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Oren: "Right now avastin and vb111 I believe doing around the same"
They're doing the same but you don't think they've reached the 105 events. So what are you saying? That avastin is performing much better than it has historically?
Assuming positive DSMC review (which I think is likely - > 50% chance), what is the next significant milestone? I am thinking it will be either the Ovarian phase 3 first patient announcement or the announcement that VB-111 is being evaluated in combination with an anti-PD-L1 checkpoint inhibitor partner.
Anything else? Facilities is good news, but perhaps not as significant? Or is it?
With CAR-T, patients that get fevers are considered "lucky" because that means the treatment is working. They usually let the fever, which can reach over 110 F, run the course to the point where the patient is in a coma-like state.
Interestingly, they also give patients acetaminophen when there is a fever because "(a)cetaminophen is used for comfort but does not usually relieve the fever." This aligns with what I said earlier: acetaminophen is an analgesic.
So I don't think it is an issue that VBL is giving patients acetaminophen when they are feverish.
Reference:
https://voice.ons.org/news-and-views/nursing-considerations-for-adverse-events-from-car-t-cell-therapy
Oren1976 .. How are they treating the fever? With acetaminophen? If so have there been research showing that acetaminophen is an immunosuppressant? My understanding is that acetaminophen is an analgesic.
imo, the immune system is also reliant on the patient's health. A healthier patient = stronger immune system. So if acetaminophen is not an immunosuppressant, I don't see the harm in giving it when the patient is feverish.
I think the thinking on this board is that 105 events have already happen and that we are waiting for the 50% with 12-month follow up. Based on the Avastin and VB-111 phase 2 survival data, it makes sense that 105 events would happen before the 12 months. But if 105 events have not happened then I can't help but think that it is mostly because of VB-111. Of course, something weird could happen during recruitment and the median survival on the Avastin side is longer than usual. Anything is possible.
Now, the reason why the interim was canceled and "replaced" with the third DSMC review is debatable. We were all surprised by the announcement. Oren has a few theories but I don't think the board has come to an agreement on what transpired. At the end of the day, outside of the DSMC folks, no one really knows (including Dror). What is known is that:
1) The change has the FDA's blessings;
2) VB-111 is doing well enough not to get stopped; and
3) There are some long-term survivors but we don't know how those survivors are divided between the two arms. Dror brought up that data in the last call. He is not blinded to the aggregate but he is blinded to the details.
Personally, I think the latest developments are good. The good news is the FDA is happy enough with VB-111 that they're okay with just the DSMC review (safety). I think there is a high chance that VB-111 will pass DSMC because it has a very safe profile, with low serious AEs. Then, the only thing left is the final results. When that day comes, it will be intense!
This is an accurate summary of the company line. I've always been positive on VB-111 and the latest news at the very least gives me more confidence in VB-111.
http://www.baystreet.ca/articles/research_reports/lifesci/VBL081417.pdf
The Company reiterated its guidance of having topline data in early 2018 from the Phase III GLOBE study evaluating the combination of VB-111 and Avastin (bevacizumab) for recurrent glioblastoma multiforme (rGBM). Notably, the interim analysis that was planned for the third quarter of 2017 will not occur due to the closeness of topline data, but a data safety monitoring committee (DSMC) analysis is expected to occur in late September.
I am still waiting for a drug that helps improve survival of rGBM patients. Even if VB-111 improves survival by only 30 days, it is far better than Avastin when you compare the side effects.
rGBM patients receive VB-111 with Avastin so when bad things happen they blame it on both drugs; they don't really know. But their side effects are very similar to patients taking Avastin alone. Furthermore, ovarian patients on VB-111 are not reporting these side effects.
What the FDA does or does not do with the VB-111 reporting process is irrelevant to me. People are dying and suffering with rGBM. Perhaps all the FDA is trying to do is determine if VB-111 is effective and get it to market asap.
I listened to the call 3 times (live and then 2 more times afterwards). I thought it was a good call for a few reasons:
1) The FDA determined that an interim report is not needed since the DSMC will review the data up to the end of August. My read is that the last DSMC data was positive enough that the FDA is comfortable with waiting for the DSMC report in September.
2) There are some patients that are being treated for a long time. Dror is blinded but his assumption is that avastin data will reflect historic results and thus, these patients are most likely being treated with VB-111.
