Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Well, here's hoping Novartis' compound achieves the type of blockbuster sales that only posters on Yahoo message boards can dream of...
Let's see... what's 3% of 20 billion in annual sales???
From osip's 10K, it appears that Novartis has since agreed to license the DP-4 use patent that the WSJ states they initially balked on.
Interesting.
Any comments on the competition in this arena, specifically the "flip-side" rationale of inhibiting dipeptyl-peptidase to increase glp-1 circulation?
yes, you're right... the A looked like a P after happy hour on friday.
my mistake.
GenoMed is a S-C-A-M... through and through. eom.
maybe the sheep are happy that goddard's online broker finally offers the "Buy" option for stocks rather than V1.0 that apparently only had a "Sell" option...
Thanks... I had clicked on the one PR that had no data on it and missed the second PR.
So their data proved that although there was no statistically significant weight loss in 12 weeks over placebo, patients on drug achieved their prospective 12 week weight at an accelerated rate.
It is also interesting that they extrapolated the mean weight loss from a linear fit to the data rather than presenting the actual mathematic mean (or median) weight loss at the 12 week time point. If you compare the graph on page 5 and the table on page 6, it is clear that this method of estimation drops the 12 week mean of the placebo group by ~20% to a mean of 0.8 kg loss rather than the 1.0 kg weight loss shown on the graph.
Wonder why they did that, because in the description of analysis on page 6, they explicity state either a comparison of the slopes, or an outright comparison of the week 12 versus week 0 numbers.
How well do patients remain on fat trials? Do they get tossed from trials if they don't adhere to the accompanying exercise protocol? I suppose that ITT analyses in this indication are also the gold standar?
Anybody have more data on this Metabolic news?
With 6 dosing groups, that ends up being about 50 per dose. Lowest dose appears to be most effective but I can't find data for the other dosing groups.
Any help?
I thought about Telik, but the problem is that they have a generous valuation right now, and with Telcyta approval, it is hard to expect more than a double in valuation. A double isn't bad (!), but some of the cheaper stocks can bring a greater multiple on your investment.
After much (5 minutes!) thought, I had to accept CTIC as the most enticing one. Over the next 24 months, they could actually see approval of 2 NDAs. It has the highest reasonable risk, in turn for the highest reward.
GTCB isn't bad, but I'm not sure if they'll have established their platform in 24 months. I think they'll probably have one approval and a pivotal trial or two by the end of 24 months. Stretch it out to 36 months...
I apologize... i was unclear in my question.
What is the failure rate for the procedure as it is currently used? Presumably this is the number that anormed is trying to improve upon.
The pixantrone trial in relapsed, aggressive non-Hodgkin's lymphoma does indeed have SPA guidance from the FDA. It's pix versus the investigator's agent of choice. The primary endpoint is an increase in complete responses, and I believe that there is to be an interim analysis in mid-2005. My memory may be faulty, but I do not think CTIC has revealed much regarding the stat penalty for the interim analysis, or the % improvement that they'll be looking for.
As for ARQL, I believe DD is accurate. My bet is that they're taking all comers in the first stage to fish for an indication that appears more sensitive than others. One annoying thing in that PR is that they refer to a clinical trial with taxotere but suggest that the preclinical basis was in models using arq501 and taxol. Sounds downright absurd. Hopefully it's just a typo...
I guess my question regarding stem cell transplatation is:
What is the failure rate?
aahhh....
my fault then
By first, I meant to convey "the first result to come out". I have a feeling that based on the results from the first one, the market will handicap the remaining 2 and adjust the share price accordingly.
Stellar 2, 3 and 4 have all completed enrollment. However, data is not out from any of the three.
For Stellar 3, they're about 40 deaths short of triggering the analysis of the trial... although i wish they would delay their analysis (but that's another story). This likely puts the trigger date for analysis sometime very early in 05.
Many seem to be expecting stellar 4 to have data ready at about the same time. So the first quarter of 2005 is going to be a hell of a ride for ctic.
I'm not sure what Stellar 1 is, if there was one. It's before my time.
Never really understood the potential of increasing stem cell harvests for transplantation. It's my understanding that the procedure has a relatively good success rate. In a very recent Velcade trial, 8 of 8 patients scheduled for stem cell harvesting underwent the trial successfully.
