Marc Anderson

Education

B.S. (1995) University of Colorado at Boulder, Computer Science
Ph.D. (2001) University of California at Santa Cruz, Organic Chemistry

Research Areas: Organic and Medicinal Chemistry

Our group uses organic synthesis as a tool to design and optimize inhibitors of therapeutically relevant drug targets in human illness. Previous targets we have pursued have been focused on various channel proteins as drug targets: TMEM16A, UT-A, CFTR, pendrin, SLC26A3, SLC26A4,  etc.  Typical projects involve multi-step organic synthesis of channel protein modulators, and then biological evaluation using cell based assays that quantify inhibition (or activation) of the function of those proteins.

Earlier synthesis campaigns of channel protein modulators to treat disease

Some channel proteins our laboratory has explored earlier at SFSU include inhibitors of TMEM16A (a target in cancer, hypertension, and chronic pain), and UT-A1 and UT-B (novel targets for diuretic drugs).  We've also explored inhibitors of SLC26A3 ("DRA"), as potential therapies for chloride-absorptive constipation and kidney stones, and SLC26A4 ("pendrin") as a novel target to reverse the effects of the disease cystic fibrosis.

In the last couple years, our lab has worked toward developing inhibitors of SLC26A6 ("PAT1"), which is a putative target for gastrointestinal symptoms of cystic fibrosis.  Our laboratory has also been developing libraries of molecules that could serve as CFTR co-potentiators.  Cystic fibrosis is a genetic disease caused by loss of function mutations in the protein CFTR (cystic fibrosis transmembrane regulator).  CFTR co-potentiators act in synergy with the clinical CFTR potentiator (VX770, or Ivacaftor).  This synergistic treatment strategy may be useful to treat certain mutations of CFTR that cause the disease CF, which are not effectively treated by VX770 alone.

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