Universiteit Leiden

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Cell Systems and Drug Safety

Allosterism

The recognition that there may be more, so-called allosteric binding sites on a given receptor has also fueled our synthetic efforts. Over the last few years we have focused on many drug targets (adenosine A1, A2A and A3 receptors, the mGlu2 receptor and a classic ‘anti-target’, the hERG channel) to explore this notion.

We have identified and designed new compounds that enhance the action of a classic agonist (a so-called positive allosteric modulator – PAM) or, very differently, act as a new class of antagonists (negative allosteric modulators – NAMs). As a PAM for the adenosine for the hERG channel (exemplified by LUF 7346) may even reverse the cardiotoxicity induced by hERG somatic mutations, and save the life of patients suffering from this genetic malfunctioning.

Such compounds would be fantastic representatives of true ‘precision medicine’. Structural evidence for compounds allosterically influencing each other came from our joint work with Tracy Handel’s team at San Diego’s School of Pharmacy, with whom we solved the structure of the chemokine CCR2 receptor bound to two small molecules at the same time. From pharmacological experiments we had already learned that the two molecules, BMS-681 and CCR2-RA-[R], reinforced their binding to the receptor.

Related publications

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