Biotech Values

[DewDiligence]

ACHN Selects ACH-1625 as Lead HCV Protease Inhibitor

[This is ACHN’s first foray back into the HCV market since ACH-806, the NS4A antagonist partnered with GILD, was killed due to liver toxicity (#msg-18754183).]

http://biz.yahoo.com/pz/080604/144093.html

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Wednesday June 4, 4:07 pm ET 


NEW HAVEN, Conn., June 4, 2008 (PRIME NEWSWIRE) -- Achillion Pharmaceuticals, Inc. (NasdaqGM: ACHN ) today announced the nomination of its first clinical candidate from the company's proprietary HCV protease program. The candidate, ACH-1625, is a highly selective inhibitor of HCV NS3 protease.

In preclinical studies, Achillion has demonstrated that ACH-1625 has an excellent safety profile and a pharmacokinetic profile characterized by rapid and extensive partitioning to the liver. ACH-1625 has also exhibited superior potency against NS3 protease in HCV replicon assays compared to protease inhibitors in more advanced stages of development. Preclinical data supporting the selection of ACH-1625 for clinical development will be presented at a future scientific meeting.

``The inherent nature of HCV to mutate rapidly necessitates a therapeutic approach that utilizes a combination of drugs with complementary mechanisms of action in order to suppress viral resistance,' said Milind S. Deshpande, Executive Vice President and Chief Scientific Officer of Achillion. ``Our HCV protease inhibitor program has focused on the discovery of potent and safe, orally bioavailable therapeutics with potential for once a day dosing. Inhibition of NS3 protease is complementary to NS4A antagonism, on which we are collaborating with Gilead Sciences. We have leveraged our robust drug discovery capabilities to create a portfolio of inhibitors of NS3 protease to which we retain all commercial rights.'

Michael D. Kishbauch, Achillion's President and CEO, stated, ``We are very encouraged by the excellent safety, potency and PK profile exhibited by ACH-1625 to-date, and we expect to initiate a Phase 1 study in the first half of 2009. We are quite excited by the potential to have two HCV candidates operating by distinct mechanisms in the clinic next year.'
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