Member Info for inanaco

I have laid it out as I see it .. using the evidence provided by RNS

Val have reported correctly .. it's just that you are not reading what is written ...

understand the difference with words 10Th Dec 2018

“Pharmacokinetics is how a body processes a drug. ... It's really mostly focused on the drug and the body.

---------------------------------------------------- from RNS-------------------------------------------------------------------------------

In addition to the independent analysis, the pharmacokinetics information collected from the clinical evaluation of ValiRx's more recent patients, shows that ValiRx is addressing the protocol's primary and secondary endpoints - as well as all the exploratory tertiary end points.
Further information about the endpoints is to be found posted on the NIH website, www.ClinicalTrials.gov, under: 'Dose Finding Safety Study of VAL201 in Cancer Patients (VAL201-001)'

and yet again VAL highlights ... """" Dose Finding Safety Study of VAL201 """"

so these RNS is at best Vague in that its a repeat of old RNS dressed up to appear as if something new has been discovered ... when in reality they are hiding behind """" pharmacokinetics"""" which is what they did in the 401 peer review release paper

Rather than ........

""" Pharmacodynamics """"

which takes into account the complex interactions between the drug, the human body, and then the pathogen that might be causing an infection in the patie

Val already accepts that its competing against Current standard of care ... from 2018 RNS

The molecule is a peptide that inhibits the interaction between the androgen receptor and/or the oestrogen receptor complex with Src Kinase complex Domain 3. This very specific mode of action has been shown in pre-clinical studies to provide a potent therapeutic benefit with """fewer side effects compared to the standard hormone therapy"""". VAL201 is potentially and uniquely able to treat prostate cancer without many of the other debilitating side effects associated with other therapies

To do that on efficacy the Phase 2 part of the trial has to run for a number of years, and what we have at the moment is the Dose escalation stage to find that efficacy which started approx in Oct 2019 despite having the agreement to start in late 2018, nearly a year went missing with no patients treated. Dec 2017 to Oct 2018

which is why in the 18Th Dec 2017 RNS

they set 3 Goals

·     To substantially raise the dosing level in patients in order to reach therapeutic levels and reduce disease progression;Â

·     To assess at what stage in disease development the compound can be most effectively deployed in subsequent, larger, outcome-oriented clinical trials; and

·     To determine which route and with whom to take the project to its next stage - by the Company or with a partner.

so you are still at the first Goal ... ie VAL has to demonstrate that it can get as close as possible to the current standard of care on efficacy and win on a "" Safety profile ""

Until you see actual data with a statement from the Lead Trial Investigator (not VAL) the evidence of efficacy is still sketchy ... because of the need to dose escalate !! Having a statistical report done by somebody who is close to VAL carries no weight.considering they fail to mention "current standard of care"

It really is a tough call as to why they have not RNS the Trial investigators report .. that also applies to Val 401 no Doctor on the actual trial has put a signature to the data ... why ? because they cannot 7 patients will not give you any conclusive evidence other than Palliative care, and that in context to risperidone is worthless

you mean the modi1 trial .. dose escalation of 3+3+3 = 9 patients ......... phase 1 ..

then we move to the phase 2 ...

why not read Vals Web Site ...

ValiSeek:-

which gives you all the Value Drivers .............. """" the great Cancer cure """"

""""Data from the completed Phase II clinical trial indicated a palliative effect and an improvement of quality of life in the patients treated. """"

we have been telling you since 7p .......... what data ? 7 patients .. ? worthless

ValiSeek is ValiRx’s joint venture company with Tangent Reprofiling Limited (a SEEK group company), which was formed in 2014 and has progressed product VAL401 through pre-clinical development and through a pilot Phase II clinical trial for the treatment of non small cell lung cancer. VAL401 is a reformulation of risperodone which has a well-established safety record derived from decades of clinical use in the treatment of psychosis. The reformulation enables anti-cancer activity, and this is the subject of multiple granted patents in US and other world territories.

