A fun but off-topic note: "behave the same chemically" is only approximately true. For heavy atoms like the ones discussed in the article, it's basically true. But for hydrogen, adding one neutron doubles its mass and you can get real effects on chemical reaction rates.

https://en.wikipedia.org/wiki/Kinetic_isotope_effect

And of course, an obligatory "In The Pipeline" link on how it's used in drug discovery: https://www.science.org/content/blog-post/isotopes-get-your-...

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A great example of this in relatively recent history is the treatment of hepatitis C. The treatments pre-circa-2011 were pretty crappy: interferon/ribavirin had poor cure rates and bad side effects. But it was still better than hepatitis destroying your liver, so people dealt with it.

Then, in 2011, as the culmination of years of trials, telaprevir (from Vertex/J&J) [1] and boceprevir (Schering-Plough/Merck) [2] were approved and were DRAMATICALLY BETTER than interferon/ribavirin.

...and then just two years later both of these drugs got nuked by the approval of sofosbuvir (aka Sovaldi, from Pharmasset/Gilead) [3], which has _cure_ rates in excess of 90%. Telaprevir and boceprevir were pulled from the market because there was simply no more market for them once sofosbuvir hit. Scientific competition at its finest.

There is absolutely a dark side to pharmaceutical pricing and licensing, but please don't let the existence of that dark side cloud your vision of the transformative impact that those of us in biotech R&D want to have (and in many cases, have had). I was at Vertex when the early trial data on telaprevir started coming out and it became clear that we might be able to offer patients real hope who did not have it before.

[1] https://en.wikipedia.org/wiki/Telaprevir [2] https://en.wikipedia.org/wiki/Boceprevir [3] https://en.wikipedia.org/wiki/Sofosbuvir

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Those typically have a "stem" which indicate the mechanism by which the drug works. In this case, it's "-glipron", which you can parse as "glipr" -- GLP-1 receptor -- and "on" -- it's an "agonist", or something that turns "on" the receptor. So "-glipron"s are drugs which agonize, or activate, the GLP-1 receptor. There are other gliprons in trials, including danuglipron (https://en.wikipedia.org/wiki/Danuglipron) from Pfizer, and many others that don't have assigned INNs.

Semaglutide and liraglutide also agonize GLP-1, so why aren't they gliprons? Because chemically they are analogs of the naturally occurring GLP-1 peptide, so they get the -glutide (GLUcagon-like pepTIDE) stem.

I don't know why tirzepatide got that name. It's a peptide, so "-tide" makes sense, but it's actually listed as a "various" exception in the master document of INNs: https://iris.who.int/bitstream/handle/10665/379226/978924009....

The Wikipedia pages are decent -- the picture makes it fairly obvious how much smaller orforglipron is than tirzepatide even if you don't know how to read chemical structures; just count atoms!

https://en.wikipedia.org/wiki/Orforglipron

https://en.wikipedia.org/wiki/Tirzepatide

https://job-boards.greenhouse.io/recursionpharmaceuticals

Note that "video" is a little different here than the way we all usually think of it - think "minutes or hours between frames" not "frames per second".

But the biggest challenge for these tests is that this "tumor fraction" can be very very low in early stage cancers, which is why stage I sensitivity tends to be quite poor.

*"Below" meaning "on the opposite side from the objective" - you illuminate _through_ the sample.

1. How does your technology or product offering distinguish itself from prior attempts like NeoPrep (née Advanced Liquid Logic) from Illumina or Voltrax from ONT?

2. How "hackable" is the offering for power users to implement custom protocols on the instrument and consumables?

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