3) Some other positive flags. New facilities are on schedule to support production. BLA being discussed.
I'm cautiously optimistic. No worries based on my due diligence.
Of note:
PFS will be censored at the time of initiation of alternative anticancer therapy, date of last radiologic assessment, or time of last contact.
For subjects who have not died, survival data will be censored at the subject's last known alive date. The Kaplan-Meier method will be used to estimate the distribution and median OS for subjects treated at the MTD level.
For patients who do not progress or die, PFS will be censored at the time of initiation of alternative anticancer therapy, date of last tumor assessment, or time of last contact.
Patients will be followed for survival status after completion or removal from the study for progression or toxicity until death. For patients who have not died at the time of analysis, survival data will be censored at the patient's last known alive date.
VB-111 was safe and well tolerated, 53 adverse events were reported, 14 were classified as possibly related to VB-111. All events were of CTCAE grade 1-2 except one grade 3 pulmonary embolism (PE). There were no study related deaths.
While we're waiting for the quarter and interim results, check out the patent filed in May 2016. A good read.
https://www.google.com/patents/US20160121001?cl=enAn
VB-111 and bevacizumab are both anti-angiogenic agents that target the tumor vasculature. However, they do so based on two distinct MOAs: Bevacizumab antagonizes VEGF while VB-111 directly disrupts the angiogenic vessels.
Expected Adverse Events with Bevacizumab
- Serious and sometimes fatal GI perforation occurs at a higher incidence in bevacizumab-treated patients compared to controls
Surgery and Wound Healing Complications
- The incidence of wound healing and surgical complications, including serious and fatal complications, is increased in bevacizumab-treated patients
Additional patients were subsequently added to the study and the data were recalculated accordingly. Forty six patients aged 27-76 years at 4 medical centers in the US and Israel received up to 13 repeat doses of VB-111. Of these, 30 patients received the high dose (1×1013 VPs). There were 22 related adverse events, 19 CTCAE grade 1-2; grade 3 included pulmonary embolism, peri-tumoral edema and DVT. The median overall survival was 360 [range: 70-574] and 266 days [range: 28-664] for patients receiving at least one high dose vs. subjects who received lower doses, respectively (p NS). Progression free survival was 63 vs. 55 days for patients who received high vs. lower doses, respectively (p=0.01). Median follow-up was 232 days. Six patients had a partial response and/or prolonged disease stability (?180 days). Tumor growth rates showed a statistically significant dose response. Eleven patients received combination therapy of up to 4 doses of VB-111 together with bevacizumab after progression on VB-111 monotherapy. Median time to second progression was 93 days. These data are shown in FIG. 2. FIG. 3 provides an example of a patient who was treated with a combination of VB-111 and bevacizumab upon disease progression. VB-111 was safe and well tolerated both as monotherapy and combined therapy.
[0639]
Conclusions:
VB-111 was safe and well tolerated in patients with recurrent GBM with repeat doses of up to 1×1013 VPs. Tumor responses were seen. Overall survival was about 3 months longer compared to historical data in recurrent GBM including standard of care anti-angiogenic agents. Data suggests that VB-111 potentiates the response to bevacizumab given at further progression.
Looking forward to the VB-111 combo announcement later this year and hope they consider more than lung. With all the failures in gbm, it looks like treatment is moving towards combo as well.
https://www.washingtonpost.com/news/to-your-health/wp/2017/07/26/these-experimental-treatments-target-brain-cancer-like-john-mccains/?utm_term=.d3912d2da5e0
Researchers say they are learning from the failures. They now believe, for example, that it will take a combination of treatments to make progress against the disease. One reason: Glioblastoma tends to have subpopulations of different cancer cells that require different lines of attack.
The immunotherapy approaches include checkpoint inhibitors, genetically engineered cellular therapies, vaccines and viruses that infect and kill cancer cells.
Also, just for conversational purposes. Anyone familiar with KB (Katherine Barnett) Peters? She works in the Neuro-Onc dept at Duke and published this research.
Look who is funding her research.
http://www.tandfonline.com/doi/full/10.1080/21678707.2016.1235971
Utilizing PubMed and MEDLINE® databases, we identified key preclinical and clinical data pertaining to VB-111. We then reviewed ClinicalTrials.gov to determine the status of ongoing research.
