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Initial Discovery |

The Acquist prototype drug (ACQT1001) was tested in more than 370 U.S. patients. Acquist investigators first observed that the drug was associated with marked reduction of serum uric acid.  Acquist pursued this lead by identifying the underlying biologic mechanisms that caused the effect.

Bi-functional Mechanism |

For more than 50 years, standard treatment for gout has started with a drug that reduces uric acid production (allopurinol) – an inhibitor of an enzyme known as xanthine oxidase.  However, a large percentage of patients do not respond to allopurinol, and then a second drug is added that promotes urinary excretion of uric acid by inhibiting an enzyme known as URAT1.

Acquist found that the marked reduction in serum uric acid with ACQT1001 owed to its bifunctional inhibition of both enzyme targets – a unique effect never before described.  Moreover, the level of inhibition against both targets with ACQT1001 exceeded the standard agents that inhibited only one target. The Company has synthesized a library of novel compounds that optimize these activities and reduce potential adverse effects.  (See the diagram for consequences of bifunctional activity.)

bifunctional

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