If so, what is the utility of recovering that extra 10% of cells?
Tough one to get excited about right now, in my opinion.
I don't think any DNA-decoy method will work. I didn't think cgtk's trial would show anything, but i was too chicken to say anything or put my money down.
I feel like the lion in the wizard of oz.
>Does CPOP expand the potential for such regimens? <
I have no hard data to answer this question right now. However, I do project that the answer will be yes. The important factor is the tolerability of pixantrone versus doxorubicin. The latter is well known to have cumulative cardiac toxicity in humans due to exacerbation of free radical-derived damage. This has seriously limited doxorubicin use / retreatment in the clinic. To date, pix appears to be much more benign with respect to this serious side effect. Therefore, approval of pix may open up retreatment regimens that were not previously an option with dox.
Additional commercial opportunities lie in breast, ovarian and some blood cancers. CTIC has some heavy lifting to do in order to introduce pix as a softer, gentler doxorubicin. However, the economic benefits will be worth the effort.
I have a modest position in CTIC that I plan to increase following the results from the first Stellar trial. I figure if the stellar trials work, then i'll be buying for xyotax and pix. If Stellar fails, I'll be able to buy relatively more but just for pix. I realize it makes just as much sense to buy right now, but for some reason, I don't want to hold a large position ahead of the Stellar uncertainty. Gut feeling, not objective reasoning...
Oncolytics:
I have no position. An undergraduate friend of mine worked with Dr. Lee for a summer. I chose another lab. He said it was intense and Lee had a reputation for being smart and doing great work. The data from his lab are first rate. However, I've been spooked by the fact that he doesn't appear to be very involved in the company... at least as far as i know. That has kept me on the sidelines somewhat. And for some reason, I just don't trust the company. Don't ask me why because I can't give you solid reasons... just a gut feeling that is strong enough to keep me away for the time being.
Apparently I make most of my decisions based on my gut, not on the data
For Rituxan + CHOP in untreated NHL, response rates approach 100%, with CRs in the 60% range. For the CTIC trial, many had already failed CHOP, so the observation that 41% of those achieved a CR with CPOP looks pretty encouraging.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_...
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_...
I look for pixantrone to effectively replace doxorubicin, so it's really a CHOP versus CPOP competition at the beginning. Hopefully that will be enough for physicians to replace Rituxan + CHOP with Rituxan + CPOP.
>As I said before, this is starting to look suspiciously like a vehicle for management enrichment.<
Exactly. Management and the traders / investors that they're in bed with.
The big boys are playing that stock now. It's a joke of a company, but you don't need products to make traders rich in the market. Thanks to future dilutions, it is guaranteed that any honest investor will not make a good return off Genta.
However, Dew's point is valid: Don't be left holding the bag when the big boys decide that the Genta game is over.
For the record, Allen's explanation that BMY dropped the drug because it was singularly focused on objective response rates really didn't go over with me. Basically, he was saying that BMY didn't bother to look at the survival data at all once they saw the response rates were unchanged. I find this type of talk to be common for drugs that have been cast off from big pharma and rescued by smaller biotechs.
Also, I'm not touting response rate as a 100% reliable predictor of clinical benefit. It is an arbitrary measure. However, for a drug that is hypothetically able to increase the time that a cytotoxic sticks around the cell, it is reasonable to expect an increase in RR. My preference would be to focus on the PFS data as a reliable predictor of survival. Anyways...
On another topic: Yes, you're quite right. AMEV was fiddling with the variable portion of antibodies in order to screen for better binding clones.
>In a case like this it is helpful to see the K-M curves themselves. Comparing only the median values of the active-arm PFS and OS to their placebo-arm counterparts can be misleading.<
For overall survival i definitely agree. I've already seen the k-m curves for the finished phase III. In the subgroup of interest, there is no evident treatment influence on the k-m until 8 months. Also from the look of the k-m curves, it looks clear that the lack of PFS improvement isn't simply due to a consideration of a single point.
Heck what do i know? I'm sure the trial will work.
My point with the BIOM data is that it can be easy to dismiss impressive prior data *knowing* that the follow-up failed. However, had you read BIOM's phase II data at the time of its release, would you have invested?