Expert opinion: Demonstrating safety and showing signs of efficacy in early phase clinical trials, VB-111 is being studied in combination with and without bevacizumab in a large phase 3 trial for recurrent glioblastoma. Given the data, VB-111 is a unique viral-mediated, antiangiogenic approach that has significant potential to make an impact in the field of oncology and neuro-oncology. We agree with the continued study of this agent in expanded and randomized cohorts to determine if VB-111 can indeed impact survival in glioblastoma.
KEYWORDS: VB-111, virotherapy, angiogenesis, adenovirus, glioblastoma, glioma
Additional information
Funding
KB Peters research is funded by Eisai, Merck, Genentech, Amgen, BioMimetix Pharmaceutical, Inc., VBL Therapeutics and Agios.
I think you're right, wcopeland. I was using the fact that there are 52 weeks / year and that averages to 4.33 weeks / month. Also, the Hebrew / solar calendar alternates between 29 and 30 days per month.
Using 4 wks (28 days) / month is reasonable but opens up the data to accuracy questions. Perhaps that is why they changed the data from months to weeks; to be more accurate.
I'm not too concerned about it. 59 weeks is still a heck of an improvement from 32 weeks. Even if the interim data comes back with 55 weeks, that would be amazing. Anything above 50 weeks would be amazing, imo (especially considering how many others have failed).
It used to be 15 months (or 64 weeks). 59 weeks (almost 14 months) is 5 weeks less. Do you recall why the numbers changed?
http://www.vblrx.com/vbl-therapeutics-announces-launch-of-the-first-israeli-site-as-part-of-the-globe-international-pivotal-trial-for-vb-111/
In November 2015, at the Society for Neuro-Oncology (SNO) conference, VBL reported data from its recently-completed Phase 2 multi-center study of VB-111 in rGBM, which showed that VB-111 almost doubled the historical median overall survival for rGBM. Patients treated with continuous exposure of VB-111 had median overall survival (OS) of 15 months, compared to 8 months in patients with limited VB-111 exposure (p=0.048).
Thoughts on the differences between median overall survival numbers in 2016 and 2017? If you ask, "What differences?" then you have not been paying attention.
Notice the wording "a better planned randomized phase 2 BRAIN trial". You would think a company like Genentech/Roche have extensive experience in designing trials .... unless they intentionally designed the trial so that the data worked favorably for them. Seems like that strategy work for them ... billions for them and no improvement in mOS for the patients. This is all about greed and nothing to do with improving healthcare.
Biosimilars are taking their market share and hopefully VB-111 does too.
Interesting comment from Cloughesy, who is leading the GLOBE trial, regarding avastin:
“This is the first prospective, randomized clinical trial to address the question of bevacizumab continuation in recurrent glioblastoma,” Dr. Hovey said. “Continuing bevacizumab after progression of recurrent glioblastoma did not improve PFS,” nor did it confer “any apparent clinical benefit.” She said that these results must be placed in context with a variety of other data, but this study suggests that bevacizumab should not routinely be continued beyond disease progression.
Discussant Timothy Cloughesy, MD, of the University of California, Los Angeles, called the data compelling. “We have been evaluating bevacizumab for 10 years, and we don’t have a really clear idea of where we’re going,” he said.
https://am.asco.org/no-benefit-continued-bevacizumab-recurrent-glioblastoma
Also, it looks like avastin achieved some crazy results in early trials that drove the FDA approval. Its median OS of 9.2 months in one phase 2 but subsequent trials have shown mOS to be in the range of 8 months (32 weeks).
Several phase I/II studies reported high responses and improved 6-month progression-free survival with Bevacizumab. Based on these results Bevacizumab, a vascular endothelial growth factor inhibitor received FDA approval for use in recurrent gliomas. Subsequently, a better planned randomized phase 2 BRAIN trial investigated bevacizumab alone and in combination with irinotecan did not show a convincing benefit of Bevacizumab compared with historical series [42]. The trial randomly allocated 167 patients with first or second relapse to receive Bevacizumab monotherapy or in combination with Irinotecan. The primary end points were 6-months PFS and overall response rate. The trial reported 6 months PFS 42.6% and 50.3% in the monotherapy and combination arm, and ORR 28.2% and 37.8% respectively. Median Overall survival was 9.2 months and 8.7 months respectively.
http://www.sciencedirect.com/science/article/pii/S111003621630036X
If VB-111 comes close to its phase 2 results (59 weeks mOS) then it would be an amazing accomplishment.
