And keep dreaming about pancreatic, or any other cancer.
"Active at a stage in the cell cycle during which telomere length is not relevant."
Let me repeat that, you are an IDIOT!
Well ruxo already looked good in the high-CRP subset of Recap (Janus-1 is ALL high-CRP). And the futility checkpoint on Janus-1 was passed in the Summer. There was an observation that if patients had been screened for probability of 4-week survival rather than level of function at first treatment, the low-CRP part of Recap would very likely have succeeded too--that's been done for Janus-1. I give it a very good chance of success, and it is being done under SPA so success is sufficient. And as I love to point out, Recap was the only trial on R/R PaCa patients in which they generally gained weight (turns out that families and friends care a lot about that, but patients don't).
As I pointed out elsewhere, a tumor type with low-ish incidence of paraneoplastic syndromes and a partnered-agent acting on supporting tissues rather than the cancer cells themselves is an unfavorable case for ruxo and its presumed action.
There are some odd things going on here. First, 373 patients sounds large for a phase 2. Second: I don't recall a lot of cases in which a futility judgment on a phase 2 got announced, and absolutely none in which futility of a subset did. Third and more: we heard little when the inflammation-targeted JAK-1-specific candidate was killed, and even less when the PI3K-delta program was diverted. And yeah, the logic behind ruxo for solid tumors favors partnering it with an agent that was used previously, and that generally loses its effectiveness because it is no longer absorbed. Some of this is the sort of stuff that stopped when Mr Daly came on board, and he doesn't seem to have been replaced effectively.
Note that while the MPNs are never thought of as solid tumors, the dividing cells stay at home and expand in the marrow, so they have an intermediate nature.
The CRC p2 was a bit of a Hail Mary. Regorafenib is a fairly #$%$ drug and the combo with ruxolitinib not particularly promising.
I agree that this has little bearing on the panc ca studies, but panc is a tough nut to crack. Ruxolitinib has an uphill battle in solid tumours.
Frankly, your posting identity puts me off. but I'll answer you seriously this once. I refer to the articles in NEJM of last Sept 3. It is unlikely, and very nearly ruled out, that Imetelstat works by inhibiting telomerase. The editors picked up on evidence from measured telomere lengths. I add that in MF, Imetelstat had a favorable clinical effect ONLY on patients bearing the V617F JAK-2 always-on mutation and with wild type histone-binder ASXL1. Both of these are active at a stage in the cell cycle during which telomere length is not relevant. Since we don't know what it does, it's hard to say how IM might interact with other agents. (there's also an old objection to the proposed mechanism from timing of action) Again, with the beautiful Nobel-Prize-winning story removed, I see no reason to suppose that Imetelstat will do anything useful that it has not been directly shown to do. I am not aware of specific plans to do the solid tumor trials.
I have seen claims that IM is sure to be approved if it performs the same in the IMBARK study as it did in the demonstration series. From the on-line appendix to the MF paper (it's a little tricky, but possible, to reconstruct these numbers from the main body of the paper), there were 48 grade 3 or worse adverse events among the 33 subjects during a nominally 9-month study. Approval is uncertain with that rate of serious adverse events. So IM will need to do better than it has in the past.
In direct contrast, ruxolitinib in combination with capecitabine has passed the RECAP phase 2 trial and in the Janus 1 phase 3 trial has passed a futility checkpoint like the one a different combination failed today; in April we will have good evidence on whether that combination is effective against pancreatic cancer.
You do know that when they set a $145 target, it means they're proving cover for their clients to get out at any price possible?
The fear is that the phase 3 pancreatic cancer study and solid tumors in general are doomed.
Piper Jaffray analysts said while it would be premature to write off the pancreatic cancer studies, the risk of success of Jakafi, or Ruxolitinib, had gone up.
"Jakafi for solid tumors is one of the key pillars to support Incyte's valuation and potential upside, so we are not surprised to see the after-market weakness,"
it simply means that all valuation above $70 was hot air and meaningless. you'll be giving back another 50% to sub 30s within a year.
There have been multiple recent preclinical research conducted at universities that has shown telomerase inhibition (Imetelstat used as the inhibitor) enhances other already approved therapies. Telomerase is expressed by 90% of all cancer. The solid tumor studies the jacosa is referring to were not successful as it appears that telomerase inhibition alone is not effective in solid tumors. Imetelstat may not be a cure for cancer but it has potential as a combo therapy for a broad range of cancers as Janssen further develops Imetelstat. The hope being that Imetelstat can limit the spread of cancer while the standard of care attacks the tumor. I'm not a INCY hater. I hope their therapies are successful but Imetelstat has a completely different mode of action and than Jakafi so they are more likely complimentary than competitive.
INCY is the poster child of Biotech Bubble. When this is all said and done, INCY market cap will likely be under 7Billion and under $35/share.