San Diego-based Conatus Pharmaceuticals ($CNAT) has scored another big surge in its stock price after a short, small midstage study provided bragging rights to a success in treating an indicator for liver damage that afflicts patients suffering from NASH and hepatitis C.
Among 22 patients with damage to their livers, investigators tracked what they called a statistically significant improvement in hepatic venous pressure gradient (HVPG)--a measurement of pressure in the portal vein--and an improvement from baseline in cleaved cytokeratin 18 (cCK18), a biomarker of excessive cell death that contributes to chronic inflammation, after being dosed with emricasan.
Emricasan is an oral caspase protease inhibitor that's being used to tackle enzymes which play a role in liver disease.
The biotech painted the data as another proof-of-concept example of the potential that this drug has in a hot market. And investors were happy to jump in, pushing the company's share price up more than 40% on the data Wednesday evening.
This isn't the first time that Conatus has scored a big increase in its stock price on POC results from small studies. The same thing happened last March, when it produced biomarker data for nonalcoholic fatty liver disease.
Company executives were happy to herald these new results as clear support for more advanced studies with their drug. But the company has a long way to go before it can come up with the kind of data that will convince regulators of its benefits.
"We were excited to demonstrate that a drug candidate with the potential to achieve long-term resolution of fibrosis and cirrhosis also has the ability to induce a rapid and clinically meaningful reduction of severe portal hypertension," noted Dr. David Hagerty, executive vice president of clinical development at Conatus. "The reduction of portal pressure over a relatively short time frame in the patients with therapeutically relevant portal hypertension may reflect the initial impact of emricasan on the hyperdynamic circulation that is the predominant contributor to portal hypertension as cirrhosis progresses and/or a direct effect upon intrahepatic vasculature resistance. Future studies will be needed to assess the relative contribution of these mechanisms to the observed clinical effect. Decreasing HVPG has been identified by the FDA (U.S. Food and Drug Administration) as a validated, objective measure that may be acceptable as a surrogate endpoint for clinical trials of patients with liver cirrhosis. These results set the stage for future Phase 2b clinical trials in patients with cirrhosis and therapeutically relevant portal hypertension."
- here's the release