VAL401 completed its first clinical trial in Q3 2017 an oral treatment of late stage non-small cell lung cancer, adenocarcinoma in a pilot Phase II Clinical Study in Tbilisi, Georgia. The study measured the impact of VAL401 treatment on measures of progression-free survival, quality of life and overall survival of the patients. Further to this recording the pharmacokinetics, drug metabolism, safety and tolerability of the VAL401 formulation in comparison to historical clinical records for risperidone were conducted.

Data from the completed Phase II clinical trial indicated a palliative effect and an improvement of quality of life in the patients treated. ValiSeek is in receipt of confirmation of acceptance of its Clinical Study Report. ValiSeek is currently in discussions with potential partners for starting the next clinical trial. In January 2019, an independent peer reviewed article published in the European Journal of Drug Metabolism and Pharmacokinetics analysed the pharmacokinetic data acquired during the Phase II clinical trial and considered the clinical significance of the VAL401 results in comparison to previously reported data for conventional risperidone, thereby providing a theoretical scientific insight into the activity of the therapeutic.

why would you buy any share in this sector without some idea if its commercial ? are you just talking punts ?

the post highlighted that .... ie ... why ? what was the driver ? spooky

Auditors audit to a HMRC standard ... it makes no difference who you use ... apart from the price you pay hence it went out to tender.
Scancell has no sales ...
hardly rocket science to add up expenditure

so C7 is right........... don't pay any attention ...

The question you have to ask here .... is length of trial at the Highest dose which started i believe in October 2018 to gauge it against the competition requires to treat for extended periods and because Val have only done dose escalation, who is actually going to run the phase 2 part of the trial and for how long ?

Adding abiraterone acetate (Zytiga) plus prednisone to standard hormonal therapy for men newly diagnosed with high-risk, metastatic prostate cancer lowers the chance of death by 38%. In a phase III clinical trial of 1,200 men, abiraterone also more than doubled the median time until the cancer worsened, from 14.8 months to 33 months. These data were presented today by Fizazi et al at the 2017 ASCO Annual Meeting (Abstract LBA3).

Hardest to Treat Cancer

cs_surv_common_males.png. Testicular cancer has the highest ten-year survival in men at 98%, and five year survivors of this disease may be considered 'cured'.

Pancreatic cancer has the lowest ten-year survival in men at just 1%

why on earth would Scancell be confident to build a moditope against pancreatic . the most difficult to treat cancer

Modi 3

says it all in my book.

Its also a very different cancer to Scancells Targets

https://en.wikipedia.org/wiki/Follicular_lymphoma

Median survival is around 10 years, but the range is wide, from less than one year to more than 20 years. Some patients may never need treatment. The overall survival rate at five years is 72–77%.[16] Recent advances and addition of rituximab improved median survival. Recent reports for the period 1986 and 2012 estimates median survival of over 20 years

well .. ipad

just list out the pipeline of Modi1/2/3 Immunobody scib1./2 plus others plus the glycans

appreciate the Karolinska Institutet (expanded program) and BioNtech nearly completed program

have remained positive indeed by BioNtech staying in the Modi3 program

its a competitor to Oncosec il-12 (cytokine injections) one of its pipeline , and its using the "adjuvant" that is used with vaccines directly injected into tumours

so it you look the pipeline you will see the TRL4 ....

if you look scancell you will find tests already done with Trl4

Days post tumour implant. P e rce n t su rviva l. Control. 1 nmol TLR9/TLR4 mix. 0.1 nmol TLR9 linked. 0.1 nmol TLR1/2 linked. 1 nmol TLR1/2 ..

which is why its only $300m ... the issue as ever is the Stock market just puts no value on Scancell .. even thou its pipeline quality is 10 x immunedesign ...