The way phase 2 worked, as I understand it, is that everyone (n=46) was given VB-111 as a monotherapy. Then upon progression (median of 1 dose) they were put in 1 of the 2 cohorts: 1) Avastin alone or 2) Combo. Here's a link for review:
http://ir.vblrx.com/news-releases/news-release-details/new-phase-2-patient-data-presented-asco-strengthen-evidence-anti
A total of 46 patients were enrolled in two sequential cohorts. In the first cohort, patients were treated with VB-111 as monotherapy for a median of only one dose and, upon disease progression, switched to Avastin (bevacizumab) alone as standard of care (Limited Exposure cohort). This cohort behaved like an Avastin historical control with a median Overall Survival (mOS) of 8 months.
In the second cohort, patients continued to receive treatment with VB-111 after progression, in combination with Avastin as the standard of care (Treatment Through Progression cohort). This cohort received in median 4 doses of VB-111, about 8 months of treatment.
While we wait for the results, this deck is worth revisiting. From slides 48-53 (download presentation at bottom of page):
https://sigport.org/documents/pca-based-algorithm-longitudinal-brain-tumor-stage-classification-and-dynamicalmodeling
Figures illustrates how the therapeutic Fas-c protein successfully controls the trajectory of Tumor Cells to an equilibrium state that approaches zero (y=0.77). Treatment proved also successful in controlling TNF-a which approaches zero (x=0.0018). These results agree with the findings in actual biological experiments between Tumor cells, Effector cells and TNF-a. With virotherapy treatment, the system moved from a pathological state (Tumor cells ?0) to a normal state where Tumor cells, effector cells and TNF-a are approaching zero
Figure 32 compares cells dynamics between two cases: with and without VB-111 treatment and for different antigenic tumors. It is apparent that our model captured the therapeutic properties of Fas-c on tumor cells, effector cells and TNF-a. In the case gene therapy is not administered , regardless of the level of tumor antigenicity , the cell dynamics exhibit oscillatory behavior alternating between different states (fig c,d). When VB-111 gene therapy is administered, however, the previously perturbed states are stabilized with a Fas-c protein killing rate of ß=10 (fig a,b).
-it is apparent that our model successfully captures the decay and stabilization of tumor cells by VB-111 monotherapy
I hear ya - there can be good and bad outcomes when it comes to mitochondrial dysfunction.
With avastin, I think it's more bad for the following reasons:
1) There is no fever associated with avastin (like VB-111) so it makes me wonder if the immune cells are being recruited.
2) Avastin side effects (like severe weakness) points to mitochondrial malfunction and the body not getting the energy it needs.
While not conclusive, the research does provide an interesting perspective.
oren ... more fuel for your "avastin devil" fire
CONCLUSIONS:
TMZ and BEV can directly cause the dysfunction of mitochondria isolated from human brain tumors. However, BEV has a greater ability to disturb mitochondrial function in mitochondria isolated from human brain tumors than either TMZ or calcium overload conditions.
https://www.ncbi.nlm.nih.gov/pubmed/27078710
I read that as him saying that he thought the DSMC review would happen sooner than it did. After the DSMC review he said, "Based on enrollment trends and events that triggered the DSMC review, we currently expect the GLOBE Trial interim analysis to occur in mid-2017." This aligns with what you quoted.
Estimating when X number of deaths will happen (to trigger the DSMC review) is harder than estimating the deaths that occur in the mean OS metric, imo. The math that I provided earlier is not accurate, but it is more accurate than estimating when X number of deaths will happen.
Doing the math, I can see why Dror thinks that the number of deaths will happen before the 12-month follow up for 50% of the patients.
Avastin median OS = 32 weeks (this has been established from pooled data of prior Avastin trials)
VB-111 median OS = 59 weeks (from phase 2)
Based on the above numbers, 105 deaths out of 252 patients should happen before the 12-month/52-week follow up for 50% of the patients.
This is an educated guess from Dror/VBL. It is highly likely to play out this way but it does not mean that they know the data. They are blinded to the data.
Dror gave the reason for his estimate and it was pretty clear for me:
"So first everybody should understand that we are completed blinded on the data. And we have no way to know much on the data and that clearly is only the data monitoring committee that can take look at the data. And we insist on being completed blinded and we never try or allow anybody to tell us anything different that can hint anything. We know when we recruited patients and of course we know when we are going to get to the 12 months follow up of half of the patients. And that's not going to happen before Q3 2017."
