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Discovery of a first-in-class inhibitor of the PRMT5-substrate adaptor interaction

McKinney, D. C.; McMillan, B. J.; Ranaghan, M.; Moroco, J. A.; Brousseau, M.; Mullin-Bernstein, Z.; O'Keefe, M.; McCarren, P.; Mesleh, M. F.; Mulvaney, K. M.; Singh, R.; Bajrami, B.; Skepner, A.; Timm, D. E.; Porter, D.; Kaushik, V.; Sellers, W. R.; Ianari, A.

2021-02-03 cancer biology
10.1101/2021.02.03.429644 bioRxiv
Show abstract

PRMT5 and its substrate adaptor proteins (SAPs), pICln and Riok1, are synthetic lethal dependencies in MTAP-deleted cancer cells. SAPs share a conserved PRMT5 binding motif (PBM) which mediates binding to a surface of PRMT5 distal to the catalytic site. This interaction is required for methylation of several PRMT5 substrates, including histone and spliceosome complexes. We screened for small molecule inhibitors of the PRMT5-PBM interaction and validated a compound series which binds to the PRMT5-PBM interface and directly inhibits binding of SAPs. Mode of action and structure determination studies revealed that these compounds form a covalent bond between a halogenated pyridazinone group and cysteine 278 of PRMT5. Optimization of the starting hit produced a lead compound, BRD0639, which engages the target in cells, disrupts the PRMT5-RIOK1 complex, and reduces substrate methylation. BRD0639 is a first-in-class PBM-competitive small molecule that can support studies of PBM-dependent PRMT5 activities and the development of novel PRMT5 inhibitors that selectively target these functions.

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