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QURE:
I've been away. Is there a data presentation for this?
TIA.
MDVN:
What company-specific events (if any) caused MDVN to fall 40% from its high? I haven’t followed the company closely during the past year or so.
QURE:
This seems to be accompanied by BMY optioning 3 new targets for the CV collaboration.
They were already working on S100A1 together, and they have repeatedly dubbed this protein a "master regulator" for heart function.
I guess this means the 3 new targets are not as important because they were already working on the master regulator. Language is important.
GLPG:
Appreciate the comments. I was going by the pretty charts and thought the 2x100 mg was significantly enough better that they (or Abbvie) would prefer that despite GLPG saying the QD dosing was the way to go.
GLPG / ABBV:
I thought the data especially for ACR-70 were particularly strong.
TRVN:
I think I've babbled about the heart drug before. I think the science is sound, but there is a subtle aspect to it that is amplified by the models used. In other words, the cell lines overexpressing various signaling proteins and the analogous transgenic mice create a model system that likely over-estimates the impact and magnitude of the "biased" protective signaling mechanisms they're targeting.
Also, it should be noted that one of their papers many years ago suggested that carvedilol was effectively a biased antagonist of the beta-adrenergic receptor unlike a classical b-blocker like propranolol. If their hypothesis is clinically relevant, carvedilol should be able to outperform other b-blockers. To date, I do know of a meta-analysis that has suggested such a finding (24.1% versus 28.5% all cause mortality).
If this is the magnitude of the treatment effect, they'll have to run relatively large trials for the AT receptor drug.
re: MDVN
At what point do we start to worry about potential competition for MDVN? Could any of TKAI, EPIX, Aragon, etc. wind up with better drugs in this space?
MDVN:
The Cowen analyst has been pounding his shoe on the table for weeks saying MDVN is overvalued. He claims peak enzalutamide sales expectations are $3 billion but that it will be closer to $1 billion. Cites lack of penetration into urologist offices.
Sales are currently running at ~$1 billion per year.
LOXO:
The paper gives a relatively thorough breakdown on this patient. The CT scans of the response are rather impressive.
Only issue is that these data were previously disclosed. Maybe today's reaction suggests that the market is valuing peer reviewed publications more highly than meeting abstracts and talks?
Probably wishful thinking on my part.
I think LOXO and RXDX is a good TRK basket for now. Their lead drugs have some differences which make them overlapping but not identical assets.
Re: INCY
Can't say the sales are too surprising. Levy has been there a long time and at some point deserves to cash out.
But as we talked before, the company is fully valued and has some significant risks over the next year. Baricitinib data in RA against the biologic comparator is probably the next meaningful datapoint. Not surprising to see them protect their net worth ahead of that uncertainty.
OT:
After 14 years and spending $1.3 Billion on a childhood Study which was to enroll 100,000 kids was cancelled last week after only enrolling 5700 kids.
Spend more!
QURE:
Sort of plays off the monogenic comment you had made on Twitter and which I had been thinking about in regards to preclinical models of HF.
I think QURE is doing everything right so far. I've been looking at their preclinical data and comparing it to other similar models that have progressed to (and failed in) the clinic with the hope of finding a differentiator or observation that can set them apart. Not really seeing one.
This is no different a quandary than all the preclinical cancer models that are successful yet flop in the clinic. Hopefully I'll live long enough to see what the underlying mechanism is that blocks the successful translation of many treatments.
SGYP:
I'm wondering why you said Linzess might have a slight edge in efficacy? Did you compare Phase 3 trial results?
SGYP:
With a $.85 billion market cap, this now seems a little rich as the sales ramp will be slow but steady. After all, this isn't a cancer drug.
SGYP:
Definitely too early to presume first in class. The competition between plecanatide and linaclotide may be a prescriber's preference type situation. If we're being generous to both sides, right now linaclotide may have a small hint of an efficacy edge while plecanatide has an edge in side effect / AE profile. That may leave it to the patient and prescriber to choose the trade-off they prefer.
Jq noted on twitter that there is a trial testing linaclotide at half the current dose. That may signal the diarrhea / AE profile to be meaningful enough that the company is willing to spend money to address it. In turn, it suggests there is a real place for plecanatide on the market.
BCDA:
This is a failure waiting to happen.
This type of cell has already been tried in 2 different, randomized trials and failed miserably and conclusively.
AAVL:
Crazy after hours action on aavl
OT: Med School
I'm a Ph.D. but have contributed to med school admissions and have been heavily involved in residency and fellowship admissions and training. I've heard all the lines of bs by applicants and have had multiple conversations with fellows and residents on the brink. I didn't train as an MD but arguably PhD training is as long with less certain career prospects, so in that regard I think I have a relevant view on the length of training and the value it offers.
I think the paperwork concern is something you should shelve. No job is going to be without it, and I agree with a previous poster who noted that electronic systems are establishing and evolving.
Regarding training and the length: there is a very strong trend towards niche specialization at the more prominent academic centers. As such, this can be a long training and involves multiple fellowship years and likely some research component. It can certainly be long hours, so it is important to be intellectually interested in it. The best way to do that is to enter medical training with an open mind towards all specialties and see which one you actually practically enjoy. I've seen many enter with the intention of being a cardiologist or whatnot and struggle as they force themselves into a field they're not enjoying.
