alive and kicking
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I recognize the accomplishment(s) that Enanta has had, and I think Enanta has at times overstated its wins and understated its losses. I was very much bothered many years ago when at least in my mind Enanta dropped a program without providing much information at all. Today it feels like Enanta may be utilizing a "let it linger" approach with regard to EDP 305 and 297.
Also there is information on the internet about a new building for Enanta operations, this has been intermittently discussed on this board, but I think this is actually a big deal as far as interrupting operations and probably financially as well. The talk with Jeffries this week was not uplifting. However, I did think I heard Jay say he has drug for the phase 3, please correct me if I am wrong, if that is true that there is right now sufficient drug to conduct the phase 3, then this is a big deal.
I disagree
but to be clear enta didn't state if the data is stat sig or not (i presume if you combine the 2 drug arms to placebo to up the N that it is stat sig but again I don' think it matters)
ENTA Pfizer Case One can sort of follow the case from a site called PacerMonitor. Also, there is a May 5th, 2023 document from the case available to view by searching in Google Case 1:22-cv-10967-DJC
ENTA reports additional post-hoc EDP-235 analyses_from_ phase-2_trial—details_in_new_corporate_slide_set:
ENTA reports additional post-hoc EDP-235 analyses_from_ phase-2_trial—details_in_new_corporate_slide_set:
I point out several of your contradictions in your own writings, where you actually lay out your thoughts but you don't or cant explain the error, contradiction or weakness in your argument.
Instead, you change the subject with pure whataboutism.
And in that you seem to feel that the next gen Pfizer drug has great potential I infer you must also agree. What I cannot grasp is how in your mindset that approval is possible for competitors, but also somehow impossible for Enanta's EDP 235.
Nice interview of the IMGN CEO at ASCO after the presentation of the MIRASOL data in PROC. He also talks about why ADCs appear to be making a nice comeback as anti-cancer therapies. Worth watching and encouraging for IMGN investors.
https://www.biotechtv.com/post/mark-enyedy-june-4-2023
Nice interview of the IMGN CEO at ASCO after the presentation of the MIRASOL data in PROC. He also talks about why ADCs appear to be making a nice comeback as anti-cancer therapies. Worth watching.
https://www.biotechtv.com/post/mark-enyedy-june-4-2023
I generally don't because most of what I am doing with what has been a reduced exposure over the last few years has generally been short term opportunities. A significant portion of that has been with options, which isn't for most people on this board. I don't want to come off as facetious or flippant to a serious inquiry, but the few things I am holding for longer periods are probably fairly priced or slightly rich right now.
Then why do SARS patients still get very sick, sometimes hospitalized, and sometimes die still?
The same holds for flu, rsv
Good luck. As I said, other opportunities exist. I've also said that if ENTA goes to 100 without me, that's okay. Can't get more clear than that.
I appreciate your taking the time to explain why you think ENTA will do well. I don't care at all about your tax strategies based on other holdings that have done well, but if you are happy then that's wonderful!
I never said they didn’t see an anti-viral effect why are you twisting my words. I said they didn’t see viral load reductions (as we all know in nasal swabs relative to placebo but I didn’t think I had to spell all that out)
You are also avoiding my point altogether that you use baseline levels to explain away the aligos HBV data but poo poo that when explaining entas viral load data. It’s classic confirmation bias
I just don't see value in a long or a short at this time. Other opportunities exist.
I don't disagree that we will get there eventually for all diseases, but oncology is "easy" because in an increasing number of cases you can identify single-gene drivers.
The causes of metabolic or inflammatory diseases, on the other hand, are highly polygenic and are not going to be incredibly amenable to targeted approaches for a long time, although of course there will be a slow and increasing drip of targeted approaches over time.
Keep looking, there are more :)
As far as I know GSK is the only company to show sustained declines (off treatment) without interferon thus far at rates greater than current standard of care, and this was only in 9-25% of patients depending on baseline surface antigen levels
Bought more ENTA today and have added 20% since the EDP-235 data release. When a deal happens ENTA shareholders will have reason to smile again.
I bought more IMGN this morning under $14. I did it in part due to the impending release of the poster describing data from the Glorioso phase 3 trial, which will be presented at ASCO and released this afternoon. This open label trial is assessing Elahere + Avastin in platinum sensitive ovarian cancer (PSOC). This population comprises ~75% of the patients with ovarian cancer whereas the MARISOL trial was in PROC. IMGN also has two other trial for Elahere in PSOC, one as a single agent and another in combination with carboplatin, an anti-cancer drug that uses platinum.
Let’s see where we are in 12-18 months and let it be this thread is juvenile
I didn't imply negative or lack of confidence unless they leave it on the shelf.
So it wouldn't matter what hey said before. That's my point.
And what if no one partners?
You can certainly feel that EDP-235 is a dead end and that ENTA won't be able to get a partner but that is distinct from the point I am making.
It doesn't matter what they sa[d, If they thought that 235 was superior they'd run a ph3. They've spent millions in research with nothing to show for it.