This is an interesting list. 3 on the list were phase III. 3 were angiogenic inhibitors. This is why avastin, even though it sucks, is the SOC. Many have tried but none have been able to beat avastin as the SOC.
Still, VB-111 looks promising and I'm looking forward to the interim in Sept/Oct.
http://www.sciencedirect.com/science/article/pii/S111003621630036X
Table 3. Summarizes different agents used for the treatment of rGBM alone or in combination failed to achieve significant response in phase I/II/III trials.
Drug/Phase Type of drug
Verubulin/Phase II Microtubule destabilizer and Vascular disrupting agent
Erlotinib + temsirolimus/PhaseII Epidermal growth factor receptor (EGFR) and the mechanistic target of rapamycin (mTOR)
Sunitinib/Phase II Inhibitor of several receptor tyrosine kinases
Fotemustine/Phase I; Phase II VEGF inhibitor with Nitrosurea
Enzastaurin/Phase II, Phase III Selective oral inhibitor of protein kinase Cß
Cediranib/Phase III [monotherapy or in combination with Lomustine] Vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor
Dasatinib/Phase II Multitargeted tyrosine kinase inhibitor
Bosutinib/Phase II Kinase inhibitor of Src and Abl
Cilengitide/Phase II av integrin antagonist
CT-322/Phase II Inhibitor of VEGFR-2
Veliparib/Phase I PARP inhibitor
Pazopanib + Lapatinib/Phase II Antiangiogenic pazopanib; ErbB inhibitor lapatinib
Gimatecan/Phase II Lipophilic oral camptothecin analog
Nintedanib/Phase II Triple angiokinase inhibitor
Vandetanib/Phase II Multi targeted tyrosine kinase inhibitor
Patupilone/Phase II Natural microtubule-stabilizing cytotoxic agent
Vorinostat/Phase II; Romidepsin/Phase II Histone deacetylase (HDAC) inhibitor
TLN-4601/Phase II Ras-MAPK signaling pathway inhibitor
Aflibercept/Phase II VEGF Trap
Sagopilone/Phase II Lipophylic and synthetic analog of epothilone B
Rilotumumab/Phase II A fully human monoclonal antibody against hepatocyte growth factor/scatter factor (HGF/SF)
Imatinib + hydroxyurea/Phase II Protein-tyrosine kinase inhibitor that inhibits the BCR-ABL tyrosine kinase
Didemnin B/Phase II Natural product derived from the Caribbean Tunic inhibit all phases of the cell cycle
Induces rapid and wholesale apoptosis through dual inhibition of PPT1 and EEF1A1
KRN8602(MX2)/Phase II A novel morpholino anthracycline with capacity to cross BBB
Thalidomide/Phase II Putative inhibitor of angiogenesis
Paclitaxel/Phase II Enhances the polymerization of tubulin to stable microtubules
Cystemustine/Phase II Nitrosourea
Marimastat/Phase II Matrix metalloproteinase inhibitor
XR5000/Phase II Tricyclic carboxamide that intercalates DNA and inhibits both topoisomerase I and II
Gefitinib/Phase II; Erlotinib/Phase II Epidermal growth factor receptor tyrosine kinase inhibitor
Cloretazine/Phase II Novel alkylating agent belonging to 1,2-bis(sulfonyl)hydrazines class
Cetuximab/Phase II Anti EGFR monoclonal Antibody
Trabedersen/Phase II TGF-ß2 inhibitor
Bortezomib/Phase II Proteasome inhibitor
Convection-enhanced delivery (CED) of cintredekin besudotox (CB) was compared with Gliadel wafers (GW)/Phase III Nitrosurea in Wafer
Thanks for that, Valueinvestor12. I think the key part is "we know that we won't be able to talk about interim analysis before the second part of Q3 2017." We had a big discussion here when that came out. I think the way we read it was that the earliest we will hear about the interim is mid-August. It doesn't mean that it will happen in August but he is saying that it certainly will not happen before then.