One thing to keep an eye on for tesmilifine: it's noted to enhance chemotherapy cytotoxicity possibly by modulating p450 or interfering with MDR. If that's the case, my little mind suggests that an arm with cytotoxic X + tesmilifine should have a higher response rate than the cytotoxic alone. This is likely to be accompanied by higher toxicity for the cytotoxic + tesmilifine arm.
I note that from the JCO paper, tesmilifine did not increase the number of objective responses but did increase toxicity (note that an MDR inhibitor has failed phase III NSCLC due to toxicity). Also interesting is that the ASCO abstract for this trial suggests that an interim analysis looking for increased response rate failed to show it, but did show increased toxicity.
The other red flag with the phase III described in the JCO article is that overall survival was increased by the addition of tesmilifine without an increase in PFS. If this increased survival is a drug effect attributable to tesmilifine, then why isn't PFS significantly increased? As described (if you imagine the kaplan-meier curves), the data suggests a long-term survival bias for the tesmilifine arm well past the time that treatment ended... which begs the question about patient treatment following their progression *off* the trial. I haven't had time yet to comb over the JCO paper, so these questions may be answered. If not, they may be reason for caution.
This used to be a Bristol Myers drug? Any idea how it landed into YM's lap? Interesting to note that BMS is in the ASCO abstract, but their name is missing from the JCO publication. Did they drop it for toxicity?
25 patients. Median survival for those patients was 26.5 months compared to 9.2 months for a historical control.
Suffice to say it didn't pan out.
>BIOM - Their drug would be used after chemo so not a competitor to YMI<
I wasn't mentioning Theratope as a possible competitor. Rather as a drug that showed a doubling of median survival in phase II.
check out biom and theratope. eom.
Part assumption, part deduction...
(actually, handicapping this ISEL result is an interesting exercise)
The underlying assumption is that both molecules are metabolized at the same maximum catalytic rate by the cytochrome enzymes involved... therefore, the only variable influencing overall clearance of the two drugs is total enzyme activity. Both Iressa and Tarceva are cleared primarily by Cyp3A4 and additionally by Cyp1A2. The latter, Cyp1A2, is induced by smoking. Therefore, clearance in smokers should proceed at a faster rate assuming that clearance is proportional to the sum of the total activities of Cyp3A4 and Cyp1A2. Since Iressa is less potent, and maintains lower Cmax and Css values than Tarceva, the clearance of both drugs under conditions of normal Cyp3A4 and Cyp1A2 activity should give Tarceva the edge. With Cyp1A2 induction in smokers, the overall clearance for both drugs (dictated by Cyp3aA4 + Cyp1A2 activities) should increase, giving an additional neck-up for Tarceva in the PK/PD race.
All theoretical, mind you... but if ISEL fails to match BR21, I'm going to pretend as if the above explanation was the clincher
Some interesting Iressa data from the Moffitt cancer centre that I had not previously seen:
http://www.moffitt.usf.edu/pubs/ccj/v10n5/pdf/388.pdf
They ran their own prospective Iressa study in 183 patients. The population is about 50% adeno, but did not restrict enrollment to those having previously received chemo. 18% were chemo naive, 40% had received 1 prior therapy. Most were PS0-1 (32%:43%), and 7.7% were PS3. Generally a healthier population than in the BR21 study. Nice data to have handy for those handicapping the Iressa versus Tarceva battle.
One aspect that may be in Tarceva's favor with respect to the ISEL trial is smokers. Goddard has mentioned that Tarceva is cleared faster in smokers than in nonsmokers; possibly a reason for the lower efficacy in this group. Rapid clearance of the drug really hits Iressa harder than Tarceva, since Iressa has a lower affinity for the EGF-R target.
Although Tarceva didn't show great efficacy for smokers (HR = 0.87), if Iressa bombs on this subpopulation, it could account for the small difference that OSIP needs at this point to shed itself of the Iressa shadow.
And after looking at the participating countries, I feel pretty good about there being sufficient smokers in the ISEL trial
Thanks for the paper.
With Tarceva hitting the EGF receptor with an IC50 of 2 nM, a 500 fold reduced specificity for the IGF-IR would mean that it is getting hit when Tarceva reaches about 1 micromolar in the blood. At that point, half of the IGF-IR signaling would be shut down whereas 99.9999% of the EGF-R signaling would be shut down.
