Fair, preclinical drug candidate more like

“hey what if we tried to make cancer grow faster” is not a great pitch

they got funding because it wasn’t what they were trying to do, but it did ended up being the case, but it worked anyway so, so far, all is good. but don’t expect that it will become a new drug, because 90% of clinical trials fail, and here maybe there is some other less malformed cancer line that will grow faster after administration of that drug, which is sort of what was could be expected now that we know mechanism

cells have different enzymes, enzymes do different things, to keep everything in order you need some way to control these enzymes. there are many, many ways in nature to do this, but the one relevant here is that some enzymes have tyrosine residue sticking out in a specific way. when phosphate is attached to them, extra charge appears, which can bend enzyme out of or into shape, switching it on or off or changing something about the way it works.

the job of flipping these switches belongs to tyrosine kinases, and in many cancers something is wrong about these. the ones relevant here are from RAS/MAPK pathway and PI3K/AKT/mTOR pathway, and these are involved in many things, but among them is cell growth and division. blocking one or other tyrosine kinase from working is something that many of anticancer drugs do, and it works pretty well, because overactive (for whatever reason) or mutated tyrosine kinase is often present. in many cancer cells, if for some reason MAPK is made to be more active, cancer cells might grow faster.

now the thing is, there is something peculiar about the specific way in which RAS/MAPK cascade is broken in that cancer type, that when it’s cranked up cells stop spreading and break apart. this is something that this new drug seems to be doing (through a couple of layers of other enzymes), and it’s weird, and unexpected, and in no way you’d get funding for that, but it works apparently

just give your cancer cancer ez gg