Are you reading it the same way?
wcopeland ... good post! My thoughts are:
1) I think the partnership can be either/both PD-L1 or/and PD-1. Here's an interesting research related to this topic:
"A 2015 review of all studies published on PD-1/ PD-L1 blockade showed that approximately 15% of patients with PD-L1–negative tumors responded to anti-PD-1 therapy. While this was significantly lower than the response rate in patients who had PD-L1–positive tumors (45%), Topalian stated that PD-L1 status alone is insufficient to exclude patients from receiving anti-PD-1/PD-L1 therapy."
http://www.onclive.com/publications/oncology-live/2016/vol-17-no-14/biomarker-combos-may-hold-key-to-antipd1pdl1-therapy-response
I have thought that AZ may be the partner but I'm leaning more towards BMS now for these reasons:
a) The COO hire. As I've said when the hire was announced, she has the pedigree to go anywhere. Why go to VBL? It has limited funds. It is a small company HQ'ed in Israel. Basically, her strengths don't match well with the company's current needs. Unless ... something else is going on here between BMS and VBL. We shall see but I think BMS is going to be the partner.
b) BMS (Opdivo) lost big time to Merck (Keytruda) - it lost 20% of its market cap when the failed data was announced. So it's taking a shotgun approach (with its significant resources) to get back in the $15B market that is lost out on to Merck. If not NSCLC, BMS can be targeting VB-111 for glioblastoma or other solid tumors (check out this summary of where BMS is involved: http://info.evaluategroup.com/rs/607-YGS-364/images/epv-pdct17.pdf)
2) I think the big pharma will foot the bill. But a what cost? Dror is not going to give the business away no matter what the COO recommends. I get a feeling she will be negotiating as much for BMS as she will for VBL. Basically with her inside VBL, BMS gets a view to which no other big pharma has. She will know exactly what BMS is looking for and look to determine how strongly VBL fits with BMS's needs.
3) If big pharma foots the bill then why not start? It is something that VBL wants to do but has put off due to limited budget, imo. VBL is at a point at which it wants to discover other capabilities of VB-111 (now that multiple trials have indicated that VB-111 is safe in combo and comes with limited AEs).
As for the timing of the interim report. It will take some time to prepare, analyze and approve the interim data before reporting out. So I think interim will be triggered in Aug/Sep but we won't hear about it until Sep/Oct.
Interesting development on an oncoprotein GT198, which these researchers are targeting.
http://chronicle.augusta.com/news/2017-06-18/au-researcher-looking-way-choke-cancer-tumor-blood-supply
Here's an earlier article on targeting GT198:
https://www.sciencedaily.com/releases/2016/03/160318111445.htm
More from the same session:
"Michael Gilman, whose company Stromedix licensed a fibrosis drug from Biogen Idec and was later acquired by the biotech giant, shed light on how other companies viewed Stromedix’s drug. As Stromedix tried to partner the asset, the drug was seen as “damaged goods,” with suspicious potential partners wanting to know why the big biotech had out-licensed it in the first place. Gilman noted that big companies drop collaborations and outlicense development programs frequently these days, and that the stigma associated with these events is abating. Corinne Epperly, Global Mergers and Acquisitions Lead at BMS echoed his sentiments, explaining that a program that does not mesh strategically with one company’s portfolio could fit perfectly in another company’s pipeline.
The panelists agreed that in some cases, a small biotech’s big pharma partner does have a slight information advantage over other potential acquirers. However, Epperly noted that sometimes companies are able to act on this information, as in the case of BMS’ acquisition of partner Medarex (and melanoma cancer drug Yervoy) in 2009, and sometimes their incremental advantage over other companies does not matter, as in the case of Eli Lilly’s 2008 acquisition of BMS’ drug development partner ImClone, despite BMS’ own efforts to acquire the company."
http://www.biotech-now.org/business-and-investments/2013/02/putting-a-ring-on-it-advice-on-successful-drug-development-collaborations
Insight on Epperly. Here's a snippet on her thoughts regarding "things to consider to position your biotechnology startup for an acquisition" (hint, hint) at the 2013 BIO CEO conference in NY (the same one at which VBL/Dror presented ... ROTH is also there):
"Epperly said it depends on the data. Good data is key and strong data speaks volumes. As long as your product is generating good data it can attract capital and help you outlast any unforeseen partner breakups. Without it, the product’s future is in jeopardy, not to mention the company."
http://medcitynews.com/2013/02/4-things-to-consider-to-position-your-biotechnology-startup-for-an-acquisition/
Good to see that she is focussed on data. That's what counts at the end and hopefully she saw something in the data that convinced her to take the COO job.
