Key result
Compound 4b selectively inhibited ADAMTS-5 proteoglycanase activity (IC50 9.4 μM) by binding to a novel exosite in the disintegrin-like domain, without targeting the active site zinc.
Why the study?
ADAMTS-5 is a therapeutic target for osteoarthritis, but existing inhibitors target its active site and lack selectivity.
The development of compound 4b demonstrates that targeting the ADAMTS-5 disintegrin-like domain exosite is a viable strategy for achieving selective inhibition, with potential implications for osteoarthritis therapy.
Answers are grounded in this paper and cite their sources.
Advances selective ADAMTS-5 inhibition strategies; leaves open in vivo efficacy for osteoarthritis.
ADAMTS-5 is a major protease involved in the turnover of proteoglycans such as aggrecan and versican. Its aggrecanase activity has been directly linked to the etiology of osteoarthritis (OA), identifying ADAMTS-5 as a pharmaceutical target for OA treatment. However, most existing ADAMTS-5 inhibitors target its active site and therefore suffer from poor selectivity. Here, using a novel approach, we have designed a new class of sugar-based arylsulfonamide inhibitors, which are selective for ADAMTS-5 through binding to a previously unknown substrate-binding site (exosite). Docking calculations combined with molecular dynamics simulations demonstrated that our lead compound is a cross-domain inhibitor that targets the interface of the metalloproteinase and disintegrin-like domains. Targeted mutagenesis identified disintegrin-like domain residues K532 and K533 as an exosite which is critical for substrate recognition. Furthermore, we show that this exosite acts as major determinant for inhibitor binding and, therefore, can be targeted for development of selective ADAMTS-5 inhibitors.
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Santamaria et al. (2020) studied Osteoarthritis. Compound 4b (glycoconjugated arylsulfonamide) vs. DMSO / ADAMTS-4 was evaluated on Inhibition of ADAMTS-5 versicanase activity (IC50 9.4 μM). Compound 4b selectively inhibited ADAMTS-5 proteoglycanase activity (IC50 9.4 μM) by binding to a novel exosite in the disintegrin-like domain, without targeting the active site zinc.
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