If I remember correctly, Tarceva does readily achieve 1 micromolar concentration in the blood, so some inhibition of IGF-IR signaling is reasonable to expect. Unfortunately, I think it is near impossible to reliably handicap the impact of the EGF-R inhibition versus the IGF-IR inhibition. However, a theoretical 50% inhibition of a kinase is pretty shabby. Perhaps a very small percentage of the patients may have responded in part due to IGF-IR inhibition. But across a large sample, 50% inhibition of kinase activity is unlikely to demonstrate much effect in aggressive cancers.
insulin-like growth factor receptor?
I'm ashamed to admit that my DD never uncovered this... i'm also drawing a blank on Pubmed.
Care to elaborate?
Show that to Bio-guyo on the Imclone thread...
I'm encouraged by such data. In the absence of a definitive test for the EGF-R mutation, it only makes sense that Iressa be tried in case the patient carries the mutation.
Kinda cheap for AZN to be gripping the "class-effect" mantra though. When I'm talking to some of the cardio reps from AZN over lunches, they speak about Crestor being better than Lipitor and how you can't just judge it by class (their attempt to differentiate themselves from Merck's drug).
Anyways, I'm sure the market will sort all this out soon enough.
I rarely make outright purchase recommendations, but I really think OSIP is a gift here.
The Package Insert is available at Tarceva.com
It does have a mention of insterstitial lung disease, however, the incidence on the Tarceva arm is exactly the same as the control group. If this is part of what people are basing their selling on, then they're going to regret it imo.
My opinion is that the only way Iressa matches up to OSI is if they've excluded PS3 patients from their large registry. Dunno if that kind of a trick will work on oncologists, but it would surely work on the public.
However I've not followed this Iressa trial very closely so I do not know the entry criteria... I'm shooting from the hip.
Dunno if it was halted or not, but yahoo is showing osip up 3 bucks and change. My real-time shows nada...
Since T/A is often revisionist, I would like to retro-actively claim victory for this at-the-time ill-fated call.
Never, ever doubt the validity of retro-active T/A.
>Ferris makes it sound like they've seen the FDA response to GNVC. Awfully positive when GNVC hasn't even responded to the FDA yet.<
Hack job by a seemingly hack outfit. They need to be more careful with the way that they phrase their opinions.
>I’ll give you an A for effort, but I’m not convinced that watching the tick-by-tick movements confers any prognostic value.<
Probably not, and it doesn't seem like you would have believed any explanation And with OSIP's price taking a $1 dollar dive in about 30 minutes, needless to say that I'm keeping my day job!
>Re: MLNM’s PROTECT results (Integrilin vs Angiomax): the market’s initial response seemed more consistent with my assessment of a draw rather than your qualified assessment of a clear win for Integrilin. Cardiology is not my strong suit but, from the limited DD I’ve done, it would seem that Angiomax does crimp the prospects of the GP2b/3a inhibitors in the cath lab.<
MLNM's Integrilin is really a product that has saturated its marketplace. I don't think that these recent trial results have given anyone just cause to significantly expand Integrilin use. Market seems to be yawning, as you note. However, if I had a cardiac episode, I'd want a drug that increased myocardial perfusion and reduced myocyte necrosis. And so would you. That's why I thought Integrilin had the upper hand in those results.
dunno if this qualifies as "operational" or pure "laymen":
When a stock with sufficient liquidity (ie. doesn't trade 50K per day) opens the day down 3% from the previous close on very little volume, and then climbs in a step-wise fashion towards the previous day's close on relatively higher than average volume... that's accumulation in my book
OSIP closed yesterday at 65.71. Opened today at 64.38 and hit the day's low of 63.80 in the first 5 minutes of trading. Since then, it has recovered almost all of the day's losses. Is now down only 0.5% for the day on roughly 1 million shares at 1 pm. Average volume is ~1.3 mill a day.
Shaping up to be a big accumulation day for OSIP... volume is also looking above average. For those interested in playing an approval pop, it may be time to keep a closer eye on the stock.
OSIP completed their NDA filing for Tarceva on July 30th, and the PDUFA deadline is Jan 30, 2005. However, many expect approval before the deadline. In fact, OSIP, in a recent 8K, noted that they too expect an FDA decision before the PDUFA data. It's not often that I read those types of comments in an SEC filing.
Volume isn't especially heavy today, fwiw...