I found that the efficacy of neratinib is not that great in comparison to other approved therapies (targeting oncogenic alterations in EGFR, ALK, ROS1 and BRAF ) and may not work as a good monotherapy to treat wide variety of HER2- and HER3-mutant cancers.
Yep, I made a point to mention that they stated this, but they also mentioned its potential in use in combination therapy with other HER inhibitors. So it could still find a way to prove more useful then traditional therapies yet, onward for more research.
For clarity I mentioned this in the following paragraph:
Still, the information presented in this study is of high impact as it suggests that targeting these mutations specifically could be effective especially in combination with other chemotherapy techniques. It also opens the door to the study of combination therapies where neratinib is used at the same time as another HER kinase inhibiting compound to determine whether more potent anti-cancer effects are observed on the various mutations identified as positive hits here.
Using neratinib as a monotherapy would be a hard sell
Indeed, its just not efficacious enough. However, I think the more important information here came from the identification of a whole host of new information on which HER mutations are gain of function. This will allow for a better, more targeted application of inhibitors to those people with cancers having these gain of function mutations.
Thanks for clarifying. I was skimming through. I forwarded this nature paper to my PhD friend who works on protein engineering to enhance the efficacy of HER-targeted therapeutics. I will point this post to him. Looking forward for your research news series.
Thanks, I was trying to write this for a slightly more general audience. Your friend would likely get much more out of the original research article then my small discussion about it :)