We are in the same situations as Storm. They can’t measure if their METTL3 inhibitor is directly inhibiting METTL3 in human cancers, just if the level of m6A goes down in white blood cell RNA. This is the expected response to METTL3 inhibition, but it could be due to some other complex biological effect. It is remarkably hard to prove what your drug is doing in patients.
Ultimately this doesn’t really matter too much as it is changing the m6A level that matters, not how it occurs. This is the same for bisantrene and FTO - it doesn’t matter to the patient with a cancer that overproduces FTO how bisantrene is able to increase m6A RNA levels, just if it can return the cancer cells with low levels of m6A to normal m6A levels.
Industry news, page-1687
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