TARGETING FIBROSIS ALONE IS A NONSENSE IN NASH 

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Reading analysts since the Allergan/Tobira deal, we are surprised by their monomania on fibrosis. They compare items after items Tobira, and Intercept's results in fibrosis, regardless the differences in the studies protocols.

Investors pin other drug candidates specifically targeting fibrosis as the GR-MD-02 Galectin the Emricasan of Conatus or Simtuzumab of Gilead.

Market-induced fibrosis NASH seems the most profitable and most accessible market to day, but analysts seem blinded by this fact, they seem to forget that fibrosis is one of the consequences of NASH and focus on the effects rather than the cause, it is a very short-term vision.

It is as if one wanted to treat fibrosis induced by hepatitis C without treatment for hepatitis C.

In the long term it makes no sense, the drug that had the most success is not the one that processed the complications of hepatitis C but the one who treated hepatitis C because by removing the cause we removed the complications, the reverse is not true.

It is the same in the NASH or it is established that treatment of metabolic disease affecting the ballooning and inflammation of hepatocytes spontaneously regress induced fibrosis.

If the cause is treated with a drug, fibrosis will regress by itself and pure NASH induced antifibrotic will become a very limited market.

This is especially true if the systemic drug reach the market before the antifibrotic.

It is curious that analysts do not see that.

They also suggest to readers that the problem of NASH is essentially fibrosis, whereas this is not true, by far.

NASH kills 4 times its cardiovascular consequences as cirrhosis, and against all these dead, antifibrotic are ineffective.

As for hepatitis C market will eventually focus on the treatment of the disease and not its consequences.

When fashion antifibrotic is over, he will remain the real market, the drugs really treat patients in time and it is these drug candidates that should be monitored closely by savvy investors.

G. Divry



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