Good to see ENTA starting to rebound as it breaks $28/share. Obviously a long way to go but eventually the impulsive moves that cause market over-reactions, like the drop ENTA suffered, are countered by cold hard and rational assessment.
ENTA will likely be able to run a non-inferiority trial of EDP-235 vs Paxlovid because Paxlovid is sson expected to receive full-fledged FDA approval (rather than a mere EUA), enabling ENTA to obtain Paxlovid through commercial channels for use in the phase-3 trial. AVIR did not have this option when its own phase-3 trial commenced.
CEO is Jim Bianco, making his public comeback, he of private jets and running CTIC into the ground for years and years.
Good to see ENTA starting to rebound as it breaks $28/share. Obviously a long way to go but eventually the impulsive moves that cause market over-reactions, like the drop ENTA suffered, are countered by cold hard and rational assessment.
I had used very little margin, however I'm sure that some people who've used substantial margin are being forced to sell or bring in substantial cash in spite of having more equity in their account perhaps than even.
Why does Tang want to acquire AVIR? Presumably for AVIR’s COVID drug, AT-527, such as it is. AT-527 is a polymerase inhibitor that is similar to an HCV drug BMY dropped several years ago due to toxicity. AVIR is conducting a phase-3 trial in high-risk COVID patients using a daily dose of 1100 mg (550mg BID); the trial listing is at: https://www.clinicaltrials.gov/ct2/show/NCT05629962 .
No way this stays at 200% gains without a correction, doesn’t happen - just be ready
Gonna do this all the way until asco
Some more observations on why viral RNA levels in the nose aren't a good metric for anti-Covid efficacy. I also point to data from the Shionogi's drug trial isn't as impressive as they would like you to believe or some ENTA critics here assert.
The link to the Shionogi presentation (provided by dewophile). If you notice on slide 9 there is once again is NOT a dose dependent response as the 250mg dose is LESS effective in reducing viral titer than the 125mg dose. In fact, by day 6 the 250mg dose is no better than placebo.
https://www.shionogi.com/content/dam/shionogi/global/investors/ir-library/presentation/2022/ECCMID%20Ph2b%20presentation%20final2.pdf
The same is true for slide 12, total symptom change from baseline as the 250mg dose was LESS effective than the 125mg dose. Something weird is happening, and it sure doesn't inspire confidence.
In slide 14 the middle panel assesses systemic symptoms. It looks like the 250mg dose is essentially a placebo and the 125mg dose had at best a minor effect. Once again NOT a dose dependent response. The only one is a clear separation was respiratory symptoms but not digestive symptoms.
Some last thoughts about the disconnect between viral levels in nasal swabs. The first a general one that people often keep testing positive for RNA long after their symptoms are gone. The second is the issue of the faster viral clearance in the placebo arm in the ENTA study (see slide 22 of the ENTA presentation for SPRINT below). For placebos at day 3, the Shionogi phase 2b study showed maybe a 0.8 log decline but for SPRINT is was already 1.5 log decline. By day 5, the Shionogi phase 2b study showed a 2 log decline whereas the ENTA placebo had a 3.5 log decline. If the decline of viral RNA in the nasal swab correlates with symptom improvement, then the placebo group in the SPRINT study should have reduced their symptoms faster than in the Shionogi phase 2b study.
However, look at slide 17 of the ENTA presentation. The left side is ENTA's SPRINT data and the right side is Shionogi phase 2b study. By 3 days, total symptom score in Shionogi's placebo is down just over 4 log (~4.5 log) whereas in SPRINT, there is a bit less than a 4 log drop. By 4 days, total symptom score in Shionogi's placebo is down 6 logs as is in the SPRINT study. So it sure looks like the more rapid clearance in the SPRINT trial doesn't correlate with more rapid patient symptom improvement. This once again points to nasal swabs not being a good metric for drug efficacy.
https://ir.enanta.com/static-files/c9eca2f1-296c-4a0c-9ce4-d668229f1ec5
“The FTC won’t hesitate to challenge mergers that enable pharmaceutical conglomerates to entrench their monopolies at the expense of consumers and fair competition,” FTC Bureau of Competition Director Holly Vedova said.
ENTA made that point on today's JMP webcast.
Remdesivir also showed clinical efficacy despite no effect on viral loads in the nasopharynx in the outpatient setting. Enta mentioned this on the call but here’s the link for reference.
Ok now I see that the baseline “viral titer” (infectious not rna) was only 2.5 or so. The sensitivity of a positive vs negative viral titer is above 1.0. So a reduction on day 4 of -1.49 on drug vs -1.08 on placebo turns the viral titer from positive to negative even though there is only a -.41 log difference in viral titer on day 4
This graph assessed *infectious* viral titer not total RNA (which can pick up RNA from dead virus). Enta only showed results for total viral RNA not infectious RNA in their presentation.
