibiting this pathway using the FDA-approved small molecule, CHD could be prevented in mouse models. This chemical has been shown to cross the placental barrier and is non-toxic and efficacious at the dose used in this method.


其他

State Of Development

Preliminary experiments have been carried out in mice. This chemical has been shown to prevent congenital heart disease without detectable side effect.


Background

Congenital heart disease (CHD) is a heterogeneous group of structural anomalies in the heart that is present in 0.8% of newborn infants worldwide. Although the advance in pre-natal diagnosis allows us to detect CHD and assess the risk early during pregnancy, corrective surgery is currently the only effective option and there is no way to prevent the progression of CHD. Therefore, the financial, emotional and social burden of the families with a baby with CHD is huge. While the cause of CHD may vary, maternal hyperglycemia is associated with a 5-fold increase in CHD risk. Careful monitoring and control of the mother’s blood glucose level has not been proven to be effective in preventing CHD. With rapidly increasing prevalence of diabetic pregnancy and high incidence of CHD, how to treat CHD will be an urgent issue in medical practice and medical economy in the next few decades.


Related Materials

Nakano, H.; Minami, I.; Braas, D.; Pappoe, H.; Wu, X.; Sagadevan, A.; Vergnes, L.; Fu, K.; Morselli, M.; Dunham, C.; Ding, X.; Stieg, A. Z.; Gimzewski, J. K.; Pellegrini, M.; Clark, P. M.; Reue, K.; Lusis, A. J.; Ribalet, B.; Kurdistani, S. K.; Christofk, H.; Nakatsuji, N.; Nakano, A. Glucose inhibits cardiac muscle maturation through nucleotide biosynthesis. eLife. 2017.


Tech ID/UC Case

29355/2017-725-0


Related Cases

2017-725-0


國家/地區

美國

欲了解更多信息,請點擊 這裡
Business of IP Asia Forum
桌面版