Marc Anderson

Marc Anderson

Associate Professor
At SF State since 2007
Phone: (415) 338-6495
Location: TH 636


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.

*** note: we are moving into a new building (Spring/Summer 2024).  Our laboratory is being massively compressed (1200 sq ft --> 600 sq ft).  This will drastically impact our work space, which includes the ability to set up and perform experiments, computer resources to prepare experiment protocols and analyze data, etc.  Our current space allows us to accommodate a larger number of students, and this will simply not be the case in the new building.  Our lab, in particular, has acquired and uses a variety of major pieces of equipment (2 x HPLC, 2 x MSD, nitrogen generator, Biotage Isolera automated chromatography, Biotage Initiator microwave, BMG FLUOstar Omega plate reader, servers for computational drug discovery, etc) that will take up most of the provided lab space.   Because of these factors, and since the lab is currently full of students, we are pausing the intake of new undergraduate and graduate student research assistants until the lab is established into the new building.

Previous synthesis campaigns of channel protein modulators

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.

marc project 3a

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.

marc project 3b


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