The fact the infectious viral titer looked so good would lead you to think there would be better efficacy on symptoms despite the modest total viral RNA difference on day 4 which was only -.41 log in this study
I have had the chance to go over the data from the published phase 2 data of Shionogi's anti-Covid drug Ensitrelvir and somethings stand out that just don't make sense, but provides some hope for ENTA's EDP-235. We see that a dose dependence effect for Ensitrelvir doesn't read true and that there isn't a correlation between viral tier in the nose and symptom relief. Keep in mind that Ensitrelvir failed to show a significant relief of Covid-19 symptoms.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10110269/pdf/ciac933.pdf
Figure 2 compares viral changes in placebo and drug (125mg in blue & 250mg in red). In 2B (viral titer decrease log10), the day 4 and day 6 improvement is greater in the 125mg arm than the 250mg arm.
Table 2 shows the same, the lower dose was better.
Table 3 shows patients with treatment related AEs were higher in the 250mg arm (22.1%) than the 125mg arms (13.6%) vs placebo (5.0%). That means the higher dose is doing something, but not doing something beneficial. Still, it provides confidence they didn't mis-label the graphs from Figure 2 or in the supplemental figures following.
Supplementary Figure 1. Mean total symptom changes (A) and change form baseline (B). Keep in mind that Ensitrelvir failed to show a significant relief of Covid-19 symptoms. In looking at the data from B, the 250mg arm looks identical to placebo until 48hrs. The 250mg arm did worse than the 125mg arm until 72hrs then goes back to being worse. None of this is statistically significant but it looks puzzling to me and or shows the weakness of the drug in improving symptoms.
Supplementary Figure 2. Graph of the percentage of patients positive for viral titer in nasal swabs. This is where Ensitrelvir really shines but a disconnect between nasal viral levels and symptom relief becomes clear. By day 4, 54% of patients in the placebo arm are still positive for viral titer. Positive titers are found in only 2% of patients in the 125mg arm and in 6% in the 250mg arm. The difference between the drug arms are likely meaningless but it follows the pattern where dose dependence doesn't follow. However, the major point I am making and that is clear is that a drop in viral titer from nasal swabs does NOT correlate with symptom relief/improvement.
Taking this all to its logical conclusion, if nasal viral titer is NOT a metric for a drug's ability to serve as a anti-covid treatment, then it isn't such a stretch to accept that EDP-235 showed a dose dependent statistical improvement in symptom relief despite not showing a viral reduction in nasal swabs. While not a guarantee, it is food for thought. ENTA will almost certainly present the full data set parsed out in far more detail in a future conference than they did in the press releases. That will be something to look forward to analyzing.
I have had the chance to go over the data from the published phase 2 data of Shionogi's anti-Covid drug Ensitrelvir and somethings stand out that just don't make sense, but provides some hope for ENTA's EDP-235. We see that a dose dependence effect for Ensitrelvir doesn't read true and that there isn't a correlation between viral tier in the nose and symptom relief. Keep in mind that Ensitrelvir failed to show a significant relief of Covid-19 symptoms.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10110269/pdf/ciac933.pdf
Figure 2 compares viral changes in placebo and drug (125mg in blue & 250mg in red). In 2B (viral titer decrease log10), the day 4 and day 6 improvement is greater in the 125mg arm than the 250mg arm.
Table 2 shows the same, the lower dose was better.
Table 3 shows patients with treatment related AEs were higher in the 250mg arm (22.1%) than the 125mg arms (13.6%) vs placebo (5.0%). That means the higher dose is doing something, but not doing something beneficial. Still, it provides confidence they didn't mis-label the graphs from Figure 2 or in the supplemental figures following.
Supplementary Figure 1. Mean total symptom changes (A) and change form baseline (B). Keep in mind that Ensitrelvir failed to show a significant relief of Covid-19 symptoms. In looking at the data from B, the 250mg arm looks identical to placebo until 48hrs. The 250mg arm did worse than the 125mg arm until 72hrs then goes back to being worse. None of this is statistically significant but it looks puzzling to me and or shows the weakness of the drug in improving symptoms.
Supplementary Figure 2. Graph of the percentage of patients positive for viral titer in nasal swabs. This is where Ensitrelvir really shines but a disconnect between nasal viral levels and symptom relief becomes clear. By day 4, 54% of patients in the placebo arm are still positive for viral titer. Positive titers are found in only 2% of patients in the 125mg arm and in 6% in the 250mg arm. The difference between the drug arms are likely meaningless but it follows the pattern where dose dependence doesn't follow. However, the major point I am making and that is clear is that a drop in viral titer from nasal swabs does NOT correlate with symptom relief/improvement.
Taking this all to its logical conclusion, if nasal viral titer is NOT a metric for a drug's ability to serve as a anti-covid treatment, then it isn't such a stretch to accept that EDP-235 showed a dose dependent statistical improvement in symptom relief despite not showing a viral reduction in nasal swabs. While not a guarantee, it is food for thought. ENTA will almost certainly present the full data set parsed out in far more detail in a future conference than they did in the press releases. That will be something to look forward to analyzing.