The data is intriguing: "in all three indications over 50% of patients have achieved long term survival following treatment with VB-111". It is not statistically significant but it is positive directionally.
Will we see a repeat in ph3? I hope so. That's all that really matters at this point. Ph1 and ph2 data can show wonderful things but they won't matter if ph3 fails.
Watch the 6/20, 11:45 am pt, webcast here:
https://www.veracast.com/webcasts/bio/internationalconvention2017/17205139583.cfm
Someone with her background (dual degree, Goldman, BMS) is joining a small company like VBL for a reason. We'll find out soon enough.
Btw, she has a (twin?) sister, Melissa, who also has an impressive background: https://www.linkedin.com/in/melissa-epperly-1053b3/
It is a very significant announcement, imo.
1) This board has long projected that BMS could be a partner, and now it's looking more likely.
2) The assumption is that VB-111 will be successful, in order for her to fulfill her "responsibilities in forming VBL's marketing strategy and commercialization plan for its Phase 3 candidate VB-111 and will work with VBL's leadership team to advance corporate strategy and U.S. activities".
All around very positive.
oren ... "it has nothing to do with the antiangiogenesis- all the activity curing the cancer in some patients and the regression in tumor is only because the immune response"
Do you think this is also true in ovarian, thyroid and other solid tumors?
Waiting for the terms of the grant. For example, Nano received a grant from the same organization, and these were the terms. I suspect it would be similar for VBL. If so, the $2.5 mil grant gives the company more options and the terms are reasonable.
Nano Dimension Technologies Ltd., has received a grant approval from the Israel Innovation Authority to finance further development of the Company's flagship 3D printer for printed circuit boards. The total approved budget for this project is approximately $1.4 million (NIS 5.2 million), of which the Israel Innovation Authority will finance 30%. The terms of the grant require Nano Dimension to pay royalties on future sales of any technology developed with these funds, up to the full grant amount.
This is the third consecutive year Nano Dimension has received a grant approval from the Israel Innovation Authority to support its flagship development project, which is focused on developing a complete solution for printing printed circuit boards using 3D printers and proprietary nano-inks.
https://www.accesswire.com/463574/Nano-Dimension-Receives-Grant-Approval-from-the-Israel-Innovation-Authority-for-a-Budget-of-14M-NIS-52M-to-Continue-Development-of-Flagship-3D-Printer
From ASCO, it is good to see that the continuous exposure (CE) group had lower KPS and higher rate of 2nd recurrence BUT achieved longer median OS.
Notes from ASCO:
The overall response rate (ORR) for the continuous exposure group was 29% (7/24), and 2 patients experienced complete responses. (CRs) One of the CRs occurred using single-agent VB-111, and the patient remains in remission as of 39 months. Notably, patients in the continuous exposure group had an overall lower Karnofsky performance status (KPS), a less successful initial resection, and had a higher rate of second recurrence than the limited exposure group at baseline, increasing our confidence in the prior survival results with VB-111.
See page 2:
http://baystreet.ca/articles/research_reports/lifesci/ASCO2017Presentations2060717.pdf
oren, avastin is the SOC. Everyone is treated with avastin because it is the only drug approved for rgbm.
The bold part is key, imo. If there was no difference found in the 2 cohorts except for what was reported, then that is pretty significant. Phase 3 interim is a few weeks away so we'll see.
Whereas brief exposure to VB-111 was associated with tumor progression in most patients, longer exposure to VB-111 (median= 4, mean=4.7 doses) led to attenuation of tumor growth kinetics (median % increase (MPI) per 30 days: 0.6 vs 14.1, p=0.0032). Furthermore, tumor regression was more frequent upon longer exposure to VB-111; only 16% of patients with limited exposure to VB-111 had tumors shrink below baseline dimensions during the first 100 days, compared to 61% of patients who continued to receive VB-111 through progression (p=0.002; McNemar’s test). Except for longer treatment with VB-111 leading to favorable OS, there was no evidence for difference between the two cohorts in any of the criteria tested, including patient characteristics, initial tumor growth kinetics, and Avastin treatment of both groups.
http://ir.vblrx.com/phoenix.zhtml?c=253311&p=irol-newsArticle&ID=2278715