Scientists at Tokyo Institute of Technology have discovered the primary mechanism by which thalidomide causes malformed limbs in developing embryos.

After many affected children were born to mothers who had been prescribed the drug for morning sickness, the drug's side-effect gained recognition.

The research says that thalidomide binds to and renders inactive the protein cereblon, which is very important in limb formation.

The fact that it causes birth defects means that for women, use of drug thalidomide remains risky and controversial, though it may be effective in the treatment of certain cancers and leprosy.

The negative effects of the "potentially useful" drug were isolated in the study by the research team, led by Takumi Ito from the Tokyo Institute of Technology in Japan.

They set out to discover which target molecules thalidomide bound to in the body. This was done by them using tiny beads that extracted each individual molecule the drug bound to.

The conclusion was confirmed after the usage of genetic techniques to reduce the production of the cereblon protein in developing zebra fish and chick embryos. The embryos with reduced cereblon had similar developmental defects to those that were treated with thalidomide.

The researchers wrote in their Science article, "We have shown that cereblon is a primary target of thalidomide teratogenicity".

"Although the mechanism for the teratogenic effect was made clear, the mechanism for its therapeutic effects remains unknown. If we want to develop a new drug devoid of teratogenic activity, it is important to understand this mechanism. This is what we are heading for," Dr Ito told BBC News. (With Inputs from Agencies)