I think it is also worth having a view of what type of area you'd like to live in. In larger cities, opportunities lie more in teaching hospitals and private practices where they'll expect you to have a fellowship record preferably from a "prestigious" location. Some trainees even do 2 fellowships. However, if you and/or your significant other have always dreamed of returning to your childhood city of 100K people, you won't need to do 5 years of fellowship to be an expert in small, specific populations.
The extra work is worth it provided you have a final goal (work and home lifestyle / location) in mind. IMO avoiding paperwork shouldn't factor into that decision.
OT: Med School
Couple of questions that may help me better comment on your concerns:
- ultimately, are you thinking you'd be working at a teaching hospital / academic center or private practice?
- if not med school (due to paperwork etc), then what is the alternate? Perhaps the alternate has even more paperwork and pays less on top of it all
Preconditioning:
This is actually an interesting phenomenon that seems to have benefits in a variety of settings. Not sure there are great explanations yet, and better controlled trials are slowly coming online, but it's a very cheap / no-effort intervention that deserves study.
Celyad may also fit on your list, unless you think it too early. If I recall, they've dosed their first patient in their NK cell program.
Re: ONTY and the like...
I think every agrees it is far from a slam dunk, but valuation matters and phase 1 data provides enough rational for phase 2.
IPH:
As of no ORR, what can I say? Do people read carefully before they write? The study included mostly patients who had experienced CR/PR by previous treatments!
FGEN / ENTA:
And what number do you plan to use for "Y" that makes this easier?
ENTA/FGEN:
FGEN is a marathon compared to ENTA ph3 clinical programs, which is why it is harder to quantify risk, for me anyway.
GLPG:
Since male is much smaller RA population (20-25%), it wouldn't be much different from other dose reduction implemented under different circumstances, for example renal impairment to use 2mg QD for baricitinib and 5mg QD for tofacitinib.
GLPG:
To be clear, I'm inclined to think that the dosing for men will be sorted out prior to the phase 3. I don't see them doing a phase 3 in the US with men dosed at 100 mg. The efficacy at this level seemed unremarkable.
But with the current status quo, I agree that it would provide a challenge in the marketplace. Even though most RA sufferers are women, the 100 mg total dose seemed a poor efficacy proposition for men. That would suggest that specialists wanting the best for their male and female patients would prescribe separate drugs. This makes it all the more vital that GLPG have very strong efficacy results in the female population, otherwise convenience may prompt prescribers to just stick to one drug.
On the other hand, the GLPG drug may have advantages in the AE profile that may urge docs to preferentially stick with it.
GLPG:
I think their RA drug looks pretty good. I'm a bit curious about what will happen at the higher doses if it remains contraindicated for men in the US. Although not statistically significant, the 200 mg doses did look stronger than the lower doses. This could send the overall ACR response rates a touch lower if men are not able to be dosed much above 100 mg. However, I suspect that this small caveat will be addressed before the company submits an NDA in the US.
It will be interesting to see how the JAK inhibitors compete. Tofacitinib doesn't seem to excite many people, leaving a possible opening for the competitors GLPG and INCY.
Right now I own INCY, MDVN, SGYP, TRIL, ENTA, PFE. Up until a few weeks ago I also owned Innate.
AGEN:
I don't really follow them, sorry. I only watch indirectly via INCY.
INCY
Perhaps you should say that it’s fully valued (rather than over-valued) :- )
INCY:
Good to catch you....I entered INCY, 9-20-2000, at $8.95. I see no reason to sell...any suggestions?
While i question my understanding of the science , i feel that the lack of interest from this board is almost a negative for owning the stock....and i resigned myself to just post info gleaned on other boards in case some find it usefull here
CLDN:
I appreciate it. Honestly, this is exactly where I was expecting it. The ITT HR is probably 1, which would be consistent with the fact that they're not producing any protein in the heart.
I don't think this speaks to AAV use in other organs, but does speak to AAV use in the heart via intracoronary delivery, and also speaks to the credibility of the academic labs that pushed the preclinical work.
QURE:
Sorry if I missed it, but are you generally more optimistic on what BMY aims to do in collaboration with QURE on the gene therapy cardio front or are you as skeptical on that approach as you are with what CLDN is doing?
CLDN:
What, exactly, did the control-arm patients receive?
CLDN:
My point is that if Serca2 was found in biopsyes of the higher dose individuals and non in the placebo group, so the vector works
CLDN:
I believe the company knows what they are doing in therms of type of vectors and transcriptional controls.
CLDN:
By the way I read you have referred to an old article to discuss about the vector, published in 2008. Bear in mind CLDN uses AAV1, which is different to AAV2, it is not the same.
CLDN:
Do you think the basis for this could be endothelial expression of SERCA, or simply cardiomyocyte expression of SERCA that simply loses expression over time? I do understand at least partly the potential issues with AAV and potential carbohydrate recognition mismatch between species.
Having said that, this SERCA isoform is one of the best ways (if not THE best) to deal with CHF if expression can be directed and exist for the long haul.
In a similar vein, do you have a view on QURE?