The first involves disabling CTGF with human antibodies, the guided missiles of the immune system.

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When studying slides from animal trials, he kept noticing a mysterious protein that he later identified as CTGF.

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The latest work revolves around two culprit proteins, transforming growth factor beta (TGF-beta) and connective tissue growth factor (CTGF).

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He found that once TGF-beta activated a cell, it triggered the CTGF gene to make its protein (see chart).

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Fibrogen researchers spent two years painstakingly screening 150 antibodies, and found 2 that hinder CTGF's ability to bind with cell receptors.

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The best part: CTGF, concerned primarily with spreading collagen production to neighboring cells, had a much more limited role than TGF-beta.

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An experimental new class of drugs is aimed at rendering TGF-beta and CTGF ineffective by blocking their ability to bind with cell receptors.

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By 1992 Grotendorst, who had done work at the University of South Florida and is now at the University of Miami, concluded that it was CTGF, not TGF-beta, that triggers collagen production by binding to specific cell receptors.

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Fibrogen's other approach, a joint effort with Japan's Sankyo , is to screen thousands of small-moleculeproteins on their shelves and those of other firms to see whether one or two will block CTGF from binding with receptors or knock out one of the collagen-producing signals that CTGF sends into a cell nucleus.

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