Just shows you how cheap Scancell is ........... when you look at the pipelines and how fr we have already gone into trial .

https://www.fda.gov/downloads/AboutFDA/CentersOffices/CDER/ManualofPoliciesProcedures/ucm082022.pdf

I assume we are in a "clinical Hold"

An IND goes into effect 30 calendar days after FDA receives the IND, unless
FDA notifies the sponsor that the trials described in the IND are subject to a
clinical hold, or on earlier notification by FDA that the trials may proceed
(21 CFR 312.40(b)).

we Know Ichor medical and Scancell have responded

For complete responses to clinical holds (responses that address all the
deficiencies identified in the clinical hold letter), FDA has 30 calendar days to
respond in writing. FDA’s response will either remove the hold or maintain the
hold, and will provide the reason for such a determination (21 CFR 312.42(e)).

so the next letter I assume is to release the Clinical hold or explain why they are still holding ..

This may be the wrong procedural page, but not found any other but if they follow this guideline pretty sure that the IND will be approved soon

anyone else looked ?

Maduro Corbyn ... LOL

Immunobody CD4+T cell is very important as not only its activity is to promote inflammation ...But when subject to the pd-1 ligand it actually promotes T cell regulation ..

causing the immune system to go into reverse !!

These results suggest that the PD-1/PD-L1 pathway plays a role in Treg induction and is associated with impaired adaptive immunity. In the tumor microenvironment, PD-1 expressed on Tregs accelerates CD4+ T cells differentiating into Foxp3+ Tregs under the circumstances of CD3 and TGF-ß. Foxp3 is a critical transcription factor of Tregs, which suppress Th1 responses [94]. Foxp3+ Tregs is a highly immunosuppressive subset of CD4+ T cells that is critical in suppressing proliferation and cytokine production of other T cells, inhibiting tumor-specific immune responses and maintaining peripheral immune tolerance in cancer patients [114]. Meanwhile, Treg cells express constitutive high levels of PD-1, which enhance Treg functional response or proliferation and inhibit T cells responses

this is another area that Can be blocked by Keytruda ...

which is why every bit of data i find tells me .. Keytruda Plus SCIB1 = Synergy

just bought at 6.7 £800

What they have got ... keytruda history

Pembrolizumab was invented by scientists Gregory Carven, Hans van Eenennaam and John Dulos at Organon after which they worked with Medical Research Council Technology (now known as LifeArc) starting in 2006 to humanize the antibody; Schering-Plough acquired Organon in 2007 and Merck & Co. acquired Schering-Plough two years later.[18] Carven, van Eenennaam and Dulos were recognized as Inventors of the Year by the Intellectual Property Owners Education Foundation in 2016.[19]

The development program for pembrolizumab was seen as high priority at Organon, but low at Schering and later Merck. In early 2010 Merck terminated development and began preparing to out-license it.[20] Later in 2010 scientists from Bristol Myers Squibb published a paper in the New England Journal of Medicine showing that their checkpoint inhibitor, ipilimumab (Yervoy) had shown strong promise in treating metastatic melanoma and that a second Bristol-Myers Squibb checkpoint inhibitor, nivolumab, (Opdivo) was also promising.[20] Merck at that time had little commitment or expertise in either oncology or immunotherapy, but understood the opportunity and reacted strongly, reactivating the program and filing its IND by the end of 2010.[20] As one example, Martin Huber was one of the few senior people at Merck with strong experience in lung cancer drug development, but had been promoted to senior management and was no longer involved in product development. He stepped down from his role to lead clinical development of pembrolizumab for lung cancer.[20]

So let's Cut through the Crap that Big Pharma BOD actually Know this market

"""""""""""" In early 2010 Merck terminated development and began preparing to out-license """""""""

just shows you how close Merck was to closing the program !!!! Ouch !!

only two things we need to know .......... C7 ..

"""The paper concludes that "SCIB1 is a novel class of anti-cancer immunotherapy that induces T cells which can cause tumour regression in patients with melanoma.""" 12 February 2018 RNS

and

Mechanism of action. Pembrolizumab (keytruda) is a therapeutic antibody that binds to and blocks the PD-1, programmed cell death protein 1 located on lymphocytes (t cells inc.)

thats it in a nutshell ...

We have T cells that work

Keytruda locks onto those T cells blocking the ligand that can stop them working ... that is why the mechanism of failure is so difficult to identify ...